hypretension kc043 gdg

“Evaluation of the efficacy of Shilajatu Guggulu

Rasayana in Pittavruta Udana w.s.r. to

Essential Hypertension” By

SANJEEV KUMAR

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore

In partial f

Ayurved

KUnd

Dr. RagM.D. (Ayu), As

DepartmPost Graduate

D.G. MELMALAGI AY

ulfillment of the degree of

a Vachaspati M.D. In

ayachikitsa er the Guidance of havendra V. Shettar st. Professor in Kayachikitsa

ent of Kayachikitsa Studies & Research Center URVEDIC MEDICAL COLLEGE,

GADAG 2006-2009

Ayurmitra

TAyComprehended

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTER

GADAG, 582 103

This is to certify that the dissertation “Evaluation of the efficacy of Shilajatu

Guggulu Rasayana in Pittavruta Udana w.s.r. to Essential Hypertension”

is a bonafide research work done by Sanjeev Kumar in partial fulfillment of the

requirement for the post graduation degree of “Ayurveda Vachaspati M.D.

(Kayachikitsa)” Under Rajiv Gandhi University of Health Sciences, Bangalore,

Karnataka.

Date:

Place: Gadag.

Guide

Dr. Raghavendra V. Shettar, M.D. (Ayu),

Asst. Professor. Dept. of Kayachikitsa DGMAMC,

PGS&RC, Gadag

J.S.V.V. SAMSTHE’S

D.G.M.AYURVEDIC MEDICAL COLLEGE

POST GRADUATE STUDIES AND RESEARCH CENTER

GADAG, 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

Shilajatu Guggulu Rasayana in Pittavruta Udana w.s.r. to Essential

Hypertension” is a bonafide research work done by Sanjeev Kumar under the

guidance of Dr. Raghavendra V. Shettar, M.D. (Ayu), Asst. Professor, Dept. of

Kayachikitsa in partial fulfillment of the requirement for the post graduation degree of

“Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajiv Gandhi University of

Health Sciences, Bangalore, Karnataka.

.

D

Dat

Pla

(Dr. G. B. Patil) Principal,

DGM Ayurvedic Medical College, Gadag

Date:

.

Professor & HOD ept. of Kayachikitsa

PGS&RC e:

ce: Gadag
Place:Gadag

Declaration by the candidate

I here by declare that this dissertation / thesis entitled “Evaluation of the

efficacy of Shilajatu Guggulu Rasayana in Pittavruta Udana w.s.r. to Essential

Hypertension” is a bonafide and genuine research work carried out by me under the

guidance of Dr. Raghavendra V. Shettar, M.D. (Ayu), Asst. Professor, Dept. of

Kayachikitsa, DGMAMC, PGS&RC, Gadag.

Date:

Place:

Sanjeev Kumar

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:

Sanjeev Kumar

© Rajiv Gandhi University of Health Sciences, Karnataka

Acknowledgement

Acknowledgement

First of all I would like to pay grateful thanks to my lord i.e. my parents Shri

Raghubir Singh Choudhary and Smt. Raj Kumari, who made me mentally strong and

capable to face and solve the problems in the life without any tension and fear and

made me able to fulfill my duties. I am enormously happy to articulate my deepest sense of gratefulness to my

dearly loved and respected guide Dr. Raghvendra V. Shettar, Ass.Prof. (M.D.Ayu).

He has been very kind to guide me in the preparation of compilation and for whose

extraordinary efforts, tremendous encouragement and most valuable thoughts

provoking advice made me to complete this work.

I would like to thank specially to my Grand parents with whose blessings, I was

able to do this work successfully.

I have no words to express my feelings towards my brother: Er. Gaurav Kumar

Choudhary and sisters: Er. Vendana, who always provided me great support in all the

situations. I am thankful to my relatives who always gave me support and

encouragement.

I express my gratitude to Dr. V. V. Varadacharyulu (Professor & H.O.D.) for

his good suggestions and encouragement in every step of this work.

I pay my humble respects to Honorable Principal Dr. G. B. Patil for providing

all the essential facilities to make this study success.

I extend my gratefulness to my Co-guide Dr. Shankar Gouda for his guidance

and untiring effort for this work.

I am extremely thankful to Prof. Dr. K. Shiva Rama Prasad M.D., C.O.P.

(German), M.A., [Ph.D.] and Dr. B.M. Mulkipatil M.D. for his encouragement and

co-operation throughout my study period.

I

Acknowledgement

I extend my gratitude to Dr. G. Purushottamacharyulu, Dr. Mulgund, Dr. P.

Shivaramudu, Dr. M. C. Patil, Dr. G. S. Hiremath, Dr. B.G .Swami, Dr. Purad,

Dr. G.N. Danappagoudar, Dr. S. N. Belawadi, Dr. Nedugundi, Dr. Kuber sankh,

Dr. J. G. Mitti. Dr. Mulki Patil. Dr. Yasmin A.P, Dr. Samudri, for their kind help.

I express my enormous thanks to my statistician Mr. P.M. Nandakumar, Mr.

Tippanagoudar (Lab), Sri. V.M. Mundinamani (librarian), Shyavi and Kerur for

facilitating me in collection and production of my thesis.

I take this moment to express my thanks Dr Ashok M.G. Dr. Kamalaxi,

Dr.Ratna, Dr. Shivaleela, Dr. Sulochana, Dr. Shekhar Sharma, for their constant help

during the study.

“Faithful friends are the medicine of life” Dr.Prassan V.Joshi, Dr.Neeraj Kumar,

Dr.Vijayalakshmi, Dr. Veena. Jigalur, Dr. Anupama, Dr.Ishawar, Dr. Bodake, Dr.

Praveen, Dr. V S Kanti, Dr Trupti, Dr. Adarsha, Dr. Nataraja, Dr. Udaya, Dr Shaileja,

Dr. Ravi, Dr. Shivakumar, Dr. Sanat, Dr. Shabareesh, Dr. Rajesh, Dr.Deepak, Dr.

Jaishankar, Mr. Shakti, Dr. Joshi, Dr. Bhagyesh, Dr. Aneesh, Dr. Baba, Dr. Dash, Dr.

Vinod, Dr. Patil, Dr. Vijay, Dr. Surej, Dr. Kavitha. Dr. Sarvamangala, Dr Savitha,

Dr. Bhopesh, Dr. Gorpade, Dr. Deepa and Dr. Asha, deserves special thanks to their

affection and constant help throughout my study.

I would like to thank all my patients without whose co-operation this work

could not have been completed.

Last but not least I express my deepest thankfulness whose names are not

taken here but helped me a lot along with my kit and kins to my family members

Dr. Sanjeev Kumar Choudhary

II

Abstract

Abstract

“Evaluation of the efficacy of “Shilajatu Guggulu Rasayana in

Pittavruta Udana w.s.r. to Essential Hypertension”

Key words: Pittavruta udana, Essential hypertenshion, Shilajatu Guggulu Rasayana.

Avarana is the obstruction to movement of Vata, Avaraka is the cause for it. In

this regard Hypertension is compared to that of Pittavruta udana, which is having

symptoms Bharama, Kalama, Moorcha and Daha by Acharya Shusruta and others

whereas Acharya Charka add Ojobharamsha and Avasada in the above symptoms. As

this symptomatology manifest later stages of Hypertension hence taken for

comparison.

Although hypertension is usually asymptomatic for the first 10-20 yrs, it

slowly but surely strains the heart and damages the arteries. For this reason

hypertension is often called as silent killer.

The pathogenesis of essential hypertension is not clearly understood. Thus the

present study was undertaken to evaluate the efficacy of Shilajatu Guggulu Rasayana

in the management of Pittavruta udana with respect to Essential hypertension.

The symptoms, which are expressed in Essential hypertension, are very nearer

to the symptoms of Pittavruta udana. Pittavruta udana is explained as disease in

Ayurvedic classics. So the sign and symptoms of Pittavruta udana are simulate to that

of essential hypertension at the present context.

In this regard Shilajatu Guggulu Rasayana is best for the treatment of

Avarana. Guggulu is having its effect over atherosclerosis, obesity and is proven anti-

inflammatory drug. Shilajatu is presumed to posses the unique drug for the Dhatu

poshana and Tridosha prashamana. Hence this medicine if used wisely will account

for samprapti vightana, nullifies avarana pathology and generates healthy tissues.

III

Abstract

The subjective parameter Bhrama and Daha showed 100% response, where as

Shirah shoola shown 91% result and Klama shown 86% result. The objective

parameters like Systolic blood pressure shown 92% result where as Diastolic blood

pressure shown 83% result in this study. The present study revealed that the mean

difference of Serum cholesterol was found 36.86 i.e. lower than the before treatment

mean, mean difference of Serum triglycerides was found 29.94 i.e. lower than the

before treatment mean, mean difference of Low density lipoprotein was found 26.72

i.e. lower than the before treatment mean whereas mean difference of Very low

density lipoprotein was found 06.00 i.e. also lower than the before treatment mean.

Net mean results of the therapies (All subjective and objective in to the consideration)

= 92% i.e. Good response.

Totally Shilajatu Guggulu Rasayana has shown good response in Pittavruta

udana w.s.r. to Essential hypertension in the present study.

IV

Contents

Contents

Sl. No. Contents Page no.

01. Introduction 1 - 5

02. Objectives 6 – 8

03. Literary review 9 – 102

04. Materials and methods 103 - 107

05. Observations and results 108 – 134

06. Discussion 135 – 162

07. Conclusion 163 – 165

08. Summary 166 – 167

09. Bibliography I - XXVIII

10. Annexure i - vi

V

List of Tables Table No.

Content Page No.

01. Showing the opinion of Acharyas regarding Sira, Dhamani & Srotas 27 02. Showing samanya prakopaka karanas 48 03. Showing possible reason for manifestation of disease 48 04. Showing the Lakshana and Dosha involvement 60 05. Showing the Vyavachedaka nidana of Pittavruta udana 65 06. Showing the Vyavachedaka nidana of Hypertension 66 07. Showing the classification of blood pressure 74 08. Showing the classification of secondary hypertension 76 09. Showing the Korotkoff Sounds 83 10. Showing the classification of Chikitsa 86 11. Showing the efficacy of Non-Pharmacological management 90 12. Showing the treatment of Hypertension 92 13. Showing the Pathyapathya in Pittavruta udana 93 14. Showing the properties of Ingredients 102 15. Showing the composition of Shilajatu Guggulu Rasayana 103 16. Showing Age wise distribution of total 30 patients 108 17. Showing Sex wise distribution of total 30 patients 109 18. Showing Religion wise distribution of total 30 patients 109 19. Showing Occupation wise distribution of total 30 patients 110 20. Showing Economical Status wise distribution of total 30 patients 110 21. Showing Marital Status wise distribution of 30 patients 111 22. Showing Intake Rasa predominance wise distribution of 30 patients 111 23. Showing Nidra wise distribution of total 30 patients 112 24. Showing Malapraviti wise distribution of 30 patients 112 25. Showing Addiction wise distribution of 30 patients 113 26. Showing Ahara wise distribution of total 30 patients 113 27. Showing Manasika Prakriti wise distribution of total 30 patients 114 28. Showing Shareera Prakriti wise distribution of total 30 patients 114 29. Showing Sara wise distribution of total 30 patients 115 30. Showing Samhanana wise distribution of total 30 patients 115 31. Showing Satmya wise distribution of total 30 patients 116 32. Showing Satwa wise distribution of total 30 patients 116 33. Showing Vyayama Shakti wise distribution of total 30 patients 117 34. Showing Vaya wise distribution of total 30 patients 117 35. Showing Pramana wise distribution of total 30 patients 118

36-A. Showing Abhyvarana (AS) wise distribution of total 30 patients 118 36-B. Showing Jarana (AS) wise distribution of 30 patients 119 37. Showing Jatharagni Bala wise distribution of total 30 patients 119 38. Showing Koshta wise distribution of total 30 patients 120 39. Showing Family History wise distribution of total 30 patients 120 40. Showing Chronicity wise distribution of 26 patients (Previously

diagnosed) 121

41. Showing Onset History wise distribution of 30 patients 121 42. Showing Intensity wise distribution of total 30 patients 122 43. Showing Relieving Factors wise distribution of total 30 patients 122

VI

Table No.

Content Page No.

44. Showing Aggravating Factors wise distribution of total 30 patients 123 45. Showing Drug History wise distribution of total 30 patients 123 46. Showing Symptoms wise distribution of total 30 patients 124 47. Showing Associated complaints wise distribution of total 30 patients 124 48. Showing Systolic Blood Pressure (Average) of 30 patients 125 49. Showing Diastolic Blood Pressure (Average) of 30 patients 125 50. Showing the effect of therapy on Bhrama 127 51. Showing the effect of therapy on Klama 127 52. Showing the effect of therapy on Shirah shoola 127 53. Showing the effect of therapy on Daha 128 54. Showing the effect of therapy on Systolic hypertension 128 55. Showing the effect of therapy on Diastolic hypertension 128 56. Showing the over all response on Subjective and Objective parameters 129 57. Showing the effect of therapy on Biochemical Parameters 129 58. Showing the effect of therapy on Bhrama 130 59. Showing the effect of therapy on Klama 130 60. Showing the effect of therapy on Shirah shoola 130 61. Showing the effect of therapy on Daha 131 62. Showing the effect of therapy on Moorcha 131 63. Showing the effect of therapy on Systolic hypertension 131 64. Showing the effect of therapy on Diastolic hypertension 132 65. Showing the effect of therapy on Serum Cholesterol 132 66. Showing the effect of therapy on Serum triglycerides 132 67. Showing the effect of therapy on High density lipoprotein 133 68. Showing the effect of therapy on Low density lipoprotein 133 69. Showing the effect of therapy on Very Low density lipoprotein 133 70. Showing overall result of the therapy 156 71. Showing the effect of therapy on Pittavruta udana (Essential

hypertension) 160

72. Showing Demographic Data i 73. Showing Subjective parameters Before and After treatment ii 74. Showing Objective parameters Before and After treatment iii 75. Showing Lipid Profile values Before and After treatment iv 76. Showing Scoring Before and After the Treatment of all the parameters v 77. Showing Net Response of the Treatment (all the parameters) vi

VII

List of Figure & Photo Figure No.

Content Page No.

01. Showing the Blood Pressure Regulation 33 02. Showing the role of Renin-Angiotensin System 36 03. Showing the diagramatic presentation of concept of Avarana 41 04. Showing the Environmental factors and Cardiovascular events 52 05. Showing Obesity and Sodium sensitivity in Hypertension 53 06. Showing Samprapti chart of Pittavruta udana 62 07. Photo showing the Shilajatu Guggulu Rasayana 103 08. Showing Age wise distribution of total 30 patients 108 09. Showing Sex wise distribution of total 30 patients 109 10. Showing Religion wise distribution of total 30 patients 109 11. Showing Occupation wise distribution of total 30 patients 110 12. Showing Economical Status wise distribution of total 30 patients 110 13. Showing Marital Status wise distribution of 30 patients 111 14. Showing intake Rasa Predominance wise distribution of 30 patients 111 15. Showing Nidra wise distribution of total 30 patients 112 16. Showing Malapraviti wise distribution of 30 patients 112 17. Showing Addiction wise distribution of 30 patients 113 18. Showing Ahara wise distribution of total 30 patients 113 19. Showing Manasika Prakruti wise distribution of total 30 patients 114 20. Showing Shareera Prakriti wise distribution of total 30 patients 114 21. Showing Sara wise distribution of total 30 patients 115 22. Showing Samhanana wise distribution of total 30 patients 115 23. Showing Satmya wise distribution of total 30 patients 116 24. Showing Satwa wise distribution of total 30 patients 116 25. Showing Vyayama Shakti wise distribution of total 30 patients 117 26. Showing Vaya wise distribution of total 30 patients 117 27. Showing Pramana wise distribution of total 30 patients 118 28-A. Showing Abhyvarana (AS) wise distribution of total 30 patients 118 28-B. Showing Jarana (AS) wise distribution of 30 patients 119 29. Showing Jatharagni Bala wise distribution of total 30 patients 119 30. Showing Koshta wise distribution of total 30 patients 120 31. Showing Family History wise distribution of total 30 patients 120 32. Showing Chronicity wise distribution of 26 patients (Previously

diagnosed) 121

33. Showing Onset History wise distribution of total 30 patients 121 34. Showing Intensity wise distribution of total 30 patients 122 35. Showing Relieving Factors wise distribution of total 30 patients 122 36. Showing Aggravating Factors wise distribution of total 30 patients 123 37. Showing Drug History wise distribution of total 30 patients 123 38. Showing Symptoms wise distribution of total 30 patients 124 39. Showing Associated Complaints wise distribution of 30 patients 124 40. Showing Systolic Blood Pressure (Average) of 30 patients 125 41. Showing Diastolic Blood Pressure (Average) of 30 patients 126 42. Showing overall result of the therapy 157

VIII

Introduction

Introduction

Research is a process of finding out the old hidden facts from the old theories

and concepts as well as discovery of new facts. The chief goal of any medical

research will be clinical application. Ayurveda, the science of life is an amicable

dictum of life principles, which benefits health, happiness and harmony to the

humanity.

The aim of Ayurveda is “to maintain the health in the healthy person and to

alleviate the disorders in the diseased”1. This supports the fact that any research taking

place in the world of Ayurveda must be having its impact or role in the clinical field.

Blood pressure is the pressure exerted by the blood on the walls of blood

vessels. Persistent high arterial blood pressure without a known cause is essential

hypertension when the elevation of systolic blood pressure is more than 140 mm of

Hg and diastolic blood pressure is above 90 mm of Hg2.

Our Acharyas have described the various kinds of ailments in Ayurveda i.e.

more than thousands of diseases, Ayurveda, an ancient medical science has a rich

literature regarding a plenty of disorders. Hypertension in Ayurveda may fall under

Pittavruta udana3, Raktagata vata4, Pittavruta vata5, Raktavruta vata6, Pranavruta

udana7, Rakta vega vridhi, Rasa bhara, Rakta Samvardhana, Vyanabala,

Uccharaktachapa, Siragata vata8, Bhrama9,10,11, Raktamada12, Moorcha13,14,

Sanyasa15,16 and Dhamanipratichaya17 etc.

As Ayurveda is a technical science, yukthi pramana is a pre-requisite in

pragmatic practice, to achieve the talent a vaidya should process unbeatable

knowledge of the scriptures and discriminating skill in handling the patients therefore,

Ayurveda emphasizes on efficiency and discrete knowledge of the physician.

Shilajatu Guggulu Rasayana in Pittavruta Udana ( Essential Hypertension)

1

Introduction

In this competitive world, time becomes more precious for human being. The

20th century described as the age of anxiety and stress. People don’t have time to think

about themselves, so they are becoming less concerned regarding health and are

taking more stress and strain. Therefore, these irregularities regarding health and

mental stress leads to many physical and mental disorders, out of these hypertension

is one of the alarming diseases.

The great physiologist of modern science, Dr. Chaudhury18 has told

hypertension is an ancient disease. More then 2500 years ago Acharya Charka, the

Father of Hindu system of medicine describes the condition admirably. Essential

hypertension cannot be permanently cured but the level of blood pressure in such

patients can substantially reduce by drugs and measures. A large number of

hypertensives in the early stages have no symptoms often with high blood pressure is

detected on a routine check up and physical examination 19, 20.

Until now, the cause of majority of types of hypertension is unknown. All the

anti hypertensive drugs reduce the blood pressure without correcting the cause.

Hypertension is an established risk factor for all clinical manifestations of

atherosclerosis. It is a common and powerful independent predisposing factor for

development of coronary heart disease (C.H.D.), stroke, peripheral arterial disease

and heart failure. The high prevalence of hypertension, its powerful impact on the

incidence of cardiovascular disease (C.V.D.) and the potential impact on control

justify high priority efforts to detect and treat elevated blood pressure (BP) 21.

Nearly 15% of the world population is labeled hypertensive, either knowing or

unknowingly by doctors. In India approximately 14% of people suffer from

hypertension and majority of them had essential hypertension, which is indicated its

significance and prevalence. In the recent survey in Mumbai, diagnosis of


2

Introduction

hypertension (SBP >140 mm of hg & DBP > 90 mm of Hg) 22 was based on the

average of three readings a confirmed on two subsequent occasions.

Indian council of medical researches (ICMR) All India institute of medical

science (AIIMS) study declared India as a nation of hypertension. 40-45 million

Indians are believed to be suffering for the disease that are a key risk factor for

coronary artery disease, diabetes and renal failure.

Thus considering the prevalence and significance of the problem it should be

of academic interest to Ayurvedic clinician to diagnose and treat it through Ayurveda.

So the concept of hypertension, when clearly understood can be used as an effective

tool for various purposes.

The modern life style, stress, smoking, etc. that interferes with homeostatic

mechanism and circadian rhythmic patterns, thus manifests its ill effects.

The ill effects of faulty regimens of Triupastambha23, Asatmendriyanrtha

sanyoga, Pragnyaparadha and Parinama24 etc. influence the Rajodosha in Manas, thus

directly bring out the dosha vitiation so as it cause the ailment.

The faulty regimens i.e. deviating from dinacharya, ritucharya an extreme

competitive life thus directly predisposes hypertension.

The symptoms, which are expressed in essential hypertension, are very nearer

to the symptoms of Pittavruta udana. Pittavruta udana is explained as disease in

Ayurvedic classics. So the sign and symptoms of Pittavruta udana are in resemble to

that of hypertension at the present context.

Although hypertension is usually asymptomatic for the first 10-20 yrs, it


hypertension is often called as silent killer 25.


3

Introduction

The adverse effects of hypertension principally involve the blood vessels, the

CNS, the retina, the heart and the kidneys 26, ending in organ damage.

The pathogenesis of essential hypertension is not clearly understood in

Ayurveda. Thus, the present study was undertaken to evaluate the efficacy of

Shilajatu Guggulu Rasayana in the management of Pittavruta udana with respect to

Essential hypertension.

Explanation of Hypertension is not at all found in Ayurvedic literature.

Acharya Charaka has mentioned that due to the time and geographical change disease

would occur and the physician of that era should diagnose and treat disease according

to dosha, dushya vichara 27. Therefore, Ayurveda provides three-fold approach to

manage any disease i.e. Hetu, Linga and Aushadha28.

Avarana is the obstruction to movement of Vata, Avaraka is the cause for it 29.

Hypertension is compared to that of Pittavruta udana, which is having symptoms like

Bhrama, Klama, Moorcha and Daha, which resembles sign and symptoms of

Hypertansion. Acharaya Sushruta30 and others 31, 32, 33 opines the same while Acharya

Charaka34 added Ojobharamsha and Avasada to the above symptoms. As these

symptomatology manifests later stages of Hypertension, for this reason taken for

assessment.

In general for all the Avarana, Rasayana is the best treatment as it pacify the

vitiated doshas and conducive to the dhatus35, 36.

In this regard, Shilajatu Guggulu Rasayana is best for the treatment of

Avarana37. Guggula38 is having its effect over atherosclerosis, obesity and is proven

anti-inflammatory drug. Shilajatu39, 40 is presumed to posses the unique drug for the

dhatu poshana and tridosha prashamana. Hence, this medicine if used wisely will


4

Introduction

account for samprapti vighatana, nullifies avarana pathology and generates healthier

tissues.

Apart from this, the medicine proposed for this study is cost effective and

easily available hence present clinical study; “Evaluation of the efficacy of

Shilajatu Guggulu Rasayana in Pittavruta udana” with special reference to

Essential hypertension” was undertaken.

Study hypothesis:

Diseases always takes new form from their original existing diseases may not

be there in olden days vis-à-vis olden day’s diseases may not exist now.

In this regard Acharya Charaka has told, one should diagnose the diseases on

the basis of dosha dushya vivechana. Many of recent researchers have made attempt

to correlate Hypertension with many conditions told in Ayurveda.

In the present study an attempt was made to correlate the Essential

hypertention with Pittavruta udana.

Vata is responsible factor for the gati, the blood flow. So dosha dushya

vivechana in Essential hypertension fit for Vata dosha vikriti. In Vidhishoniteeya

Adhyaya of Charaka, we get plenty of refferences regarding Raktadusti, which are

simulates to the probable etiological factors for Essential hypertension. On the basis

of Ashrayaashrayi sambandha, vitiation of Rakta is mainly because of Pitta. Pitta

vikruti thus assumed in Essential hypertension. This hypothesis built in the present

study and justified. The clinical symptoms of Pittavruta udana are mimic the Essential

hypertension at one or the other stages of Hypertension.


5

Objectives

Objectives of the study

Essential hypertension with special reference to Pittavruta udana is a very

significant as its symptoms are not explained separately in our classics, so we can

compare it with the other symptomatically diseases. Then why this problem has been

taken for Research work. There are so many positive reasons behind the selection of

this topic because every one wants to do something different and get success.

Therefore, it becomes necessary that each and everyone should have some

extra qualities, which make his or her personality special to others. Success is depends

upon hard work. Thus to achieve the goals it is very important to develop some

different characteristics and personality.

Objectives of the study:

1. To evaluate the efficacy of the Shilajatu Guggulu Rasayana in the management of

Pittavruta udana.

2. To evaluate the efficacy of the Shilajatu Guggulu Rasayana in the management of

Essential hypertension.

3. To evaluate the anti hypertensive effect of Shilajatu Guggulu Rasayana.

4. To evaluate the efficacy of Rasayana effect of Shilajatu and Guggulu.

1. To evaluate the efficacy of the Shilajatu Guggulu Rasayana in the

management of Pittavruta udana:

Avarana is the obstruction to movement of Vata, avaraka is the reason for it.

The symptoms of Pittavaruta udana are Bhrama, Klama, Moorcha and Daha,

according to Acharaya Sushruta and others, while Acharya Charaka further adds

Ojobhramsha and Avasada to it. As this symptomatology manifest later stages of

Hypertension, hence taken for comparison.

Shilajatu Guggulu Rasayana in Pittavruta Udana ( Essential Hypertension) 6

Objectives

In general for all the Avarana, Rasayana is the best treatment as it pacify the

vitiated doshas and conducive to the dhatu’s. In this view, Shilajatu Guggulu

Rasayana is the best treatment for Avarana.

2. To evaluate the efficacy of the Shilajatu Guggulu Rasayana in the

management of essential hypertension:

High Blood Pressure is not a disease in itself. It is only; at best, a risk factor

for future vascular accidents in the various target organs like the heart, brain, kidney,

eyes, etc. It carries the same significance as other risk factors for vascular diseases.

Hypertension is a symptomatic but is having a direct relation to that of vasculature.

Atherosclerosis and arteriosclerosis are the phenomena, which affects the individuals

if neglected accounts for morbidity and mortality, which needs an effective of careful

approach.

Now it is the time to highlight the Ayurveda in the world of hypertension with

its unique aspects. The adverse reactions of modern antihypertensive and higher cost

of therapy are also one of the causes to look towards Ayurveda for its humeral

approach.

The pathogenesis of essential hypertension is difficult to understand. Thus, the

present study was conduct to evaluate the efficacy of Shilajatu Guggulu Rasayana in

the management of Essential hypertension.

3. To evaluate the anti hypertensive effect of Shilajatu Guggulu Rasayana:

A multiplicity of treatment modalities exist and newer ones are continuously

being introduced to undertake the hypertensive problems in modern era. Until now,

the cause of majority of types of Hypertension is unknown. All the anti hypertensive

drugs reduce the blood pressure without correcting the cause.


Objectives

Guggulu is having its effect over atherosclerosis, obesity and is established

anti-inflammatory drug. Shilajatu is presumed to posses the unique drug for the Dhatu

poshana and Tridosha prashamana. Hence, this medicine if used wisely will account

for samprapti vightana, nullifies Avarana pathology and generates healthier tissues.

4. To evaluate the efficacy of Rasayana effect of Shilajatu and Guggulu:

The modern life style, stress, smoking, alcohol etc. interfere with homeostatic

mechanism and circadian rhythmic patterns, thus manifests its ill effects.

The ill effects of faulty regimens of Triupastambha, Asatmendriyanrtha samyoga,

Pragnyaparadha, Parinama etc. influence the Rajodosha in Manas, thus directly brings

out the dosha vitiation so as it cause the ailment.

Acharya Charka has laid down the code of good conduct by which one can

remains healthy and long life. The Charka Samhita shows the path by which we can

avoid the ailment and enjoy the normal life span.

Rasayana gives the strength to all the dhatus of the body and refreshes the vital

organs of the humankind. Rasayana gives longevity, intelligence, good memory,

health, good complexion, luster and strength to the body.

Rasayana chikitsa maintains equilibrium of doshas and dhatus. Makes strong and

healthy dhatus of the body and prevents the diseases.

Apart from this, the medicine proposed for this study is cost effective and

easily available hence present clinical study; to evaluate the efficacy of Rasayana

effect of Shilajatu Guggulu.


Literary review

Historical Review

History says that past paves the way for future & knowing about past events,

aids in a having a better present. Thus, history study is important to know about the

systematic growth and improvement of the subject to decide plans for further

establishment and research designing. Here are some Historical facts regarding

Hypertension.

The division of Historical aspect is:

A) Vedic Kala B) Pre-samhita Kala C) Samhita Kala.

A) Vedic Kala:

In Vedas, the references are in a scattered manner. Some of the references

regarding Heart and blood flow are found which are as follows:

In Rigveda:

Hridaya as a organ described & also give description about Hridroga in

Mantras form.

In Yajurveda:

In human being Hridaya - Heart is considered to be seat of Shubha - Ashubha

Sankalpa.

In Athervaveda:

The flow of Rasa in body has been stimulated to the rivers flowing towards the

sea. The direction of flow of this Ragayukta fluid (red colored) has been described in

terms of Urdhwa Dhaminis or Lohini.

These vessels carrying Lohitas are stated as ‘HIRA’. These are hollow organs

i.e. having lumen.


Literary review

B) Pre-Samhitas Kala:

Brahmanas & Upanishads

In Brihad - Aranyaka Upanishad:

Here ‘Hridaya’ is formed by three words - Hri-da-ya. Hri is to take (Aharana),

Da is to give (pana), Ya is to control or move constantly (yachhati).

It means that the Hridaya receives Rasa and Rakta from whole body &

supplies the Suddh Rasa, Rakta, gives nutrition and controls the circulation by its

specific action of Sanckocha and Vikasa. Hridaya is the origin of five Indriyas i.e.

Shabda, Sparsha, Rupa, Rasa and Gandha. Hridaya is situated in the middle of the

chest wall and connect with various Nadies.

In Chhandogya Upnishada:

One hundred and one nadies emerge from Heart & towards whole body.

In Mandakopnishad:

Hridaya collect Rasa and circulate the Rasa in all over body.

Hridaya is stated to be seat of kapha.

In Vayu Purana:

Hridaya situated in mid body and it is considers as the seat of Manas (mind) &

Panchbhutas- seat of Pran & Agni are discussed in new perspective.

In Skanda Purana:

Hridaya is the seat of Sadhaka Agni.

C) Samhita kala:

The description of Heart, Blood Circulation, Dhamanis, Shiras etc. are found

in Samhita Kala.


Literary review

Charaka Samhita:

Hridaya is the Adhistana and root of the Pranavaha, Rasavaha41, Manovaha,

Sangnyavaha srotas. Hridaya is said as the seat of Ojas42.

Hridaya is root cause for the maintenance of six organs Mana, Atma, Vigyana,

Indriya, Pancha-artha and Trigunas including it various Vishaya43 and also explains

the Hridaya roga prakarana separately44.

Sushruta Samhita:

Hridaya is the Adhistana and root of the Pranavaha and Rasavaha srotas45.

Hridaya is said to be seat of Chetana46 and is to be found adhomukha just like lotus

flower47.

Astanga Samgraha & Astanga Hridaya:

Here more description about Hridaya, Dhamani, Siras, Srotas etc. are found.

Hridaya is said to be place of Chetana, shleshma rakta prasadat and is to be found

adhomukha just like lotus flower48. Hridaya is the sthana of ojus and the origin of

dashamoola shiras49.

Kashyapa Samhita:

Hridaya is said to be the seat of Shonitha and it motivates the Mana and

Indriyas50.

Sharangdhar Samhita:

Sharangadhar visualize the significance of Oxygen is extensively distributed

through the body from Heart and give description about rasa, rakta, blood circulation

with Hridaya51. He was the first Physician to incorporate Nadi pariksha into orthodox

medicines, mentioned different types of pulses on the bases of Doshas and certain

physiological condition52.


Literary review

Historical milestone in blood pressure:

In modern medicines normal Blood Circulation & Pulse tension is known

since very early period. But the name of Hypertension & specifically Essential

hypertension is given a little more then one century.

First time Blood circulation was described by Galen. He also established the

Autonomous movements without the control of Nervous system.

1559: Calsalpino (ITALY) introduced term circulation with reference to movement of

blood in Arteries & Veins.

1628: The inventor of blood circulation “William Harvey” was the first to learn the

whole structure.

1731: Blood circulation described by Galen first time. He also established the

autonomous movement without the control of nervous system.

1789: The English clinician Richard Bright (1789-1858) made an important

contribution to the understanding of the link between Hypertension and renal disease,

based on his observations of patients. In a paper published in 1836, Bright noted that

pathological changes in the kidney are often accompanied by hypertrophy of the left

ventricle of the heart, although he did not link the two conditions to Hypertension.

However, he did speculate that the presence of small vessels disease in the

tissues might require a greater cardiac force to overcome the increased resistance to

blood flow.

The condition that Bright described where nephritis and albuminuria were

usually accompanied by edema and elevated blood pressure became known as

Bright’s disease. Bright’s work led others to realize the significance of Hypertension

as a cause of some of the pathological changes in the kidneys and other organs and

hence, to recognize Hypertension as disease.


Literary review

1836: Richard Bright (England) established association of blood pressure in Kidney

diseases.

1852: Charles Brown-Sequard (1817-1894) outlined the effects of sympathetic

innervations on the vasculature. He demonstrated that cutting of the sympathetic

nerve leads to vasodilatation, whereas stimulating the peripheral sympathetic nerve

endings causes vasoconstriction.

1855: Introduction of the Sphygmograph by Kari Vicrodt.

