bhrama kc026 gdg

Evaluation of the efficacy of

“KAKUBHADI LEHYA” AS HRIDYA RASAYANA IN

“BHRAMA” (HYPERTENSION)By

“Chetan Sangappa Minajigi”

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial fulfilment of the degree of

Ayurveda Vachaspati M.D.In

KayachikitsaUnder the Guidance of

Dr. Shiva Rama Prasad KethamakkaM.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)]

Department of Kayachikitsa

Post Graduate Studies & Research CentreD.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG

2002-2005

Ayurmitra

TAyComprehended

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTREGADAG - 582 103

This is to certify that the dissertation entitled “EVALUATION OF THE

EFFICACY OF “KAKUBHADI LEHYA” AS HRIDYA RASAYANA IN

“BHRAMA” (HYPERTENSION)” is a bonafide research work done by

“Chetan Sangappa Minajigi” in partial fulfilment of the requirement for the

post graduation degree of “Ayurveda Vachaspati M.D. (Kayachikitsa)”

Under Rajiv Gandhi University of Health Sciences, Bangalore, Karnataka.

Dr. SHIVA RAMA PRASAD KETHAMAKKA

M.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)]Guide

READER IN KAYACHIKITSADGMAMC, PGS&RC, Gadag

Date:

Place: Gadag

J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTREGADAG, 582 103

Endorsement by the H.O.D, Principal/ head of the institution

This is to certify that the dissertation entitled “EVALUATION OF THE

EFFICACY OF “KAKUBHADI LEHYA” AS HRIDYA RASAYANA IN “BHRAMA”

(HYPERTENSION)” is a bonafide research work done by “Chetan Sangappa

Minajigi” under the guidance of Dr. SHIVA RAMA PRASAD KETHAMAKKA, M.D.

(Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)], Reader in Kayachikitsa, DGMAMC,

PGS&RC, Gadag, in partial fulfilment of the requirement for the post graduation

degree of “Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajeev Gandhi

University of Health Sciences, Bangalore, Karnataka.

.

(Dr. G. B. Patil)Principal,

DGM Ayurvedic Medical College,Gadag

Date:Place:

(Dr. V. Varada charyulu)Professor & HOD

Dept. of KayachikitsaPGS&RC

Date:Place: Gadag

Declaration by the candidate

I here by declare that this dissertation / thesis entitled “EVALUATION

OF THE EFFICACY OF “KAKUBHADI LEHYA” AS HRIDYA RASAYANA IN

“BHRAMA” (HYPERTENSION)” is a bonafide and genuine research work

carried out by me under the guidance of Dr. SHIVA RAMA PRASAD

KETHAMAKKA, M.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)], Reader in

Kayachikitsa, DGMAMC, PGS&RC, Gadag.

Date

Place

(Chetan Sangappa Minajigi)

Copy right

Declaration by the candidate

I here by declare that the Rajiv Gandhi University of Health Sciences,

Karnataka shall have the rights to preserve, use and disseminate this

dissertation/ thesis in print or electronic format for the academic / research

purpose.

Date

Place

(Chetan Sangappa Minajigi)

© Rajiv Gandhi University of Health Sciences, Karnataka

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” I

I express my deep gratitude to my guide Dr. K. Shiva Rama Prasad, M.D. (Ay),

M.A. (Jyo) [Ph.D. (Jy)] for his timely advises and encouragement in every step of my

success. His ideologies have been exemplar to my further career.

I express my gratefulness to my professor H.O.D., Dr. V. Varadacharyulu,

M.D.(Ayu), and Dr R. V. Shettar, M.D (Ayu) lecturer in Kayachikitsa, for their time to time

help and critical suggestions associated with expert guidance at the completion of this

dissertation.

I express my thankfulness to beloved principal Dr. G. B. Patil, for his

encouragement as well as providing all necessary facilities for this research work.

I express my profound sense of acknowledgement to various departments

H.O.D.s, teachers and colleagues of sister concern departments along with the ministerial

and sub staff of the D.G.M. Ayurvedic Medical College & Hospital, Gadag.

I express my sincere thanks to Dr. Shashidar. H. Doddamani, Dr. Kuber Sankh,

Dr. P. Shivaramudu, Dr. M.C. Patil, Dr. Danappagoudar and Dr. Santhosh Belavadi. I

express my sincere thanks to Mr. Nandakumar for his help in statistical analysis of

results. I am thankful to Dr. Nagi Reddy for his assistance in preparing the medicine and

Dr Kona for the lab assistance.

I express my sincere conceding to Dr. Shashikant Nidagundi, Dr. Jagadeesh Mitti,

Dr. Mulkipatil, Dr. U.V. Purad, Dr. Paraddi, Dr. Sajjan and Dr. B.G. Swami.

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” II

I discharge my salute to my beloved Grand mother - smt. Susheela Bai Subbayya

Gudur and express my humble heart filled gratitude that stood strong to support me at my

calamities. Present existence of mine is because of my beloved parents, Late Sangappa

Chanabassappa Minajigi, and Smt. Shobha Devi, I am at their remembrance at every

movement of my success.

Behind my success, the pillars are my brothers, Dr. Ananad and Sachin, a warm

thanks to them on this regard. I am extremely thankful and obliged to Dr. Pranesh S. Gudur

and Smt. Rekha Pranesh and Ramanna S Gudur, and Smt Savitri R Gudur, who always

watched me and shaped my career. Its only their support and encouragement which made

me possible to achieve my goal. .

My sincere thanks to Dr. Chandrashekhar, Yapal Parvi, Anil Menasinakai, S.C.

Biradar and Dr.D.P.Joshi - my friend of all times, with out of their support I am always

incomplete.

My relatives and well wishers, those were supporting all the time - Jyothi,

Venkatesh, and Dr. Sudhakar. T.B, Dr. Suhashini Telang, Dr. Srinivasa Reddi, Swaroopa

Rani, Dr. Varsha Kulakarni, Dr. Pattanshetti, Dr. Mangala Patil, Dr. Jaggal, Dr. Santoji, Dr.

Bingi, Dr. Santosh Yadahalli, Dr. V.S. Hiremath, Dr. K. Hiremath, Dr. Veena Kori, Dr.

Shankaragouda, Dr. Yasmeen, Dr. Hadimani, Dr. Hanamanthagoudar, Dr. Pradeep, Dr.

Koteswar Rao, Dr. B.Y. Ghanti, Spoorti JT, Priya KR, Asha P, Shivkumar LT, Anil Biradar,

Anil Ratod, Manish jain and Harun Kowshik – I express deep thankfulness for their

inspiration during the study.

At last my sincere thanks to the subjects who cooperated at my dissertation, with

out of them it would have been not a success.

Place:

Date: Chetan Sangappa Minajigi

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” III

Abstract

Bhrama vis-à-vis essential hypertension in which the causes of increase in blood

pressure is unknown. It constitutes about 90-95% patients of hypertension. Angiotensin II

alters blood pressure by increasing both peripheral resistance and blood volume. Many

patients have a family history of high blood pressure. Lifestyle changes can significantly

improve a patient’s blood pressure. The factors influencing the relationship between

blood pressure and cardiovascular risk include systolic blood pressure, diastolic blood

pressure, circadian blood pressure patterns blood pressure variability, and cardiac and

vascular hypertrophy. Retention of sodium will cause an increase in the blood volume,

which in turn increases the blood pressure.

Evidence supports treatment of systolic high blood pressure in older persons.

Local endothelial factors may play a role in blood pressure. High blood pressure lowers

cognitive function. Increased T.P.R. + increased cardiac output = increased blood

pressure. Hypertension increases the viscosity of blood.

Treatment of the disease reduces the symptoms of high blood pressure.

Shirodhara is claimed to reduce high blood pressure. Present study registers 30 patients,

out of 68 approached patients. Parameters of co-morbidity in Bhrama are serum

creatinine, Serum cholesterol and associative LDL, VLDL with S.Triglycerides. Study of

Kakubhadi Lehya on Bhrama vis-à-vis hypertension show marked drop of 20 mm Hg of

systolic hypertension by inducting the Rasayana effect. All the objective parameters

show highly significance. After through study of the entire parameters and materials

available for the assessment of results it was drawn a conclusion of results as - 9

(30.02%) well responded, 6 (20.02%) moderately responded, 10 (33.33%) responded, 3

(10%) patients not responded and the last 2 (6.63%) patients discontinued in the study.

Thus it is concluded that the Kakubhadi Lehya is effective as Hrudya Rasayana in

the disease condition Bhrama vis-à-vis hypertension. This is recommended for the

regulation and prophylactics of Bhrama vis-à-vis hypertension.


“Kakubhadi Lehya” as Hridya Rasayana in “Bhrama”

(Hypertension)

By – Chetan Sangappa Minajigi

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” IV

Table of contents


“KAKUBHADI LEHYA” AS HRIDYA RASAYANA

IN “BHRAMA” (HYPERTENSION)

Heading Page number

Chapter -1 Introduction 1 to 12

Chapter –2 Objectives 13 to 15

Chapter –3 Review of literature 16 to 67

Chapter –4 Methodology 68 to 85

Chapter –5 Results 86 to 114

Chapter –6 Discussion 115 to 178

Chapter –7 Conclusion 179 to 185

Chapter –8 Summary 186 to 189

Bibliographic References I to XIV

Annex – Case sheet 1 to 6

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” V

List of tables

Sno Table Heading Page

1 3

2 Dushyadi Vivechana of Bhrama in comparison to 38

3

in the patients with mild or moderate Hypertension - Symptoms

49

Step care treatment of hypertension 57

Showing the Pathyapathya in Hypertension (Bhrama)

6 Key items of the baseline physical and laboratory examinations 79

7 82

8 83

9 84

10 85

11 87

12 87

13 88

14 90

15 91

16 93

17 94

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” VI

18 Distribution of patients by presenting complaints 95

19 Distribution of patients by Associated features 97

20 Distribution of patients by mode of on set 98

21 Distribution of patients by Intensity 99

22 Distribution of patients by Aggravating factors 100

23 Distribution of patients by relieving factors 102

24 Distribution of patients by Shareerika Prakruti 103

25 Distribution of patients by Manasika Prakruti 105

26 Assessment of Lab investigations in Bhrama 106

27 Assessment of Subjective parameters in Bhrama 108

28 Results of Kakubhadi Lehya in Bhrama vis-à-vis Hypertension 110

29 Statistical analysis - Subjective parameters 111

30 Statistical analysis - Emotional parameters 112

31 Statistical analysis - Objective parameters 112

32 Statistical analysis - Blood pressure variances 113

33 Blood pressure levels 124

34 Four stages wherein cardiac involvement takes place 127

35 The World Health Organisation (WHO) Classification of Hypertension 127

36 Cardiovascular responses to stimulation 134

37 Apo-fraction representation of the lipoproteins 145

38 Blood pressure variances of Before to After 172

39 BMI Vs Blood Pressure 176

40 Male BMI with lipid profile variations 177

41 Female BMI with lipid profile variations 177

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama”VII

List of figures

Sno Figures heading Page

1 Showing the Blood Pressure Regulation 33

2 Showing the Role of Renin-Angiotensin System 36

3 Diagrammatic expression showing dietary intake and CVD 43

4 Showing the Schematic Representation of Samprapti 50

5 Initiation of Modern Treatment in Patients with Hypertension 59

6 Showing the Approach to the Hypertensive Patient after Initiating

Anti-hypertensive Drug Treatment

60

7 Algorithm for Treating Hypertension 61

8 Ingredients of Kakubhadi Lehya 82

9 Comparison of the benign and malignant hypertension 121

10 Speculative current theory of hypertension 123

11 Summary of the aetiology 128

12 Measurement of Blood Pressure 138

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama”VIII

List of graphs

Sno Graph heading Page

1 Distribution of patients by Age – Gender 89

2 Distribution of patients by Gender in Bhrama 90

3 Distribution of patients by Religion 92

4 Distribution of patients by occupation 93

5 Distribution of patients by Economic status 95

6 Distribution of patients by presenting complaints 96

7 Distribution of patients by Associated features 97

8 Distribution of patients by mode of on set 98

9 Distribution of patients by Intensity 100

10 Depicting the Aggravating factors of Bhrama 101

11 Distribution of patients by relieving factors 102

12 Distribution of patients by Shareerika Prakruti 104

13 Distribution of patients by Manasika Prakruti 105

14 Distribution by presenting complaints 109

15 Results of the Kakubhadi Lehya 111

16 Linear graph of Blood Pressure – Systolic hypertension 173

17 Linear graph of Blood Pressure – Diastolic hypertension 174

18 BMI with systolic blood pressures 175

19 BMI with diastolic blood pressure 175

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” 1

Chapter-1

Introduction

iddiness or Dizziness (Bhrama), headache (Sirahsoola), fatigue

(Angasada), insomnia (Nidranasha) and palpitation (Hritdrava) are common complaints

for an Ayurvedic practitioner occasionally get confused with the presented symptoms to

correlate. As the nomenclature of Hypertension or similar was not included in classical

texts and neither of Acharyas has affirmed such a condition elaborately, undertaking the

support of the contemporary medical system is unavoidable.

Hypertension is a major risk factor for many serious health problems. We have

many weapons to combat it: prevention, lifestyle changes, and increasing knowledge

about how best to employ a growing arsenal of medications. Yet, as many as half the

patients who start hypertension treatment stop within a year. Treatment is expensive, it

can have uncomfortable side effects. When the condition itself is asymptomatic and

physicians and patients may not remain fully vigilant through lengthy treatment 1.

The Hypertension, called as “Salient Killer”, drawn the attention of W.H.O. in

over decreasing the life span of 10 to 20 years causing cardiac or renal troubles. Further it

can be said, as it is an important factor in increasing the morbidity and mortality due to


As there is no definitive definition universally accepted, the Joint National

Committee (JNC-4) of United states on detection, evaluation and treatment of high blood

pressure defines Hypertension as systolic blood pressure (SBP) of 140 mm Hg or more

and diastolic blood pressure (DBP) of 90 mm Hg or more.

Definition and classification

Arterial or systemic hypertension in a patient is defined clinically as ‘borderline’

if the systolic blood pressure is more than 140 mm Hg and diastolic pressure is above

90mmHg (currently labeled as mild hypertension), and ‘hypertensive’ when the elevation

of systolic and diastolic pressure exceeds 160 and 95mmHg respectively (now termed as

moderate hypertension). The diastolic pressure is often considered more significant.

However, blood pressure varies with many factors such as age of the patient, exercise,

emotional disturbances like fear and anxiety. Therefore, it is important to measure blood

pressure at least twice during two separate examinations under least stressful conditions.

A clinically useful classification of hypertension has been recently described by the Joint

National Committee of the WHO/International society of Hypertension, by means of

these criteria, the prevalence of hypertension is observed in about 25% of population.

Hypertension is generally classified into 2 types 2

1. Primary or essential hypertension in which the causes of increase in blood

pressure is unknown. Essential hypertension constitutes about 90-95%

patients of hypertension.

2. Diseases of the kidneys, endocrines or some other organs cause secondary

hypertension, in which the blood pressure is increased. Secondary

hypertension comprises 5-10% cases of hypertension.


According to the clinical course, both essential and secondary hypertension may

be benign or malignant. Benign hypertension is moderate elevation of blood pressure and

the rise is slow over the years.

Clinical classification of hypertension

Table -1

Category Systolic (mmHg) Diastolic (mmHg)

Normal <130 <85

High normal 130-139 85-89

Hypertension

Mild (stage1) 140-159 90-99

Moderate (stage2) 160-179 100-109

Severe (stage3) 180-209 110-119

Very severe (stage4) >210 >120

Malignant hypertension >200 >140

About 90-95% patients of hypertension have benign hypertension

Malignant hypertension

Malignant hypertension is marked and rapid increase of blood pressure to 200/140

mmHg or more and the patients have papilloedema, retinal haemorrhages and

hypertensive encephalopathy. Less than 5% of hypertensive patients develop malignant

hypertension and life expectancy after diagnosis in these patients is generally less than 2

years if not treated effectively.

Essential (primary) hypertension

By definition the cause of essential hypertension is unknown but a number of

factors are related to its development. These are as under -


1. Genetic factors: The role of heredity in the etiology of essential hypertension has

long been suspected. The evidences in support are the familial aggregation,

occurrence of hypertension in twins, epidemiologic data, experimental animal studies

and identification of hypertension susceptibility gene (angiotensinogen gene)

2. Racial and environmental factors: Surveys in the US have revealed higher

incidence of essential hypertension in black than in whites. A number of

environmental factors have been implicated in the development of hypertension

including salt intake, obestity, skilled occupation, higher living standards and patients

in high stress.

3. Risk factors modifying the course of essential hypertension: There is sufficient

evidence to show that the course of essential hypertension that begins in middle life is

modified by a number of factors. These are as under -

a) Essential hypertension (90%)

(a) Genetic factors

(b) Racial and environmental factors

(c) Risk factors modifying the course

b) Secondary hypertension (10%)

1. Renal

(a) Renovascular

(b) Renal parenchymal diseases

2. Endocrine

(a) Adrenocortical hyperfunction

(b) Hyperparathyroidism

(c) Oral contraceptives

3. Coarctation of aorta

4. Neurogenic


Younger the age at which hypertension is first noted but left untreated, lower the

life expectancy. Females with hypertension appear to fare better than males. Accelerated

atherosclerosis invariably accompanies essential hypertension. This could be due to

contributory role of other independent factors like cigarette smoking, elevated serum

cholesterol, glucose intolerance and obesity. Other factors, which alter the prognosis in

hypertension, include; smoking, excess of alcohol intake, diabetes mellitus, persistently

high diastolic pressure above 115 mm Hg and evidence of endorgan damage ((i.e. heart

eyes, kidney and nervous system).

The pathogeneic mechanism in essential hypertension is explained by many

theories. These are -

High plasma level of catecholamines

Increase in blood volume i.e., arterial overfilling (volume hypertension) and

arteriolar constriction (vasoconstrictor hypertension)

Increased cardiac out put

Low-renin essential hypertension found in approximately 20% patients due to

altered responsiveness to renin release. High renin essential hypertension seen in about

15% cases due to decreased adrenal responsiveness to angiotensin II

Blood pressure is a continuous physical variable and is complex, being influential

by many factors. An individual can show variations through out the day depending on

physical activity, body posture, mental activity, emotional status, the environment and

consumption of drugs, alcohol and tobacco. Dynamic or isometric exercise can also risk

blood pressure in normal subjects3.


Ayurveda is based on the humoral theory and establishes that the Tridoshas have

its effect over the body. These humors move all over the body. The Vata, Pitta and Kapha

rule the ages of child, youth and old age4. It also has its effect on the divisions of the day

and night, and also to the food; where dosha vitiation is seen naturally contributed by the

external factors.

The clinical entity of hypertension is not available as such in the classical

literatures of Ayurveda. However, according to the directions of Acharyas regarding the

approach for the study of new diseases, 5-6-7 various contemporary Ayurvedic scholars

have made efforts to findout the proper nomenclature, etio-pathogenesis and treatment of

the disease.

It is very interesting to note that Acharya Charaka says about the complication of

Avrithavata as, Avrithavata if neglected leads to Hridroga, vidradi, pleeha, gulma and

Atisara8.

Thus by understanding the Dosha state, site of appearance and its signs and

symptoms, we have to come for conclusion and treat the state of disease or illness on the

basis of vikalpa i.e. combinations and permutations of doshas9.

In recent times many Ayurvedic scholars have tried to give an appropriate term to

hypertension in Ayurveda. Following are the different correlation and different

terminology suggested by various scholars-

Avrita Vata Roga Vaidya R.K. Sharma

Dhamani Atipurana Acharya Yogendranath Sen

Dhamani Prapoornata Vaidya G.N. Saraswathi

Dhamani Praticchaya Vaidya A.D. Athawale; Vaidya Ranajit Rai Desai


Dhamani Upalepa Prof. G. N. Chaturvedi and Dr. K.N. Shastri

Mada,Murcha, Sanyasa Kaviraj Kumud Ranjan Roy

Rakta Peedanadhikyata Prof. Dr.V.V.S. Sastry, Dr.K.S.R.Prasad,

Dr.S.S.Hiremath (Gadag), et.al.

Raktagata Vata Prof. Yadunandana Upadhyaya. And Shri.

Sudarshana Shasrti; Bhupenra Pal. (Varanasi)

Rakta Sammardhana Prof. G.N. Chaturvedi

Rakta Sampeeda Vaidya S.P. Panday

Rakta Vata Prof. Yadunandana Upadhyaya. And Shri.

Sudarshana Shasrti; Dr. Sharma (Puri)

Raktatimardam Dr. John K. George

Rakta Vega Vriddhi Vaidya V.B. Athawale

Rasa Bhara Vaidya T.S. Mishra

Roudira Mada Acharya Vishwanath Dwivedi

Siragata Vata Prof. G. N. Chaturvedi and Dr. K.N. Shastri

Sleshamavrita Vyana Dr. Gupta H.C. (Varanasi)

Uccha Rakta Bhara Dr. Pathak U.C. (Jaipur)

Uccha Rakta Nipeedana Acharya Vidyadhara Shukla

Uccha Raktachapa Prof. Madan Gopal Sharma and Dr. Ajay Kumar

Sharma

Vyana Bala Vaishamya Vaidya Brihaspati Triguna

Some of the other terminologies used by other authors are Raktavruta Vata, Rakta

Pradoshaja Vikara, Bhrama, Rakta chapadhikyata, Raktabhigarshana, Rakta vikshepa etc.


Essential hypertension when symptomatic will have one or few vague symptoms.

Similarly when we consider many avrita vatas they contain one or few symptoms of

essential hypertension, those are Raktavrita Vata, Pittavrita Udana, Pittavrita Prana,

Pranavrita Udana, Samanavrita Vyana, Sleshmavrita Vyana, Apanavrita Udana,

Vyanavrita Prana, Pranavrita Vyana, Udanavrita Prana, Kaphavrita Udana, Pittavrita

Vyana, Udanavrita Apana, Kaphavrita Prana etc. In these the involvement of Vyana,

Udana and Prana seems to be more prominent.

After considering all these, when we look at the symptoms explained in Rakta

gata vata, Sira gata vata, Roudhiramada, Dhamanipratichaya etc., and the various

Avrithavata’s, it seems that each pathological entity contains one or few symptoms

explained in essential hypertension. It may be because of the fact that usually in essential

hypertension, different patients will be manifested with different symptoms. Our ancient

Acharyas diagnosed the disease on the basis of symptoms available. But when we collect

all these symptoms, it directly coincides with the symptoms explained in essential

hypertension. This indicates that our Acharyas considered this disease under Vata roga.

On close observation, it is very much evident that different scholars tried to

identify the disease on the basis of following;

1. On the basis of vitiated dhatu – like Raktapradoshaja vikara, Rakta

chapadhikyata, Rakta samvardhana etc.

2. On the basis of vitiation of Vata – like Vyana bala vaishamya etc.

3. On the basis of vascular changes – like Dhamanipraticchaya, Dhamani

prapoornata, Sira gata vata etc.

4. On the basis of Avarana – like Raktavrita vata, Pittavrita udana, Sleshmavrita

Vyana etc.


Historical review:

In ancient days the Hypertension was not described as an individual disorder. It

may be because of less prevalence as they followed strict daily and seasonal regimens

and also not much psychological interference in daily routine. But they were not ignorant

of the conditions developed by the psychological pressure disturbances. There by they

placed them under the nanatmaja vyadhis, related to their cause and mode of

development. Much more such symptoms are explained and tagged with Vata, which can

be said as that to be under neural control impairment and very few conditions are with

Pitta and Kapha.

Until 1920’s, Hypertension was considered that as beneficial, even though in

1733 Stephen Hales measured first time Atrial blood pressure and demonstrated in a

dramatic fashion, that the blood in arteries is under a great deal of pressure. His work was

published by Royal society in 1733 as two volumes.

The instrument developed by Stephen Hales 10 were improved by Karl Ludwig

(1816-1895) improved the Instrument developed by Stephen Hales by adding a float in

the measuring cylinder. Karl Vierodt (1818-1884) constructed a sphegmograph tracking

the human pulse, which estimates the blood pressure by puncturing the vessel. It was

difficult and also painful for the patient. This method was greeted by British medical

journal and followed by Samual Von Bach (1880) and later developed by Scipione Riya

Rocci in 1896.

In 1905, Karokoff a Russian, introduced the auscaltatory method of estimating

blood pressure. With in few years Sphygmomanometer took place with the stethoscope.

The mercury column and spring dial Sphygmomanometers were introduced in 20th


century. Late 20th century with advancements in electronics has presented digital

Sphygmomanometer to the medical community apart from ECG and Doplar studies,

which will provide scope to measure blood pressure.

Proposal:

When the lakshanas of Hypertension are observed with its patho-physiology, the

present proposed name “Bhrama” will be relatively clear to explain state of

Hypertension.

As Charaka explained, there may be only one cause for one disease or same cause

may give rise many diseases. Some times we may find so many causes gives rise or

develops one disease or many causes develops many diseases 11. Thus, the present

selected disease has many synonyms, according to the state of development of the disease

or with respect to that of the disease development.

The Vata nanatmaja vyadhi consists of three conditions that appear in the process

of Hypertension pathogenesis. They are Bhrama (Dizziness), Hritdrava (palpitation), and

Aswapna (sleeplessness) 12. The appearance of the above said in Vata age and rutukala is

of physiological and if it appears with Pitta and Kapha association or age and rutukala, it

becomes pathological. If Dhamani pratichaya is (atherosclerosis) 13 one out of twenty

Kaphaja diseases appears or associates with the ageing factor have more responsibility to

give rise Hypertension or Bhrama.

Role of Rasayana Chikitsa in Bhrama vis-à-vis Hypertension

Rasayana Chikitsa not only strengthens Dhatus but also works as a “Vajikarana”

i.e. youthful vigor and vitality. This is attributed to the “Sukrala” effect of Rasayana

dravyas. The dissimilarity of Vajikarana drugs is only limited to and restricted to


‘sukrala’ effect and it can not nourish and strengthen the other Dhatus. Here it is worth

mentioning the increased activity of controlled cell-division if it can replace the old cells

by new in a short spell, will also constitute the rejuvenation of the body leading to a

longer life, i.e. the Rasayana effect.

In Ayurveda any treatment that increases the immune power and life force is

considered as Rasayana or rejuvenate. This can include herbs, food, diet or activities that

restore vitality, youthfulness and cure disease. Rasa is the juice of life, the vital fluid that

sustains health and life. As we grow older we gradually lose this "juiciness", our tissues

begin to dry out and our joints lose their lubrication and ease of movement. Rasayana

replenishes this innermost sap of the body promoting clarity of perception, physical

strength, endurance and longevity of tissues.

Rasayana's are more subtle and specific in their action than simple nutritive tonics

as they promote and sustain the optimum functioning of the body, assisting not only

longevity but also awakening of the mind. They restore youthfulness in old age and

improve memory, mental clarity and vitality. Rasayanas' nourishing and rejuvenating

action at the cellular level of the tissues promotes continued production of lives vital

essences enabling to remain active and full of enthusiasm for the entire duration of life.

Rasayana herbs are being continuously explored for their effects on immune

system. Available evidence shows that, these drugs can be used to modulate the immune

functions. At one hand they may work to enhance immune functions and build us from

deep within, or they might pacify an angry immunity cell to be in its limits on the other.

Thus, a Rasayana drug favours the host in both ways.


Rasayana therapy is defined as “the means by which one gets the excellence of

Rasa, Rakta etc., (tissue elements). This Rasa is the only source of nourishment to all the

tissue of the body. This is cyclical through out day and night without interruption

supplying nutrition to all living cells of the body through the Rasa-Rakta admixture. Rasa

(essence of food) is known to be the premier nutrition of the body tissue is capable to

progress/ limit the blood-related diseases, such as hypertension.

The Rasa vitiation is one of the major situations in case of Bhrama, thus the

removal of impurities and proper transportation of the Rasa-Raktavaha srotogata dravaya

i.e. Rakta with its related components in the minute vessels and capillaries is possible

through Rasayana. Dhaturupa Rasa (plasma and such other fluid constants of the body in

association with Rakta (blood constituents), which makes the imbalance through the Rasa

are to be rectified in the same route following the most best procedure of safeguarding

the Preenana and Jeevana kriyas by the Rasayana.


Chapter-2

Objectivesresent study bears the following objectives -

(a) To evaluate the efficacy of “KAKUBHADI LEHYA” in

BHRAMA (Hypertension)

(b) To evaluate the efficacy of Rasayana effect of “KAKUBHADI

LEHYA” in BHRAMA (Hypertension).

(c) To evaluate the effect of “KAKUBHADI LEHYA” over disease

predisposing factors such as Lipids.

Their detail discussion is as under -

1) To evaluate the efficacy of “KAKUBHADI LEHYA” in BHRAMA

(Hypertension)

Bhrama is a pathetic condition in which the patient has a feeling of reeling head.

This could be because of humour vitiation as in association with the Rasa and Rakta

stated in Ayurveda or because of the impaired haemo-dynamics.

In such condition the Kakubhadi Lehya is said as better by its contents. It can be

substantiated that the rational combination made in Ayurvedic text, Bhaisajya Ratnavali

at Hrudroga Chikitsa Prakarana, can establish its identity by normalising the components

of Bhrama vis-à-vis high blood pressure and equilibrating the Dosha involved. Present

study evaluates the efficacy of the Kakubhadi Lehya under the lime light of the

contemporary medical parlance.


2) To evaluate the efficacy of Rasayana effect of “KAKUBHADI LEHYA” in

BHRAMA (Hypertension)

Since the need for primary and secondary health care is paramount, the

Government will direct most of its spending towards this sector14. Every individual is

responsible for the entire cleanliness of himself, his house and surroundings. When once

this is recognised and, carried out, he is sure to attain freedom from sickness. Personal

cleanliness of the body, of dwelling apartments and of surroundings, good habits, good

food, exercise, recreation and sleep are all important factors in determining the strength,

luster, happiness and long life of individual 15.

Charaka has also laid down the code of good conduct by which one can remain

healthy and long-lived. He has also emphasised on prevention of diseases for which he

has devoted a number of chapters dealing with daily routine, seasonal living etc. in the

first section of the Samhita. The Charaka Samhita shows the path by which a man,

devoid of any ailment, can live happily and enjoy the normal life span (100 years) 16.

Aswins treat Maharshi Chyavana and Nandana with Rasayana therapy and made them

young by all means. This story was said in Rigveda17.

In the present context of Rasayana the word Rasa has the sense of end products of

digestion, which influence the metabolism of the body under the influence of the daily

stress and strain undertaken in the walking food running duties society. All the herbs

have the Rasa, which influence the Ahara Rasa, very specifically the preenana function.

Thus the Kakubhadi Lehya embedded Rasas cumulative effect on the body especially as

Rasayana over the body is evaluated here in this study.


3) To evaluate the effect of “KAKUBHADI LEHYA” over disease predisposing

factors such as Lipids

Carbon monoxide causes perivascular oedema of the blood vessels and hypoxia.

This alters the permeability of the endothelium and increases the deposition of lipids in

the vessel wall. Reduction or stoppages of smoking helps to reduce blood pressure even.

Obesity contributes to blood lipid abnormalities and impaired glucose tolerance; it has

particular significance as a factor underlying the increased prevalence of coronary artery

disease in hypertensive patients. For every 10% increase in weight a rise of 6.5-mm Hg

in systolic pressure was observed in Framingham study.

Susruta has mentioned medoroga leads to vatavikara. Dalhana explained that

vatavikara is produced due to medavrita marga18. Apart from this in Astauninditeeya

adhyaya of charaka sutra sthana, Charaka has described the complications of sthoulya.

Here the apakva medas when deposited in rasavaha srotas may lead to dhamani

pratichaya 19-20-21 (atherosclerosis), which is the main factor responsible for hypertension.

Kakubhadi Lehya is a medicine in which, associations of Ghee with sugar candy exists.

The medicines with the edible fats are supplied to promote good fats in the body and to

excavate the fats responsible for disturbing the Srotas and Dhatu even. At this juncture

there is a need of evaluation of such medicament study in relation to that of the lipid

profile. Thus the present objective is carried out.


Chapter-3

Review of literature

here is no definite information regarding the normal or abnormal

conditions of Hypertension in Ayurvedic classics. But this especially in an abnormal

state is presently recognised as a disease state, which requires immediate attention of the

physician 22.

HYPERTENSION IN ANTIQUITY

If you just look back to the past days, the clinical entity of hypertension is not

available as such in any of the classical literatures of Ayurveda. We find more than

thousands of diseases described in Ayurveda which can be correlated or resembles one or

the other modern diseases, like Jwara, Rajayakshma, Visarpa, Switra etc., to that of

Fever, Tuberculosis, Herpes, Leucoderma etc., respectively. On the contrary it is difficult

to find a clear-cut correlation to that of hypertension in our science. But looking to the

description of hridaya, the diseases like Hridroga, Pakshaghata which can be taken as the

complications of hypertension and the drugs like Sarpagandha, Arjuna etc., we can think

of hypertension to be present in those days.

