cardiovascular nursing

Lecture Notes on Cardiovascular System

Prepared By: Mark Fredderick R Abejo R.N, MAN

Medical and Surgical Nursing Abejo 1

MEDICAL AND SURGICAL NURSING

Cardiovascular System

Lecturer: Mark Fredderick R. Abejo RN, MAN

Anatomy and Physiology of the Heart

Cardiovascular system consists of the heart, arteries,

veins & capillaries. The major function are circulation of blood,

delivery of O2 & other nutrients to the tissues of the body &

removal of CO2 & other cellular products metabolism

Heart

Muscular pumping organ that propel blood into the arerial

system & receive blood from the venous system of the body.

Hollow muscular behind the sternum and between the lungs

Located on the middle of mediastinum

Resemble like a close fist

Weighs approximately 300 – 400 grams

Has heart wall has 3 layers

Endocardium – lines the inner chambers of the

heart, valves, chordate tendinae and papillary

muscles.

Myocardium – muscular layer, middle layer,

responsible for the major pumping action of the

ventricles.

Epicardium – thin covering(mesothelium),

covers the outer surface of the heart

Pericardium – invaginated sac

Visceral – attached to the exterior of

myocardium

Parietal – attached to the great vessels and

diaphragm

Papillary Muscle

Arise from the endocardial & myocardial surface of the

ventricles & attach to the chordae tendinae

Chordae Tendinae

Attach to the tricuspid & mitral valves & prevent eversion

during systole

Separated into 2 pumps:

right heart – pumps blood through the lungs

left heart – pumps blood through the peripheral

organs

Chamber of the Heart

Atria

2 chambers, function as receiving chambers, lies

above the ventricles




Upper Chamber (connecting or receiving)

Right Atrium: receives systemic venous blood

through the superior vena cava, inferior vena cava &

coronary sinus

Left Atrium: receives oxygenated blood returning to

the heart from the lungs trough the pulmonary veins

Ventricles

2 thick-walled chambers; major responsibility for

forcing blood out of the heart; lie below the atria

Lower Chamber (contracting or pumping)

Right Ventricle: contracts & propels deoxygenated

blood into pulmonary circulation via the aorta

during ventricular systole; Right atrium has

decreased pressure which is 60 – 80 mmHg

Left Ventricle: propels blood into the systemic

circulation via aortaduring ventricular systole; Left

ventricle has increased pressure which is 120 – 180

mmHg in order to propel blood to the systemic

circulation

Heart Valves

Tricuspid

Pulmonic

Mitral

Aortic

Coronary artery – 1st branch of aorta

Right Coronary

SA nodal Branch – supplies SA node

Right marginal Branch – supplies the right border

of the heart

AV nodal branch – supplies the AV node

Posterior interventricular artery – supplies both

ventricles

Left Coronary

Circumflex branch – supplies SA node in 40 % of

people

Left marginal – supplies the left ventricle

Anterior interventricular branch aka Left anterior

descending(LAD)–supplies both ventricles and

interventricular septum

Lateral branch – terminates in ant surface of the

heart

Coronary Veins

Coronary sinus – main vein of the heart

Great Cardiac vein – main tributary of the coronary sinus

Oblique vein – remnant of SVC, small unsignificant

Heart Circulation

Cardiac Conduction System

Properties of Heart Conduction System

• Automaticity

• Excitability

• Conductivity

• Contractility

Structure of Heart Conduction System

Nodal tissues

SA Node( Sino-atrial, Keith and Flack)

Primary Pacemaker

Between SVC and RA

Vagal and symphatetic innervation

Sinus Rhythms




AV Node( Atrioventricular , Kent and Tawara)

At the right atrium

3 zones

AN Zone(atrionodal)

N Zone (nodal)

NH zone (nodal –HIS)

Internodal and Interatrial Pathways

Connects SA and AV Node

Ant. Internodal(bachman) tract

Middle Internodal(wenkebach) tract

Posterior internodal(Thorel) tract

Bundle of His/ Purkinje Fibers

Provides for ventricular conduction system

Fastest conduction among cardiac tissues

Right bundle

Left Bundle

Cardiac Action Potential

Depolarization: electrical activation of a cell caused by

the influx of sodium into the cell while potassium exits

the cell

Repolarization: return of the cell to the resting state

caused by re-entry of potassium into the cell while

sodium exits

Refractory periods:

Effective refractory period: phase in which cells

are incapable of depolarizing

Relative refractory period: phase in which cells

require a stronger-than-normal stimulus to

depolarize

Anatomical Sequence of Excitation of the Heart

(right atrium)

sinoatrial node (SA)

(right AV valve)

atrioventricular node (AV)

atrioventricular bundle (bundle of His)

right & left bundle of His branches

Purkinje fibers of ventricular walls

(from SA through complete heart contraction = 220 ms = 0.22 s)

a. Sinoatrial node (SA node) "the pacemaker" - has the

fastest autorhythmic rate (70-80 per minute), and sets the

pace for the entire heart; this rhythm is called the sinus

rhythm; located in right atrial wall, just inferior to the

superior vena cava

b. Atrioventricular node (AV node) - impulses pass from

SA via gap junctions in about 40 ms.; impulses are

delayed about 100 ms to allow completion of the

contraction of both atria; located just above tricuspid

valve (between right atrium & ventricle)

c. Atrioventricular bundle (bundle of His) - in the

interATRIAL septum (connects L and R atria)

d. L and R bundle of His branches - within the

interVENTRICULAR septum (between L and R

ventricles)

e. Purkinje fibers - within the lateral walls of both the L and

R ventricles; since left ventricle much larger, Purkinjes

more elaborate here; Purkinje fibers innervate “papillary

muscles” before ventricle walls so AV can valves prevent

backflow

The Normal Cardiac Cycle

General Concepts

Systole - period of chamber contraction

Diastole - period of chamber relaxation

Cardiac cycle - all events of systole and diastole during one

heart flow cycle

Events of Cardiac Cycle

1. mid-to-late ventricular diastole: ventricles filled

the AV valves are open

pressure: LOW in chambers; HIGH in

aorta/pulmonary trunk

aortic/pulmonary semilunar valves CLOSED

blood flows from vena cavas/pulmonary vein INTO

atria

blood flows through AV valves INTO ventricles

(70%)

2. ventricular systole: blood ejected from heart

filled ventricles begin to contract, AV valves

CLOSE

contraction of closed ventricles increases pressure

ventricular ejection phase - blood forced out

semilunar valves open, blood -> aorta & pulmonary

trunk

3. isovolumetric relaxation: early ventricular diastole

ventricles relax, ventricular pressure becomes LOW

semilunar valves close, aorta & pulmonary trunk

backflow

TOTAL CARDIAC CYCLE TIME = 0.8 second

(normal 70 beats/minute)

atrial systole (contraction) = 0.1 second

ventricular systole (contraction) = 0.3 second

quiescent period (relaxation) = 0.4 second

Cardiac Output - Blood Pumping of the Heart

General Concepts

• Stroke volume: the amount of blood ejected with each

heartbeat

• Cardiac output: amount of blood pumped by the

ventricle in liters per minute

• Preload: degree of stretch of the cardiac muscle fibers at

the end of diastole

• Contractility: ability of the cardiac muscle to shorten in

response to an electrical impulse

• Afterload: the resistance to ejection of blood from the

ventricle

• Ejection fraction: the percent of end-diastolic volume

ejected with each heartbeat




General Variables of Cardiac Output

1. Cardiac Output (CO) - blood amount pumped per minute

CO (ml/min) = HR (beats/min) X SV (ml/beat)