1874: Frederick Mohamed (1849-1884) - was the first to notice “high tension in the

arterial system” occurs “previous to the commencement of any kidney change, or to

the appearance of albumin in the urine.

1876: Sir William Richard Gower’s (1845-1915) - a neurologist and one of the

pioneers of the ophthalmoscope, noted the presence of vascular changes in the retina

in patients with Bright’s disease. He published a paper in which he demonstrated a

close correlation between constrictions of retinal arterioles and raised arterial

pressure.

1880: Introduction of the Sphygmograph by Vas Basch.

1896: Albutt introduced the term ‘Hyperplesia’ in to distinguish patients with

elevated blood pressure alone from those with Bright’s disease. The disease was later

renamed ‘Essential Hypertension’.

1897: Hill & Barnard developed an arm occluding sphygmomanometer.

1904: Theodore Janewaydrew attention to the striking response to stresses such as

surgery, tobacco and anxiety.

1911: Frank first gave the name Essential Hypertension.

1920: McLeod (1876-1935) - produced his acclaimed text on physiology, in which he

outlined the major factors controlling blood pressure. Later, in 1934, Goldblatt and


Literary review

colleagues demonstrated that Hypertension could be induced in dogs by clamping the

renal artery.

1939: Keith and colleagues published a paper in which they showed a correlation

between retinal abnormalities and prognosis in Hypertension. The relation between

Hypertension and arteriosclerosis was appreciated in 1948, although its nature was not

fully understood at that time.

1940: Anyuman & Gold shine established that Blood Pressure measured at home was

lower then in clinic.

1944: Smirk assessed blood pressure behavior in the individual by measuring based

blood pressure.

1955: Pereira described the natural history of Hypertension and its frequent

progression to end-organ complications, largely resulting from acceleration of the

processes of arteriosclerosis. He was one of the first to question the existence of

benign form of Hypertension.

1964: George Pickering showed for first time profound fall Blood Pressure record

during sleep.

1970: Physiology & pharmacology of B.Adrenergic Receptor by Black for which he

got noble prize in 1998.

1994: Smik assessed Blood Pressure Behavior in the individual by measure basal

Blood Pressure.

Review of previous research work:

Ahamedabad:

Shah J.R. - Studied appraisal of dosha in H.T.N. (1984)

Solanki P.V.-An effect of Virechana & Shaman on Essential Hypertension. (1987)


Literary review

Vashishta A.G. - A clinical study on the role of Basti-Chikitsa in the management

of E.H.T.(1994)

Bhupendra Pal- A clinicopathological study of Raktagata Vata (H.T.N.) &

management by Jatamansi Churna. (1994)

Banaras Hindu University (B.H.U.):

S.P.Pande- Study of Arterial H.T.N. and role of Japapushpa (Hibiscus Rosa

sine sis) in its management. (1977)

Ram Singh- A Clinical & experimental evolution of certain indigenous dugs

and its significance in the management of E.H.T. (1993)

G.J.Sayakarars- Study of Avritta in the light of H.T.N. (1993)

Murti Krishana.P.- A clinical study in Ayurvedic management of H.T.N. with

specific reference to some non-pharmacological measures. (1993)

Ph.D. Thesis:

H.C.Gupta- A new care treatment of H.T.N.(Shleshmavrita Vayana). (1990).

Ritu Bhardwaj- A clinical & competitive study Shodhana (Virechana) purvaka

shaman & shamana chikitsa in the management of E.H.T. (1998)

Hyderabad Govt. Ayurvedic collage:

Anjanedya.S- A clinical study of the effect of Vacha on H.T.N. (1985).

J.V. Rao- A study on the effect of Jyothishmati & Punarnava in H.T.N. (1985)

K.Bhushan- Effect of Sarpagandhadi yoga on H.T.N. (1989)

I.P.G.T & R.A. Jamnager:

G.B.Pandey- Avarut Vata Vigyana. (1960)

O.C.Birla- Abhivridha Raktachapa par Sirodhara. (1973)

P.D.Joshi- Role of Dosha-Dushya in H.T.N. (1979)


Literary review

Maheshwar Shukla- Effect of Shirodhara by Takra in patients suffering from

H.T.N. (1983)

A.R.Dev (MRS)- A comparative study on the Rasayana drug & Jaladhara in

the management of Uccharaktachapa. (1988)

Jay Krishana Jani- A study on the Etiopathogenesis of E.H.T. and its

management with certain Ayurvedic drugs. (2000)

Mahopty K.- Critical study of Srotovijananam in Brihatrayi w.s.r. to

Raktavaha Srotodusti & its management B.P. (2000)

Sumit Pathania- Role of Takradhara & Sarpangandha Ghanvati in the

management of Uccharaktachapa. (2000)

Dhananjay Patel- The role of Mansikbhavas in the Etiopathologenesis of

Uchharaktachapa & its management with Medhya-rasayan & shirodhara. (2003)

Ramesh Bhayala- The role of Virechana & Shaman Chikitsa in the

management of E.H.T. (2003)

Govt. College of Indian Medecine Mysore:

R.Mohammed - A study of H.T.N. on Ayurvedic apporach. (1987)

Titlak Ayurved Mahavidhayalaya Pune:

P.P.Patil - Efficiency of Rasgandha vati in H.T.N. (1995)

H.D.Datkhile - Study of H.T.N. according to Ayurveda. (1994-95)

Ahiv Rao B.G.- Relation of B.P.(Raktabhar) & Prakrati. (1984-85)

Gopa Bandhu Ayurvada Mahavidhyalaya Puri:

Chandra B. - Management of H.T.N. with Jatanmansi. (1993)

G.C.D.Sharma - Study on the effect of Sarpagandha churna with Jatamansi

kwatha on Benign Arterial H.T.N. (1989)


Literary review

Govt. Ayurvedic College-Raipur (P.T. Ravishankar University):

Tamrakar B.C.- Comparative therapeutic evolution of shirodhara

(Panchakarma therapy) in H.T.N. (1987)

N.Mishara - Ayurvedic drishtikon se Uccharaktachap ka nidanik evam

vaignyanik adhyayana. (1985)

Anil Singhai-A clinical study of Ayurvedic compound in arterial H.T.N. (1987)

Govt. Ayurveda College (Kerala University) Trivendram:

Ravindranath M. N. - Management of H.T.N. (1984)

P.N.Jaya Singh - Management of H.T.N. with Shodashanga kashaya. (1993)

N.I.A. Jaipur:

J.P.Pathak - Raktachap evam Bramhi Rasayana-uccha raktachap ka nidan

chikitsatamak adhyayana. (1983)

S. Malik - Avrit Vyan udan vayu (Uccharaktachapa) per Rasona Guggulu ka

chikitsatmak adhyayana. (1996)

Views of ayurvedic scholars

Vidya Ranjit Rai Desai:

In his book Nidana Chikitsa Hasthamalaka, he has opined that the disease

hypertension is a raktaja Vyadhi. Langhana, virechana and Raktamokshana etc,

samanya chikitsa sutras of raktajavyadhi can give fruitful results in the management

of Hypertension. He has clearly stated that the hypertension is due to Raktavruta

Vyana vata.

Vaidya Shri.Sudarshan Shastri, Shri.Yadunanda Upadhyaya:

They have opined that hypertension is due to Raktagata vata and is to be taken

as pravruddha raktachapa.


Literary review

Vaidya Shri.Gananath Sen:

He has opined that high blood pressure is Raktagata vata or Raktavruta vata.

Here vitiated vata will become Raktagata or Raktavruta and manifests the disease.

Here the symptoms are not only due to the Hridaya but also due to the vikriti of

vrukka also.

Vaidya Shri.V.V.Shastry:

In his paper, he has considered raktapeedanadhikya as hypertension and

dhamanipratichaya to be one of the major causes for causing the high blood pressure.

He has given the following causes, which cause the dhamani pratichaya:

As this is a shlaishmika disease, a shlaishmika and snigdha substance may be

smear or added to the vessel wall, consequently producing a growth and increase in

the thickness of the vessel wall. This may finally lead to the obstruction of srotas

(srotorodha).

The dhamani which loose the elasticity due to the increase in the thickness of

the vessel wall, also loose the quality of dhamana, thereby necessitating an increased

force in the contraction of the hridaya to maintain the preenana and jeevana kriyas. As

a consequence there is rakta peedanadhikyata.

Vaidya Shri. M.Mahadevashastry:

He has suggested the following treatment during the management of rakta

samurdam (hypertension).

Shodhana and shamana as in vatashonita and medasavrita Vata, Anavarana

vata, Sudation and cleansing, use of purana guggulu with tila taila, internal use of

unsaturated seed oils, Ksheerabalataila, shilajatu, guduchi, in atheroma and

atherosclerosis. Brihat Vatachintamani, Agatsya hareetaki etc. strengthen hridaya,

brain, arterioles and renal vessels.


Literary review

Vaidya Shr. D.T.Giri and Vaidya Smt. Jayashree.R.Shah:

In the Aug. 85 issue of Ayu magazine, Dr.Giri and Dr.Jayashree have

considered hypertension as uchcha raktachapa. They have classified hypertension into

three categories, namely, i) Vataja, ii) Pittaja, iii) Kaphaja, according to do dosha on

the basis of dosha vriddhi lakshana.

As per their opinion Chinta, Bhaya, Shoka, Vegadharanadi, Vatavriddhi

karanas are the nidanas for vataja uchcharaktachapa, Krodha, Shoka, Mamsa sevana,

Katurasa sevana, Dhumra pana etc, are said to be the nidana for pittaja uchcha

raktachapa, And Diwaswapna, Alasya, Amlarasa, Lavanarasa, Guruahara sevana,

Madhura rasa sevana, Masha etc, are the nidanas for Kaphaja Uchcha Rakta Chapa.

In Vataja uchcharaktachapa- dhamani kathinyata and rakta vahi sankocha is

the main pathogenesis. In paithika uchcharaktachapa rajoguna vriddhi are due to

ushna teekshna gunas of pitta. Then vata vriddhi and paithika uchcharaktachapa is

manifested.

They have stated that shodhana chikitsa in uchcharaktachapa should be

according to doshas involved.

In vatapradhana uchcharaktachapa, basti karma is indicated. In pitta pradhana

uchcharaktachapa, virechana is indicated and in Kapha pradhana raktachapa, vamana

is indicated. They have told that this shodhana karma in uchcharaktachapa is only an

upashaya, which gives the knowledge of predominant dosha in the patients suffering

from uchcharaktachapa.

Hypertension in Ancient Period:

Ayurveda an ancient medical science has a rich literature regarding a plenty of

disorders but it is difficult to find a clear-cut correlation to that of hypertension in our

science. However, looking to the description of hridaya, the diseases like Hridroga,


Literary review

Pakshaghata that can be taken as the complications of hypertension. We can think that

hypertension might be present in those days.

Diseases considered under the heading Hypertension by 20th Century Authors is as

follows –

1) Pittavruta udana vata, 2) Pittavruta prana vata, 3) Pittavruta vata, 4)

Dhamani pratichaya, 5) Mada, 6) Moorcha, 7) Bhrama, 8) Sanyasa, 9) Rakta gata

vata, 10) Raktachapadhikyata, 11) Raktapradoshaja vikara, 12) Raktavruta vata, 13)

Roudhiryamada, 14) Siragata vata, 15) Ucharakta bhara, 16) Ucha rakta chapa,

17) Pranavruta udana vata, 18) Raktamada, 19) Vyanabala, 20) Raktasamvardhana,

21 )Raktavega vridhi, 22) Rasabhara.

Pittavruta udana vata

The Pittavruta udanavata lakshana are - Murcha, Daha, Bhrama, Klama,

Avasada, daha in the nabhi and urah region and Ojobhransha53.

Pittavrutha prana vayu

The lakshanas are- Murcha, Daha, Bhrama, Shoola, Vidaha, Chardi and

Sheeta kamatwa54.

Pittavruta vata

In Pittavruta vata, the following symptoms are- Daha, Trishna, Shoola,

Bhrama, Tama, aggravation of daha by the use of Katu, Amala, Lavana, Ushana and

Sheetakamita55.

Raktavruta vata

Acharya Charaka has described the disease Raktavruta Vata36 under the

context of Vatavyadhi but no other Acharyas have mentioned regarding this disease.

In Raktavruta vata, the symptoms are - Daha in between twak, Mamsa, Raga,

Mandalas and Kshavathu56.


Literary review

Raktapradoshaja vikaras

Raktapradoshaja vikaras are explained under the vidhishonita adhyaya. In

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

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

diseases are considered57.

Raktagatavata

The lakshanas of Raktagatavata, according to Acharya Charaka- Teevraruja,

Santapa, Vaivarnya, Krishata, Aruchi and Stambhata soon after having food58.

Acharya Vagbhata also explained almost all the symptoms, which are explained by

Acharya Charaka, in addition with – Swapam, Raga and Bhrama59.

Sri Sudarshan Shastri and Sri Yandunandanopadhya conferred opinion, as

Raktagata Vata is nothing but hypertension.

Siragata Vata

The Lakshanas of siragata vata are- Mandaruja, shopha, Shushyati, Spandyate,

Suptasatanvyo in siras60.

Bhrama:

It is one of the symptoms of Pittavruta udana. It is one of the vataja nanatmaja

vyadhi61. The shareerika doshas vata, pitta and manasika dosha rajas are considered as

the causative factors for the Bhrama. Bhrama means Giddiness or rotation, a person

feels the fast rotation in the shirah62.

Dhamani Pratichaya

It is one of the kaphaja nanatmaja vikara63. Due to adhika poshana especially

Rasa and Rakta dhatus the dhamanis in which these dhatu circulates get dilated.

Because of these, the gati becomes manda and guru. The Dhamani will not be guru,

manda and mrudu as seen in Atipoornata but it will be Katina and Teekshna due to


Literary review

vitiation of Vata. It will sometimes be Teekshana, Manda, Poorna and Ksheena due to

the vitiation of Vata.

Roudhira Mada

Mada is one of the rakta dushti vikaras. In the seven type of mada the

Roudhira mada is considered as hypertension and stated that the dushya involved in

this disease is Rakta whereas Vata, Pitta, and Kapha plays an important role in the

formation of Roudhira Mada64.

Raktachapadhikyata

Raktachapadhikyata is created by three words - Rakta, Chapa and Adhikyata.

Rakta’ refers to – Vishesha dhatu among all dhatus and rakta indicates life.

‘Chapa’- refers to pressure or squeezing.

‘Adhikyata’-refers to, high or increased.

Raktachapadhikyata” means high blood pressure65.

Moorcha

Madhava Nidana66, 67 has explained the moorcha in detail. It is due to vitiated

Vatadidosha, rakta dusti and tama dosha. It can be considered as syncope. Lose of

consciousness induced by a temporarily insufficient flow of blood to the brain.

Acharya Vagbhata68 mentioned the mada, moorcha and sanyasa. Acharya

Charka and Acharya Sushruta explained the types of moorcha.

Sanyasa

It is the disease of rakta dushti and samjnya vaha srotas. It is due to the

vitiated doshas. If moorcha is not treated properly, it leads to Sanyasa. According to

contemporary science coma is a state of unnatural heavy deep and prolonged sleep

often accompanied by slow irregular breathing and consequently ending in to death69.


Shareera

Shareera Vivechana

Anatomy-Physiology of the heart and blood vessels with physiology of blood

circulation is very much indispensable in Pittavruta udana w.s.r.t. Essential

hypertension before going to discussion part.

Hridaya

The word ‘Hridaya’ in Ayurveda is a synonym for the word Heart. Hridaya is

derived from two verbs. ‘Hri’ which means to bring back forcibly and ‘Da’ which

means to donate. 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 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- and the physicians or Vaidyas denote the word hridaya to

Urohridaya or Muscular heart.

The anatomy and physiology of Hridaya is not explained under one heading or

at one place in classics, we get lot of quotes and descriptions based on which we

should appreciate 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 shleshma 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 Sushruta.


Shareera

Hridaya is the moola of pranavaha and rasavaha Srotas70. It is the seat of

manas and para-apara ojus71. Hridaya is the sthana of dashadhamani’s which spreads

all over the body and which carries rasa, ojas and does tarpana karma72, 73. Hridaya

continues to work whether the person is in jagrutavasta or swapatavasta74.

The particular function of hridaya is conceded out by particular dosha. These

functions are discussed below:-

Doshas related to Hridaya

The three doshas are related with Hridaya i.e. among vata, the Udana vata,

Prana vata and Vyana vata75related to Hridaya. Among pitta, the Sadhaka pitta76, and

among kapha, the Avalambaka kapha is related to Hridaya77.

Udanavata with Hridaya

Acharya Charaka and Vagbhata have mentioned the uras as the sthana of

Udana vata78, 79, 80 and is related to hridaya. The functions of Udana vata are prayatna

(Endeavour or effort), urja (enthusiasm) and bala (strength)81, with respect to hridaya,

we can think of the conductive system of the heart, i.e. Udana vata by the functions

like prayatna and bala initiates and helps in the conduction of the cardiac impulses in

the heart. It is the coordinator of speech, memory, strength etc82, 83.

Pranavata with Hridaya

Acharya Charaka and Vagbhata have mentioned the Shiras84, 85 are the sthana

of Pranavata and acc. to Acharya Sharangadhara, Prana is situated in hridaya86.

Acharya Vagbhata states that Prana vata maintains the activities of hridaya and does

dharana of dhamanis87. Thus, Prana vata is situated in murdha and sends impulses to

hridaya, there by overriding the sympathetic and parasympathetic actions or functions.

Prana is central controller of all the motor activities of body88.


Shareera

Vyanavata with Hridaya

Acharya Vagbhata stated that Vyana vata is situated in hridaya89,90 and it

moves quickly all over the body91,92. Vyana vata is responsible for circulation of Rasa

(Rasadhatu) all through the body93, 94. Acharya Sushruta has also mentioned asruk

sravana to be one of the functions of Vyana vata95. Acharya Vagbhata summarizing

all functions of Vyana vata by the statement that Vyana vata96 conducts all the actions

or movements of the body.

Even Acharya Charaka has mentioned that Vyana vata is responsible for the

continuous flow of rasadhatu to all parts of the body throughout the life by using the

words like ajasram and sada97 and controls the circulation of Rasa, Rakta and Sweda

in the body98.

Sadhakapitta with Hridaya

Acharya Sushruta and Vagbhata stated that Sadhaka pitta is situated in

hridaya99, 100, 101 and is responsible for attainment of buddhi, medha, abhimana, utsaha

and abhipretartha.

Therefore, it is connected with some of the higher mental faculties and

emotional states. Hence, Sadhaka pitta related with psycho-physiological actions.

Avalambaka Kapha with Hridaya

Acharya Vagbhata and Sushruta stated that Avalambaka kapha is situated in

uras102, 103, 104. It does avalambana of hridaya i.e. with the help of rasa it gives bala to

hridaya. It also does tarpana and kledana of Hridaya.

Manas with Hridaya

Acharya Charka and Acharya Sushruta stated that hridaya is the adhistana of

Manas105, 106. Acharya Charaka while mentioning measures to protect hridaya and oja


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say to avoid the thing that produces dukha to the Manas. Even in Unmada chikitsa

adhyaya also Acharya Charaka mentions about manovaha srotas.

Ojas with Hridaya

Ojas has been classified in to two types, i.e. para ojus and apara ojus. Para

ojus is located in hridaya107 and pramana is ashta bindu. It is said to be uttama

pranayatana even, if a very little is destroyed the body cannot exist. Apara ojus is

located 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.

Rasa Rakta Paribhramana

Hridaya is the srotomula of rasavaha and pranavaha srotas108 and responsible

for rasa samvahana in the shareera. Samanavata brings the ahara rasa that is fashioned

to hridaya, and in hridaya it is called as rasa dhatu. At the present with the help of

Udana vata and Vyana vata the sankocha and vikasa i.e. the praspandana of hridaya

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

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

Prana vata 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 further109.

As per kedarakulyanyaya, the rasa moves to all parts of the body and

nourishes the whole body. This function is conceded constantly all over the life

Afterwards this rasa is brought back to the hridaya by Vyana vata, Samana

vata 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 denote the continuous function of hridaya in circulation of rasa110.


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Blood Vessels and Shareera

The concept of blood vessels in Ayurveda has not been cleared till today.

Different Acharyas have different opines regarding this. The three terms i.e. Sira,

Dhamani and Srotas are used with different meanings depending on the context at

different places. Dalhana in Dhamaneevyakarana adhyaya has described regarding

sira, dhamani and srotas, elaborately. He has differentiated these three based on four

pramanas, i.e. lakshana, moola, karma and agama. Dalhana giving the reason for

these three being read together says, though they are differentiated, however has

similarity in vahana karma.

Table-01: Showing the opinion of Acharyas regarding Sira, Dhamani and Srotas

Sira Dhamani Srotas Definition:

“Saranat Siraha”111

Chakrapani, Gangadhara,

Gananathsen’s opinion goes in

favour of vein.

Ashuddha raktavahini’s are

considered as sira and can be

referred as vein (Atharvaveda).

Pandit Hariprapannaji considers

sira to be vein. Pittavaha siras

can be considered as vein.

The word sira has been used

with the meaning of kandara.

The word sira has been used

with the meaning of dhamani.

The word sira denotes vein,

artery and lymphatics.

Definition:

“Dhmand Dhamanyaha” 112



favour of artery. Shuddha

raktavahini’s are considered as

dhamani and can be referred as

artery (Atharvaveda). The word

dhamani has been used with the

meaning of Jnyanatantu.

At parishad shabdartha it was

concluded that dhamani can be

considered as artery, nerve or

vein, or any vessel in the body.

The word dhamani has been

used with the meaning of

rasavahini.

The word dhamani has been

used with the meaning of sira.

Definition:

“Sravanat Srotamsi” 113



favour of capillaries.

It has paryayas like sira,

dhamani, rasayanya, nadi,

pantha, marga etc.

Therefore, by the above, it is very difficult to come in a conclusion that

whether sira is considered as artery or dhamani is considered as artery.


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Acharya Charaka is more of the opinion of considering dhamani to be as

artery, while Acharya Sushruta considers rohini sira or asrugvaha sira as the artery.

Even the parishad that was conducted on shabdartha could not conclude on this

controversy. Therefore, now based on pulsatile feature, dhamani is taken as artery in

this study. Acharya Sushruta has used the word sira pratana to describe the plexus of

arteries or veins.


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The Heart (Anatomy)

Greek name is cardia from which we have the adjective cardiac, Latin name

is cor from which we have the adjective coronary.

The heart is a conical, hollow muscular organ, situated in the middle

mediastinum. It is enclosed within the Pericardium. It pumps the blood to various

parts of the body. The heart is placed obliquely behind the body of the sternum and

adjoining parts of the costal cartilages, so that 1/3rd of it lies to the right, 2/3rd to the

left of the median plane. The direction of blood flow, from atria to the ventricles, is

downwards, forwards and to the left. The heart measures about 12×9 cm (5×3 or 3 ½

inches) and weighs about 300 gms in males, 250 gms in females114.

External features

The human heart has four chambers. These are right and left atria and the right

and left ventricles. The atria lie above and behind the ventricles. On the surface of the

heart, they are separated from the ventricles by an atrioventricular groove. The atria

are separated from each other by an interatrial groove. The Ventricles are separated

from each other by inter-ventricular groove, which is subdivided into anterior and

posterior parts. The upper part of each atrium has an appendage called the auricle.

The heart has an apex directed downwards, forwards and to the left; a base (or

posterior surface) directed backwards; and anterior, inferior and left surfaces. The

surfaces are demarcated by upper, lower, right and left borders115.

Arteries and veins of the heart

The heart is supplied by two coronary arteries, arising from the ascending

aorta. Both arteries run in the coronary sulcus116.

The venous blood is drained by great cardiac vein, the middle cardiac vein, the

small cardiac vein, the posterior vein of the left ventricle, the oblique vein of the left


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atrium, the right marginal vein, the anterior cardiac veins, and the venae cordis

minimae. All these except last two drain into the coronary sinus which opens into the

right atrium. The anterior cardiac veins and the venae cordis minimae open directly

into the right atrium117.

Lymphatic and the nerve supply of the heart

Lymphatic of the heart accompany the coronary arteries and from two trunks.

The right trunk ends in the brachiocephalic nodes, and the left trunk ends in the

tracheobronchial lymph nodes at the bifurcation of the trachea.

Parasympathetic nerves reach the heart via the vagus. These are cardio

inhibitory; on stimulation they slow down the heart rate. Sympathetic nerves are

derived from the upper 3-5 thoracic segments of the spinal cord. These are

cardioaccelaratory, and on stimulation they increase the heart rate, and also dilate the

coronary arteries. Both parasympathetic and sympathetic nerves form the superficial

and deep cardiac plexuses, the branches of which run along the coronary arteries to

reach the Myocardium118.

Anatomy of Artery and Arterioles

The whole circulatory system from the finest capillaries up to and including

the heart is lined by a smooth, continuous single layered endothelium. The walls of all

vessels except capillaries and sinusoids are formed by three analogous zones (coats)

i.e., from inside outwards the tunica intimae, tunica media, and tunica adventitia.

These coats confer on the vessels a number of important properties, including an

endothelial lining low in friction and connective tissue components able to withstand

longitudinal and circumferential stress due to prevailing blood pressure.

The smallest arteries terminate in muscular arterioles 100-50 µm in diameter,

which branch into terminal arterioles less than 50 µm in diameter. Metarterioles are


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branches of terminal arterioles, 10-15 µm in diameter at their origin and decreasing

over 5-100 µm to as little as 5 µm, where they open in to the capillary bed. They are

surrounded by a strong circular layer of non striated myocytes forming precapillary

sphincters, which affect the final control of blood flow through the capillaries. Pre

capillary sphincters have been seen to open and close periodically with a cycle of 2-8

seconds.

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 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, then to the arterioles, capillaries, and the

veins of the whole body, and finally to the two venacavae 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 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


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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 utilized 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 fibers 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 venacava 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.


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Regulation of Blood Pressure

Physiologically the magnitude of the arterial pressure depends on two

fundamental homodynamic variables; cardiac 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 FACTORS

Constrictors Dilators

BLOOD VOLUME -Angiotensin II -Prostaglandins

-Sodium -Catecholamines -Kinins

-Mineralocorticoids -Thromboxane -NO/EDRF*

-Atriopeptin -Leukotrienes

-Endothelin

BP = CARDIAC X PERIPHERAL LOCAL FACTORS

OUTPUT RESISTANCE -Autoregulation

-Ionic (pH, hypoxia)

CARDIAC FACTORS NEURAL FACTORS

-Heart rate Constrictors Dilators

-Contractility -α-adrenergic -β-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


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blocks the excretion of sodium and water into the urine.

It appears that most patients with established hypertension have abnormal

cardiac output and blood pressure is mainly sustained by increased peripheral vascular

resistance.

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),


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

blood pressure by adjusting the amounts 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


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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

Renin Renin Substrate

Angiotensin I

Converting 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


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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.


Disease Review

Disease Review

Importance of Avruta vata

Vata is most significant and commanding among three doshas in many ways, for

example Pitta, Kapha and Dhatus are pangu without Vata consequently Vata regulates

their functions, another one is its ashukaritwa.

Gati is the unique feature of vata, whenever its gati is disturbed due to Avarana or

other cause then its vitiation occurs. According to chakrapani, because of avarana, the

speed of the moment of vata gets arrested which leads to its aggravation.

Vata gets vitiates in to two ways i.e. by marga Avaranas or by the dhatu kshaya,

whereas Pitta have single rout of its vitiation. Before going to the Avarana aspect of vata,

first its various pathological conditions are being discussed.

Pathological Conditions of Vata:

Acharya Sushruta had point out the three pathological condition of Vata i.e.

Kevala vata

Dosha-Yukta Vata &

Avruta Vata119

Kevala Vata Disordrders:

Kevala Vata indicate Shudha Vata. The word kevala refers to Dosha-Asamsrista

i.e pathological state of Vata without association of other Dosha120.

Due to the nidanas of Vata, the body tissues under goes destruction resulting in

increase of Akasha i.e.Vaccum and to fill this vaccum, by marga Avaranas Vata leads to

its prakopa. The treatment can be given to Vata only. However, certain care has taken for

this disorder. Here it may produce both Nanatmaja and samanyaja types of Vata


Disease Review

disorders. The nanatmaja disorders are produced only by vata not by other dosha. On the

other hand, its samanyaja disorders are produced by the the dosha, which may be of vata

type only or may be due to samasarga and sannipata with other Dosha.

Doshayukta Vata i.e. Samsarga and sannipata:

Doshayukta vata indicate the association of other Doshas, which is different from

Avarana121. It is a pathological state of Vata due to the association of Pitta or Kapha or

both, which may be caused by the mutual hetus. Clinical manifestations of Vata as well

as of the associated Dosha as Anubandha may be there. In that case, generally the

primary Dosha i.e Vata dominates in all the sphere of hetu, symptoms and treatment.

Usually, with the treatment of primary Dosha, the secondary Dosha or

complications is also relieved provided a care is taken because the treatment is not

opposed to associated Dosha.

The Samsarga or Sannipata may occur in the simple way of prakriti sama

samaveta i.e like physical mixture of Dosha, where the mixed symptoms of both the

involved Dosha are manifested. On the other hand, when the combination of Dosha is in

the form of Vikriti Vishama Samaveta then there may be some peculiar symptoms, which

may not be belonging to either of the Dosha.

Gata Vata: The word GATA has 2 meanings-

• Related with movement

• Related to Destination / Site /Adhishthana122

Initially Vata is vitiated by its own nidanas, afterward, following the specific

path of its pathogenesis, when involves some specific site i.e Dhatu, Upadhatu or Ashaya,


Disease Review

then such condition is termed by adding adjective of that site (Dhatu or Ashaya e.g

Pakvashaya Gata Vata or Rakta Gata vata and so on123.

The symptoms developed according to the severity, site of participation etc. Pain

is the common and chief complaint in all the conditions of Gatavata. On the other hand,

character of the pain varies according to the site of localization. For example, unbearable

pain associated with burning sensation is the symptom of Rakta Gata Vata, deep-seated

aching pain is the typical feature of Mamsa Gata Vata124.

Avruta Vata:

Like Ama, the Avarana is also a unique concept of disease pathogenesis,

especially of Vata vyadhis. Term Avarana means; achhadana, avarodha, obstruction,

occlusion, to cover or to mask. Gati is unique feature of Vata, whenever the gati of vata

gets arrested which leads to its aggravation125. Avarana of vata is a characteristic

pathological condition, where obstruction to its Gati occurs due to the nidanas other then

its own, leading to its Prakopa resulting into various Avaranas. The Dosha, Dhatu, Mala,

Anna, Ama & sub type of Vata can cause the Avarana.

Synonyms of Avaranas:

Avintah

Samyuktah126.

Meaning of term used in Avarana:

The three terms are used to understand the Avarana i.e. Avarana, Avarka and

Avruta described below:-


Disease Review

Avarana:

Avarana denotes the obstruction of vata movements. This obstruction can be due

to Pitta, Kapha, Rasadi dhatus, Malas or even by panchavidha vata.

Avaraka:

The factor, which causes obstruction of vata, is called Avaraka. For example if

Pitta cause obstruction of Vata, then Pitta is called Avaraka.

Avruta:

The gati of Vata, which is affected by the Avaraka is known as Avruta.

The substance, which obstructs the pathway of Vata, is termed as Avaraka while Vata

whose avarana occurs is termed as Avarita.127.

Figure 3: Showing the diagramatic presentation of concept of Avarana

VATA PITTA PITTA (Avaraka) (Avaraka) (Avruta)

This concept of Avarana is particularly stated for Vata.

According to Chakrapani, the excessively strong Avaraka suppresses the normal

dealings of Vata. The excessively increased Avaraka manifests its actions. Avarana of

Vata leading to its prakopa, thus the symptoms is also manifested depending upon its site

involvement128.

In the initial stage of the situation, as the Avaraka is strong and Vata is nearly in

the normal status, there will be decrease in the functions of Vata, in the beginning with


Disease Review

increase in the function of Avaraka. When the obstruction is complete, it leads to Prakopa

of Vata resulting in its disorder129.

Hence, it is clear that Vata is initially in its normal state, but development of

Avaraka occurs. The Vata Prakopa occurs after the obstruction is completed. Hence the

Vata disorders are produced without indulging of its own nidana.

How to know Avruta-Avraka:

Charak samhita describes certain guidelines to identify the affected Avruta, and

Avaraka, the causative factor of Avarana in 28th chapter cikitsa sthana.

i) If Avaraka is stronger than Avruta, i.e. Avruta dosha looses its functions and

there is increase in the activity of the Avaraka factor (it may be vata, kapha or pitta etc.).

ii) However, if the Avruta dosa (Vata) is stronger due to sanchaya, prakopa etc.

than the Avaraka, then there is increase in the functions of Avruta and decrease in the

functions of Avaraka.

iii) According to some scholars, the decrease of the functions of the Avruta,

increase in the functions of the Avaraka130.

By observing these lakshanas in a particular case of Avarana one has to analyze

them to identify Avruta-Avraka etc.

Indicator composite in Avruta Vata:

Repeatedly the symptoms manifested are comprised of disturbed function of the

obstructing factor as well as the obstructed Vata. The symptoms produced are based on

the principles of Karma Hani (Rupahani), Karma Vriddhi (Rupa Vriddhi) and Anya

Karma (Rupantara)131.


Disease Review

These are depending upon the intensity of the obstruction i.e. partial or complete,

functional or organic, acute or chronic, transient or persistent, etc. For example, the less

strong obstruction of Vata will lead to its aggravation, where as the very powerful

obstruction may make it weak and like wise.

The symptomatology of the Avarana depends up on the place where the Dosha-

Dushya Sammurchana has takes place. For instance, the symptom of Shoola of Avruta

Vata may occur in the different parts like head, ears, abdomen, back, depending upon the

organ involved in the process of Avarana.

Avarana Bhedas:

Avarana may be innumerable132. However, 42 types of Avarana of Vata have

been described in the texts; these are categorized under the following hading.

