Angina pectoris

Angina pectoris is a term used to describe chest pain, characterized by transient and paroxysmal. The
chest pain is produced by insufficient blood flow to the myocardium resulting in myocardial ischemia.

Risk factors

■ HTN, atherosclerosis, CAD, DM

■ Thromboangiitis obliterans, aortic insufficiency

■ Severe anemia, exertion, emotion, exposure to cold

Pathophysiology

Atherosclerotic changes in coronary artery

Obstruction of coronary artery

Decrease in blood flow to the heart

Decrease in oxygen supply

Ischemia of the tissues

Chest pain (angina)

1. Decrease supply

- Disorder of the coronary vessels-], circulation and blood supply

- Atherosclerosis and arterial spasm ^resistance to flow

- Disorder of the circulation

❖ Hypotension (Spinal anesthesia, drugs, blood loss)- | blood return to the heart

❖ Aortic stenosis or insufficiency- Filling pressure of the coronary arteries

2. Increased demand:
- Increase cardiac output e.g., exercise, emotion, digestion of a large meal, anemia and hyperthyroidism

- Increased myocardial need of 02 e.g. HTN, hypertrophy of the myocardium, thyrotoxicosis, strong
emotion, heavy exertion

3. Reduced oxygen-carrying capacity of the blood for example anemia

Classifications

■ Stable angina: it is also called exertional angina. It occurs with activities that involve

exertion or emotional stress and is relieved with rest or nitroglycerine

■ Unstable angina: It is also called pre-infarctional angina. It occurs with an

unpredictable degree of exertion or emotion and increases in occurrence, severity and

duration over time. Pain may not be relieved by nitroglycerine

■ Variant angina: Also called Prinzmetal’s or vasospastic angina. It results from

coronary artery spasm and may occur at rest. The attacks may be associated with ST

segment elevation noted on the ECG

■ Intractable angina: A chronic, incapacitating angina that is unresponsive to

interventions

Signs and symptoms

■ Angina usually causes chest pain that is like pressure, crushing, tightness, squeezing

substemally with possible radiation to the neck, jaw, back, and arms and relieved by

rest.

• Other clinical manifestations are palpitation and tachycardia, hypertension, dyspnea,

diaphoresis, pallor, dizziness and faintness.

■ Complications of angina pectoris include unstable angina, MI, and death.

Diagnosis

• History of chest pain, aggravating factors (e.g. exercise, emotion, heavy meal),

alleviating factors (e.g. rest, nitroglycerine)

■ ECG and ambulatory ECG, TMT

• Cardiac enzymes, TC, DC

• Chest X -ray

■ Cardiac catheterization or angiography

Management

The objectives of the management of angina are: (1) Relief from acute attack (2) Prevention of

further attack for reducing the risk of MI. The treatment is focused on decreased oxygen demand

of the myocardium, increased oxygen supply and relieved symptoms.

1. Pharmacological management

► Vasodilators e. g. Nitroglycerines, GTN, nitrates, mononitrate, isordil may be

given by different routes such as sublingual, oral, IV, topical to reduce myocardial

oxygen demand by reduction heart load.

► Antiplatelet agents e.g. aspirin, clopidogrel; prevent thrombus formation by

inhibiting platelet aggregation.

> Beta-Blocking agents e.g. metoprolol, atenolol, propranolol); reduce myocardial

oxygen by decreasing heart rates and reductions in myocardial contractility and

afterload.

► Calcium channel blockers e.g. amlodipine, verapamil, diltiazem; cause smooth

muscle relaxation- peripheral vasodilation and f afterload.

► Anti-ischemic agents

► Angiotensin-converting enzyme (ACE) inhibitors help to relax blood vessels.

2. Dietary management: low saturated fat and low cholesterol diet. Increase the intake of

fruits, vegetables and whole grains

3. Surgery: Revascularization therapy can be considered in patients with left main artery

stenosis greater than 50%, 2- or 3-vessel disease and LV dysfunction (ejection fraction,

< 45%), poor prognostic signs during noninvasive studies, or severe symptoms despite

maximum medical therapy.