Normal CO = 75 beats/min X 70 ml/beat

= 5.25 L/min

2. Heart Rate (HR) - cardiac cycles per minute

Normal range is 60-100 beats per minute

Tachycardia is greater than 100 bpm

Bradycardia is less than 60 bpm

Sympathetic system INCREASES HR

Parasympathetic system (Vagus) DECREASES HR

3. Blood pressure - Cardiac output X peripheral resistance

Control is neural (central and peripheral) and

hormonal

Baroreceptors in the carotid and aorta

Hormones- ADH, aldosterone, epinephrine can

increase BP; ANF can decrease BP

Regulation of Stroke Volume (SV)

End diastolic volume (EDV) - total blood collected in

ventricle at end of diastole; determined by length of

diastole and venous pressure (~ 120 ml)

End systolic volume (ESV) - blood left over in ventricle

at end of contraction (not pumped out); determined by

force of ventricle contraction and arterial blood pressure

(~50 ml)

SV (ml/beat) = EDV (ml/beat) - ESV (ml/beat)

Normal SV = 120 ml/beat - 50 ml/beat = 70 ml/beat

Frank-Starling Law of the Heart - critical factor for stroke

volume is "degree of stretch of cardiac muscle cells";

more stretch = more contraction force

increased EDV = more contraction force

slow heart rate = more time to fill

exercise = more venous blood return

Regulation of Heart Rate (Autonomic, Chemical, Other)

1. Autonomic Regulation of Heart Rate (HR)

Sympathetic - NOREPINEPHRINE (NE) increases heart

rate (maintains stroke volume which leads to increased

Cardiac Output)

Parasympathetic - ACETYLCHOLINE (ACh) decreases

heart rate

Vagal tone - parasympathetic inhibition of inherent rate

of SA node, allowing normal HR

Baroreceptors, pressoreceptors - monitor changes in

blood pressure and allow reflex activity with the

autonomic nervous system

2. Hormonal and Chemical Regulation of Heart Rate (HR)

epinephrine - hormone released by adrenal medulla

during stress; increases heart rate

thyroxine - hormone released by thyroid; increases heart

rate in large quantities; amplifies effect of epinephrine

Ca++, K+, and Na+ levels very important;

hyperkalemia - increased K+ level; KCl used to

stop heart on lethal injection

hypokalemia - lower K+ levels; leads to

abnormal heart rate rhythms

hypocalcemia - depresses heart function

hypercalcemia - increases contraction phase

hypernatremia - HIGH Na+ concentration; can

block Na+ transport & muscle contraction

3. Other Factors Effecting Heart Rate (HR)

normal heart rate - fetus 140 - 160 beats/minute

female 72 - 80 beats/minute

male 64 - 72 beats/minute

1. exercise - lowers resting heart rate (40-60)

2. heat - increases heart rate significantly

3. cold - decreases heart rate significantly

4. tachycardia - HIGHER than normal resting heart rate

(over 100); may lead to fibrillation

5. bradycardia - LOWER than normal resting heart rate

(below 60); parasympathetic drug side effects; physical

conditioning; sign of pathology in non-healthy patient

Vascular System

Major function of the blood vessels isto supply the tissue

with blood, remove wastes, & carry unoxygenated blood

back to the heart

Types of Blood Vessels

Arteries

Elastic-walled vessels that can stretch during systole &

recoil during diastole; they carry blood away from the

heart & distribute oxygenated blood throughout the body

Arterioles

Small arteries that distribute blood to the capillaries &

function in controlling systemic vascular resistance &

therefore arterial pressure

Capilliaries

The following exchanges occurs in the capilliaries

O2 & CO2

Solutes between the blood & tissue

Fluid volume transfer between the plasma &

interstitial space

Venules

Small veins that receive blood from capillaries &

function as collecting channels between the capillaries &

veins

Veins

Low-pressure vessels with thin small & less muscles than

arteries; most contains valves that prevent retrograde

blood flow; they carry deoxygenated blood back to the

heart. When the skeletal surrounding veins contract, the

veins are compressed, promoting movement of blood

back to the heart.




Assessment of the Client with Cardiovascular

Disorders

Nursing History

Risk Factors

A. Non – Modifiable Risk Factor

Age

Gender

Race

Heredity

B. Modifiable Risk Factor

Stress

Diet

Exercise

Sedentary lifestyle

Cigarette smoking

Alcohol

Hypertension

Hyperlipidemia

DM

Obesity

Type A personality

Contraceptive Pills

Common Clinical Manifestations of Cardiovascular Disorders

a. Dyspnea

- Exertional

- Orthopnea

- Paroxysmal Noctural Dyspnea

- Cheyne-stokes

b. Chest Pain

c. Edema

- Ascites

- Hydrothorax

- Anasarca

d. Palpitation

e. Hemoptysis

f. Fatigue

g. Syncope and Fainting

h. Cyanosis

i. Abdominal Pain

j. Clubbing of fingers

k. Jaundice

Physical Assessment

Inspection:

– Skin color

– Neck vein distention

– Respirations

– Pulsations

– Clubbing

– Capillary refill

Palpation:

Heart Sounds: Stethoscope Listening

Overview of Heart Sounds (lub-du ; lub, dub )

lub - closure of AV valves, onset of ventricular systole

dub - closure of semilunar valves, onset of diastole

Tricuspid valve (lub) - RT 5th intercostal, medial

Mitral valve (lub) - LT 5th intercostal, lateral

Aortic semilunar valve (dub) - RT 2nd intercostal

Pulmonary semilunar valve (dub) - LT 2nd intercostals

S1 - due to closure of the AV(mitral/tricuspid) valves

- timing: beginning of systole

- loudest at the apex

S2 - due to the closure of the semi-lunar (pulmonic/aortic) valves

- timing: diastole

- loudest at the base

S3 – Ventricular Diastolic Gallop

Mechanism: vibration resulting from resistance to rapid

ventricular filling secondary to poor compliance

Timing: early diastole

Location: Apex (LV) or LLSB (RV)

Pitch: faint and low pitched

S4 - Atrial Diastolic Gallop

Mechanism: vibration resulting from resistance to late

ventricular filling during atrial systole

Timing: late diastole ( before S1)

Location: Apex ( LV) or LLSB (RV)

Pitch: low ( use bell)

Heart Murmurs

Murmur - sounds other than the typical "lub-dub"; typically caused

by disruptions in flow

Incompetent valve - swishing sound just AFTER the

normal "lub" or "dub"; valve does not completely close,

some regurgitation of blood

Stenotic valve - high pitched swishing sound when blood

should be flowing through valve; narrowing of outlet in

the open state

Pericardial Friction Rub

It is an extra heart sound originating from the pericardial sac

Mechanism: Originates from the pericardial sac as it moves

Timing: with each heartbeat




Location: over pericardium. Upright position, leaning

forward

Pitch: high pitched and scratchy. Sounds like sandpaper

being rubbed together

Significance: inflammation, infection, infiltration

Classification of Clients with Diseases of the

Heart ( Functional Capacity )

Class I. Patients with cardiac disease but without

resulting limitations of physical activity.

Class II. Patients with cardiac disease resulting to slight

limitation of physical activity

Class III. Patients with cardiac disease resulting in

marked limitation of physical activity. They are

comfortable at rest.