Murta Avarana133,134:

Pitta & Kapha Dosha, Dhatus, Mala and Anna are the Murta substances, which

obstruct the gati of Vata and this state is called as Murta Avarana. These are 22 in

numbers i.e.

Doshavruta Panchabedha of Vata

Pittaavruta Udana-1,

Pittaavruta Apana -1,

Pittaavruta Samana-1,

Pittaavruta Vyana-1,

Pittaavruta Prana-1,

Kaphavruta Udana-1,

Kaphavruta Prana-1,


Disease Review

Kaphavruta Apana-1,

Kaphavruta Samana-1,

Kaphavruta Vyana-1 &

Pitta avruta Vata-1,

Kapha avruta vata-1.

Dhatavarita Vata

Rakta avruta Vata-1,

Mamsa avruta Vata-1,

Meda avruta Vata-1,

Asthi avruta Vata-1,

Majja avruta Vata-1,

Shukra avruta Vata-1,

Sarva Dhatvarita Vata -1 &

Malavruta Vata -1,

Mutravruta Vata -1,

Anna vrita Vata -1.

Amurta Avarana135,136:

When sub-type of Vata obstruct the function of each other, is called Amurta or

Anyonya Avarana. It is of 20 in number i.e.

Vyana avruta Udana-1,

Vyana avruta Prana-1,

Vyana avruta Samana-1,

Vyana avruta Apana-1,


Disease Review

Udana avruta Prana-1,

Udana avruta Apana-1,

Udana avruta Samana-1,

Udana avruta Vyana-1,

Samana avruta Prana-1,

Samana avruta Apana-1,

Samana avruta Udana-1,

Samana avruta Vyana-1,

Apana avruta Prana-1,

Apana avruta Samana-1,

Apana avruta Udana-1,

Apana avruta Vyana-1,

Prana avruta Samana-1,

Prana avruta Apana-1,

Prana avruta Udana-1 &

Prana avruta Vyana-1.

Mishra Avarana:

In this, two or more factors are involved in the pathogenesis of Avarana, here

variation and combinations of Pitta and Kapha and sub-type of Vata resulting in

innumerable numbers of Pathologies of Avarana137,138.

Avarana and Sama Dosha:

Sama state of Dosha and Dushya is very important to produce Margavarana in the

srotas and avayava. The sama Dosha or Mala is capable of producing srotosanga, which


Disease Review

in turn obstruct the Gati of Vata. In this way, Ama may also help in producing the

Avarana of Dosha and Dushya etc. indirectly.

Avarana-As atypical Clinical presentation:

The symptom complex produced by Avarana is always an analytic challenge. To

identify the accurate cause and pathogenesis of Avarana requires a special diagnostic

skills and expertise. Some time it misleads the physician because of its complex atypical

presentation.

Acharya Charaka alarms about its atypical presentation by mentioning that vata

obstructed by Meda and Kapha produced pain (shula), Numbness (supti) and Oedema

(shvayathu)

The Physician ignorant of the condition of Avarana, thinking that vata prakopa is

there, may prescribe unctuous enema, which may further decline the conditions139. All

these references indicate towards its atypical presentation, which may lead to diagnostic

error resulting in mismanagement too.

Diagnostic Method of pathologies of Vata:

Kshaya, Vriddhi and Gatatva condition of Vata can be diagnosed easily with the

help of symptomatology’s mentioned in the text.

The Avarana requires a special diagnosis between the conditions of Kevala Vata,

Samsarga Vata and Avruta Vata. The diagnosis can be made based on their symptoms

and by applying reasoning.

Some times it may not be possible to diagnose the Avarana and Anyonya-Avarana

straightforwardly and in that case it can be diagnosed with the help of the exclusion

methods with proper reasoning on the basis of its altered physiology 140.


Disease Review

Diagnosis of Avarana

Some times it is very hard to analyze that condition of Avarana so it requires

repeated clinical examination and frequent administration of Upashaya before getting to

proper clinical diagnosis141.

For example madhumeha is described in two types in Charaka Samhita. Among

which one type is due to Vata avaruta by Kapha, Pitta, Medas and Mamsa142. and another

type is due to Dhatukshaya or Shuddha Vata143.

The etiological factors described in the sutra sthana are of Avaraka i.e of Kapha,

Pitta etc. and in the nidana sthana is due to dhatu kshayajanya. The descriptions of

etiological factors of both these varieties are:

A) Etiological factors of Madhumeha due to Avarana:

By taking excess heavy, unctuous, sour, and salty articles; by using new cereals

and drinks, by over indulgence in sleep, sedentary habits, by not undergoing seasonal

purification, the Kapha, Pitta, Meda and Mamsa increases excessively leading to

Madhumeha144.

B) Etiological factors of Madhumeha due to Kevala Vata:

The habitual use of astringent, pungent, bitter, dry, light and cold articles; over

indulgence in sexual act, exercise, emesis, purgation, enema and errhines; suppression of

natural urges, fasting, trauma, sun-heat, worry, grief, depletion of blood, waking in the

night and unwholesome postures of the body, lead to immediate provocation of vata145.

Finally, the Madhumeha is same but fashioned by different nidanas.


Nidana

Nidana

Nidana (etiological factor) is defined as a cause of the disease. Lacking of

nidana, disease can not be manifested. In Ayurvedic as well as Modern texts, the

exact cause for Pittavruta udana w.s.r.t. ETH is not explained. The samanya

prakopaka karana are given below:

Table2: Showing samanya prakopaka karanas Factors Vata Pitta Rakta

Rasa Katu, Tikta and

Kashaya146.

Katu, Amla, and

Lavana147.

Lavana, Amala,

Katu and Kshara148.

Guna Ruksha, Laghu, Sheeta,

Khara, Sukshma, Daruna

and Chala149.

Ushna, Teekshna,

Laghu, Vidahi, and

Kshara150.

Drava, Snigdha &

Guru161.

Aharaja Pulses like Uddalaka,

Masha, Adaki, Kalaya,

Nishpava and Harenu.

Dried leafy vegetables,

Vallura, millets like

Varaka, Koradusha,

Syamaka and Neevara.

Peenyaka, Atasi,

Kulatha, Sarshapa,

Greenleafy vegetables

like Harenuka, the

flesh of Godha, fish or

goat, curds, whey,

buttermilk and sura.

Dushita, adhika,

atiteekshna,

atiushna, Madira

sevana, Kulatha,

Masha, Nishpava,

Pindalu, Moolaka,

Dadhi, Kanji, Sura,

Mastu, Saktu and

Souveera.

Table3: Showing possible reason for the manifestation of disease

Nidana Possible reasons

Excess amala rasa Pittakarka, agni vardhaka and rakta dushtikara. Produces daha,

shotha and other Pitta vikaras152.

Excess lavana rasa Causes Pitta prakopa, Rakta dushti, Vidaha, moorcha, santapa,

trishanakarka, indriya glani, vivarnta and other Pittaja &

Raktaja vikaras153.

Excess katu rasa It is vata and agni guna bahulya and pittakaraka. Produces

avasada, moorcha, bhrama, tama, santapa, trishana, daha, bala

kshaya, kampa, toda, bhedavat vedana and vata vikaras154.


Nidana

Nidana Possible reasons

Excess tikta rasa It produces shira shoola, bhrama, toda, bheda, moha, vata

vikaras and causes bala kshaya155.

Excess kashaya rasa Causes hrudaya vedana, rasavahi srotas avarodha, trishna,

stambhata, akunchana, akshepaka, tingling sensation,

convulsions and is khara, vishada, rooksha guna pradhana156.

Excess Teekshna

guna ahara

It is agni mahaboota pradhanya and pittakara, it produces daha,

paka, etc. and it results in bala ksheenata157.

Excess Ushana guna

ahara

It is pitta vardhaka, agni guna pradhana and sweda pravartaka.

It produces daha, paka, moorcha, trishana etc158.

Excess Laghu ahara It is vata vardhaka and agni vardhaka159.

Excess Drava ahara It is pitta vardhaka160.

Excess Rooksha

guna ahara

It is vata vardhaka and agni vardhaka. It produces moorcha,

bhrama etc161.

Excess Snehayukta

ahara

It is pitta and kapha vardhaka162.

Atimatrahara Leads to ama dosha163, causes durvipaka.

Viruddha ahara This ahara cause tejo, bala, smruti, indriyan, chitta nasha and

causes mrityu just like visha164. According to Acharya Charka,

it acts like “visha” and can cause moorcha, napunsakata etc.

Such ahara could cause mrityu165.

Tila sevana The properties of tila taila are Ushna veerya, Madhura, Tikta,

Kashaya, Katu rasa. It is Raktapitta karaka, vata kapha hara.

With excessive intake, Pitta vardhana166.

Kshara Kshara possesses the following qualities: ushana,

teekshana,laghu and pitta vardhaka167.

Mamsa Hamsa, Kukkuta, Mahisha Tittira, mamsa and matsaya are

Ushna and Kaphapittakaraka. Shushka mamsa is Kashaya,

Amla rasa Katu vipaka, Ruksha, Sheeta168.

Sarshapa Guru, Ushna, Sarvadoshakrit, Baddha vinmootram169.

Madya pana Madya is Amla Rasa, Katu in vipaka, has Teekshna, Vidahi

guna and Ushna virya170.


Nidana

The some expected nidanas are:

Adhyashana, Ajeerna, Anashana, Kulatha, Vidahi ahara, Vishma ahara, Vega

dharana, Krodha, Chinta, Bhaya, Samprahara, Udvega, Kshobha, Deenata, Ati

maithuna, Shoka, Ati vyayama, Kriya atiyoga, Atapasevana etc.

Dosha prakopa Karana:

Pitta prakopka nidana: Katu, teekshana, ushana, Krodha and vidahi anna171.

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

ahara, bhara vahana, ati rodana, ati hasya172 etc.

Srotodusti Karanas:

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

chinta173 etc.

Rakta vaha Srotodusti Karanas: Vidahiannapanani, ushna, snigdha, drava ahara,

adhika atapa and vata sevana174 etc.

Manovaha Srotodusti Karanas: Krodha, shoka, bhaya, harsha, kama, lobha, moha,

chinta, ayasa, udvega and aghata175 etc.

Margavarodha:

The site or sthana of margavarodha176 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 (Rasavaha

srotas) results in "Hypertension" as one of the manifestations.


Nidana

Etiology:

In 90–95% of hypertension cases, the etiological factors that are responsible

for the blood pressure increase remain unknown177i.e. the cause of disease is not

known; however in recent years, experimental, epidemiological and therapeutic

evidence seems to indicate that essential hypertension is due to one or combination of

etiological factors. The probable factors which are responsible for the development of

essential hypertension are:-

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 susceptibility gene (angiotensinogen gene).

Acharya Charaka while describing the genetic influence in disease says, at the

time of conception, if the beeja (shukra or ovum), beeja bhaga (chromosome) or beeja

bhaga avayava (genes) get vitiated, It is likely to travel in subsequent generations178.

Dalhana has also commented that beeja dushti does not mean whole dushti, but

there may be a dushti of a part of beeja, that is the organ developing from that

particular part are also defective or abnormal179.

Acharya Sushruta, while classifying the diseases, has mentioned adibala pravrutta

vyadhi and is said to originate due to deformity of raja or veerya of the parents at the

time of conception180.

2) Racial and Environmental Factors:

Surveys in the US have revealed higher incidence of essential hypertension in

blacks than in whites. But in rural Africa hypertension is relatively rare, suggesting

that the high prevalence in the US is not because of the genetic tendency, rather, it


Nidana

might be due to adaptation of western life style by American blacks181. There is a lot

of controversy in the environmental factors. One of the evidence showing that, the

environment in which a person lives affects his blood pressure.

Figure-4: Showing the Environmental factors and Cardiovascular events182

3) Salt Intake:

For a long time salt is suspected, to have an etiological influence on the blood

pressure. It is also known that only an increased salt content of diet intake alone will

not lead to high blood pressure. Invariably there are some predisposing factors like

heredity or renal diseases. In such patients alone increased intake of salt more then 10

grams per day leads to renal retention of salt and water, which in turn increases the

plasma and extravascular fluid volume.


Nidana

Ultimately peripheral resistance increases, which leads to increase blood

pressure. Excessive use of Lavana causes rakta dushti and leads to shonitaja roga183.

since rakta dhatu is one of the important dushya in the etiopathogenesis of

hypertension, it is given more importance. Therefore salt should not be consumed in

excess and for longer duration184. When excessively used, it produces fatigue and

weakness of the body185, which are the symptoms usually found in patients of

hypertension.

4) Obesity:

There is a strong link between excess body fat, blood pressure levels and

prevalence of hypertension. As obesity contributes to blood lipid abnormalities and

impaired glucose tolerance. Acharya Sushruta has mentioned medoroga leads to vata

vikara186.

Figure-5: Showing Obesity and Sodium sensitivity in Hypertension187


Nidana

5) Stress:

The stressful stimuli certainly raise blood pressure and may be more

argumentative in subjects who have familial hypertension. Sustained or repeated

emotional stress (anger, frustration, envy, hatred, fear and worry) causes arteriolar

contraction through an outpouring of nor-epinephrine from the sympathetic

vasomotor nerve endings and epinephrine from the adrenal medulla. In some persons,

the blood pressure increases due to the presence of a doctor (white coat hypertension).

This is possibly due to the temporary emotional stress.

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

caused by them are kama, krodha, lobha, mada, bhaya etc188. Acharya Charaka has

advised to suppress these factors189, because they tend to elevate raja and tama gunas

which cause manodusti resulting in manovikara with involvement of samjnavaha or

manovaha srotas190.

Further, Chakrapani commenting on srotomula says, hridaya and

dashadhamani are the manovaha srotomula191. In this way the arteries of the heart

may get afflicted by these manovikara and therefore they also afflict oja which is also

ashirta of hridaya192,and vitiation of Vata193 and Pitta also takes place.

Hence it may be concluded that all the psychological factors directly provoke

Vata and Pitta which can produce hypertensive state.

6) Meals:

After meals the blood pressure is little higher.

7) Emotion:

Anger and fear raise the blood pressure. However, there may be fainting

attacks.


Nidana

8) Sleep:

Sleep causes a fall of blood pressure. However, sleep associated with

frightening dreams may cause rise of blood pressure.

9) Exposure to cold:

It causes rise of blood pressure. This is due to hypothalamic stimulation.

There is cutaneous vasoconstriction leading to increased resistance to the blood flow

and elevation of blood pressure (cutaneous vasoconstriction causes conservation of

heat within the body).

10) Geographic factors:

Several studies have shown that high altitude residents have lower blood

pressure. Possible constituting factors include -

Lower peripheral resistance due to increased capillarisation of tissues.

Hypoxia causing reduced thyroid activity and

Primitive conditions.

11) Physical activity:

Several population studies have suggested that individuals who undertake

regular physical exercise have lower blood pressures.

Regarding exercises, dynamic exercise raises blood pressure and isometric

exercise raises it a lot more. Despite this, there is good evidence that people who take

regular exercises are healthier and have lower blood pressures than those who take

none.In Ayurveda idle sitting is told to be one of the astamaha doshakarabhava194.

12) Other Trace Metals:

More hypertension has been seen in association with long-term exposure to

arsenic and carbon disulfide. Long-term exposure to even low levels of lead may lead

to hypertension, perhaps by increased production of reactive oxygen species beyond


Nidana

the probability that increased intracellular calcium is involved in the pathogenesis of

hypertension195. The following findings usually are noted in uncomplicated, untreated

primary hypertension:

Lower dietary intake of calcium

Increased urinary calcium excretion, which is likely the reason for an

increased incidence of kidney stones.

Lower plasma ionized calcium levels.

Increased levels of parathyroid hormone in some, likely related to reduced

intake of calcium. Parathyroid hormone levels are even higher in Blacks than

Whites and are potentially able to raise BP.

Intake of more sodium leads directly to an increase in calcium excretion.

13) Socio-economic status:

A very large study in Mumbai found no difference between high and low

socio-economic groups. So higher or lower socio-economic status does not have

significant effect on blood pressure.

14) Age:

Older people tend to have higher blood pressure than young people. Almost

all surveys show that blood pressure rises with age in both men and women. Due to

the thickening of vessel wall, an increase in sub-endothelial layer and the media,

which increase collagen content and elastic fragmentation. In Vriddhavasta vata is

predominant and in Youvana avastha Pitta is predominant196.

15) Sex:

Though Hypertension affected both sexes, the incidence is slightly lower in

the female up to 40 years. However after that females are more prone to

Hypertension.


Nidana

16) Smoking:

The nicotine in cigarette smoke acutely raises blood pressure(BP), even in

addicted smokers. No tolerance develops, so the BP remains high as long as the

patient continues to smoke. However, the effect of each cigarette is transient and is

over within 30 minutes; if the BP is taken in a smoke-free environment, as in most

physicians' offices and clinics, the pressure effect may be missed. Cigars, if inhaled,

and smokeless tobacco also raise BP, but nicotine replacement therapies do not appear

to do so. Cross-sectional data on smokers and nonsmokers are not consistent: Some

studies find smokers to have a higher BP, whereas others find smokers to have a

lower BP. Regardless, all who smoke should be strongly advised to quit. Smoking is

associated with insulin resistance and an attenuation of endothelium-dependent

relaxation. These multiple adverse effects obviously add to the major cardiovascular

damage induced by smoking197.

17) Caffeine:

Acutely, consumption of the caffeine contained in 3 cups of coffee will raise

BP an average of 4/3 mm Hg. Some develop tolerance to this effect and only an

average 2.4/1.2 mm Hg higher pressure has been noted in those who drink 5 cups or

more of coffee per day compared to nondrinkers. In contrast, increasing caffeine

intake, ascertained by multiple careful dietary recalls, was associated with lower BP

among the participants in the Multiple Risk Factor Intervention Trial. Three cups of

black tea raised the BP even more than seen with 3 cups of coffee, but the pressure

effect was prevented when the tea was accompanied with food198.

18) Alcohol:

The possible role of alcohol, in amounts consumed by a large part of the

overall population, needs special emphasis. In contrast to its immediate vasodepressor


Nidana

effect, chronic consumption, even of only moderate quantities, may raise the BP; in

larger quantities, alcohol may be responsible for a significant amount of

hypertension199.

In madatyaya chapter, Acharya Charaka has explained that, when madya is

taken in large quantity, it shall affect channels of rasa (rasavaha srotas) and by

entering hridaya it affect the dhatus situated in hridaya (rasa, oja, rakta). The gunas of

alcohol like ushna, teekshna, sukshma, vyavayi etc. are exactly opposite to the gunas

of oja200, which also provoke vata-pitta dosha.

Acharya Charaka has also described pradusta, bahu (excessive), ushna,

teekshna madyapana and surapana as causative factors of shonita dusti201. Further, it

is the shelter to moha, krodha, shoka and mrityu202.


Poorvaroopa

Poorvaroopa

The Purvaroopa manifests in the Sthana Samshraya stage of Shatkriya kala.

Charaka has quoted that avyakta lakshanas of vata vyadhi are to be taken as its

Poorvaroopa203.

Commentator Vijayarakshita explains the term Avyakta as the symptoms

which are not manifested clearly204.

Hence Mild exhibition of actual features of the disease Pittavruta udana prior

to the manifestation of Pittavruta udana may be taken as purvaroopa.

According to most of the 20th century authors and with the available references

we can compare essential hypertension to that of Avruta Vata. Since the poorvarupa

of Vata vyadhi are avyakta, the poorvarupa of Hypertension are also avyakta. In

modern science also prodromal symptoms have not been explained.


59

Roopa

Roopa

A disease is produced on the completion of dosha dushya sammurchana.

Signs and symptoms of the fully manifested disease indicating the specific

characteristics of the disease (in the vyaktavastha) are called roopa. These become

evident in the fifth stage of kriyakala i.e. vyaktavastha.

Pittavruta udana:

The Pittavaruta udana having symptoms Bhrama, Klama, Moorcha, Daha.

Acharya Sushruta205 and others206, 207, 208 opine the same while Acharya Charaka209

added ojobhramsha and avasada to the above symptoms. Shira shoola added to above

according to contemporary texts.

Table-4: Showing the lakshana and Dosha involvement

Lakshana Dosha involvements

Acc. to Acharya Susruta, Bhavaprakasha, Gadanigraha and Madhava Nidana

Klama Fatigueness, languor, it is due to Rakta210, 211.

Daha Burning, conflagration. It is due to Pitta and Rakta212, 213, 214.

Bhrama Confuse, perplex, giddiness. It is due to Vata and Pitta215, 216, 217.

Moorcha Fainting, delusion, swooning. It is due to Pitta218, 219.

Acharya Charka some more added in the above symptoms

Daha in nabhi

and uras

Burning sensation in nabhi and uras. It is due to Pitta220, 221, 222.

Avasada Fainting, exhaustion. It is due to Vata223, 224.

Ojobharamsha Bhramsha means decline, losing, falling down225.

According to contemporary text books explanation with Ayurveda

Shiroshoola. Headache. It is due to Vata and Rakta226, 227, 228, 229.

According to contemporary texts:

A large number of hypertensives in the early stages have no symptom i.e., why

it is called as the silent killer230. Most patients with hypertension have specific


Roopa

symptoms referable to their blood pressure elevation and are identified only in the

course of a physical examination231.

Mild to moderate essential hypertension is usually associated with normal

health and well being for many years. So essential hypertension may be-

• Asymptomatic or

• Symptomatic.

The first and foremost symptom of essential hypertension is headache later the

other symptoms like dizziness, easy fatigability, insomnia, chest pain, and palpitation

can be seen232, 233.


Samprapti

Samprapti

The whole sequence of manifestation of disease starting from the causative

factors, dosha dushti till the appearance of lakshanas is known as Samprapti234.

Direct reference regarding the samprapti of Pittavruta udana is not

available in the classics. Hence to understand the samprapti of Pittavruta Udana,

the general samprapti of avarana can be considered.

By observing the lakshanas of Pittavruta udana, the doshas and dooshyas

involved in the samprapti to cause this condition can be assessed as follows.

Figure-6: Showing Samprapti chart of Pittavruta udana

Pitta prakopaka Nidana

Pitta prakopa

Vata prakopaka Nidana

Vata Prakopa

Vata Avarana

Avarodha of UdanaVata by Pitta

Nidana Nidana

Pittavruta udana


62

Samprapti

Samprapti:

The Pittavruta udana comes under Vata vyadhi chapter. If Pitta Vitiated

and then obstruct the Udana vata comes under samanyaja vyadhi. Hence in the

samprapti of Pittavruta udana, Vata and Pitta vitiates by their own nidanas and

then vitiated Vata comes in contact with vitiated Pitta which causes more Pitta

vikruti, resulting in the obstruction of Udana vata leading to the Pittavruta udana.

Samprapti-Ghatakas:-

Doshas: Vata (Udana) – Shirashoola and bhrama235,236.

Pitta (anubandi) – Daha, bhrama and moorcha237, 238, 239.

Dushyas: Rakta – daha, klama and Shira shoola240.

Agni: Jatharagni.

Srotas: Rasavaha, Raktavaha & Manovaha.

Srotodushti-Prakara: Sanga type of srotodusti.

UdbhavaSthana: Pakvashaya-Amashaya Samudbhava.

Avayava: Hridaya, Dhamani.

Adhisthana: Manodaihika (Psychosomatic, Sira, Dhamani, Srotas).

Sanchara-sthana: Sarva Sharira.

Rogamarga: Madhyama Rogamarga.


63

Upshaya and Anupshaya

Upshaya and Anupshaya

For Vata dosha:

Upashaya of Avruta Vata is not at hand; on the contrary, Upshaya of Avaraka

is present.

For Example in Pittavruta vata, the patient gets Vidaha from the Upshaya of

Vata i.e, Amla, Lavana and Ushna. In Kaphavruta Vata there is Upashaya from Katu

etc and patient shows desire for Fast, Exercise, Ruksha etc. things which are Upshaya

for Kapha and Anupshaya for Vata241.

For Pitta dosha:

In Pittavruta vata, patient feels Daha, Trishana, Shoola, Bhrama, Tama and

gets Vidaha from Amla, Lavana, Katu and Ushna veerya dravyas. On the other hand,

the patient shows the desire for cold (sheeta) things, which is Upashaya for Pitta242.


64

Vyavachedaka Nidana

Vyavachedaka Nidana

Vyavachedhaka Nidana or differential diagnosis plays a prime role in arriving

at an exact decision between diseases presenting a similar clinical feature. While

making the diagnosis of Pittavruta vata the following disorders that are having similar

features has to be excluded.

Table-5: Showing the Vyavachedaka nidana of Pittavruta Udana

Sl.

No

Laxanas Pittavruta

Udana243

Pittavruta

Vyana244

Pittavruta

Prana245

Pittavruta

Samana246

1. Klama + + - -

2. Bhrama + - + -

3. Daha + + + +

4. Moorcha + - + +

5. Avasada + - - -

6. Ojobhramsha + - - -

5. Gatravikshepana - + - -

6. Santapa - + - -

7. Vedana - + + -

8. Vidaha - - + -

9. Chardana - - + -

10. Aruchi - - - +

11. Atisweda - - - +

12. Agni upaghata - - - +


65

Vyavachedaka Nidana

In modern science essential hypertension should be differentiated from

secondary hypertension given below:

Table-6: Showing the Vyavachedaka nidana of Hypertension Factors Essential Hypertension Secondary Hypertension Incidence 95% 5% Etiology Unknown etiology Known etiology Pathology Pathogenesis is not clearly

understood. Pathogenesis depends on the disease that has caused hypertension.

Blood Pressure Recording

A rise in diastolic pressure when the patient goes from the supine to the standing position is most compatible with essential hypertension.

A fall in the absence of antihypertensive medication with the treatment of the cause, suggest secondary forms of hypertension.

Symptoms Symptomatic or asymptomatic. If symptomatic, vague symptoms like headache, dizziness, easy fatigability etc., will be present.

Symptoms will be present with the underlying disease.

Investigations Sr. creatinine, Blood urea, Lipid profile, fasting blood sugar, ECG and chest X-ray. ECG and chest X-ray will be normal.

Depending on the basic disease, the values of these laboratory investigations, ECG and chest X-ray varies. Some other investigations are needed to rule out the secondary hypertension.

Prognosis It is controllable with proper treatment. It requires life long monitoring and treatment may require periodic adjustments.

It is curable. When cause is treated, the elevated blood pressure comes down to normal.

Treatment Treatment comprises of Drug and Non Drug therapy

Treatment depends on the cause and requires drug therapy during severe condition.


66

Sadhyasadhyata

Prognosis of Avarana

In Dosha Avarana, the Avarana of Prana and Udana by Pitta and Kapha

are more severe and difficult to treat (Gurutaram) because of their vital function in

the body physiology i.e. to provide life (Jivana-Ayu) and strength (Bala).

Among the Dhatu avarana conditions, Medavruta Vata is comparatively

more difficult to treat due to its complications and poor therapeutic

response247,248,249,250.

In Anyonya Avarana conditions Udanavruta prana, the condition of

occlusion of Prana by Udana leads to loss of all sensory and motor functions

(Karma Kshaya), loss of vital essence (Oja Kshaya), loss of strength (Bala,

kshaya) and complexion, and it may result even in death of the patient251. So

depending on the type of Avarana and Avaraka prognosis of the Avarana

pathology varies.

Similarly if the condition persists for one year, its management is delayed

or improper, then it may land up in difficult to cure or incurable state. So early

diagnosis and timely management make the prognosis good252.


67

Upadrava

Upadrava

Improper diagnosis and delayed treatment of different Avarana conditions or

of one year chronicity lead to complications like Hridroga (heart disease) due to

Pranavruta udana vata, udavarta, Gulma (Localized enlargement of abdomen) due to

Vyanavruta apana253. There are many conditions like Sthaulya, Prameha, Urustambha,

which occur through the pathogenesis of Avarana. Additionally, Dalhana mentions

that in sthaulya and many other types of Vata vikara may occur as complications due

to avarana type of pathology. For example, Medavruta vata in which meda obstructs

the Gati of Vata leads to the vitiation of Vata resulting in different Vata disorders254.

In this way, it can be stated that Avarana may occur as independent disease as

well as part of the pathogenesis of certain diseases. It may also help in understanding

the pathogenesis of many conditions described in modern medicine as well as to

decide their management on Ayurvedic lines. Further it has been mentioned that there

may be innumerable Avarana disorders255. It means the few conditions of Avarana

mentioned in the texts are just for example and by involving different sites other

specific condition of Vata may be produced. For instance, the Pittavruta and

Kaphavruta incident occurs in different organs like stomach, head, heart256 etc.

resulting in the symptomatology pertaining to that particular organ. In this way by

considering the findings of the modern medicine the diseases like cerebral thrombosis

and embolism leading to hemiplegia, coronary thrombosis and embolism leading to

myocardial infraction etc can be interpreted by the Avarana pathology of Ayurveda

and accordingly their management may also be evolved purely based on Ayurvedic

principles. Acharya Charaka has mentioned the use of Rasayana drugs particularly

Shilajatu and Guggulu in the management of Avarana257. So the globe of indications

of these drugs may be widened to treat such conditions.


Hypertension

Essential hypertension

A large number of hypertensive in the early stages have no symptoms often

with high blood pressure is detected on a routine check up and physical

examination258, 259.

Hypertension is a major risk factor for the development of cardiovascular

disease260.

Definition of Essential Hypertension

Varieties of factors are responsible for Blood Pressure261. These factors are

interconnected with each other and difficult to find out the particular causes for

hypertension. Thus, when a specific cause of Hypertension can not be identified, then

the hypertension is called as essential hypertension262.

In more than 95% of cases, a specific underlying cause of hypertension cannot

be found such patients are said to have essential hypertension263. Hypertension is said

to be an essential when the cause is unknown264.



hypertension, when the elevation of systolic blood pressure is more than 140 mm Hg

and diastolic blood pressure is above 90 mm Hg upon repeated

sphygmomanometric265, 266.

Till now the cause of majority of types of hypertension is not known. All the

anti hypertensive drugs reduce the blood pressure without correcting the cause.

Unfortunately there was no clinical or laboratory tests which can give an

affirmative diagnosis of essential hypertension. However, essential hypertension is a

clinical entity in itself, though its pathogenesis is not known.


69

Hypertension

Even though hypertension is usually asymptomatic for the first 10-20 yrs, it


hypertension is often called as silent killer267.

The difficulty in studying a disease process such as hypertension begins with

the fact that the etiology of hypertension is heterogeneous. Hypertension can be

primary or secondary to a defined process, such as renal artery stenosis268.

According to 7th Report of the Joint National Committee, the “normal” or

“high normal” blood pressure is called as “prehypertension which differs from

European Society of Hypertension/European Society of Cardiology. The definitions

of hypertension proposed by the 2003 European Guidelines and the 7th Report of the

Joint National Committee incorporate aspects of disease characterization that are not

previously defined. One is the classification of patients into different categories at

blood pressure values, 140/90 mmHg, which is based on the continuous relationship

to cardiovascular risk in the normotensive range269.

Classification

The sign and symptoms of Essential Hypertension are not explained separately

in our classics. But According to modern medicine Hypertension can be classified in

number of ways i.e.

A. Systolic and Diastolic Hypertension.

B. Essential or Primary and Secondary Hypertension.

C. Accelerated and Malignant Hypertension.

D. On the basis of Severity.

A. Systolic and Diastolic Hypertension

Since the mid-1920s, a relationship has been known to exist between diastolic

and systolic blood pressures and life expectancy. Highly elevated blood pressure was


70

Hypertension

called malignant hypertension because 79% of affected individuals died within 1 year

of this diagnosis. From the 1920s until the 1980s, the risks of coronary heart disease

and stroke have been attributed predominantly to elevated diastolic blood pressure.

Diastolic blood pressure would be a better predictor of cardiovascular risk270.

Systolic hypertension

a) Increased cardiac output

• Aortic valvular insufficiency

• Atrioventricular fistula, patent ductus arteriosus

• Thyrotoxicosis

• Paget’s disease of bone

• Beriberi

• Hyperkinetic circulation

b) Rigidity of aorta or small arteries271.

B. Essential and Secondary Hypertension

Essential Hypertension is said in which the cause of increases in blood

pressure is unknown272.

Secondary Hypertension is said in which the increase in blood pressure is

caused by disease of the kidney, endocrine gland, central nervous system, aorta or

some other organs273.

A. Primary, essential or idiopathic:

B. Secondary:-

Renal :

a) Renal parenchymal disease:

• Acute glomerulonephritis

• Chronic nephritis


71

Hypertension

• Polycystic disease

• Diabetic nephropathy

• Hydronephrosis

b) Renovascular

• Renal artery stenosis

• Intrarenal vasculitis

c) Renin-producing tumors

d) Renoprival

e) Primary sodium retention (Liddle’s syndrome, Gordon’s syndrome)

Endocrine :

a) Acromegaly

b) Hypothyroidism

c) Hyperthyroidism

d) Hypercalcemia (hyperparathyroidism)

e) Adrenal

i. Cortical

Cushing’s syndrome

Primary aldosteronism

Congenital adrenal hyperplasia

Apparent mineralocorticoid excess (licorice)

ii. Medullary pheochromocytoma

f ) Extra-adrenal chromaffin tumors

g) Carcinoid

h) Exogenous hormones

Estrogen


72

Hypertension

Glucocorticoids

Mineralocorticoids

Sympathomimetics

Tyramine-containing foods and monoamine oxidase inhibitors

Coarctation of the aorta

Pregnancy-induced hypertension

Sleep apnea

Neurologic disorders

a) Increased intracranial pressure

Brain tumor

Encephalitis

Respiratory acidosis

b) Quadriplegia

c) Acute porphyria

d) Familial dysautonomia

e) Lead poisoning

f) Guillain–Barre´ syndrome

Acute stress, including surgery

a) Psychogenic hyperventilation

b) Hypoglycemia

c) Burns

d) Pancreatitis

e) Alcohol withdrawal

f) Sickle cell crisis

g) Postresuscitation


73

Hypertension

h) Postoperative

Increased intravascular volume

Alcohol274

Drug use eg. Oral contraceptives containing oestrogens, anabolic steroids,

carbenoxolone, corticosteroids, sympathomimetic agents, NSAIDs275 etc.