► Percutaneous transluminal coronary angioplasty, with or without coronary

stenting,

► Coronary artery bypass grafting (CABG)

Nursing management

1. Assess pain, vital signs, dysrhythmias, cardiac output, anxiety, dyspnea, level of

consciousness, pallor, and diaphoresis. During pain assessment, find out the
information about location, intensity, radiation, frequency, aggravating factors,

alleviating factors.

Pain can be assessed by using the acronym ‘PQRST”

P Position, location, provocation Where is the pain? Can you point it? What were you
doing when pain began?

Q Quality and quantity How would you describe the pain? Has the pain been
constant or relieved with rest?

R Radiation and relief Had pain radiated to another site? Had pain relieved
after rest?

S Severity and symptoms How much do you rate your pain in 0-10 pain scale or
mild, moderate, severe? Did you notice any other
symptoms with pain?

T Timing When did you first feel pain or pain started?

2. Provide bed rest and place the patient in semi to high Fowler’s position

3. Administer 02 at 3L/min by nasal cannula as prescribed

4 Administer nitroglycerine or narcotic analgesic for prompt pain relief as prescribed

5. Obtain a 12 lead ECG

6. Monitor ECG continuously

7. Provide emotional support

8. Instruct the client to notify the physician if pain occurs and persists, despite rest and

medication

9. Provide teaching

■ Purposes of diagnostic procedure, management, assessment of pain

■ Proper use of nitrates

> Nitroglycerine sublingual

❖ Allow the tablet to dissolve

❖ Relax for 15 minutes after taking the tablet to prevent dizziness

❖ If no relief with 1 tablet, take additional tablets at 5-minute intervals, but no more than 3
tablets within 15 minutes.

❖ Transient headache is a common side effect.

❖ Keep the bottle tightly capped and prevent exposure to air, light, heat

❖ Ensure tablets are always within reach

❖ Check shelf life and expiry date of the medicine

> Nitroglycerine ointment: rotate sites to prevent inflammation and remove

previously applied ointment. Avoid massaging or rubbing because that increases

absorption and interferes with the drug's sustained action.

■ Ways to minimize precipitating event

> Reduce stress and anxiety by relaxation techniques

> Avoid smoking, over exertion, extreme temperature, extreme cold

> Eat small frequent meal

■ Gradually increase activities and exercise. Can participate in regular exercise program

but maintain rest periods.

■ Diet: low cholesterol and low saturated fat

■ Maintain ideal weight

Evaluation

■ The patient remains free of pain.

" The patient does not exhibit manifestations that indicate high level of anxiety

“The patient remains free of complications

Myocardial infarction
Myocardial infarction (MI), commonly known as a heart attack, is the irreversible necrosis of heart
muscle secondary to prolonged ischemia.

MI usually results from an imbalance in oxygen supply and demand, which is most often caused by
plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood
supply to a portion of the myocardium when myocardial tissue is abruptly and severely deprived of 02.

Risk factors

Nonmodifiable

• Advance age

• Male

• Positive family history

Modifiable factors

• Smoking or other tobacco use

• Diabetes mellitus

• Hypertension

• Hypercholesterolemia & hypertriglyceridemia

• Dyslipidemia

Contributing factors

• Obesity

• Sedentary lifestyle

• Psychosocial stress

• Type A personality

Pathophysiology

Changes in the condition of plaque in the coronary artery

I
 Activates the platelets

Formation of thrombus

Coronary arteries occlusion

Myocardial ischemia

Decreased coronary artery blood supply than demand

Myocardial cell death -> Anaerobic glycolysis -> lactic acid production -> severe chest pain.

Myocardial irritability -> arrhythmias

Decreased myocardial contractility -> stimulation of CNS -> HR -> O2 demands? Afterload

Decreased left ventricular function

Decreased cardiac output

Shock

Death

Signs and symptoms

The degree of symptoms ranges from asymptomatic (in diabetic patient) to sudden cardiac death.