Class IV. Patients with cardiac disease resulting in

inability to carry on any physical activity without

discomfort

Diagnostic Assessment

Purposes:

1. To assist in diagnosing MI

2. To identify abnormalities

3. To assess inflammation

4. To determine baseline value

5. To monitor serum level of medications

6. To assess the effects of medications

A. Blood Studies

1. Complete Blood Count

a. RBC count- # of RBCs/ mm3 of blood, to diagnose anemia and

ploycythemia

b. Hemoglobin- # of grams of hgb/ 100ml of blood; to measure the

oxygen-carrying capacity of the blood

c. Hematocrit – expressed in %; measures the volume of RBCs in

proportion to plasma; used also to diagnose anemia and

polycythemia and abnormal hydration states

d. RBC indices- measure RBC size and hemoglobin content

a. MCV (mean corpuscular volume)

b. MCH (mean corpuscular hemoglobin)

c. MCHC (mean corpuscular hemoglobin concentrarion)

e. Platelet count- # of Platelet/ mm3; to diagnose

thrombocytopenia and subsequent bleeding tendencies

f. WBC count- of WBCs/ mm3 of blood; to detect infection or

inflammation

g. WBC Differential count- determines proportion of each WBC

in a sample of 100 WBCs; used to classify leukemias

Normal Values

RBC: Women – 4.2-5.4 million/mm3

Men – 4.7-6.1 million/mm3

Hgb: Women – 12-16 g/dl

Men – 13-18 g/dl

Hct : Women – 36-42%

Men – 42-48%

WBC: 5000-10,000/mm3

Granulocytes Neutrophils: 55-70%

Eosinophils: 1-4%

Basophils: 0.5-1.0%

Agranulocytes Lymphocytes: 20-40%

Monocytes: 2-8%

Platelets: 150,000-450,000/mm3

2. Coagulation Screening Test

a. Bleeding Time – measures the ability to stop bleeding after

small puncture wound

b. Partial Thromboplastin Time (PTT) – used to identify

deficiencies of coagulation factors, prothrombin and fibrinogen;

monitors heparin therapy.

c. Prothrombin Time (Pro-time) – determines activity and

interaction of the Prothrombin group: factors V (preacclerin), VII

(proconvertin), X (Stuart-Power factor), prothrombin and

fibrinogen; used to determine dosages of oral anti-coagulant.

Normal Values

Bleeding Time: 2.75-8 min

Partial Thromboplastin Time (PTT): 60 - 70 sec.

Prothrombin Time (PT): 12-14 sec.

3. Erythrocyte sedimentation rate ( ESR)

It is a measurement of the rate at which RBC’s settle out

of anticoagulated blood in an hour

It is elevated in infectious heart disorder or myocardial

infarction

Normal Values

Male: 15-20 mm/hr

Female: 20-30 mm/hr

4. CARDIAC Proteins and enzymes

a. CK- MB ( creatine kinase)

Most cardiac specific enzymes

Accurate indicator of myocardial dammage

Elevates in MI within 4 hours, peaks in 18 hours and

then declines till 3 days

Normal value is 0-7 U/L or males 50-325 mu/ml

Female 50-250 mu/ml

b. Lactic Dehydrogenase (LDH)

Most sensitive indicator of myocardial damage

Elevates in MI in 24 hours, peaks in 48-72 hours

Return to normal in 10-14 days

Normally LDH1 is greater than LDH2

Lactic Dehydrogenase (LDH)

MI- LDH2 greater than LDH1 (flipped LDH pattern)

Normal value is 70-200 IU/L (100 – 225 mu/ml)

c. Myoglobin

Rises within 1-3 hours

Peaks in 4-12 hours

Returns to normal in a day

Not used alone

Muscular and RENAL disease can have elevated

myoglobin

d. Troponin I and T

Troponin I is usually utilized for MI

Elevates within 3-4 hours, peaks in 4-24 hours and

persists for 7 days to 3 weeks!

Normal value for Troponin I is less than 0.6 ng/mL

REMEMBER to AVOID IM injections before

obtaining blood sample!

Early and late diagnosis can be made!

e. SERUM LIPIDS

Lipid profile measures the serum cholesterol,

triglycerides and lipoprotein levels

Cholesterol= 200 mg/dL

Triglycerides- 40- 150 mg/dL

LDH- 130 mg/dL

HDL- 30-70- mg/dL

NPO post midnight (usually 12 hours)




B. Non-Invasive Procedure

1. Cardiac Monitoring / Electrocardiography (ECG)

A non-invasive procedure that evaluates the electrical

activity of the heart

a. Limb Leads

b. Precordial Leads

The precordial leads VI –V6 are part of the 12 lead EKG.

They are not monitored with the standard limb leads

c. 12 lead ECG

ECG Paper

Deflection Waves of ECG

1. P wave - initial wave, demonstrates the depolarization from SA

Node through both ATRIA; the ATRIA contract about 0.1 s after

start of P Wave.

2. QRS complex - next series of deflections, demonstrates the

depolarization of AV node through both ventricles; the ventricles

contract throughout the period of the QRS complex, with a short

delay after the end of atrial contraction; repolarization of atria also

obscured

3. T Wave - repolarization of the ventricles (0.16 s)

4. PR (PQ) Interval - time period from beginning of atrial

contraction to beginning of ventricular contraction (0.16 s)

5. QT Interval - the time of ventricular contraction (about 0.36 s);

from beginning of ventricular depolarization to end of

repolarization.

2. Holter Monitoring

A non-invasive test in which the client wears a Holter

monitor and an ECG tracing recorded continuously over

a period of 24 hours

Instruct the client to resume normal activities and

maintain a diary of activities and any symptoms that may

develop




3. Stress Test

A non-invasive test that studies the heart during

activity and detects and evaluates CAD

Exercise test, pharmacologic test and emotional test

Treadmill testing is the most commonly used stress

test

Used to determine CAD, Chest pain causes, drug

effects and dysrhythmias in exercise

Pre-test: consent may be required, adequate rest , eat

a light meal or fast for 4 hours and avoid smoking,

alcohol and caffeine

During the test: secure electrodes to appropriate

location on chest, obtain baseline BP and ECG

tracing, instruct client to exercise as instructed and

report any pain, weakness and SOB, monitor BP and

ECG continuously, record at frequent interval

Post-test: instruct client to notify the physician if

any chest pain, dizziness or shortness of breath .

Instruct client to avoid taking a hot shower for 10-12

hours after the test

4. Pharmacological stress test

Use of dipyridamole

Maximally dilates coronary artery

Side-effect: flushing of face

Pre-test: 4 hours fasting, avoid alcohol, caffeine

Post test: report symptoms of chest pain

5. ECHOCARDIOGRAM

Non-invasive test that studies the structural and

functional changes of the heart with the use of ultrasound

Client Preparation: instruct client to remain still during

the test, secure electrodes for simultaneous ECG tracing,

explain that there will be no pain or electrical shock,

lubricant placed on the skin will be cool.

6. Phonocardiography

Is a graphic recording of heart sound with simultaneous

ECG.

C. Invasive Procedure

1. Cardiac Catheterization ( Coronary Angiography /

Arteriography )

Insertion of a catheter into the heart and surrounding

vessels

Is an invasive procedure during which physician

injects dye into coronary arteries and immediately

takes a series of x-ray films to assess the structures

of the arteries

Determines the structure and performance of the

heart valves and surrounding vessels

Used to diagnose CAD, assess coronary atery

patency and determine extent of atherosclerosis

Pretest: Ensure Consent, assess for allergy to

seafood and iodine, NPO, document weight and

height, baseline VS, blood tests and document the

peripheral pulses

Pretest: Fasting for 8-12 hours, teachings,

medications to allay anxiety

Intra-test: inform patient of a fluttery feeling as the

catheter passes through the heart; inform the patient

that a feeling of warmth and metallic taste may

occur when dye is administered

Post-test: Monitor VS and cardiac rhythm

Monitor peripheral pulses, color and warmth and

sensation of the extremity distal to insertion site

Maintain sandbag to the insertion site if required to

maintain pressure

Monitor for bleeding and hematoma formation

2. Nuclear Cardiology

Are safe methods of evaluating left ventricular muscle

function and coronary artery blood distribution.

Client Preparation: obtain written consent, explain

procedure, instruct client that fasting may be required for

a short period before the exam, assess for iodine allergy.

Post Procedure: encourage client to drink fluids to

facilitate the excretion of contrast material, assess

venipuncture site for bleeding or hematoma.