C. Accelerated and Malignant Hypertension

These forms of Hypertension have become less common with the widespread use

of antihypertensive therapy. It represents a sudden acceleration in the vascular disease

associated with essential hypertension276.

D. Based on Severity

A commonly accepted classification would be the one adopted from “The Sixth

Report of the Joint National Committee on Detection, Evaluation, and the Treatment

of High Blood Pressure (JNC-VI)” Archives of Internal Medicine 1572413-2446,

1997.

Table-7: Showing the classification of blood pressure277

Classification Systolic (mm Hg) Diastolic (mm Hg)

Optimal* <120 <80

Normal <130 <85

High normal 130-139 85-89

HYPERTENSION**

Stage I. HTN (Mild) 140-159 90-99

Stage II. HTN (Moderate) 160-179 100-109

Stage III. HTN (Severe) ≥180 ≥ 110

Stage IV. HTN (Very Severe) >210 >120

JNC of WHO/International society of HTN (ISH).


74

Hypertension

*Optimal BP with respect cardiovascular risk is <120/80 mm of Hg. However,

unusually low reading should be evaluated for clinical significance.

**Based on the average of > 2 readings taken at each of two or more visits

after an initial screening.

Hypertension in some other forms:

Borderline Hypertension:

If the SBP is more than 140 mm of Hg and DBP is above 90 mm of hg278.

Isolated Systolic Hypertension:

The systolic B.P is 160mm Hg and above, and fluctuates from time to time, high

in the morning and low at night279.

Benign Hypertension:

Is moderate elevation of B.P, and the rise is slow over the years280.

Malignant Hypertension:

The marked and rapid increase of blood pressure to 200/140 mm of Hg or

more, the complications like papilledema, retinal exudates, haemorrhage281 are seen.

White coat Hypertension:

White coat hypertension is the most commonly used term to describe patients

whose blood pressure is high only in a medical setting. The concept of White coat

hypertension has been widely adopted in the lay press as well as professional

publications. White coat hypertension should be distinguished from the white coat

effect, which is a measure of the pressure response to the clinic visit and is generally

defined as the difference between the average clinic blood pressure and the daytime

ambulatory blood pressure. The white coat effect is present to a greater or lesser

degree in most hypertensive patients and is greatest in patients with the highest clinic

pressures282. The causes of Secondary hypertension are as follows:-


75

Hypertension

Table-8: Showing the classification of secondary hypertension

Renal endocrinal Cardiovascular Miscellaneous

Glomerulonephritis

Pyelonephritis

Pregnancy

gs: Dru

Polycystic kidney Oral

Contraceptives

Diabetic Nephropathy Liquorice

Rini Produceing

Tumour

Cortico Steroids

Renal Artery Stenosis

Adrenal Cortex

Cushing Syndrome

Hyper Aldosteronism

ADERNAL

MEDULLA

Pheorochromocytoma

Coarctation of

Aorta

Amphetamines


76

Blood Pressure Measurement

Blood pressure measurement

The blood pressure should be taken lying, sitting and standing positions and

can be recorded directly or indirectly. There are three common devices used for the

indirect recording of blood pressure –

Sphygmomanometers, either mercury column or aneroid

Electronic devices

Automated ambulatory blood pressure devices

On the other hand, mercury Sphygmomanometer remains the gold standard for

recording

Indirect Blood Pressure Measurement:

Indirect blood pressure measurement is safe, painless, and provides reliable

information when performed accurately. These guidelines based on BP’s, obtained by

American Heart Association (AHA) standardized indirect measurement method.

Health professionals base crucial clinical decisions on these measurements;

therefore, the proven benefits of treating high BP can be completed only when BP

measurement is taken accurately. The accurate BP measurement requires the ability to

hear, interpret, record Korotkoff sounds and operate the equipment properly.

Selecting the Blood Pressure Measurement Equipment:

The manometer is mercury or an aneroid instrument calibrated to the nearest 2

mm Hg. The mercury manometer’s reading is at the top edge (the meniscus) of the

mercury column. It is the most accurate measurement device available.

The aneroid manometer consists of a metal bellows that expands as the

pressure in the cuff increases and its reading is at the point indicated by a needle on its

dial. The accuracy of the mercury manometer is assessed by noting whether the



mercury meniscus rests at zero. Users cannot be certain that it is accurate even when

the needle is positioned at zero.

The use of automated devices is discouraged in most clinical settings because

they are often difficult to calibrate, fail to give accurate readings on many individuals,

and do not eliminate human error.

Steps Needed to Obtain Accurate and Reliable Readings283:

Step 1: Environment:

The setting should be private and quiet, with a comfortable room temperature.

To get the best estimate of the patient's usual BP, environmental factors that may

cause BP variation or interfere with hearing Korotkoff sounds must be controlled.

The manometer must be positioned so the observer can view it at eye level.

Viewing the manometer above or below the observer's eye, level results in inaccurate

readings. The room should have a straight-backed chair to seat the patient next to a

table or desk with feet flat on the floor.

A seat for the BP observer should be provided along with an adjustable

surface to support the arm at heart level during standing measurements. The height of

the table should be such that the midpoint of the cuff is in place on the patient's right

arm (or the arm that is known to produce the higher BP reading) and is supported at

heart level.

It is important to avoid errors induced by differences in hydrostatic pressure

between the point of artery compression by the cuff and the heart.

If the center of the cuff on the arm or leg is above the heart level, the reading

will be falsely low by 0.8 mm Hg for each 1 cm above the heart level. If below heart

level, it will be falsely high by a similar amount. Supporting the back in the seated



position and the arm in any position avoids increases in BP due to isometric muscle

contraction.

Step 2: Preparation and rest period:

Inquire about biologic factors that may affect the reading at this time,

including the time and dose of medications. If not wearing short, loose sleeves,

patients should nude their arm.

To get the best estimate of the patient's usual BP, biologic factors that may

cause BP variation such as pain, stress, full urinary bladder, and recent meal should be

minimized. Recent ingestion of prescription, over-the-counter or street drugs,

caffeine, and nicotine can affect BP readings. Clothing interferes with cuff placement,

pressure, and sound transmission. Proper preparation avoids elevated readings due to

anxiety about the procedure. Repeated readings increase accuracy.

Instruct patients to sit up straight with legs uncrossed, back resting against the

chair, and feet flat on the floor, and to remain silent until after BP readings.

Allow a 5-minute rest period before the first reading. The lack of back and

foot support, such as occurs when the patient is seated on an examination table, causes

BP elevation averaging 5 mm Hg diastolic. Talking or active listening during

measurement causes BP elevation.

Step 3: Proper cuff (bladder) size:

To get an accurate reading, the width of the cuff bladder should encircle at

least 40% of the arm circumference; the length of the cuff bladder should encircle at

least 80% of the arm circumference.

At the first visit, measure circumference at the midpoint of the upper arm,

between the olecranon and acromion processes. Chart the arm circumference for

future reference. Arms >53 cm in circumference should have the BP measured with a



cuff of the appropriate size on the forearm. When arm circumference measurement is

not practical, as during screening situations, it is acceptable to estimate the proper cuff

size by comparing the bladder width and length to arm circumference.

When BP is not measured in both arms, the reading should be taken in the

right arm unless it is known that BP in the left arm is higher.

Note the appropriate cuff and bladder size on each chart. Using a bladder that

is too narrow or short for the limb is a common error that is serious because it yields

false high readings.

Step 4: Cuff placement:

Locate the patient's brachial artery at the midpoint of the upper arm by

palpating between the biceps and triceps muscles on its inner surface. Wrap the cuff

smoothly and snugly around the arm with its bladder center directly over the palpated

artery and the lower edge of the cuff 2.5 cm above the antecubital fossa.

This technique avoids false high readings that occur when cuff pressure is not

equally distributed over the artery and avoids errors that result from extra sounds

when the stethoscope is exposed to the cuff or tubing.

Step 5: Determine the maximum inflation level:

Before listening for the BP, determine the inflation level necessary to obtain

an accurate systolic reading, the maximum inflation level. To do this, locate the radial

pulse and note the heart rate and rhythm. When the heart rate is irregular, systolic BP

may vary beat to beat, and additional readings are needed to get the best estimate of

the systolic BP.

Continue feeling the pulse and rapidly inflate the cuff to 60 mm Hg, and then

by 10-mm increments until the pulse is no longer palpable. This is the first estimate of

the palpated pressure. Stop inflating the cuff.



Begin deflation at 2 mm Hg per second. Note the pressure at which the pulse

reappears. This is the palpated systolic pressure and is usually within 10 mm Hg of

the level at which the pulse disappeared.

Immediately release all pressure. Add 30 mm Hg to the palpated systolic

reading to determine the maximum inflation level. This maneuver determines the

minimum pressure needed to get an accurate systolic BP on a patient, decreases

patient discomfort, and avoids errors that result from failure to inflate above systolic

BP reading, including an inaccurately low systolic BP reading, which occurs when the

observer begins listening during an auscultatory gap.

Step 6: Stethoscope placement284:

Position the stethoscope earpieces pointing forward in your ears. Sound is not

transmitted well when the ear tips fail to point into the ear canal. Find the point at

which the brachial artery pulse is the strongest, usually just above the antecubital

fossa on the inner aspect of the arm.

Using light pressure, position the chest piece over this point with all edges

gently touching the skin surface. The stethoscope bell or a low-frequency detector is

recommended. The loudest sounds can be heard over this pulse and errors owing to

difficulty hearing and interpreting Korotkoff sounds are minimized along with errors

from too much stethoscope pressure that may cause artery occlusion and distortion of

BP sounds.

Do not allow the stethoscope head to touch the cuff or tubing because

extraneous sounds mask and confuse Korotkoff sounds.



Step 7: Inflation and Deflation:

Rapidly inflate the cuff to the maximum inflation level. If sounds are heard

immediately, completely release all pressure and repeat step five to repeat the

palpated pressure.

Rapid inflation to the correct maximum inflation level ensures listening above

systolic BP. Slow inflation traps venous blood in the arm and may result in pain and

diminished or distorted sounds. Release the air from the cuff so that the mercury falls

at a rate of 2 mm Hg per second until Korotkoff sounds are heard.

Continue deflation at the rate of 2 mm Hg per beat. If unable to hear sounds

clearly, quickly release all pressure and check position of ear tips and stethoscope.

Repeat the procedure. Slow deflation is necessary to allow the observer to hear the

systolic and diastolic pressures at the point of onset. A reading can be no more

accurate than the rate of deflation (i.e., a deflation rate of 10 mm Hg/second results in

a pressure accurate to only 10 mm Hg, and if 1 beat, is missed, to only 20 mm Hg).

Step 8: Systolic blood pressure:

Read to the nearest 2 mm Hg mark. Remember the systolic pressure at the

onset of Korotkoff phase 1. Forgetting the reading is a very common source of errors

of 8 to 10 mm Hg, especially in the presence of a wide pulse pressure (difference

between the systolic and diastolic pressures).

Concentrate and remember the reading by silently repeating the systolic

number with every heartbeat until you confirm disappearance. Observers must learn

to rule out sound artifacts. Single sounds inconsistent with heart rate are insignificant

artifacts unless the pulse was irregular during palpation. In the case of arrhythmia,

additional readings are needed to get the best estimate of the systolic BP.



Table-9: Showing the Korotkoff Sounds The Korotkoff Sounds are classified under five phases*

Phase 1 The pressure level at which the first faint, consistent tapping sounds are

heard. The sounds gradually increase in intensity as the cuff is deflated.

The first of at least 2 of these sounds is defined as the systolic pressure.

Phase 2 Times during cuff deflation when a murmur of swishing sounds are heard.

Phase 3 The period during which sounds are crisper and increase in intensity.

Phase 4 The time when a distinct, abrupt muffling of a sound (usually of a soft

blowing quality) is heard. This is defined as the diastolic pressure in anyone

in whom sounds continue to zero.

Phase 5 The pressure level when the last regular blood pressure sound is heard and

after which all sound disappears. This is defined as the diastolic pressure

unless sounds are heard to zero.

*To avoid error, the observer must be prepared to recognize two normal Korotkoff

sound variations associated with BP readings.

The auscultatory gap is a period of silence occurring during Korotkoff phases

1 and 2. This disappearance of sound is temporary and is usually short, but the gap

can occur over a period of 40 mm Hg. It seems to be associated with higher BP

readings. An absent Korotkoff phase 5 occurs when sounds are heard to zero. When

this is the case, phase 4 should be recorded along with phase 5. In this case, phase 4 is

the best reference for diastolic pressure.

Step 9: Diastolic blood pressure:

Remember the point at which the last regular Korotkoff sound is heard.

Korotkoff sounds are designated as K1 through K5. When the sounds continue to very

low diastolic levels or zero, remember the reading at the onset of K4, the point at

which sounds begin to muffle, as well as the last sound heard.

The onset of K5 is more reliably interpreted when observers listen for the last

sound heard. The absence of K5 occurs often in children, during pregnancy, and in

other high-cardiac-output states. In these cases, the onset of K4 is the most accurate



diastolic indicator. If the diastolic BP is heard above 90 mm Hg, listen for an

additional 40 mm Hg. Otherwise, listen for 10 to 20 mm Hg below the last sound to

confirm disappearance to avoid inaccurately high diastolic BP owing to failure to

listen until sounds reappear after a period of silence (auscultatory gap).

Step 10: Recording:

Immediately record the reading, the arm used, the position of the patient, and

the cuff size used to avoid recall artifact. Record the reading as K1/K5. If K4 is

recorded, write the three numbers as K1/K4/K5.

If sounds do not cease, record K5 as zero. Standardized recording methods are

necessary to correctly interpret and compare readings by different observers. When

phase 5 is absent, Korotkoff phase 4 is the best indication of diastolic pressure.

Step 11: Repeat the reading:

Make certain all air is out of the cuff and wait 1 to 2 minutes, then repeat steps

6 through 10. BP normally changes from minute to minute, especially during clinical

measurements. The average of two or more BP readings in a single arm is more

reliable and a better indicator of usual readings than is a single reading or one reading

in each arm.

Step 12: Repeat the process285:

Repeat the measurements in the other arm during initial workup and standing

or supine as dictated by the patient's situation. Postural changes in BP are measured

after 1 and 3 minutes of standing. Note the arm with the higher reading for future

comparisons. BP can differ by >10 mm Hg between arms. The higher pressure more

accurately reflects intra-arterial pressure.

Special Techniques and Populations286:

Absence of Korotkoff phase 5: When cardiac output is high, as in some children,



in thyrotoxicosis, during fever, and in pregnant women, K5 is often absent. In this

event, Korotkoff sounds are heard until the mercury column falls to zero. BP should

be recorded as three numbers (K5/K4/0).

Blood pressure measurement in children287:

The principles of measurement are the same in newborns, infants, and

children. A most important consideration is the selection of a cuff that is appropriate

for the arm circumference, as described above.

Blood pressure measurement in the elderly288:

In the elderly, the brachial arteries occasionally become very thickened and

stiff. When this happens, the indirect cuff pressure may overestimate intra-arterial

pressure, because higher cuff pressure is required to compress such a rigid vessel.

The presence of a radial artery that is still palpable after the cuff is inflated

above the systolic BP should be a warning of this error. If the artery feels excessively

thick when rolled back and forth under the finger, the BP reading measured with

indirect techniques may be falsely high. Recheck the pressure by palpation in the

forearm. If the palpated systolic pressure differs by >15 mm Hg, then a direct arterial

puncture may be needed to be certain of the true pressure, although this is rare.

Very large, cone-shaped, and muscular arms289:

If the patient's arm is >41 cm in circumference or if it is shaped so that a cuff

does not fit on it well, then accurate pressure measurement may be impossible. In this

case, palpated and auscultator readings should be attempted, with a cuff of the

appropriate size, in the upper arm and forearm. If these differ by greater than 15 mm

Hg, then a better estimate of true pressure is the palpated systolic pressure with the

cuff on the forearm.


Chikitsa

Chikitsa

The aim of chikitsa is not only to remove of the causative factors of the disease,

but also the restoration of doshik equilibrium. The prime importance of chikitsa is to

breakup the samprapti ghatakas290. Here the specific chikitsa as well as chikitsa sutra of

Pittavruta udana has not been mentioned in classics. Therefore our Acharyas have

mentioned towards the new diseases i.e. understanding the prakruti, adhistana of doshas,

immediately the chikitsa should be started291, 292.

Because of the above explanation, the chikitsa can be planed under following headings:

Table-10: Showing the classification of chikitsa

Chikitsa

Dravyabhoota chikitsa Adravyabhoota chikitsa

Vyadhi pratyaneeka chikitsa

Dosha pratyaneeka chikitsa

Nidana parivarjana

Satvavajaya chikitsa

Yoga and other practices

Adravyabhoota chikitsa:

i) Nidana parivarjana:

Nidana parivarjana refers to abstaining from samanya karanas responsible for the

vitiation of vatadi dosha293 etc. and other risk factors like excess salt intake, over weight,

smoking, alcohol etc. These are highlighted in the later part.

ii) Satwavajaya chikitsa:

The manasika karanas also play a 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.

iii) Yoga and other practices:

The most important cause is stress, strain, anxiety, tensions etc. So Yoga helps to


Chikitsa

elevate the capacity of mind and removes the stress and strain. Some of the important

yogas like Bhujangasana, Shalabhasana, Vajrasana, Pranayama, Shavasana, Yoganidra,

and sudarshana kriya, etc., have shown hopeful results in recent times.

Dravyabhoota Chikitsa:

i) Dosha Pratyanika Chikitsa

In Pittavruta udana, main importance is to be given for the treatment of Pitta and

Vata. Some of the shodhana chikitsa can be adopted, these are basti and virechana. Basti

corrects the vata where as virechana corrects the pitta. Following are the general

shodhana measures that can be used:

a) Virechana:

Virechana is a special treatment for pitta294. It can also be given in pitta pradhana

dosha295. Virechana is advised in rakta pradoshaja vikaras296.

b) Basti:

Basti is the pradhana chikitsa for vata297. It is also useful in pitta, kapha, rakta,

samsarga dosha and sannipata dosha298. The tailas which are used in basti suppress the

ruksha, laghu and khara gunas of vata and helps in reducing the katinyata and produces

mardavata of blood vessels

c) Raktamokshana:

Sushruta recommends raktamokshana for vatavyadhi299. Charaka explains

raktamokshana chikitsa for rakta pradoshaja vikara300.

ii) Vyadhi Pratyaneeka Chikitsa

Following are the dravyas and yogas that can be preferred.

Dravyas: Shilajatu, Guggulu, Gomutra, Brahmi, Jatamamsi, Shatavari, Hareetaki etc.

Yogas: Shilajatuguggulu rasayana, Brahmi vati, Brahma rasayana, Pravala pisti, Brihat

vata chintamani rasa, Chandrakala rasa etc.


Chikitsa

Apart from these, certain hridya and rasayana dravyas and yogas can be used.

Shirodhara is used to reduce high blood pressure.

General Management for Avarana:

The principles of avarana chikitsa are as follows-

In avruta vata301 first avaraka is to be treated. When both kapha and pitta are

avaraka, first pitta is to be treated then kapha and care should be taken not to

provoke the avaruta.

General principles of Vatopakrama can be adopted302.

The oushadha and ahara which are not Pitta prakopa and does vatanulomana

should be used303.

The Avarana should be treated by measures, which are Anabhishyandi (Non-

obstructive), Snigdha (unctuous) and sroto-Shudhi Karaka (depuration of body

channels)304.

In case, Vata is obstructed at all the places (Sarva Sthana Avarita), prompt (Ashu)

measures, which are regulative of Vata and at the same time not antagonistic to

Pitta and Kapha are beneficial305.

A vitiated Dosha attains great strength in its natural seats, hence it should be first

subdued by suitable medications such as emesis, purgation, enema and

sudation306.

Madhura anuvasana basti with yapana basti can be given or depending on the bala

of rogi, mridu virechana can be given307.

In Avarana the drugs that are snigdha and srotoshuddhikaraka are to be used and

at the same time these should not increase kapha308.

In condition of Pittavruta Vata, the treatment of Pitta, which is not antagonistic to

vata, should be prescribed. In the condition of Kaphavruta Vata, the treatment of


Chikitsa

Kapha, which is anulomana to Vata, should be prescribed309.

In case of Raktagata vata according to therapeutic response towards blood letting,

one has to decide the associated Avarana Pathology and should be continued

accordingly310.

Rasayana therapy: All the palliative and preventive Rasayana drugs are useful for

the prevention and treatment of avrita induced disorders. Especially Shilajitu,

Guggulu, Chyavanaprasha and Bramha Rasayana are indicated after proper

Shodhana311.

According to specific pathologies of Doshavarana, Dushyavarana, and

Mishravarana treatment modalities varies. For example, alternative administration

of cold and hot therapeutics in case of Pittavruta Vata312.

Anyonya Avarana

When one type of Vata obstructs the function of other types of Vata is called

Anyonya Avarana e.g. Prana avruta vyana313.

They should be treated by means of massage, unctuous potion, enema and all

other similar therapies and by cold and hot measures alternatively314.

Generally Udana should be regulated upward and the Apana downwards. The

Samana should be pacified and the Vyana should be treated by all these three measures.

Prana should be maintained with due care in comparison to other types of Vata, because

life depends on the proper maintenance of it. Thus the various types of Vata that are

occluded or misdirected (Vimargamana) should be established in their normal habitat315.

Treatment:

The aim of treatment is to prevent the morbidity and mortality of hypertension.

The benefits of treatment have to be considering against side effects and inconvenience


Chikitsa

Treatment of blood pressure includes non-pharmacological and pharmacological

measures. Non-pharmacological involvement through life style modification is promoter

as preliminary therapy for essential hypertension.

Non-Pharmacological Management Includes:

Relief of emotional and environmental stress.

Sodium intake: Elderly people are more sensitive to sodium intake. So advised to

reduce the sodium intake i.e. 6 gms per day is suggested.

Weight reduction: Weight reduction is most beneficial in patients who are more

than 10% over weight. However even a 5% reduction in weight will result in

significant lowering of blood pressure.

Avoidance of excessive alcohol intake.

Avoidance of excessive smoking.

Reduction of cholesterol and saturated fat intake

Regular physical exercise.

Table-11: Showing the efficacy of Non-Pharmacological management316

Modification Recommendation

Recommendation

Approximate reduction (range)

Weight reduction

Maintain normal body weight (body mass index 18.5–24.9 kg/m2)

5–20 mmHg/10 kg

Adopt eating plan Consume a diet rich in fruits, vegetables, and low-fat dairy products with a reduced content of saturated and total fat

8–14 mmHg (74)

Dietary sodium reduction

Reduce dietary sodium intake to no .100 mmol/day (2.4 g sodium or 6 g sodium chloride)

2–8 mmHg (74)

Physical activity

Engage in regular aerobic physical activity such as brisk walking (at least 30 min/day, most days of the week)

4–9 mmHg

Moderation of alcohol consumption

Limit consumption to no more than two drinks; (e.g., 24 oz beer, 10 oz wine, or 3 oz 80-proof whiskey) per day, in most men and to no more than one drink per day, in women and lighter weight persons.

2–4 mmHg


Chikitsa

Pharmacological Management:-

General Management:

1. Start with a low dose of an agent and, if blood pressure is not controlled, increase slowly

with diet control therapy.

2. Start with an agent that may also treat and/or not harm a coexisting condition.

3. Add a second agent from a different, complementary class, if blood pressure is not

controlled with a moderate dose of the first agent.

4. Start with an agent that the patient is likely to tolerate best; long term compliance is

related to tolerability and efficacy of the first agent used.

5. Use a diuretic when two agents are used, in nearly all cases.

If the blood pressure is controlled, then a slowly reduce the dose and withdrawal

of some of the agents with regular observation. In general, there are six classes of

drugs; diuretics, anti adrenergic agents, vasodilators, calcium entry blockers, angiotensin

converting enzyme (ACE) inhibitors and angiotensin receptor antagonists.

Fish Oil317:

From a physiologic viewpoint, it is attractive to propose that fish oil lowers BP.

Fish oil has highly unsaturated fatty acids that stimulate the synthesis of vasodilating

prostaglandins, inhibit platelet aggregation, and limit the release of vasoconstrictors. Fish

oil is often prescribed as capsules that contain 1 ml of purified oil or as crude cod liver

oil. Large doses of fish oil (e.g., 30 to 45 ml daily) clearly lower BP levels in

hypertensive patients. A smaller dose (e.g., 6 capsules daily) had no effect in hypertensive

and normotensive persons. The unpleasant taste of the fish oil and belching interfere with

compliance. Therefore, fish oil is not considered a practical therapy for hypertension.


Chikitsa

Table-12: Showing the treatment of Hypertension

Class of Drug

Compelling Indications

Possible Indications

Compelling Contra Indications

Possible Contra Indications

Diuretics Heart failure, Elderly patients, Systolic hypertension

Diabetes Gout Dyslipidemia, Sexually active malaes

Blockers Angina, After myocardial infarct, Tachy arrhythmias

Heart failure, Pregnancy, Diabetes

Asthma & COPD, Heart block

Dyslipidemia, Athletes & Physically active patients, Peripheral vascular disease

ACE –Inhibitors

Heart failure, Left ventricular dysfunction, After myocardial infarct, Diabetic nephropathy

Pregnancy, Hyperkalaemia, Bilateral renal artery stenosis

Calcium Antagonists

Angina, Elderly patients, Systolic hypertension

Peripheral vascular disease

Heart block Congestive heart failure

Blockers Prostatic hypertrophy

Glucose intolerance, Dyslipidemia

Orthostatic hypotension

Angiotensin IIAntagonists

ACE-inhibitor cough

Heart failure Pregnancy, Bilateral renal artery stenosis, Hyperkalaemia


Pathya-Apathya

Pathya- Apathya

That which is not against the srotas and priya to manas318. Srotas is always an

important integral part of samprapti of a disease, which needs to be corrected by the

means of chikitsa. Pathya sevana along with the proper Aushada will always reduce

the recovery phase of a disease. Acharya Lolimbaraja who was known as the best poet

physician was the first to explain the significance of pathya in his work Vaidhya

Chintamani. He feels that if a person knows all about pathya then there is no necessity

of taking the oushadha for the disease319.

The specific Pathya-Apathya is not mentioned for Pittavruta udana, but the

general Pathya-Apathya mentioned for Pittavruta vata and Vatavyadhis are good for

Pittavruta udana. In the treatment of diseases, diet and other habits are given equal

importance with drugs and therapeutic measures.

The pathyapathya that can be suggested are as follows,

Table-13: Showing the Pathyapathya320 in Pittavruta udana

Pathya Apathya

Ahara Mamsa of jangla pradesha

animals and birds, Yava,

Shalee.

Other than Jangala mamsa, Dadhi,

Tobacco, Tea, Coffee, Salt, Fatty

substances, Alcohol, Amala, Lavana,

Katu rasa, stored food 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.


93

Drug Review

Drug Review

Shilajatu:

Shilajatu is an exudation from rock during hot sunny days. Though it may be

occurring in many parts of the world but India was the first to highlight its wonderful

therapeutic value for many centuries. Ayurveda mentions it as wonderful medicine. It

describes that shodhita Shilajatu can cure even the assadhya diseases. Acharya

Charaka says “there are hardly any curable diseases which can not be controlled or

cured with the help of Shilajatu321”.

Names according to Language322:

Sanskrit: Shilajatu, Hindi: Shilajita, Nepali: Kalo Shilajita, Arabic: Hajar–ul–Musa,

Bengali: Shilajita, English: Black Bitumen or Mineral Pitch, Gujarati: Shilajita,

Marathi: Shilajita Latin: Asphaltum punjabinum, Malayalam: Kanmadam, Unani:

Momiye and Shilajita, Parsi : Momiya Phacyral Yahud.

Synonyms of Shilajatu323, 324,325:

Adrija, Adreyam, Ashmaja, Ashmotham, Girija, Gaireya, Shaila, Shilodbhava,

Jatu, Adrijatu, Ashmajatuka, Girijatu, Shilajatu, Shilaniryasa, Shilasveda, Shilamaye,

Shiladhatu, Shaildhatuja, Shaileya, Shilaya, Shilaj, Ashamlaksha, Atithi, Shilaha,

Shail, Ashamsara, Dhatuja, Ashamajatu, Ashamj-jatu, etc.

Test: The testing techniques for Shilajatu are as follows:

i. Shilajatu put on fire it erects perpendicularly and burn with out smoke.

ii. If pure Shilajatu put in water, through the tip of a thin erect glass it will come down

slowly after spreading like fibre326.

Properties:

Rasa, Guna, Virya, Vipaka, Karma can be considered as the properties of the

drug.


94

Drug Review

The texts like Rasa Ratna Samucchaya believed that Shilajatu possess all the

properties of rasa, uparasa, parada, ratna and lauha together in itself327.

Rasa328: Tikta, Katu

Guna: The samanya guna of Shilajatu is considered to be sheeta by Rasa Paddhati,

where as Acharya Charaka mentions it to be of natiushna-sheeta329 whereas another

place Acharya Charka mentioned the types of shilajatu as sheeta Veerya330.

Virya: Ushna virya331.

Vipaka: Katu vipaka332

Karma: Mutrala, Yogavahi, Rasayana333, Chedana, Tridosha hara334 etc.

Uses:

According to Charaka Samhita there is no curable disease on earth which

Shilajatu can not perforce subdue. When administered at right time, well prepared and

in the right manner, it will secure for the healthy subject the optimum measure of

vitality. It removes old age and disease, gives great firmness of the body, increases

intelligence and memory and promotes prosperity335.

Pathya–Apathya:

While taking a course of Shilajatu care should be taken to see that, irritating

and heavy articles are excluded form the dietary. Exercise, sun light, direct air and

chittsantapa should be avoided. During the administration of Shilajatu the following

materials are contraindicated:

1. Vidahi 2. Guru 3. Kulatha 4. Kapota mamsa.

Kulatha is kashaya rasa, ushna virya, kapota mamsa is alo ushana veerya.

Shilajatu is katu, kashaya, Tikta rasa and ushna virya. So the above properties cause

untoward effect in the body. Therefore should be avoided double the days of

administration336.


95

Drug Review

Chemical Composition337:

Analyzed by Hooper it yielded:

Water = 09.5%, Organic matter = 36.20%, Mineral matter = 34.65%, Nitrogen =

01.3%, Lime = 07.80%, Potash = 09.07%, Phosphoric acid = 00.16%, Silica =

01.35%.

Guggulu:

Guggulu gum is used to produce standardized or purified extracts called

guggulipids or guggulsterones. Heart drugs based on Guggulu extracts are sold in

India, where almost all of the research on Guggulu has been done in the past thirty

years338.

Vernacular name:

Sanskrit: In Sanskrit, Guggulu means “that which protects against diseases”. Another

traditional Sanskrit name for Guggulu is palnkash- pal means flesh and kash means to

reduce. It is one of the best herb for obesity339.

Latin: Commiphora Mukul.

Family: Burseracae340.

English: Indian bedellium

Common Name: Bdellium Gum, Guggulipid, Gum Gugal, Gumgu Ggulu, Salaitree,

Commiphora mukul, Balasmodendron mukul341.

Hindi: Gugal, Guggal. Kanada: Kanthagana, Gugggula, Gugulugida, Guggulu.

Telugu: Guggipannu. Assam: Guggulu. Malayalam: Guggulu. Marathi: Guggul.

Urdu: Muqil (Shihappu). Gujarati: Gugal. Oriya: Guggulu. Punjabi: Guggal.

Kashmiri: Kanth Gan342.

Synonyms: Devdhoop, Jatayu, Koushik, Pur, Kumbholookhlak, Mahishaksh,

Kalaniryas, Natankchar, Shiv and Durg, Palnkash343,344.


96

Drug Review

Habitat Sindh, Rajasthan, Eastern Bengal, Assam, Mysore, Northeast Africa,

Afghanistan, Bihar, Bellary etc345.

Characteristics:

Guggulu is obtained from a tree, which exudes a resinous sap out of incisions,

that are remade on its bark. This resin has been used for centuries. The fresh the oleo-

gum resin is moist, viscid, fragrant and of a golden color. It burns in fire, melts in the

sun, & forms a milky emulsion with hot water346.

Gunakarma:

Rasa: Tikta, Katu, Kasaya, Virya: Usna, Vipaka: Katu, Prabhava: Tridosahara

Guna: Laghu, Ruksha, Tikshna, Vishada, Sukshma, Sara347.

Part used: Resin / Gum348.

Phytoconstituents349:

Guggulu an extract of the exudate (gum guggulu) of Mukul myrrh tree

contains phytosterols named guggulsterones, organic acids, aromatic acids,

diterpenes, lignans, sterols, steroids, esters and fatty acid alcohols. Guggulu is

preferred to crude gum guggulu because it is safer and more effective. 0.37% volatile

oil consisting chiefly myrcene, dimyrcene, gum resin & bitter principle.

Actions:

Analgesic, highly potent anti inflammatory, rejuvenator, aphrodisiac,

diaphoretic, diuretic, astringent, hypocholesterolaemic / hypolipidaemic, demulcent,

alterative, carminative, appetizer, antispasmodic, emmenagogue, antirheumatic,

antiarthritic, antisuppurative, antiseptic, hypercholestremia, enhances phagocytosis,

immunostimulant, thyroid stimulant, uterine stimulant350,351.

The pharmacological action of the oleo resin resembles in many ways with the

actions of copaiba cubebs. Its active components, Z-guggulsterone and E-


97

Drug Review

guggulsterone, have an ability to lower both cholesterol and triglyceride levels.

Specifically, gugulipid lowers VLDL and LDL cholesterol and triglycerides while

simultaneously raising HDL cholesterol. This indicates Guggulu primary use for

providing a protective effective against atherosclerosis. These effects are due to

Guggulu action on the liver and thyroid.

The thyroid is stimulated to increase the body's metabolic rate, and the liver is

stimulated to metabolize LDL cholesterol, effectively lowering the amount in the

bloodstream352.