In spite of the variation of manifestations, majority of the signs and symptoms are as follows:

■ Pain usually substernal with radiation to the neck, arm, jaw or back, severe, crushing,
viselike with sudden onset, unrelieved by rest or nitrates

■ Nausea and vomiting

■ Skin-cool, clammy ashen, pallor, cyanosis

■ Dyspnea, dysrhythmia, fever, diaphoresis

■ Apprehension; fear of death and restlessness

■ Initial increase in BP and pulse, with gradual drop in BP

■ Occasional findings; rales and crackles, pericardial friction rubs

Complications

■ Dysrhythmias, cardiogenic shock

■ Heart failure, pulmonary edema, thrombophlebitis, pericarditis, mitral valve

insufficiency, postinfarction angina, ventricular rupture

■ Dressler’s syndrome (a type of pericarditis due to immune response after damage of

heart tissues)

Diagnosis

Diagnosis criteria of MI (WHO, 2000): a cardiac troponin rise accompanied by typical symptoms,

pathological Q waves, ST elevation or depression.

■ History: chest discomfort, types, nature of chest pain, aggravating and alleviating

factors of pain, associated symptoms, prior episodes of angina, myocardial ischemia

hypertension, diabetes mellitus etc.

■ Physical examination: vital signs, heart sound, lung sound, JVP, skin condition etc

■ ECG to detect myocardial ischemia

■ Cardiac enzyme:

> CK-MB level rises within 3-12 hours of the onset of chest pain, reach peak values

within 24 hours, and return to baseline after 48-72 hours (50- 325 unit/L

> Troponin levels increase within 3-12 hours from the onset of chest pain, peak at

24-48 hours and return to baseline over 5-14 days.

> LDH level rises 24 hrs. after MI, peaks between 48-72 hours and falls to normal in
7 days (normal value- troponin I <0.6ng/ml

> Myoglobin level rises within 1 hour after cell death, peaks in 4-6 hours and return

to normal within 24-36 hours

■ Lipid profile, TC, DC, ESR

■ Echocardiogram- to evaluate ventricular function and wall-motion abnormalities

■ Cardiac catheterization or angiogram- to confirm or rule out anatomy and degree of

myocardial perfusion abnormalities

Management

Goals of management are:

1. Restoration of the balance between the oxygen supply and demand to prevent further

ischemia

2. Pain relief

3. Prevention and treatment of complications

■ Rest: reduces the myocardial oxygen demand.

■ 02 therapy: to reduce myocardial work load and maintain SP02 > 90%

■ Morphine: Usually morphine (opioid) is given I/V, to relieve pain and anxiety.

Morphine may depress respiratory center, so need to monitor respiration

■ Nitroglycerine Nitrates (nitroglycerine); Isordil, GTN, mononitrate are used for

vasodilator effects

■ Aspirin: 150-325 mg loading dose (chewed) and 75-150 mg maintenance dose.

■ Statins: high potency statins such as atorvastatin 80 mg, or rosuvastatin 40 mg and to

be continuously used to decrease cholesterol

■ Beta blockers (propanol, inderal, atenolol): Decreases myocardial 02 consumption by

decreasing heart rate & BP and force of myocardial contraction. Monitor pulse/heart

rate & BP

■ Heparin or low molecular weight heparin 1 mg/kg body weight

■ Angiotensin converting enzyme (ACE) inhibitors (Enalapril, captopril). Used to prevent

the conversion of angiotensin I to angiotensin II, causes low BP, & excrete Na+ H2O

by kidney, consequently decreases 02 demand of heart. It prevents heart failure.

■ Calcium channel blocker can be used after beta blocker and nitrates.

■ Antidysrhythmic and inotropes may be used according to the changes in ECG, BP and

pulse.

■ A defibrillator may be used to restore a normal rhythm if the patient has arrhythmias

■ A temporary pacemaker may be used if arrhythmia is not managed by medical therapy.

■ Thrombolytic/fibrinolytic therapy: Mostly streptokinase (1500,000 IU) is used, it is

administered by dissolving in 1000 ml. NS, over 30 to 60 minutes. It is effective for

chest pain of less than 12 hours, it dissolves the thrombus in a coronary artery &

reperfusion the area. Watch carefully for bleeding.

■ Stool softeners; reduce stress during defecation and reduce myocardial workload.

■ H2 antagonist

■ Sedative, anxiolytic, and hypnotic drugs at night

■ Diuretics: can help get rid of excess fluids that sometimes accumulate when the heart is

not pumping effectively. Usually taken orally, they cause the body to dispose fluids

through urination.