20th Century Authors on Hypertension

Based on the Dosha Dushya vivechana by 20th Century Authors and various

diseases are considered under the heading Hypertension. Different names are

recommended for the Hypertension or the Hypertensive States are as follows –


1. Bhrama

2. Dhamani pratichaya

3. Mada

4. Moorcha

5. Pittavrita udanavata

6. Rakta gata vata

7. Raktachapadhikyata

8. Raktapradoshaja vikara

9. Raktavriddha pittavrita vata

10. Roudhiryamada

11. Sanyasa

12. Siragata vata

13. Ucha rakta bhara

14. Ucha rakta chapa

1) Bhrama:

The literal meaning of Bhrama is rotation. As a disease, it has been explained as a

feeling that a person experiences the fast rotation in the shiras similar to that of fast

rotating wheel23. Charaka has considered the Bhrama as one out of the vataja nanatmaja

vyadhi. Here Bhrama corresponds to Giddiness and Vertigo. Bhrama is a disease not only

concerned to the shiras but also considered as Raktapradoshaja Vyadhi. Chakrapani has

explained Bhrama as a smruthi mohaha that means hallucination in his commentary24.

According him the Bhrama is a smruthimoha that means hallucination25.


Vagbhata has mentioned that this is because of vata dosha Vruddhi and Kapha

Ksheena26, where as Charaka affirmed it as sanchaya of vata dosha blocked by vitiated

pitta dosha27. Bhrama explained as a prodromal symptom of some diseases. It is also

said as symptom and complication of many diseases. It is due to disturbed vata dosha,

either alone or combined with or obstructed by vitiated pitta dosha.

Among the shareera doshas vata, pitta and manasa dosha rajas are considered as

the causative factors for the Bhrama28. When Kapha is diminished and both Vata and

Pitta are aggravated, it produces giddiness, cramps, piercing pain, burning sensation,

cracking, trembling, bodyache, wasting, distress and fuming29. In diminution of Vata and

Pitta, Kapha, blocking up the channels, produces loss of movement, fainting and

difficulty in speech.

In Astanga Hridaya Vagbhata has mentioned that it is one of the symptom caused

by vriddhi of vata Dosha and Kapha ksheena30. Charaka explained that it is caused due to

Sanchaya of vata dosha blocked by vitiated pitta Dosha31. It is due to disturbed vata

dosha, either alone or combined with or obstructed by vitiated pitta dosha.

Bhrama explained as a prodromal symptom of some diseases. It is also explained

as symptom and complication of many diseases. For example in the pittaja kasa the

Bhrama is a complaint32.

2) Dhamani Pratichaya

According to Charaka Dhamani pratichaya is one of the kaphaja nanatmaja

Vyadhi 33. The description of dhamani prathichaya as available in Nidhana Chikitsa

hastamalaka is ati poornata of dhamani. This Atipoornata of Dhamani is because of

Adhika Poshana. Due to adhika poshana especially Rasa and Rakta dhatus the damanis in


which these dhatu circulates get dilated. Because these Dhamanis get stretched by the

fullness of the Rasa, Rakta (Vriddhi) dhatu in them, simultaneously the velocity of the

Rasa Rakta Dathu (i.e, the gati becomes manda and guru) is hampered. The stretching

i.e., increase in the circumference of the dhamani is also caused by vayu, but in those

cases where in the increase in elasticity on circurmference of the damanis is due to vayu

in them.

The Dhamani will not be guru, manda and mrudu as in the Atipoornata of

Dhamanis by Rasa, Rakta. But infact, it will be hard (Katina) and Teekshna due to

vitiation of vayu on chalatwa of vayu and because of vitiation and chalatwa of Vata it

will sometimes be Teekshana, Manda, Poorna and Ksheena depending on the vitiation of

any one of these may be present in intervals.

This description is recorded in Nidana Chikitsa Hastamalaka clubbing the views

of Chakrapani, Gangadhara, Yogendranath commentaries on the word Dhamani

pratichaya the description also include the views of Astanga Sangrahakara and

Hridayakara on the word Dhamani Pratichaya. Most of these Acharyas have used

Dhamaniupalepa to denote Dhamani Pratichayaya i.e. Atherosclerosis.

3) Raktagatavata:

The disease Raktagata Vata, which is mentioned under the context of Vatavyadhi,

can be correlated with essential hypertension. Separate nidana have not been mentioned

for Raktagatavata, so samanya nidana mentioned for Vatavyadhi can be considered as

etiology for the Raktagata Vata. Some Ayurvedic scholars have mentioned that Raktagata

Vata as Raktavata. Charaka broached lakshanas as - Teevraruja, Santapa, Vaivarnya,

Krishatha, Aruchi., Stambata soon after having food34 and Vagbhata also mentions


almost all the symptoms, which are mentioned by Charaka, in addition with – Swapam,

Raga and Bhrama35.

Shri sudarshan shastri and shri yandunandanopadhya commenting on Raktagata

Vata says that the word Raktachapa can be considered as hypertension. Acording to

Kaviraj Gananathsen, the conditions Raktagata Vata and Vata Rakta are one and the

same. But Sri Sudarshan Shastri and Sri Yandunandanopadhya conferred opinion, as

Raktagata Vata is nothing but hypertension.

4) Raktavrita Vata:

Charaka has described the disease Raktavrita Vata under the context of

Vatavyadhi but no other Acharyas have mentioned regarding this disease. Raktavrita vata

resembles to that of Raktagata vata. They are Daha in between twak, mamsa and Vedana

saragayukta shotha and mandala.

The lakshanas mentioned under Raktavrita Vata 36 resembles to that of Raktagata

vata, they are Daha in between twak and mamsa, vedana saragayukta shotha and

mandala.

5) Siragata Vata:

Siragata vata is described under Vatavyadhi. Charaka, Susrutha and Vagbhata

describe it. When there is vata prakopa in siras, it causes many diseases such as vata

sambava vyadhies. Lakshanas mentioned under siragata vata are -

Ø Mandaruja, shopha, kampa no spandana in siras but there will be

akunchana in them 37.

Ø Susrutha and Yogaratnakar supported Charaka in all aspects. While

sushruta mentioning lakshanas, shoola, sira akunchana, and purana are being


mentioned i.e akunchana means sankocha in siras and purana means stoolatwa

in siras. In Yogaratnakar, it is mentioned that when there is vata prakopa in

sira there will be shoola akunchana in siras it will be filled with vata, which in

turn causes Bahyayama and Antarayama, khalli and kubjatwa.

6) Roudhira Mada: 38

Mada is one of the Raktaja disorders. Mada is nothing but, mado

Harshaglanopanaya i.e. in this disease. Harsha and Glani of that particular dhatu takes

place.i.e; increased gati and matra of rakta takes place or utkarsha or apakarsha of rakta is

called mada.

Mada is – “Mado harshaglanopanayh” it means, Harsha and glani of Rakta takes

place, i.e. increased gati and matra of rakta takes place or other wise utkarsha or aakarsha

of rakta is called mada. In charaka samhita 43 types of raktaja vydhies are mentioned and

mada is one among them 39. In Charka Samhita 43 types of raktaja vyadhies are

mentioned and mada is one among them 40.

There are seven types of madas explained vataja, pittaja, kaphaja, sannipataja,

vishaja and roudhiramada. Roudhira mada is considered as hypertension, by Acharya

Shree Viswanath Dwivedi and clarified that the dushya involved in this disease is Rakta.

In Roudhira mada, the vitiation of Rakta results in to increase Blood by the

vitiated Rakta altered Akunchana and Purana of Raktavaha and siras takes place then

leads to Roudhira mada.

On the other hand there are seven types of madas explained - Vataja, pittaja,

kaphaja, sannipataja, vishaja and roudhiramada. Roudhira mada is considered as


hypertension by Acharya shree Vishwanath Dwivedi and clarified that the dushya

involved in this disease is Rakta.

In Roudhira mada, initially the vitiation of blood results into increased Rakta, and

there by altered Akunchana and Purana of Raktavaha and siras takes place. Then it

confers to Roudhira mada.

7) Raktapradoshaja vikaras:

In charaka samhita totally 43 diseases are mentioned in vidhishonita adhyaya all

these diseases come under the rakta pradoshaja vikara. In this group mada, raktapitta etc.,

diseases are considered 41-42-43. Hypertension is considered under the Raktapradoshaja

vikara, due to the involvement of Rakta Dhatu.

Vatashonita, Raktapitta etc., diseases are mentioned in Sushruta Samhita under

the rakta vikara 44. Mada, Bhrama etc., diseases are considered under the Raktopradoshaja

diseases in Astanga Hridaya 45. But in Astanaga Sangraha, Mada, Murcha and Sanyasa

are explained in Rakta pradoshaja vikara 46.

8) Avruta Vata

The disorders of Vata are nomenclated as many as 80. Some of the avrutha vata

disorders are also considered under the heading of hypertension. They are Pittavruta

pranavata and Pittavruta udanavata.

8a) Pittavrutha prana vayu: The lakshanas mentioned are - Murcha,

daha, bhrama, soola, vidaha, chardi and sheeta kamatwa 47.

8b) Pittavruta udana vata : The pittavruta udanavata lakshana are -

Murcha, daha, shoola, daha in the nabhi and urah region, ojobransha,

shwasa, and klama 48.


8c) Pitta Avrithavata 49: If vayu is covered by Pitta the following

symptoms arise – burning sensation, thirst, pain, giddiness, feeling of

darkness, aggravation of burning sensation by the use of pungent, sour,

salty and hot things and desire for cold.

In case of covering with Kapha there are coldness, heaviness and pain, suitability

of pungent etc. and particular desire for fasting exertion, rough and hot things.

• If vayu is covered with Rakta, there is burning sensation with distress,

the space between skin and muscle becomes red and swollen and

rashes appear.

9) Murcha and Sanyasa:

Murcha is disease of raktavaha srothas which is due to vikrutha pitta and tamo

guna i.e, both sharirika and manasika vyadhi. Murcha can be considered as syncope,

which is mentioned, in modern science. A simple faint or temporary loss of

consciousness due to cerebral and it is important to note that giddiness, faintness or actual

syncope is much more frequently due to peripheral circulatory failure.

According to Astanga hridaya mada, murcha and sanyasa are the diseases of rasa,

rakta and samjnavaha sroto dusti. Acharya Susruta explained 6 types of murcha vataja,

pittaja, kaphaja, raktaja, madyaja and vishaja. While explaining about the raktaja murcha,

it is due to smell of blood or by seeing the blood it occurs. Sri sudarshan shastri and sri

Yadundana Upadhyaya opined that murcha occurring in rakta vata or high blood pressure

can be raktaja murcha.


9a) Murcha:

Murcha is considered as disease entity in Madava Nidana and explained in details

with nidana panchakas. Murcha is disease of raktavaha srotas, which is due to vikruta

pitta and tama guna i.e., both sharirika and manasika Vyadhi 50. On the literacy base

murcha is nothing but syncope which is mentioned in modern science.

A simple faint or temporary loss of consciousness due to cerebral, anaemia often

caused by dilatation of the peripheral blood vessels and a sudden fall in blood pressure 51.

It is proved that it is loss of consciousness due to cerebral and it is important to note that

giddiness, faintness or actual syncope is much more frequently due to peripheral

circulatory failure.

According to Astang Hridaya – Mada, Murcha and Sanyasa are the diseases of

rasa, rakta and samjnavaha sroto-Vikruti 52. Acharya Sushruta explained 6 types Murcha

viz. Vataja, Pittaja, Kaphaja, Raktaja, Madyaja and Vishaja. While explaining about the

raktaja murcha, it is due to smell of blood or by seing the blood it occurs. Commenting

on this statement Hindi commentator of madavanidana Sri Sudarshana Shastri and Sri.

Yadunandana Upadhyaya opined that murcha occuring in rakta vata or high blood

pressure can be taken, as raktaja murcha after considering raktaja murcha is Raktavaha

Sroto Vyadhi.

9b) Sanyasa:

Sanyasa is disease of samajnavaha srotas and also called as gambhira murcha. If

murcha is not treated properly it leads to Sanyasa. According to modern science coma is a

state of unnatural heavy deep and prolonged sleep often accompanied by slow irregular

breathing and consequently ending in to death 53.


10) Raktachapadhikyata

The word Raktachapadhikyata is formed by three words - Rakta, Chapa and

Adhikyata.

‘Rakta’ refers to - Shareerastha saptadhatwantargata dhatu vishesha: l

Raktam sarvashareerastham jeevasyadhara uttamaha: l S.T.M. 4

v ‘Chapa’- refers to pressure or squeezing.

v ‘Adhikyata’-refers to, high or increased.

So the meaning of “Raktachapadhikyata” is the high blood pressure or increased

blood pressure. Here it does not specify whether it is essential hypertension or secondary

hypertension. But here in this, the word Raktachapadhikyata is used to denote essential

hypertension.

Vata-caused hypertension often leads to a blood pressure that often fluctuates for

many years, until it begins to aggravate Pitta and Kapha, respectively, and becomes

increasingly more constant and more difficult to treat. Pitta-caused hypertension is the

most common in a classic Pitta body type (sometimes demonstrated through a red face

and bloodshot eyes). The patient may have quick temper with an aggressive and

competitive nature that incessantly drives him. Kapha-hypertension is often associated

with obesity and edema. This imbalance is usually long-standing and chronic. The Dosha

of Kapha can act as a storage site for all the circulatory Ama created in the doshas of

Vata and Pitta. The herbs for Vata and pita may be necessary as needed, and some

pungent and astringent herbs to detoxify accumulated Ama are important. Garlic,

cayenne (capsicum frutescens), and pippali (piper longum) or trikatu, a combination of

long pepper, black pepper and ginger are useful 54.


SHAREERA VIVECHANA

Before discussing the disease Bhrama, it is very much essential to know the

functional anatomy of the heart and blood vessels with physiology of blood circulation.

Hridaya

The word ‘Hridaya’ explains and signifies only the functional aspect of an organ.

According to Shatapatabrahmana the word hridaya is made up of three dhatu’s, Hri, Da,

and Ya. These dhatus by the combination of the pratyaya and adesha, forms the dhatus,

as Hrit, Dana and Ayana.

The dhatu Hrit gives the meaning of Hanane, Apatirite i.e., to take or to receive.

The dhatu Dana gives the meaning of Tyage, Palane, Chedane i.e. to give or to eject or to

nourish. The dhatu Ayana having the paribhasha of Kayam, gives the meaning of Gati,

Chalana, or Movement.

The word hridaya has been attributed to mainly two organs, namely Mastishka or

Shirohridaya and Hridaya i.e. Urohridaya. Generally yogis attribute the word hridaya to

Mastishka or Brain, and the physicians or vaidyas denote the word hridaya to Urohridaya

or Muscular heart.

In classics the anatomy and physiology of hridaya is not explained under one

heading or at one place, we get lot of quotations and similies based on which we should

understand the anatomy and physiology of heart.

Hridaya is considered as one of the kostanga. It is situated in vaksha pradesha in

between the two stanas. It is formed by sleshma and rakta, having the shape of inverted

lotus and according to Arunadatta it is made up of mamsapeshi and rakta. It measures

two angula according to Chakrapani and four angula according to Susruta. Hridaya is the


moola of pranavaha and rasavaha Srotas 55. It is the seat of manas and para-apara ojus56.

Hridaya is the prabhava sthana of dashadhamani’s which spreads all over the body and

which carries rasa, ojas and does tarpana karma 57-58. According to Palakapya, from

hridaya siras arise and spreads all over the body just like a network, and like all rivers

join ocean, in the same fashion all siras opens in to hridaya 59. Hridaya continues to work

whether the person is in jagrutavasta or swapatavasta 60.

Many of its functions can be attributed to the doshas that are concerned to it, i.e. a

particular function of hridaya is carried out by particular dosha. These functions are

discussed below with respect to concerned doshas.

Relation of Hridaya with Doshas

Hridaya is related with all the three doshas. Among vata, it is related with

udanavayu, prana vayu and vyana vayu. Among pitta, it is related with sadhaka pitta and

pachaka pitta, and among kapha it is related with avalambaka kapha.

Hridaya and Udanavata

Charaka and Vagbhata have mentioned the uras as the sthana of udana vayu 61-62-

63. This indicates that, it is related to hridaya also. When we look at the functions of

udana vayu, the functions like prayatna (endeavour or effort), urja (enthusiasm) and bala

(strength) 64, with respect to hridaya, we can think of the conductive system of the heart,

i.e. udana vayu by the functions like prayatna and bala initiates and helps in the

conduction of the cardiac impulses in the heart.

Hridaya and Pranavata

According to Charaka and Vagbhata Pranavata is situated in Shiras 65-66. And

according to the Sharangadhara it is situated in hridaya67. Vagbhata states that pranavata


maintains the activities of hridaya (heart and circulatory system), and supports or does

dharana of dhamanis (probably the vasomotor functions) 68-69. Looking to the above

description it can be said that prana vata situated in murdha sends impulses to hridaya,

there by governing the sympathetic and parasympathetic actions / functions.

Hridaya and Vyanavata

Vyana vayu is situated in hridaya 70-71 and it pervades swiftly throughout the body

72-73. Vyana vayu is responsible for circulation of Rasa (rasadhatu) through out the body

74-75, by the regular contraction and relaxation of the heart 76. Sushruta has also

mentioned asruk sravana to be one of the functions of Vyanavata 77. Vagbhata concised

all functions of vyana vata by the statament that all the actions or movements of the body

are conducted by vyana Vata 78.

In Nadee-gnyanam, it is mentioned that the rhythmic tendency of the heart is

responsible for continuous contraction and dilatation of the hridaya and which is the

inherent tendency and capacity of hridaya.

Even Charaka has mentioned that vyana vayu is responsible for the continuous

flow of rasadhatu to all parts of the body through out the life by using the words like

ajasram and sada 79.

Hridaya with relation to Sadhakapitta

Sadhaka pitta is situated in hridaya 80-81-82, and it is responsible for achievement of

buddhi, medha, abhimana, utsaha and abhipretartha.

From this it is understood that, it is essentially connected with some of the higher

mental faculties and emotional states. The concept of sadhaka pitta therefore,

encompasses psycho-physiological actions.


Hridaya and Avalambaka Kapha

Avalambaka kapha is situated in uras 83-84. It does avalambana of hridaya i.e. with

the help of rasa it gives bala to hridaya. In other way it does tarpana and kledana of

Hridaya and there by helping it to function properly.

Hridaya with relation to Manas

It is also seen that hridaya is the adhistana of Manas 85-86-87-88. Acharya Charaka

while mentioning measures to protect hridaya and oja says to avoid the thing that

produces dukh to the Manas 89. Even in Unmada chikitsa adhyaya also acharya Charaka

mentions about manovaha srotas. Chakrapani commenting on it says the dhamani’s that

originate from hridaya or the dhamani’s that are related to hridaya desha, are to be taken

as manovaha Srotas 90-91. From all these it is clear that hridaya, sadhaka pitta and manas

are related to each other and the vitiation of one causes the vitiation of other.

Relation of Hridaya with Ojas

In shareera ojas has been classified in to two types, i.e. para ojus and apara ojus.

Para ojus is situated in hridaya 92. It is asta bindu in pramana and it is said to be uttama

pranayatana (most important vital part). Even, if little of it is destroyed the body cannot

exist. Apara ojus is situated in hridaya and dhamani, and circulates all over the body. It

is ardhanjali in pramana and the deficiency of this ojus does not cause death but diseases

like prameha are likely to set in.

Looking to all these above references we cannot get a clear cut picture of anatomy

and physiology of heart. But it gives a clear idea that, the hridaya that is described is

nothing but the muscular heart or cardia. Even the classical quotations and similies given

for hridaya almost fulfil the modern description that has been given for heart.


Rasa Rakta Paribhramana

Hridaya is the srotomula of rasavaha and pranavaha srotus 93. It is responsible for

rasa samvahana in the body. Samanavata brings the ahara rasa that is formed to hridaya,

and as it enters the hridaya it is considered as rasa dhatu. Now with the help of vyana

vayu and udana vayu the sankocha and vikasa i.e. the praspandana of hridaya starts.

Praspandana of hridaya can be correlated to the conductive system of the heart. Here

sankocha can be considered as systole and vikasa can be considered as diastole.

Pranavata maintains the actions of hridaya and does dharana of dhamanies. This

indicates that it governs the vasomotor functions. Once the sankocha takes place the rasa

moves in to dashadhamani, and proceeds further 94.

Here by prasarana akunchana karma, and as per kedarakulya nyaya, the rasa

moves to all parts of the body and nourishes the whole body. This function is carried out

continuously through out the life 95. Even Bhela explains that rasa samvahana takes place

through sira dhamani, which are spread all over the body and owes their origin and

insertion to hridaya. Sharangadhara while explaining rasa samvahana explains that, rasa,

rakta, oja, sneha are carried from hridaya to all parts of the body, and does tarpana karma.

Avalambaka kapha gives bala to hridaya, to carry out these functions.

Regarding rasa samvahana acharya Susruta gives a simily i.e. “Shabdarchi

Jalasantanavat” 96. This indicates that rasa moves in all directions. Dalhana commenting

on it says, urdhwagamitwa of rasa occurs like archi, adhogamitwa of rasa like jala and

tiryagamitwa of rasa like shabda.

Again this rasa is brought back to the hridaya by vyana vayu samana vayu and

hridaya vikasana takes place, followed by sankocha and rasa moving towards sarva


shareera. This cycle continues and acharya Charaka uses the word ajasra to denotes the

continuous function of hridaya in circulation of Rasa 97.

PHYSIOLOGY OF BLOOD CIRCULATION

The activity of the organs of the circulatory system, that is, of the heart and blood

vessels, ensures a constant flow of blood in the organism. Because of its movement, the

blood can perform numerous transport functions, in particular, supplying oxygen and

nutrients to the tissues, and removing waste substances formed as the result of

metabolism.

The movement of blood in the organism follows a complicated course known as

the systemic, or greater circulation, and the pulmonary or lesser. The systemic

circulation starts at the left ventricle of the heart, passes to the aorta, to the arteries,

originating from it and to all their branches, thence to the arterioles, capillaries, and the

veins of the whole body, and finally to the two venae cavae which enter the right atrium.

The pulmonary circulation begins from the right ventricle, continues along the pulmonary

artery and all its branches, then along the pulmonary arterioles, capillaries, and veins and

terminates in to the pulmonary veins, which empty into the left atrium.

The flow of blood in the vessels is due to the work of the heart. Contraction of

the ventricular myocardium ejects blood under pressure from the heart into the aorta and

pulmonary arteries. The movement of the blood further along the vessels, and its return

to the heart, is conditioned by its pressure in the large arteries being higher than in the

small arteries, the pressure in the latter being higher than in the capillaries, and the

pressure in the capillaries being higher in turn than in the veins and atria. In this way

there is difference in pressure all along the blood stream that determines its circulation in


the vascular system, blood flowing from the vessels with higher pressure to those with

lower. The gradual drop in the pressure along the blood stream (from the arteries to the

capillaries and veins) is brought about by the fact that the energy imparted by the heart is

utilised to overcome the resistance of the vessels to the movement of the fluid arising

from friction between the fluid particles and the vascular wall and between the particles

themselves.

The function of the heart is rhythmic pumping of blood that it receives from the veins

in to the arteries. It is performed by alternate rhythmic contraction and relaxation of the

muscular fibres that forms the walls of the atria and ventricles. Contraction of the

myocardium of these chambers is known as their systole, and relaxation as their diastole.

In normal physiological conditions systole and diastole occur in a definite co-

ordination and constitute the cardiac cycle. Each cycle is considered to start with the

atrial systole. The contraction begins as a wave in that part of the right atrium where the

orifices of the venecavae are, and then involves both atria, which have a common

musculature with a cardiac rhythm of 75 contractions per minute, an atrial (auricular)

systole lasts 0.1 second. As it ends, the ventricular systole begins, the atria then being in

a state of diastole, which lasts 0.7 second. The contraction of the two ventricles occurs

simultaneously, and their systole persists for about 0.3 second. After that, ventricular

diastole begins and lasts about 0.5 second. One-tenth second before the end of the

ventricular diastole a new atrial systole occurs, and a new cycle of cardiac activity begins.

Regulation of Blood Pressure

Physiologically the magnitude of the arterial pressure depends on two

fundamental hemodynamic variables; cardiacs out put and total peripheral resistance. In


other words, the arterial blood pressure is a product of cardiac out put and peripheral

vascular resistance.

Figure -1

Showing the Blood Pressure Regulation

HUMORAL FACTORSConstrictors DilatorsBLOOD VOLUME -Angiotensin II -

Prostaglandins-Sodium -Catecholamines -Kinins-Mineralocorticoids -Thromboxane -NO/EDRF*-Atriopeptin -Leukotrienes

-Endothelin

BP = CARDIAC X PERIPHERAL LOCAL FACTORSOUTPUT RESISTANCE -Autoregulation

-Ionic (pH, hypoxia)

CARDIAC FACTORS NEURAL FACTORS-Heart rate Constrictors Dilators-Contractility -�-adrenergic -�-adrenergic

* Nitric oxide / endothelium - derived relaxing factor

The Blood Pressure can be raised by increased peripheral resistance and by

increased cardiac output.

The cardiac output depends upon the heart rate, its contractibility and the blood

volume. The blood pressure can be raised by an increase in the volume of fluid

absorption of water and water retaining sodium from the intestine in to the vascular

system or an increased production of the adrenocortical hormonal aldesterone, which

blocks the excretion of sodium and water into the urine.


It appears that most patients with established hypertension have abnormal cardiac

output and increased peripheral vascular resistance mainly sustains blood pressure.

The peripheral vascular resistance is determined by the arteriolar lumen, which

may expand or contract depending on the state of muscular cells in the vessel wall. This

is known as local vascular tone. Normal vascular tone depends on the competition

between vasoconstricting influences and vasodilators. Peripheral resistance depends on

the size of the lumen of some vessels. A decrease in the inner (lumen) diameter will

raise the Blood Pressure. The decrease in the lumen could be brought about by an

anatomical thickening of vessel walls (eg., intimal thickening of arteries), by their

mechanical compression from outside or most commonly by their active muscular

contraction which can be induced by a variety of vasoconstrictor mediators. The

common vasoconstricting mediators are epinephrine, norepinephrine and renin- activated

angiotensin-II. The other recently described vasoconstrictors include endothelin-I,

thromboxane and leucotrienes. Resistance vessels also exhibit auto regulation, a process

by which increased blood flow to such vessels induces vasoconstriction, an adaptive

mechanism that protects against hyperperfusion of tissues. The vasodilators include

kinins, prostaglandins and nitric oxide. Certain metabolic products such as lactic acid,

hydrogen ions, adenosine and hypoxia can also function as local vasodilators.

Recently it has been discovered that haemoglobin plays an important role in

regulation of blood pressure. In the body tissues, haemoglobin releases oxygen and

super nitric oxide (SNO) and picks up carbon dioxide. The released SNO causes

vasodilatation. At the tissue level haemoglobin also picks up excess nitric oxide (NO),

which tends to cause vasoconstriction. Thus haemoglobin helps in regulating the blood


pressure by adjusting the amonts of SNO and NO to which blood vessels are exposed.

This newly appreciated role of haemoglobin may influence development of drugs to treat

hypertension.

Further the arteriolar smooth muscle contraction can be increased by increased

sympathetic tone and also by increased sodium load and extra cellular fluid load.

The kidneys play an important role in the blood pressure regulation, and there is

considerable evidence that renal dysfunction is essential for the development and

maintenance of both essential and secondary hypertension.

The kidney influences both peripheral resistance and sodium homeostasis, and the

renin-angiotensin system appears central to these influences. Renin elaborated by the

juxtaglomerular cells of the kidney transforms plasma angiotensinogen to angiotensin-I,

and the latter is converted to angiotensin II by angiotensin converting enzyme (ACE).

Angiotensin II alters blood pressure by increasing both peripheral resistance and blood

volume. The former effect is achieved largely by it’s ability to cause vasoconstriction

through direct action on vascular smooth muscle, the latter by stimulation of aldosterone

secretion, which increases distal tubular reabsorption of sodium and thus of water.

The renin-angiotensin system

The renin-angiotensin system has been extensively studied since the introduction

of practicable essay methods for plasma renin and angiotensin patients with essential

hypertension have been subdivided into subgroups with low, normal and high plasma

renin on the grounds of the elevated pressure. The different mechanisms and in particular

those patients with low plasma renin might have excess, mineralocorticoid activity.

Plasma renin and angiotensin ii values are continuously distributed in the hypertensive


population. Further peripheral levels of plasma renin and angiotensin –II is found in

relation inversely to age in essential hypertension. Peripheral levels of anti diuretic

hormone have been reported as being slightly suppressed in uncomplicated essential

hypertension.

Figure -2

Showing the Role of Renin-Angiotensin System

J G

Renin

Renin Substrate

Angiotensin IConverting Enzyme

Angiotensin II

Vasoconstriction Increased Aldosterone Synthesis

Sodium retention

Increased Blood Pressure

• The kidney produces a variety of vasodepresser or antihypertensive substances that

presumably counter balance the vasopressin effects of angiotensin. These include the

prostaglandins, a urinary kallikrein-kinin system, platelet-activating factor, and nitric

oxide.

• When blood volume is reduced, the glomerular filtertation rate (GFR) falls, this, in

turn, leads to increased reabsorption of sodium by proximal tubules in an attempt to

conserve sodium and expand blood volume.


• GFR- independent natriuretic factors, including atrial natriuretic factor (ANF), a

peptide secreted by heart atria in response to volume expansion, inhibit sodium

reabsorption in distal tubules and cause vasodilation. Abnormalities in these renal

mechanisms are implicated in the pathogenesis of secondary hypertension in a variety of

renal diseases, but they also play an important role in essential hypertension.

Approach to Clinical features of HTN

All acharyas have directed us to understand an anukta roga in terms of dosha

dushyadi bhava 98 and also they have mentioned about pratitantra siddhanta 99 i.e.

regarding the concepts of other science, with these guidelines an interdisciplinary attempt

has been made to analyse the dosha dushya in Hypertension to understand the Nidana

panchaka and for better management of it. And for this the signs and symptoms of

essential hypertension are analysed with special reference to that of Bhrama. The analysis

is undertaken on the basis of available data from contemporary medicine, where yukti

Pramana is invoked.

From the analysis made below in the chart is seen that among shareerika doshas,

all the three doshas are involved, and in manasika doshas both raja and tama are

involved, and in dushya rasa, rakta, mamsa, and medas are involved, and regarding

srotas, rasavaha, raktavaha, mamsavaha, medovaha and manovaha srotas are involved.

And it also reveals that among shareerika doshas vata is the pradhana dosha that gets

afflicted followed by pitta and kapha. Among dushya rakta is the pradhana dushya that

gets afflicted. Thus from this study it can be concluded that Bhrama (essential

hypertension) is vata pradhana tridoshaja vyadhi with rakta as the pradhana dushya.


Table -2

Showing Dosha Dushyadi Vivechana of Bhrama in comparison to hypertensionSHAREEKADOSHA

MANASIKADOSHA

DUSHYASl.No.

CLINICALFEATURES

V P K Raj Tam R Ra

Ma

Me

SROTAS

1. Giddiness + + - + - + + - - RasavahaRaktavaha

2. Headache + - - - - - + - - Raktavaha3. Vertigo + + - + - - + - - Raktavaha4. Palpitation + - - - - + - - - Rasavaha5. Fatigue + + - - - - + - - Raktavaha6. Chest pain + - - - - + - + - Rasavaha7. Insomnia + + - + - - - - - Manovaha8. Irritability + + - + - - - - - Manovaha9. Anxiety + - - + - - - - - Manovaha10 Dyspnoea + - - - - + - - - Pranavaha,

Rasavaha11 Delirium + - - + - - - - - Manovaha12 Anger - + - + - - + - - Raktavaha13 Fainting + + - - + - - - - Manovaha14 Epistaxis - + - - - - + - - Raktavaha15 Tinnitus + - - - - + - - - Rasavaha16 Bounding pulse + + - - - - + - - RaktavahaNOTE: V – Vata; P – Pitta; K – Kapha; Raj – Rajas; Tam – Tamas; R – Rasa;

Ra – Rakta; Ma – Mamsa; Me - Medas

Nidana

Observation and analysis of the scriptural references of Bhrama vis-à-vis

Hypertension, a Hridroga concern reveals that the Nidana, Samprapti and Lakshana can

be categorised into three groups 100:

1. Mityahara Vihara,

2. Pragnaparadha,

3. Marmaghata.


1) Mityahara Vihara:

Improper diet like consumption of excessively pungent, heavy, dry, incompatible,

unaccustomed, un-digestive foods which are basically dhatu produshaka, viruddha,

apatarpaka and ahridya ahara and also improper regimen like chintanamati chintanam

(strong emotional stress) intermittent eating, faulty therapeutic measures like

Bastivyapath, Virechana Vyapath etc., These factors are by nature rasa dhatu

pradooshaka and also rasavaha srotho dushti karakas.

These nidanas cause apatarpana of rasa dhatu which leads to Hridayavayava

Dushti by being nourished by dushita rasadhatu. And even the santarpana nidanas

mentioned like tila, guda, guru aharas also do not cause proper nourishment; but cause

amasandharana which accumulates in rasavaha srotas and proper hridaya in the form of

Upalepa (fat disposition as in cholesterol and atherosclerosis) leading to granthi

formation, which in turn hampers vyana vata sanchara, creating vyshamya in its gati.

2) Prajnaparadha:

The causative factors like instigation and inhibition of natural urges especially of

Adhovata, Trishna, Ashru, Chardi, Shramashwasa, Udgara etc., Physical exertion, Grief,

Fasting, Sexual abuse, Awakening at night, Excessive sleep etc., which are volitional

transgression of body and mind, these also include violation of Dinacharya, Ritucharya

and Swastha Vritha.