Theraputic uses:

Obesity, nervous diseases, arthritis, diabetes, hemiplegia, leprosy, leucorrhea,

marasmus, muscle spasms, neuralgia, neurasthenia, ophthalmia, pertussis, pneumonia,

pyelitis, pyorrhea, rheumatism, scrofula, skin disorders, sore throat, spongy gums,

ulcerative pharyngitis, hypertension, ischemia, heart diseases, urinary disorders, skin

diseases, applied locally in hemorrhoids, abscesses, bad ulcers. A number of studies

have supported the claims that Guggulu extracts can help to reduce heart disease risk

factors, with reductions in both blood fats and total cholesterol of 15-30 percent over

three months.

Guggulu extracts have been shown to lower overall blood fats, reduce "bad"

LDL cholesterol, and raise "good" HDL cholesterol. If it is also true, as some studies

suggest, that guggulu extracts can reduce platelet stickiness, this herb would rank

among the most important since few substances have a positive impact on both blood

fats and platelets353.

Triphala354:

This includes three drugs: (a) Haritaki (b) Vibhitaki (c) Amalaki.

Synonyms355: Phalatrika, Vara.


98

Drug Review

Rasa: Kshaya Pradhana.

Vipaka: Madhura.

Veerya: Anushna.

Properties : Tridoshahara, Chakshushya, Dipana, Vrishya, Sara.

1) Haritaki356:

Latin name - Terminalia chebula Retz.

Family - Combretaceae

Paryaya357:

Sanskrit - Abhaya, Pathya, Shiva, Girija, Pramthya, Amrita.

Hindi – Harad, Kannada – Anilekayi, Gujarati – Harde, Marathi – Harda.

English – Chebulic myrobalan.

Fruit: Drupe, glabrous, pendulous 1-2 inch long, ellipsoid ovoid from a broad base,

more or less five ribbed.

Test of genuine Haritaki: It should be fresh, smooth, dense, heavy and round in

shape, when put into water it should sink.

Chemistry: Fruits contain about 24.6-32.5% of tennin and also contains chebulagic

acid, glucose, corilagin, amino etc.

Guna Karma:

Rasa - Kashaya pradhana Tikta, Katu, Madhura, Amla, Virya – Ushna, Guna -

Laghu, Ruksha, Vipaka - Madhura, Prabhava - Tridoshahara.

Action and uses: Medhya, Rasayana, Brimhana, Anulomana, Ayushya, Chakshushya,

Mootrala etc. and used in Prameha, Sopha, Hridroga, Eye diseases, Tvakroga etc.

Part used – Fruit

2) Vibhitaki358:

Latin name – Terminalia bellirica Roxb.


99

Drug Review

Family – Combretaceae

Paryaya359:

Samskrita- Kalidruma, Kasaghna, Aksha, Karshaphala, Kalpavriksha

Hindi – Baheda, Gujarati – Beheda, Kannada – Tarekayi, Marathi – Behda

English – Belliric myrobalan.

Fruit: 10-25 mm in diameter, ovoid, grey suddenly narrowed into a very, short stalk,

velvety, obscurely 5 angled when dried.

Chemistry – Fruits contain about 21.4% B-sitosterol, gallic acid, ellagic acid,

chebulagic acid, galloyl, glucose, Mannitol, galactose, ethyl gallate, fructose,

rhamnose, a new cardiac glycoside, belliricanin, and kernels yielded yellow fatty oil.

Guna Karma:

Rasa – Kashaya. Guna – Ruksha, Laghu

Virya – Ushna, Vipaka – Madhura, Doshaghnata – Tridosha, mainly Kaphahara.

Action and uses: Dipana, Anulomana, Grahi, Chakshushya, Kanthya, Swasakasahara,

Raktashodhana. It is used in Kasa, Swasa, Swarabheda, Vatavyadhi, Arsha etc.

Part used – Fruit

3) Amalaki360:

Latin name – Emblica officinalis Gaertn.

Family – Euphorbiaceae

Paryaya361:

Samskrita – Dhatri, Vayastha, Amruta phala etc.

Hindi – Amla, Anvla, Kannada – Nellikayi, Gujarati – Anvla, Marathi – Awle,

English – Emblic myrobalan.

Gana: Virechnopag, Vayahsthapana etc.

Distribution: This tree is common in the mixed deciduouis forests of India


100

Drug Review

Fruit: 1.3-1.6 cm in diameter, fleshy, globosely, with 6 obscure vertical furrows. The

fruit is green, changing to light yellow when mature; it is sour and astringent in taste.

Chemistry: Fruit contains mineral matter (0.7%), fiber (3.4%), Protein (0.5%)

carbohydrate (14.1%), fat (0.1%) calcium (0.05%), phosperous (0.02%), ferrous (1.2

mg), vit.C, nicotinic acid (0.2mg/100gm), tenic acid, gelic acid etc.

Guna Karma:

Rasa – Amla (Pradhana), Kashya, Tikta, Katu, Madhura., Guna – Guru, Ruksha,

Sheeta, Vipaka – Madhura, Virya – Sheeta, Doshaghnata –Tridoshaghna

Action and uses – Rasayana, Vrishya, Shonita and Garbha sthapana, Mootrala etc.

Part used – Fruit (without seed)

Gomutra:

Gana, Guna and Karmadi of Gomutra:

Gana : Acharya Charaka has described Gomutra in Katuskanda362. Sushruta in

shirovirechana gana363.

Guna Karmadi364, 265:

Rasa – Katu, Tikta, Kashaya, Madhura, Lavana, Guna – Tikshna, Laghu, Virya –

Ushna.

Karma366,367 – Kaphavata shamaka, Pitta janaka, Agni pradeepaka, Medhya.

Other properties:

According to Bhava Prakasha, the simple mutra is taken as Gomutra. Different

types of mutras are used in the treatment of different diseases but Gomutra is highly

effective in all the mutras368. Acharya Sushruta has advised to use Shilajatu, Guggulu,

Gomutra and Triphala in the treatment of Sthaulya369.


101

Table-14: Showing the properties of Ingredients

Sl no

Drug Latin name Paryoga RasaAnga

Guna Veerya Vipaka Doshaghnata Karmukata

1 Shilajatu Asphaltumpunjabinum

Ishat- Amla MriduKashaya

Sama-Sheetoshna

Katu Balya, Yogavahi, Vrishya, Rasayana, Medhohara, Hritshoolanashaka

2 Guggulu Commiphora Niryasa mukul

Tikta, Katu Laghu ,Ruksha, Teekshna,Vishada Sukshma,

Ushana Katu Vata Kapha Shamaka

Hridya,Rakta prasadana, Mutrala,Shothahara, Medohara,

3 Hareetaki Terminaliachebula

Phala Lavanavarjita- Pancharasa Kashaya

Laghu ,Ruksha

Ushana Madhura Tridosha hara Hridya,Shonitasthapana, Mutrala Shotha hara,

4 Vibhitaki Terminaliabellarica

Phala Kashaya Laghu , Ruksha

Ushana Madhura Tridosha hara Rakta stambhana, (Kapha hara) Sleshama hara

5 Amalaki Emblicaofficinalis

Phala PpancharasaLavanavarjita Amla

Guru , Ruksha Sheeta

Sheeta Madhura Tridosha hara Hridya, Shonita sthapana, Pittashamaka Rasayana, Mutrala

6 Gomutra Katu, Tikta,Kashaya, Madhura, Lavana (anurasa)

Tikshna, Ushna, Laghu

Ushna Katu Kaphavatashamaka, Pitta prakopaka

Deepana, Pachana, Anulomana, Amapachana, Malashodhana, used in Shula, Vataroga, Shopha etc.

102

Material & Methods

Materials and Methods

Source of data

Patients:

Patients suffering from Essential hypertension were selected from department

of Kayachikitsa Post graduation studies and research O.P.D. of Shri D.G.M

Ayurvedic medical college and hospital by preset inclusion and exclusion criteria.

Literary:

Literary aspects of study were collected from classical Ayurvedic and Modern

texts, updated with recent journals.

Composition of Trial Drug:

Table-14: Showing the composition of Shilajatu Guggulu Rasayana

Sl.No Sanskrit Name Botanical Name Proportion

1 Shilajatu Black bitumen 1 Part

2 Guggulu Commiphora mukul 1 Part

Preparation of yoga:

All the drugs were identified and collected from local area, Good

manufacturing practice was followed for the preparation.

Method of collection of data

Study design:

Present study is prospective clinical study. The patients with Pittavruta udana

w.s.r. to Essential Hypertension within the age group of 35 yrs to 70 yrs. were

selected randomly from O.P.D of D.G.M. A M.C.,H.& Research Center after

fulfilling the inclusion and exclusion criteria irrespective of their sex, occupation and

socio-economic status.


Material & Methods

Sample size:

A minimum of 30 patients was taken excluding the dropouts. The present

study is a single group study where as patients were assigned in one group. It is a

Simple random sampling technique clinical trial.

Exclusion criteria: -

Following were the criteria to exclude the patients from the study: -

Essential hypertension with diabetes.

Essential hypertension with ischaemic heart diseases.

Secondary hypertension.

Left ventricular hypertrophy.

Left ventricular failure.

Renal hypertension.

Patient with malignant hypertension.

Lactating and pregnant females.

Hypertension secondary to malignancy.

Inclusion Criteria

The selection of the patient for clinical study was done with following criteria:

Patients were selected between the age group of 35 to 70 years.

Patients of both sexes were selected indiscriminately.

Patients with following conditions were considered for the clinical trial:

• Freshly detected and untreated case of essential hypertension.

• Established and treated case of essential hypertension and who had

discontinued the treatment before the clinical trial was taken for the

study.

• Asymptomatic and symptomatic cases were taken for the study.


Material & Methods

• Both mild and moderate cases.

• Racial of environmental factors.

• No discriminations of chronicity and severity of disease.

• Other than the exclusive criteria mentioned above.

Criteria of Diagnosis

The symptomatology of Pittvaruta udana mentioned in Ayurvedic text were

the basic diagnostic criteria.

The symptomatology of essential hypertension explained in modern text were

the basic diagnostic criteria.

Estimation of high blood pressure according to American Heart association

(A.H.A) diagnostic criteria.

Diagnosis is made on the basis of measurements of sphygmomanometer.

Posology

Abhyantara 6 gms per day/24 hrs, in three divided doses. Sadhyo virechana

has been carried out with 30 ml of Gandharvahastadi castrol prior to the initiation of

the treatment.

Study Duration

Study: 30 days.

Follow-up: The duration of follow up was 30 days.

Assessment of Result

The subjective and objective parameters of base line data to pre and post

medication were compared for assessment of the results. All the result were analyzed

statistically for “p” value using student‘t’ test, Paired t- test.


Material & Methods

Subjective parameters

The symptoms of Pittavruta udana mentioned in classical text as Daha,

Moorcha, Bhrama, Klama, and symptoms of hypertension mentioned in contemporary

text were the subjective parameters.

Objective Parameters

Blood pressure:-

Standing

Sitting

Laying down posture

These have been recorded regularly during study duration.

Investigations

Diagnostic and exclusion:-

Lipid profile:

• Very low density lipoprotein cholesterol (VLDL)

• Low-density lipoprotein cholesterol (LDL)

• High-density lipoprotein cholesterol (HDL)

• Serum cholesterol

• Serum triglycerides

Chest X-Ray

Electro cardiogram (E.C.G)

Fasting blood sugar (F.B.S)

Blood urea

Serum creatinine


Material & Methods

Preparation of medicine:

1. Shilajatu shodana370:

The Shilajatu which was exuded from the stones was collected, powdered and

kept immersed in hot water for three hours. Later it was vigorously squeezed and

filtered through cloth and collected in a clean mud plate and exposed to bright sun.

The scum that collects at the top is separated and dried in the sun till it becomes a

hard mass in about two months of time. This is fit to be used as medicine. The sign of

good Shilajatu when put on fire assumes the shape of a linga(round mass) and does

not emit smoke. The water which remains underneath in the earthen plate might also

yield some Shilajatu if kept in sun light for a number of days.

2. Guggulu Shodhana371:

i) Guggulu

ii) Triphala

iii) Gomutra

Guggulu must be bundled in a strong cloth and boiled in dolayantra containing 4

parts of Triphala kashaya prepared with Gomuthra. When all the guggulu dissolves in

Triphala kashaya, pottali is removed and the liquid is evaporated to collect purified

Guggulu.

Guggulu and Shilajatu are powdered and mixed properly. Then 90 gms of yoga is

stored airtight container.


Observations

Observations

In this study total 33 patients were registered, out of which 3 patients left the

study before completion and 30 no. of patients have completed their course of

treatment with Shamana Oushdha (Shilajatu Guggulu Rasayana).

Table-16: Showing Age wise distribution of total 30 patients with percentage Male patients Female patients Total patients Age

Number % Number % Number % 36-42 01 3.33% 01 3.33% 02 6.66% 43-49 04 13.33% 03 10% 07 23.33% 50-56 07 23.33% 03 10% 10 33.33% 57-63 02 6.66% 04 13.33& 06 20.00% 64-70 04 13.33% 01 3.33% 05 16.66% Total 18 12 30

Age wise distribution of all thirty patients shows that maximum patients were

from 50-56 years age group i.e. 10 (33.33%) patients, where 07 (23.33%) were male

and 03 (10%) were female. In age group of 43-49 years 07 (23.33%) patients were

reported, in these patients 04 (13.33%) were male and 03 (10%) were female, in age

group of 57-63 years 06 (20%) patients had undergone the treatment, here 02 (6.66%)

were male and 04 (13.33%) were female and in age group of 64-70 years 05

(16.67%) patient were approached, in these patients 04 (13.33%) were male and 01

(3.33%) were female and in the age group of 36-42 years total 02 (6.67%) i.e. 01

(3.33%) were male and 01 (3.33%) were female patients had completed the treatment.

Figure-08: Showing Age wise distribution of total 30 patients

1

4

7

2

4

1

3 3

4

1

2

7

10

6

5

0

1

2

3

4

5

6

7

8

9

10

MALE FEMALE TO TAL

36-42 Years43-49 Years50-56 Years57-63 Years64-70 Years


Observations

Table-17: Showing Sex wise distribution of total 30 patients with percentage Sex Total no. of Patients % age

Male 18 60.00% Female 12 40.00% Total 30

In the present study 18 (60%) of the patients were male and 12 (40%) were

female.

Figure-09: Showing Sex wise distribution of total 30 patients

18

12

0

2

4

6

8

10

12

14

16

18

MaleFemale

Table-18: Showing Religion wise distribution of total 30 patients with percentage Religion Total no. of Patients % age

Hindu 26 86.67% Muslim 04 13.33% Christian 00 00 Others 00 00 Total 30

In this study 26 (86.67%) of the patients belongs to Hindu category and 04

(13.33%) belongs to Muslim.

Figure-10: Showing Religion wise distribution of total 30 patients

26

4

0 0

0

5

10

15

20

25

30

HinduMuslimChristianOthers


Observations

Table-19: Showing Occupation wise distribution of total 30 patients Male patients Female patients Total patients Occupation

Number % Number % Number % Sedentary 08 26.66% 12 40.00% 20 66.67% Active 06 20.00% 00 - 06 20.00% Labour 04 13.33% 00 - 04 13.33% Total 18 - 12 - 30 -

In the occupation wise distribution 20 (66.67%) of the patients had sedentary

life style where 08 (26.66%) male and 12 (405) were female, 06 (20%) were male

patients had active occupation and 04 (13.33%) were male patients are of labour class.

Figure-11: Showing Occupation wise distribution of total 30 patients

86

4

12

0 0

20

64

2

0

4

6

8

10

12

14

16

18

20

MALE FEMALE TO TAL

SedentaryActiveLabour

Table-20: Showing Economical status wise distribution of 30 patients Economical status Total no. of Patients % age

Poor 04 13.33% Middle 24 80.00% Higher class 02 6.67% Total 30

Here, 04 (13.33%) of the patients comes from Poor Class, 02 (6.67%) of the

patients come from Higher Class and 24 (80.00%) of the patients comes from Middle

Class.

Figure-12: Showing Economical status wise distribution of total 30 patients

4

24

2

0

5

10

15

20

25

PoorMiddleHigher class


Observations

Table-21: Showing Marital status wise distribution of 30 patients with percentage Marital Status Total no. of Patients % age

Unmarried 00 00 Married 30 100% Total 30

All the 30 patients i.e. 100% approached are married.

Figure-13: Showing Marital status wise distribution of total 30 patients 30

0

5

0

10

15

2 0

2 5

3 0

MarriedUnmarried

Table-22: Showing Intake Rasa predominance wise distribution of 30 patients Rasa predominance Total no. of Patients % age

Madhura 20 66.67% Amala 08 26.67% Lavana 17 56.67% Katu 30 100.00% Tikta 00 00 Kashaya 00 00

In this study maximum 30 (100%) patients have taken Katu Rasa

predominantly in their diet, followed by 20 (66.67%) Madhura Rasa, 17 (56.67%)

Lavana Rasa and 08 (26.67%) Amala Rasa. Excessive use of Katu, Lavana and Amala

Rasa may be the etiological factors of this disease.

Figure-14: Showing Intake Rasa predominance wise distribution of 30 patients

20

8

17

30

0 0

0

5

10

15

20

25

30

MadhuraAmalaLavanaKatuTiktaKashaya


Observations

Table-23: Showing Nidra wise distribution of total 30 patients with percentage Nidra Total no. of Patients % age

Sound sleep 12 40.00% Disturbed sleep 18 60.00% Total 30

The present study shows that maximum 18 (60%) of the patients had disturbed

sleep and 12 (40%) of the patients had sound sleep.

Figure-15: Showing Nidra wise distribution of total 30 patients

12

18

0

2

4

6

8

10

12

14

16

18

Sound sleepDisturbed sleep

Table-24: Showing Malapraviti wise distribution of 30 patients with percentage Malapraviti Total no. of Patients % age

Prakruta 22 73.33% Constipated 08 26.67% Total 30

In this study 08 (26.67%) of the patients had constipated stool where as 22

(73.33%) of the patients had normal stool.

Figure-16: Showing Malapraviti wise distribution of total 30 patients

22

8

0

5

10

15

20

25

PrakrutaConstipated


Observations

Table-25: Showing Addiction wise distribution of 30 patients with percentage Addiction Total no. of Patients % age

Tea 20 66.67% Coffee 22 73.33% Smoking 06 20.00% Alcohol 10 33.33% Tobacco Chewing 06 20.00%

The present study shows 22 (73.33%) of the patients had addiction to Coffee,

20 (66.67%) of the patients to Tea, 06 (20%) of the patients to Tobacco, 10 (33.33%)

of the patients to Alcohol and 06 (20%) patients had Smoking addiction.

Figure-17: Showing Addiction wise distribution of total 30 patients

Table-26: Showing Ahara wise distribution of total 30 patients with percentage

Ahara Total no. of Patients % age Vegetarian 14 46.66% Mixed 16 53.33% Oil 17 56.66% Ghee 11 36.66% Stored Food 16 53.33%

In the present study 14 (46.66%) of the patients had vegetarian diet, 16

(53.33%) of the patients had mixed diet where as 17 (56.66%) of the patients had

more oily diet, 11 (36.66%) of the patients had used ghee and 16 (53.33%) of the

patients had used stored food.

Figure-18: Showing Ahara wise distribution of total 30 patients

2022

6

10

6

0

5

10

15

2 0

2 5

TeaCoffeeSmokingAlcoholTobacco Chewing

1416 17

11

16

0

2

4

6

8

10

12

14

16

18

VegetarianMixedOilGheeStored Food


Observations

Table-27: Showing Manasika Prakruti wise distribution of total 30 patients Manasika Prakruti Total no. of Patients % age

Bhaya 09 30.00% Kopa 17 56.67% Deenata 19 63.33% Udvega 08 26.67% Kshobha 20 66.67% Samprahara 09 30.00% Mada 06 20.00%

In this study 20 (66.67%) of the patients had Kshobha, 19 (63.33%) of the

patients had Deenata, 17 (56.67%) of the patients had Kopa, 09 (30%) of the patients

had Bhaya, 09 (30%) of the patients had Samprahara, 08 (26.67%) patients had

Udvega and 06 (20%) of the patients had Mada.

Figure-19: Showing Manasika Prakruti wise distribution of total 30 patients


9

1719

8 9

6

20

Table-28: Showing Shareera Prakriti wise distribution of total 30 patients

0

Shareera Prakriti Total no. of Patients % age VP 18 60.00% VK 10 33.33% PK 02 06.66% Total 30

The above table shows 18 (60%) of the patients had vatapitta prakriti, 10

(33.33%) of the patients had vatakapha prakriti and 02 (6.66%) of the patients had

pittakapha prakriti.

Figure-20: Showing Shareera Prakriti wise distribution of total 30 patients

2

4

6

8

10

12

14

16

18

2 0BhayaKopaDeenataUdvegaKshobhaSampraharaMada

18

10

2

0

2

4

6

8

10

12

14

16

18

VPVKPK

Observations

Table-29: Showing Sara wise distribution of total 30 patients with percentage Sara Total no. of Patients % age

Twak 02 06.66% Rakta 10 33.33% Mamsa 12 40.00% Meda 05 16.66% Asthi 01 03.33% Majja 00 00 Shukra 00 00 Satwa 00 00 Total 30

The above table shows 12 (40%) of the patients had Mamsa Sara, 10 (33.33%)

of the patients had Rakta Sara, 05 (16.66%) of the patients had Medha Sara, 02

(6.66%) of the patients had Twak Sara and 01 (3.33%) of the patients had Asthi Sara.

Figure-21: Showing Sara wise distribution of total 30 patients

2

1012

5

10 0 0

0

2

4

6

8

10

12 TwakRaktaMamsaMedaAsthiMajjaShukraSatwa

Table-30: Showing Samhanana wise distribution of total 30 patients Samhanana Total no. of Patients % age

Susamhita 25 83.33% Madhyama samhita 05 16.66% Heena samhita 00 00 Total 30

The above table shows 25 (83.33%) of the patients had Susamhita and 05

(16.66%) of the patients had Madhyama Samhanana. Even single patient also has not

had Heena Samhanana.

Figure-22: Showing Samhanana wise distribution of total 30 patients

25

5

0

0

5

10

15

2 0

2 5

Susamhita

Madhyama samhitaHeena samhita


Observations

Table-31: Showing Satmya wise distribution of total 30 patients with percentage Satmya Total no. of Patients % age

Pravara 05 16.66% Madhyama 20 66.66% Avara 05 16.66% Total 30

The above table shows 20 (66.66%) of the patients were having Madhyama

Satmya and 05 (16.66%) of the patients were having Pravara Satmya and 05 (16.66%)

of the patients were having Avara Satmya.

Figure-23: Showing Satmya wise distribution of total 30 patients

5

20

5

0

2

4

6

8

10

12

14

16

18

20

PravaraMadhyamaAvara

Table-32: Showing Satwa wise distribution of total 30 patients with percentage Satwa Total no. of Patients % age


The above table shows 19 (63.33%) of the patients had Madhyama Satva and

07 (23.33%) of the patients had Avara Satva and 04 (13.33%) of the patients were

having Pravara Satva.

Figure-24: Showing Satwa wise distribution of total 30 patients

4

19

7

0

2

4

6

8

10

12

14

16

18

20



Observations

Table-33: Showing Vyayama Shakti wise distribution of total 30 patients Vyayama shakti Total no. of Patients % age


The above table shows 06 (20.00%) of the patients had Madhyam

Vyayamashakti, 20 (66.66%) of the patients had Avara Vayamashakti and 04

(13.33%) of the patients had Pravara Vyayamashakti.

Figure-25: Showing Vyayama Shakti wise distribution of total 30 patients

4

6

20

02

4

6

8

10

12

14

16

18

20


Table-34: Showing Vaya wise distribution of total 30 patients with percentage

Vaya Total no. of Patients % age Balya 00 00 Madhya 23 76.66% Vruddha 07 23.33% Total 30

The above table shows 23 (76.66%) of the patients had Madhyama Vaya and

07 (23.33%) of the patient’s had Vruddha Vaya.

Figure-26: Showing Vaya wise distribution of total 30 patients

0

23

7

0

5

10

15

20

25

BalyaMadhyaVruddha


Observations

Table-35: Showing Pramana wise distribution of total 30 patients Pramana Total no. of Patients % age

Supramanita 28 93.33% Adhika 01 03.33% Heena 01 03.33% Total 30

The above table shows 28 (93.33%) of the patients Supramanita, 01 (3.33%)

of the patients had Adhika Pramana and 01 (3.33%) of the patients had Heena

Pramana.

Figure-27: Showing Pramana wise distribution of total 30 patients

28

1 1

0

5

10

15

2 0

2 5

3 0

SupramanitaAdhikaHeena

Table showing Ahara Shakti (AS) wise distribution:- Table-36-A: Showing Abhyvarana (AS) wise distribution of total 30 patients

A) Abhyvarana Total no. of Patients % age Pravara 00 00 Madhyama 30 100.00% Avara 00 00 Total 30

The above table shows 30 (100%) patients had Madhyama Abhyvarana Shakti

and no patients were seen in Pravara and Avara kind of Ahara Shakti.

Figure-28-A: Showing Abhyvarana (AS) wise distribution of 30 patients

0

30

0

0

5

10

15

20

25

30



Observations

Table-36-B: Showing Jarana (AS) wise distribution of 30 patients B) Jarana Total no. of Patients % age

Pravara 00 00 Madhyama 30 100.00% Avara 00 00 Total 30

The above table shows 30 (100%) patients had Madhyama Jarana Shakti and

no patients were seen in Pravara and Avara kind of Ahara Shakti

Figure-28-B: Showing Jarana (AS) wise distribution of 30 patients

0

30

0

0

5

10

15

20

25

30


Table-37: Showing Jatharagni Bala wise distribution of total 30 patients

Jatharagni bala Total no. of Patients % age Manda 19 63.33% Teekshna 02 6.66% Vishama 09 30.00% Sama 00 - Total 30 -

The above table shows 19 (63.33%) of the patients had Manda Agni, 09 (30%)

of the patients had Vishama Agni and 02 (6.66%) of the patient had Teekshana Agni

Not even the single patint Sama Agni.

Figure-29: Showing Jatharagni Bala wise distribution of total 30 patients

19

2

9

0

0

2

4

6

8

10

12

14

16

18

20

MandaTeekshnaVishamaSama


Observations

Table-38: Showing Koshta wise distribution of total 30 patients with percentage Koshta Total no. of Patients % age

Krura 09 30.00% Madhyama 19 63.33% Mrudu 02 6.66% Total 30 -

The above table shows 02 (6.66%) of the patients had Mrudu Koshta, 19

(63.33%) of the patients had Madhyama Koshta and 09 (30%) of the patients had

Krura Koshta.

Figure-30: Showing Koshta wise distribution of total 30 patients

9

19

2

0

2

4

6

8

10

12

14

16

18

20

KruraMadhyamaMrudu

Table-39: Showing Family History wise distribution of total 30 patients

Family history HTN Total no. of Patients % age Yes 13 43.33% No 17 56.67% Total 30

In this study 13 (43.33%) of the patients had family history of

Hypertension and 17 (56.67%) of the patients’ family were devoid of Hypertension.

Figure-31: Showing Family History wise distribution of total 30 patients

13

17

0

2

4

6

8

10

12

14

16

18

YesNo


Observations

Table-40: Showing Chronicity wise distribution of 26 patients (Previously diagnosed) with percentage

Chronicity Total no. of Patients % age Up to 6 Month 06 20.00% Up to1 Years 12 40.00% Up to2 Years 06 20.00% Up to3 Years 02 6.66% Total 26 -

In this study 06 (20%) of the patients had minimum of 6 months Chronicity,

12 (40.00%) of the patients had 6 months to 1 year Chronicity, 06 (20.00%) of the

patients had 1 to 2 years Chronicity, and 02 (6.67%) of the patients had 2 to 3 years

Chronicity.

Figure-32: Showing Chronicity wise distribution of total 30 patients

6

12

6

2

0

2

4

6

8

10

12

Up to 6 MonthUp to1 YearsUp to2 YearsUp to3 Years

Table-41: Showing Onset history wise distribution of total 30 patients Onset history Total no. of Patients % age

Acute 04 13.33% Chronic 26 86.67% Total 30

The study shows that 26 (86.67%) of the patients had Chronic Onset and 04

(13.33%) of the patients had Acute Onset of history.

Figure-33: Showing Onset history wise distribution of total 30 patients

4

26

0

5

10

15

2 0

2 5

3 0

AcuteChronic


Observations

Table-42: Showing Intensity wise distribution of total 30 patients Intensity Total no. of Patients % age

Mild 02 6.66% Moderate 14 46.66% Severe 14 46.66% Total 30 -

Here in this study 14 (46.66%) of the patients had Moderate Intensity of

Hypertension, 14 (46.66%) of the patients had Severe Intensity of Hypertension and

02 (6.66%) of the patients had Mild Intensity of Hypertension.

Figure-34: Showing Intensity wise distribution of total 30 patients

2

14 14

14

12

4

10MildModerateSevere

8

6

2

0 Table-43: Showing Relieving Factors wise distribution of total 30 patients

Relieving factors Total no. of Patients % age Rest 23 76.67% Sleep 28 93.33% Tranquillizer 01 3.33% Anti Depressants 06 20.00%

In the present study, Relieving factors of 28 (93.33%) of the patients had

Sleep, 23 (76.67%) of the patients had Rest, 06 (20%) of the patients had Anti

Depressants and 01 (3.33%) of the patients had Tranquillizers.

Figure-35: Showing Relieving Factors wise distribution of total 30 patients

23

28

1

6

0

5

10

15

20

25

30

RestSleep TranquillizerAnti Depressants


Observations

Table-44: Showing Aggravating Factors wise distribution of total 30 patients Aggravating factors Total no. of Patients % age

Traveling 02 6.67% Anxiety 07 23.33% Emotion 15 50.00% Stress 28 93.33% Physical stress 14 46.67%

In the present study, Aggravating factors of 28 (93.33%) of the patients had

Stress, 14 (46.67%) of the patients had Physical Stress, 15 (50%) of the patients had

Emotions, 07 (23.33%) of the patients had Anxiety and 02 (6.67%) of the patients had

Travelling.

Figure-36: Showing Aggravating Factors wise distribution of total 30 patients

2

7

15

28

14

0

5

10

15

20

25

30

TravelingAnxietyEmotionStressPhysical stress

Table-45: Showing Drug History wise distribution of total 30 patients Drug history Total no. of Patients % age

Allopathic Medicine 19 63.33% Ayurvedic Medicine 00 - Discontinued Medicine 07 23.33% Others 00 -

In this study 19 (63.33%) of the patients had Allopathic Medicine where as 07

(23.33%) patients had discontinued the medicine.

Figure-37: Showing Drug History wise distribution of total 30 patients

19

0

7

0

0

2

4

6

8

10

12

14

16

18

20

Allopathic MedicineAyurvedic MedicineDiscontinued MedicineOthers


Observations

Table-46: Showing Symptoms wise distribution of total 30 patients Symptoms Total no. of Patients % age

Shirah shoola 25 83.33% Klama 27 90.00% Bhrama 24 80.00% Daha 05 16.67% Moorcha 00 00

The present study revealed that maximum 27 (90%) of the patients had

Klama following 25 (83.33%) of the patients had Shirah Shoola, 24 (80%) of the

patients had Bhrama and 05 (16.67%) of the patients had Daha but Moorcha was not

seen in any patient.

Figure-38: Showing Symptoms wise distribution of total 30 patients

2527

24

5

0

0

5

10

15

20

25

30

Shirah shoolaKlamaBhramaDahaMoorcha

Table-47: Showing Associated Complaints wise distribution of total 30 patients Associated complaints Total no. of Patients % age

Avsada 04 13.33% Dourbalya 19 63.33% Ati-sweda 00 - Daha in nabhi and uras 00 - Others 00 -

In this study, the associated complaints of 19 (63.33%) of the patients had

Dourbalya and 04 (13.33%) of the patients had Avsada. The rest of the complaints

were not seen in any patient.

Figure-39: Showing Associated Complaints wise distribution of total 30 patients

4

19

0 0 0

0

2

4

6

8

10

12

14

16

18

20

AvsadaDourbalyaAti-swedaDaha in nabhi and urasOthers


Observations

Table-48: Showing Systolic Blood Pressure (Average) of 30 patients Systolic blood pressure Total no. of Patients % age

Normal 00 - Stage I (140-159) 02 6.67% Stage II (160-179) 14 46.67% Stage III (180-209) 14 46.67% Stage IV >210 00 00 Total 30

The above table revealed that maximum 14 (46.67%) of the patients were

recorded Stage II and Stage III Average Systolic Blood Pressure followed by 02

(6.67%) of the patients were suffer from Stage I Average Systolic Blood Pressure. No

patients were recorded of Stage IV.

Figure-40: Showing Systolic Blood Pressure (Average) of 30 patients

0

2

14 14

0

0

2

4

6

8

10

12

14

NormalStage I (140-159)Stage II (160-179)Stage III (180-209)Stage IV >210

Table-49: Showing Diastolic Blood Pressure (Average) of 30 patients Diastolic blood pressure Total no. of Patients % age Normal 08 26.67% Stage I (90-99) 15 50.00% Stage II (100-109) 07 23.33% Stage III (110-119) 00 - Stage IV >120 00 - Total 30

The above table revealed that maximum 15 (50%) of the patients were

recorded Stage I Average Diastolic Blood Pressure followed by 07 (23.33%) of the

patients were suffering from Stage II Average Diastolic Blood Pressure and 08

(26.67%) of the patients were in Normal Stage. No patients were recorded of Stage III

and IV Average Diastolic Blood Pressure.


Observations

Figure-41: Showing Diastolic Blood Pressure (Average) of total 30 patients

8

15

7

0 0

8 6

4

2

0

10

12

14

16

Normal

Stage I (90-99)

Stage II (100-109)

Stage III (110-119)

Stage IV >120


Results

Results

Results of any research work are like always a new outcome in the medical

field. The results are obtained by the different observations which are collected during

the clinical trial. All these findings are tabulated in different headings.

Table-50: Showing the effect of therapy on Bhrama

Parameter Score Percentage Net result (BT - AT)

Response

Total scoring (Bhrama) BT

36 100%

Total scoring (Bhrama) AT

00 00%

100%

Good response.