■ Antipyretics to reduce fever

If ST elevation seen in ECG; Thrombolysis IV immediately or Primary PCI should be made as

soon as possible.

Medicines; The “MONABHAI” principle

■ M- morphine

■ O-oxygen

■ N- nitrate

■ A- antiplatelets

■ B- beta blockers

■ H- heparin

■ A- atorvastatin
■ I- inotropes (dopamine, dobutamine)

Surgical management

■ Percutaneous coronary intervention/ percutaneous transluminal coronary angioplasty

(PC1/PTCA).

■ Coronary artery bypass graft (CABG)

Nursing management

The focus of the plan of care tor MI patient includes Recognize and treat potentially life

threatening dysrhythmias. Monitor for complications from decreased output. Maintain a

therapeutic critical care environment. Identify the psychosocial impact of the MI on the client and

significant others. Educating the client in lifestyle changes and rehabilitation after the MI.

Assessment

■ History of chest pain, discomfort, difficulty in breathing, palpitation, faintness etc.

■ Physical examination- position of the patient, sweating, BP, pulse, temperature, heart

sound

■ ECG, Cardiac enzyme

Nursing diagnosis

■ Acute chest pain may be related to myocardial ischemia resulting from coronary artery

occlusion with loss/restriction of blood flow to an area of the myocardium and necrosis

as manifested by typically substernal pain, tightness, pressure or heaviness, pain

radiating to the arms, diaphoresis, nausea, vomiting, palpitation etc

■ Decreased cardiac output may be related to myocardial injury as manifested by changes

in LOC, dizziness, weakness, loss of peripheral pulse etc

■ Impaired gas exchange may be related to decreased cardiac output as manifested by

changed heart rate, |BP, jtemperature, changed skin color, dyspnea, impaired capillary

refill, reduced PaO2

■ Ineffective coping may be related to acute illness, anticipated life style change
■ Anxiety may be related to hospitalization, fear of death

■ High risk for activity intolerance may be related to imbalance between 02 supply and

demand

■ Risk for constipation may be related to bed rest, medication, NPO, soft diet

■ Altered health maintenance may be related to inadequate knowledge, inappropriate

adaptation in lifestyle change after MI

■ Knowledge deficit RT diagnosis, medication etc.

Nursing interventions

■ Establish a patent IV line

■ Provide pain relief, morphine sulfate IV as prescribed

■ Administer 02 as prescribed to relieve dyspnea and prevent dysrhythmias

■ Provide bed rest with semi-Fowler’s position to cardiac workload

■ Monitor ECG and hemodynamic procedures

■ Administer antiarrhythmics as prescribed

■ Perform complete pulmonary/cardiovascular assessment

■ Monitor urinary output

■ Maintain full liquid diet with gradual increase to soft, j Na diet

■ Maintain quiet environment

■ Administer stool softeners as prescribed to facilitate bowel evacuation and prevent

straining

■ Relieve anxiety associated with CCU environment

■ Administer anti-coagulants as prescribed

■ Administer thrombolytics (streptokinase) and monitor for side effects.

■ Provide teaching on:

1. Effects of MI, healing process, and treatment regimen

2. Medication regimen including name, purpose, schedule, dosage, side effects

3. Dietary restriction: low sodium, low cholesterol, avoidance of caffeine

4. Importance of participation in a progressive activity program

 5. Resumption of sexual activity according to physician’s order (usually 4-6 weeks)

6. Need to report the following symptoms; increased persistent chest pain, dyspnea,

weakness, fatigue, palpitation, light headedness

7. Enrollment of the patient in cardiac rehabilitation program

Rehabilitation: The overall goal of the cardiac rehabilitation is to help the patient (1) Live as full,

vital and productive life as possible (2) Remain within the limits of the heart’s ability to respond

to increase in activity and stress. This program has six important sub goals which are as follows:

1. Develop a program of progressive physical activity

2. Teach the patient and significant others concerning cause, prevention and

treatment of CAD

3. Help the patient accept the limitations imposed by illness

4. Aid the patient in adjusting changes in occupational goals

5. Lessen avoidable risk factors

6. Change the psychosocial factors adversely affecting the recovery from CAD

A heart healthy life-style includes; a low-fat diet, regular exercise, maintaining a healthy weight,

no smoking, moderate drinking, no illegal drugs, controlling hypertension and managing stress.