All these factors when analysed show that they are basically related with the

functioning of Pranavata, Apanavata, Udana Vata which gets vitiated simultaneously

vitiating Vyanavata, which functions in association with the rest of the vatas, leading to

Hridayavayava Dushti by gati vyshamya of vayanavata leading to Hridroga.


3) Marmaghata :

Hridaya is an important Marmanga the reason why it is specially designed for

sensitivity. Any injury to this organ externally or by the internal doshas proves to be

fatal. Hence, it should be protected with care.

1) Dosha prakopa Karana

a) Vyanavata Prakopa Karanas: Atigamana, chinta, vishama chesta, viruddha ahara,

ruksha ahara, bhaya, harsha, vishada etc 101.

b) Pranavata Prakopa Karanas: Ruksha ahara, vyayama, langhana, atyahara,

abhighata, vegadharana, adhwahata etc 102.

c) Udanavata Prakopa Karanas: Kshavathu, udgara, chardi, nidra vegadharana, guru

ahara, bhara vahana, ati rodana, ati hasya etc 103.

Here all these three vata are in relation to hridaya and rasa rakta paribhramana.

So any impairment in these leads to the disturbance or impairment in the normal function

of heart and blood circulation.

2) Srotodusti Karanas

Some of the other karanas that can be held responsible are-

a) Rasa vaha Srotodusti Karanas: Guru, sheeta, atisnigdha, atimatra bhojana, adhika

chinta etc.

b) Rakta vaha Srotodusti Karanas: Vidahi, ushna, snigdha, drava bhojana, adhika

atapa and vayu sevana etc.

c) Mamsa vaha Srotodusti Karanas: Abhishyanda, sthoola, guru ahara sevana, day

sleep after bhojana etc.


d) Medovaha Srotodusti Karanas: Avyayama, deewaswapna, excess of fat containing

meat, adhika madira etc.

e) Manovaha Srotodusti Karanas: Krodha, shoka, bhaya, harsha, vishada, irsha, asuya,

dainya, matsarya, kama, lobha, iccha, dwesha etc.104.

Excessive use of Lavana is described in Charaka samhita as the cause of Rakta

vriddi and leads to shonitaja roga 105. Since rakta dhatu is one of the important dushya in

the etiopathogenesis of hypertension, it is given more importance. The symptoms of

shonitaja roga are similar to this essential hypertension. Again Charaka has told that

lavana should not be consumed in excess and for longer duration 106. When excessively

used, it produces fatigue, lassitude and weakness of the body 107, which are the symptoms

usually found in the patients of hypertension.

Sushruta has mentioned medoroga leads to vatavikara 108 Dalhana explained that

vatavikara is produced due to medavrita marga. Apart from this in astauninditeeya

adhyaya of charaka sutra sthana, acharya has described the complications of sthoulya.

Here the apakva medas when deposited in rasavaha srotas may lead to dhamani

pratichaya (atherosclerosis), 109-110-111, which is the main factor responsible for

hypertension. In Ayurveda seat of manas shira and hridaya, which are in turn related to

prana and vyana vayu respectively, which have influence over function of maintaining

the blood pressure. So aggrevated vata will initiate the process of hypertension 112-113.

Raja and tama are the doshas pertaining to the mind and the types of morbidity

caused by them are kama, krodha, lobha, mada, bhaya 114 etc. Acharya Charaka has

advised to suppress these factors, 115 because they tend to elevate raja and tama gunas

which cause manodusti. These obnoxious state of mana produces manovikara with


involvement of samjnavaha or manovaha Srotas 116. Further, Chakrapani commenting on

srotomula says, hridaya and dashadhamani are the manovaha srotomula 117. In this way

this manovikara may afflict the arteries of the heart and therefore they also afflict oja

which is also asirta of hridaya, 118 and vitiation of vata and Pitta, 119-120 also takes place.

3) The causes of high blood pressure

The causes of high blood pressure are a bit of a mystery. About 5% of patients

requiring hypertension treatment can trace their high blood pressure to a physical cause

such as kidney disease. Treatment of the disease reduces the symptoms of high blood

pressure 121.

But for 95% of patients who undergo hypertension treatment, the causes of high

blood pressure are unknown. Diet and stress are suspected as prime contributors to

hypertension, but medical experts aren’t exactly certain of all the mechanisms involved.

There is a close relationship between blood pressure and weight. This applies to

all ages and groups. Studies have established that individuals who gain more weight show

more increase in blood pressure. Moreover, weight reductions have been accompanied by

a fall in arterial pressure. This is not exclusively a dietary consideration, subsequently

heredity and exercise are also the influencing factors.

Aetiology 122:

1. Occupation: Persons who are involved in nervous and mental overstrain like

scientific workers, engineers, physicians, drivers etc.,

2. Heredity: Chances of developing hypertension is greater in persons whose one of

both parents are hypertensives.


3. Stress: Chronic psychological stress may lead to hypertension and acutely stressful

stimuli may cause transient rise of blood pressure.

4. Sodium intake: Excessive intake of salt in diet may be important. Hypertension

may be associated with low potassium diet.

5. Alcohol: Alcoholics are often hypertensive. Alcohol however is not a direct

pressure agent and hypertension develops during alcohol withdrawal, mediated by

sympathetic nervous system.

6. Obesity: Possible mechanisms of hypertensive effect of obesity include high food

intake such as refined carbohydrates, fats etc.,

Figure - 3

Diagrammatic expression showing dietary intake and CVD

CardiovascularDiseases

Stress

DiabetesObesity

Hypertension Hyperlipidemia

Smoking

High fat,High calorie diet

Lows fiber and high fat,high calorie diet,Glucose intolerance

Stress, high fat, high caloriediet, high salt intake, Alcoholconsumption and smoking

High intake of saturated fat andanimal foods


Causes of Moorcha attributed to Bhrama

Persons who are emaciated or debilitated, in whom the doshas have undergone

profound increase, those who indulge in incompatible foods and suppression of the urges,

those who are injured and those who are mentally weak, become afflicted with the

disease Moorcha, when the doshas invade the external and internal organs of the mind.

When sanjnavaha Srotas (channels that carry sensations) are blocked by the increased

Dosha the person goes in to the condition of Tamah pravesha 123.

As the Bhrama is also associated and affirmed in the same chapter the above

etiological factors said can be attributed to that of the Bhrama undoubtedly and

conditionally as involvement of the Dosha Vata and Pitta in associations with that of

Rajodosha. In other words it can be stated that the Bhrama, is a psycho (Rajo Dosha) and

somatic (Vata and Pitta) disease with a determinative and resoling sign of Bhrama.

Samprapti

The pathogenesis of essential hypertension is not yet cleared, a hypothetical

pathogenesis have been mentioned in many of the modern texts. But when we look in

terms of Ayurveda, it seems to be a tridoshaja vyadhi with vata pradhana, pitta

kaphanubandha and pradhana dushya involved to be as rakta. So here with the guidance

of pratitantra siddhanta 124 i.e. regarding the concepts of other science, an attempt is made

to study the samprapti of Raktachapadhikyata in the language of Ayurveda with modern

paralance.

Role of Vitiated Vata

Because of the vitiation of vata which is lodged in the blood vessels, the khara

and laghu guna causes kathinya, leading to reduction in the elasticity, as a result of it


margavarodha is produced. This may be taken as arteriosclerosis. Even the age,

vriddhavastha, which is predominant of vata, contributes to the pathology.

Because of the vitiation of vata, which is lodged in hridaya, the chalana or

praspandana karma of vyana vayu, prayatna karma of udana vayu and dharana karma of

prana vayu will be impaired.

Because of this there will be impairment in the initiation of contraction and

relaxation, conduction of impulses, as a result of which the increased doshas alter the

functions of hridaya and increases the heart rate and contraction and relaxation, there by

increasing the cardiac out put. When doshas get’s lodged in dhamani’s of vrikka, kleda

samvahana is hampered thus it adds to the blood volume resulting in to increased cardiac

out put.

Role of Vitiated Pitta

By the Drava - guna vriddhi of pitta, the rakta vriddhi takes place due to

ashrayashrayi sambandha. Pitta is considered to have the identical qualities of that of

catacholamines. Since here the pitta vriddhi takes place, this can be attributed to increase

in catacholanimes. Then, when found in increased level are liable to increase blood

pressure by increasing the peripheral resistance and cardiac output.

Role of Vitiated Kapha

The picchila guna of kapha increases the viscosity of blood, which is also one of

the factor responsible in the mechanism of high blood pressure.

Role of Ama and Medas

The snigdha, picchila, guru etc, guna of ama, excessive medas and apakwa medas

(improperly converted fat) accumulates in the blood vessels causing narrowing of lumen


of blood vessels, leading to margavarodha. This can be taken as hypercholestraemic

condition of the plasma.

The increased medas can also cause mechanical compression over the blood

vessels from out side, which is also one of the factor for increased peripheral resistance.

Role of Mamsa Dhatu

Ultimately Raktachapadhikyata in course of time produces thickening of the walls

of heart to cope up with the increased function of it. This can be taken as cardiac

hypertrophy and this condition can be taken as adhimamsata, which is the preliminary

symptom of mamsavaha srotodusti.

Thus a combined effect of all these pathological events, contribute to increased

peripheral resistance and increased cardiac output leading to Raktachapadhikyata.

At this stage the premonitory symptoms will arise, but here since it being a

vatavyadhi the poorva roopa are said to be avyakta and some vague symptoms like

shirashoola, bhrama, anidra etc., may be seen with very mild intensity.

After this, the disease progresses and the complete manifestation of disease takes

place and as a result of these pathological events the signs like raktachapadhikyata,

bounding pulse etc., are seen. And symptoms may or may not be present. If present, a

symptom comprises of shirashoola, bhrama, anidra etc. Even at this stage, if the treatment

is not started, the further vitiation of doshas takes place and land up in to complications

or upadrava.

This depends on the sthana or the organ that gets affected i.e., when mastishka is

affected, the condition or diseases like ardita, pakshaghata etc., are produced. When


vrukka is affected, shotha etc., are produced. When netra is affected, it causes drishti

mandya etc., and when hridaya is affected, it causes hridroga etc.,

Pathological Anatomy 125:

Essential hypertension gradually affects permeability of vascular walls and their

protein content. At later or grave forms of the disease, this causes sclerosis or necrosis of

small arteries and secondary changes in the tissues of organs. Walls of large vessels are

usually affected by atherosclerotic changes. The extent of vascular affection differs in

various organs and various clinicoanatomical variants of the disease therefore arise, with

a prevalent affection of the vessels of the heart, brain and kidneys.

1) Margavarodha

If kayagni/dhatvagnimandya is the prime cause in the former, rasavahasrotodushti

and of course Doshasanchaya (Kapha/Pitta) are the prime causes in the latter. However,

the site or sthana of margavarodha could be anywhere in the body. For instance, stenosis

of one or both of the renal arteries can cause hypertension and so also the coarctation of

the aorta. Examples of margavarodha are many; including, the pheochromocytoma (the

chromaffin tissue tumours of the adrenal medulla), atherosclerosis, other endocrine

tumours, Glomerulonephritis, pylonephritis etc., Any kind of obstruction anywhere in the

body affecting the flow of nutrients (Rasavahasrotas) results in "Hypertension" as one of

the manifestations 126-127.

2) DHATUKSHAYA:

v · Dhatukshaya can be a result of

v · Deficiency of the corresponding nutrients

v · Agni vikriti [Metabolic aberrations]


In either condition the resultant Vata prakopa can manifest itself in a variety of

forms 128. For instance, Hypertension is due to vaso-constriction due to neural factors.

Hypertension in which stress and electrolyte imbalance are identified as prime causes,

high B.P due to arteriolar necrosis, fatty degeneration etc., The neural factors causing

hypertension, mainly involve the sympathetic vasoconstrictor system.

Signs:

Signs or physical findings depend up on the cause of hypertension, its duration,

severity and the degree of effect on target organs. The signs of essential hypertension will

reflect the stage and duration of the disease process. These includes,

v Elevated blood pressure.

v Forcible pulse.

v Thcikened and hardened arteries.

v The apex beat will reflect the underlying hypertrophy. It will be sustained or

heaving but will not be displaced.

v 4th heart sound, due to left atrial hypertrophy.

v Loud aortic second sound.

v Aortic-ejection click and aortic or apical ejection systolic murmur caused by

turbulence secondary to aortic dilatation may also be present.

v The optic fundi may show changes of hypertension; these needs to be

differentiated from those associated with arteriosclerosis.

v Cotton wool exudates, oedematous retina, pappiloedema etc. are other specific

signs of involvement of the heart, kidney and brain that may be present.


Table –3 : Key items of the base line history

in the patients with mild or moderate Hypertension - Symptoms

Blurred vision

Brochospasm

Chest pain

Claudication

Cold extremities

Cough

Depression

Dizziness

Dyspnoea

Fatigue

Flushing

Headache

Hematuria

Impotence

Joint pains

Muscle cramps

Nocturia

Palpitation

Polyuria

Skin rash

Sweating

Unsteadiness

Weakness

Weight loss or gain

Past disease History

Angina

Asthma

Diabetes

Congestive heart attack

Glomerulonephiritis

Gout

Heart block

Hepatitis

Hypertension

Lupus erythematosus

Myocardial infraction

Peptic ulcer

Pyelonephritis

Toxemia

Transient ischemic attacks

Diet and Drug History

Alcohol

Aspirin

Blood pressure medications

Cigarettes

Cocaine

Cold remedies

Chewing tobacco

Cyclosporine

Licorice

Nasal sprays

Nonsteroidal antiinflammatory agents

Oral contraceptives

Potassium (dietary)

Salt (dietary)

Tricyclic antidepressants

Family History

Coronary heart disease

Diabetes

Hereditary nephritis

Hyper lipidemia

Hyperparathyrodism

Hypertension

Phechromocytoma

Polycystic kidney disease

Renovascular hypertension

Thyroid disorders


Figure - 4. Showing the Schematic Representation of Samprapti

Prolonged indulgence in Nidana

Tridosha gets Vitiatied

Agni Dushti

Ama

Samadosha

Sahaja Karana Spreads to Hridaya and Shakhagra

Khavaigunya, any where between theRasavaha Srotomula Hridaya and Shakahgra

Dosha Dushya Sammurcchana

Resulting in to following sequalae

Vitiated Dusta Vitiated Vitiated Vitiated Vitiated Vata Medas Vata Pitta Rakta Kapha______Ama________ ___________ ________________ ___________

Narrowing of lumen Increases Heart Increases the Blood Increases theof Blood Vessels Rate Volume Viscosity ofBlood

Bhrama vis-à-vis Essential Hypertension

Increased Cardiac Output

Increased Peripheral Resistance


Chikitsa

There are three types of basics mentioned in Ayurveda, are Dinacharya,

Ritucharya and Sadvritha, which also form a part of non-drug therapy in the management

modalities.

The disease is vatapradhana tridoshaja vyadhi along with the aggravated rakta

dhatu and anubanda of pitta and kapha. Hence the general measures suggested for

Rakthadhisthita vyadhis can be adopted. The general line of treatment suggested for

raktaja vyadhi’s are:

v Virechana

v Upawasa

v Raktamokshana 129

v Hrudya Rasayana

Understanding the prakruti, adhisthana of doshas, immediately the chikitsa should be

started. With this guideline, with the view of samprapti vighatana, the ideal principles of

chikitsa of Raktachapadhikyata can be planned accordingly in the following manner –

1. Nidana parivarjana

2. Amahara chikitsa

3. Dosha pratyaneeka chikitsa

4. Vyadhi pratyaneeka chikitsa

5. Satvavajaya chikitsa

6. Yoga and other practices

These principles of chikitsa can be grouped in to two categories as,

1. Adravyabhoota chikitsa or Non pharmacological management

2. Dravyabhoota chikitsa or Pharmacological management


Adravyabhoota Chikitsa:

This includes –

(a) Nidana parivarjana

(b) Satvavajaya chikitsa

(c) Yoga and other practices

a) Nidana parivarjana:

Nidana parivarjana refers to abstaining from samanya karanas responsible for the

vitiation of vatadi dosha, dushya 130-131 etc., and other risk factors like excess salt intake,

over weight, smoking, alcohol etc. These are highlited in the later part.

b) Satwavajaya chikitsa:

In Raktachapadhikyata manasika karanas also play an important role. Raja and

tama along with tridoshas vitiates hridaya and raktavaha dhamani’s. So Achara rasayana

is advised to prevent mana getting indulged in ahita arthas.

c) Yoga and other practices

The association between ongoing life stress and hypertension is very complex and

somewhat controversial. The most important measure is to combat sresses, strains,

anxiety and tensions. So Yoga helps in raising the capacity of mind to withstand pressure

of stresses and strains. Some of the yogas that can be advised are asanas that loosens the

joints like Bhujangasana, Shalabhasana, Vajrasana, etc. Pranayama and certain

relaxation techniques like Shavasana, Yoganidra etc. Other practices such as

Transcendental meditation, progressive muscle relaxation, self hypnosis, bio–feed back,

sudarshana kriya, etc., have also shown some promising results in recent times. Apart


from these upavasa that is told in Raktapradoshaja vikara can be adapted since it is

Raktadhistita roga 132.

Dravyabhoota Chikitsa

This includes –

(a) Amahara chikitsa

(b) Dosha pratyaneeka chikitsa

(c) Vyadhi pratyaneeka chikitsa

a) Amahara Chikitsa

In Raktachapadhikyata the ama produced due to agnidusti is one of the

contributing factor in the samprapti. So amahara chikitsa is to be adopted with the help

of deepana and pachana measures and even it is very much essential before any shodhana

procedure. For this the drugs that are having laghu, ruksha guna and that are pradhana in

katu, tikta rasa should be used.

b) Dosha Pratyanika Chikitsa

Since Raktachapadhikyata is a tridoshaja vatavyadhi, prime importance is to be

given for the treatment of vata. It is seen that most of the correlations points towards

avarana. So the principles of avarana chikitsa are as follows-

� In avrita vata first avaraka is to be treated. When both kapha and pitta are avaraka,

first pitta is to be treated 133 and care should be taken not to provoke the avaraka.

� In avarana the drugs that are snigdha and srotoshuddhikaraka are to be used and at the

same time these should not increase kapha.134

� The oushadha ahara which are not kapha pitta viruddha and which does vatanulomana

should be used. 135


� Madhura anuvasana basti with yapana basti can be given or depending on the bala of

rogi, mridu virechana can be given. 136

� Sarpi, taila, vasa, majja pana, abhyanga, basti can be done. Snehana, swedana,

nivatasthana nivasa, guru pravarana, madhura, amla rasa yukta ahara sevana,

dugdhadi brihmana dravya can be taken.

The shodhana chikitsa that can be adopted here are basti and virechana due to the

involvement of vata, virechana due to the involvement of pitta, lekhana basti 137 due to

the involvement of kapha and medas. Above all it is a Raktadhistita vyadhi, so the

shodhana procedures that can be adopted are virechana and raktamokshana. Following

are the general shodhana measures that can be thought of in Raktachapadhikyata.

1) Virechana: Virechana is a special treatment for pitta.138 It can also be given in certain

conditions like pitta pradhana dosha, kapha samsrusti and pitta sthanagata kapha139. It is

not only given in these conditions, but it is also a line of treatment for Vata 140. Virechana

is advised in rakta pradoshaja vikaras too 141. Thus virechana corrects the vata and pitta

there by reducing the blood volume and ultimately reducing the increased heart rate and

cardiac output. The drugs that can be used for virechana are trivrit, shyama, danti,

dravanti, saptala etc.

2) Basti: It is the pradhana chikitsa for vata. It is also useful in pitta, kapha, rakta,

samsarga dosha and sannipata Dosha 142. The tailas, which are used in basti, subdues the

ruksha, laghu and khara gunas of vata and helps in reducing the katinyata and produces

mardavata of blood vessels. Niruha helps in elimination of malas and doshas from all the

srotases. Lekhana basti told by Susruta 143 helps in reducing medas and in shareera

lekhana.


3) Raktamokshana: Sushruta recommends raktamokshana for vatavyadhi 144. Charaka

explains raktamokshana chikitsa for shonitaja roga or rakta pradoshaja vikara, as it is

raktadhistita vyadhi it can be recommended 145.

c) Vyadhi Pratyaneeka Chikitsa

Following are some of the Raktachapadhikyata shamaka dravyas and yogas, that

can be preferred.

Dravyas: Sarpagandha, Gokshura, Guggulu, Gomutra, Arjuna, Punarnava, Bala,

Pushkaramula, Brahmi, Jatamamsi, Musta, Shigru, Shatavari, Rasona, Kantakari, Vacha,

Erandamula, Shankhapuspi, Japa, Hareetaki, Vishnukranti, Parnayavani, Jyotishmati,

Bhringaraja etc.

Yogas: Prabhakara vati, Rasa sindhura, Shodashanga kashaya, Saraswatarista, Brahmi

vati, Brahma rasayana, Yogendra rasa, Amara sundaree vati, Pravala pisti, Rasaraja rasa,

Hridayeshwara rasa, Gokshuradi guggulu, Brihat vata chintamani rasa, Maha vata

vidhwamsa rasa, Chandrakala rasa etc.

Apart from these certain hridya and rasayana dravyas and yogas can be used.

Shirodhara is claimed to reduce high blood pressure. So by adopting the above line of

chikitsa, samprapti vighatana can be achieved, and also the prevention of the vyadhi can

be attained by non-pharmacological or adravyabhoota chikitsa. Thus by all these the

silent killer can be silenced to a great extent.

Single drugs used in treatment of hypertension:

Sarpagandhaa, punarnavaa, balaa, puskara moola, eranda moola, shankhapuspee,

guggulu, haritaki, gomootra, braahmi, mandookaparni, gokshura, jataamaansi, vachaa,

shigru, rasona etc.


Compound drugs used in treatment of hypertension:

Rasaraaja rasa, hridayeshvara rasa, pravaalapisti, chintaamani chaturmukha rasa,

brihata vata chintaamanirasa, amara sundari vati, yogendra rasa, brahma rasaayana,

brahmi vati, choona saarvasvataarista etc.

Management of contemporary medicine

There are numerous anti hypertensive drugs. According to their mode of action, the

blood pressure lowering drugs may be broadly classified into five major groups;

1. Diuretics (drugs that effect the electrolyte and water balance and

secondarily, the total peripheral resistance)

2. Betablockers and other adrenergic receptor blockers; (drugs that interfere

with the activity of the sympathetic system, including the a-b

adrenoreceptors)

3. Calcium antagonises

4. Vasodilators (acting directly on smooth muscle of arterioles)

5. A.C.E.Inhibitors (angiotensin convertor enzyme) (Drugs that interfere

with the renin angiotensin system)


Table -4STEP CARE TREATMENT OF HYPERTENSION

Step 4others, betablockers anddiuretics

Step 3Methyldopa

ACE inhibitors and Diuretics

Step2Betablockers

Calcium antagonists

Step 1vasodilators

A step care approach has been devised to use these drugs in a rational manner,

taking into account the characteristics of the patient and the degree of elevation of blood

pressure.

The simplest and most effective drugs are used first, in step 1. If they don’t

control blood pressure, step 2 drugs are used, and then those of step 3 and 4. In most

patients, it will not be necessary to reduce blood pressure rapidly. Indeed a gradual

lowering of blood pressure may be preferable, and a “stepped care” program may

simplify therapy and reduce side effects.

Treatment options for high blood pressure

Lifestyle changes can significantly improve a patient’s blood pressure. Definite

steps that can and should be taken to lower and control blood pressure include.

Quitting smoking is perhaps the most important thing a smoker can do to

promote his or hier own health. Among many other side effects, smoking elevates blood

pressure.


Loss of weight in the abdominal area can immediately reduce blood pressure and

helps to reduce the size of the heart. Weight loss accornpained by salt restriction may

allow mild hypertensives to reduce or eliminate their need for medication.

Following the DASH diet: Well –controlled studies have shown that people on

the DASH diet for only eight weeks experienced a significant reduction in blood pessure.

Hypertensive crises diagnosis and management 146

Severe hypertension is a common clinical problem encountered in various clinical

setting. Although various terms have been applied to severe hypertension, such as

hypertensive crises, emergencies, or urgencies, they are all characterised by acute

elevations in BP that may be associated with end-organ damage. The immediate

reduction of BP is only required in the patients with acute end-organ damage. Today,

wide ranges of pharmacologic alternatives are available to the practitioner to control

severe hypertension. Three quarters of those affected do not have their BP well

controlled. Less than 1% of these patients will develop one or multiple episodes of

hypertensive crises.

Headache, altered level of consciousness, and less-severe degrees of CNS

dysfunction are the classic manifestations of hypertensive encephalopathy. Advanced

retinopathy with arteriolar changes haemorrhages and exudates, as well as papilloedema,

are commonly seen on examination of fundi in the patients with hypertensive

encephalopathy. Cardiovascular manifestations of hypertensive crises may include angina

or acute myocardial infarction. Cardiac decompensatio mayleada to symptoms of

dyspnoea, orthopanoea, cough fatigue or frank fulmonryoedema. Severe injury to the

kidney may lead to renal failure with oliguria and or haematuria.


Figure 5

Initiation of Modern Treatment in Patients with Hypertension

Source – 1999 WHO

Assess other risk factors. TOD & ACC

Initiate life style measures

Stratify absolute risk

SBP 140 – 180 mm Hg or DBP 90 – 110 mm Hgon several occasions

(Stage I & II Hypertension)

Begin drugtreatment

Begin drugtreatment

Monitor BP &other risk factorsfor 3 – 6 months

Monitor BP &other risk factorsfor 6-12 months

SBP � 140 orDBP � 90Begin drugtreatment

SBP < 140 orDBP < 90Continue tomonitor

SBP � 150 orDBP � 95Begin drugtreatment

SBP < 150 orDBP < 95(Borderline)Continue tomonitor

Very High High Medium Low


Figure - 6

Showing the Approach to the Hypertensive Patient after Initiating

Antihypertensive Drug Treatment

Source – 1999 WHO

Stabilization, maintenance and follow up after initiation of drug therapy.Antihypertensive drug treatment initiated

Goal blood pressure achievedHigh & Very

High RiskMedium & Low

Risk

- See every 3months- Monitor BP& risk factors- Reinforcelife stylemeasures

- See every 6months- Monitor MonitorBP & risk factors- Reinforce lifestyle measures

Not at goal blood pressureafter 3 months

- If no response, substitute a drug orlow-dose combination from otherclasses.- If partial response, increase dose,add a drug from another class, orchange to low dose combination.- Intensify life style measures.

Significant sideeffects

- Substitute a drug orlow-dose combinationfrom other classes OR- Reduce dose and add adrug from another class

Hypertension difficult to manage

* Refer to specialist physician orclinic


Figure – 7

Algorithm for Treating Hypertension

Rasayana effect 147

A most important key for a long life according to Ayurveda is to follow aachara

rasayanas, meaning code of behaviour or code of ethics. According to Charaka, the

ancient authority on Ayurveda, the one who follows all codes of conduct, need not take

other rasayanas, and those who take other rasayanas without following this code of

conduct, do not receive the optimum benefits.


The traditional behavioral rasayanas help create a harmonizing effect in the

physiology and increase the production of Ojas. Ojas is the finest material that is

produced when digestion is flawless. Ojas is the link between consciousness and matter

and is responsible for establishing and maintaining balance among Vata, Pitta and Kapha.

The more the Ojas the body produces, the better the health and immunity from disease,

and happiness.

Achara Rasayana, as spoken of by Charaka emphasises on always speaking the

truth, not getting angry not indulging in alcoholic drinks, observing celibacy and the

sexual act according to the code. It insists on not being violent, avoiding over-exertion,

being calm and peaceful in mind and not hurting others with speech; speaking pleasantly.

One should always clean the ody by bathing and regular washing. One should be

courageous and not lose patience in any situation. One should donate always to others;

follow religious and virtuous acts according to one’s beliefs, respect teachers, priests,

elders, gurus, and all animals. One should not be cruel to any one and be merciful to all

those in need of help. Balance in waking and sleeping in the night must be maintained

and staying awake long in the night and sleep in daytime both must be avoided.

Several studies involving small numbers of people with hypertension showed a

reduction I blood pressure with the use of acupuncture, while these clinical trials were

conducted over a short period of time, the encouraging results suggest that it would be

worth while for scientists to conduct long term research of acupuncture for treating high

blood pressure.

Preliminary evidence suggests that people with high blood pressure who receive

chiropractic spinal manipulation experience a significant reduction in blood pressure, but


more research is needed to confirm its use for hypertension. In fact, on rare occasions, a

spinal manipulation session may actually cause extremely low blood pressure leading to

dizziness or light-headedness.

Massage may be particularly helpful for people with hypertension brought on by

stress. This is because the beneficial effects of massage are due, at least in part, to a

reduction in stress. One recent study revealed that people with hypertension who receive

massage, showed significant reductions in blood pressure and steroid hormones, an

indicator of stress. Although more studies are needed to evaluate the long-term safety and

effectiveness of massage, people with hypertension who tend to have high levels of stress

in their lives may benefit from massage therapy.

Although the association between ongoing life stress and hypertension is complex

and some what controversial many believe that relaxation techniques may be helpful in

alleviating feelings of stress, which is often a contributing factor to hypertension. While

the results of studies investigating this relationship have been mixed, one study of older

african americans living in an urban setting, found that those who participated in a

trancendental meditation (TM) or progressive muscle relaxation (PMR) programs had a

significant reduction in blood pressure compared to those who participated in a lifestyle

education program. While both techniques were beneficial. TM was twice as effective as

PMR.

In addition to TM and PMR other mind/body techniques such as self hypnosis and

biofeedback have shown promising results in recent studies. Biobeedback in particular

may reduce elevated blood pressure from stress and help individuals achieve healthy

lifestyle modifications, such as stopping smoking and losing weight.


Yoga treats stress in a holistic (body and mind) concept of the entire person.

Stress is stated to be a result of bad interaction between different layers, called koshas, of

human existence yoga aims to achieve a totally stress free state. According to yoga, the

mind plays the most imortant part in causing hypertension and does so in the following

ways.

Mental causes

Worries of any nature stagnating in the mind for a long time produce tension in

the mind, therefore causing disturbances in the emotional state of mind.

Pranic causes

Prana means breath of life. If prana is disturbed, it will in turn cause disturbance

in the energy systems of the body, known as the chakras. The chakras produce cyclic

changes in the hormones of the body and these in turn cause disturbances in the energy

systems of the body.

Physical causes

Abnormalities in lifestyle, such as sedentary habits, sleep disturbances,

unbalanced diet, smoking, and drinking alcohol, as well as others also disturbances in the

metabolic and circulatory systems.

Yoga offers a comprehensive and integrated approach for the treatment, as well as

the prevention of essential hypertension. The practice of yoga integrates the activities of

the mind with those of the body. Ayurvedic yoga describes a meeting between

physiology and consciousness nd focusses on vital locations called marma points in order

to achieve relaxation and peace of mind.


Breathing techniues for channel purification called nadi Shodhana can be used for

cleaning and detoxification. Finally, as the skin is the largest organ of the body and rich

in healing substances, panchakrama massage can be performed. When stimulated by

massage the skin produces anti-depressant, anti-cancer, anti-ageing substances and

promotes hormone release and healthy circulation. Last, but not least, don’t forget that

affection can always have strong emotional healing and stress reduction power.

A spiritual perspective 148

Life is the music played by soul the instrument of body. In this metaphor the body

is the instrument of the soul if the piano player is sick, does it help to repair his piano?

What an instrument produces depends not only upon the state of the instrument, but also

upon the musician. If the musician plays the blues, or soars with joy the instrument

follows. Even a tuned and polished instrument cannot soar with joy if the musician

chooses sadness or grief. In the case of our soul and body, the instrument becomes the

blues, or soars with joy. If the musician becomes consumed with grief, or anger, or

sadness, the instrument disintegrates. In some cases a broken instrument can be repaired,

but a repair at that level cannot cure what caused the breakdown.

All schools of medicine are silent on the root cause of hypertension. However it is

universally seen as a resistance to the flow of the blood and through it the life energy.

What could have caused this resistance? Clogged arteries? Increased viscosity of the

liquid of the blood? Is it is extra burden to the pump of the heart? Every school tells to

live align the way to minimise this resistance to reduce blood pressure. Allopathy calls it

life style modification, Ayurveda aachar Rasayana and numerous other names are given

to the same thing by different other schools.


A personality that walks along the path of its soul creates the human experience

that is healthy, harmoniums and full of growth and joy. Everything serves that.

Hypertension is true SOS- sound of soul – to save our lives from drowning in the sea of

sufferings. It must be heard and acted upon with responsibility. Drugs exercises, life style

modifications are important but insufficient. The core of the issue is the alignment of

splintered personality with the soul.

PATHYAPATHYA

In the treatment of diseases, diet and other habits are given equal importance with

drugs and therapeutic measures. The pathyapathya that can be recommended on the basis

of dosha dushyadi are as follows,

Table -5

Showing the Pathyapathya in Hypertension (Bhrama)

PATHYA APATHYA

AHARA Mudga, Masoora, Yava, Palaka,

Methica, Jambeera, Carrot, Papaya,

Dry grapes, Orange, Ardraka,

Rasona, Hingu, Jeeraka, Mareecha,

Jangala pakshi mamsa, Godugda,

Ajadugda, Takra etc.

Anupa desha pashu pakshi mamsa,

Dadhi, Dugda vikara, Tobacco, Tea,

Coffee, Salt, Fatty substances,

Alcohol, etc.