The present study revealed that 36 score was found before the treatment

whereas 00 score was found after the treatment. This study illustrated that the effect

of Shilajatu Guggulu Rasayana on Bhrama gives 100% result i.e. Good response.

Table-51: Showing the effect of therapy on Klama


Response

Total scoring (Klama) BT

42 100%

Total scoring (Klama) AT

06 14%

86%

Good response.

The present study shows that 42 score was found before the treatment whereas

06 score was found after the treatment. This study demonstrated that the effect of

Shilajatu Guggulu Rasayana on Klama gives 86% result i.e. it also comes under Good

response.

Table-52: Showing the effect of therapy on Shirah shoola


Response

Total scoring (Shirah shoola) BT

45 100%

Total scoring (Shirah shoola) AT

04 09%

91%

Good response.


Results

The present study revealed that 45 score was found before the treatment

whereas 04 score was found after the treatment. This study illustrated that the effect

of Shilajatu Guggulu Rasayana on Shirah shoola gives 91% result i.e. Good response.

Table-53: Showing the effect of therapy on Daha


Response

Total scoring (Daha) BT

06 100%

Total scoring (Daha) AT

00 00%

100%

Good response.

The present study shows that 06 score was found before the treatment whereas

00 score was found after the treatment. This study demonstrated that the effect of

Shilajatu Guggulu Rasayana on Daha gives 100% result i.e. it also comes under Good

response. As the symptom Daha was found only in 5 patients.

Table-54: Showing the effect of therapy on Systolic hypertension


Response

Total scoring (SBP) BT

72 100%

Total scoring (SBP) AT

06 8%

92%

Good response.

The present study revealed that the highest 72 score was found before the

treatment whereas 06 score was found after the treatment. This study illustrated that

the effect of Shilajatu Guggulu Rasayana on Systolic blood pressure gives 92% result

i.e. the result comes under Good response.

Table-55: Showing the effect of therapy on Diastolic hypertension


Response

Total scoring (DBP) BT

29 100%

Total scoring (DBP) AT

05 17%

83%

Good response.

The present study revealed that 29 scores was found before the treatment

whereas 05 score was found after the treatment. This study demonstrated that the


Results

effect of Shilajatu Guggulu Rasayana on Diastolic blood pressure gives 83% result i.e.

it shows Good response.

Table-56: Showing the over all response on Subjective and Objective parameters

Net Result Percentage Net results of all therapies (X/N)

Response

Systolic B.P. 92% Diastolic B.P. 83% Shirah shoola 91%

Klama 86% Bhrama 100%

Daha 100% N = 6 X = 552

92%

Good response.

Net mean results of the therapy on all parameters (all subjective and objective

in to the consideration) showed 92%. This study demonstrated that the effect of

Shilajatu Guggulu Rasayana on all parameters showed Good response.

Table-57: Showing the effect of therapy on Biochemical Parameters

Mean score Biochemical Parameters

BT AT

Mean difference Net Relief

Serum cholesterol 193.81 156.95 36.86

Serum triglycerides 172.94 143.00 29.94

High density lipoprotein 47.63 43.39 4.24

Low density lipoprotein 111.69 84.97 26.72

Very low density lipoprotein 34.54 28.54 06.00

The present study revealed that the mean difference of Serum cholesterol was

found 36.86 i.e. lower than the before treatment mean, mean difference of Serum

triglycerides was found 29.94 i.e. lower than the before treatment mean, mean

difference of High density lipoprotein was found 4.24 i.e. lower than the before

treatment mean, mean difference of Low density lipoprotein was found 26.72 i.e.

lower than the before treatment mean whereas mean difference of Very low density

lipoprotein was found 06.00 i.e. also lower than the before treatment mean, hence

this shows that the effect of Shilajatu Guggulu Rasayana on Lipid Profile.


Results

Statistical Analysis

Table-58: Showing the effect of therapy on Bhrama

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 1.2 0.80 - - Bhrama

AT 0.0 0.0 1.2 0.805

0.147 29 8.163 <0.001 HS

In order to assess the Parameter the patients were examined according to the

clinical findings and the results were analysed from the statistical analysis.

In parameter Bhrama Mean ±SD before was 1.2 ±0.8 and after the treatment it

is reduced to 0.0 ±0.0 with Mean difference 1.2 and standard of mean 0.147 and test

shows more highly significant before and after the treatment as P<0.001.

Table-59: Showing the effect of therapy on Klama

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 1.44 0.77 - - Klama

AT 0.2 0.40 1.2 0.664

0.121 29 9.917 <0.001 HS

In parameter Klama Mean ±SD before was 1.44 ±0.77 and after the treatment

it is reduced to 0.2 ±0.40 with Mean difference 1.2 and standard of mean 0.121 and

test shows more highly significant before and after the treatment as P<0.001.

Table-60: Showing the effect of therapy on Shirah shoola

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 1.5 0.86 - - Shirah

shoola AT 0.13 0.34 1.366 0.764

0.139 29 9.827 <0.001 HS

In parameter Shira shoola Mean ±SD before was 1.5 ±0.86 and after the

treatment it is reduced to 0.13±0.34 with Mean difference 1.366 and standard of mean


Results

0.139 and test shows more highly significant before and after the treatment as

P<0.001.

Table-61: Showing the effect of therapy on Daha

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 0.2 0.48 - - Daha

AT 0.0 0.0 0.2 0.484

0.0884 29 5.475 <0.001 HS

In parameter Daha Mean ±SD before was 0.2 ±0.48 and after the treatment it



Table-62: Showing the effect of therapy on Moorcha

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 0.0 0.0 - - Moorcha

AT 0.0 0.0 0.0 0.0

0.0 29 - - -

In parameter Moorcha before and after the treatment is not seen.

Table-63: Showing the effect of therapy on Systolic hypertension

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 2.4 0.62 - - Systolic

B.P. AT 0.2 0.55 2.2 0.664

0.121 29 18.18 <0.001 HS

In parameter Systolic B.P. Mean ±SD before was 2.4 ±0.62 and after the

treatment it is reduced to 0.2 ±0.55 with Mean difference 2.2 and standard of mean


P<0.001.


Results

Table-64: Showing the effect of therapy on Diastolic hypertension

Para

Meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 0.96 0.71 - - Diastolic

B.P. AT 0.16 0.37 0.8 0.55

0.1 29 8.00 <0.001 HS

In parameter Diastolic B.P, Mean ±SD before was 0.96 ±0.71 and after the


0.55 and test shows more highly significant before and after the treatment as P<0.001.

Effect of therapy on Biochemical Parameters:

Table-65: Showing the effect of therapy on Serum Cholesterol

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE D

F

T-

Value

P-

Value

Rem

arks

BT 193.81 29.22 - - Choleste

rol AT 156.95 29.7 37.63 18.29

3.34

1

29 11.26 <0.001 HS

In parameter Cholesterol Mean ±SD before was 193.81 ±29.22 and after the

treatment it is reduced to 1560.95 ±29.70 with Mean difference 37.63 and standard of

mean 18.298 and test shows more highly significant before and after the treatment as

P<0.001.

Table-66: Showing the effect of therapy on Serum Triglycerides

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 0.96 0.71 - - Trigly

ceride AT 0.16 0.37 0.8 0.55

4.72 29 8.73 <0.001 HS

In parameter Triglyceride Mean ±SD before was 172.94 ±60.41 and after the



Results


P<0.001.

Table-67: Showing the effect of therapy on High Density Lipoprotein

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 47.63 10.03 H.D.L.

AT 43.39 8.03 4.813 3.619

0.66 29 7.29 <0.001 HS

In parameter H.D.L Mean ±SD before was 47.63 ±10.03 and after the



P<0.001.

Table-68: Showing the effect of therapy on Low Density Lipoprotein

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Valu

e

Rem

arks

BT 111.69 30.13 - - L.D.L

AT 84.97 24.64 29.09 16.29

2.974 29 9.781 <0.0

01

HS

In parameter L.D.L. Mean ±SD before was 111.69 ±30.13 and after the



P<0.001.

Table-69: Showing the effect of therapy on Very Low Density Lipoprotein

Para

meter

Dura

tion

Mean

± SD

Mean

differ

ence

SD of

Differ

ence

SE DF T-

Value

P-

Value

Rem

arks

BT 34.54 12.10 - - V.L.D.L

AT 28.54 11.46 8.694 5.201

0.949 29 9.16 <0.001 HS


Results

In parameter V.L.D.L. Mean ±SD before was 34.54 ±12.10 and after the



P<0.001.


Discussion

Discussion Discussion is the most important part of any research where the observations

are discussed and given reasons by the researcher. Here researcher conveys the

practical experience with special reference to textual explanations. The significant

results and insignificant results will be discussed in the same section with reasons.

Hence it becomes important to discuss the clinical study in detail.

Discussions on this study are made under the following headings:

1) Discussion on Disease Review

2) Discussion on Drug Review

3) Discussion on Clinical study.

4) Discussion on Results

1) Discussion on Disease Review:

Pittavruta udana is explained as disease in Ayurvedic classics. The symptoms,

which are expressed in essential hypertension, are similar to the symptoms of

Pittavruta udana. As Ayurveda explains, Pitta pangu, Kapha pangu without vata, so

vata plays an important role in the formation of diseases. Vata is a unique Dosha as it

differs from other Doshas in many ways, for example Vata regulates the functions of

Pitta and Kapha. In the pathological state also it has double path of its vitiation i.e its

vitiation may occur by the depletion of dhatus or by the obstruction, while Pitta and

Kapha have a single route of vitiation. Most of the hypertensive patients show

minimal cause in vascular integrity. Acharya Vagbhata clearly states that vascular

integrity is maintained by Vata (Prana). In one word he says “Dhamani dharana” is a

function of Prana Vata.

Nearly 15% of the world population is labelled hypertensive, either knowing

or unknowingly by doctors. In India approximately 14% of peoples suffer from


Discussion

hypertension and majority of them had essential hypertension which indicates its

significance and prevalence. At present, Indian Council of Medical Research (ICMR)

and All India Institute of Medical Sciences (AIIMS) also have declared India as a

nation of hypertension. Although hypertension is usually asymptomatic for the first

10-20 yrs, it slowly but surely strains the heart and damages the arteries. For this

reason hypertension is often called as silent killer5 because mild to moderate levels

usually ignored by patient until serious damage has been done.

Epidemiological studies revealed that it is the most important single factor

responsible for death from cardiovascular and cerebro-vascular disease. Therefore its

epidemiology has drawn the attention of W.H.O in 1978 and declared that year as

“Hypertension Year”.

So far hypertension in various systems of medicines likes 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 systems of medicines

Ayurveda adopts the treatment for the benefit of life and life is nothing but the feeling

of self or self-consciousness. Ayurveda is eternal and ever lasting principle.

Ayurvedic drugs have shown re-constructive or rejuvenate effect.

So many Allopathic medications like beta-blockers, calcium channel blockers,

ACE inhibitors etc. are invented, to keep the blood pressure in normal ranges. But all

these medicines have big adverse effects, where as Ayurvedic medicines cure the

disease without producing the adverse effects and give side benefits as a substitute of

side effects. Therefore, the Ayurvedic therapeutics has attracted considerable glamour

for providing safe and effective remedies. Several researches have been done to tell


Discussion

off the significance of medication. However, it is necessary to conduct the further

research to find out some safe and effective therapy with no adverse effects and

protect the hypertensive population. In Ayurvedic literature, the disease essential

hypertension is not described by its name. But, from compilation of scattered

references it is concluded that Essential hypertension is a condition that simulates the

Pittavruta udana vyadhi. After understanding essential hypertension on the basis of

Ayurvedic fundamentals, the treatment selected was more effective and also cost

effective. The clinical trial was conducted in a randomized sample of 30 patients. The

drugs and doses have already been described in the clinical study. The results were

assessed individually on various parameters, monitored carefully; subjected to bio

statistical analysis.

Nidana Panchaka

I. Nidana:

In the classics there are no direct references regarding nidanas of Pittavruta

udana. Vriddhi of avaraka along with avaruta dosha is essential to cause avarana. So

the nidanas which causes mainly Pittavriddhi along with vatavriddhi to some extent

be considered as the hetus for Pittavruta udana. Many of Raktadustikara Nidanas

contribute to the Pitta vruddhi, intern’s manifestation the Avarana to Vata producing

clinical manifestation. While discussing about Nidana of Vata prakopa, Acharya

clearly mentioned that viruddha/vishama ahara leads to margavrodha. This can be

understood as obstructive pathology, the prime factor of Essential hypertension.

In the present study majority of patients have irregular and incompatible food

style. Tea/Coffee may contribute to agni vaishamya interns Pitta and Vata prakopa

takes place. Particularly Pitta makes the margavarana to Vata leads to Hypertension.


Discussion

II. Poorvaroopa:

The Poorva roopa for this condition is not described in the classics. Charaka

has quoted that avyakta lakshanas of vata vyadhi are to be taken as its Poorvaroopa.

III. Roopa:

Shirah shoola: is due to the Vata, shiro daha is due to Vata and Pitta. Here

Vata as well as Pitta vitiation occurs.

Klama: is due to vitiation of Rakta

Daha: is due to the vitiation of Pitta

Bhrama: is due to vitiation of Vata and Pitta

Moorcha: is due to the vitiation of Pitta

IV. Upashaya and Anupshaya

For Vata: Upashaya of Avruta Vata is not at hand; on the contrary, Upashaya

of Avaraka is present. For Example in Pittavruta vata, the patient gets Vidaha from

the Upashaya of Vata i.e, Amla, Lavana and Ushna. In Kaphavaruta Vata there is

Upashaya from Katu etc and patient shows desire for Fast, Exercise, Ruksha etc.

things which are Upashaya for Kapha and Anupashaya for Vata.

For Pitta: In Pittavruta vata, patient feels Daha, Trishana, Shoola, Bhrama,

Tama and gets Vidaha from Amla, Lavana, Katu and Ushna veerya dravyas. On the

other hand, the patient shows the desire for cold (sheeta) things, which is Upashaya

for Pitta.

V. Samprapti:

The whole sequence of manifestation of disease starting from the causative

factors, dosha dushti till the appearance of lakshanas is known as Samprapti. The

samprapti ghatakas i.e. dosha, dushya, srotas, agni etc. having great significance in

this process, whereas Acharya Sushruta’s describes the stages of the development of a


Discussion

disease. The shatkriyakala’s are chaya, prakopa, prasara, sthanasanshraya, vyakti and

bheda avasthas372. To understand the samprapti of Pittavruta udana (Essential

hypertension), it is necessary to know about the nidana factors of the disease because

the three chief events of the healthy human being towards the disease happen only

from the fractions of nidana factors. These chief events are

a). Dosha Prakopa

b). Kha Vaigunya

c). Dhatu Shaithilya

In this perspective, it is necessary to take note of the involved factors i.e.

samprapti ghatakas viz ; dosha, dushya, srotas, agni, ama etc. Direct reference

regarding the samprapti of Pittavruta udana is not available in the classics. Hence to

understand the samprapti of Pittavruta udana, the general samprapti of avarana can be

considered.

Like ama, the Avarana is also unique concept of disease pathogenesis,

especially of Vata vyadhis. Vata dosha is the chief among Tridoshas373, because of its

asukaritwa & its ability to carry on the all life process in association with Pitta,

Kapha, Saptadhatus & Trividha mala. It is composed of “Rajo guna bahulya374”

which is the “Pravartaka-sarvabhavanam” and other two doshas are of turn described

as Pangu without the involvement of Vata dosha375. Such dynamic factor Vata,

naturally causes more number of diseases in the body than the other doshas. One of

the reasons behind causation of the 80 diseases by Vata376 is because it is provoked

by two principle factores:

1. Dhatus kshaya (Emaciation of body tissues)

2. Margasya Avarana (by the occlusion of its channel of circulation)


Discussion

Acharya Chakrapani377 mentions that Vata get aggravated in two different

ways. Because of second type of cause Avarana, the speed (vega) of Vata gets

arrested which leads to its aggravation. However, when Vata is obstructed in the

same way, it is specifically called Avarana.

Explanation of the word Avarana:

The words Avarana means– Achhadana i.e covering or avarodha i.e

obstruction. The three terms are used to understand the Avarana i.e. Avarana, Avarka

and Avrutah.

i. Avarana: Avarana denotes the obstruction of vata movements. This obstruction

can be due to Pitta, Kapha, Rasadi dhatus, Malas or by the panchavidha vata.

ii. Avaraka: The factor, which causes obstruction of vata, is called Avaraka or the

main sources which cause the obstruction is Avaraka. For example if Pitta cause

obstruction of Vata, then Pitta is called Avaraka.

iii. Avruta: The gati of Vata, which is affected by the Avaraka is known as Avruta or

which is arrested by other dosha is known as Avruta. The substance, which obstructs

the pathway of Vata, is termed as Avaraka while Vata whose avarana occurs is termed

as Avruta.

To understand the samprapti of Pittavruta udana, it is necessary to know about

the nidana i.e. karanas of the disease because the disease Pittavruta udana comes

under Vata vyadhi chapter. If Pitta Vitiated and then obstruct the Udana vata comes

under samanyaja vyadhi. Hence in the samprapti of Pittavruta udana, Vata and Pitta

vitiates by there own nidanas and then vitiated Vata comes in contact with vitiated

Pitta causes more Pitta vikruti and results the obstruction of Udana vata. So by seeing

this samprapti Avarana comes under Vata vyadhi chapter (nanatmaja vikara).

By observing the lakshanas of Pittavruta udana, the doshas and dooshyas involved in


Discussion

the samprapti to cause this condition can be assessed as follows:

Samprapti-Ghatakas:-

Doshas: Vata (Udana) – Shirashoola and bhrama.

Pitta anubandi– Daha, bhrama and moorcha

Dushyas: Rakta – daha, klama and Shira shoola

Agni: Jatharagni

Srotas: Rasavaha, Raktavaha & Manovaha

Srotodushti-Prakara: Sanga type of srotodusti

UdbhavaSthana: Pakvashaya-Amashaya Samudbhava

Avayava: Hridaya, Dhamani

Adhisthana: Manodaihika (Psychosomatic, Sira, Dhamani, Srotas)

Sanchara-sthana: Sarva Sharira

Rogamarga: Madhyama Rogamarga.

Prognosis:

In dosha avarana, the Avarana of Prana and Udana by Pitta and Kapha are

more severe and difficult to treat because of their vital function in the body

physiology i.e. to provide life and strength. Therefore Pittavruta udana is difficult to

treat.

If the condition continues for one year, its management is delayed or improper

and then it may difficult to treat or is incurable. So early diagnosis and timely

management make the prognosis good.

Modern concept of Essential Hypertension:




Discussion

hypertension when the elevation of systolic blood pressure is more than 140 mm Hg

and diastolic blood pressure is above 90 mm Hg.

Arterial pressure depends on the cardiac out put and total peripheral resistance.

The Blood Pressure can be raised by increased cardiac output and increased peripheral

resistance. 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 hormone 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 blood pressure is mainly sustained by increased peripheral vascular

resistance.

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 vasoconstriction 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 (e.g. 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


Discussion

vasoconstriction, an adaptive mechanism that protects against hyper perfusion 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 amounts 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


Discussion

tubular reabsorption of sodium and thus of water. 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 re-absorption 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 re-absorption in distal tubules and cause vasodilatation. 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.

Chikitsa:

In classics several treatment modalities are explained for Pittavruta vata. The

dravyas which are not abhishyandi but having snigdha and srotoshodhaka gunas

should be used. The oushadhi drayas which are not virudha to Pitta, which causes

Vatanulomana and Vatashamana are to be administered. In Vata enclosed by Pitta,

alternative application of cold and hot things is desirable. Jeevaneeya sarpi, meat of

wild animals, barely, shali rice, sustaining milk enema, purgation, intake of milk

boiled with panchamoola and bala are employed. Then sprinkling with madhu yasti

taila, bala taila, ghee, ksheera panchamoola decoction or cold water are useful.

Recent studies’ shows significant improvement of Essential hypertension by

chikitsa like Virechana, Shirodhara, Rasayana. If we look in to the chikitsa principles

of Avarana, Virechana is the best shodhana chikitsa. Pitta and Vata both are regulised


Discussion

by Virechana. Shirodhara also had beneficial role in management of Essential

hypertension.

In all encircled conditions, the regular use of Rasayana such as Shilajathu

Guggulu with milk would be beneficial or use of chyavana prasha should be

employed with milk diet. In Pithavrutha panchavata the measures to be adopted are

Pittaghna remedies which never derange Vata.

Treatment of Vata is not effective whereas the treatment of Avaraka is

effective. When Vata is occluded by Pitta, it leads to Vata Prakopa manifested by the

symptom of Shula. It may be the main symptom disturbing the patient very much. In

addition other symptoms of Pitta like burning, thirst, giddiness and darkness before

eyes may be there. Here to relive dominant symptom of Vata i.e Shula, Pitta

alleviating treatment should be undertaken as the basic pathology is due to the

increased Pitta. Hence the administration of Vata alleviating treatment such as use of

hot, sour and salt substances, which are antagonist to Pitta, may deteriorate the

condition. If Kapha occludes Vata, it leads to Vata prakopa manifested by the

symptom of Shoola. It may be the main symptom disturbing the patient very much. In

addition other symptoms of kapha such as cold, heaviness, pronounced desire to

pungent and similar other articles and carving for fasting, exertion, dry and hot things.

Here to relive dominant symptom of Vata i.e Shoola, Kapha alleviating treatment

such as katu, kashaya etc. articles should be used, as the basic pathology is due to the

increased Kapha though this therapy is antagonist to Vata.

2. Discussion on Drug Review:

Shilajatu:

By its tikta rasa and naatiushna gunas, acts on Pitta dosha and by ushna verya

act on Vata dosha. Because of tikta rasa, it removes avarana of Vata dosha and their


Discussion

by Vata anulomana occurs. As it is having rasayana property, hence does Vata

shamana.

Shilajatu is one of the best mootrala dravya. Its diuretic property is

established. Because of its mootrala properties, it reduces the blood volume

automatically blood pressure reduced. In Essential hypertension diuretic property is

very beneficial. By its virtue of diuretic property Shilajatu showed significant best

result in the present study.

Guggulu:

By its tikta and kashaya rasas it makes Pitta shamana, by its tikta rasa, ushna

and teekshna gunas it removes the Avarana of Vata. Because of Ushna veerya and

Rasayana properties it is Vatashamaka.

The Guggulu shodhana was done with the Triphala kwatha, which is prepared

with Gomutra. Consequently it is necessary to consider the effects of these dravyas on

Pittavruta udana. A number of studies have supported the claims that Guggulu

extracts can help to reduce heart disease risk factors, with reductions in both blood

fats and total cholesterol of 15-30 percent over three months. Guggulu extracts have

been shown to lower overall blood fats, reduce "bad" LDL cholesterol and also

normalizing the weight. It also reduces blood triglycerides which are known to

contribute to atherosclerosis and heart attack. As some studies suggest, that Guggulu

extracts can reduce platelet stickiness, this herb would rank among the most important

since few substances have a positive impact on both blood fats and platelets. These

effects are due to Guggulu action on the liver and thyroid. The thyroid is stimulated to

increase the body's metabolic rate, and the liver is stimulated to metabolize LDL

cholesterol, effectively lowering the amount in the bloodstream and is


Discussion

antihypertensive. Due to its diuretic action it reduces the blood pressure. Although the

use of Guggulu is appears to be safe and non-toxic.

Triphala is mainly Pitta shamaka and Vatanulomaka. Hareetaki and Vibhitaki

by their Kashaya, Tikta and Madhura rasa and by Madhura vipaka it acts on Pitta

dosha. Amalaki, by its Kashaya and Madhura rasa, Madhura vipaka and Sheeta

veerya, does Pitta shamana. Hareetaki and Vibhitaki by their Madhura rasa and

vipaka, Ushna veerya and anulomana properties it acts on Vata dosha. Amlaki by its

Amla, Madhura rasa and vipaka and Rasayana properties it pacifies Vatadosha.

Gomutra has srotoshodhaka property. We have made Guggulu shodhana by

Gomutra siddha Triphala kwatha. Because of Gomutra shodhita Guggulu, it may act

as Vatanulomaka and srotoshodhaka although Gomutra is Pitta prakopaka but because

of the Triphala, it may not aggravate Pitta. By its Ushna guna and veerya, Lavana and

Madhura rasa it dose Vata shamana.

By summarising all these factors, this yoga is effective in Pittavruta udana

because of sroto shodhaka, Vata and Pitta shamaka, Vatanulomaka and Rasayana

properties.

3) Discussion on Clinical study:

In this study total 33 patients were registered, out of which 3 patients left the

study before completion and 30 no. of patients have completed their course of

treatment with Shamana Oushadha (Shilajatu Guggulu Rasayana). All 30 patients are

screened for hypertension before and after the clinical trial. Before to initiation of the

treatment, all patients are screened for cardiac abnormalities, renal abnormalities,

metabolic abnormalities like diabetes, hypo/hyper thyroidism etc. Patient’s blood

lipids are assessed before and after the treatment. For the safety purpose X-ray and

ECG are taken before to include in the trial. Once he/she found with normal findings


Discussion

of X-ray, ECG then included in the study. Throughout the clinical trial, all patients are

closely observed for any adverse changes. Telephonic communication was kept

through the clinical trial. After the clinical trial, patients are put on control drug i.e.

Sarpagandha Ghana vati 1 TID for further management, with consent of the

Physician. Some patients are referred to concerned Physician for further management.

Observations:

Age:

Age wise distribution of all thirty patients shows that maximum patients were

from 50-56 years age group i.e. 10 (33.33%) patients where 07 (23.33%) were male

and 03 (10%) were female. In age group of 43-49 years 07 (23.33%) patients were

reported, in these patients 04 (13.33%) were male and 03 (10%) were female, in age

group of 57-63 years 06 (20%) patients were undergone the treatment, here 02

(6.66%) were male and 04 (13.33%) were female and in age group of 64-70 years 05

(16.67%) patient were approached, in these patients 04 (13.33%) were male and 01

(3.33%) were female and in the age group of 36-42 years total 02 (6.67%) i.e. 01

(3.33%) were male and 01 (3.33%) were female patients had completed the treatment.

The age is the important factor in the manifestation of the disease because

hypertension is establish mostly in middle and senile age group. In Ayurveda, the

Vaya has been significant factor in the manifestation and prognosis of the disease.

Seeing that the hypertension normally occurs in middle and senile age, hence it can

mainly related to Pitta and Vata pradhana378 because of the dosha pradhanyata

according to the age. Essential hypertension is more prevalent in the middle and old

age. According to Acharya Vagbhata, the dosha pradhanyata according to age makes

difficult to treat379.


Discussion

Sex:

The present study showed that 18 (60%) of the patients were male and 12

(40%) were comes under female category. In female, occurrence is mainly due to age,

hormonal changes and increase in blood pressure take place due to menopause also.

Thus in the present study the percentage of females is less than that of males.

Religion:

In this study 26 (86.67%) of the patients belongs to Hindu category and 04

(13.33%) belongs to Muslim. It may be due to Hindu dominant population. As the

sample size is too small, it is difficult to rule out the exact difference in their life style

concern to etiology of hypertension as both communities had taken lavana, katu,

amala etc. rasa yukta ahara.

Occupation:

In the occupation wise distribution 20 (66.67%) of the patients had sedentary

life style where 08 (26.66%) male and 12 (405) were female, 06 (20%) were male

patients had active occupation where as 04 (13.33%) were male patients are of labour

class. In the sedentary life style patients have taken heavy diet, excessive fat meal,

excessive salty diet and having more tension. The active occupation related strain and

stressful work where as in the labour occupation also having the stressful work. Even

though physical exercise is beneficial to Essential hypertension but dynamic exercise

raises blood pressure and isometric exercise raises it a lot more. These are the

important cause for increase in blood pressure.

Marital Status:

The present study showed that all the 30 patients i.e. 100% approached are

married. Stress and tension was the most common factor observed in married life.

Oppositions of opinion between the partners, the worry for their children and family


Discussion

etc. after marriage these could be the reason for the high blood pressure.

Economical Status:

Here, 04 (13.33%) of the patients comes from Poor Class, 02 (6.67%) of the

patients come from Higher Class and 24 (80.00%) of the patients comes from Middle

Class. The middle class peoples suffer with more anxiety. Stress may because of

financial insecurity or work tension and the negligence to proper Ahara and Vihara

may be the cause of hypertension.

Ahara:

In the present study 14 (46.66%) of the patients had vegetarian diet, 16

(53.33%) of the patients had mixed diet where as 17 (56.66%) of the patients had

more oily diet, 11 (36.66%) of the patients had used ghee and 16 (53.33%) of the

patients had used stored food. The geographical population takes more oily food, salt,

chillies, stored food, mixed food, ghee etc., therefore it can be concluded that patients

were taken the ahara which have been the nidana of hypertension so leads to

hypertension.

Intake of dominant Rasas:

In this study maximum 30 (100%) patients have taken Katu Rasa

predominantly in their diet, followed by 20 (66.67%) Madhura Rasa, 17 (56.67%)

Lavana Rasa and 08 (26.67%) Amala Rasa. The more use of Katu, Lavana and Amla

Rasa may be the nidana of this disease and these provokes the Pitta also, where as

Madhura rasa was used for the taste or after food. To make diet tastier Katu, Lavana

and Amla are used and they have taken spicy food.

Addictions:

The present study shows 22 (73.33%) of the patients had addiction to Coffee,

20 (66.67%) of the patients to Tea, 06 (20%) of the patients to Tobacco, 10 (33.33%)


Discussion

of the patients to Alcohol and 06 (20%) patients had addiction with Smoking. Coffee

and tea becomes a most commonly used in this era, so it should not be considered as

addiction. On the other hand in liable persons nicotine and caffeine in higher

concentration may work as nidanas. Tobacco is toxic thing and having Vyavayi,

Vikasi, Ushna and Tikshna gunas, can vitiate Rakta Dhatu. Alcohol also vitiates the

Rakta and Pitta.

Family History:

In this study 13 (43.33%) of the patients had family history of Hypertension.

This was important factor in the formation of disease because of involvement of

genetic factors in this disease.

Prakriti

Sharirika:

The study shows 18 (60%) of the patients had vatapitta prakriti, 10 (33.33%)

of the patients had vatakapha prakriti and 02 (6.66%) of the patients had pittakapha

prakriti. This shows that Vata and Pitta plays more important role in the formation of

disease. The Samprapti of hypertension is having the route of Avarana. The Vata

always gets vitiated by Avarana Pitta and Pitta Prakriti persons are more susceptible

Pittaja Vikaras. So in Pitta prakruti person the Vata get aggravating themselves. If the

Dosha matches with Prakriti and other factors like Dushya, Desha, Kala, Bala etc.

then the curability of disease becomes very difficult380.

Manasika:

In this study 20 (66.67%) of the patients had Kshobha, 19 (63.33%) of the

patients had Deenata, 17 (56.67%) of the patients had Kopa, 09 (30%) of the patients

had Bhaya, 09 (30%) of the patients had Samprahara, 08 (26.67%) patients had

Udvega and 06 (20%) of the patients had Mada. The stressful stimuli certainly raise


Discussion

blood pressure. Mada, Bhaya, Kama, Krodha, Lobha etc. elevate raja and tama gunas

which cause manodusti results in manovikara with involvement of samjnavaha or

manovaha srotas381. These factors are responsible for the disease formation because

stress, strain like nidanas are plays majour role in Hypertension. Hence it may be

concluded that all the psychological factors directly provoke Vata and Pitta which can

produce hypertensive state.

Satva:

The study shows 19 (63.33%) of the patients had Madhyam Satva and 07

(23.33%) of the patients had Avara Satva and 04 (13.33%) of the patients were having

Pravara Satva. Hypertension is stated as psychosomatic disease. Acharya Charka has

toled that satva is nothing but mana382. The Pravara Sattva patients have less attention

to exposing the disease because tension plays a major role in the formation of disease.

The stress and strain contribute highly in Essential hypertension. So Pravara satva

when reduces, the person will be victim for stress and strain hence Madhyama and

Avara Satva patients have more chances to get the disease.

Satmya:

The study shows 20 (66.66%) of the patients were having Madhya Satmya and

05 (16.66%) of the patients were having Pravara Satmya and 05 (16.66%) of the

patients were having Avara Satmya. Sarva Rasa intake is designate to accomplish

equipoise state of Dhatus383, but further Chakrapani has make clear that it does not

mean to take all Rasas in equal quantity. For example Vata Prakriti persons may

require more diet of Madhura, Amla and Lavana Rasa. Thus the part of Rasa requires

according to the bodily constitution, season, and dietetic properties384. So it is difficult

to look for the effect of Satmyata of Rasa in the manifestation of disease.


Discussion

Agni:

The present study shows 19 (63.33%) of the patients had Manda Agni, 09

(30%) of the patients had Vishama Agni and 02 (6.66%) of the patient had Teekshana

Agni not even a single patient had Sama Agni. Manda Agni385 is major cause for all

disorders. Dooshya Rasa and Rakta which are involved in Essential hypertension

depend on Agni. Mandagni always responsible for srotoavarodha and is the

predominant factor in manifestation of Pittavruta Udana.

Koshtha:

The present study shows 02 (6.66%) of the patients had Mrudu Koshta, 19

(63.33%) of the patients had Madhyama Koshta and 09 (30%) of the patients had

Krura Koshta. Koshatha is also related to Agni hence also plays an important role in

the formation of disease.

Onset history:

The study shows that 26 (86.67%) of the patients are known hypertensive

among them 19 are on medication, 7 are discontinued. Before to the initiation of the

treatment, all were advised to taper down the previous medications. Data was

collected after the withdrawal of medication and found hypertensive and 04 (13.33%)

of the patients are newly diagnosed. After observation of the patients and monitoring

of the blood pressure, they were found hypertensive and were included in the clinical

trial with pre requisite inclusion criteria.