Types of Nuclear Cardiology

o Multigated acquisition (MUGA) or cardiac

blood pool scan

Provides information on wall motion

during systole and diastole, cardiac

valves, and EF.

o Single-photon emission computed

tomography (SPECT)

Used to evaluate the myocardium at

risk of infarction and to determine

infarction size.

o Positron emission tomography (PET)

scanning

Uses two isotopes to distinguish

viable and nonviable myocardial

tissue.




o Perfusion imaging with exercise testing

Determines whether the coronary

blood flow changes with increased

activity.

Used to diagnose CAD, determine

the prognosis in already diagnosed

CAD, assess the physiologic

significance of a known coronary

lesion, and assess the effectiveness of

various therapeutic modalities such

as coronary artery bypass surgery,

percutaneous coronary intervention,

or thrombolytic therapy.

D. Hemodynamics Monitoring

1. CVP ( Central Venous Pressure )

Reflects the pressure of the blood in the right atrium.

Engorgement is estimated by the venous column that can

be observed as it rises from an imagined angle at th point

of manubrium ( angle of Louis).

With normal physiologic condition, the jugular venous

column rises no higher than 2-3 cm above the clavicle

with the client in a sitting position at 45 degree angle.

CVP is a measurement of:

- cardiac efficiency

- blood volume

- peripheral resistance

Right ventricular pressure – a catheter is passed from a

cutdown in the antecubital, subclavian jugular or basilica

vein to the right atrium and attached to a prescribed

manometer or tranducer.

NORMAL CVP is 2 -8 cm h20 or 2-6 mm Hg Decrease indicates dec. circulating volume, increase

indicates inc. blood volume or right heart beat failure.

To Measure: patient should be flat with zero point of

manometer at the same level of the RA which

corresponds to the mid-axillary line of the patient or

approx. 5 cm below the sternum.

Fluctuations follow patients respiratory function and will

fall on inspiration and rise on expiration due to changes

in intrapulmonary pressure. Reading should be obtained

at the highest point of fluctuation.

2. Pulmonary Artery Pressure ( PAP) Monitoring

Appropriate for critically ill clients requiring more

accurate assessments of the left heart pressure

Swan-Ganz Catheter / Pulmonary Artery Catheter is use

Client Preparation: obtain consent, insertion is under

strict sterile technique, usually at the bedside, explain to

client the sterile drapes may cover the face, assists to

position client flat or slight T-postion as tolerated and

instruct to remain still during the procedure

Nursing Care During Insertion: Monitor and document

HR,BP and ECG during the procedure

CARDIAC DISORDER

CORONARY ARTERIAL DISEASE

ISCHEMIC HEART DISEASE

Results from the focal narrowing of the large and

medium-sized coronary arteries due to deposition of atheromatous

plaque in the vessel wall

Stages of Development of Coronary Artery Disease 1. Myocardial Injury: Atherosclerosis

2. Myocardial Ischemia: Angina Pectoris

3. Myocardial Necrosis: Myocardial Infarction

I. ATHEROSCLEROSIS

ATHEROSCLEROSIS ARTERIOSCLEROSIS

Narrowing of artery

Lipid or fat deposits

Tunica intima

Hardening of artery

Calcium and protein

deposits

Tunica media

A. PRESDISPOSING FACTORS 1. Sex: male

2. Race: black

3. Smoking

4. Obesity

5. Hyperlipidemia

6. Sedentary lifestyle

7. Diabetes Mellitus

8. Hypothyroidism

9. Diet: increased saturated fats

10. Type A personality

B. SIGNS AND SYMPTOMS

1. Chest pain

2. Dyspnea

3. Tachycardia

4. Palpitations

5. Diaphoresis

C. TREATMENT

Percutaneous Transluminal Coronary Angioplasty and

Intravascular Stenting

Mechanical dilation of the coronary vessel wall by

compresing the atheromatous plaque.

It is recommended for clients with single-vessel

coronary artery disease.




Prosthetic intravascular cylindric stent maintain

good luminal geometry after ballon deflation and

withdrawal.

Intravascular stenting is done to prevent restenosis

after PTCA

Coronary Arterial Bypass Graft Surgery

Greater and lesser saphenous veins are commonly used for

bypass graft procedures

Objectives of CABG

1. Revascularize myocardium

2. To prevent angina

3. Increase survival rate

4. Done to single occluded vessels

5. If there is 2 or more occluded blood vessels CABG is

done

Nursing Management:

Nitroglycerine is the drug of choice for relief of pain

from acute ischemic attacks

Instruct to avoid over fatigue

Plan regular activity program

For Saphenous Vein Site:

Wear support stocking 4-6 week postop

Apply pressure dressing or sand bag on the site

Keep leg elevated when sitting

3 Complications of CABG

1. Pneumonia: encourage to perform deep breathing,

coughing exercise and use of incentive spirometer

2. Shock

3. Thrombophlebitis

II. ANGINA PECTORIS

Transient paroxysmal chest pain produced by insufficient

blood flow to the myocardium resulting to myocardial

ischemia

Clinical syndrome characterized by paroxysmal chest

pain that is usually relieved by rest or nitroglycerine due

to temporary myocardial ischemia

Types of Angina Pectoris

Stable Angina: pain less than 15 minutes, recurrence is less

frequent.

Unstable Angina : pain is more than 15 mins.,but not less

than 30 minutes, recurrence is more frequent and the

intensity of pain increases.

Variant Angina ( Prinzmetal’s Angina ): Chest pain is on

longer duration and may occur at rest. Result from coronary

vasospasm.

Angina Decubitus: paroxysmal chest pain that occur when

the client sits or stand.

A. PRESDISPOSING FACTORS 1. Sex: male

2. Race: black

3. Smoking

4. Obesity

5. Hyperlipidemia



8. Hypertension

9. CAD: Atherosclerosis

10. Thromboangiitis Obliterans

11. Severe Anemia

12. Aortic Insufficiency: heart valve that fails to open &

close efficiently

13. Hypothyroidism



B. PRESIPITATING FACTORS

4 E’s of Angina Pectoris

1. Excessive physical exertion: heavy exercises, sexual

activity

2. Exposure to cold environment: vasoconstriction

3. Extreme emotional response: fear, anxiety,

excitement, strong emotions

4. Excessive intake of foods or heavy meal

C. SIGNS AND SYMPTOMS 1. Levine’s Sign: initial sign that shows the hand

clutching the chest

2. Chest pain: characterized by sharp stabbing pain

located at sub sterna usually radiates from neck,

back, arms, shoulder and jaw muscles usually

relieved by rest or taking nitroglycerine(NTG)

3. Dyspnea

4. Tachycardia

5. Palpitations

6. Diaphoresis




D. DIAGNOSTIC PROCEDURE 1. History taking and physical exam

2. ECG: may reveals ST segment depression & T wave

inversion during chest pain

3. Stress test / treadmill test: reveal abnormal ECG

during exercise

4. Increase serum lipid levels

5. Serum cholesterol & uric acid is increased

E. MEDICAL MANAGEMENT 1. Drug Therapy: if cholesterol is elevated

Nitrates: Nitroglycerine (NTG)

Beta-adrenergic blocking agent: Propanolol

Calcium-blocking agent: nefedipine

Ace Inhibitor: Enapril

2. Modification of diet & other risk factors

3. Surgery: Coronary artery bypass surgery

4. Percutaneuos Transluminal Coronary Angioplasty

(PTCA)

F. NURSING INTERVENTIONS 1. Enforce complete bed rest

2. Give prompt pain relievers with nitrates or narcotic

analgesic as ordered

3. Administer medications as ordered:

A. Nitroglycerine(NTG): when given in small

doses will act as venodilator, but in large doses

will act as vasodilator

Give 1st dose of NTG: sublingual 3-5

minutes

Give 2nd dose of NTG: if pain persist after

giving 1st dose with interval of 3-5

minutes

Give 3rd& last dose of NTG: if pain still

persist at 3-5 minutes interval

NTG Tablets(sublingual)

Keep the drug in a dry place, avoid

moisture and exposure to sunlight as it

may inactivate the drug

Change stock every 6 months

Offer sips of water before giving

sublingual nitrates, dryness of mouth may

inhibit drug absoprtion

Relax for 15 minutes after taking a tablet:

to prevent dizziness

Monitor side effects: orthostatic

hypotension, flushed face. Transient

headache & dizziness: frequent side effect

Instruct the client to rise slowly from

sitting position

Assist or supervise in ambulation

NTG Nitrol or Transdermal patch

Nitropatch is applied once a day, usually

in the morning.