VIHARA Samyak vishrama, Upavasa,

Shavasana, Samyak vyayama,

Sadvritta palana, Nitya abhyanga,

Krodha-Irsha-Bhaya-Chinta-

Shokadi dharaneeya vega dharana,

etc.

Divaswapna, Ativyayama,

Avyayama, Vegadharana,

Adhyashana, Atichintana,

Atikrodha, Atishrama,

Atisukhasana, Ratri jagarana, etc.


Dietary recommendations 149

High blood pressure is mainly found in industrial rations that consume a diet high

in sugar animal protein and fat. Vegetarians have a much lower incidence of

hypertension.

A diet high in naturally occuring potassium and low in artifical sodium is

important in lowering blood pressure. Increase fruits and vegetables; apples, banas,

carrots, organes, potatoes zucchini and celery are all excellent foods to balance potassium

and sodium levels. Limit the use of table salt and food that high in sodium.

Cold water fish such as salmon, halibut, mackerel and herring have been shown to

reduce blood pressure. Consume fresh fish three times weekly.

Eat less red meat. Instead focus on legumes and vegetable protein foods. Eat more

garlic, onions, basil, oregano and gingerroot. These foods all have mild blood pressure

lowering effects.

Reduce or eliminate caffeine-it constricts the blood vessels walls and may

increase blood pressure. Some people with high blood pressure do well on a high protein-

low to medium carbohydrate diet. This is the premise of books such as the zone by Barry

sears and the atkins diet by Dr. Robert atkins. Check with your natural healthcare

practitioner before making radical diet changes.


Chapter-4

Methodologyn the present day mechanical life style individual is often put under

Stress 150 mood upsets, worries dietic irregularities, which becomes essential etiology to

impair rajoguna and aggravate Tridosha and causes corruption in rasavaha srotas. The

symptom which are expressed as Bhrama (Vertigo), Anga sada (Body pain), Shiroruja

(Headache), Nidra Nasha (Insomnia) shriaghoornam (dizziness), chittavasada (lack of

concentration), gatrasupta (numbness in the body), etc which makes one, day today

problems disturbance in body physiology 151.

In all the above said signs and symptoms, Bhrama becomes the major presenting

symptom, Brama 152 is explained as disease in Ayurvedic classics and also as symptom

under different context viz pittavruta vata 153, Rajapittanilahmaka 154 etc.

The signs symptoms of ‘Bhrama’ are in resemble to that of Hypertension at the

present context. Hypertension 155 represents a major public health concern. It affects

about a billion people worldwide and is the most common treatable risk factor for

cardiovascular disease in the patients aged over 50. Although 156 Hypertension is usually

a symptomatic for the first 10 to 20 years, it slowly but surely strains the heart and

damages the artery .For this reason Hypertension is often called as silent killer.

The adverse effects of Hypertension principally involve the blood vessels 157, the

central nervous system, the retina, the heart and the kidneys, with 158 this ends at organ

damage, mainly 159 in more than 95% of cases a specific underlying cause of

Hypertension cannot be found. Such patients are said to have Essential hypertension.

The pathogenesis of Essential hypertension is not clearly understood.


Large benefits, in terms of avoided cardiovascular disease, are expected from the

treatment of Hypertension 160. Thus the present study was proposed to check the effects

Bhramahara, Hypotensive, Cardio vascular restorative properties of herbal compound

“Kakubhadi lehya” with special reference to hypertension.

Till now about hypertension accepted dictums of the modern day that, the cause

of a majority of types of Hypertension is not known and the antihypertensives once

started are a must throughout the life for the management of Symptoms obviously

indicate the need of the day with this, all the Hypertensive drugs reduce the Blood

pressure without correcting the cause. Under such circumstances, the Ayurvedic

understanding and curative line of treatment gains much confidence.

In Veda’s and in Samhita granthas there is no direct reference or specific

nomenclature available in relation to Hypertension from classical textbooks. Even

though some of signs and symptomatologies mimic the situational condition of

Hypertension Therefore explanation of Hypertension in the language of Ayurveda is a

moot point till today.

So far nomenclature claimed as Hypertension in Ayurveda are Raktachapa,

Raktabharadhikyata, Raktapeedanadhikyata etc. But as a matter of translation or

transliteration from English, the word and condition at Hypertension refers to “Bhrama”

approximately as it implies to the condition giddiness.

Moreover, charaka12 has very clearly expressed all the diseases (Disorders) or

states of illness, may not be known with specific modalities of classification and offered

as way to introduce new diseases or conditions in to the nomenclature there by no

definite and permanent name can be attributed to a particular condition as it is expected


to change with the time to time according to its presentation 161. Thus understanding the

dosha state, site of appearance and its signs and symptoms may have to treat the

conditions on the basis of vilkalpa i.e combinations and permutations.

But Ayurveda 162 mainly speaks and considers Bhrama as a disease entity, it’s

literal meaning is rotation. In 163 charaka sutrasthna has considered Bhrama as one out of

the vataja nanatmaja Vyadhi, here Bhrama Correspond to giddiness and Vertigo. Bhrama

is a disease not only concerned to the Shiras 164 but also considered in Raktapradoshaja

Vyadhi's. As Tamasascha atidarshanam, Chakra panidatta has explained Bhrama as a

Smruti mohna that means hallucination in his commentary. Vagbhata has mentioned that

this is because of Vradhi 165 of vata dosha and kshaya 166 of kaphadosa, where as Charaka

affirmed 167 it as sanchaya of vata dosha blocked by vitiated pitta dosha. Therefore

Bhrama explained as a Nidanarthakaravyadhi of some diseases. It is also said as signs

and symptom (Lakshana), and upadrava (complication) of many diseases as like

Hypertension.

Hypertension is the other major risk factor in the development of atherosclerotic

IHD and cerebro-vascular disease. It acts probably by mechanical injury to the arterial

wall due to increased blood pressure. A systolic pressure of over 160 mm Hg or a

diastolic pressure of over 95mmHg is associated with five times higher risk of developing

IHD than in people with blood pressure with blood pressure within normal range (140/90

mm Hg or less) 168.

In contemporary medicine the principle etiological factor of Hypertensive disease

is psychological factor. Psychological over strain leads to impaired regulation of the

vascular tone. In general this hypothesiss is at the support of Ayurvedic dosha, Vata

interference in producing Bhrama. Thus the Hridhya, Bhramahara, Vatanulomaka,


srotosodhaka as well as Rasayana modalities are grouped under “KAKUBHADI

LEHYA” as Hridya Rsayana from Bhaisjya Ratnavali is to be undertaken for the study.

METHODS OF STUDY

I) Source of data:

a) Patient suffering from “Bhrama” (Hypertension) will be selected from

PGSandR Department of Kayachikitsa OPD/IPD of D.G.M. Ayurvedic

Medical College and Hospital under pre-set inclusion and exclusion criteria.

b) Literary: Literary aspect of study will be collected from classical Ayurvedic

text’s updated with recent medical journals, Magazines and Meddler search.

c) Trial Drug: “KAKUBHADI LEHYAM” 169

II) Method of Collection of Data:

a) STUDY DESIGN

Prospective Clinical Trial

b) SAMPLE SIZE:

Minimums of 30 patients are taken in randomized selection.

c) EXCLUSION CRITERIA: 170

i) Secondary Hypertension patients --

1) Renal complication. --

A) Reno vascular.

B) Renal parenchymal diseases.

2) Endocrine --

A) Adrenocortical hyperfuction.

B) Hyperparathyoidism.

C) Oral contraceptives.


3) Coarctation of Aorta.

4) Neurogenic.

ii) Severe (stage 3) very severe (stage 4) Maligant HTN

iii) Below 25 years and above 65 years.

iv) Alcohol abuses.

v) Left ventricular hypertrophy.

vi) Left ventricular failure.

vii) Essential Hypertension with I.H.D.

viii) Essential hypertension with diabetes.

x) Lactating and pregnant females.

xi) Iatrogenic hypertension – Hypertension due to administration of drugs--

1) Estrogen.

2) Abuse of Compounds containing glycyrrhetive acid – (Liquorice

biogastrone).

3) Abuse of vaso – Constrictive nasal drops.

4) Abuse of analgesics, which may lead to renal lesions--

- Hormonal Contraceptives.

- Liquorice and Carbenoxolone.

- ACTH and cortico steroids.

d). INCLUSION CRITERIA:

i) Other than that of exclusive criteria mentioned above and

ii) A patient of both sexes indiscriminately.

iii) No discriminations of chronically and severity of disease.

iv) Patients with recently detected.


v) Both mild and Moderate, Hypertension that is – 171

1. High normal – 130-139/85-89 mm Hg

2. Mild (stage –I) – 140-159 /90-99 mm Hg

3. Moderate (stage –2) – 160-179 /100-109 mm Hg.

vi) Essential Hypertension with --

i. Genetic factors

ii. Racial and environmental factors.

iii. Risk factors modifying the course

iv. Untreated cases of Essential hypertension

e) CRITERIA OF DIAGNOSIS 172

1) Diagnosis is made on the basis of measurements of

sphygmomanometer.

2) Diagnosis as described by the joint national committee of the WHO/

International society (ISH) of Hypertension (1995)

Approach to the patients with hypertension methods 173

Since there is no dividing line between normal and high blood pressure, arbitrary

levels have been established to define persons who have an increased risk of developing a

morbid cardiovascular event and/or will clearly beniefit from medical therapy. These

definitions should take into account not only the level of diastolic pressure but also

systeolic pressure, age, sex, and race. For example, patients with a diastolic pressure

greater than 90 mm Hg have a significant reduction in morbidity and mortality rate if

they receive adequate therapy. These, then, are patients who have hypertension and who

should be considered for treatment.


The level of systolic pressure is also important in assessing the influence of

arterial pressure on cardiovascular morbidity. Males with normal diastolic pressure

(<82mmHg) but elevated systolic pressures (>158mmHg) have a cardiovascular mortality

rate 2.5 times higher than individuals who have similar diastolic pressures but whose

systolic pressures clearly are normal (<130mmHg). A reduction in mortality and

morbidity with treatment, specifically in the elderly, has been documented in these

patients. This beneficial effect results mainly from a reduction in strokes and occurs in

women as well. Other significant factors that modify the influence of blood pressure on

the frequency of morbid cardiovascular events are age, race, and sex, with young black

male being most adversely affected by hypertension.

When hypertension is suspected, blood pressure should be measured at least twice

during two separate examinations after the initial screening. In adults a diastolic pressure

below 85mmHg is considered to be normal; one between 85 and 89mmHg is high

normal; one of 90 to 104mmHg presents mild hypertension; one of 105 to 114mmHg

represents moderate hypertension; and one of 115 mmHg or greater represents severe

hypertension. When the diastolic pressure is below 90 mmHg, a systolic pressure below

140 mmHg indicates normal blood pressure; one between 140 and 159 mmHg indicates

borderline isolated systolic hypertension and one of 160 mmHg or higher indicates

isolated sstolic hypertension. Increasing use of 12 or 24 hours blood pressure monitoring

may provide additional useful information in the patients who are difficult to classify.

However normal values for this procedure and its usefulness in relation to therapeutic out

come are not currently known.


Patient evaluation

In evaluating patients with hypertension the initial history, physical examination,

and laboratory tests should be directed at

1. uncovering correctable secondary forms of hypertension

2. establishing a pretreatment baseline

3. assessing factors that may influence the type of therapy or be changed

adversely by therapy

4. determining if target organ damage is present and

5. determining whether other risk factors for the development of arteriosclerotic

cardiovascular disease are present

Ideally, this evaluation also would determine the underlying mechanisms in

essential hypertension, particularly if such information leads to a more specific

therapeutic program. Unfortunately, at present this aspect of the evaluation is limited by

lack of knowledge of some of the underlying mechanisms, by uncertainty as to the

correct treatment for a distinct subset even if the underlying mechanisms are known, or

by the prohibitive cost of defining a subset of hypertensive patients even if specific

therapy were available. However with the accumulation of additional information, this

sixth component of the evaluation of patients with hypertension may become increasingly

important.

Symptoms and signs most patients with hypertension have no specific symptoms

referable to their blood pressure elevation and are identified only in the course of a

physical examination. When symptoms do bring the patient to the physician, they fall

into three categories. They are related to -


1. the elevated pressure it self,

2. the hypertensive vascular disease and

3. The underlying disease, in the case of secondary hypertension.

Though popularly considered a symptom of elevated arterial pressure, headache is

characteristic only of severe hypertension; most commonly such headaches are localized

to the occipital region and are present when the patient awakens in the morning but

subside spontaneously after several hours. Other complaints that may be related to

elevated blood pressure include dizziness, palpitations, easy fatigability and importance.

Complaints referable to vascular disease include epistaxis, hematuria, blurring of vision

owing to retinal changes, episodes of weakness of dizziness due to transient cerebral

ischemia, angina pectoris, and dyspnea due to cardiac failure. Pain due to dissection of

the aorta or to a leaking aneurysm is an occasional presenting symptom.

Examples of symptoms related to the underlying disease in secondary

hypertension are polyuria, polydipsia, and muscle weakness secondary to hypokalemia in

patients with primary aldosteronism or weight gain and emotional lability in patients with

cushing’s syndrome. The patient with a pheochromocytoma may present with episodic

headaches, palpitations, diaphoresis, and postural dizziness.

History

A strong family hostory of hypertension, along with the reported finding of

intermittent pressure elevation in the past, favors the diagnosis of essential hypertension.

Secondary hypertension often develops before the age of 35 or after 55 or after 55. A

history of use of adrenal steroids or estrogens is of obvious significance. A history of

repeated urinary tract infections suggests chronic pyelonephritis, although this condition


may occur in the absence of symptoms; nocturia and polydipsia suggest renal or

endocrine disease, while trauma to either flank or an episode of acute flank pain may be a

clue to the presence of renal injury. A history of weight gain in compatible with

Cushing’s syndrome, and one of weight loss is compatible with pheochromocytoma. A

number of aspects of the history aid to determining whether vascular disease has

progressed to a dangerous stage. These include angina pectoris and symptoms of

cerebrovascular insufficiency. Congestive heart failure, and or peripheral vascular

insufficiency. Other risk factors that should be asked about include cigarette smoking,

diabetes mellitus. Lipid disorders, and a family history of early deaths due to

cardiovascular disease. Finally, aspects of the patients’s lifestyle that could contribute to

the hypertension or affects its treatment should be assessed, including diet, physicl

activity, family status, work, and educational level.

Physical examination

The physical examination starts with the patients’ general appearance. For

instance are the round faces and truncal obesity of cushing’s syndrome present is

muscular development in the upper extremities out of proportion to that in the lower

extremities, suggesting coarctation of the aorta? The next step is to compare the blood

pressure and pulses in the two uper extremities and in the supine and standing positions

(for at least 2 min). A rise in diastolic pressure when the patient goes from the supine to

the standing position is most compable with essential hypertension; a fall, in the absence

of antihypertensive medications, suggests secondary forms of hypertension. The patient’s

height and weight should be recorded. Detailed examination of the ocular fundi in

mandatory, as funduscopic findings provide one of the best indications of the duration of


hypertension and prognosis. A useful guide is the keith-wagener barker classification of

funduscopic changes the specific changes in each fundus should be recorded nd a grade

assigned. Palpation and ausculatation of the carotid arteries for evidence of stenosis or

occlusion are important narrowing of a carotid artery may be a manifestation if

hypertensive vascular disease and it also may be a clue to the presence of a renal arterial

lesion, since these two lesions may occur together. In examination of the heart and lungs,

evidence of left ventricular hypertrophy and cardiac decompensation should be sought. Is

there a left ventricular lift? Are third and fourth heart sounds present? Are there

pulmonary rales? A third heart sound and pulmonary rales are unusual in uncomplicated

hypertension. Their presence suggests ventricular dysfunction. Chest examination also

includes a search for extracardiac murmurs and palpable collateral vessels that may result

from coarctation of the aorta.

Basic test for intial evaluation

Always included

1. urine for protein, blood and glucose

2. hamatocrit

3. serum potassium

4. serum cretinine and /or blood urea nitrogen

5. electrocardiogram

- Usually included, depending on cost and other factors

1. microscopic urinalysis

2. white blood cell count

3. plasma/blood glucose, cholesteril, HDL cholesterol, and

triglycerdes

4. serum calcium phoshate and uric acid

5. chest x-ray echocardiogram

-Special studies to screen for secondary hypertension


v Renovascular disease angiotension coverting enzyme inhibitor renogram,

renal duplex ultrasound.

v Pheochromocytoma; 24-h urine assay for cretinine, metaephrines, and

catecholamines or plasma catecholamines

v Cushing’s syndrome; overnight dexamethasone suppression test or 24-h urine

cortisol.

Tabel - 6

Key items of the baseline physical and laboratory examinationsin patients with mild or moderate hypertension

Physical examination

GENERALAppearanceBloodpressure(supine orsiting;standing;both arms)heart rate(supine orsitting;standing)

HEENT #

Carotid bruitFundiNeck veinsTemporalarteriesThyroidgland

CHEST

AorticregurgitationApeximpulseBreastRalesS3, S4

SystolicmurmurWheezes

ABDOMEN

BruitPalpablekidneys

EXTREMITIESEdemaPeripheralpulsesPeripheralbruits

NEUROLOGICFocal signsProximalmusclestrength

Laboratory examination

GENERAL

HemoglobinHematocritWhite blood cellcount

KIDNEYS

Blood urea nitrogenCreatinineUrine dipstickUrine sediment

METABOLIC

CalciumCholesterol *Glucose (fasting)PotassiumUric acid

MISCELLANEOUS

Chest x rayECGEchocadiogram

* Also obtain fasting triglyceride and high density lipoproteine cholestrol levels if theserum cholestrol level is 200mg/dl or more in patients with other cardiovascular risk factoror 240 mg/dl or more in patients with out other cardivascular risk factors.# HEENT = head, eyes, ears, nose, and throat.


Patients who monitor their blood pressure at home have a lower clinic blood

pressure than those whole blood pressures is monitored in the healthcare system 174. A

greater proportion of them also achieves blood pressure targets when assessed in the

clinic.

f) POSOLOGY –

Internal 5gms twice daily.

g) STUDY DURATION –

30 Days.

h) FOLLOW UP –

15 days.

Assessment of Result:

The clinical data and sphygmomanometer studies assess results. Subjective and

objective parameter to the baseline data compared to after treatment data for the

assessment of results.

i) Subjective parameter:

As shown in the classical (Bhrama) and Contemporary texts (Hypertension)

j) Objective parameters:

1) BLOOD PRESSURE

A) Standing

B) Sitting

C) Lying down posture – These have been recorded in seven

visits, under study duration.


2) LIPID PROFILE

Laboratory investigations

a) Serum cholesterol

b) Serum triglycerides

c) High-density lipoprotein cholesterol (HDL)

d) Low density lipoprotein cholesterol (LDL).

e) Very low density lipoprotein cholesterol (VLDL)

k) Investigations for exclusion:

X-ray.

Electro cardio gram (ECG)

Random Blood sugar (R.B.S) -- Are to be under taken.

By these above parameters, in order to assess the severity of illness and

the effect of treatment each case will be evaluated prior to commencement of treatment

and periodically during the course of treatment and also after the completion of treatment

respectively. The assessment was made with systolic, diastolic and with mean arterial

blood pressure and the results will be assessed based on the lipid profile and Blood

pressure findings and also the signs and symptoms of Bhrama as per classics for which

students paired t-test will be applied.

III) MATERIALS OF TRAIL

Preparation of Medicine:

All the drugs will be identified and collected from local area. Good manufacturing

practice will be followed for preparation of Avalehya. As above mentioned Kakubhadi

Lehya is explained in choorna kalpana, but for easy administration and to attain the

Rasayana effect it is formulated in the form of avalehya.


The detailed study of the Kakubhadi Lehya with its content analysis and

preparation of the Kakubhadi Lehya is as follows. The combination and properties of

Kakubhadi Lehyam is as Follows.

Table – 7

Contents and Proportion of Kakubhadi Lehya

Sanskrit name Latin name Family Proportion

1. Arjuna 175-340-341 Terminalia arjuna Combretaceae 1 Part

2. Vacha 176-342-343 Acorus calamus Araceae 1 Part

3. Rasna 177-344-345 Pluchea lanceolata Zingiberaceae 1 Part

4. Bala 178-179-180 Abatilon indicum Malvaceae 1 Part

5. Nagabala 181-183 Grewia hirsute Tiliaceae 1 Part

6. Abhaya 184-186 Terminalia chebula Combretaceae 1 Part

7. Shati 187-189 Curcuma zedooria Zingiberaceae 1 Part

8. Pushkaramula190-192

Innula vacemosa Compositteae 1 Part

9. Pippali 193-195 Piper longum Piperaceae 1 Part

10. Vishwabheshaja196-198

Zingiber officinale Scitaminae 1 Part

The chosen drug “Kakubhadi Lehya” assumed as the best Hrudya Rasayana

because of its contents and in further its action towards the Bhrama vis-à-vis

hypertension. The ingredients are botanically identified and under the GMP stipulations

with equal quantities of the ingredients are formulated as Lehya. The individual drug

pharmaco dynamics are tabulated as under –


Table – 8

Describing the pharmacological properties of Kakubhadi Lehya

Name of theingredient

Rasa Guna Veerya Vipaka Prabhava

1) Arjuna Kashya Rookshalaghu

Sheeta Katu HrudyaMutrala

2) Vacha Katu tiktha Laghutikshnasara

Ushna Katu MedhyaKaphaharaMootrakruchrahara

3) Rasna Tikta Guru Ushna Katu VishagnaKaphavataharaSwasaharaUdarahara

4) Bala Madhura Guru,Snigdha,picchila

Madhura Madhura VatapittaharaAnulomakaMutralaNidrakaram

5) Nagabala Madhura,kashaya

Guru,Snigdha,picchila

Sheetha Madhura VatapittaharaMutralaMutrakruchrahara

6) Abhaya Kashaya,Tikta, katu,madhura,Amla

Laghu,Rooksha

Ushna Madhura TridoshaharaRechakaRasayanamAyushyamHrudrogaharamTwakdoshaharamShothaharam

7) Shati Katu, tikta,kasaya

Laghu,tikshna

Ushna Katu MutralaDeepanaPachanaKasa-Swasa hara

8) Pushkaramula Tikta katu Laghu,Tikshna

Ushna Katu VatakaphaharaKasa-Swasa haraPanduhara (RN)

9) Pippali Katu Laghu,Snigdha,tiksshna

Anushnasheeta

Madhura VatakaphaharaYogavahiDeepanaPachanaRechanaUdarahara

10) Vishwabheshaja Katu Guru,rooksha,tikshna

Ushna Katu Kapha haraAmavataharaHrudrogaharaGrahiPanduhara


Table – 9

Describing the therapeutic values of Kakubhadi Lehya


Indications Preparations

1) Arjuna Bhagna, hrudroga, kshaya,trushna, sadhyavruna, prameha

Kakubhadi Churna, arjunarishta,arjunagrutha

2) Vacha Unmada, apasmara, jwara Saraswatha Churna, medhyaRasayana

3) Rasna Shotha, Swasa, vatashoola ,kasa, jwara

Rasnadi kwatha, rasnadi taila,rasnadi ghruta

4) Bala Vrunashotha, pakshaghata,Ardhita, gruhani, hrudroga,hrudourbalya, raktapitta,urahkshata, Mootrakrichra jwara

Baladi kwata, baladi ghruka,baldhyarishta, chandana balalakshadi taila

5) Nagabala Rakta srava, kshata vruna,vatavyadhi, amlapitta,hrudhroga, Rakta Pitta, kasa,Swasa, urakshata, yakshma,mootra kruchra,vishmajwara,dourbalya

Naga bala ksheera, nagabalapayasa, naga baala Rasayana

6) Abhaya Gulma,arsha, kamala, gruhani,hrudhdaurbalya, vatarakta,shoota, kasa, Swasa hika,Mootrakricchra, mootraghata,visharpa

Abhaya modhaka, abhuya rishta,pathyadi vati, vyaghri haritaki,chitraka haritaki, pathyadi Churna

7) Shati Swasa kasahika, udarashoola,hruddourbalya, arsha, rakthaviksheena, twakdosha,

Satyadi Churna, satyadi Vata.

8) Pushkaramula

Agnimandhya, vatavikara,hrudhyashoola, hika swasa,parshwa shoola, jwara, shotha,pandhu, meda vrudhi.

Pushkara mooladhi Churna,pushkaradhi Churna

9) Pippali Hrudhadourbalya, pandu,raktavikara, kasa, Swasa, aruchi,Agni mandhya, kshata.

Guda pippali, pippali khada,pippalyasava

10) Vishwabheshaja

Hrudourbaya, hrutshoola,shlipadha, shota, amvata ,sheethaPitta

Ardrakakhanda, panchasamaChurna, samasharkara Churna,rasnadi kwatha, soubhagya shunthi ,shunthi sura


Table – 10

Describing the Chemical constituents of Kakubhadi Lehya


Chemical constituents

11) Arjuna B-sitostirol, elagic acid, arjunoic acid, arjuna glycosides, arjunetin,fridelin, Tenin – 20-25%, Calcium – 0.33%, Magnesium – 0.78%,Alumunim – 0.076%,In fruits – 7-20% tannin present

12) Vacha In rhisome 1.5-3.5 volatile oil is present in that asaryl aldehyde inthat two active acidic that is A-asarone B-asarone are present otherchemical components like acorin, augenol, caffine

13) Rasna In leaves – kwarsitin and aisoraimanetin, and in panchanga pluchinis present

14) Bala Ksharabha (acidic) 0.085%, in seed 0.32% Ksharabha (acidic)present main Ksharabha (acidic) i.e., eqhdrine with these steroied,phaitostirol, ral, ral acid, musin, and potassium nitrate.

15) Nagabala B- phenenthylamines quinazoline, gossypol, steroculic acid,linoleic acid etc/

16) Abhaya Tanin – 24.6-32.5 in that chebumagic acid corilagin and 18 aminoacids phosphoric, succinic, clinic, shikimic acid, and yellow colouroil. Is present about 36.4%

17) Shati The dried rhizomes of commerce yield, 4% of an essential oil withthe characteristic odour and pungent taste of rhizomes. It containsstarch 52% carbonic acid a glycocide, and ash 46% the principleconstituent of the oil is the ethyl ester of p- methoxy cinnamic acid.

18) Pushkaramula Inulin-10%, Volatile -1.3%, Contents:- oiland alantolactone and itis called as teevra krimighna.

19) Pippali Volatile oil – 0.8%, Piperine – 4-5%, Pipalatine and sesamine andpiplasterol- 0.15- 0.18% and pipalartin-0.13-0.20% piperlanguminon, steroid, glycoside

20) Vishwabheshaja Dry Ness 80.9, protein 2.6, fat 0.9, fibre 2.4, carbohydrate 12.3,metals 1.2%, calcium 20, phosphorus 60, iron 2.6 mg, each 100 gmother then these iodine chlorine are also present vitamin A,B,C arealso present

Preservation of the Medicine:

The prepared medicine is preserved in the glass jars of 500 gms quantity with air tight

sealing. As on the patients approached and fit under the norms of the trail the Kakubhadi

Lehya is distributed at regular intervals.

Periodical check-ups are under taken as par the norms and pre-determined

parameters.


CHAPTER-5

RESULTSresent study registers 30 patients, out of 68 approached patients.

Out this, 2 patients were discontinued hence their data has not been included in the

assessment. The remaining 28 patients of Bhrama viz. Hypertension, fulfilling the criteria

of diagnosis and inclusive criteria were included in the study.

All the patients were examined before and after the trail, according to the case

sheet format given in the annex. Both the subjective and objective criteria were recorded.

The data recorded are presented under the following headings.

A. Demographic data

B. Evaluating disease Data

C. Result of the Kakubhadi Lehya in Bhrama viz. Hypertension and

D. Statistical analysis of the clinical and objective parameters

A) Demographic data:

The details of Age, Gender, Religion, and Occupation etc. of the 28 patients is as

follows.

A1) distribution of patients by Age

Age – gender distributions Observation and Results:

An interval of 10 has considered from the ages 25 to 65 as discussed in the

methods. In the study it is revealed that stress is continued from the ages of 25 onwards

and as age advances the sample are settled. At the older age group of 55-65 only 2

(10.52%) patients are reported. Where in 25-35 and 35-45 age groups reported with 6

(31.5%) patients in each group. 45-55 age group reported with the 5 (26.4%) patients


with the symptoms of Bhrama vis-à-vis hypertension. The tabulations are depicted as

under.

Table- 11

Distribution of patients by Age- gender

Male patients Female patients Total patientsAge

Number % Number % Number %

25-35 6 31.5 0 0 6 20

35-45 6 31.5 1 9.1 7 23.4

45-55 5 26.4 1 9.1 6 20

55-65 2 10.6 9 81.8 11 36.6

Total 19 100 11 100 30 100

Table- 12

Distribution of Male patients by Age

Age

Tot

al n

o of

patie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

% Not

Res

pond

ed%

Dis

cont

inue

d

%

25-35 6 31.5 4 66.6 2 33.3 0 0 0 0 0 0

35-45 6 31.5 1 16.6 2 33.3 2 33.3 0 0 1 16.6

45-55 5 26.4 4 80 0 0 0 0 0 0 1 20

55-65 2 10.6 0 0 0 0 1 50 1 50 0 0

Total 19 100 9 4 3 1 2

Here in this study an attempt is made to understand the male female responses to

the management with respect to that of the age groups.


Observations of well-responded group in the Male gender comparison is, 25-35

interval 4 (66.6%) patients, 35-45 interval 1 (16.6%) patient, 45-55 interval 4 (80%)

patients and 55-65 interval no patients in the study. Observations of Moderately

responded results group in Male gender comparison is, 25-35 interval 2 (33.3%) patients

and 35-45 interval and 2 (33.3%) patients. Observations of responded results group in

Male gender comparison is 35-45 interval 2 (33.3%) patients and 1 (50%) in 55-65

interval and no patients in other groups of the study. Observations of not-responded

group in the Male gender comparison are 1 patient of 55-65 is found. One each of the

males discontinued from the age groups of 35-45 and 45-55.

Table- 13

Distribution of Female patients by Age

Age

Tot

al n

o of

patie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

% Not

Res

pond

ed

%

Dis

cont

inue

d

%

25-35 0 0 0 0 0 0 0 0 0 0 0 0

35-45 1 9.1 0 0 0 0 1 100 0 0 0 0

45-55 1 9.1 0 0 1 100 0 0 0 0 0 0

55-65 9 81.8 0 0 1 11.1 6 66.6 2 22.2 0 0

Total 11 100 0 2 7 2 0

At the female side of the results major number (9 cases – 81.8%) of the cases are

from the 55-65 age group. No patients reported at the 25-35 class of age group. One

patient (9.1%) reported from that of 35-45 age group responded to the treatment. Out of 1

(9.1%) patient of the age group of 45-55 has moderately responded to the treatment. The


major group of the 55-65 in females has the no patients of well responded and

discontinued. Many i.e. 6 (66.66%) patients responded to the treatment and 1 (11.1%)

patient moderately responded and 2 (22.22%) patients have not responded to the

management in the study.

Graph – 1

DISTRIBUTION OF PATIENTS BY AGE – GENDER

The observation of this study suggests that the hypertension is directly

proportional to that of age in the females and inversely proportional in the male

populations. The pictorial representation is as under.

DISTRIBUTION OF PATIENTS

BY AGE - GENDER1

1

92

6

5

60

0 2 4 6 8 10

25-35

35-45

45-55

55-65

Female 0 1 1 9

Male 6 6 5 2

25-35 35-45 45-55 55-65


A2) Distribution of patients by Gender

Table- 14

Distribution of patients by Gender in Bhrama

GenderT

otal

no

ofpa

tient

s% W

ell

Res

pond

ed

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Female 11 36.67 1 9.09 2 18.2 5 45.4 3 27.3 0 0

Male 19 63.33 8 42.1 4 21.1 5 26.3 0 0 2 10.5

Total 30 100 9 6 10 3 2

Graph - 2

Distribution of patients by Gender in Bhrama

GENDER DISTRIBUTION

Male63.33%

Female 36.67%


Gender distributions Observation and Results:

The male female ratio in the study is 19:11 patients. The percentage of the

distribution does not show any gender differentiation to get this anxiety-related disease.

The observations are 19 Patients i.e. (63.33%) male and 11 patients i.e. (36.67%) were

female.

As the results observed, out of 19 (63.33%) males, 8 (42.1%) patients well

responded, 4 (21.05%) patients moderately responded, 5 (26.31%) patients responded, 2

(10.52%) patients of discontinued are recorded. As the results observed, out of 11

(36.67%) female, 1 (9.09%) patient well responded, 2 (18.18%) patients moderately

responded, 5 (45.45%) patients responded and 3 (27.27%) patients of not responded are

recorded.

A3) distribution of patients by Religion

Table- 15

Distribution of patients by Religion

Religion

Tot

al n

o of

patie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

% Not

Res

pond

ed

%D

isco

ntin

ued

%

Hindu 25 83.3 8 32 6 24 7 28 2 8 2 8

Muslim 5 16.7 1 20 0 0 3 60 1 20 0 0

Christian 0 0 0 0 0 0 0 0 0 0 0 0

Others 0 0 0 0 0 0 0 0 0 0 0 0

Total 30 100 9 6 10 3 2


Religion distributions Observation and Results:

At the results observed, out of 25 (83.3%) of Hindu patients, 8 (32%) patients

well responded, 6 (24%) patients moderately responded, 7 (28%) patients responded, 2

(8%) patients of each not responded and discontinued are recorded. On the other hand the

results observed at Muslim community are, out of 5 (16.7%), 1 (20%) patient well

responded, 3 (60%) patients responded and 1 (20%) patient not responded. The graphical

representation is as under.