Intensity:

Here in this study 14 (46.66%) of the patients had Moderate Intensity of

Hypertension, 14 (46.66%) of the patients had Severe Intensity of Hypertension and

02 (6.66%) of the patients had Mild Intensity of Hypertension. The present clinical

trial was mainly aimed on antihypertensive effect of the trial drug. Majority of


Discussion

patients approached are known cases. As we discussed earlier all patients who are

taking medications for hypertension advised to stop the pervious medication. Because

of that majority of patients comes under the category of moderate and severe

intensity.

Vaya

In this study 23 (76.66%) of the patients had Madhya Vaya and 07 (23.33%)

of the patient’s had Vruddha Vaya. The Vaya is also plays an important role in the

manifestation of disease because hypertension is mostly found in Madhya and

Vruddha Vaya. In Ayurveda, the Vaya has been significant factor in the manifestation

and prognosis of the disease. In Madhya Vaya Pitta pradhanta and in Vruddha Vaya

Vata pradhanta occures. Essential hypertension is more prevalent in the Madhya and

Vruddha Vaya.

Vyayama shakti

The above table shows 06 (20.00%) of the patients had Madhyam

Vyayamashakti, 20 (66.66%) of the patients had Avara Vyamashakti and 04 (13.33%)

of the patients had Pravara Vyayamashakti. In observation, table no 33, showed that

66.67% patients are of sedentary life style. Global survey of the hypertension confine

that, sedentary life style may contribute to hypertension.

Nidra:

The present study shows that maximum 18 (60%) of the patients had disturbed

sleep and 12 (40%) of the patients had sound sleep. Majority of the patients with

disturbed sleep showed imbalanced condition of mind due to some psychological

conditions like anxiety, stress etc.


Discussion

Aggravating & Relieving factors:

In the present study, emotional and physical stress was observed as

aggravating factor. Aggravating factors of 28 (93.33%) patients had Stress, 14

(46.67%) patients had Physical Stress, 15 (50%) of the patients had Emotions, 07

(23.33%) of the patients had Anxiety and 02 (6.67%) of the patients had Travelling.

Whereas sleep and rest was observed as a relieving factor in the patients. Relieving

factor of 28 (93.33%) patients had Sleep, 23 (76.67%) of the patients had Rest, 06

(20%) of the patients had Anti Depressants and 01 (3.33%) of the patients had

Tranquillizers. Therefore stress i.e. manovikaras plays a major role in Essential

hypertension.

Symptomatology:

The present study revealed that 27 (90%) of the patients had Klama following

25 (83.33%) of the patients had Shirah Shoola, 24 (80%) of the patients had Bhrama

and 05 (16.67%) of the patients had Daha but Moorcha was not seen in any patient.

As klama and shirashoola are raktapradoshaja vikaras which were observed in 90%

and 83.33% patients respectively and Daha in 16.67%, indicates predominance of

Pitta. The presence of Bhrama in 80% of patients indicates vataprakopa in present

condition. As shirashoola is the laxana of both Raktadusti and Vataprakopa, it

indicates involvement of both Vata and Pittadosha in Pittavruta vata.

Associated complaints:

Regarding the associated complaints of 19 (63.33%) of the patients had

Dourbalya and 04 (13.33%) of the patients had Avsada. The rest of the complaints

were not seen in any patient.


Discussion

Systolic Blood Pressure:

The study revealed that maximum 14 (46.67%) of the patients were recorded

Stage II and Stage III average Systolic Blood Pressure followed by 02 (6.67%) of the

patients were of Stage I average Systolic Blood Pressure. No patients were recorded

of Stage IV. As the Allopathic medicine were withdrawn from the patients who had

undergone the Allopathic treatment. This may be the reason that maximum patients

were having stage II and stage III systolic hypertension.

Diastolic Blood Pressure:

Table no 49 revealed that maximum 15 (50%) of the patients were recorded

Stage I average Diastolic Blood Pressure followed by 07 (23.33%) of the patients

were suffering from Stage II average Diastolic Blood Pressure and 08 (26.67%) of the

patients were in Normal Stage. No patients were recorded of Stage III and IV average

Diastolic Blood Pressure. Here also by the same reason patients having stage I and

stage II diastolic hypertension.

4) Discussion on Results:

Results are drawn on cumulative effects of therapy on subjective and objective

parameters. In the present study 25 patients showed good response and 5 responded

moderately.

Table-70: Showing Overall Result of the therapy

Result No of patients Percentage

Good response 25 83.33%

Moderate response 05 16.66%


Discussion

Figure-42: Showing Overall Result of the therapy

83%

17%

goodresponsemoderateresponse

Effect of Therapy on Bhrama:

The present study illustrated that the effect of Shilajatu Guggulu Rasayana on

Bhrama gives 100% result. As Bhrama is due to Vata and Pitta dosha, the Shilajatu

and Guggulu having the rasayana properties hence act on the Vata dosha whereas

Guggulu having kashaya rasa act on Pitta dosha., the drug Triphala having the

properties of Pitta hara and madhura rasa hence act on Vata and Pitta. Gomutra

having the properties of anulomana with madhura and hence give the effect to

Shilajatu and Guggulu to act on Vata dosha. Like this Shilajatu and Guggulu

Rasayana, helps in regulating Bhrama.

In parameter Bhrama Mean ±SD before was 1.2 ±0.8 and after the treatment it



Effect of Therapy on Klama:

The present study demonstrated that the effect of Shilajatu Guggulu Rasayana

on Klama gives 86% result. As Klama is due to Rakta dushti, the drug Triphala

having the properties of Pitta hara and madhura rasa hence acts on Pitta. The Shilajatu


Discussion

having sheeta guna and Guggulu having kashaya rasa hence acts on Pitta dosha. By

these properties Shilajatu and Guggulu Rasayana, helps in reducing Klama.

In parameter Klama Mean ±SD before was 1.44 ±0.77 and after the treatment

it is reduced to 0.2 ±0.40 with Mean difference 1.2 and standard of mean 0.121 and

test shows more highly significant before and after the treatment as P<0.001.

Effect of Therapy on Shirah shoola:

The present study revealed that the effect of Shilajatu Guggulu Rasayana on

Shirah shoola gives 91% result. As Shirah shoola is due to Vata dosha and Rakta

dushti, , the Shilajatu and Guggulu having the rasayana properties hence act on the

Vata dosha whereas Guggulu having kashaya rasa and Shilajatu having sheeta guna

act on Pitta dosha. Triphala having the properties of Pitta hara and madhura rasa

hence act on Vata and Pitta. Gomutra having the properties of anulomana with

madhura hence give the effect to Shilajatu and Guggulu to act on Vata. By these

properties Shilajatu and Guggulu Rasayana helps in subsiding Shirah shoola

In parameter Shira shoola Mean ±SD before was 1.5 ±0.86 and after the

treatment it is reduced to 0.13±0.34 with Mean difference 1.366 and standard of mean


P<0.001.

Effect of Therapy on Daha:

The present study shows that the effect of Shilajatu Guggulu Rasayana on

Daha gives 100% result. As Daha is due to Pitta dosha, the drug Triphala having the

properties of Pitta hara and madhura rasa whereas Shilajatu having sheeta guna and

Guggulu having kashaya rasa hence acts on Pitta dosha. Therefore Shilajatu and

Guggulu Rasayana, regulates Daha.


Discussion

In parameter Daha Mean ±SD before was 0.2 ±0.48 and after the treatment it



Discussion on Moorcha:

In the present study none of the patient gives the history of moorcha. It

develops in the later stage of the hypertension and mostly observed during malignant

hypertension, where reduction in blood supply to the brain was established.

Effect of Therapy on Systolic hypertension:


Systolic blood pressure gives 92% result. As Shilajatu and Guggulu having the

mutrala properties hence reduces the blood pressure.

In parameter Systolic B.P. Mean ±SD before was 2.4 ±0.62 and after the



P<0.001.

Effect of Therapy on Diastolic hypertension:


Diastolic blood pressure gives 83% result. As Shilajatu and Guggulu having the

mutrala properties hence reduces the blood pressure.

In parameter Diastolic B.P, Mean ±SD before was 0.96 ±0.71 and after the


0.55 and test shows more highly significant before and after the treatment as P<0.001.

Over all response on Subjective and Objective parameters:

Net mean results of the therapy on all parameters (all subjective and objective

in to the consideration) showed 92%. This study demonstrated that the effect of


Discussion

Shilajatu Guggulu Rasayana on all the parameters. The drug Shilajatu and Guggulu

having the Rasayana affects hence Vata shamka, whereas Guggulu having kashaya

rasa and Shilajatu having sheeta guna hence Pitta shamka. Triphala having Pittahara

properties with madhura rasa hence act on Vata and Pitta dosha. Gomutra having the

properties of anulomana with madhura and hence give the effect to Shilajatu and

Guggulu to act on Vata dosha. Therefore by these properties Shilajatu and Guggulu

Rasayana, act on all parameters.

Table71: Showing the effect of therapy on Pittavruta udana (Essential

hypertension)

Net Result Percentage Net results of all therapies (X/N)

Response

Systolic B.P. 92% Diastolic B.P. 83% Shirah shoola 91%

Klama 86% Bhrama 100%

Daha 100% N = 6 X = 552

92%

Good response.

Effect of therapy on Biochemical Parameters:

Effect of Therapy on Serum Cholesterol:

In parameter Cholesterol Mean ±SD before was 193.81 ±29.22 and after the



P<0.001.

Effect of Therapy on Serum Triglycerides:

In parameter Triglyceride Mean ±SD before was 172.94 ±60.41 and after the



P<0.001.


Discussion

Effect of Therapy on High Density Lipoprotein:

In parameter H.D.L Mean ±SD before was 47.63 ±10.03 and after the



P<0.001. Although HDL is highly significant in statistical analysis but clinically it is

insignificant.

Effect of Therapy on Low Density Lipoprotein:

In parameter L.D.L. Mean ±SD before was 111.69 ±30.13 and after the



P<0.001.

Effect of Therapy on Very Low Density Lipoprotein:

In parameter V.L.D.L. Mean ±SD before was 34.54 ±12.10 and after the



P<0.001.

Over all effect of therapy on Biochemical Parameters:


found 36.86 i.e. lower than the before treatment mean, mean difference of Serum

triglycerides was found 29.94 i.e. lower than the before treatment mean, mean

difference of High density lipoprotein was found 4.24 i.e. lower than the before

treatment mean, mean difference of Low density lipoprotein was found 26.72 i.e.

lower than the before treatment mean whereas mean difference of Very low density

lipoprotein was found 06.00 i.e. also lower than the before treatment mean. As

Guggulu is the best drug to act on Serum cholesterol and Serum triglycerides where as


Discussion

Guggulu promotes the High density lipoprotein but in this study High density

lipoprotein mean difference was found 4.24, lower than the before treatment, this may

be due to the other cause. Even though it is highly significant in statistical analysis but

clinically it is insignificant. The Low density lipoprotein and Very low density

lipoprotein are the calculation of the rest of lipid profile. Hence the action of Shilajatu

Guggulu Rasayana on Lipid Profile has been seen.

OVER ALL RESPONSE:

Overall in almost all parameter the drug shows highly significant except HDL

cholesterol before and after the treatment. Majority of patients showed significant

control in the blood pressure. Except HDL, Serum Cholesterol, Serum Triglyceride,

LDL and VLDL are significantly reduced.


Conclusion

Conclusion

Following conclusion can be drawn from the present study:

The symptoms of Pittavruta udana is correlated to certain extent with essential

hypertension.

Avarana means the obstruction to movement of Vata, avaraka is the cause for

it. In this regard hypertension is compared to that of Pittavruta udana, which is

having symptoms Bhrama, klama, moorcha daha opined by Acharaya Sushruta

and others Acharya Charaka added ojobhramsha and avasada to the above

symptoms.

Mainly in more than 95% of cases a specific underlying cause of hypertension

cannot be found such patients are said to have essential hypertension.

Hypertension usually asymptomatic for the first 10-20 yrs, slowly but surely

strains the heart and damages the arteries often called as silent killer.

Hypertension is asymptomatic but is having a direct relation to that of

vasculature. Atherosclerosis and arteriosclerosis are the phenomena, which

affects the individuals if neglected accounts for morbidity and mortality, which

needs an effective of careful approach.

Dr. Chaudhury great physiologist has mentioned hypertension is an ancient

disease, even Acharya Charaka; the Father of Hindu system of medicine

described the condition admirably more than 2500 years ago.

In the present study most of the patients had symptoms like bhrama, klama and

shirashoola.

Among the patients of present study only five had daha as one of the symptom.

Moorcha one of the symptom of Pittavruta udana, not observed in any of the

patients.

Shilajatu Guggulu Rasayana in Pittavruta Udana (Essential Hypertension) 163

Conclusion

In the present study 13 patients had the family history of hypertension it

suggests that there is strong involvement of genetic factors.

Among the 30 patients 4 patients newly diagnosed and rest 26 patients were

previously suffering with the hypertension.

Life style also have significant role in the manifestation of hypertension as 20

patients of the present study had sedentary life style.

A minimum of 2 months to maximum of three years chronic was noticed in the

present study.

14 patients had moderate to severe intensity of hypertension.

6 patients had the habit of smoking followed by 10 patients had alcohol

consumption as habit which are the triggering factors of hypertension.

Even 22 and 20 patients respectively had frequent intake of coffee and tea as

they contain certain triggering factors.

In the present study all patients were taking katu rasa pradhana ahara followed

by 17 patients were consuming lavana rasa pradhana ahara as which are the

pitta, vata and rakta prakopaka rasas.

As all patients had involvement of manovaha sroto vikruti as stress and strain is

the strong etiology behind the screen.

Shilajatu Guggulu Rasayana is best for the treatment of Avarana.

Guggulu is having its effect over atherosclerosis, obesity and is proven anti-

inflammatory drug.

Guggulu is the best drug to act on Serum cholesterol and Serum triglycerides

where as Shilajatu is presumed to posses the unique drug for the Dhatu poshana

and Tridosha prashamana.


Conclusion

Both Shilajatu and Guggulu having the property of mootrala hence act as

diuretics as per modern system of medicine. Diuretic is the first aid in some

cases of hypertension.

The subjective parameter bhrama and daha shown 100% response, where as

shirah shoola shown 91% result and klama shown 86% result.

The objective parameters like systolic blood pressure shown 92% result where

as diastolic blood pressure shown 83% result in this study.


found 36.86 i.e. lower than the before treatment mean, mean difference of

Serum triglycerides was found 29.94 i.e. lower than the before treatment mean,

mean difference of Low density lipoprotein was found 26.72 i.e. lower than the

before treatment mean whereas mean difference of Very low density

lipoprotein was found 06.00 i.e. also lower than the before treatment mean.

Overall in almost all parameter the drug shows highly significant before and

after the treatment i.e., good response.

Net mean results of the therapies (All subjective and objective in to the

consideration) = 92% i.e. Good response

Totally Shilajatu Guggulu rasayana has shown good response in Pittavruta

udana (essential hypertension) in the present study.

Suggestion for future study:

Present study showed encouraging results. The same study if done with large

sample more data can be obtained.

Present study showed good response on lipid profile. Further research may

show hopeful out come in hyperlipidaemia.


Summary

Summary

The thesis entitled “Evaluation of the efficacy of “Shilajatu Guggulu

Rasayana in Pittavruta udana” with special reference to Essential hypertension”

comprises following parts.

1. Introduction

2. Objectives of the study

3. Review of literature

4. Methodology

5. Observation and results

6. Discussion

7. Conclusion

1. Introduction:

This part includes importance of the disease entity Pittavruta udana

comparison with Essential hypertension with its prevalence and about the importance

of Shilajatu Guggulu Rasayana in all type of Avarana with its individual effects.

2. Objectives of the study:

It includes importance of Avarana and our acharyas opinion on Pittavruta

udana, effect of Shilajatu Guggulu Rasayana on Avarana with its anti hypertensive

effects, effects of Essential Hypertension in modern life style, objectives of the study,

and reasons behind the selection of drug for this disease.

3. Review of literature:

This part includes historical review, description of Hridaya in ancient time,

review of previous research works, views of Ayurvedic scholars; Review of Pittavruta

udana includes disease etymology description of Avarana with classifications,

Description regarding nidana, lakshanas, nidana, poorvaroopa, roopa, samprapti,


Summary

upashaya-anupashaya, pathya-apathya etc., Description regarding the Hypertension

and its classification and different types of treatments. In the drug review description

concerning about the properties and preparation of Yoga.

4. Methodology:

This includes the selection criteria, study design, plan of the study, subjective

and objective parameters, posology, preparation of yoga, sample size, literary aspect,

criteria of diagnosis, inclusion and exclusion criteria and preparation of drug.

5. Observation and result:

It includes observation on all demographic data with their percentage and

graphical representation, regarding the observation nidanas, poorvaroopas, lakshanas

and results of individual symptoms followed overall response of the treatment.

6. Discussion:

Shilajatu Guggulu Rasayana vis-à-vis of Essential Hypertension, Discussion

on disease review, Discussion on drug review, Discussion on clinical study,

Discussion on results, Discussion on the patients of Pittavruta udana (Essential

Hypertension) who underwent the trial, Mode of Action of Shilajatu Guggulu

Rasayana.

7. Conclusion:

This is the last part of the present study. This section comprises of the

Conclusion on the whole study.


Bibilography

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I

Bibilography

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Bibilography


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teekya samvrita, 5th edition, Chapter-24/222, Published by: Choukhambha Sanskrit sansthan

varanasi, pp-260.

32) Ganga sahaya pandeya edited Gadanigraha, Vydyotini hindi commentary, 1st edition 1969,

Chapter-21/26, Published by Chaukhambha Sanskrit series, Varanasi-1, pp-474/475



Sudarsana sastri, 15th edition 1985, Chapter-22/23, Published by: Choukhamba Sanskrit

sansthan Varanasi, pp-419.




35) Ibid, Chapter-28/241-242, pp-981.

36) Ibid, Chapter-1/1/7-8, pp-5.

37) Ibid, Chapter-28/241-242, pp-981.

38) Dr. J.L.N. Sastry edited Dravyaguna vijnana-II, 1stedition 2004, S. no.-18, Published by

Choukhambha Orientalia Varanasi, pp-116,117.


commentary, Reprint 2002, Chapter-1/3/49, Published by: Chaukhambha Surbharati


40) Ibid, Chapter-1/3/61, pp-58.

41) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Vimana Sthana, with the

Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-5/8, Published

by Chaukhambha Sanskrit Santhan, Varanasi, pp- 250.

42) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Sutra Sthana, with the Ayurveda-

Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-30/7-8, Published by

Chaukhambha Sanskrit Santhan, Varanasi, pp- 184.



III

Bibilography

44) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Chikitsa Sthana, with the

Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-26/78-103,

Published by Chaukhambha Sanskrit Santhan, Varanasi, pp- 602.

45) Vaidya Jadavji Trikamji Acharya edited Susruta Samhita, Shareera Sthana, with the

nibandhasangraha commentary of Sri Dalhnacharya, reprinted 2008, Chapter-9/12, Published

by Chaukhamba Surbharati Prakashan,Varanasi, pp- 386.


47) Ibid, Chapter-4/32, pp-358

48) Dr. Shivprasad Sharma edited Astanga Samgraha, Shareera Sthana, Sasilekha Sanskrit

Commentary by Indu, Reprint 2006, Chapter-5/47, Published by: Chaukhamba Sanskrit

Series Office, Varansi, pp-304.

49) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Shareera Sthana,

Sarvangasundara of Arunadatta & Ayurvedarasayana of Hemadri Commentaries, Reprint

2007, Chapter-3/18-19, Published by: Chaukhambha Surbharati Prakashana Varanasi, pp-

389.

50) Sri Satyapala Bhisagacharya edited Kashyapa Samhita, Garbhakrantishareera adhyaya, The

Vidyotini Hindi Commentary and with Sanskrit Introduction, 3rd edition, Shaloka-5-10,

Published by: Chaukhamba Sanskrit Sansthan, Varansi, pp-74.

51) Pandit Parasurama Sastri, Vidyasagar edited Sarngadhara Samhita, Prathma Khanda, with the

commentary of Adhamalla’s Dipika and Kasirama’s Gudhartha Dipika, 6th edition 2005,

Chapter-6/9-10, Published by Chaukhambha Orientalia Varanasi, pp-68.

52) Pandit Parasurama Sastri, Vidyasagar edited Sarngadhara Samhita, Prathma Khanda, with the

commentary of Adhamalla’s Dipika and Kasirama’s Gudhartha Dipika, 6th edition 2005,

Chapter-3, Published by Chaukhambha Orientalia Varanasi, pp-28.




54) Ibid, Chapter-28/221-222, pp-626.

55) Ibid, Chapter-28/61-62, pp-619.

56) Ibid, Chapter-28/63-64, pp-619.


Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-24, Published by



IV

Bibilography


Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-28/31,


59) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Nidana Sthana,


2007, Chapter-15/10, Published by: Chaukhambha Surbharati Prakashana Varansi, pp-531.



Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-20/11, Published by


62) Prof. Yadunandana Upadhyaya edited Madhava Nidana, with Madhukosha Sanskrit

commentary by Sri Vijayaraksita and Srikantha Datta with the Vidyotini hindi commentary

by Sri Sudarsana Sastri, Part-1, 30th edition 2000, Chapter-17/1, Published by Chaukhambha

Sanskrit Santhan, Varanasi, pp- 346.




64) Ibid, Chapter-24/15,34, pp-124,126.

65) Arun.K.Tiwari, details on Hypertension, Heritage healing, Professional publications pvt. Ltd,

Madhurai, May 2002, pp-14.



by Sri Sudarsana Sastri, Part-1, 30th edition 2000, Chapter-17/1-3, Published by



Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-24, Published by




2007, Chapter-6, Published by: Chaukhambha Surbharati Prakashana Varanasi, pp-485.


Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-24/42-44, Published by



V

Bibilography



by Chaukhambha Sanskrit Santhan,Varanasi, pp- 250.



Chaukhambha Sanskrit Santhan,Varanasi, pp- 184.

72) Ibid, Chapter-30/3-4, pp-183.

73) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Shareera Sthana,


2007, Chapter-3/13-15, Published by: Chaukhambha Surbharati Prakashana Varansi, pp-388.






Published by Chaukhambha Sanskrit Santhan,Varanasi, pp- 616.

76) Vaidya Jadavji Trikamji Acharya edited Susruta Samhita, Sutra Sthana, with the

nibandhasangraha commentary of Sri Dalhnacharya, reprinted 2008, Chapter-21/10,

Published by Chaukhamba Surbharati Prakashan,Varanasi, pp- 101.


78) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Sutra Sthana,



79) Dr. Shivprasad Sharma edited Astanga Samgraha, Sutra Sthana, Sasilekha Sanskrit






81) Ibid





VI

Bibilography

83) Vaidya Jadavji Trikamji Acharya edited Susruta Samhita, Nidana Sthana, with the









86) Pandit Parashurama Shastri and Vidyasagar edited Sharangadhara Samhita, Poorvakhanda,

Anonymous Adhamalla Dipika Sanskrit commentary, Edition 3rd 1983, Chapter-5/27-28,

Published by Chaukhambha Orientalia,Varanasi-01, pp-50



















93) Ibid, Chapter-1/17-18, pp-260.





VII

Bibilography











nibandhasangraha commentary of Sri Dalhnacharya, reprinted 2008, Chapter-1/17-18,











102) Ibid, Chapter-21/14, pp-102.



2007, Chapter-12/15-16, Published by: Chaukhambha Surbharati Prakashana Varansi, pp-

194.




105) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Sutra Sthana, with the

Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-30/4,13,

Published by Chaukhambha Sanskrit Santhan,Varanasi, pp- 183,185.


VIII

Bibilography





Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-30/7














112) Ibid.

113) Ibid.

114) B.D. Chaurasia edited Human Anatomy Regional and Applied, Section-2 Chapter-18,

Vol-1, 3rd edition, Fourth Reprint 1999, published by: CBS Publishers and Distributors, New

Delhi pp-216.

115) Ibid.

116) Ibid, pp-226.

117) Ibid, pp-228.

118) Ibid, pp-229.

119) Vaidya Jadavji Trikamji Acharya edited Susruta Samhita, Chikitsa Sthana, with the


by Chaukhamba Surbharati Prakashan, Varanasi, pp- 429.

120) Ibid

121) Ibid

122) Raja Radhakanta Deva edited Shabda-Kalpadrum, Part-2, 3rd edition 1967, Published by

Chaukhamba Sanskrit Series Office, Varanasi-1, pp- 298.


IX

Bibilography

123) Brahmanand Tripathi edited Charaka samhita, Chikitsa Sthana, Charaka chandrika Hindi



124) Ibid, Chapter-28/31-32, pp-942.

125) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Chikitsa sthana, with the



126) Dr. S. Suresh Babu edited The Principles and Practice of Kaya Chikitsa (Ayurveda’s

Internal Medicine), Vol-1, Edition:1st 2003,Jaikrishnadas Ayurveda Series No. 116, Chapter-

14, Published by Chaukhambha Orientalia,Varanasi-1, pp- 141.

127) Ibid, pp-142.




129) Ibid, Chapter-28/215, pp-626.

130) Ibid, Chapter-28/215-216, pp-626.

131) Dr. Shivprasad Sharma edited Astanga Samgraha, Nidana Sthana, Sasilekha Sanskrit



















X

Bibilography







139) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Sidhi Sthana, with the












143) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Nidana Sthana, with the






145) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Nidana Sthana, with the






147) Ibid.

148) Ibid Chapter-24/5, pp-429.




XI

Bibilography


152) Ibid Chapter-26/42-2, pp-482.

153) Ibid Chapter-26/42-3, pp-483.

154) Ibid Chapter-26/42-4, pp-483.

155) Ibid Chapter-26/42-5, pp-484.

156) Ibid Chapter-26/43, pp-484

157) Prof. P.V. Sharma edited Dravyaguna Vijnana, Vol-1, 2nd part, Chapter-2, Reprint 2001,

Published by: Chaukhambha Bharati Academy Varansi, pp-142.

158) Ibid , pp-139.

159) Ibid , pp-138.

160) Ibid , pp-147.

161) Ibid, pp-140.



2007, Chapter-1/11-12, Published by: Chaukhambha Surbharati Prakashana Varansi, pp-9-

10.




164) Dr. Ravidutt Tripathi edited Astanga Samgrah, Sutra sthana, Saroja Hindi Vyakhya Sahit,

Reprint 2001, Chapter-9/29, Published by: Chaukhambha Sanskrit Pratishthan Delhi, pp-193.




166) Sri Brahmasankara Misra and Sri Roop lal ji edited Bhava Prakasha Nighantuh,

Poorvardham, Tailaverga, Shaloka-2-6, 5th edition 1969, Published by Chaukhambha Sanskrit

Series office Varanasi-1, pp-779.

167) Brahmanand Tripathi edited Charaka samhita, Vimana sthana, Charaka chandrika Hindi





Prakashana Varansi, pp-509-511.


XII

Bibilography

169) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Sutra sthana,




Poorvardham, Sandhanaverga, Shaloka-19-20, 5th edition 1969, Published by Chaukhambha

Sanskrit Series office Varanasi-1, pp-785.

171) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Nidana sthana,




173) Brahmanand Tripathi edited Charaka samhita, Vimana sthana, Charaka chandrika Hindi




175) Brahmanand Tripathi edited Charaka samhita, Nidana sthana, Charaka chandrika Hindi

commentary, Reprint 2003, Chapter-7/4, Published by: Chaukhambha Surbharati Prakashana

Varansi, pp-639.

176) Pt. Hari Sadasiva Sastri Paradakara Bhisagacarya edited Astanga Hrdaya, Sutra sthana,



216.

177) Edouard J. Battegay, Gregory Y. H. Lip, George L. Bakris edited Hypertension Principles

and Practice, Published in 2005, Chapter-2, Published by Taylor & Francis Group, new York,

pp-16.

178) Brahmanand Tripathi edited Charaka samhita, Shareera sthana, Charaka chandrika Hindi






180) Ibid.




XIII

Bibilography

182) Norman M. Kaplan edited Kaplan's Clinical Hypertension, 9th copyright 2006, Chapter-3,

Printer: Quebecor World –Taunton, pp-173.



















190) Ibid, Chapter-24/25, pp-125.

191) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Indriya Sthana, with the









194) Vaidya Jadavji Trikamji Acharya edited Charaka Samhita, Siddi Sthana, with the




XIV

Bibilography






197) Norman M. Kaplan edited Kaplan's Clinical Hypertension, 9th copyright 2006, Chapter-

3, Printer: Quebecor World –Taunton, pp-183.

198) Ibid, pp-183.

199) Ibid, pp-183.


















nibandhasangraha commentary of Sri Dalhnacharya, reprinted 4th edition 1980, Chapter-1/35,

Published by Chaukhambha orientalia Varanasi, pp- 263.

206) Sri Harihar prasad pandeyen edited Bhavaprakasha, Udradhah, Udradhah, Vidhyotani

namikya bhasha teekya samvrita, 5th edition, Chapter-24/222, Published by: Choukhambha

Sanskrit Sansthan Varanasi. pp-260.

207) Ganga Sahaya Pandeya edited Gadanigraha, Vydyotini hindi commentary, 1st edition

1969, Chapter-21/26, Published by Chaukhambha Sanskrit Series, Varanasi-1, pp-474/475


XV

Bibilography

208) Yadunandana Upadhyaya edited Madhava Nidana-I, with Madhukosha Sanskrit

commentary by Shri Vijayaraksita and Srikanthadatta, with the Vidyotin hindi commentary

by Shri Sudarsana Sastri, 15th edition 1985, Chapter-22/23, Published by: Choukhamba

Sanskrit Sansthan Varanasi, pp-419.


Aurveda dipiaka commentary of Chakrapanidatta, reprinted 2004, Chapter-28/223,224,

Published by Chaukhambha Sanskrit Sthana Varanasi, pp- 626.


Aurveda dipiaka commentary of Chakrapanidatta, reprinted 2004, Chapter-24/11-16,

Published by Chaukhambha Sanskrit stahan Varanasi, pp-124.

211) Vaman Shivram edited The Student Sanskrit-English Dictionary, reprint 1976, Published

by Motilal Banarsidass, Delhi, Printed at Shri Jainendra press, Delhi-7, pp-169.




213) Ibid. Chapter-20/14, pp-114.




Aurveda dipiaka commentary of Chakrapanidatta, reprinted 2004, Chapter-20/11, Published

by Chaukhambha Sanskrit stahan Varanasi, pp-113.








nibandhasangraha commentary of Sri Dalhnacharya, reprinted 4th edition 1980, Chapter-

15/13, Published by Chaukhambha orientalia Varanasi, pp- 70.




XVI

Bibilography









223) Ibid, pp-62.















229) Anthony S. Fauci, Joseph B. Martin, Eugene Braunwald, Kurt J. Isselbacher, Jean D.

Wilson, Dan L. Longo, Stephen L. Hauser, Dennis L. Kasper edited Harrison’s Principles of

internal medicine-I, 14th edition 1998, Part 8th section 4-246, Published by: McGraw- Hill

Health Professions Division New York. pp-203.

230) Daryl Fox edited Elaine N. Marieb Human anatomy and physiology, 4th edition 1998,

Unit-IV, Chapter-20, Published by Benjamin/Cummings science California pp-. 709.





232) Ibid.


XVII

Bibilography






2007, Chapter-1/8, Published by: Chaukhambha Surbharati Prakashana Varanasi, pp-443.
























242) Ibid, Chapter-28/61, pp-619.




244) Ibid, Chapter-28/227-228, pp-626.


XVIII

Bibilography

245) Ibid, Chapter-28/222-223, pp-626.

246) Ibid, Chapter-28/221-222, pp-626.










206.







252) Ibid, Chapter-28/235,236, pp-626.


Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-28/206-

207,211-212, Published by Chaukhambha Sanskrit Santhan,Varanasi, pp- 625.














XIX

Bibilography










261) Harsh Mohan edited Textbook of pathology, 5th edition 2005, Chapter-20, Published by:

Jaypee brother’s medical publishers (P) Ltd. New Delhi, pp-708.




263) Ibid.

264) Harsh Mohan edited Textbook of pathology, 5th edition 2005, Chapter-20, Published by:

Jaypee brother’s medical publishers (P) Ltd. New Delhi, pp-708.




and Practice, Chapter-2, Published in 2005, Published by Taylor and Francis Group, New

york, pp-16.

267) Daryl Fox edited Elaine N. Marieb Human anatomy and physiology, 4th edition 1998,

Unit-IV, Chapter-20, Published by Benjamin/Cummings science California pp-. 709.

268) Izzo, Joseph L.; Black, Henry R.; Goodfriend, Theodore L.; Sowers, James R.; Weder,

Alan B.; Appel, Lawrence J.; Sheps, Sheldon G.; Sica, Domenic A.; Vidt, Donald G. edited

Hypertension Primer: The Essentials of High Blood Pressure, 3rd Edition 2003, Chapter A41,




York, pp-16-17.

270) Ibid.Chapter-3, pp-37.

271) Ibid.Chapter-14, pp-217.


XX

Bibilography

272) Harsh Mohan, Textbook of pathology, 5th edition 2005, Chapter-20, Published by: Jaypee

brother’s medical publishers (P) Ltd. New Delhi, pp-709.

273) Ibid.



York, pp-217.




276) Robert C. Schlant, R. Wayne Alexander edited The Heart, 8th international edition,

Copyright 1994, Vol.-2, Chapter-75, Published by McGraw-Hill,Inc Health Professions

Division, New York, pp-1397.



278) Ibid, pp-708-709.





281) Ibid.



Hypertension Primer: The Essentials of High Blood Pressure, 3rd Edition 2003, Chapter

B101, Published by Lippincott Williams & Wilkins, New York, pp-296.



Hypertension Primer: The Essentials of High Blood Pressure, 3rd Edition 2003, Chapter

C109, Published by Lippincott Williams & Wilkins, New York, pp-322.

284) Ibid, pp-323.

285) Ibid, pp-324.

286) Ibid.

287) Ibid.

288) Ibid.

289) Ibid.


XXI

Bibilography


Commentary by Indu, Reprint 2006, Chapter-2/4, Published by: Chaukhamba Sanskrit Series

Office, Varansi, pp-358.