Avoid placing near hairy areas as it may

decrease drug absorption

Avoid rotating transdermal patches as it

may decrease drug absorption

Avoid placing near microwave ovens or

during defibrillation as it may lead to

burns (most important thing to remember)

B. Beta-blockers: decreases myocardial oxygen

demand by decreasing heart rate, cardiac output

and BP

Propanolol

Metropolol

Pindolol

Atenolol

Assess PR, withhold if dec.PR

Administer with food ( prevent GI upset )

Propanolol: not given to COPD cases: it causes

bronchospasm and DM cases: it cause

hypoglycemia

Side Effects: Nausea and vomiting, mental

depression and fatigue

C. Calcium – Channel Blockers: relaxes smooth

cardiac muscle, reduces coronary vasospasm

Amlodipine ( norvasc )

Nifedipine ( calcibloc )

Diltiazem ( cardizem )

Assess HR and BP

Adminester 1 hour before meal and 2 hours

after meal ( foods delay absorption )

4. Administer oxygen inhalation

5. Place client on semi-to high fowlers position

6. Monitor strictly V/S, I&O, status of

cardiopulmonary fuction & ECG tracing

7. Provide decrease saturated fats sodium and caffeine

8. Provide client health teachings and discharge

planning

Avoidance of 4 E’s

Prevent complication (myocardial infarction)

Instruct client to take medication before

indulging into physical exertion to achieve the

maximum therapeutic effect of drug

Reduce stress & anxiety: relaxation techniques

& guided imagery

Avoid overexertion & smoking

Avoid extremes of temperature

Dress warmly in cold weather

Participate in regular exercise program

Space exercise periods & allow for rest periods

The importance of follow up care

9. Instruct the client to notify the physician

immediately if pain occurs & persists despite rest &

medication administration

III. MYOCARDIAL INFARCTION

Death of myocardial cells from inadequate oxygenation,

often caused by sudden complete blockage of a coronary

artery

Characterized by localized formation of necrosis (tissue

destruction) with subsequent healing by scar formation &

fibrosis

Heart attack

Terminal stage of coronary artery disease characterized

by malocclusion, necrosis & scarring.

Types of M.I

Transmural Myocardial Infarction: most dangerous type

characterized by occlusion of both right and left coronary

artery

Subendocardial Myocardial Infarction: characterized by

occlusion of either right or left coronary artery

The Most Critical Period Following Diagnosis of

Myocardial Infarction

6-8 hours because majority of death occurs due to

arrhythmia leading to premature ventricular contractions

(PVC)

A. PREDISPOSING FACTORS 1. Sex: male

2. Race: black

3. Smoking

4. Obesity

5. CAD: Atherosclerotic

6. Thrombus Formation

7. Genetic Predisposition

8. Hyperlipidemia






11. Hypothyroidism



B. SIGNS AND SYMPTOMS 1. Chest pain

Excruciating visceral, viselike pain with sudden

onset located at substernal& rarely in

precordial

Usually radiates from neck, back, shoulder,

arms, jaw & abdominal muscles (abdominal

ischemia): severe crushing

Not usually relieved by rest or by

nitroglycerine

2. N/V

3. Dyspnea

4. Increase in blood pressure & pulse, with gradual

drop in blood pressure (initial sign)

5. Hyperthermia: elevated temp

6. Skin: cool, clammy, ashen

7. Mild restlessness & apprehension

8. Occasional findings:

Pericardial friction rub

Split S1& S2

Rales or Crackles upon auscultation

S4 or atrial gallop

C. DIAGNOSTIC PROCEDURED

1. Cardiac Enzymes

CPK-MB: elevated

Creatinine phosphokinase(CPK):elevated

Heart only, 12 – 24 hours

Lactic acid dehydrogenase(LDH): is increased

Serum glutamic pyruvate transaminase(SGPT):

is increased

Serum glutamic oxal-acetic

transaminase(SGOT): is increased

2. Troponin Test: is increased

3. ECG tracing reveals

ST segment elevation

T wave inversion

Widening of QRS complexes: indicates that

there is arrhythmia in MI

4. Serum Cholesterol & uric acid: are both increased

5. CBC: increased WBC

D. NURSING INTERVENTIONS

Goal: Decrease myocardial oxygen demand

1. Decrease myocardial workload (rest heart)

Establish a patent IV line

Administer narcotic analgesic as ordered: Morphine

Sulfate IV: provide pain relief(given IV because

after an infarction there is poor peripheral perfusion

& because serum enzyme would be affected by IM

injection as ordered)

Side Effects: Respiratory Depression

Antidote: Naloxone (Narcan)

Side Effects of Naloxone Toxicity: is tremors

2. Administer oxygen low flow 2-3 L / min: to prevent

respiratory arrest or dyspnea & prevent arrhythmias

3. Enforce CBR in semi-fowlers position without bathroom

privileges(use bedside commode): to decrease cardiac

workload

4. Instruct client to avoid forms of valsalva maneuver

5. Place client on semi fowlers position

6. Monitor strictly V/S, I&O, ECG tracing & hemodynamic

procedures

7. Perform complete lung / cardiovascular assessment

8. Monitor urinary output & report output of less than 30 ml

/ hr: indicates decrease cardiac output

9. Provide a full liquid diet with gradual increase to soft diet:

low in saturated fats, Na & caffeine

10. Maintain quiet environment

11. Administer stool softeners as ordered:to facilitate bowel

evacuation & prevent straining

12. Relieve anxiety associated with coronary care

unit(CCU)environment

13. Administer medication as ordered:

a. Vasodilators:Nitroglycirine (NTG), Isosorbide

Dinitrate, Isodil (ISD): sublingual

b. Anti Arrythmic Agents: Lidocaine (Xylocane),

Brithylium

Side Effects: confusion and dizziness

c. Beta-blockers: Propanolol (Inderal)

d. ACE Inhibitors: Captopril (Enalapril)

e. Calcium Antagonist: Nefedipine

f. Thrombolytics / Fibrinolytic Agents: Streptokinase,

Urokinase, Tissue Plasminogen Activating Factor

(TIPAF)

Side Effects:allergic reaction, urticaria, pruritus

Nursing Intervention: Monitor for bleeding

time

g. Anti Coagulant

Heparin

Antidote: Protamine Sulfate

Nursing Intervention: Check for Partial

Thrombin Time (PTT)

Caumadin(Warfarin)