Graph – 3

Distribution of patients by religion

A4) Distribution of patients by Occupation

At the results observed, out of 8 (26.6%) of sedentary patients, 1 (12.5%) patient

is well responded, 1 (12.5%) patient moderately responded, 4 (50%) patients responded

and 2 (25%) patients not responded. At the active group, out of 20 (66.6%) patients, 8

Christian 0.00%

Hindu83.33%

Muslim16.67%

Others0.00%


(40%) patient well responded, 4 (20%) patients moderately responded, 6 (30%) patients

responded and 2 (10%) patients discontinued. At the results observed, out of 2 (6.67%) of

Labour patients, 1 (50%) patient moderately responded and another patient (50%) is not

responded. The tabulation and graphical representation is as under.

Table- 16

DISTRIBUTION OF PATIENTS BY OCCUPATION

Occ

upat

ion

Tot

al n

o of

patie

nts

%W

ell R

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Sedentary 08 26.6 1 12.5 1 12.5 4 50 2 25 0 0

Active 20 66.6 8 40 4 20 6 30 0 0 2 10

Labour 02 6.67 0 0 1 50 0 0 1 50 0 0

Total 30 100 9 6 10 3 2

Graph - 4

DISTRIBUTION OF PATIENTS BY OCCUPATION

PATIENTS BY OCCUPATIONActive66.67%

Sedentary26.67%

Labour6.67%


A5) Distribution of patients by economic status

Table- 17

Distribution of patients by Economic statusE

cono

mic

sta

tus

Tot

al n

o of

patie

nts

%

Wel

l Res

pond

ed

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Poor 2 6.6 0 0 1 50 0 0 1 50 0 0

Middle 15 50 5 33.3 2 13.3 6 40 2 13.3 0 0

Higher

Middle13 43.4 4 30.7 3 23.1 4 30.7 0 0 2 15.4

Higher 0 0 0 0 0 0 0 0 0 0 0 0

Total 30 100 9 6 10 3 2

Economic status distribution Observation and Results:

At the results observed, out of 2 (6.6%) of poor patients, 1 (50%) patient is

moderately responded and 1(50%) patient is not responded. Out of 15 (50%) of Middle

class patients, 5 (33.3%) patient is well responded, 2 (13.3%) patients moderately

responded, 6 (40%) patients responded and 2 (13.3%) patients not responded. From

higher middle class 13 (43.4%) patients reported and out of them 4 (30.7%) patients are

well responded, 3 (23.1%) patients moderately responded, 4 (30.7%) patients responded

and 2 (15.4%) patients are discontinued. No patients are reported from the higher class of

classification. The pictorial graph is as follows.


Graph- 5

DISTRIBUTION OF PATIENTS BY ECONOMIC STATUS

B) Data related to the disease.

B1) Distribution of patients by presenting complaints

Table-18

Presenting complaints Patients Before Percentage

Bhrama 30 100

Shira shoola 20 66.6

Angasada 14 46.6

Nidranasha 13 43.33

Hrudrava 7 23.33

Klama 6 20.0

Urah shoola 2 6.7

2

15

13

00

2

4

6

8

10

12

14

16

Poor Middle Higher Middle Higher

by economical statusPatients


As the above table explains about the different symptoms evaluated at the study

under the heading of Bhrama vis-à-vis hypertension with the presenting complaints are

foot forth here. The first and fore most complaint is Bhrama i.e. giddiness. All the

patients in the study (100%) reported the Bhrama. The next most common complaint is

shira shoola i.e. headache. 20 patients (66.6%) reported with the headache. The third

complaint is angasada, with the 14 (46.6%) patients and associated with the nidranasha

(Sleeplessness) of 13 (43.3%) patients. Not at the least but still the patients reported with

the complicate complaints such as Hrudrava (7 patients – 23.33%), Klama (6 patients –

20%) and Urah shoola (2 patients – 6.7%). The graphical representation is as under.

Graph – 6

Distribution of patients by presenting complaints

B2) Distribution of patients by Associated features

As many as features are associated with the study Bhrama vis-à-vis hypertension

with the associated complaints are foot forth here. Many complaints of associative are not

Distribution by Presenting Complaints

30

20

14

13

7

6

2

0 5 10 15 20 25 30 35

Bhrama

Shira shoola

Angasada

Nidranasha

Hrudrava

Klama

Urah shoola


observed in the study. Toxemia, Transient Ischemic attack, Pakshaghatha and Ardita vata

is not observed in the study. Common complaint is medoroga with 7 patients (23.33%)

followed by Asthma with 5 (16.6%) patients and the last associated complaint observed is

Gout (1 patient – 3.33%). The tabulations and graphical representation are as under.

Table- 19

Associated features Total no of patients Percentage

Asthma 5 16.6

Gout 1 3.33

Toxemia 0 0

Transient Ischemic attack 0 0

Pakshaghatha 0 0

Ardita vata 0 0

Medoroga 7 23.33

Graph – 7Distribution of patients by Associated features

Distribution by Associated features

5

1

7

0

0

0

0

0 1 2 3 4 5 6 7 8

Asthma

Gout

Toxemia

Transient Ischemic attack

Pakshaghatha

Ardita vata

Medoroga


B3) Distribution of patients by mode of on set

Table- 20

DISTRIBUTION OF PATIENTS BY MODE OF ON SET

Modeof onset

Tot

al p

atie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Gradual 17 56.67 4 23.5 1 5.8 8 47 3 17.6 1 5.8

Sudden 13 43.33 5 38.4 5 38.4 2 15.3 0 0 1 7.6

Total 30 100 9 6 10 3 2

Graph –8

DISTRIBUTION OF PATIENTS BY MODE OF ON SET

The modes of onset of the Bhrama vis-à-vis hypertension results observed are as

under. Out of 17 (56.67%) of Gradual onset patients, 4 (23.5%) patients are well

responded 1 (5.8%) patient is moderately responded and 8 (47%) patients responded, 3

(17.6%) patients are not responded and 1 (5.8%) patient discontinued. Out of 13

PATIENTS BY MODE OF ON SET

Gradual 56.67%

Sudden43.33%


(43.33%) of Sudden onset patients, 5 (38.4%) patients are well responded 5 (38.4%)

patients are moderately responded and 2 (15.3%) patients responded and 1 (7.6%) patient

discontinued. There were no patients from the category of discontinued.

B4) Distribution of patients by Intensity

Table- 21

Distribution of patients by Intensity

Intensity

Tot

al p

atie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Mild 11 36.7 5 45 3 27.2 2 18.2 0 0 1 9.1

Moderate 14 46.7 4 28.5 3 21.4 4 28.5 2 14.3 1 7.1

Severe 5 16.6 0 0 0 0 4 80 1 20 0 0

Total 30 100 9 6 10 3 2

The intensity distributions of the Bhrama vis-à-vis hypertension results are

observed as under. It classified under three headings as mild, moderate and severe. Out of

11 (36.7%) of mild intensity patients, 5 (45%) patients are well responded 3 (27.2%)

patients are moderately responded, 2 (18.2%) patients are responded and 1 (9.1%) patient

is discontinued. No patients reported from the category of not responded. Out of 14

(46.7%) of moderate intensity patients, 4 (28.5%) patients are well responded 3 (21.4%)

patients are moderately responded, 4 (28.5%) patients responded, 1 (7.1%) patient

discontinued and 2 (14.3%) patients are not responded to the management. Out of 5

(16.6%) of severe intensity patients, 4 (80%) patients are responded and 1 (20%) patient

is not responded to the management. The graphical expression is as under.

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama”100

Graph – 9

DISTRIBUTION OF PATIENTS BY INTENSITY

B5) Distribution of patients by Aggravating factors

Table -22

Agg

rava

ting

fact

ors

Tot

al p

atie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Travel 16 53.34 4 25 3 18.7 6 37.5 2 12.5 1 6.25

Anxiety 27 90 8 29.7 6 22.2 9 33.3 2 7.5 2 7.5

Emotion 19 63.34 5 26.4 4 21.1 6 31.6 3 15.8 1 5.3

Stress 23 76.6 7 30.5 3 13.1 8 34.8 3 13.1 2 8.7

Physicalstress

5 16.67 1 20 1 20 2 40 1 20 0 0

The aggravating factorial distributions of the Bhrama vis-à-vis hypertension

results are observed as under. It classified under three headings as Travel, Anxiety,

PATIENTS BY INTENSITY

Severe16.67%

Mild 36.67%

Moderate46.67%


Emotions and stress. Out of 16 (53.34%) of Travelling patients, 4 (25%) patients are well

responded 3 (18.7%) patients are moderately responded, 6 (37.5%) patients are responded

and 1 (6.25%) patient is discontinued. 2 (12.5%) patients reported from the category of

not responded. Out of 27 (90%) of Anxiety referred patients, 8 (29.7%) patients are well

responded 6 (22.2%) patients are moderately responded, 9 (33.3%) patients responded, 2

(7.5%) patients discontinued and 2 (7.5%) patients are not responded to the management.

Out of 19 (63.34%) of emotional referred patients, 5 (26.4%) patients are well

responded 4 (21.1%) patients are moderately responded, 6 (31.6%) patients responded, 1

(5.3%) patient discontinued and 3 (15.8%) patients are not responded to the management.

Out of 23 (76.6%) of stress referred patients, 7 (30.5%) patients are well responded 3

(13.1%) patients are moderately responded, 8 (34.8%) patients responded, 2 (8.7%)

patients discontinued and 3 (13.1%) patients are not responded to the management. Out

of 5 (16.67%) of physical stress referred patients, 1 (20%) patient is well responded, 1

(20%) patient is moderately responded, 2 (40%) patients are responded and 1 (20%)

patient is not responded to the management. The graphical expression is as under.

Graph – 10

Depicting the Aggravating factors of Bhrama

16

27

19

23

5

0

5

10

15

20

25

30

Travel Anxiety Emotion Stress Physicalstress

Depicting the Aggravating factors of Bhrama


B6) Distribution of patients by relieving factors

Table -23Relieving

factors

Tot

al p

atie

nts

%

Wel

l Res

pond

ed

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

%

Not

Res

pond

ed

%

Dis

cont

inue

d

%

Rest 18 60 6 33.3 2 11.1 7 38.8 1 5.55 2 11.1

Tranquilliser 0 0 0 0 0 0 0 0 0 0 0 0

Sleep 28 93.3 8 28.5 6 21.4 9 32.1 3 10.7 2 7.14

Anti

Depressants0 0 0 0 0 0 0 0 0 0 0 0

Graph – 11

Depicting the relieving factors of Bhrama

18

0

28

0

0

5

10

15

20

25

30

Depicting the relieving factors of Bhrama

3-D Column 1 18 0 28 0

Rest Tranquilliser SleepAnti

Depressants


The relieving factorial distributions of the Bhrama vis-à-vis hypertension results

are observed as under. It classified under three headings as rest, tranquilliser, sleep and

anti-depressants. Out of 18 (60%) of resting patients, 6 (33.3%) patients are well


and 2 (11.1%) patients are discontinued. 1 (5.55%) patient is reported from the category

of not responded. The second category of well slept patients of 28 (93.3%), 8 (28.5%)

patients are well responded 6 (21.4%) patients are moderately responded, 9 (32.1%)

patients are responded and 2 (7.14%) patients are discontinued. 3 (10.72%) patients are

reported from the category of not responded. No patients have reported getting the

tranquillisers or anti-depressants.

B7) Distribution of patients by Shareerika Prakruti

Table- 24

Distribution of patients by Shareerika Prakruti

ShareerikaPrakruti

Tot

al n

o of

patie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

% Not

Res

pond

ed%

Dis

cont

inue

d

%

Vata Pitta 11 36.6 5 45.4 2 18.2 3 27.2 0 0 1 9.1

Pitta Kapha 15 50 3 20 3 20 6 40 2 13.3 1 6.56

Kapha Vata 04 13.4 1 25 1 25 1 25 1 25 0 0

Tridosha 00 0 0 0 0 0 0 0 0 0 0 0

Total 30 100 9 100 6 100 10 100 3 100 2 100

The Shareerika Prakruti distributions of the Bhrama vis-à-vis hypertension results

are observed as under. It classified under four headings as Vata Pitta, Pitta Kapha, Kapha

Vata and Tridoshaja. Out of 11 (36.6%) of Vata Pitta patients, 5 (45.4%) patients are well



and 1 (9.1%) patient is discontinued. No patients are reported from the Vata Pitta

category of not responded. The second category is of Pitta Kapha Prakruti with the 15

number (50%) of patients, out of well-responded 3 (20%), moderately responded 3 (20%)

patients and responded are 6 (40%). 1 (6.56%) patient is discontinued and 2 patients

(13.3%) are not responded. Out of 4 (13.4%) of Kapha Vata Prakruti patients, 1 (25%)

patient is well responded 1 (25%) patient is moderately responded, 1 (25%) patient is

responded and 1 (25%) patient is not responded. No patients are reported from the Kapha

Vata category of discontinued. It is practically difficult to ascertain the Tridosha Prakruti,

thus there is no candidature recorded. The pictorial expression of the shareerika Prakruti

is as under.

Graph -12

Distribution of patients by Shareerika Prakruti

Distribution by Shareerika Prakruti

Kapha Vata13.33%

Vata Pitta36.67%

Pitta Kapha50.00%

Tridosha0.00%


B8) Distribution of patients by Manasika Prakruti

Table -25

ManasikaPrakruti

Tot

al n

o of

patie

nts

% Wel

lR

espo

nded

%

Mod

erat

ely

Res

pond

ed

%

Res

pond

ed

% Not

Res

pond

ed

%

Dis

cont

inue

d

%

Raja Guna 21 70 7 33.3 4 19.1 7 33.3 1 4.76 2 9.52

Raja TamoGuna

9 30 2 22.2 2 22.2 3 33.3 2 22.2 0 0

Total 30 100 9 6 10 3 2

Graph -13

Distribution of patients by Manasika Prakruti

The Manasika Prakruti distributions of the Bhrama vis-à-vis hypertension results

are observed as under. It classified under two headings as rajoguna and rajotamoguna.

Out of 21 (70%) of rajoguna, 7 (33.3%) patients are well responded 4 (19.1%) patients

are moderately responded, 7 (33.3%) patients are responded, 1 (4.76%) patient is not

responded and 2 (9.52%) patients are discontinued. Out of 9 (30%) of rajotamoguna, 2

Distribution by Manasika Prakruti

Raja Guna 70.00%

Raja Tamo Guna

30.00%


(22.2%) patients are well responded 2 (22.2%) patients are moderately responded, 3

(33.3%) patients are responded, 2 (22.2%) patients are not responded and no patients of

discontinued.

C) Result of the Kakubhadi Lehya in Bhrama vis-à-vis Hypertension

C1) Assessment of Lab investigations in Bhrama

Table -26

Investigation Mean Before Mean After Mean Difference1. Temperature 98.02 97.78 0.24

2. Weight 63.61 63.37 0.24

3. Hemoglobin % 12.397 12.84 0.443

4. RBC count 4.328 4.579 0.251

5. Serum Creatinine 0.8623 0.8703 0.008

6. Serum Cholesterol 202.446 196.653 5.793

7. HDL Cholesterol 46.18667 46.93333 0.74666

8. LDL Cholesterol 117.0393 111.8067 5.2326

9. VLDL Cholesterol 40.27333 37.98 2.29333

10. Serum Triglyceride 199.0667 189.9867 9.08

It is put forth for the assessment many parameters in the study. The direct

significant parameters are included along with the parameters, which are helpful to assess

the co-morbid conditions, such as lipid profile. Some parameters that can influence the

blood pressure through its physiological or patho-physiological nature also included, such

as temperature. The variances are observed not only to assess the regression of the


disease but also to assess the Rasayana effect induced in the body by the chosen

medicament. The data analysis is as follows.

The factors that have the influence on the physiology (temperature, weight) are

decreased with the baseline mean data in the study. The temperature shows the mean

difference of 0.24 in the study, which is a point of observation to assess the Rasayana

effect induction in the body. The second factor weight has reduced by 0.24 mean value,

suggesting the induction of good health through Rasayana, there by the regulation of the

Bhrama vis-à-vis hypertension.

The third factor of objective parameter observed is haemoglobin percentage. It

shows marked increase of 0.443 mean value. Which is suggestive of inducting Rasayana

effect and also capacitating the oxygen exchange ratio and there by the controlling the co-

morbid conditions or associative such as hypoximea. The associate factor of haemoglobin

is RBC count. This has shown 0.251 mean value increase in the study reflects to the

percentage rise of the haemoglobin and there by regulating the Bhrama vis-à-vis

hypertension.

The next parameter of co-morbidity in Bhrama vis-à-vis hypertension is serum

creatinine. It has shows a rise in the study with a mean value of 0.008. It suggests that the

Angiotensin and Renin involvement in the Bhrama vis-à-vis hypertension have been

successfully reduced and provide the Rasayana effect not only at the cardiac but also in

the renal area. The small amount changes are as a process of regulation in the KUB

system.

Serum cholesterol and associative LDL, VLDL with S.Triglycerides are risk

factors in the pathology of Bhrama vis-à-vis hypertension. Out of these associated the


HDL cholesterol is good for the body and all the rest offers co-morbidity. As the results

observed except the HDL cholesterol all other cholesterol drop in the study in

comparison of mean values. The mean value of HDL is 0.74666-difference rise in the

study. The rest of co-morbid influencing factors enumerated are LDL (5.2326), VLDL

(2.29333), Serum cholesterol (5.793) and S. Triglyceride (9.08), show the significant

drop and suggest that the effect of the Kakubhadi Lehya on Bhrama vis-à-vis

hypertension with reference to its Rasayana effect over the Bhrama vis-à-vis

hypertension.

C2) Assessment of Subjective parameters in Bhrama

Table- 27

Presenting complaints Patients Before % Patients After %

Bhrama 28 100 0 0

Shira shoola 19 67.85 2 7.14

Angasada 14 50 1 3.57

Nidranasha 13 46.42 2 7.14

Hrudrava 7 25 0 0

Klama 6 21.42 2 7.14

Urah shoola 2 7.14 0 0

The presenting complaints of the Bhrama vis-à-vis hypertension are enumerated

here under the limelight of the contemporary and Ayurvedic methods. The first fore most

complaint is Bhrama, which is a pratyatma niyata Lakshana of the Bhrama. All the 28

(100%) patients included and received full-length treatment are exhibiting this symptom

and relieved 100 % at the end of the schedule.


The second major complaint expressed in the study is shira shoola by 19 (67.85%)

and outs of them 2 (7.14%) patients’ shows the persistence of the shira shoola at the end.

Angasada, a complaint observed in the study for 14 (50%) patients and one (3.57%)

patient hang on with the complaint at the end of the study. Next complaint is nidranasha,

which is always associated is observed on 13 (46.42%) patients and found that the same 2

(7.14%) patients are having the complaint at the end of the study. Hrudrava, another

relative complaint of the corresponding organ is observed in 7 (25%) patients and at the

end the Rasayana effect of the Kakubhadi Lehya made them not to have the complaint.

The klama is observed in 6 (21.42%) patients and at the end 2 (7.14%) patients are

assiduous with the complaint. The last subjective parameter observed in the study is urah

shoola for 2 (7.14%) patients and both were relieved with the complaint at the end of the

study of Kakubhadi Lehya on Bhrama vis-à-vis hypertension. The graphical

representation is as under.

Graph - 14

Distribution by Presenting Complaints

28

19

14

13

7

6

2

2

1

2

2

0

0

0

0 5 10 15 20 25 30

Bhrama

Shira shoola

Angasada

Nidranasha

Hrudrava

Klama

Urah shoolaAfter

Before


C3) Results of Kakubhadi Lehya in Bhrama vis-à-vis Hypertension

The result in the study ascertains the best activity of the Kakubhadi Lehya over

the Bhrama vis-à-vis hypertension. For the convenience the results are grouped as five

categories, viz. Well-Responded, Moderately Responded, Responded, Not responded and

Discontinued.

The result declaration is done following the norms and conditions of the inclusive

factors and study of the subjective parameters in association with the sphygmomanometer

studies of three postures. The co-morbid stimulating factors especially LDL, VLDL and

S. Triglycerides are considered in while declaring the results. The factors which make the

Rasayana effect over the body also included to assess the results.

After through study of the entire parameters and materials available for the

assessment of results it was drawn a conclusion of results as - 9 (30.02%) well responded,

6 (20.02%) moderately responded, 10 (33.33%) responded, 3 (10%) patients not

responded and the last 2 (6.63%) patients discontinued in the study. The tabulation and

graphical expression pi-diagram is as under.

Table-28

Result Number of patients Percentage

Well Responded 9 30.02

Moderately Responded 6 20.02

Responded 10 33.33

Not Responded 3 10.00

Discontinued 2 6.63

Total 30 100


Graph – 15

Results of the Kakubhadi Lehya

D) Statistical analysis of the clinical and objective parameters

D1) Subjective parameters

Table -29

Subjectiveparameters

Mean SD SE t-Value p-Value

sign

ific

ance

Bhrama 0.964 0.188 0.0357 27 <0.001 HS

Shira shoola 0.928 0.262 0.049 18.398 <0.001 HS

Angasada 0.285 0.46 0.086 3.31 <0.001 HS

Hrudrava 0.214 0.417 0.078 2.743 <0.001 HS

Klama 0.107 0.314 0.059 1.813 >0.05 NS

Urah Shoola 0.071 0.262 0.049 1.44 >0.05 NS

Results of Kakubhadi Lehya in Bhrama vis-à-vis Hypertension

Not Responded 10.00%

Moderately Responded

20.00%

Well Responded 30.00%

Responded 33.33%

Discontinued6.67%


D2) Emotional parameters

Table -30Emotionalparameters Mean SD SE t-Value p-Value Significance

Fear 0.537 0.692 0.131 4.09 <0.001 HS

Anger 1.0 0.72 0.136 7.35 <0.001 HS

Depression 0.571 0.79 0.149 3.83 >0.001 NS

Anxiety 0.8571 0.650 0.122 7.02 <0.001 HS

Irritability 0.428 0.69 0.13 3.29 <0.001 HS

Aggressiveness 0.321 0.475 0.089 3.606 <0.001 HS

Delirium 0.428 0.634 0.119 3.59 <0.001 HS

D3) Objective parameters

Table -31Objective

parameters Mean SD SE t-Value p-Value Significance

Temperature 0.278 0.428 0.080 3.475 <0.001 HS

Weight 0.443 0.291 0.055 8.054 <0.001 HS

Haemoglobin % 0.532 0.326 0.061 8.721 <0.001 HS

RBC count 0.287 0.178 0.033 8.696 <0.001 HS

Serum Creatinine 0.071 0.079 0.014 5.071 <0.001 HS

Serum Cholesterol 8.3 6.47 1.22 6.803 <0.001 HS

HDL Cholesterol 2.692 2.826 0.534 5.041 <0.001 HS

LDL Cholesterol 8.063 6.501 1.228 6.565 <0.001 HS

VLDL Cholesterol 3.201 5.85 1.107 2.891 <0.001 HS

Serum Triglyceride 9.71 7.22 1.36 7.139 <0.001 HS


D4) Blood pressure variances

Table -32

Blood pressurevariances

Mean SD SE t-Value p-Value

Sign

ific

ance

Standing Systolic 18.857 8.868 1.675 11.2579 <0.001 HS

Standing Diastolic 9.5 3.911 0.7391 12.85 <0.001 HS

Supine Systolic 17.92 8.476 1.6 11.2 <0.001 HS

Supine Diastolic 9.5 3.595 0.679 13.99 <0.001 HS

Sitting Systolic 18.5 8.478 1.6 11.56 <0.001 HS

Sitting Diastolic 9.428 4.1 0.775 12.165 <0.001 HS

All the subjective parameters except Klama and Urah shoola show highly

significance. Consider hypothesis that the drug is not responsible for the changes in the

readings of the patients, before and after the treatment, i.e. reducing the Bhrama vis-à-vis

hypertension. To test the hypothesis paired t-test is used. The parameter Bhrama shoes

highly significance with more mean effect and with least variation and it is also having

the uniform effect on the patients (by comparing the t-value) as p is <0.05 and coefficient

of variation. The parameter Urah shoola shows the non-significant with less mean effect.

The parameter Angasada is having more variation. The parameter Anger and Anxiety

shows more significant than fear and rest of the parameters. The parameter Anxiety is

having the more net mean effect and Depression having with more variation. Where as

the parameter Aggressiveness have less mean effect with less variation.


All the objective parameters show highly significance. The haemoglobin, weight,

RBC shows more or less highly significance. The parameter Serum Cholesterol is having

less mean effect with less variation. Where as the parameter serum Triglyceride having

high net mean effect with more variation. The diastolic blood pressure in all the three

different positions, the mean net effect is the same, but the supine position there is high

significance witnessed. There is much variation observed in the sitting position. The

mean effect after the treatment of diastolic blood pressure is more in the position of

standing is more with more variation.

The mean net effect of the systolic blood pressure in the standing position is

more, but there is high significance of systolic blood pressure in sitting position. The

mean effect systolic blood pressure in sitting position is more, where as standing position

show the uniform effect. In the diastolic blood pressure again the standing position show

more uniformity.


Chapter – 6

Discussionertigo 199resembles giddiness or Dizziness by all means, but the difference

is vertigo is because of the Auditory nerve impairment and the Dizziness is a systemic

malfunction expression. As Ayurveda explains, the Majja Dhatu dusti i.e. a nervous

system intervention or Rasa Dhatu dusti i.e. mal-nourishment, which impacts the

Hrudaya and Dashadhamani or a Medo Dhatu dusti which involves the associative pre

disposing factors to generate dizziness are also to be considered. It is evident from that of

pathology expressions of Ayurveda, as example in Vataja Arshas the Karan nada is

witnessed and associated even with that of dizziness. All the above conditions are to be

ruled out and only a hypertensive concerns are to considered as Bhrama, with a special

reference to that of psycho-metabolic pathological condition Bhrama vis-à-vis

hypertension.

Demographic information of Hypertension represents a major public health

concern. It affects about a billion people worldwide and is the most common treatable

risk factor for the cardio vascular disease. In patients aged over 50 and also affecting the

10 to 15 percent of adult population and nearly 50 percent of all deaths in elderly people

is related to hypertension or its complications.

Here high blood pressure (hypertension) has often been called the “silent killer of

man kind” because mild to moderate levels usually go unnoticed by patient until serious

damage has already been done. Epidemiological studies revealed that it is the most

important single factor responsible for death from cardiovascular and cerebro-vascular


disease. Therefore its epidemology drawn the attention of W.H.O in 1978 and declared

that year as “HYPERTENSION YEAR”.

Because of the threshold of 21st century is plagued with reward of fast living,

insatiable needs fanned by easy obsolescence slick marketing and industrialization. The

science at the service of mankind has its own pros and cons. The advancement of medical

science and technology is touching new horizons each day, but with each dawn serious

health hazards are creeping in to our lives, with strange pathological complications.

Hypertension is one such ailment.

So far hypertension in various system of medicines like Ayurveda, Unani,

homeopathy and allopathic-claim success in preventing, controlling hypertension. But the

fundamental factor that blood pressure is not a disease but a reaction is manifested by the

cardiovascular system against unnatural behaviours in relation to one’s Ahara and Vihara

(mithya hara vihara). Among these system of medicines Ayurveda adopts the treatment

for the benefit of life “chikitsaachayausho hitayopadishyate” and life is nothing but the

feeling of self or self-consciousness “ttrayusho chetananu vruttihi” Ayurveda is eternal

and ever lasting principle. Ayurvedic drugs have shown re-constructive or rejuvenate

effect.

So far scientists call blood pressure a child of modern civilisation. The word

civilisation as it is understood to day implies deviation from nature. For the present life is

most artificial eating food which is never meant for “natural” human being food

especially manufactured processed and tinned which acts partly as stimulating and partly

as nourishment. Out of these tobacco, alcohol, tea, coffee, cold drinks and ice cream,

flesh and spices are most important, adding insult to the injury are the present day toxic


medicines. The strain of these artificialities hammers the resistance power, vitality and

susceptibility of man. Having lost his health man resorts to modern chemical drugs

knowing not ultimate hazards of it.

Stress and strain are supposed to be the major causes for hypertension and their

effects are clinically widely seen. In other words hypertension is one of the gross and

material manifestation in individuals caused by their own mind and mind of the society.

Thinking process ideas, concepts, attitude, philosophies, convictions etc., are all abstracts

but they very much affect and alter the matter is clearly seen in hypertension

World wide, though the rates of hypertensive admission are not stabilised, there is

a evidence of increasing in hospitalisation or mortality. Death rates continue to cause

concern. In the context of an increase in hypertensive patients and in deaths it is crucial

that we should gain more in sight in to its causation and management.

The overall picture of health of the present civilised man is very gloomy. He is

still being kept under illusion, that filling his stomach with drugs is the only way back to

health. Drugs have only proved to be acting and palliative and none of them is without its

toxic bad effects. In fact correcting blood pressure disorders by drugs is to in correct it

even the simple innocent example is tranquilliser fed under this category of modern

drugs. These drugs when given to pregnant woman produced such shocking results that

the drugs are known as “Generation killer”, because hypertension in pregnancy remains

as a major cause of maternal and foetal morbidity and mortality. It is a late manifestation

of a multi-factorial multi-system disease inhibited very early in pregnancy, the feature of

which suggests an inadequate maternal response to pregnancy. So the patient of


hypertension is expected to be on medication for long tem and also high blood pressure is

more a controllable factor than a curable one.

Therefore in the present era cardio-vascular disorders from the largest group of

fatal diseases. Framingham prospective study first focussed attention by bringing about

the fact that 37 percent men and 51 percent women who died of cardiovascular disease

had an arterial pressure above 140/90-mm Hg on at least three occasions. This normal

blood pressure that is hypertension is one such disease, which is chief contributory cause

for arterial degeneration in advanced age. High blood pressure may be produced by

increased cardic out put in the pressure of normal peripheral resistance on increased

peripheral resistance in the presence of normal cardiac out put. The latter is by for the

common situation arterial hypertension can be broadly divided into two forms primary on

essential where the cause is unknown and secondary where there is some associated

lesions such as chronic nephritis or adrenal cortial tumour etc.

Thus it is high time that we should release the gravity of the situation. Turn our

backs to the chemical drugs and return backs to the nature to find out physiological

measures for the understanding and controlling blood pressure disorders.

Though there is no difficulty in understanding the disease of hypertension from

modern point of view, there are some difficulties in identifying the condition with a

known disease entity of Ayurveda. The general tendency even among the scholars to

equate a disease mentioned in Ayurveda with some of the diseases mentioned in modern

medicine on vice versa cannot be totally resisted. It may not be desirable to equate a

disease from one system with that of the other system. On the basis of superficial

similarity as there is fundamental difference in the approach of each system in describing


the pathogenesis still the above tendency may help to some extent to communicate ones

ideas regarding the diseases.

Like wise, regarding hypertension, to have the investigative part and knowledge

of complication in modern days is very appreciable and adaptable. The comprehensive

and wholesome approach of Ayurveda to understand the problem and treat it on the same

lines is the admirable features.

Patients with mild to moderate hypertension require only a simple schedule of

investigation, especially if there is a history of hypertension in first degree relatives. Tests

are necessary to profile other cardio-vascular risk factors and to detect target organ

damage with only limited screening for secondary hypertension. Careful history, physical

examination, repeated blood pressure measurements over months and measurements of

body mass index complete lipid profile, haemoglobin, serum Creatinine serum glucose,

ECG and red blood cells are all that are required.

More over till explanation of hypertension in the language of Ayurveda is a root

point till to day. A number of renowned Ayurvedic physicians and academicians have

made an attempt to explain this condition and its effective treatment in hypertension

according to the mortality of Dosha.

The affliction of different Dhatus is argued in the pathogenesis of hypertension.

Few names of the disease are suggested representing the essential hypertension. Easiest

way of translating hypertension in to Sanskrit it also tried. The different names suggested

embodying the hypertension in Ayurveda.

So in this context on the basis of theoretical and clinical symptomatology

“Bhrama” studied only restricting on comparing only to the hypertension, occurring in


the cardiovascular system. But so far nomenclature claimed in Ayurveda are Rakta chapa,

Rakta bharadhikyata, Rakta peedanadhikyata and raktasammardhan etc. As a matter of

fact the translation or transliteration of English is “the word and condition at hypertension

refers to Bhrama approximately”, which implies to that of Bhrama i.e. a condition of

giddiness. Here Ayurveda mainly speaks and considers Bhrama as a disease entity.

Charaka has considered Bhrama as one out of the vataja nanatmaja Vyadhi.

Chakrapani on that explained Bhrama is a disease not only concerned to that of Shiras but

also for Rakta as its pradoshaja Vyadhi. As “tamasacha atidarsharam” and also said it as

Smruti mohaka, Bhrama also explained as nidanarthaka Vyadhi of some diseases. It is

also said as signs and symptoms (Lakshana) and upadrava (complications) of many

diseases as like hypertension.

The principle etiological factor of hypertension is psycho-emotional overstrain

this factor leading to impaired regulation of the vascular tone. In general this hypothesis

is at the support of Ayurvedic Dosha Vata interference in producing Bhrama.