7.2.2 Valvular disorder

Valvular heart disease occurs when the heart valves cannot fully open (stenosis) or close

completely (insufficiency or regurgitation). Valvular heart disease prevents efficient blood flow

through the heart. Chronic valvular heart disease develops in at least half of those affected by

rheumatic fever with carditis. Two thirds cases occur in women. Mitral valve is affected in more

than 90% cases, followed by aortic, tricuspid and then pulmonary valves in decreasing order of

frequency. Valvular heart disease is categorized according to the anatomical name and functional

Insufficiency.
Mitral stenosis (MS)

Mitral stenosis occurs if valvular tissue thickens and narrows the valves MS is characterized by

obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of

the mitral valve apparatus.

Primarily a result of rheumatic fever and rarely congenital. Rheumatic heart disease causes

scarring & fusion of valve apparatus. Pure or predominant MS occurs in approximately 40% of

all patients w.th rheumatic heart disease and two-thirds of all patients with MS are female.

• Normal mitral valve area (MVA) is 4-6 cm2.

• Mild mitral stenosis: MVA 1.5-2.5 cm2, minimal symptoms

• Moderate mitral stenosis: MVA 1.0-1.5 cm2 usually does not produce symptoms at rest

• Severe mitral stenosis: MVA <1.0 cm and 2 symptoms occur even at rest.____________

Pathophysiology

Group A beta-hemolytic Streptococcus infection

Inflammation and scarring of the heart valve

Progressive fibrosis, calcification in the valve leaflets

Fusion of valvular apparatus (mitral stenosis)

Obstruct blood flow from atrium to ventricles

Increased left atrial pressure

Pulmonary hypertrophy, pulmonary venous congestion and breathlessness

I
 Decreased cardiac output

Activity intolerance

Effects of Mitral valve stenosis

• Left atrium hypertrophy

• Left heart failure (LAH)

• Pulmonary edema

• SOB/Cough

Effects of pulmonary valve stenosis

• Pulmonary stenosis/Tricuspid regurgitation

• Right atrium hypertrophy

• Right heart failure

• Increased JVP

• Edema

Signs and symptoms

■ Cough, fatigue, SOB, palpitation, hemoptysis

■ Left sided failure

> Orthopnea

> Paroxysmal nocturnal dyspnea (PND)

■ Right sided failure

> Hepatic Congestion

> Edema

■ Systemic embolism

■ Worsened by conditions that T cardiac output such as exertion, fever, anemia,

tachycardia, intercourse, pregnancy, thyrotoxicosis

■ Atrial fibrillations

■ Auscultation: loud first heart sound, mid diastolic murmur

■ Pulmonary effusions, pulmonary edema, crepitation and infection

Diagnosis

■ ECG: LAH, LVH

■ Chest X-ray: LAH, pulmonary venous congestion.

■ ECHO: Thickened immobile cusps; reduced valve area, reduced rate of diastolic filling

of LV

Management of mitral stenosis

■ Medical management in early and less severe case

> Diuretics for LHF/RHF

> Digitalis/Beta blockers/CCB: Rate control m a fibrillation

> Anticoagulation: In a fibrillation to reduce the possibility of embolism

■ Balloon valvuloplasty: is an invasive nonsurgical procedure. A ballon catheter is

passed from the femoral vein through the arterial septum to the mitral valve. The

balloon is inflated to enlarge the orifice. It is effective for long term improvement.

■ Surgical management (1) Mitral commissurotomy (2) Mitral Valve Replacement;

Mechanical or Bioprosthetic

Nursing management

■ Administer prescribed treatment for heart failure

■ Administer oxygen as prescribed

■ Provide a low sodium diet

■ Administer diuretics and digitalis as prescribed

■ Administer antibiotics as prescribed if infective endocarditis is present

■ Administer antidysrhythmics and anticoagulants for atrial fibrillation as prescribed

■ Prepare the client for surgery as necessary

■ Post-operative interventions:

> Monitor closely for signs of bleeding, cardiac output, sings of heart failure.