Antidote:Vitamin K

Nursing Intervention: Check for

Prothrombin Time (PT)

h. Anti Platelet: PASA (Aspirin): Anti thrombotic

effect

Side Effects:Tinnitus, Heartburn, Indigestion /

Dyspepsia

Contraindication:Dengue, Peptic Ulcer Disease,

Unknown cause of headache

14. Provide client health teaching & discharge planning

concerning:

a. Effects of MI healing process & treatment regimen

b. Medication regimen including time name purpose,

schedule, dosage, side effects

c. Dietary restrictions: low Na, low cholesterol,

avoidance of caffeine

d. Encourage client to take 20 – 30 cc/week of wine,

whisky and brandy:to induce vasodilation

e. Avoidance of modifiable risk factors

f. Prevent Complication

Arrhythmia: caused by premature ventricular

contraction

Cardiogenic shock: late sign is oliguria

Left Congestive Heart Failure

Thrombophlebitis: homan’s sign

Stroke / CVA

Dressler’s Syndrome(Post MI Syndrome):client

is resistant to pharmacological agents:

administer 150,000-450,000 units of

streptokinase as ordered

g. Importance of participation in a progressive activity

program

h. Resumption of ADL particularly sexual intercourse:

is 4-6 weeks post cardiac rehab, post CABG &

instruct to:




Make sex as an appetizer rather than dessert

Instruct client to assume a non weight bearing

position

Client can resume sexual intercourse: if can

climb or use the staircase

i. Need to report the ff s/sx:

Increased persistent chest pain

Dyspnea

Weakness

Fatigue

Persistent palpitation

Light headedness

j. Enrollment of client in a cardiac rehabilitation

program

k. Strict compliance to mediation & importance of

follow up care

IV. CARDIOGENIC SHOCK ( POWER/PUMP FAILURE )

Is a shock state which result from profound left

ventricular failure usually from massive MI.

It result to low cardiac output, thereby systemic

hypoperfusion.

A. SIGNS AND SYMPTOMS

1. Decrease systolic BP

2. Oliguria

3. Cold, clammy skin

4. Weak pulse

5. Cyanosis

6. Mental lethargy

7. Confusion

B. MEDICAL MANAGEMENT

1. Counterpulsation ( mechanical cardiac assistance /

diastolic augmentation )

Involves introduction of the intra – aortic

balloon catheter via the femoral artery

Intra Aortic Balloon Pump augments

diastole, resulting in increased perfusion

of the coronary arteries and the

myocardium and a decrease in left

ventricular workload.

The balloon is inflated during diastole, it

is deflated during sytole.

Indications:

Cardiogenic shock

AMI

Unstable Angina

Open heart surgery

C. NURSING INTERVENTIONS

1. Perform hemodynamic monitoring

2. Administer oxygen therapy

3. Correct hypovolemia. Administer IV fluids as

ordered

4. Pharmacology:

a. Vasodilators: Nitroglycerine

b. Inotropic agents:Digitalis, Dopamine

c. Diuretics : Furosemide

d. Sodium Bicarbonate, Relieve lactic acidosis

5. Monitor hourly urine output, LOC and arrhythmias

6. Provide psychosocial support

7. Decrease pulmonary edema

a. Auscultate lung fields for crackles and wheezes

b. Note for dyspnea, cough , hemoptysis and

orthopnea

c. Monitor ABG for hypoxia and metabolic

acidosis

d. Place in fowler’s position to reduce venous

return

e. Administer during therapy as ordered:

Morphine sulfate to reduce venous

return.

Aminophylline to reduce

bronchospasm caused by severe

congestion.

Vasodilators to reduce venous return

Diuretics to decrease circulating

volume

V. PERICARDITIS / DRESSLER’S SYNDROME

Is the inflammation of the pericardium which occurs

approximately 1 – 6 weeks after AMI.

Results as an antigen – antibody response. The necrotic

tissues play the role of an antigen, which trigger antibody

formation. Inflammatory process follows.

Constrictive Pericarditis is a condition in which a chronic

inflammatory thickening of the pericardium compresses

the heart so that it is unable to fill normally during

diastole.

A. SIGNS AND SYMPTOMS

1. Pain in the anterior chest, aggravated by coughing,

yawning, swallowing, twisting and turning the torso,

relieved by upright, leaning forward position.

2. Pericardial friction rub – scratchy, grating or

cracking sound

3. Dyspnea

4. Fever, sweating, chills

5. Joints pains

6. Arrhythmias

B. NURSING INTERVENTIONS

1. Elevate head of bed, place pillow on the overbed

table so that the patient can lean on it.

2. Bed rest

3. Administer prescribed pharmacotherapy.

a. ASA to suppress inflammatory process

b. Corticosteriods for more severe symptoms

4. Assist in pericardiocentesis if cardiac tamponade is

present.

5. Pericardiocentesis is aspiration of blood or fluid

from pericardial sac.

VI. CARDIAC TAMPONADE

Also known as pericardial tamponade, is an emergency

condition in which fluid accumulates in the pericardium

(the sac in which the heart is enclosed).

If the fluid significantly elevates the pressure on the heart

it will prevent the heart's ventricles from filling properly.

This in turn leads to a low stroke volume.

The end result is ineffective pumping of blood, shock,

and often death.

A. PREDISPOSING FACTORS

1. Chest trauma ( blunt or penetrating )

2. Myocardial ruptured

3. Cancer

4. Pericarditis

5. Cardiac surgery ( first 24 – 48 hours )

6. Thrombolytic therapy


1. Beck’s Triad Hypotension

Jugular venous distension

Muffled heart sound

2. Pulsus paradoxus ( drop of at least 10 mmHg in

arterial BP on inspiration )

3. Tachycardia

4. Breathlessness

5. Decrease in LOC




C. NURSING INTERVENTIONS

1. Administer oxygen

2. Elevate head of bed, place pillow on the overbed

table so that the patient can lean on it.

3. Bed rest

4. Administer prescribed pharmacotherapy.

c. ASA to suppress inflammatory process

d. Corticosteriods for more severe symptoms

5. Assist in pericardiocentesis and thoracotomy

6. Pericardiocentesis is aspiration of blood or fluid

from pericardial sac.

CONGESTIVE HEART FAILURE

Inability of the heart to pump blood towards systemic

circulation

I. LEFT-SIDED HEART FAILURE


1. 90% - Mitral valve stenosis

RHD

Inflammation of mitral valve

Anti-streptolysin O titer (ASO) – 300 todd

units

Penicillin, PASA, steroids

Aging

2. MI

3. IHD

4. HPN

5. Aortic valve stenosis


1. Pulmonary edema/congestion

Dyspnea, PND (awakening at night d/t

difficulty in breathing), 2-3 pillow orthopnea

Productive cough (blood tinged)

Rales/crackles

Bronchial wheezing

Frothy salivation

2. Pulsus alternans (A unique pattern during which the

amplitude of the pulse changes or alternates in size

with a stable heart rhythm.)This is common in

severe left ventricular dysfunction.)

3. Anorexia and general body malaise

4. PMI displaced laterally, cardiomegaly

5. S3 (ventricular gallop)

C. DIAGNOSTICS

1. CXR – cardiomegaly

2. PAP – pulmonary arterial pressure

Measures pressure in right ventricle

Reveals cardiac status

3. PCWP – pulmonary capillary wedge pressure

Measures end-systolic and end-diastolic

pressure (elevated)

Done through cardiac catheterization (Swan-

Ganz)

4. Echocardiograph – reveals enlarged heart chamber

5. ABG analysis reveals elevated PCO2 and decreased

PO2 (respiratory acidosis) hypoxemia and

cyanosis

Tracheostomy for severe respiratory distress and laryngospasm

performed at bedside within 10-15 minutes

CVP reveals fluid status; Normal = 4-10cm H2o; right atrium

PAP – cardiac status; left atrium

ALLEN’S test – collateral circulation Cardiac Tamponade: pulsus paradoxus, muffled heart sounds, HPN

II. RIGHT SIDED HEART FAILURE


1. Tricuspid valve stenosis

2. COPD

3. Pulmonary embolism (char by chest pain and

dyspnea)