Thus one among such formulation which was not even established any where,

which is Bhrama hara, Hrudaya vatanulomaka, srotoshoodhaka as well as Rasayana

modalities are grouped under “Kakubhadi Lehya” as Hrudya Rasayana from Bhaisajya

Ratnavali is to be under taken for the study. These by helping the person to have an

overall sense of well being. So drug therapy and this prevention of mortality and

morbidity arising out of its complications can control it.

Spectrum of disease

Hypertension is a major risk factor for many serious health problems. As there is

no definitive definition universally accepted, the joint National committee (JNC-4) of


United states on detection, evaluation and treatment of high blood pressure defines

Hypertension as systolic blood pressure (SBP) of 140 mm Hg or more and diastolic blood

pressure (DBP) of 90 mm Hg or more. Dynamic or isometric exercise can also risk blood

pressure in normal subjects.

Figure-9

Comparison of the benign and malignant hypertension


About 90% to 95% of all high blood pressure cases are what is called primary, or

essential, hypertension.

There will be an increased risk of high blood pressure if a person is -

• Have a family history of high blood pressure.

• African Americans develop high blood pressure more often than whites, and it

tends to happen earlier in life and be more severe.

• Are male. Women are at an increased risk after age 55.

• Are older than 60. Blood vessels become more brittle with age and are not as

flexible.

• Face high levels of stress. In some studies, stress, anger, hostility, and other

personality traits have been shown to lead to high blood pressure, but the findings

have not always been consistent. Emotional factors most likely add to the risk of

high blood pressure for people who also have other risk factors.

• Are overweight or obese.

• Use tobacco products. Smoking damages your blood vessels.

• Use oral contraceptives. Women who smoke and use oral contraceptives greatly

increase their risk.

• Eat a diet high in saturated fat.

• Eat a diet high in salt (sodium).

• Drink more than a moderate amount of alcohol. Experts say that moderate intake

is an average of one to two drinks per day for men and one drink per day for

women. One drink is defined as 1½ fluid ounces (fl oz) of 80-proof spirits (such


as bourbon, Scotch, vodka, gin, etc.), 1 fl oz of 100-proof spirits, 4 fl oz of wine,

or 12 fl oz of beer.

• Are physically inactive.

• Have diabetes.200

That means the real cause of the high blood pressure is not known, but a number

of factors are associated with the condition.

Figure –10

Figure –

Aetiology of hypertension

Ayurvedic management for Unknown disease

Ancient Acharyas had suspected that new diseases could manifest in the future,

owing to the various changes in environmental, cultural and socio-economic factors.

They have guided us on how to manage such diseases, when not mentioned in the

classics, “The physician should not get disheartened at not knowing the name of a


disease”, instead, he should research and try to collect information with regard to the

signs.

New high blood pressure guidelines

New recommendations for tighter control of high blood pressure may drastically

reduce the number of individuals who die each year from hypertension-related illnesses,

according to the Seventh Report of the Joint National Committee on Prevention,

Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII). A summary

report is published in today’s JAMA Express, and the full report will be published this

summer in Hypertension: Journal of the American Heart Association.

The new classification – “pre-hypertension” – describes people with blood

pressures between 120-139 millimeters of mercury (mm Hg) systolic (the top number in a

blood pressure reading) or 80-89 mm Hg diastolic (bottom number) 201. This is

considered as Poorvaroopa of Ayurvedic literature.

Table-33BLOOD PRESSURE LEVEL (mm Hg)202

Category Systolic Diastolic

Optimal** less than 120 less than 80

Normal less than 130 less than 85

High Normal 130-139 85-89

High Blood Pressure

Stage 1 140-159 90-99

Stage 2 160-179 100-109

Stage 3 Greater than or equal to 180 greater than or equal to 110

* For those not taking medicine for high blood pressure and not having a short-termserious illness. These categories are from the National High Blood Pressure EducationProgram.** Optimal blood pressure with respect to heart disease risk is below 120/80 mm Hg.However, unusually low readings should be evaluated for clinical significance.


Current Guidelines

JNC VI 203 is our most recent and comprehensive guide to treating hypertension.

Its recommendations introduced several innovations and new directions for treatment,

placed a new emphasis on both prevention and the efficacy of lifestyle changes, and

established several important goals.

Guidelines of most other groups identify two threshold pressures, one for the

diagnosis of hypertension, which for diastolic pressure is 90 mm Hg or higher and for

systolic pressure, 140 mm Hg or higher, and one for the initiation of drug treatment based

on BP level alone 204-208. The drug treatment threshold for diastolic BP alone differs

considerably amongst the guidelines 209 being 90, 95, 210-212 or 100 mm Hg. Most

guidelines suggest that factors other than BP should influence the decision to begin drug

treatment of patients with pressures between the thresholds for diagnosis and routine

treatment of hypertension 213.

There are few differences amongst the guidelines on factors that interact with

hypertension to increase the likelihood of cardiovascular risk and include older age, male

gender, smoking cigarettes, hyper-cholesterolemia, diabetes, hypertensive target organ

damage, and the presence of cardiovascular disease. Most guidelines recommend

diuretics or beta-blockers as initial drug therapy for patients in whom there are no

specific contradictions; 214-218 the World Health Organisation /International Society of

Hypertension guidelines suggest, however, that any particular class of anti-hypertensive

agent may be chosen 219. The primary goal of treatment in most guidelines is a diastolic

BP below 90 mm Hg, and even lower levels in certain situations such as the presence of

renal disease in diabetic patients 220. All guidelines recommend a more individualised


therapeutic approach in special circumstances although even here the American Joint

National Committee guidelines still tend to favour diuretics and beta-blockers as initial

therapy in most instances 221. The Preventive Services Task Force recommends that BP

be measured regularly in all persons aged 3 and above 222-223.

PRIMARY OR ESSENTIAL HYPERTENSION

About 80% hypertensive cases belong to this category wherein aetiology is not

known. The primary function of the heart is to supply blood and thereby oxygen to every

cell of the body. In doing so, blood pressure rises. This essential rise to meet the demand

of adequate supply of oxygen of the cell is perhaps designated as essential hypertension

224. Normal systolic blood pressure is maintained as 110 - 140 (mm Hg) and normal

diastolic blood pressure is maintained as 70 to 90 mm Hg. Blood pressure = cardiac

output x peripheral resistance Hence, the mean arterial pressure is the product of cardiac

output and the total peripheral resistance. If one of the factors is affected, it results into a

change of blood pressure 225-228.

Cardiac output is the product of stroke volume (the quantity of blood ejected by

each left ventricular contraction) and the number of contraction per minute (heart rate).

Hence cardiac output depends on stroke volume, heart rate and venous capacitance.

Venous dilatation causes less return or pre-load to heart while venous constriction causes

more volume to return to the heart. Total peripheral resistance (TPR) depends on calibre

of arteriolar bed, elasticity of aortic and arterial walls and the viscosity of blood.

Vasoconstriction results in increased TPR, while vasodilatation results in decreased TPR

229-230. The traditional concept that the elevated arterial pressure is caused by increased

total peripheral resistance with normal cardiac output needs to be modified 231.


TABLE - 34

Four stages wherein cardiac involvement takes place

Stage I Normal size heart with no evidence ofcardiac involvement by ECG or chest X-ray.

Stage II Early left ventricular hypertrophy, detectedleft arterial abnormality (ECG) and fourthheart sound.

Stage III Clinical evidence of left-ventricularhypertrophy by chest X-ray and by ECG.

Stage IV Left ventricular failure

TABLE -35

The World Health Organisation (WHO) Classification of Hypertension

Stage Clinical characteristicsWHO 1 Latent hypertension. Uncomplicated after

labile elevation of blood pressure usually inyounger individuals.

WHO 2 Established hypertension - Stable elevationof blood pressure with signs ofcardiovascular hypertrophy usually inmiddle-aged individuals.

WHO 3 Advanced hypertension - associated withsigns of organic damage caused byelevation of blood pressure e.g. cerebralsclerosis, coronary sclerosis, myocardialinsufficiency and nephrosclerosis.

Borderline hypertension

The haemo-dynamic changes in this group demonstrate increased cardiac output

with normal peripheral resistance where increased heart rate and increased oxygen

consumption is observed. The mechanism behind these changes is still obscure. Probably

an imbalance between sympathetic and parasympathetic nervous system takes place.

Drugs acting on sympathetic system are very effective in achieving control over such

hypertension.


Definite hypertension

Blood pressure climbs consistently above 160/95 mm Hg. Elevation of diastolic

pressure is classified further as -232 -

1. Mild 95 to 104 mm Hg

2. Moderate 105 to 114 mm Hg

3. Severe or malignant 115 mm Hg or above

Figure –11Summary of the aetiology

There is fair evidence to measure BP in young and middle-aged adults (B

Recommendation). Case finding should be considered in all persons aged 21 to 64 years;


individual clinical judgement should be exercised in all other cases. Accurate BP

measurement by sphygmomanometer in the physicians’ office remains the principal

method of diagnosis. There is insufficient evidence to recommend the routine use of

echocardiography, self-measurement of BP or ambulatory BP monitoring in diagnosis.

While there is good evidence to recommend anti-hypertensive therapy for young

and middle-aged adults (ages 21 to 64 years) with diastolic pressures of 90 mm Hg or

over. There is insufficient evidence to evaluate therapy in persons –

1) with elevated pressure aged under 21 years; or

2) with isolated systolic hypertension defined as a systolic pressure of 140 mm

Hg or higher and diastolic pressure less than 90 mm Hg 233.

Bhrama at the evaluation:

Vagbhata has mentioned that this is because of vata dosha 234 where as Charaka

affirmed it as sanchaya of vata dosha blocked by vitiated pitta Dosha 235. Bhrama

explained as a prodromal symptom of some diseases. Vagbhata has mentioned that it is

one of the symptoms caused by vriddhi of Vata Dosha 236. Charaka explained that it is

caused due to Sanchaya of Vata Dosha blocked by vitiated Pitta Dosha 237. Bhrama

explained as a prodromal symptom of some diseases.

Major factors responsible for the development of the disease are -

1. On the basis of vitiated Dhatu

The Dhatu interrelated in this condition are Rasa and Rakta. Rasa’s main function

is Preenana i.e. nourishment. Essential elements for the body also to be considered here

as the Rakta transports it. The interference of the calcium is such thing in this concern.


Apart from the above, the Ca ion is compared with the Vata functions, which regulates

and makes the Rakta to move all around the body i.e. Vyanavata.

Regulation of intracellular calcium

Calcium in the free form as ions is referred to as activator calcium. This forms a

complex with calmodulin for the phosphorylation of contractile proteins, which helps

actinmyosin bridging. Thus, calcium brings about the vascular smooth muscle cell

contraction. This mechanism could be mediated by the influx of calcium via slow

calcium channels. Putting calcium into the cell brings about the second mechanism by

sodium/calcium exchange mechanism.

However, this exchange mechanism may not be operative in smooth muscle cell,

although we know that this exchange mechanism has a great importance in the

myocardial muscle cell. Mobilising calcium from sub-cellular pools can also increase

intracellular calcium. The effective concentration of calcium extrusion pumps that takes

care of calcium extrusion. It is not very clear how the plasma natriuretic factor blunts the

pump action 238. The receptors of the sympathetic nervous system, specifically the alpha-

1 and alpha-2 adreno receptors move calcium into the cell by opening up the slow

calcium channels and thereby increasing the intra cellular calcium 239-240, and by the

prostaglandins.

Normally, the sodium/calcium exchange pump operates as shown below.

With three ions of sodium moving from lumen to cytoplasm, one ion of calcium and two

ions of potassium move from cytoplasm to lumen side. The Ca++ dependent ATPase or

calcium pumps embedded in the sarcoplasmic reticulum membrane is responsible for

active transport of Ca++ ions against its concentration gradient from cytoplasm to the


lumen. There are two types of responses responsible for the influx of calcium ions. The

tonic response is induced by acetylcholine, serotonin, histamine, nor-adrenaline on the

transmembrane activation of myofibrillar ATPase.

The histamine, noradrenaline, acetylcholine and serotonin also produce phasic

response on the calcium stores. This phasic response is via calcium release from the

calcium stores activating thereby myofibrillar ATPase. Both these responses result in

vasoconstriction in addition to the effects of high extracellular potassium, cardiac

glycosides and electrical stimuli. Acetylcholine does not initiate the vasculature

originating from systemic arteries. However, noradrenaline produces contraction of extra-

mural coronary vasculature only after previous beta-receptor blockade. Vasoconstriction

occurs if the free intracellular calcium concentration is elevated and binding to

calmodulin leads finally to the splitting of ATP and to mechanical tension development.

This increase of intracellular calcium concentration can be produced by the

transmembrane calcium influx through so called potential or receptor operated membrane

calcium channels and generally leads to contractions of tonic characters. Calcium

antagonists in minute concentrations inhibit this transmembrane calcium influx into

smooth muscle cells, producing thereby vasodilatation.

The second mode of delivery of activated calcium in vascular smooth muscle cell

consists of calcium liberation from cellular stores heading to the phasic contraction.

Calcium antagonists do not directly block the cellular release but seem to interfere with

transmembrane replenishment of the cellular calcium stores thus eventually, both tonic

and phasic vascular smooth muscle activity can be damped by calcium antagonists.

During the excitation of the heart muscle fibres, an increase in transmembrane calcium


influx occurs together with liberation of calcium from endoplasmic stores resulting in a

rapid rise in intracellular concentration of free calcium ions. This initiates the splitting of

ATP by the calcium dependent ATPase of the myofibrils, so that phosphate bond energy

is transformed into mechanical energy. In other words, calcium ions act as mediators

between the excitatory processes at the surface and the intracellular biochemical

reactions, which involve ATP utilization for contraction. In short, a positive ionotropic

influence on the contractile tension development is developed by the various

mechanisms, which helps the contraction. However, calcium channel blockers resulting

in vasodilatation produce a negative ionotropic effect. Calcium glycosides improve the

availability of calcium to the contractile system.

2. On the basis of vitiation of Vata

The Vata involvement in the process of hypertension is evaluated in the literary

review. Out of the factors involved is compared with the nervous system of contemporary

medicine is as follows.

Vata verses old age:

Evidence supports treatment of systolic high blood pressure in older 241-242

persons. A review of the medical literature suggests that older persons with systolic

hypertension (and systolic blood pressure of at least 160 mm Hg) should receive

treatment.

Over activity of the Sympathetic Nervous System

Over activity of the sympathetic nervous system may be a fundamental

mechanism in hypertension. Plasma norepinephrine in the heart and kidneys is elevated

in young individuals with hypertension 243-244. Heightened activity of the renal


sympathetic nerves contributes to increased renal vascular resistance in essential

hypertension.6 Increased muscle nerve sympathetic overactivity is seen in mildly

hypertensive patients 245. Renal vascular disease or vascular remodeling follows

sympathetic overactivity in the early stages of hypertension. Hypoxia-driven arterial

chemoreceptors are potent stimulators of sympathetic activity. Recurrent episodic

hypoxia stimulates carotid chemoreceptors and, thus, sympathetic activity. Subsequently,

adrenal and renal sympathetic nerves maintain this heightened sympathetic activity 246.

Local endothelial factors may play a role in blood pressure.

The neural control

Experimentally, stimulation of several areas in the central nervous system

(Medulla, nucleus tractus soliterius, vasomotor centre and vagal nuclei) has shown to

raise or lower blood pressure. The CNS pressure impulses that are transmitted through

the autonomic nervous system network and finally through the sympathetic

postganglionic nerve fibres, affect the heart and vascular structure, due to the release of

norepinephrine. This norepinephrine - stimulates the adrenergic receptors in the

cardiovascular system. When the alpha-receptors located primarily in the vascular tissues

are stimulated, the vasoconstriction in arteriolar and venular region takes place. When

beta-2 receptors of blood vessels are stimulated a slight degree of vasodilatation takes

place.

While, stimulation of beta-1 receptors, which are, located in myocardium increase

the heart-rate, thereby increasing the force of myocardial contraction, it shortens the

ejection rate. Sinus node is also stimulated causing thereby an increase in heart rate.


Therefore, 247-250 over-activity of central nervous system leads to a hyperadrenergic state,

i.e. hypersecretory state of adrenal-medulla 251-254.

TABLE 36Cardiovascular responses to stimulation

Adreno receptors Organ affected Response

Alpha-1 Arterial and venous tissues Vaso constriction

Beta-2 Arterial and venous tissues Slight vasodilatation

Shortening of ejection rate.Beta-1 Myocardium sinus node

Increase in force

myocardial contraction

(From Cards : A Clinical Guide to Hypertension, 1985)

Overall effect of CNS stimulation

1. Alpha receptor - stimulation results in

v Arteriolar vasoconstriction resulting in increase in total peripheral resistance

(T.P.R.).

v Venous constriction resulting in increased preload.

2. Beta receptors - stimulation results in

a. Increased heart rate

b. Increased myocardial contraction

c. Increased cardiac output

3. Increased T.P.R. + increased cardiac output = increased blood pressure

Adrenergic neural activity affects the plasma renin activity.

Effect of adrenaline and nor-adrenaline could be summarised as follows.

Adrenaline

1. Stimulates beta-receptors of the Heart

2. Increases heart rate

3. The force of contraction is increased

4. Cardiac output is increased

5. Metabolism of the myocardium is increased which increases oxygen

consumption.


6. It abbreviates cardiac systole. Due to high cardiac rate, there is an incomplete

filling of blood during cardiac diastole, therefore, a fall in cardiac output (volume)

is decreased.

7. It enhances conduction across AV node and may produce ventricular arrhythmia.

Nor Adrenaline:

Has similar action like that of Adrenaline, however, 2-10 times less than that of

Adrenaline.

Effect on blood pressure

1. It produces vaso-constrictive effect on blood vessels of skin and mucous

membrane.

2. It dilates the vessels of skeletal muscles on account of preponderance of beta-

receptors.

3. The net effect of the above two is the decrease in peripheral resistance.

4. Thus adrenaline raises the systolic blood-pressure by its cardiac action, and it

lowers the diastolic pressure by its peripheral action. The myocardial effects of

these two hormones could be blocked by beta receptor blocking agents like

propranolol etc. AV conduction is suppressed with the result that the contraction

of the heart is delayed.

3. On the basis of vascular changes

An adult can counter prenatal and childhood influences on blood pressure by

adopting a healthy lifestyle. But she added that research has uncovered the beginnings of

clogged arteries even in children, and this may not be completely reversed by healthy

habits later in life 255.


MODULATORS OF VASOCONSTRICTORY MECHANISMS

Calcium plays an important role in the vasoconstrictory mechanism and therefore

should be treated as an important modulator. An intracellular calcium role in the trans

induction of the hormone action will have to be attributed special importance in

development of high blood pressure.

4. On the basis of Avarana

Pittavrutha Pranavata lakshanas includes Murcha and Bhrama, Pittavruta

Udanavata lakshana also included Murcha and Pitta Avrithavata exhibits the giddiness

and feeling of darkness. In case of covering with Kapha there are coldness, heaviness and

pain, suitability of pungent etc. and particular desire for fasting exertion, rough and hot

things. If Vata is covered with Rakta, there is burning sensation with distress, the space

between skin and muscle becomes red and swollen and rashes appear.

The above conditions exhibit because of either Dhatu kshaya or Avarana, the

different planes of the aetiology discussed and the psycho-pathological condition Bhrama

vis-à-vis hypertension is precipitated, for which the Rasayana treatment is ultimate.

Role of Rasayana Chikitsa in hypertension vis-à-vis Bhrama

Rasa (essence of food) is known to be the premier nutrition of the body tissue is

capable to progress/ limit the blood-related diseases, such as hypertension.

v Reduction or stoppage of smoking helps to reduce blood pressure.

v Atherosclerosis, which is the main factor responsible for hypertension.

Vyanavata is situated in hridaya, 256-257 and it pervades swiftly throughout the

body 258-259. Vyanavata is responsible for circulation of Rasa (rasadhatu) through out the

body 260-261. Sadhakapitta is situated in hridaya 262-265. Even in unamada Chikitsa adhyaya

also acharya Charaka mentions about manovaha Srotas 266.


Concept and management of hypertension in Ayurveda

Charaka provides us opportunity to comprehend the nature of the disease by

detailed evaluation of vikaraprakriti adhisthana and samuthana visesha and recommends

treating them accordingly. So in the forgoing illustration we have drawn the conceptual

pathogenesis of hypertension and the plan of its treatment.

Spectrum of Setting

High blood pressure lowers cognitive function 267, researchers say,

• High blood pressure in adults between the ages of 18 and 83 is associated with a

measurable decline in cognitive powers, according to a report published today by

University of Maine researchers.

• In their study, younger individuals (18-47 years) performed at a higher level than

older individuals (48-83 years), but they, like older individuals, showed blood

pressure-related decline in cognitive function over time.

• Subjects in the study exhibited a normal range of cognitive functioning, as

determined by the Wechsler Adult Intelligence Scale (WAIS).

• The researchers analysed data from four types of cognitive function tests focusing

on visualisation-fluid ability, memory, crystallised-verbal ability and speed.

• Other studies have related high blood pressure to cognitive decline but have not

compared younger and older individuals and have not measured cognitive

performance over an extended time period.

• The results emphasise the importance of reducing high blood pressure even in

younger adults, the researchers said.

• "To the extent that BP (blood pressure) effects on cognition are not reversible, it

is important to prevent an increase in BP levels as early as possible in the life

cycle," they added.


Measurements of BP 268

Figure -12

Accurate BP measurement by sphygmomanometer in the physicians’ office

remains the principal method of diagnosis. There is insufficient evidence to recommend

the routine use of echocardiography, self-measurement of BP or ambulatory BP

monitoring in diagnosis 269. While there is good evidence to recommend anti-

hypertensive therapy for young and middle-aged adults with diastolic pressures of 90 mm

Hg or over, the clinical decision to initiate pharmacologic treatment should take into


account the individual’s absolute risk for cardiovascular disease, particularly when the

average diastolic pressure is in the range of 90 to 99 mmHg and there is no hypertensive

target organ damage or other concomitant diseases 270.

Incidence:

Despite many recommendations, poor control of SH is increasing. A recent study

examining trends in hypertension control found that isolated elevation of SBP was the

most common finding among patients being treated for hypertension (high blood

pressure), occurring in 76 percent of patients in 1999 compared with 57 percent in 1990-

1995.

Three out of every 10 Chinese adults have high blood pressure, one of the highest

rates of hypertension in the world. The prevalence of hypertension among people aged 35

to 74 has reached 27.2 percent, putting the blood pressure of 130 million adults above the

normal level 271. A recent study of 111 African-American people with high blood

pressure found that a meditative technique lowered blood pressure on par with anti-

hypertensive drugs 272. With 50 million adults suffering from high blood pressure in the

United States, worries about the state of the nation's health are increasing. And your

pressure being just a little more than 120 over 80 may not be good enough any more.

Millions of people do not even know if they have hypertension. That is why it is called

the silent killer 273. Research has shown that hypertension is on the rise in India,

especially in urban populations where it has been linked to lifestyle changes and the

stress of urban living 274.

Around 10 million people in the UK have high blood pressure, in which one in

five of UK living 275. In 90 to 95 percent of high blood pressure cases, the cause is


unknown, when the cause is unknown, you have what's called essential or primary

hypertension 276. As many as 60 percent of American adults have hypertension or are

borderline under revised thresholds for high blood pressure. Chicago researchers,

published in the Archives of Internal Medicine, reported that 58.2 percent of adults in a

1999- 2000 government survey either suffered from high blood pressure or were pre-

hypertensive under new guidelines set last year. New Jersey researchers - estimated that

as many as two-thirds of people between the ages of 45 and 64 and 80 percent of those

between 65 and 74 might have pre-hypertension or residual hypertension -- having a top-

number blood pressure of 140 millimetres of mercury or higher despite treatment. High

blood pressure affects about 50 million Americans, and contributes to more than 250,000

deaths each year. But researchers believe only about a third of people with high blood

pressure have it controlled by medication 277.

Hereditary:

The researchers found that parents' BMI -- before pregnancy for mothers, and

during pregnancy for fathers -- was related to their 5-year-old's blood pressure, as was the

child's own BMI. In addition, both parents' weights influenced their child's blood

pressure, which rose in tandem with mothers and dad's body mass index (BMI) 278.

Tobacco usage

Tobacco smoking or chewing not only causes the nicotine deposition in the

respiratory endothelial system and in the gastrointestinal system but also elevates the

blood pressure significantly to cause circulatory disorders resulting in an infarct. Besides

this, it also creates its carcinogenic effects. Some studies were conducted in AMI

patients, who were smokers or non-smokers in order to visualise the effect of nicotine on


lipid parameters. It was concluded that the lipid parameters are not altered by the nicotine

concentration. The aetiology of infarct in these cases may be other than the smoking or

chewing of tobacco.

Co-morbid conditions

Cholesterol

Cholesterol is a chemical that is made in the liver from fatty foods that you eat. A

certain amount of cholesterol is present in the bloodstream. We need some cholesterol to

keep healthy. However, if you have a high blood cholesterol level, you have an increased

risk of developing atheroma. A build up of atheroma can cause heart diseases such as

angina and heart attacks, stroke, transient ischaemic attack (TIA or 'mini-stroke'), and

peripheral vascular disease (narrowing of the arteries to the legs). Patches of atheroma are

like small fatty lumps which develop within the inside lining of arteries (blood vessels).

A patch of atheroma makes an artery narrower, which may reduce the blood flow. Over

time, patches of atheroma can become larger and thicker.

Causes of atheroma development

The following are the causes of atheroma development.

• Smoking.

• Hypertension (high blood pressure).

• High cholesterol level.

• Diabetes.

• Obesity.

• Lack of exercise.

• An unhealthy diet.


• A strong family history. This means if you have a father or brother who

developed heart disease or a stroke before they were 55, or in a mother or sister

before they were 65.

• Being male.

• Ethnic group (for example, southern Asians in the UK have an increased risk.)

Some risk factors are more 'risky' than others. For example, smoking causes a greater risk

to health than a lack of exercise. Also, risk factors interact. So, if you have two or more

risk factors, your health risk is much more increased than if you just have one.

'High’ cholesterol level 279

As a rule, the higher the cholesterol levels the greater the risk to health. As a

guide, a level less than 5 mmol/l is considered 'good', and is often the target advised to

aim for. A 'risk factor calculator' is used by doctors and nurses to predict the health risk

for an individual. The calculated score takes into account all your risk factors. Current

guidelines advise that you should lower your cholesterol level if your score gives you a 3

in 10 risk (or more) of developing heart disease within the next 10 years, and your

cholesterol level is higher than 5.0 mmol/l.

Causes high cholesterol

• In most people, your cholesterol level reflects the amount of fat that you eat. This

is not the full story as different people who eat the same amount of fat can make

different amounts of cholesterol. However, in general, if you eat less fat your

cholesterol level is likely to go down.


• In some people a high cholesterol level is due to another condition. For example,

an underactive thyroid gland, obesity, drinking a lot of alcohol, and some rare

kidney and liver disorders can raise the cholesterol level.

• In a small number of people a very high level of cholesterol runs in the family due

to an inherited genetic problem. One example is called familial

hypercholesterolaemia.

Importance of lipids

Cholesterol occurs as the alcohol (free cholesterol) and in the esterified form, in a

proportion that is fairly constant. About 70% of the cholesterol are esterified except in

obstructive disease of the liver and some rare diseases. Practically all the sterol in plasma

is 280-281 cholestene - 3 beta-ol.

Cholesterol is deposited in the intima of artery. In the later stages, calcium gets

deposited along with cholesterol in the vascular system. This deposition is referred to as

sclerosis of the arteries. This causes a greater resistance to the flow of blood. In order to

comply with the demand of oxygen from the body cells, the heart has to pump with more

force of contraction and in doing so the blood pressure increases due to the increase in the

heart rate. As a result of this in the prolonged state of uncontrolled hypertension, the left

ventricular hypertrophy occurs and the size of the heart is also increased.

The level of cholesterol in plasma is decided mainly by the following factors :

a. Dietary intake of cholesterol

b. Cholesterol catabolism of hormones

c. Endogenous biosynthesis of cholesterol

d. The excretion of cholesterol


The net result of these four factors is the cholesterol level in the blood. It will be

therefore appropriate to discuss the above factors.

It has been observed that uncontrolled diabetes leads to the abnormal deposition

of cholesterol producing thereby atherosclerosis and circulatory disorders. Apart from

this, it creates, hazards viz. impotency in the sexual system, especially in the males, by

excessive production of prostaglandins due to uncontrolled intake of unsaturated fatty

acids. Intake of aspirin daily not only prevents the clot formation but also overcomes the

sexual hazards.

Excessive intake of triglycerides in the diet elevates the plasma triglyceride

concentration due to the absorption of lipids. In diabetes mellitus, when there is a total

failure of the pancreas, both in the production of insulin and that of pancreatic lipase,

triglycerides of the diet are not hydrolysed. With the result, they are accumulated in the

blood causing thereby an increase of plasma triglyceride concentration. This increases the

viscosity of blood. Such viscous blood will affect the blood flow and the pressure and

eventually will affect the blood circulation, which in turn affects the oxygen supply to

various tissues of the body. High triglyceride concentrations are associated with an

increased risk of ischaemic heart diseases. However, the increased risk cannot be

attributed to triglycerides alone, since these values are associated with high total

cholesterol concentration and lower values of HDL concentration 282. It has been said

before that the intake of small chain fatty acids in limited amounts and their esterification

with glycerol (butter) will help the requirements of fat in the diet. This may restrict the

consumption of saturated fatty acids.


Lipoproteins: Lipoproteins are characterised by the presence of one or more proteins or

polypeptides known as apoproteins. As per the “A B C” nomenclature, the corresponding

apo-fractions represent the lipoproteins carried with them as follows:

Table – 37Apo-fraction representation of the lipoproteins

Apo AI

Apo AIIHDL

Apo B LDL,VLDL and chylomicronsApo CI

Apo CII

Apo CIII

(Smaller polypeptides) VLDL, HDL Chylomicrons

To summarise therefore, Factors responsible for blood pressure would be -

1. Hormones of adrenal medulla

a) Adrenaline

b) Nor-adrenaline

Their effect on heart

function

2. Cardiac output x peripheral resistance

3. Heart rate Na : K ratio(intracellular)

* Intracellular Na+

* Intracellular Ca++

Effective K+ action

4. Effective renin-angiotensin system (Effective blocking)

Angiotensin I

Converting EnzymeAlpha-2 globulin Renin

Angiotensin II

Angiotensin III

5. Dietary intake of sodium and potassium

Atrial natriurectic Factor : Aldosterone Angiotensin III

6. Dietary intake of lipids

Role of CholesterolTriglyceridesSaturated and unsaturatedFatty acids freefatty acidsLipoproteinsApolipoproteins

7. Prostaglandins and oxygen free radicalsFormation depends upon

phospholipids and arachidonic acid.


8. Degree of atherosclerosis

Adipose tissue Catabolism

Cyclic AMP FFA formation

9. Dietary intake of serotonin, tryptophan etc.

10. Ratio of testosterone to oestradiol

However, if one estimates the HDL-cholesterol, LDL cholesterol and VLDL

cholesterol, the risk factor can also be concluded. Various people in this field have

observed that decrease in concentrations of HDL-cholesterol with simultaneous rise in

the concentration of LDL-cholesterol indicates the risk of ischaemic heart disease.

Apolipoprotein B-100 (Apo B) is the major structural compound of very low-density

lipoprotein (VLDL) and low-density lipoproteins (LDL). Therefore, VLDL apo-B and

LDL apo B determination could be a good diagnostic index for the risk involved in the

development of CAD. As there is one molecule of apo-B per lipoprotein particle,

determination of total serum levels of apo B provides a measure of total number of

VLDL and LDL particles in the circulation 284-290.

Episodic Hypoxia and Sympathetic Output

Acute hypoxia contributes to an acute rise in blood pressure during and following

apnea. In fact, the level of oxygen-hemoglobin desaturation during acute apnea is directly

related to the magnitude of blood pressure change associated with apnea. Supplemental

oxygen provided to subjects with simulated recurrent apneas ameliorates the blood-

pressure increase in response to apnea 291-292.

Syndrome Z

The features of syndrome Z include hypertension, central obesity, insulin

resistance, hyperlipidemia, and OSA. The factors influencing the relationship between

blood pressure and cardiovascular risk include systolic blood pressure, diastolic blood


pressure, circadian blood pressure patterns (dippers vs nondippers), blood pressure

variability, and cardiac and vascular hypertrophy. Abnormal vascular endothelial

function has been reported in hypertension, diabetes mellitus, and hyper-lipidemia. This

may precede the onset of cardiovascular disease symptoms by many years. As discussed

above, abnormal endothelial function may be present in the patients with sleep apnea and

hypertension. Whether sleep apnea affects endothelial function independently of

hypertension and insulin resistance requires further research.

OSA is closely linked to the cluster of cardiovascular risk factors known as

syndrome X (a cluster of risk factors including systemic hypertension, insulin resistance,

hyperlipidemia, and central obesity) and the converse is also likely but has not yet been

proven (syndrome Z) 293-294.