293) Sri Satyapala Bhisagacharya edited Kasyapa Samhita, Garbhakrantishareera adhyaya,

The Vidyotini Hindi Commentary and with Sanskrit Introduction, 3rd edition, Chapter-16/42,

Published by: Chaukhamba Sanskrit Sansthan, Varansi, pp-338.
























XXII

Bibilography

302) Ibid, Chapter-28/75,183, pp-620,624.

303) Ibid, Chapter-28/239, pp-627.

304) Ibid.

305) Ibid.

306) Ibid, Chapter-28/198, pp-625.

307) Ibid, Chapter-28/240, pp-627.

308) Ibid, Chapter-28/239, pp-627.

309) Ibid, Chapter-28/245, pp-627.







312) Ibid, Chapter-28/183-184, pp-624.

313) Ibid, Chapter-28/200-202, pp-625.

314) Ibid, Chapter-28/218, pp-626.

315) Ibid, Chapter-28/219,221, pp-626.



york, pp-361.



Hypertension Primer: The Essentials of High Blood Pressure, 3rd Edition 2003, Chapter B95,





319) Dr. In Dradeva Tripathi edited Lolimbaraja, Vaidhyajeevanam, prathama vilasa, 10th

shloka, 3rd edition 2005, Chawkhambha Orientalia Varanasi, pp-4.





XXIII

Bibilography


Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-1/3/65,

Published by Chaukhambha Sanskrit Santhan,Varanasi, pp-59.

322) Dr. Chanderbhooshan jha edited Ayurved Rasashastra, , reprint 2003, Chapter-6,

Published by Chaukhambha Surbharti Prakashan Varanasi, pp- 225.

323) Prof. Priyavrat Sharma edited Dhanvantari Nighantuh, Tritya verga-73, First edition

1982, Published by Chaukhambha Orientalia Varanasi, pp-117.

324) Pandit Kashinath Shastri edited Rasatrangini,11th edition 1979, Chapter-22/60-61,

Published by Motilal Banarsidas Varanasi, pp-582.

325) Dr. Chanderbhooshan jha edited Ayurved Rasashastra, , reprint 2003, Chapter-6,

Published by Chaukhambha Surbharti Prakashan Varanasi, pp- 225.

326) Dr. Indra Dev Tripathi edited Rasaratna Samuchchaya, with Rasaprabha hindi

commentary, 2nd edition 2003, Chapter-2/207, Published by Chaukhambha Sanskrit

Bhawan,Varanasi, pp- 20.

327) Ibid, Chapter-2/208-209, pp-20.




Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-1/3/48-49,


330) Ibid, Chapter-1/3/58-59, pp-57.




Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-1/3/48-49,


333) Pandit Kashinath Shastri edited Rasatrangini,11th edition 1979, Chapter-22/84, Published

by Motilal Banarsidas Varanasi, pp-588.

334) Pandit Shiva Sharma edited Ayurveda Prakasha, with the Arthavidyotini and

Arthaprakasini Sanskrit and Hindi commentaries, reprinted 1999, Chapter-4/100-104,

Published by Chaukhambha Bharati Academy Varanasi, pp- 428.


Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-1/3/65,

Published by Chaukhambha Sanskrit Santhan,Varanasi, pp-59.


XXIV

Bibilography

336) Pandit Shiva Sharma edited Ayurveda Prakasha, with the Arthavidyotini and

Arthaprakasini Sanskrit and Hindi commentaries, reprinted 1999, Chapter-4/126-127-104,

Published by Chaukhambha Bharati Academy Varanasi, pp- 433.

337) Pandit Kashinath Shastri edited Rasatrangini,11th edition 1979, Chapter-22, Published by

Motilal Banarsidas Varanasi, pp-582.

338) file:///F|/tmp/Ayuherbal/Guggulu -Medicinal Plant of India.htm.

339) Ibid.

340) Prof. P.V.Sharma edited Dravya Guna Vijnana, Vol.-2, reprint: 2005, Vedanasthapana-

20, Chapter-1, Published by Chaukhambha Bharati Academy Varanasi, pp-54.



Karpooradiverga-25, 5th edition 1969, Published by Chaukhambha Sanskrit Series office

Varanasi-1, pp-205.

343) Ibid, pp-204.




Karpooradiverga-25, 5th edition 1969, Published by Chaukhambha Sanskrit Series office

Varanasi-1, pp-205.



347) Ibid, pp-55.

348) Ibid, pp-57.




351) file:///F|/tmp/Ayuherbal/Guggulu -Medicinal Plant of India.htm

352) Ibid.

353) Ibid.

354) Prof. P.V.Sharma edited Dravya Guna Vijnana, Vol.-1, Pratham Khanda, reprint: 2001,

Chapter-9, Published by Chaukhambha Bharati Academy Varanasi, pp-99-100.


Haritkyadiverda, 5th edition 1969, Shaloka-43, Published by Chaukhambha Sanskrit Series

office Varanasi-1, pp-12.


XXV

Bibilography

356) Prof. P.V.Sharma edited Dravya Guna Vijnana, Vol.-2, reprint: 2005,

Jawaraghanadiverga-340, Chapter-9, Published by Chaukhambha Bharati Academy Varanasi,

pp-753.


Haritkyadiverda, 5th edition 1969, Published by Chaukhambha Sanskrit Series office

Varanasi-1, pp-7.

358) Prof. P.V.Sharma edited Dravya Guna Vijnana, Vol.-2, reprint: 2005, Chenadiverga-93,

Chapter-4, Published by Chaukhambha Bharati Academy Varanasi, pp-239.


Haritkyadiverda, 5th edition 1969, Published by Chaukhambha Sanskrit Series office

Varanasi-1, pp-9.

360) Prof. P.V.Sharma edited Dravya Guna Vijnana, Vol.-2, reprint: 2005,

Jawaraghanadiverga-340, Chapter-9, Published by Chaukhambha Bharati Academy Varanasi,

pp-758.


Haritkyadiverda, 5th edition 1969, Shaloka-43, Published by Chaukhambha Sanskrit Series

office Varanasi-1, pp-10.







364) Sri Brahmasankara Misra and Sri Roop lal ji edited Bhava Prakasha Nighantuh, 5th

edition 1969, Mootraverga, shaloka-1-6, Published by Chaukhambha Sanskrit Series office

Varanasi-1, pp-778.


Ayurveda-Dipika commentary of Sri Chakrapanidatta, reprinted 2004, Chapter-1/94,101,



nibandhasangraha commentary of Sri Dalhnacharya, reprinted 2008, Chapter-45/220-221,



XXVI

Bibilography

367) Sri Brahmasankara Misra and Sri Roop lal ji edited Bhava Prakasha Nighantuh, 5th

edition 1969, Mootraverga, shaloka-1-6, Published by Chaukhambha Sanskrit Series office

Varanasi-1, pp-778.

368) Ibid.




370) Pandit Parasurama Sastri, Vidyasagar edited Sarngadhara Samhita, Madhyama Khanda,

with the commentary of Adhamalla’s Dipika and Kasirama’s Gudhartha Dipika, 6th edition

2005, Chapter-11/94-98, Published by Chaukhambha Orientalia Varanasi, pp-255.

371) The Ayurvedic formulary of India, Part-1, 1st edition 1978, Govt.of India, Ministry of

Health and Family Planning Department of Health, Delhi, pp-55.

372) Vaidya Jadavji Trikamji Acharya edited Susruta Samhita, `Sutra Sthana, with the









375) Pandit Parasurama Sastri, Vidyasagar edited Sarngadhara Samhita, Prathma Khanda, with

the commentary of Adhamalla’s Dipika and Kasirama’s Gudhartha Dipika, 6th edition 2005,

Chapter-5/25, Published by Chaukhambha Orientalia Varanasi, pp-50.











XXVII

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XXVIII

i

Table72: Showing Demographic Data

Sex: M- Male, F- Female, Religion: H-Hindu, M-Muslim, FS-Fiscal Status: P-Poor, M- Middle, H- Higher class, Occ-Occupation: S- Sedentary, A-Active, L-Labor, MS-Marital Status: M-Married, OS-Onset: C-Chronic, A-Acute, Intensity: S-Severe, Mo-Moderate, Mi-Mild, Diagnosis: P-Previously diagnosed, N-Newly diagnosed, FH- Family History of HTN: Y-Yes, N-No, Nidra: S-Sound, D-Disturbed, MV-Mansika Vritanta: B-Bhaya, K-Kopa, D-Deenta,, U-Udvega, Ks-Kshobha, Sa-Samprahara, M-Mada, Diet: V-Vegetarian, M-Mixed, Vyasana: T-Tea, C-Coffee, S-Smoking, A-Alcohal, Prakruti: VP-Vatapitta, VK-Vatakapha, PK-Pittakapha, Re-Remarks: GR-Good Response, MR-Moderate Response.

Sl OPD Age Sex Religion F.S. M.S. Occ. O.S. Int Diagnosis F.H. Nidra M.V. Diet Vyasana Prkruti. Re. 01. 5276 70 M H M M S C S P N D KDKs M T VP GR 02. 5285 70 M H M M S C S P N D KDKs M T VP GR 03. 5719 58 F H M M S C Mo P N D BD V C VK GR 04. 5774 55 M H M M S C S P Y S BKKsSa V TCA VP GR 05. 5735 48 M H M M S C Mo P Y D DKs V CA VK GR 06. 5892 45 M H P M L C S P N S KDSa M TA VP MR 07. 6342 50 M H M M S C Mo P Y D KKsSa M C VK GR 08. 6341 40 F M M M S C Mi P N S KKsSa M C VP GR 09. 6457 56 M H M M S C Mo P Y D KDKs V TC VP GR 10. 6529 66 M H M M S C S P Y S KKsSa M TCSA VK MR 11. 6530 58 F H M M S C Mo P Y S DUKs M C VK MR 12. 1225 38 M H H M A C Mo P N D BKKs V C VP GR 13. 4905 46 F H M M S C Mo P Y S BD M C VK MR 14. 5899 55 F M M M S C S P Y S KKsSa M TC VK GR 15. 345 55 M H P M L C Mo P Y D BDKs V TSA VP GR 16. 347 58 F H M M S C S P N S DU V T PK GR 17. 349 65 F H M M S C S P Y D DKsM V TC VP GR 18. 494 68 M H M M A C S P N S KKsSaM V T VP GR 19. 459 49 M H M M A C S P N D KDUKsSa V C VP GR 20. 496 45 M H M M S C S P N D KSaM M TSA VK GR 21. 527 57 F M M M S C Mo P N D KUKs M TC VP GR 22. 531 44 F H M M S A Mi N Y S BDKs V TC VP GR 23. 1219 53 F H M M S C Mo P N D DU V TC VP GR 24. 1218 52 M H M M A A S N N S KKsM M CSA VP GR 25. 1217 58 M H P M L C Mo P N D BDUM V TSA VK GR 26. 1445 48 F H H M S A Mo N N D BKDUM V TC VP GR 27. 1435 50 F M M M S C S P N S BDU M C VK GR 28. 1442 55 M H P M L C S P N D DKs M TSA PK MR 29. 1446 50 M H M M A A Mo N Y D D M TC VP GR 30. 1444 60 M H M M A C Mo P Y D KKs M TCA VP GR

ii

Table73: Showing Subjective parameters Before and After treatment

Bhrama Klama Shirah shoola Daha Moorcha Sl. No.

OPD NO BT AT % BT AT % BT AT % BT AT % BT AT %

01. 5276 3 0 100 3 0 100 2 0 100 0 0 - 0 0 - 02. 5285 1 0 100 2 0 100 1 0 100 0 0 - 0 0 - 03. 5719 2 0 100 2 1 50 1 0 100 1 0 - 0 0 - 04. 5774 1 0 100 2 0 100 1 0 100 0 0 - 0 0 - 05. 5735 2 0 100 0 0 - 2 0 100 0 0 - 0 0 - 06. 5892 1 0 100 2 1 100 3 1 67 0 0 - 0 0 - 07. 6342 2 0 100 1 0 100 1 0 100 0 0 - 0 0 - 08. 6341 0 0 - 2 0 100 2 0 100 0 0 - 0 0 - 09. 6457 1 0 100 2 0 100 0 0 100 0 0 - 0 0 - 10. 6529 2 0 100 3 1 67 0 0 - 0 0 - 0 0 - 11. 6530 2 0 100 2 1 50 2 1 50 0 0 - 0 0 - 12. 1225 1 0 100 1 0 100 2 0 100 0 0 - 0 0 - 13. 4905 0 0 - 2 1 50 3 1 67 0 0 - 0 0 - 14. 5899 2 0 100 1 0 100 2 0 100 0 0 - 0 0 - 15. 345 2 0 100 1 0 100 1 0 100 0 0 - 0 0 - 16. 347 2 0 100 1 0 100 2 0 100 0 0 - 0 0 - 17. 349 2 0 100 1 0 100 1 0 100 0 0 - 0 0 - 18. 494 0 0 - 1 0 100 2 0 100 0 0 - 0 0 - 19. 459 1 0 100 1 0 100 2 0 100 1 0 100 0 0 - 20. 496 1 0 100 2 1 50 2 0 100 0 0 - 0 0 - 21. 527 1 0 100 2 0 100 2 0 100 1 0 100 0 0 - 22. 531 1 0 100 1 0 100 1 0 100 0 0 - 0 0 - 23. 1219 2 0 100 1 0 100 0 0 - 0 0 - 0 0 - 24. 1218 0 0 - 1 0 100 2 0 100 0 0 - 0 0 - 25. 1217 1 0 100 1 0 100 2 0 100 0 0 - 0 0 - 26. 1445 0 0 - 0 0 - 2 0 100 2 0 100 0 0 - 27. 1435 1 0 100 1 0 100 0 0 - 0 0 - 0 0 - 28. 1442 1 0 100 0 0 - 2 1 50 0 0 - 0 0 - 29. 1446 0 0 100 1 0 100 2 0 100 0 0 - 0 0 - 30. 1444 1 0 100 2 0 100 0 0 - 1 0 100 0 0 - BT- before treatment, AT- after treatment, Total- total number of patients, % - percentage

iii

Table74: Showing Objective parameters Before and After treatment

Blood Pressure Systolic B.P.(S.B.P) Diastolic B.P.(D.B.P)

SL No.

OPD No.

BT AT % BT AT % 01. 5276 3 0 100 % 0 0 - 02. 5285 3 0 100 % 0 0 - 03. 5719 2 0 100 % 2 1 50 % 04. 5774 3 0 100 % 1 0 100 % 05. 5735 2 0 100 % 0 0 - 06. 5892 3 2 33 % 2 1 50 % 07. 6342 2 0 100 % 1 0 100 % 08. 6341 1 0 100 % 0 0 - 09. 6457 2 0 100 % 2 0 100 % 10. 6529 3 2 33 % 2 1 50 % 11. 6530 2 0 100 % 2 1 50 % 12. 1225 2 0 100 % 1 0 100 % 13. 4905 2 0 100 % 2 1 50 % 14. 5899 3 0 100 % 1 0 100 % 15. 345 2 0 100 % 0 0 - 16. 347 3 0 100 % 1 0 100 % 17. 349 3 0 100 % 1 0 100 % 18. 494 3 0 100 % 1 0 100 % 19. 459 3 0 100 % 1 0 100 % 20. 496 3 1 67 % 1 0 100 % 21. 527 2 0 100 % 0 0 - 22. 531 1 0 100 % 1 0 100 % 23. 1219 2 0 100 % 1 0 100 % 24. 1218 3 0 100 % 1 0 100 % 25. 1217 2 0 100 % 0 0 - 26. 1445 2 0 100 % 1 0 100 % 27. 1435 3 0 100 % 0 0 - 28. 1442 3 1 67 % 1 0 100 % 29. 1446 2 0 100 % 1 0 100 % 30. 1444 2 0 100 % 2 0 100 %

BT- before treatment, AT- after treatment, Total- total number of patients, % - percentage, SBP- Systolic blood pressure, DBP- Diastolic blood pressure, GR- Good Response, MR- Moderate Responce

iv

Table75: Showing Lipid Profile values Before and After treatment

LIPID PROFILE Cholesterol Triglyceride H.D.L. L.D.L. V.L.D.L. Sl.

No. OPD. No. BT AT BT AT BT AT BT AT BT AT

1. 5276 256.5 215.7 154.4 92.9 58.3 50.0 167.4 147.2 30.8 18.52. 5285 165.5 140.9 100.4 118.2 31.8 39.7 113.7 77.6 20.0 23.63. 5719 197.3 201.8 103.5 169.8 57.2 42.8 119.4 125.1 20.7 33.94. 5774 154.6 136.2 123.6 117.1 59.7 55.7 70.2 57.8 24.7 23.45. 5735 177.4 145.3 298.7 190.1 67.5 53.5 50.2 53.8 59.7 38.06. 5892 203.0 147.5 197.9 154.2 59.2 47.8 104.3 68.9 39.5 30.87. 6342 189.1 163.6 194.5 152.8 37.9 35.4 112.3 97.6 38.9 30.58. 6341 172.2 128.1 134.0 101.2 35.4 34.0 110.0 73.9 26.8 20.29. 6457 186.2 133.1 102.6 86.2 37.2 34.0 128.4 81.8 20.5 17.210. 6529 196.0 148.2 196.1 138.1 50.5 48.2 106.3 72.3 39.2 27.611. 6530 146.5 132.1 145.6 86.1 41.9 38.2 75.5 76.6 29.1 17.212. 1225 159.0 132.2 155.0 130.0 50.0 49.4 52.0 57.0 31.0 26.013. 4905 207.5 143.2 118.1 92.1 48.6 45.1 135.3 79.7 23.6 18.414. 5899 218.4 168.2 140.2 122.4 53.7 50.0 136.7 93.7 28.0 24.415. 345 198.7 163.7 192.1 165.2 39.2 35.0 121.0 95.6 38.4 33.016. 347 183.1 148.2 163.6 137.5 32.1 30.0 118.2 90.7 32.7 27.517. 349 210.2 165.1 180.1 132.7 53.7 49.5 120.4 89.0 36.0 26.518. 494 232.0 172.9 192.2 148.2 55.0 52.1 138.5 91.1 38.4 29.619. 459 225.0 232.0 308.0 382.0 35.7 30.3 157.0 125.3 61.6 76.420. 496 223.0 220.0 334.0 218.0 39.3 40.0 116.9 137.0 66.8 43.021. 527 214.1 178.9 221.7 184.2 37.4 35.2 132.4 106.8 44.3 36.822. 531 216.5 159.4 126.0 170.2 55.6 49.3 135.7 76.1 25.2 34.023. 1219 173.2 113.9 168.1 107.2 39.0 32.9 100.5 59.6 33.6 21.424. 1218 192.3 142.7 128.7 92.5 43.5 37.0 123.0 87.2 25.14 18.525. 1217 184.3 130.7 118.7 92.4 40.0 37.2 120.5 75.0 23.7 18.426. 1445 250.1 184.2 248.6 192.1 59.2 55.9 141.2 89.9 49.7 38.427. 1435 185.7 157.2 140.3 137.1 47.4 47.0 110.3 81.9 28.0 27.428. 1442 200.3 153.1 130.9 92.9 55.7 48.2 118.4 86.3 26.18 18.529. 1446 168.5 132.3 201.1 150.9 62.3 55.2 65.9 46.9 40.2 30.130. 1444 128.3 118.2 169.7 135.9 45.0 43.2 49.3 47.8 33.9 27.1 BT- before treatment, AT- after treatment, H.D.L- High density lipoprotein L.D.L. - Low density lipoprotein, V.L.D.L. - Very low density lipoprotein, Cholesterol- Total serum cholesterol, Triglyceride- Serum triglycerides

v

Table76: Showing Scoring Before and After the Treatment of all the parameters Scoring Before Treatment (all the parameters) Scoring After Treatment (all the parameters) Sl.

No OPD. No. Bhrama Klama Shirah

shoola Daha Systolic

B.P. Diastolic B.P

Total Bhrama Klama Shirah shoola

Daha Systolic B.P.

Diastolic B.P

Total

1. 5276 3 3 2 0 3 0 11 0 0 0 0 0 0 0 2. 5285 1 2 1 0 3 0 7 0 0 0 0 0 0 0 3. 5719 2 2 1 1 2 2 10 0 1 0 0 0 1 2 4. 5774 1 2 1 0 3 1 8 0 0 0 0 0 0 0 5. 5735 2 0 2 0 2 0 6 0 0 0 0 0 0 0 6. 5892 1 2 3 0 3 2 11 0 1 1 0 2 1 5 7. 6342 2 1 1 0 2 1 7 0 0 0 0 0 0 0 8. 6341 0 2 2 0 1 0 5 0 0 0 0 0 0 0 9. 6457 1 2 0 0 2 2 7 0 0 0 0 0 0 0 10. 6529 2 3 0 0 3 2 10 0 1 0 0 2 1 4 11. 6530 2 2 2 0 2 2 10 0 1 1 0 0 1 3 12. 1225 1 1 2 0 2 1 7 0 0 0 0 0 0 0 13. 4905 0 2 3 0 2 2 9 0 1 1 0 0 1 3 14. 5899 2 1 2 0 3 1 9 0 0 0 0 0 0 0 15. 345 2 1 1 0 2 0 6 0 0 0 0 0 0 0 16. 347 2 1 2 0 3 1 9 0 0 0 0 0 0 0 17. 349 2 1 1 0 3 1 8 0 0 0 0 0 0 0 18. 494 0 1 2 0 3 1 7 0 0 0 0 0 0 0 19. 459 1 1 2 1 3 1 9 0 0 0 0 0 0 0 20. 496 1 2 2 0 3 1 9 0 1 0 0 1 0 2 21. 527 1 2 2 1 2 0 8 0 0 0 0 0 0 0 22. 531 1 1 1 0 1 1 5 0 0 0 0 0 0 0 23. 1219 2 1 0 0 2 1 6 0 0 0 0 0 0 0 24. 1218 0 1 2 0 3 1 7 0 0 0 0 0 0 0 25. 1217 1 1 2 0 2 0 6 0 0 0 0 0 0 0 26. 1445 0 0 2 2 2 1 7 0 0 0 0 0 0 0 27. 1435 1 1 0 0 3 0 5 0 0 0 0 0 0 0 28. 1442 1 0 2 0 3 1 7 0 0 1 0 1 0 2 29. 1446 0 1 2 0 2 1 6 0 0 0 0 0 0 0 30. 1444 1 2 0 1 2 2 8 0 0 0 0 0 0 0 B.P.- Blood Pressure

vi

Table77: Showing Net Response of the Treatment (all the parameters)

GR- Good Response, MR- Moderate Response, MdR- Mild Response, NR– No Response.

TOTAL RESPONSE :

GOOD RESPONSE - 25

MODERATE RESPONSE - 05

MILD RESPONSE - 00

NO RESPONSE - 00

Sl. No.

OPD No.

BT (SCORE)

AT (SCORE)

BT (%)

AT (%)

NET RESPONSE (%)

REMARKS

01. 5276 11 0 100 000 100 GR 02. 5285 7 0 100 000 100 GR 03. 5719 10 2 100 20 80 GR 04. 5774 8 0 100 000 100 GR 05. 5735 6 0 100 000 100 GR 06. 5892 11 5 100 45 55 MR 07. 6342 7 0 100 000 100 GR 08. 6341 5 0 100 000 100 GR 09. 6457 7 0 100 000 100 GR 10. 6529 10 4 100 40 60 MR 11. 6530 10 3 100 30 70 MR 12. 1225 7 0 100 000 100 GR 13. 4905 9 3 100 33 67 MR 14. 5899 9 0 100 000 100 GR 15. 345 6 0 100 000 100 GR 16. 347 9 0 100 000 100 GR 17. 349 8 0 100 000 100 GR 18. 494 7 0 100 000 100 GR 19. 459 9 0 100 000 100 GR 20. 496 9 2 100 22 78 GR 21. 527 8 0 100 000 100 GR 22. 531 5 0 100 000 100 GR 23. 1219 6 0 100 000 100 GR 24. 1218 7 0 100 000 100 GR 25. 1217 6 0 100 000 100 GR 26. 1445 7 0 100 000 100 GR 27. 1435 5 0 100 000 100 GR 28. 1442 7 2 100 29 71 MR 29. 1446 6 0 100 000 100 GR 30. 1444 8 0 100 000 100 GR

Special Case sheet

Shilajatu Guggulu Rasayana in Pittavruta udana (Essential Hypertension)

I

Department of Post Graduate Studies in Kayachikitsa

D.G.M. Ayurvedic Medical College & Hospital GADAG Special case sheet for evaluation of

Shilajatu Guggulu Rasayana in Pittavaruta udana w.s.r.to Essential Hypertension Guide: Dr. R.V. Shettar, M.D (Ayu), Scholar: Sanjeev Kumar (Asst. Professor, P.G. Dept of Kayachikitsa.) 1) Name of the Patient

2) Father’s / husband’s name Sl.No

3) Sex Male Female OPD No

4) Age (in years) Birth place IPD No

5) Religion Hindu Muslim Christian Other

6) Occupation Sedentary Active Labor

7) Marital status Married Unmarried

8) Economical status Poor Middle Higher middle Higher class

9) Address

Contact No: Pin

10) Selection Included Excluded

11) Schedule Initiation Date Completion Date

Well responded Moderately responded 12) Result

Mild responded Poor responded Discontinued

13) 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.

EzÀÄ £Á£ÀÄ ²æÃ/²æÃªÀÄw ___________________________________________________

£À£Àß ¸ÀéEZÉÒ¬ÄAzÀ PÉÆqÀÄªÀ aQvÁì ¸ÀªÀÄäw. ¥Àæ¸ÀÄÛvÀ £ÀqÉ¢gÀÄªÀ aQvÁì ¥ÀzÀÞwAiÀÄ §UÉÎ £À£ÀUÉ aQvÀìPÀjAzÀ ¸ÀA¥ÀÇtð

ªÀiÁ»w zÉÆgÉwzÀÄÝ ªÀÄvÀÄÛ AiÀiÁªÁUÁzÀgÀÄ aQvÉì¬ÄAzÀ »AwgÀÄUÀ®Ä ¸ÁévÀAvÀæ÷å«zÉ JAzÀÄ w½¢gÀÄvÉÛ£É.

gÉÆÃVAiÀÄ gÀÄdÄ/Patient’s Signature

Special Case sheet


II

14) Pradhana vedana: Duration Sl.no. Complaints Present / Absent

Fresh < 1 Yrs < 5 Yrs > 5 Yrs 1 Bhrama 2 Klma 3 Shirah shoola 4 Daha 5 Moorcha

15) Anubandha vedana:

Duration Sl.no

Complaints Present/Absent Fresh <1Yrs < 5Yrs > 5Yrs

1 Daha in nabhi and uras 2 Avsada 3 Ati sweda 4 Others

16) Adhyatana vyadhi vrittanta:

Mode of onset [Atanka samutpatti]

Acute Chronic

Course of the disease [Vedana samucchaya]

Yrs / Month

Intensity Mild Moderate Severe Traveling Anxiety Emotion Aggravating

[Anupashaya] Stress Physical stress If any other Rest Tranquilizers

Fac

tors

Relieving [Upashaya] Sleep Anti depressant’s

Others 17) Poorva vyadhi vrittanta: 18) Kula vrittanta: (Write relationship)

Heart Disease Cancer Hypertension Thyroid disorders Obesity Hemiplegic Diabetes Any other

Special Case sheet


III

19) Chikitsa vrittanta:

Newly Diagnosed Previously Diagnosed Previous Medication Ayurvedic Allopathic Discontinued

1. 2. Drug used Dose Duration Dose Duration Response Controlled Not controlled Oral contraceptives

Yes No Duration Dose

Anti depressant Yes No Duration Dose 20) Vyasna:

21) Vyaktika vrittanta:

Night sleep Hrs. Day sleep Hrs. Nature of sleep Sound Disturbed

Nidra

Dreams Yes No Vegetarian Madhura Amala Mixed food Lavana Katu Oil/Ghee Tikta Kshaya

Ahara

Stored food

Rasa predominance

Kostha Krura Madhyama Mrudu Jatharagni bala Manda Teekshna Vishama Sama Occupational history Sedentary Active Labour Work involving any mental stress Yes No If yes Mild Moderate Severe Whether symptoms produced during working hours Yes No Weather symptoms relieved by change of place Yes No

22) Rutuchakra vrittanta: (For women)

Menopause attained Yes No If yes the age of attainment No.of days of flow Regular Irregular Duration of flow Normal Excessive Scanty Nature of flow Dysmenorrhoea Leucorrhoea

Duration Cigarette/Beedi Daily Beedi

Smoking

Frequency of smoking Chain smoker Duration Hot drinks / Beer Daily Quantity

Alcohol

Occasionally Tea /coffee Tobacco Chewing Duration Quentity

Special Case sheet


IV

23) Mansika vrittanta:

Sl. BT AT SI BT AT 1 Bhaya (Fear) 5 Deenata (Depression) 2 Kopa (Anger) 6 Samprahara (Aggressiveness) 3 Mada (Delirium) 7 Kshobha (Irritability) 4 Udvega (Anxiety) 24) Samanya Pareeksha: Pulse /min Temp °F Respiration rate /min

Weight /kgs Height Heart rate /min

25) Vishesha pariksha: Fundus of Eye Peripheral pulses Neck vein BMI

Pitting Non pitting Oedema Pedal Face Back

26) Aturabala pareeksha: Ashta vidha pareeksha :- 1.Nadi Rate Type 4. Jihwa

Varna Times/day 5. Shabda 2.Mala Consistency 6. Sparsha Varna 7. Druk 3.Mootra Times/day 8. Akruti

Dashavidha pareeksha:- Prakruti Shareerika V P K VP VK PK Sama

Sara Twak Rakta Mamsa Meda Asthi Shukra Majja Satwa

Samhanana Susamhita Madhyama samhita Heena samhita

Satmya Pravara Madhyama Avara

Satwa Pravara Madhyama Avara

Vyama shakti Pravara Madhyama Avara

Vaya Balya Madhya Vruddha

Pramana Supramanita Adhika Heena

Ahara shakti Abhyvarana Jarana

Special Case sheet


V

27) Systemic examination:- Cardiovascular system A) JVP Pressure B) Pulse Rhythm Volume Character C) Blood pressure - Standing Sitting Supine In mm/hg Systolic Diastolic Systolic Diastolic Systolic Diastolic Lt. Upper Rt. Upper

1) Shape of Chest wall 2) Other pulsation Para sternal Epigastric Supra sternal In the neck Second Left space On the right side

Ins

pect

ion

3) Dilated veins 4) Scars Sinuses 6) Others

1) Apex beat 2) Left Parasternal heave 3) Thrills

Palp

atio

n

4) Other pulsation

1) Left second & Intercostal space dullness 2) Upper border 3) Right border 4) Left border

Perc

ussi

on

5) Lower sternal resonance S1 S2 1) Heart sounds S3 S4

2) Murmur Systolic Diastolic Continuous 3) Rate 4) Rhythm

Aus

culta

tion

5) Other sounds Respiratory System: Inspection Palpation Percussion Auscultation

Abdomen: Inspection

Liver Palpation Spleen Percussion Auscultation

Special Case sheet


VI

Other systems (If any): 28) Laboratory investigations:

Before After Changes observed Serum Cholesterol Serum Triglycerides High Density Lipoprotein Low Density Lipoprotein Very Low DensityLipoprotein Serum Creatinine Fasting Blood Sugar Blood Urea

Other Investigations: Before After Changes observed

E.C.G.

Chest X -Ray

29) Chikitsa: Yoga: Shilajatu Guggulu Rasayana. Posology: 6 gms per day in three divided doses. Anupana: Warm Milk Medicine distributions/advises record: Day Date Systolic Diastolic Complaints if any advise

0

7

14

21

30

45

60

Special Case sheet


VII

Assessment Sheet Clinical Parameters During treatment schedule Follow up

F1 F2 a) Subjective 1 day 7 days 14 days 21 days 30 days 45 days 60 days

1. Bhrama 2. Klama 3. Shirah shoola 4. Moorcha 5. Daha

b) Objective Blood Pressure 1. Supine

2. Sitting

3. Standing

Average Systolic (SBP)

Average Diastolic (DBP)

Blood Pressure Grading Systolic (SBP)

Diastolic (DBP)

c) Lab Investigations BT AT Serum Cholesterol

Serum Triglycerides

High Density Lipoprotein

Low Density Lipoprotein

V.L.D.L.

Blood Urea

Serum Creatinine

Fasting Blood Glucose

E.C.G.

Chest X-Ray

Investigators note :- Signature of Guide: (Dr.R.V. Shettar)

Signature of Scholar: (Dr. Sanjeev Kumar)

Special Case sheet


VIII

Note:-

CLASSIFICATION SYSTOLIC (mm Hg) DIASTOLIC (mm Hg) Optimal <120 <80 Normal <130 <85 High normal 130-139 85-89 HYPERTENSION Stage I. HTN (Mild) 140-159 90-99 Stage II. HTN (Moderate) 160-179 100-109 Stage III. HTN (Severe) 180-209 110-119 Stage IV. HTN (Very Severe) >210 >120 Malignant HTN >200 >140

Joint National Committee of WHO/International society of HTN (ISH)

SUBJECTIVE PARAMETERS Criteria Score Particulars

0 No pain. 1 Pain tolerable. 2 Not disturb the normal work 3 Disturb the normal work

1) Shirah shoola

4 Intolerable. 0 No brama. 1 1-2 episodes in 24 hrs. 2 On physical work. 3 Continuous.

2) Bharama

4 Even at rest. 0 No klama. 1 Wishes to stand while walking. 2 Wishes to sit while standing. 3 Wishes to lie down while sitting.

3) Klama

4 Wishes to sleep while lying down. 0 Nil. 1 Mild. 2 Moderate. 3 Severe.

4) Daha

4 Extensive. 0 Nil. 1 Transient attack. 2 Unconscious not more than 2 to 3 second. 3 Unconscious less than 30 second.

5) Moorcha

4 Unconscious less than 1 minute. OBJECTIVE PARAMETERS

0 Normal. 1 Stage I (Mild). 2 Stage II (Moderate). 3 Stage III (Severe).

Blood Pressure

4 Stage IV (Very severe).

hypretension kc043 gdg

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