4. Pulmonic stenosis

5. Left sided heart failure

B. SIGNS AND SYMPTOMS (Venous congestion)

1. Jugular vein distention

2. Pitting edema

3. Ascites

4. Weight gain

5. Hepatosplenomegaly

6. Jaundice

7. Pruritus/ urticaria

8. Esophageal varices

9. Anorexia

10. Generalized body malaise

C. DIAGNOSTICS

1. CXR – cardiomegaly

2. CVP – measures pressure in right atrium; N = 4-

10cc H2O

During CVP: trendelenburg to prevent

pulmo embolism and to promote ventricular

filling

Flat on bed post CVP, check CVP readings

Hypovolemia – fluid challenge

Hypervolemia – diuretics (loop)

3. Echocardiography – reveals enlarged heart chamber

Muffled heart sounds cardiomyopathy

Cyanotic heart diseases

TOF “tet” spells cyanosis with

hypoxemia

Tricuspid valve stenosis

Transposition of aorta

Acyanotic

PDA – machine-like murmur

DOC: indomethacin SE: corneal

cloudiness

4. Liver enzymes

SGPT up

SGOT up

D. NURSING MANAGEMENT

Goal: increase myocardial contraction increase CO;

Normal CO is 3-6L/min; N stroke volume is 60-70ml/h2o

1. Administer medications as ordered

Cardiac glycosides

Digoxin (N=.5-1.5, tox=2)

Tox: Anorexia, N&V; A: Digibind

Digitoxin – given if (+) ARF; metabolized

in liver and not in kidneys

Loop diuretics

Lasix – IV push, mornings

Bronchodilators

Aminophylline (theophylline)

Tachycardia, palpitations

CNS hyperactivity, agitation

Narcotic analgesics

Morphine sulfate – induces vasodilation

Vasodilators

NTG and ISDN

Anti-arrhythmic agents

Lidocaine (SE: dizziness and

confusion)

Bretyllium

YOU DON’T GIVE BETA-BLOCKERS TO

THESE PATIENTS

2. Administer O2 inhalation at 3-4 L/minute via NC as

ordered high flow

3. High fowler’s, 2-3 Pillows

4. Restrict Na and fluids

5. Monitor strictly VS and IO and Breath Sounds

6. Weigh pt daily and assess for pitting edema

7. abdominal girth daily and notify MD

8. provide meticulous skin care




9. provide a dietary intake which is low in saturated

fats and caffeine

10. Institute bloodless phlebotomy

ROTATING TOURNIQUET

Rotated clockwise every 15 minutes to

promote a decrease in venous return

11. Health teaching and discharge planning

Prevent complications : Arrhythmia, Shock,

Thrombophlebitis, MI, Cor pulmonale – RV

hypertrophy

Regular adherence to medications

Diet modifications

Importance of ffup care

HYPERTENSION

Is an abnormal elevation of Bp, systolic pressure above

140 mmHg and or diastolic pressure above 90mmHg at

least two readings

WHO: BP >160/95 mmHg

AHA: BP >140/90 mmHg

In hypertension, vasoconstriction – vasospasm –

increases PVR – decrease blood flow to the organ.

Target Organs:

Heart : MI, CHF, Dysrhythmias

Eyes: blurred / impaired vision, retinopathy,

cataract.

Brain: CVA, encephalopathy

Kidneys : renal insufficiency, RF

Peripheral Bloods Vessels – aneurysm,

gangrene

CLASSIFICATION OF BP FOR ADULTS 18 YRS AND

OLDER (PHIL. SOCIETY OF HPN)

Optimal

o <120 mmHg / <80 mmHg

Recheck in 2 years.

Normal

o 120-129 mmHg / 80-84 mmHg

Recheck in 2 years.

High normal

o 130-139 mmHg / 85-89 mmHg

Recheck in 1 year.

Stage 1 (mild) HPN

o 140-159 mmHg / 90-99 mmHg

Confirm in 2 months.

Stage 2 (moderate) HPN

o 160-179 mmHg / 100-109 mmHg

Evaluate within a month.

Stage 3 (severe) HPN

o 180-209 mmHg / 110-119mmHg

Evaluate within a week.

Stage 4 (very severe) HPN

o 210 mmHg / >/=120 mmHg Evaluate

A. CLASSIFICATION

Essential / Idiophatic / Primary HPN, accounts

for 90 – 95% of all cases of HPN, cause is

unknown

Secondary HPN, due to known causes ( Renal

failure, Hypertension )

Malignant Hypertension, is severe, rapidly

progressive elevation in BP that causes rapid onset

of end organ complication

Labile HPN, intermittently elevated BP

Resistant HPN, does not respond to usual

treatment

White Coat HPN, elevation of B only during

clinic or hospital visits

Hypertensive Crisis, situation that requires

immediate blood pressure lowering 240mmHg /

120 mmHg

B. RISK FACTORS

1. Family history

2. Age

3. High salt intake

4. Low potassium intake

5. Obesity

6. Excess alcohol consumption

7. Smoking

8. Stress

C. SIGNS AND SYMPTOMS

1. Headache

2. Epistaxis

3. Dizziness

4. Tinnitus

5. Unsteadiness

6. Blurred vision

7. Depression

8. Nocturia

9. Retinopathy

D. TREATMENT STRATEGIES

Non-pharmacologic therapy

1. Low salt diet.

2. Weight reduction.

3. Exercise.

4. Cessation of smoking.

5. Decreased alcohol consumption.

6. Psychological methods: Relaxation / meditation.

7. Dietary decrease in saturated fat.

Drug therapy

Stepped Care

o Progressive addition of drugs to a regimen,

starting with one, usually a diuretic, and adding,

in a stepwise fashion, a sympatholytic,

vasodilator, and sometimes an ACE inhibitor.

Monotherapy

o Advantageous because of its simplicity, better

patient compliance, and relatively low

incidence of toxicity.

CATEGORIES OF

ANTI-HYPERTENSIVE DRUGS

Drugs that alter sodium and water balance Diuretics.

Loop diuretics

Thiazides

Spironolactone and Triamterene

Drugs that alter sympathetic nervous system function

Sympatholytic drugs.

Centrally-acting sympatholytics

Clonidine

Guanabenz

Guanfacine

Methyldopa

Peripherally-acting sympatholytics

Guanadrel

Guanethidine

Reserpine

a-blockers

Doxazosin

Prazosin

b-blockers

Acebutolol - Labetalol

Atenolol - Metoprolol

Betaxolol - Nadolol

Bisoprolol - Penbutolol

Carteolol - Pindolol

Carvedilol - Propranolol

Esmolol - Timolol




Vasodilators

Direct vasodilators

Diazoxide - Hydralazine

Minoxidil - Nitroprusside

Fenoldopam

Calcium channel blockers

Amlodipine - Nifedipine

Diltiazem - Nimodipine

Felodipine - Nisoldipine

Isradipine - Nitrendipine

Manidipine - Nicardipine

Lacidipine - Verapamil

Lercanidipine - Gallopamil

AGENTS THAT BLOCK THE PRODUCTION OR

ACTION OF ANGIOTENSIN

ACE inhibitors

Benazepril - Moexipril

Captopril - Quinapril

Enalapril - Perindopril

Fosinopril - Ramipril

Lisinopril - Trandolapril

AT1-receptor blockers

Irbesartan - Losartan

Telmisartan - Valsartan

Candesartan - Eprosartan

Olmesartan

DRUGS FOR HYPERTENSIVE EMERGENCIES OR

CRISES

Trimethaphan

o 1 mg/ml IV infusion; titrate;

instantaneous onset

Sodium nitroprusside

o 5-10 mg/L IV infusion; titrate;

instantaneous onset

Diazoxide

o 300-600 mg Rapid IV push;

instantaneous onset

Nifedipine

o 10-20 mg Sublingual or chewed;

onset within 5-30 min.