Plasma renin concept

Renin is the enzyme synthesised by juxta-glomerular cells with the help of cyclic

AMP or cyclic GMP. Cyclic AMP is formed by the action of adenylcyclase on adenosine

triphosphate (ATP). This formed cyclic AMP is destroyed by the enzyme

phosphodiesterase to produce 5’ AMP. Insulin promotes this action whereas ACTH,

TSH, glucagon, catacholamines, growth hormone and gluco-corticoids activate

adenylcyclase and promote the formation of cyclic AMP. The effective concentration of

cyclic AMP that is the availability of cyclic AMP in juxtaglomerular cell decides the

level of plasma renin formation. It will be interesting to note that prostaglandin E1 and

prostaglandin E2 block the lipolytic activity by effectively blocking the formation of the

cyclic AMP, which is under the control of bradykinins 295-299.


Renin acts on a alpha-2 globulin known as angiotensinogen and converts it to

angiotensin I which consists of 10 amino acids. Angiotensin I is further acted upon by

converting enzyme and is converted to angiotensin II which consists of eight amino acids.

Angiotensin II has a stronger vasoconstrictory action than that of angiotensin I.

Angiotensin II is further converted to angiotensin III. The action of converting enzyme is

blocked by angiotensinase. Drugs like captopril block the formation of angiotensin II and

angiotensin III. Pressor activity of angiotensin II is 200 times more than that of

norepinephrine. Both angiotensin II and angiotensin III exhibit the sodium retention

property and act like aldosterone. Therefore, plasma renin has a larger role, in handling

sodium and potassium. Patients with high renin in essential hypertension have been

considered to be of vasoconstrictory type and to have a contracted plasma volume due to

the overwhelming pressor effect of angiotensin II. Propranolol, a beta-adrenergic receptor

blocker nhibits the release of renin by the kidney.

Dr. Laragh’s associates especially Dr. Brunner suggested that renin is a

vasculotoxic substance. The vascular sequelae of high renin levels in essential

hypertension should include strokes, myocardial infarction, renal damage, retinopathy

and encephalopathy. Mroczek and Finnerty found that there were many Negro patients in

U.S.A. who had high renin levels in essential hypertension but did not suffer from

vascular sequelae. It is therefore clear that high renin alone may not be the cause of

vasculotoxicity. A sustained hypertension may be cardiogenic and vasculotoxicity may

be due to sodium and calcium load.

When the Species of anti-hypertensive drugs 300 are administered to patients with

essential hypertension, it induces a significant drop in diastolic pressure in those with


high renin, intermediate drops in those with normal renin 301-302 and very little or no

response in individuals with low renin. Patients with essential hypertension could be

classified with levels of renin as 303-304 - Low renin -30% (Approx.), High renin - 15%

(Approx.) and Normal renin - 55% (Approx.).

The possible aetiology of renin elevation in juxta-glomerular cells in renal cortex is

1. decreased arterial blood flow

2. partial ischaemia of kidney region

3. low sodium concentration in ascending limb of Loop of Henle and distal

convoluted tubule and

4. low potassium levels in plasma and in intracellular compartments.

Renal kallikrein-kinin system

Urinary kallikrein is an enzyme synthesised by the kidney 305. It is involved in the

generation of vasodilating peptides called kinins, which include bradykinin 306. Tissues

other than kidneys, viz. Pancreas and salivary glands also possess kallikrein-kinin system

307-309. All these are similar to one another, but they differ from activity of the plasma

kallikrein-kinin system 309. It is postulated that the renal kallikrein system may be

involved in the pathogenesis of hypertension 310. Kidney kallikrein reacts with kininogen

(brady-kininogen), a substrate found in liver to yield bradykinin. The action occurs in

interstitial cells of the renal medulla. Bradykinin is a vasodilator and it may be that this

effect is partially related to the ability of kinin to stimulate synthesis of prostaglandins.

Conversely, prostaglandin themselves may stimulate renal kallikrein release.


Prostaglandins 311

Prostaglandins are derived from C20 eicosanoic or arachidonic acid with

methylene interrupted bonds. Prostaglandin E2 and prostaglandin A2 produce peripheral

vasodilatation and hence lower the blood pressure. However, prostaglandin F2 constricts

arterioles and the overall circulatory system and also increases the heart rate thereby

increasing the force of heart contraction. The resultant effect of vasoconstriction and

vasodilatation decides net blood pressures. Serotonin is vasoconstrictory in action and

raises the blood pressures. Therefore, its presence in food (Ahara in Annavaha srotas) or

the presence of large amount of tryptophane in diet should therefore multiply the effects

of vasoconstriction and eventually high blood pressure will result.

It is an established fact that sodium stimulates the sinoatrial node in the

myocardium and the impulses are further carried to emphasise a systole, the magnitude of

which affects the overall resultant force of contraction of the heart. The sino-atrial node is

also governed by the presence of calcium ions. Conversely to this force of contraction, is

the inhibitory effect produced by potassium ion, which induces bradycardia and governs

a diastole.

The relationship of sodium to potassium ions is to be taken into account while

discussing the role. The retention of sodium takes place by the loss of potassium ion from

the body. Administration or intake of sodium chloride causes the excessive accumulation

of sodium intra-cellularly with the loss of potassium. It has been already established with

increase in Na++ and that of Ca++ produces a vasoconstrictory effect while potassium

nullifies this effect. Therefore, it will be worthwhile to discuss the mechanism by which

the concentration of Na+ and Ca++ is raised.


Na-K Pumping:

This is an active process of diffusion of Na+ and K+ in the opposite direction

which is described as "Antiport" process while the diffusion in the same direction is

referred to as "Symport". ATPase enzyme, present in the cell-membrane hydrolyses ATP

molecule to the aspartate residue. This reaction is coupled with removal or transference

of 3 Na+ ions from intracellular region to extracellular region, with simultaneous transfer

of 2 K+ ions from extracellular region to intracellular region. This process of active

transport, which is energy bound, is influenced by two factors namely.

1. Atrial natriuretic factor

2. Release of aldosterone or some compound produced by the kidney tissue exerting

aldosterone like activity.

Atrial-natriuretic factor

This factor was earlier reported in the 1980s in the crude extracts of atrial heart

muscles. This crude extract was from majority of atrial muscle fibres (cardiocytes in

mammalian atria) and appeared to be morphologically differentiated as both contractile

and secretory cells. These cells contain numerous membrane bound granules called as

atrial granules storing the polypeptide hormone. This polypeptide exerts its action as a

diuretic and therefore is referred to as natriuretic peptide or factor; and it contains 28

amino acids, which are identified as peptide chain. This peptide was sequenced in 1984.

On its secretion, the aldosterone production is inhibited. Therefore, it promotes the

sodium excretion. It has been observed that it increases the glomerular filtration rate and

a large amount of volume is excreted with a hypotonic urine formation 312.


The discovery of ANP led to search for other peptides with natriuretic activity. In

1988, the brain natriuretic peptide (BNP) and in 1990, the C-type natriuretic peptide

(CNP) was identified 313 ANP, BNP and CNP are structurally similar but only 12 amino

acids are common to all three peptides out of 28 amino acids for ANP, 32 amino acids for

BNP and 22 amino acids for CNP. Though, both BNP and CNP were originally identified

in porcine brain, concentrations of BNP are much more higher in the heart than in the

brain.

Normally, ANP is stored in large concentrations in atria with much less

concentrations than in the ventricles, whereas, BNP is derived from the cardiac ventricles

to a much greater extent. The ventricles secrete a large amount of BNP though they store

only a small quantity. Plasma concentrations of ANP are usually higher than the plasma

concentrations of BNP. However, it has been observed that plasma BNP concentrations

are increased in cardiac failure. In congestive cardiac failure due to a left ventricular

hypertrophy, plasma BNP concentrations exceed the plasma ANP concentrations and

therefore, plasma BNP is regarded as a very sensitive indicator of left ventricular failure.

The overall biological effects of BNP are very similar to ANP in promoting the

sodium excretion and causing vasodilatation. The inhibitory effect on aldosterone

production is through the release of GMP. Richards et al 314-315 found an inverse

correlation between plasma BNP and cardiac output. Davies et al 316 has noted high ANP

concentrations, in-patients who subsequently developed cardiac failure. However, it has

been proved that BNP is a good early marker for left ventricular failure, which can

identify hypertrophic obstructive cardiomyopathy better than echocardiography 317-319.


It would be interesting to note the exact mechanism of sodium excretion caused

by the formation of these peptides. When excessive retention of sodium occurs in the

body in the intracellular region, it stimulates the release of atrial natriuretic peptide 320.

Retention of sodium will cause an increase in the blood volume which inturn increases

the blood pressure.

The factor ANP has a direct effect on the ATPase pump mechanism in the kidney.

When the blood circulates through the hypothalamic region, the oscmoreceptors located

in this region are stimulated by the increased osmolarity of the blood, with the result the

ANP synthesis takes place. With the formation of ANP, aldosterone activity is inhibited.

As there is no or less aldosterone activity, reabsorption of sodium does not take place and

it allows excess of sodium excretion from the tubule. It may be noted that ANF formation

suppresses the aldosterone activity by suppressing the ATPase activity, thereby causing a

loss of sodium in the urine along with increased volume. Figure represents the normal

Na-K pump, which maintains the normal sodium and potassium ratio at the intracellular

level.

The overall effect of excessive intake of sodium results in the change of Na: K

ratio thereby affecting the normal physiological function of the cell. This becomes an

unexplained evident aetiology for the essential hypertensive disorders 321. Recently,

Spencer from the University of Minnesota Medical School 322, while studying the use of

diuretics in the patients with heart failure had reported studies on dietary sodium.

Normally, ingestion of 6 g/day would be matched by a loss of the same approximate

amount in the urine excluding some negligible losses in stool and in sweat - for a zero net

balance. In the patient with heart failure, consumption of 6 g of sodium/day may result in


excretion of only half that amount, leaving a net positive balance of 3 g/day. Over a long

period, this not positive balance is associated with congestion and oedema in the

pulmonary, abdominal and peripheral compartments. Retention of this 3 g/day of sodium

has been reduced to 1 g/day by the use of diuretics.

Effects of Na-restricted diet with adequate intake of K

Average consumption of adults is estimated as 9.5 gms and Adult men consume

11 gms and women 8 gm 323 per day. As pointed out earlier, a high intake of sodium will

result in high intracellular concentration of sodium and ratio of Na:K will be altered. This

creates an adverse effect on systolic and diastolic pressures 324. However in such a

condition, the intake of salt free diet meaning thereby salt is not added while cooking or

while eating, produces a change in intracellular concentration of Sodium and Potassium,

thereby correcting the altered Na:K ratio. As the intake of salt is reduced by way of diet,

the added source is eliminated, yet the body receives sodium by way of water and natural

liquid intake. It has been said before that salt restriction corrects this Na:K ratio.

A supplement of normal intake of K will facilitate this correction of ratio, which

results in achieving an early control over blood pressure 325-326. However, as the ATPase

reaction is energy bound, the authors in the above studies have added a mixture of 17

mEq of NaCl and 67 mEq of K and left the body to decide its own homeostatic

mechanism - to correct this Na:K ratio. Once the ratio is corrected on prolonged

treatment with combined regime of salt (NaCl + KCI) therapy the normal operation of the

ATPase continues in maintenance of Na:K ratio 327-329.


Ama vis-à-vis free Radicals

Free Radicals

Molecular oxygen has a very little capability of oxidising other chemical

compounds. Instead, it must be first converted into an active form of oxygen. There are

several different forms of active oxygen and these forms are often called as oxidising free

radicals. One of the most important forms is the superoxide free radical (O2-).

Even when the partial pressure of oxygen is at normal level i.e. 40 mm of Hg,

small amounts of free radicals are continually formed from the dissolved molecular

oxygen. However, the tissue contains multiple enzymes that rapidly remove the free

radicals including especially peroxidase, catalase and superoxide dismutase. Therefore,

the normal haemoglobin-oxygen buffers mechanism functions properly resulting thereby

in the maintenance of the normal tissue partial pressure of oxygen. The removal of free

radicals from this tissue under the maintenance of the tissue partial pressure of O2 is so

fast that the free radicals have practically no adverse effect on the tissue.

Treatments:

1) Virechana: Castor Oil cleansing

Castor oil cleansing is very good for hypertension because it tends to cleanse the

liver and the intestines and reduce the salt in the body 330.

2) Pancha bhoota healing for Hyper Tension 331

Hypertension has become one of the most prevalent health problems. Diet, stress

and sedentary life style are some of the most important causes. Pancha bhoota healing

uses all the five elements to bring the blood pressure to normal.


Water therapy helps to detoxify the body from toxins and eliminates the salt.

Detoxification through diet, pranayama, yoga and relaxation will facilitate the healing

better.

Reducing refined foods and eating natural foods is the best approach for

hypertension. Juicing is one of the best way to reduce pressure. Here are some

suggestions.

3) Folate Lowers High Blood Pressure Risk for Women 332

Folate, a vitamin already known for its power to prevent birth defects, also

appears to reduce the risk of high blood pressure for women both young and old. Folate

also reduced the risk of high blood pressure in older women, but to a lesser degree, the

study found. Folate is a B vitamin that is found naturally in leafy green vegetables such

as spinach and turnip greens, fruits, dried beans and peas. To consume 800 micrograms a

day, you would need to take a multivitamin plus eat three-quarters of a cup of breakfast

cereal fortified with 400 micrograms of folate, or other foods. A half cup of spinach, for

instance, has 100 micrograms, and three ounces of beef liver has 185 micrograms.

4) Stress Management

In one study, 132 healthy men and women were put under various stresses. Blood

pressures typically went up, depending on the level and type of stress.

5) Stress Reduction through Transcendental Meditation 333

127 African-American men and women attending an inner city hypertension

clinic were allocated to one of three groups. The first practised Transcendental

Meditation 334 (TM) for 20 minutes twice a day, the second used progressive muscular

relaxation for the same amount of time, and the third received an educational lifestyle


modification program. At the end of three months the blood pressure in the TM group

was lower than in the educational group (by 10/6 mm Hg mm Hg -- systolic/diastolic -- in

the women, and 13/8 in the men). Inconsistent changes were seen in the relaxation group.

The blood reductions with TM were equally big in people who had high or low levels of

stress. In both active treatment groups the compliance with the program was very high

(97% of people in the TM group and 81% in the relaxation group practiced their

technique twice a day).

At the end of three months the blood pressure in the TM group was lower than in

the educational group (by 10/6 mm Hg mm Hg -- systolic/diastolic -- in the women, and

13/8 in the men). Inconsistent changes were seen in the relaxation group. The blood

reductions with TM were equally big in people who had high or low levels of stress. In

both active treatment groups the compliance with the program was very high (97% of

people in the TM group and 81% in the relaxation group practised their technique twice a

day) 335.

6) Supplements

You can incorporate dietary supplements into your diet that specifically address

hypertension. Note that it is extremely important that the proper dosage be taken. It is

also wise to work in partnership with a qualified health practitioner. Anti-hypertensive

medications should not be abruptly discontinued.

Supplements that are known to positively influence hypertension include 336-

1) Magnesium

2) Potassium

3) Calcium

4) Coenzyme Q10


5) Garlic

6) Taurine

7) Herbs such as Hawthorn, and

8) Essential fatty acids may also help to control blood pressure.

7) Yoga and Blood pressure management 337

While practising the Pranayama i.e. Kumbhaka, if the Jalandhar Bandha is not

performed properly by contracting the neck muscles the blood pressure will rise the BP

and it may lead to permanent Hyper Tension. Hence it is essential to perform the

Jalandhar Bandha properly to keep the BP on the lower side during the practice of

Pranayama with Kumbhaka.

8) Weight therapy to lower Blood pressure

Blood pressure can be controlled by losing weight, exercising, quitting smoking,

eating less salt and consuming no more than one or two alcoholic drinks per day. If

lifestyle changes aren't enough, drugs usually can bring blood pressure under control.

However, many people stop taking medications, or take their pills intermittently.

The UIC study found that only 69 percent of adults with hypertension knew they

had the condition. And only 31 percent of patients with high blood pressure had

succeeded in getting their numbers below 140 over 90. These findings point to a "serious

problem of low awareness and inadequate management of hypertension," the researchers

wrote.

9) Treatments of Blood Pressure 338

The first course of action usually involves lifestyle changes, especially for people

with pre-hypertension.

• Start eating a low-fat and low-salt diet.


• Lose weight, if you need to.

• Begin a regular exercise program.

• Learn to manage stress.

• If you smoke, quit.

• Drink alcohol in moderation, if at all. Remember that moderate intake is an

average of one or two drinks per day for men and one drink per day for women.

Pathya:

Principles of the diet 339

• Low calories , Low sodium , Low fat , Cholesterol, Normal protein intake

Firstly, if the person is obese his weight needs to be reduced. This can be done by

reducing the intake of calories -- to 20 kcals per kg ideal body weight. And increase the

energy spent by increasing exercise, the safest being brisk walking. Protein in the form of

dals, sprouts, legumes can be taken in the normal quantity. Normal servings of chapati,

rice, pasta or other cereals are allowed. Fat intake needs to be reduced considerably. Fat

added while cooking needs to be restricted to about 2-3 tsp per day than to ghee, butter,

cream, are a strict no since they are high in cholestrol. Some foods themselves are high in

fat like animal products. The fat in them contains cholesterol, which is lethal to

hypertensives.

Foods high in cholesterol are egg yolk, ghee, butter, cream, cheese, kidney, liver,

brain, red meat. Fish and fish oils are however beneficial for hypertensives. They contain

the n-3 fatty acids, which controls hyperlipidemia, reduce incidence of blood coagulation,

thereby reducing the incidence of a blood clot and an infarct (heart attack or stroke).


A general question asked by many hypertensives is that which oil should be used.

The answer is groundnut oil is the best choice. It has the near perfect ratio of poly and

mono unsaturated fatty acids that is beneficial to maintain good cardiovascular health.

SODIUM:

Sodium is osmogenic, which means the higher the sodium content in the blood it

will draw more water from the surrounding tissues into the blood to dilute it thereby

increasing its volume and thus pressure on the walls of the arteries and veins and creating

what is commonly known as blood pressure. Thus, by reducing sodium one is

automatically reducing the blood pressure. Mild hypertension can be controlled by diet

alone that is by controlling sodium and fat. Common salt is the highest in sodium (it

chemical formula is sodium chloride).

Other foods high in sodium

are:

1) Salted butter

2) Cheese

3) Salted bread

4) Tinned foods

5) Tomato sauce

6) Soya sauce

7) MonoSodiumGlutamate

(Aginomoto)

8) Wafers

9) Cakes

10) Biscuits

11) Baking powder

12) Cornflakes

13) Pickles

14) Papad

15) Lobster

16) Shellfish

17) Beacon

18) Peanut butter

19) Frozen foods

20) All foods where salt has been added

on the top


Sodium sources

Canned, prepared, and “fast” foods are loaded with sodium; so are condiments

such as ketchup. Even some foods that don’t taste salty contain high amount sodium.

Consider the values below:

Food-----------------------Milligrams of sodium1 can tomato soup------------------------8721 hot dog-----------------------------------6391 cheeseburger----------------------------7091 tablespoon ketchup---------------------1561 dill pickle--------------------------------9281 cup corn flakes--------------------------256

Other high-sodium sources include baking powder, baking soda, barbecue sauce,

bouillon cubes, celery salt, chili sauce, cooking wine, garlic salt, onion salt, softened

water, and soya sauce. Surprisingly, many medicines and other nonfood items contain

sodium, such as alkalizes for indigestion, laxatives, aspirin, cough medicine mouthwash,

and toothpaste.

CALCIUM: Calcium is involved in the control of strength with which blood is pumped

by the heart. Increasing calcium intake reduces the incidence of hypertension and all

other cardiovascular disease.

FIBRE: A high fibre diet helps to physically entangle some amount of ingested

cholesterol and fat from the food and throw it out of the body even before it can be

digested via the faeces. Secondly it adds bulk to the diet thereby the person feels full yet

he has taken in much lesser calories than if he had ingested the same quantity of low fibre

foods. Foods high in fibre are vegetables (preferably raw and with the peel wherever

possible), leafy vegetables, legumes (again wherever possible with the skin). One

important thing all cardiovascular patients need to remember: Do not eat large meals this


will build the pressure on oxygen requirement since it is required for food digestion if

more is drawn for this function less will be available for other important functions

thereby causing breathlessness. Hence small frequent meals are advisable. Diet control

and exercise generally alone control mild to moderate hypertension. Only in cases of

severe hypertension diet, exercise and medication together can control the blood pressure.

Evaluation of the subjective parameters of Bhrama

Different symptoms evaluated at the study under the heading of Bhrama vis-à-vis

hypertension with the presenting complaints are foot forth here for discussion.

The first and fore most complaint is Bhrama i.e. giddiness. All the patients in the

study (100%) reported the Bhrama, which is said as the “Pratyatma Niyata Lakshana”.

The giddiness may be either hypoxia or mal-function of haemopoitic system including

respiratory system or even it is because of the involved neural controls. But the ultimate

cause could be attributed to that of the high salt intake. Ultimately a Symptom giddiness is

witnessed in the Bhrama is undoubted.

The next most common complaint is shira shoola i.e. headache. 20 patients

(66.6%) reported with the headache. The Shiras is also termed as Hrudaya in Ayurveda.

The Rasayana effect imposes the normal function of the head concerns i.e. and disposes

the person to attain the sleep there by the symptom sleeplessness and headache are

relieved.

The third complaint is anhgasada, with the 14 (46.6%) patients and associated

with the nidranasha (Sleeplessness) of 13 (43.3%) patients. This clearly states that the

involvement of the head and neural control in the disease. Induction of the sleep is a


function of the psychotropic drug. Here the psychotropic drug is Bala. It acts over the

condition Bhrama, which is a psychophysical state of disease.

Not at the least but still the patients reported with the complicate complaints such

as Hrudrava (7 patients – 23.33%), Klama (6 patients – 20%) and Urah shoola (2 patients

– 6.7%). All these symptoms are pertained to that of the Uro-Hrudaya, i.e. cardiac heart.

The cardiac protective phenomenons are to be induced whenever the management of the

hypertension vis-à-vis Bhrama is undertaken.

Materials (Kakubhadi Lehya) evaluation

Chiefly the composition of the “Kakubhadi Lehya” consists of pancha Rasa

except the Lavana Rasa. Predominant Rasa is Madhura added with that of the Katu Rasa.

The actions of these Rasa are emphasised as nourishing and cleansing. The chief

pathology lies in the arteries in which the “Dhamani Pratichaya” is witnessed. The

Dhamani Pratichaya i.e. aetherotic plaques can be prevented and removed by the Tikta

and Katu Rasa. The Madhura Rasa nourishes the entire body through its preenana effect

through the adyarasa Dhatu, which is circulated through out the body till to Rasayani i.e.

arterioles. The other Rasa present in the composition are Amla and Kashaya. The Amla

Rasa plays major role in the citrus acid cycle and prevents the formation of the LDL and

VLDL cholesterol in the body. In further the Amla Rasa acts over the conversion of the

Rasa in to Rakta Dhatu under the influence of the Ranjakapitta. Thus the action of the

Rasas in the “Kakubhadi Lehya” is substantiated.

Hrudya – the origin of the disease is heart, thus the medicine is expected to act on

the organ concerned. In further the heart propels the blood under the influence of the

Vyanavata and there by the blood attains the stroke volume and velocity. The normal


function of the heart to resume is the primary duty of a physician who is treating such

condition. Many a times it is drawn attention to treat symptomatically rather than

strengthening the concern organ i.e. heart. Here an attempt is made to promote the vitality

of the heart and there by regulating the blood pressure through the Hrudya property of the

Kakubhadi Lehya as Hrudya Rasayana.

Rasayana – the condition hypertension is long associated, thus the disease needs

the long tern protective management instead of the temporary symptomatic management.

In this trail it is brought in to focus as the need of the Rasayana, which helps the body in

total and also fortifies the heart and circulation. The Rasayana chronologically nourishes

the Rasa to Sukra and there by normalise the body humours and functions. Kakubhadi

Lehya is such a combination in which many Rasayana properties are embedded.

Mutrala – the primary management of the hypertension is diuresis in the

contemporary medical practice, because of the involvement of the renin – angiotensin in

renal system. A medicament, which helps to regulate the water system in the body and

there by regulating the pressure in arteries, is the basic mechanism at the first step of

management in the Bhrama vis-à-vis hypertension. In this Kakubhadi Lehya many

mutrala prabhava herbs are included as to give a proper elimination of the waste from the

body in association with regulating the renin – angiotensin mechanism.

Kasaswasahara- Acute hypoxia contributes to an acute rise in blood pressure

during and following apnea, which resembles the conditions pertaining to that of the

pranavaha Srotas and there by a pharmacological property which regulates the respiratory

system and ventilation is necessary. Proper ventilation and regulation of the haemoglobin

makes an individual to respond properly to that of Rasayana management. More over the


Kakubhadi Lehya with increased values as kasa swasahara restore the lung functions,

which are very basic of a disease concerned to blood and its circulation.

Anulomaka – is a property to control the disease-disposing factor Vata (neural

control). Experimentally, stimulation of several areas in the central nervous system

(Medulla, nucleus tractus soliterius, vasomotor centre and vagal nuclei) has shown to

raise or lower blood pressure. The anulomana makes the regulation and pacification of

the Vata there by the neural controls is regulated through the Kakubhadi Lehya, which is

a Vata Kapha hara in nature.

Panduhara – is a property directly related to that of regulation of the blood and its

contents. Many conditions may terminate in to the Pandu i.e. anaemia. Mainly the lack or

breach of the haemopoitic system can cause effect over many areas espicially on heart

and kidneys, which are directly involved in the pathology of hypertension vis-à-vis

Bhrama. Kakubhadi Lehya is such a medicine acts over the loss of haemoglobin and the

other factors in the formation of the blood either directly or indirectly.

Yogavahi – is such a property termed in Ayurveda, in which the drug penetrates

in to the micro areas of living i.e. deep in to the cellular repair. Contemporary practices

may not think of the deep root effect of the hypertension vis-à-vis Bhrama, but an

Ayurvedic practitioner mean it. Thus the property embedded Pippali is one of the

components of Kakubhadi Lehya, which permits the penetrability of the anti-

hypertensive effect deep in to the cellular level, where the real Na and K exchange and

regulation is needed.


Individual components of Kakubhadi Lehya explored

1) Arjuna

(1) The hypotensive and cardiotonic properties are reported (Hippokrates, 1982).

(2) The diuretic, hypotensive and cardiotonic properties are reported (J. Res. Edu. Ind.

Med. 1988 Oct- Dec. P.31-36).

(3) In a clinical study the role of Arjuna is studied over IHD and the drug is found to be

effective in correcting the T-wave changes (Chaturvedi, 1967).

(4) The cardiotonic activity of Arjuna (T.arjuna) is reported from NIA, jaipur (Jha,

1983)

(5) Its bark significantly decreased the elevated cholesterol and increased the HDL

cholesterol. It was also noted that the prostaglandin levels which were low have

been increased and high levels of catecholamines were brought down by the

administration of the drug besides relief from symptoms like pain, palpitation etc

(Dwivedi, 1986).

(6) Serum lipids were found to be lowered by administration of bark powder in triton-

induced hyperlipaemia. T. arjuna altered lipolytic activities in plasma, liver, heart

and adipose tissues of hyper lipidemic rats. The lipid lowering effect of this natural

product was found to be mediated through inhibition of hepatic cholesterol

biosynthesis, increased faecal bile- acid excretion and enhanced plasma lecithin:

cholesterol acyltransferse activity and stimulation of receptor mediated catabolism of

low lipoprotein (khanna et al., 1996)

(7) Marked reduction in total cholesterol and raise in the HDL are observed (Intl. J. of

Crude. Drug Res. 1990, 28 (1) : p. 43-47


2) Vacha

1) Cardiac depressant activity was observed both with asarone and B- asarone. Both

showed moderate degree of hypotensive action in anaesthetized dogs (Sharma&

Dandiya, 1962)

2) It was found that the sedative effect of asarone was dependent on the depression of

the ergotropic division of the hypothalamus (Menon &dandiya, 1967).

3) Rasna

1) An important clinical difference was that the plant extract supressed the delayed

periarticular changes more as compared to the acute inflammatory phase (Prasad D. N. cl

al. Ind. J. Meel. Res. 54: 582 (1966).

4) Bala

1) Used for Colds, high fever, mumps, hives [China] Fever [India]

2) An anti- microbial alkaloid cryptolepine, ephedrine and vasicine are reported from the

different species of Sida plant(Guntilaka, A. A. L. et al.: Plania Med. 39: 66 (1980).

5) Nagabala

1) Decoction of the root-bark and root is used in mild cases of debility and fever

2) It is alternative and restorative (promotive) and analgesic action.

3) The management of heart disease has use of Nagbala. The powder of Nagbala root

and Arjuna (bark of tree Terminalia arjuna) are mixed and used with milk.

6) Abhaya

1) Resin and a purgative principle of the nature of anthraquinone and sennoside are also

present in Abhaya. (Tripathi, V. N. et. al.: sachitra Ayurveda, 740, (1983).


2) Triphala is an important formulation in the ayurvedic pharmacopoeia containing

haritaki. Triphala and each of its constituents are well known rasayana drugs . They are

used to prevent aging and impart longevity, immunity and body resistance against

disease. They have beneficial effects on all the tissues(Abhang, R. Y.: Deerghayu, 2: 3

(1976).

7) Shati

1) Hypotensive effect of alcoholic extract of the plant was also reported and attributed to

cholinergic or histaminc responses (shaw, 1980)

2) The alcoholic extract showed spasmolytic effect on the smooth muscles and tracheal

chain. It could counteract the effect of spasmogens like acetylcholine and histamine.

The plant also showed negative inotropic and chronotropic effect on frog heart. It

induced a mild vasodilatory effect (Sharma 1974. 1975).

3) Essential oil of rhizomes showed tranquilising activity of short duration ;

4) it depressed conditioned avoidance response, rotarod performance and

potentiated pentobarbitone hypnosis (Ind. J. Pharmacol. 1979,11, 147).

8) Pushkaramoola

1) Cardiotonic activity – (a) Cordiotonic activity of ag. And adcoholic extracts were

studied on isolated frog’s heart (Sharma & Tripathi, 1986).

2) Hypotensive activity- Hypotensive activity was reported.

3) The extract showed negative inotropic and negative chronotropic effect on frog heart.

Hence indicate that I recemosa may have adranergi beta-blooking activity (Tripathi et

al., 1988).


4) Anti-platelet activity – it is reported to possess anti-platelet aggregation activity

(Dwivedi & Amrita, 1993).

5) Its serum cholesterol lowering effect was found to be highly significant (Sharma, et

al., 1983).

9) Pippali ( Neogi et al.,1971)

1) Piperene revealed a hypotensive effect in dogs and also produced a non-specific

blockade of contractions induced by acetylcholine, histamine and serotonin in

isolated intestine of guinea pig and rat. It also had mild antipyretic activity. ( Neogi

et al.,1971)

10) Viswabheshaja

1) Bio availability enhancer property of Z officinale is also reported (Zutsi., 1986)

2) In a clinical study on Grahani roga the effect of Z. officinale has been found

significant in term of control of number of motions, improvement of body weight,

appetite, Hb% etc (Nanda et., 1985).

3) (E)-8- beta, 17 – exoxylabel-12ene-15, 16-dial (ZT) showed inhibitory effect on the

cholesterol biosynthesis (Tanabe et al., 1993)

4) Significantly reduced the hyperlipidemia-induced by feeding orally on atherogenic

diet for 10 weeks in male albino rabbits (Bhandari & Sharma, 1995).

Evaluation of the objective parameters of Bhrama

It is put forth for the assessment many parameters in the study. The direst







medicament. Different objective criteria are considered to evaluate the Bhrama vis-à-vis

hypertension. The data analysis is as follows.

The factors that have the influence on the physiology (temperature, weight) are

decreased with the baseline mean data in the study. The temperature shows the mean

difference of 0.24 in the study, which is a point of observation to assess the Rasayana

effect induction in the body. The second factor weight has reduced by 0.24 mean value,

suggesting the induction of good health through Rasayana, there by the regulation of the

Bhrama vis-à-vis hypertension.

The third factor of objective parameter observed is haemoglobin percentage. It

shows marked increase of 0.443 mean value. Which is suggestive of inducting Rasayana

effect and also capacitating the oxygen exchange ratio and there by the controlling the co-

morbid conditions or associative such as hypoximea. The associate factor of haemoglobin

is RBC count. This has shown 0.251 mean value increase in the study reflects to the

percentage rise of the haemoglobin and there by regulating the Bhrama vis-à-vis

hypertension.

The next parameter of co-morbidity in Bhrama vis-à-vis hypertension is serum

creatinine. It has shows a rise in the study with a mean value of 0.008. It suggests that the

Angiotensin and Renin involvement in the Bhrama vis-à-vis hypertension have been

successfully reduced and provide the Rasayana effect not only at the cardiac but also in

the renal area. The small amount changes are as a process of regulation in the KUB

system.


Serum cholesterol and associative LDL, VLDL with S.Triglycerides are risk

factors in the pathology of Bhrama vis-à-vis hypertension. Out of these associated the

HDL cholesterol is good for the body and all the rest offers co-morbidity. As the results



study. The rest of co-morbid influencing factors enumerated are LDL (5.2326), VLDL

(2.29333), Serum cholesterol (5.793) and S. Triglyceride (9.08), show the significant

drop and suggest that the effect of the Kakubhadi Lehya on Bhrama vis-à-vis

hypertension with reference to its Rasayana effect over the Bhrama vis-à-vis

hypertension.

Analysis of disease results




Discontinued. The result declaration is done following the norms and conditions of the

inclusive factors and study of the subjective parameters in association with the

sphygmomanometer studies of three postures. The co-morbid stimulating factors

especially LDL, VLDL and S. Triglycerides are considered in while declaring the results.

The factors which make the Rasayana effect over the body also included to assess the

results. After thorough study of the entire parameters and materials available for the



responded and the last 2 (6.63%) patients discontinued in the study.


Age with systolic and diastolic blood pressures enumerated

In this study as we examine different age groups an attempt is made to understand

the linear systolic and diastolic values of baseline data to that of the final data. Whenever

two or more patients of the same age are seen mean values are considered. In this process

the age related blood pressure chart is drawn is explained as above.

Table –38Blood pressure variances of Before to AfterSystolic Blood Pressure Diastolic Blood Pressure

AgeBefore After Before After

28 144 124 92 8029 148.6 127.3 94 82.6632 154 128 86 8233 140 124 88 8234 140 122 90 8435 144 124 88 8237 154 127 96 8638 160 132 96 8439 144 126 98 8840 144 128 92 8646 148 124 92 8249 154 127 93 8451 164 134 92 8252 169 143 108 9055 165.5 145.5 104.5 9259 167 158 100 9360 168.6 149.3 104.6 9261 168 144 94 8465 170 154 108 100

As it is observed that the systolic blood pressure has taken a rise till to 32 years of

age and show a down fall to the age of 34. From that a gradual increase is observed to age

of 38 and stable to the ages of 40. From 40 a rising gradient is observed till to 52 years of

age and becomes more or less stable to the forwarded ages. A linear line drawn in

comparison to that of baseline data to final shows markedly 20 mm Hg differences in the

study. Though many may not give attention to that of the systolic hypertension, which

could be pacified with the rest and regulations needs to drag the attention. At present


study, the effect of Kakubhadi Lehya over the Bhrama vis-à-vis hypertension show

marked drop of 20 mm Hg of systolic hypertension by inducting the Rasayana effect. The

graphical expression with the linear graph is as follows.

Graph –16Linear graph of Blood Pressure - systolic hypertension

Another important reading of the blood pressure is diastolic. It is observed that the

small variances in it can cause the Bhrama vis-à-vis hypertension. The arterial diastolic

blood pressure measured in the study was put for the keen observations, as there are 28-

29, 37-39 and 52-55 age groups show marked elevations. This could be because of the

tension, anxiety, stress, strain etc, psychophysical factors. The linear line is drawn an

observed as the cumulative effect of the Kakubhadi Lehya varies from 15 mm Hg to

20mm Hg of diastolic from the early ages to late. The older people those who receive the

80

90

100

110

120

130

140

150

160

170

180

28 29 32 33 34 35 37 38 39 40 46 49 51 52 55 59 60 61 65

Age

Syst

olic

HT

N

PtsSysBeforeNor SysPtsSysyAfterLinear (PtsSysBefore)Linear (PtsSysyAfter)


Hrudya Rasayana well responded and show the marked relief for the condition. The

diastolic blood pressure graphical expression is as follows.

Graph – 17Linear graph of Blood Pressure - Diastolic hypertension

BMI with systolic and diastolic blood pressures enumerated

At this study one attempt is made to understand the relationships of the BMI with

systolic and diastolic blood pressure. As it is observed that the linear graph drawn on the

basis of data obtained show a clear evidence of the relationship to the BMI and systolic

and diastolic blood pressures. It is an observation expressed that as the BMI is increased

the response to the medicine is decreased or other wise it can be stated that the BMI is

inversely proportional to that of response to the medicine. As the people get more BMI, a

risk factor to the heart and where the depositions of the LDL and VLDL cholesterol are

anticipated is witnessed as a factor determining the result of the medicine. The

70

75

80

85

90

95

100

105

110

28 29 32 33 34 35 37 38 39 40 46 49 51 52 55 59 60 61 65

Age

Dia

stol

ic H

TN

PtsDiasBeforeNor DiastPtsDiasAfterLinear (PtsDiasBefore)Linear (PtsDiasAfter)


tabulations of BMI Vs BP and graphical expressions with linear BMI relationships are as

follows.

Graph – 18BMI with systolic blood pressure

Graph –19BMI with systolic and diastolic blood pressure

TABLE –

100

110

120

130

140

150

160

170

180

18.69

20.95

21.18

21.59

21.77

23.16

23.35

24.05

24.88

25.31

26.13

26.74

29.14

30.53

BMI

Syst

olic

HT

N

PtsSysBeforePtsSysyAfterLinear (PtsSysBefore)Linear (PtsSysyAfter)

70

75

80

85

90

95

100

105

110

115

18.69

20.95

21.18

21.59

21.77

23.16

23.35

24.05

24.88

25.31

26.13

26.74

29.14

30.53

BMI

Dia

stol

ic H

TN

PtsDiasBeforePtsDiasAfterLinear (PtsDiasAfter)Linear (PtsDiasBefore)


Table – 39

BMI vs Blood Pressure

S.No BMI SystolicBefore

SystolicAfter

DiastolicBefore

DiastolicAfter

1 18.69 144 126 98 882 19.94 154 128 86 823 20.95 158 126 98 884 21.07 160 132 96 845 21.18 170 142 110 906 21.48 164 134 92 827 21.59 162 154 100 928 21.64 172 148 110 949 21.77 144 124 88 8210 22.48 144 124 92 8011 23.16 140 124 88 8212 23.18 140 122 96 8413 23.35 158 132 92 8414 23.35 168 144 94 8415 24.05 144 122 92 8016 24.75 150 122 94 8417 24.88 154 126 98 8618 25.11 172 162 106 9819 25.31 172 154 108 9420 26.04 156 124 102 8421 26.13 160 142 98 8822 26.22 168 144 106 9023 26.74 162 138 98 8424 26.875 148 124 92 8225 29.14 172 162 100 9426 29.77 174 162 110 10227 30.53 148 134 92 8228 36.97 170 154 108 100

Mean 24.51232 158.1429 136.7857 98 87.28571

The mean difference of the systolic blood pressure is 21.3572 and that of diastolic

is 10.71429. These differences are the marked in the study as the raised BMI is directly

proportional to the systolic and diastolic blood pressures of the study.


Lipid profile with systolic and diastolic blood pressures enumerated

Table – 40Male BMI with lipid profile variations

BMI HDL LDL VLDL Sch STG0.95 -6 5.5 -6.32 -6.8 -31.6

30.53 0 -1 2 1 1018.68 1 -5 1 -3 424.88 3 -5 -3 -1 736.97 1 2 2 5 924.75 1 4 2 7 11

26.875 2 -7 1 -4 521.77 -6 19 0 13 626.21 -2 8 4 12 2019.94 -12.4 -1.4 -2.6 -16 -13.221.18 2 -5 1 2 621.48 -1 2 2 3 722.48 -1 15 0 14 023.16 0 7 2 9 923.18 0 -8 2 -6 1023.35 1 -3 2 4 926.04 -1 6 2 7 1224.05 -3 2 3 2 225.11 2 4 1 7 7

24.29395 -1.02105 2.057895 0.793684 2.589474 4.694737Table – 41

Female BMI with lipid profile variationsBMI HDL LDL VLDL Sch STG

21.07 1 -4 5 2 2521.59 -2 15 5 18 2521.64 -2 10 0 8 323.35 -3 10 1 8 325.11 -4 21 32 17 -425.31 -1 4 1 4 826.13 -3 15 -1 11 -426.22 -4 4 4 6 1226.74 0 27 1 28 729.14 9 4.88 3.72 17.6 18.229.77 -4 11 2 9 9

25.09727 -1.18182 10.71636 4.883636 11.69091 9.290909Another important observation made in this study is BMI relationships to that of

the lipid profiles of baseline data to the final data, at the gender identification. The male

Vs BMI and Female Vs BMI are tabulated as above.


Limitation of the study

1. the sample size was small

2. limited to that of one particular geographical area

3. the period of study was limited

4. longer follow up was not done

5. parameters like ECG is considered to check the co-morbid condition but

not analysed

Future Scope for the further study

The following recommendations are made on the basis of observations

and conclusions made in the study, as guidelines for the further studies, which

are made in future to over come the limitations listed.

1. Same study can be repeated by taking a large number of samples and

longer duration.

2. The effect of Rasayana can be vividly studied.


Chapter –7

Conclusion1. Primary or essential hypertension in which the causes of increase in blood pressure is

unknown. But for 95% of patients who undergo hypertension treatment, the causes of

high blood pressure are unknown.

2. Essential hypertension constitutes about 90-95% patients of hypertension.

3. Secondary hypertension comprises 5-10% cases of hypertension.

4. About 90-95% patients of hypertension have benign hypertension

5. Increase in blood volume i.e., arterial overfilling (volume hypertension) and arteriolar

constriction (vasoconstrictor hypertension)

6. Angiotensin II alters blood pressure by increasing both peripheral resistance and

blood volume.

7. About 5% of patients requiring hypertension treatment can trace their high blood

pressure to a physical cause such as kidney disease. Treatment of the disease reduces

the symptoms of high blood pressure.

8. Many patients have a family history of high blood pressure.

9. Lifestyle changes can significantly improve a patient’s blood pressure. Among many

other side effects, smoking elevates blood pressure.

10. Reduce or eliminate caffeine-it constricts the blood vessels walls and may increase

blood pressure.

11. Iatrogenic hypertension is Hypertension due to administration of drugs by physicians.

12. Evidence supports treatment of systolic high blood pressure in older persons.

13. Local endothelial factors may play a role in blood pressure.


14. Increased T.P.R. + increased cardiac output = increased blood pressure

15. High blood pressure lowers cognitive function, researchers say.

16. Hypertension increases the viscosity of blood.

17. The factors influencing the relationship between blood pressure and cardiovascular

risk include systolic blood pressure, diastolic blood pressure, circadian blood pressure

patterns, blood pressure variability, and cardiac and vascular hypertrophy.

18. Retention of sodium will cause an increase in the blood volume, which in turn

increases the blood pressure.

19. Essential fatty acids may also help to control blood pressure.

20. Shirodhara is claimed to reduce high blood pressure.

21. Present study registers 30 patients, out of 68 approached patients. Out this, 2 patients

were discontinued hence their data has not been included in the assessment. The

remaining 28 patients of Bhrama viz. Hypertension, fulfilling the criteria of diagnosis

and inclusive criteria were included in the study.

22. The temperature shows the mean difference of 0.24 in the study, which is a point of

observation to assess the Rasayana effect induction in the body.

23. Weight factor has reduced by 0.24 mean value, suggesting the induction of good

health through Rasayana, there by the regulation of the Bhrama vis-à-vis

hypertension.

24. Haemoglobin percentage shows marked increase of 0.443 mean value. Which is

suggestive of inducting Rasayana effect and also capacitating the oxygen exchange

ratio and there by the controlling the co-morbid conditions or associative such as

hypoximea.


25. The associate factor of haemoglobin is RBC count. This has shown 0.251 mean value

increase in the study reflects to the percentage rise of the haemoglobin and there by

regulating the Bhrama vis-à-vis hypertension.

26. The next parameter of co-morbidity in Bhrama vis-à-vis hypertension is serum

creatinine. It has shows a rise in the study with a mean value of 0.008. It suggests that

the Angiotensin and Renin involvement in the Bhrama vis-à-vis hypertension have

been successfully reduced and provide the Rasayana effect not only at the cardiac but

also in the renal area. The small amount changes are as a process of regulation in the

KUB system.

27. Serum cholesterol and associative LDL, VLDL with S.Triglycerides are risk factors

in the pathology of Bhrama vis-à-vis hypertension. Out of these associated the HDL

cholesterol is good for the body and all the rest offers co-morbidity. As the results



study. The rest of co-morbid influencing factors enumerated are LDL (5.2326),

VLDL (2.29333), Serum cholesterol (5.793) and S. Triglyceride (9.08), show the

significant drop and suggest that the effect of the Kakubhadi Lehya on Bhrama vis-à-

vis hypertension with reference to its Rasayana effect over the Bhrama vis-à-vis

hypertension.

28. The presenting complaints of the Bhrama vis-à-vis hypertension are enumerated here

under the limelight of the contemporary and Ayurvedic methods. The first fore most

complaint is Bhrama, which is a pratyatma niyata Lakshana of the Bhrama. All the 28


(100%) patients included and received full-length treatment are exhibiting this

symptom and relieved 100 % at the end of the schedule.

29. Another major complaint expressed in the study is shira shoola by 19 (67.85%) and

outs of them 2 (7.14%) patients’ shows the persistence of the shira shoola at the end.

Angasada, a complaint observed in the study for 14 (50%) patients and one (3.57%)

patient hang on with the complaint at the end of the study.

30. Nidranasha, which is always associated is observed on 13 (46.42%) patients and

found that the same 2 (7.14%) patients are having the complaint at the end of the

study. Hrudrava, another relative complaint of the corresponding organ is observed in

7 (25%) patients and at the end the Rasayana effect of the Kakubhadi Lehya made

them not to have the complaint.

31. The klama is observed in 6 (21.42%) patients and at the end 2 (7.14%) patients are

assiduous with the complaint.

32. Urah shoola for 2 (7.14%) patients and both were relieved with the complaint at the

end of the study of Kakubhadi Lehya on Bhrama vis-à-vis hypertension. The

graphical representation is as under.

33. The result in the study ascertains the best activity of the Kakubhadi Lehya over the

Bhrama vis-à-vis hypertension. For the convenience the results are grouped as five

categories, viz. Well-Responded, Moderately Responded, Responded, Not responded

and Discontinued.

34. The result declaration is done following the norms and conditions of the inclusive

factors and study of the subjective parameters in association with the

sphygmomanometer studies of three postures. The co-morbid stimulating factors


especially LDL, VLDL and S. Triglycerides are considered in while declaring the

results. The factors which make the Rasayana effect over the body also included to

assess the results.

35. After through study of the entire parameters and materials available for the

assessment of results it was drawn a conclusion of results as - 9 (30.02%) well

responded, 6 (20.02%) moderately responded, 10 (33.33%) responded, 3 (10%)

patients not responded and the last 2 (6.63%) patients discontinued in the study. The

tabulation and graphical expression pi-diagram is as under.

36. As it is observed that the systolic blood pressure has taken a rise till to 32 years of age

and show a down fall to the age of 34. From that a gradual increase is observed to age

of 38 and stable to the ages of 40. From 40 a rising gradient is observed till to 52

years of age and becomes more or less stable to the forwarded ages. A linear line

drawn in comparison to that of baseline data to final shows markedly 20 mm Hg

differences in the study. Though many may not give attention to that of the systolic

hypertension, which could be pacified with the rest and regulations needs to drag the

attention. At present study, the effect of Kakubhadi Lehya over the Bhrama vis-à-vis

hypertension show marked drop of 20 mm Hg of systolic hypertension by inducting

the Rasayana effect.

37. Another important reading of the blood pressure is diastolic. It is observed that the

small variances in it can cause the Bhrama vis-à-vis hypertension. The arterial

diastolic blood pressure measured in the study was put for the keen observations, as

there are 28-29, 37-39 and 52-55 age groups show marked elevations. This could be

because of the tension, anxiety, stress, strain etc, psychophysical factors. The linear


line is drawn an observed as the cumulative effect of the Kakubhadi Lehya varies

from 15 mm Hg to 20mm Hg of diastolic from the early ages to late. The older people

those who receive the Hrudya Rasayana well responded and show the marked relief

for the condition.

38. At this study one attempt is made to understand the relationships of the BMI with

systolic and diastolic blood pressure. As it is observed that the linear graph drawn on

the basis of data obtained show a clear evidence of the relationship to the BMI and

systolic and diastolic blood pressures. It is an observation expressed that as the BMI

is increased the response to the medicine is decreased or other wise it can be stated

that the BMI is inversely proportional to that of response to the medicine. As the

people get more BMI, a risk factor to the heart and where the depositions of the LDL

and VLDL cholesterol are anticipated is witnessed as a factor determining the result

of the medicine.

39. The mean difference of the systolic blood pressure is 21.3572 and that of diastolic is

10.71429. These differences are the marked in the study.

40. Another important observation made in this study is BMI relationships to that of the

lipid profiles of baseline data to the final data, at the gender identification.

41. All the subjective parameters except Klama and Urah shoola show highly

significance i.e. reducing the Bhrama vis-à-vis hypertension.

42. The parameter Urah shoola shows the non-significant with less mean effect.

43. The parameter Angasada is having more variation.

44. The parameter Anger and Anxiety shows more significant than fear and rest of the

parameters.


45. The parameter Anxiety is having the more net mean effect and Depression having

with more variation.

46. Where as the parameter Aggressiveness have less mean effect with less variation.

47. All the objective parameters show highly significance. The haemoglobin, weight,

RBC shows more or less highly significance.

48. The parameter Serum Cholesterol is having less mean effect with less variation.

Where as the parameter serum Triglyceride having high net mean effect with more

variation.

49. The diastolic blood pressure in all the three different positions, the mean net effect is

the same, but the supine position there is high significance witnessed.

50. There is much variation observed in the sitting position. The mean effect after the

treatment of diastolic blood pressure is more in the position of standing is more with

more variation.

51. The mean net effect of the systolic blood pressure in the standing position is more,

but there is high significance of systolic blood pressure in sitting position.

52. The mean effect systolic blood pressure in sitting position is more, where as standing

position show the uniform effect. In the diastolic blood pressure again the standing

position show more uniformity.

53. Thus it is concluded that the Kakubhadi Lehya is effective as Hrudya Rasayana in the

disease condition Bhrama vis-à-vis hypertension.

54. This is recommended for the regulation and prophylactics of Bhrama vis-à-vis

hypertension.


Chapter –8

SummaryPrimary or essential hypertension in which the causes of increase in blood

pressure is unknown. Essential hypertension constitutes about 90-95% patients of

hypertension. Secondary hypertension comprises 5-10% cases of hypertension.

Evidence supports treatment of systolic high blood pressure in older persons.

Local endothelial factors may play a role in blood pressure. Increased T.P.R. + increased

cardiac output = increased blood pressure. High blood pressure lowers cognitive function,

researchers say.

The factors influencing the relationship between blood pressure and

cardiovascular risk include systolic blood pressure, diastolic blood pressure, circadian

blood pressure patterns blood pressure variability, and cardiac and vascular hypertrophy.

Retention of sodium will cause an increase in the blood volume which inturn increases

the blood pressure. Essential fatty acids may also help to control blood pressure.

On close observation, it is very much evident that different scholars tried to

identify the disease on the basis of following;

5. On the basis of vitiated dhatu – like Raktapradoshaja vikara, Rakta

chapadhikyata, Rakta samvardhana etc.

6. On the basis of vitiation of Vata – like Vyana bala vaishamya etc.

7. On the basis of vascular changes – like Dhamanipraticchaya, Dhamani

prapoornata, Sira gata vata etc.

8. On the basis of Avarana – like Raktavrita vata, Pittavrita udana, Sleshmavrita

Vyana etc.


The Vata nanatmaja vyadhi consists of three conditions that appear in the process

of Hypertension pathogenesis. They are Hritdrava (palpitation), Bhrama (Dizziness) and

Aswapna (sleeplessness).

Dhamani pratichaya is (atherosclerosis) one out of twenty Kaphaja diseases

appears or associates with the ageing factor have more responsibility to give rise

Hypertension or Bhrama.

The Rasa vitiation is one of the major situations in case of Bhrama, thus the

removal of impurities and proper transportation of the Rasa-Raktavaha srotogata dravaya

i.e. Rakta with its related components in the minuet vessels and capillaries is possible

through Rasayana. Dhaturupa Rasa (plasma and such other fluid constants of the body in

association with Rakta (blood constituents), which makes the imbalance through the Rasa

are to be rectified in the same route following the most best procedure of safeguarding

the Prenana and Jeevana kriyas by the Rasayana.

The chosen drug “Kakubhadi Lehya” assumed as the best Hrudya Rasayana

because of its contents and in further its action towards the Bhrama vis-à-vis

hypertension.

The first and fore most complaint is Bhrama i.e. giddiness. All the patients in the

study (100%) reported the Bhrama, which is said as the “Pratyatma Niyata Lakshana”.

The giddiness may be either hypoxia or mal-function of hemopoitic system including

respiratory system or even it is because of the involved neural controls. But the ultimate

cause could be attributed to that of the high salt intake. Ultimately a sypotom giddiness is

witnessed in the Bhrama is undoubted.


Here an attempt is made to promote the vitality of the heart and there by

regulating the blood pressure through the Hrudya property of the Kakubhadi Lehya as

Hrudya Rasayana.

Mutrala effect – the primary management of the hypertension is diuresis in the

contemporary medical practice is observed in the study.

It is put forth for the assessment many parameters in the study. The direst






medicament.

All the subjective parameters except Klama and Urah shoola show highly

significance.

All the objective parameters show highly significance. The haemoglobin, weight,

RBC shows more or less highly significance. The parameter Serum Cholesterol is having

less mean effect with less variation. Where as the parameter serum Triglyceride having

high net mean effect with more variation.




Discontinued.


The result declaration is done following the norms and conditions of the inclusive

factors and study of the subjective parameters in association with the sphygmomanometer

studies of three postures. The co-morbid stimulating factors especially LDL, VLDL and

S. Triglycerides are considered in while declaring the results. The factors which make the

Rasayana effect over the body also included to assess the results.

After through study of the entire parameters and materials available for the



responded and the last 2 (6.63%) patients discontinued in the study.

The mean effect systolic blood pressure in sitting position is more, where as

standing position show the uniform effect. In the diastolic blood pressure again the

standing position show more uniformity.

Thus it is concluded that the Kakubhadi Lehya is effective as Hrudya Rasayana in

the disease condition Bhrama vis-à-vis hypertension. This is recommended for the

regulation and prophylactics of Bhrama vis-à-vis hypertension.

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” I

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28) Madhava Nidana, edited by Yadunandana Upadhyaya, with commentary of Madhukosha , ByVijaya rakshita, published by chaukambha Sanskrit Orientalia Varanasi, in 1980, ref. 17/19

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40) Ibid, 28/3141) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Sutra 24/942) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Sutra 24/11-1643) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

series 4), Sutra 36/744) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Sutra 24/945) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

series 4), sutra 24/2-446) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

series 4), Sutra 36/747) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Chikitsa 28/21848) Ibid, 25/22049) Ibid, 28/6150) Madhava Nidana, edited by Yadunandana Upadhyaya, with commentary of Madhukosha , By

Vijaya rakshita, published by chaukambha Sanskrit Orientalia Varanasi, in 1980, ref. 17/1-351) Bailliere’s dictionary,52) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

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Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” III

55) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (KasiSanskrit series 228), Vimana, 5 chapter

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series 4), Shareera 3/1558) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Sutra 3059) Palakapya tantra 16/4160) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Shareera 4/3261) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Chikitsa 28/762) Vagbhata, Astanga Sangraha, Prof.K.R.Shrikhantamurthy editor. Varanasi: Chaukhambha

Orientalia; 1996. (Jaikrishnadas Ayurvedic series 79), Sutra 20/463) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic


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68) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academicseries 4), Sutra 12/4,5

69) Ibid, 20/470) Vagbhata, Astanga Sangraha, Prof.K.R.Shrikhantamurthy editor. Varanasi: Chaukhambha



Sanskrit series 228), Chikitsa 28/973) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Nidana 1/1774) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Chikitsa 28/975) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Nidana 1/17-1876) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Sutra 15/377) Ibid, Nidana 178) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic


Sanskrit series 228), Chikitsa 15/3680) Vagbhata, Astanga Sangraha, Prof.K.R.Shrikhantamurthy editor. Varanasi: Chaukhambha


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Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” IV

82) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series51), Sutra 21

83) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academicseries 4), Sutra 12/15-16

84) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series51), Sutra 21/13

85) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (KasiSanskrit series 228), Sutra 30/4,13

86) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series51), Shareera 4/31

87) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academicseries 4), Sutra 12/15 Arunadutta

88) Bhela, Bhela Samhita, Literary research unit, TMSSM library, Thanjavur, CCRIM&H/pub-1,New Delhi, 1977, Chikitsa 8/4

89) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (KasiSanskrit series 228), Sutra 30/13

90) Ibid, Chikitsa 9/591) Ibid, Indriya 5/4192) Ibid, Sutra 30/793) Ibid, Vimana 594) Ibid, Chikitsa 15/3095) Ibid, 15/3696) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series


Sanskrit series 228), Chikitsa 15/3698) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda


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Academy, Banga;ore, Vol-27, no-2, Feb 2004, – pp 15-16101) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

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51), Sutra 1/24 (3)105) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

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Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” V

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115) Ibid, Sutra 7/27116) Ibid, 24/25 Chakrapani117) Ibid, Indriya 5/41118) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series


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Academy, Banga;ore, Vol-27, no-2, Feb 2004, – pp 15-16123) Madhava Nidana, edited by Yadunandana Upadhyaya, with commentary of Madhukosha , By

Vijaya rakshita, published by chaukambha Sanskrit Orientalia Varanasi, in 1980, ref. 17/1-3124) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Vimana 8/37125) Raini. S. Patil, Hypertension – in the perspective of Ayurveda, Ayurvijnana, Ayurveda

Academy, Banga;ore, Vol-27, no-2, Feb 2004, – pp 15-16126) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

series 4),sutra 13/24127) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), sutra 28/10128) Vagbhata, Astanga Hrudaya, Varanasi: Krishnadas Academy; 1982.. (Krishnadas Academic

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Sanskrit series 228), Sutra 25/40130) Kashyapa samhita Khilastana, 16/41131) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), Vimana 8132) Ibid, sutra 24/19133) Ibid, Chikitsa 28/188134) Ibid 28/238135) Ibid 28/239136) Ibid 28/240137) Susruta, Susruta Samhita, Varanasi: Krishnadas Academy; 1980. (Krishnadas Ayurveda series

51), Chikitsa 38/82138) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

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Orientalia; 1996. (Jaikrishnadas Ayurvedic series 79), Sutra 27/9140) Ibid 13/1 Arunadatta141) Agnivesa, Charaka Samhita, 4th ed. Varanasi: Chaukhambha Sanskrit Sansthan; 1994. (Kasi

Sanskrit series 228), sutra 24/18

Kakubhadi Lehya” as Hridya Rasayana in “Bhrama” VI

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SPECIAL CASE SHEET FOR EVALUATION OF“KAKUBHADI LEHYA” AS HRIDYA RASAYANA IN “BHRAMA (HYPERTENSION)”

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Dr. Shiva Rama Prasad Kethamakka,

M.D (Ayu), C.O.P.(German) M.A.(Astro), Ph.D (Astromed)

1) Name of the Patient Sl.No

2) Sex Male Female OPD No

3) Age Years IPD No

4) Religion Hindu Muslim Christian Other

5) Occupation Sedentary Active Labor

6) Economical status Poor Middle Higher middle Higher class

7) Address

Pin

8) Birth data Place of Birth

AMDate Month Year Time

Hours Minutes PM

9) Selection Included Excluded

10) Schedule Initiation Date Completion Date

Well responded Moderately responded11) Result

Responded Not responded Discontinued

12) INFORMED CONSENT

I Son/Daughter/Wife of am

exercising my free will, to participate in above study as a subject. I have been informed to my

satisfaction, by the attending physician the purpose of the clinical evaluation and nature of the drug

treatment. I am also aware of my right to opt out of the treatment schedule, at any time during the course

of the treatment.

Patient's Signature

Scholar:

Dr. Chetan Sangappa Minajigi

Annexure


13) Chief complaints with durationDuration At the treatment (day’s)No Complaints

Fres

h

< 1

Yrs

< 5

Yrs

> 5

Yrs

5 10 15 20 25 30

1 Bhrama (Dizziness)2 Sirashoola (Headache)3 Anga sada ( Body pain)4 Nidranasha (Insomnia)5 Hrit Drava (Palpitation)6 Klama (Fatigue)7 Urah shoola8 Others9

14) Associated FeaturesBefore treatmentNo ComplaintsFresh <1Yrs < 5Yrs > 5Yrs

Aftertreatment

1 Asthma2 Gout3 Toxemia4 Transient Ischemic attack5 Pakshaghatha6 Ardita vata7 Medoroga8 Other Associated features

15) History of present illnessMode of onset[Atanka samutpatti]Course of the disease[Vedana samucchaya]Frequency [Pravrutti]Intensity Mild Moderate Severe

Travel Anxiety EmotionAggravating[Anupashaya] Stress Physical stress If any other

Rest Tranquilizersfact

ors

Relieving[Upashaya] Sleep Anti depressant’s

Others

16) History of past illness if any


17) Previous treatment history if anyPrevious MedicationDrug used

Dose DurationResponse Controlled Not controlledPresent status

18) Habits and Drug historySleep time During

night /hrs Waking time /hrs

Nature of sleep Sound DisturbedDreams Yes NoDay sleep Yes No

Sleep

OtherYear of starting Cigarette / BeediDaily / occasionally Frequency of smokingChain smoker

Smoking

If left how manyday’s back

Present condition ofsmoking

Alcohol Year of starting Hot drinks / BeerDaily/ Occasionallyand qty

Present condition ofdisking

Tobacco/pan-Chewing

Year ofstarting

Daily /Occasionallyand qty

Presentcondition

Tea /coffee

Oral contraceptives Yes No Duration DoseAnti hypertensives Yes No Duration DoseOther's

19) Emotional StatusBT AT BT AT

1 Fear (Bhaya) 5 Irritability (Kshobha)2 Anger (Kopa) 6 Aggressiveness (Samprahara)3 Depression (Deenata) 7 Delirium (Mada)4 Anxiety (Udvega) 8 Other's20) Family History (Write relationship in the column)Heart Disease CancerHypertension Thyroid disordersObesity Any otherDiabetes

21) Personal historyVegetarian Salt BitterMixed food Pungent SweetOil/Ghee Sour Astringent

a) Ahara

Stored food

Taste inpredominance

others


b) vyayama shakti Heena Madhyama Uttamac) Kosta Krura Madhyama Mrudud) Jatharagni bala Manda Teekshna Vishama Samae) Pureesha pravritti Vitvibandha Dravavit Prakrita Frequencyf) Mutra pravritti Frequency day Night Mutradahag) Nidra Sukh Alpa Ati Vaishamyah) Occupational historyType of employmentWork involving any mental strain Yes NoIf yes Mild Moderate SevereWhether symptoms produced during working hours Yes NoWeather symptoms relieved by change of place Yes NoFor womenMenarche Yes No AgeMenopause Yes No AgeRegular IrregularDuration of flow Normal Excessive ScantyNature of flow Dysmenorrhoea LeucorrhoeaPregnancies Abortion Miscarriages Still birth

22) General examinationPulse /min Temp °F Respiration rate /minWeight /kgs Height heart rate /minFundus of Eye OedemaNeck vein Peripheral pulses BMI

23) Aturabala pareeksha

Prakruti Shareerika V P K VP VK PK SamaManasika S R T SR ST TR Sama

Sara Twak Rakta Mamsa Meda Asthi Shukra Majja SatwaSamhanana Pravara Madhyama AvaraSatmya Pravara Madhyama AvaraSatwa Pravara Madhyama AvaraVyamashakti

Pravara Madhyama Avara

Vaya Balya Madhya JeernaDesha Jangala Anupa Sadharana24) Systemic examination (vishesha pariksha):- Cardiovascular systemPeripheral Vascular systemA) JVP Pressure WavesB) Pulse Rate Rhythm Volume

Equality Upstroke Downstroke

Condition of vesselwall

Apex pulse deficitCharacter

Carotid bruit Radio femoral delay


C) Blood pressure - Standing Sitting SupineIn mm/hg Systolic Diastolic Systolic Diastolic Systolic DiastolicLt. upperRt. upper

1) Pericardium2) Apex impulse3) Other pulsation Para sternal Epigastric

Supra sternal In the neck

In the second Leftspace

On the right side

4) Dilated veins

Insp

ecti

on

5) Scars Sinuses 6) Others1) Apex beat2) Left para sternal heave3) Diastolic shock (palpable S2)4) ThrillsP

alpa

tion

5) Other pulsation1) Left second & Intercostal space dullness2) Upper border3) Right border4) Left border

Per

cuss

ion

5) Lower sternal resonance1) Heart sounds2) Murmur Systolic Diastolic Continuous3) Rate4) Rhythm

Aus

cult

atio

n

5) Other soundsOther systems: - (If any)25) Laboratory investigations: -

Before After Changes observedHemoglobin %Serum cholesterolSerum triglyceridesHigh density lipoproteinLow density lipoproteinVery low density lipoproteinRatio26) Subjective parameters

Before After DifferenceBhramaSirashoolaAnga sadaHrit DravaKlamaUrah Shoola


27) Objective parameters: -a) Blood pressure readings. :-

Systolic Diastolic Changes observedBefore mm/hg mm/hg mm/hgStandingAfter mm/hg mm/hg mm/hgBefore mm/hg mm/hg mm/hgSittingAfter mm/hg mm/hg mm/hgBefore mm/hg mm/hg mm/hgSupine

position After mm/hg mm/hg mm/hgBefore After Differences

Hemoglobin %TemperatureWeightE.C.GRBC countSerum CreatinineRandom Blood GlucoseHDL Cholesterol28) Medicine distributions/Advises record: - (Date in Brackets)Day Date Systolic Diastolic Complaints if any advise

051015202530354045

Investigators note :-

Signature of Guide:Dr. Shiva Rama Prasad Kethamakka,

Signature of Scholar: Dr. Chetan Sangappa Minajigi

bhrama kc026 gdg

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