Labetalol

o 20-80 mg IV at 10-minute intervals (max.dose:

300mg); immediate onset

MECHANISMS OF DRUG ACTION

PRINCIPLES OF DRUG THERAPY

Monotherapy is generally reserved for mild to moderate

HPN; it has gained popularity because of its simplicity,

fewer side effects, and improved patient compliance.

More severe HPN may require treatment with several

drugs that are selected to minimize adverse effects of

combined regimen.

Treatment is initiated with any of 4 drugs depending on

individual patient: Diuretic, b-blocker, ACEI, and a Ca-

channel blocker; if BP is inadequately controlled, a 2nd-

drug is then added.

HPN may co-exist with other disease that may be

aggravated by some of the anti-HPN agents.

Lack of patient compliance is the most common reason

for failure of anti-HPN therapy; it is important to enhance

compliance by carefully selecting a drug regimen that

minimizes adverse effects.

Therapy is directed at preventing disease that may occur

in the future, rather than in relieving present discomfort

of the patient.




E. NURSING INTERVNTIONS

1. Patient Teaching and Counselling Teaching about HPN and its risk factors

Stress therapy

Low NA and low saturated fat

Avoid stimulants ( caffeine, alcohol, smoking )

Regular pattern of exercise

Weight reduction if obese

2. Teaching about medication The most common side effects of diuretics are

potassium depletion and orthostatic

hypotension.

The most common side effect of the different

antihypertensive drugs is orthostatic

hypotension.

Take anti – hypertensive medications at regular

basis

Assume sitting or lying position for few

minutes

Avoid very warm bath

Avoid prolonged sitting and standing

Avoid alcoholic beverages

Avoid tyramine – rich foods ( proteins ) as

follows: ( this may cause hypertensive crisis )

Aged cheese

Liver

Beer

Wine

Chocolate

Pickles

Sausages

Soy sauce

3. Preventing Non-compliance Inform the client that absence of symptoms

does not indicate control of BP

Advise the client against abrupt withdrawal of

medication, rebound hypertension may occur.

Device ways to facilitate remembering of

taking medications

PERIPHERAL VASCULAR DISORDERS

ANEURYSM

It is the localized, irreversible dilatation of an artery

secondary to an alteration in the integrity of its wall.

Most common type is AAA ( abdominal aortic aneurysm )

The most common cause is hypertension

A. CLASSIFICATIONS

Fusiform Aneurysm , involves outpouching of the

both side of the artery

Saccular Aneurysm , outpouching of only one side

of the artery.

Dissecting Aneurysm, involves separation or tear in

the tunica intima and tunica media

B. RISK FACTOR

1. Age

2. Tobacco use

3. HPN

4. Atherosclerosis

5. Race

6. Gender

7. Family history

C. SIGNS AND SYMPTOMS

1. Pulsating mass over abdomen (AAA)

2. Presence of the bruit sound

3. Low back pain

4. Lower abdominal pain

5. Flank pain

6. Shock

D. MEDICAL / SURGICAL MANAGEMENT

1. Hypertensive Medication

2. Surgery if aneurysm is greater than 4 cm

Teflon graft

Dacron graft

Gortex graft

E. NURSING INTERVENTIONS

1. Monitor the following

VS

Hemodynamic measurements

Urine output

BUN and creatinine

Bowel sounds

Passage of flatus

Peripheral pulses

2. Promoting Fluid Volume

Check dressing for excessive drainage

Assess for abdominal pain or backpain

Assess Hgb and Hct values

ARTERIAL ULCERS

I. THROMBOANGITIS OBLITERANS ( Buerger’s Dse. )

– acute inflammatory condition affecting the smaller and

medium sized arteries and veins of the lower extremities.

IDIOPATHIC


1. High risk group men 30 years old above

2. Chronic smoking

B. SIGNS AND SYMPTOMS Consistent to all arterial

diseases

1. Intermittent claudication – leg pain upon strenuous

walking r/t temporary ischemia

2. Cold sensitivity and skin color changes

White/pallor bluish/cyanosis red/rubor

(+) especially post smoking

3. Decreased peripheral pulses’ volume particularly in

dorsalis pedis and posterior tibial

4. Trophic changes

5. Ulceration

6. Gangrene formation

C. DIAGNOSTICS

1. Oscillometry – reveals a decrease in peripheral

pulse volume

2. Doppler UTZ – decrease in blood flow to affected

extremity

3. Angiography – site and extent of malocclusion





1. Encourage slow progressive physical activity

Walking 3-4x/day

Out of bed 3-4x/day

2. Medications as ordered

Analgesics

Vasodilators

Anticoagulants

3. Instruct patient to avoid smoking and exposure to

cold environment

4. Institute foot care management

Avoid barefoot walking

Straight nails

Lanolin cream for feet

(-) constricting clothes

5. Assist in surgery: BKA

II. REYNAULD’S DISEASE – characterized by acute episodes

of arterial spasms involving the digits of hands and fingers


1. High risk group women 40 years old up

2. Smoking

3. Collagen diseases

SLE

RA

4. Direct hand trauma

Piano playing

Excessive typing (tsk tsk! Lagot!)

Carpal tunnel syndrome

Operating chainsaw (nyek!)

Writing (tsk tsk, kaya dapat may module eh!

Grr!)


1. Intermittent claudication

2. Cold sensitivity and skin color changes

White/pallor bluish/cyanosis red/rubor

(+) especially post smoking

3. Trophic changes

4. Ulceration

5. Gangrene formation

C. DIAGNOSTICS

1. Oscillometry – reveals a decrease in peripheral

pulse volume

2. Angiography – site and extent of malocclusion



Analgesics

Vasodilators

2. Encourage pt to wear gloves

3. Instruct: avoid smoking and exposure to cold

environment

VENOUS ULCERS

I. VARICOSE VEINS – abnormal dilation of the veins of the

lower extremities d/t incompetent valves leading to increased

venous pooling and venostasis decreased venous return


1. Hereditary

2. Congenital weakness of veins

3. Thrombophlebitis

4. Cardiac diseases

5. Pregnancy

6. Obesity

7. Prolonged immobility prolonged standing and

sitting


1. Pain after prolonged standing

2. Dilated tortuous skin veins which are warm to touch

3. Heaviness in the legs

C. DIAGNOSTICS

1. Venography

2. Trendelenburg’s test – reveals that veins distend

quickly < 35 seconds incompetent valves

D. NURSING MANAGEMENT (consistent to all venous

ulcers)

1. Elevate legs above heart level increased venous

return (2-3 pillow elevation)

2. Measure circumference of leg to determine swelling

3. Anti-embolic stocking, full support panty hose

4. Medications as ordered analgesics

5. Assist in surgery

Vein stripping and ligation (more effective, no

recurrence)

Sclerotherapy

For spider-web varicosities

Cold solution injection

SE: thrombosis

II. THROMBOPHLEBITIS / DEEP VEIN THROMBOSIS

(DVT)


1. Smoking

2. Obesity

3. Prolonged use of OCPs

4. Chronic anemia

5. Diet high in saturated fats

6. DM

7. CHF

8. MI

9. Post-cannulation (insertion of various catheters)

10. Post-surgical operation



1. Pain at the affected extremity

2. Presence of cyanosis

3. Dilated tortuous veins

4. (+) HOMAN’S pain on calf on dorsiflexion

C. DIAGNOSTICS

1. Venography

2. Doppler UTZ

3. Angiography


1. Elevate the legs above heart level

2. Apply warm moist pack to relieve lymphatic

congestion

3. Measure circumference of leg muscles to determine

if it is swollen

4. Anti-embolic stockings


Analgesics

Anticoagulants – heparin

6. Prevent complications

Pulmonary embolism

cardiovascular nursing

Documents

superior vena cava

partial thromboplastin time

administer prescribed pharmacotherapy

cardiac disease resulting

serum cholesterol

stroke volume

cardiac output

side effects