> Administer medications as prescribed and monitor incision and report any redness

and discharge from the wound.

> Provide health education

❖ fatigue is expected, so take adequate rest

❖ If a mechanical valve is inserted, anticoagulation therapy is necessary

❖ Avoid: any dental procedure for six months. Heavy lifting (>10 lb) and

activities that have chance of injury to the sternal region,

❖ Instruct the patient about: side effects of anticoagulants, if bleeding and

bruising occur notify the physician. Importance of good oral hygiene to

reduce risk of infective endocarditis. Brush teeth twice daily with a soft

toothbrush, followed by oral rinse. Importance of prophylactic antibiotics

before any invasive procedure. Obtain a medical id card.

Aortic stenosis

Aortic stenosis is a narrowing of the aortic valve in the heart. This restricts the blood flow through

the valve. The heart then needs to squeeze (contract) harder to pump blood into the aorta.

Causes

■ Congenital bicuspid valve

■ Idiopathic degenerative sclerosis with calcification

■ Infective endocarditis and rheumatic fever.

Pathophysiology

Normally the aortic valve consists of three cusps or leaflets and has an opening of 3-42cm. When

the left ventricle contracts, it forces blood through the valve into the aorta When the left ventricle

expands again, the aortic valve closes and prevents the blood in the aorta from regurgitating into

the left ventricle.

 Aortic stenosis

Aortic valve does not open fully

Partial restriction of blood flow from the left ventricle into the aorta

Increased ventricular pressure and compensatory left ventricular hypertrophy

Left ventricular hypertrophy

Reduced ejection fraction and decreased cardiac output

Angina, arrhythmia, left ventricular failure

Signs and symptoms

■ Dyspnea on exertion, chest pain (angina), pressure or tightness, fainting (syncope)

■ Orthopnea, fatigue and activity intolerance

■ Palpitations, heart murmur

Diagnosis

■ Aortic stenosis is diagnosed by heart murmur, chest X-ray (calcification around the

aortic valve), ECG, echocardiogram.

Management

Management of the patient depends upon the clinical manifestation, if there is no symptom then

may not need any treatment. If the patient develops symptoms or complications, medicines and

even surgery may be needed to ease the symptoms.

■ ACE inhibitors and diuretics may be used.

■ Surgical intervention includes valvotomy, valvuloplasty and valve replacement.

Nursing management

■ Administer prescribed treatment for heart failure

■ Administer 02, diuretics, digitalis, antibiotics as prescribed

■ Prepare the patient for valve replacement

■ Provide a low sodium diet.

■ Provide nursing care according to physical status of the patient and pre-post operative

care if surgery is recommended

Aortic regurgitation

Regurgitation is due to incompetence of the aortic valve or any disturbance of the valvular

apparatus. Blood is leaked each time from the aortic valve when the left ventricle relaxes.

Regurgitation of aortic valve allows the blood to flow in two directions. Oxygen-rich blood flows

out through the aorta to the body as it should, but some flows backwards from the aorta into the

left ventricle when the ventricle relaxes.

Incompetent closure of the aortic valve can result from intrinsic disease of the cusp, diseases of

the aorta, or trauma. An increase in systolic stroke volume and low diastolic aortic pressure

produces an increased pulse pressure. The heart will have to do more work to compensate for the

blood leaked back into the left ventricle. The walls of the ventricle will sometimes thicken

(hypertrophy), and a thickened heart muscle is a less effective pump. Eventually, the heart maybe

unable to pump enough to meet the body’s need for blood, leading to heart failure.
Mild aortic regurgitation may be treatable with medications to reduce blood clotting and reduce

the risk of stroke, but surgical repairs are often needed.

Cardiomyopathy

Cardio: heart Disease of the heart muscles (myocardium) which inhibit effective

Myo: muscles pumping

Pathy: disease

Cardiomyopathy is a subacute or chronic disease of the heart muscle, associated with cardiac

dysfunction (heart loses effectiveness as a pump). In cardiomyopathy, the heart muscle becomes

enlarged, thick or rigid. When condition becomes worse, the heart becomes weaker and less able

to pump blood through the body and maintain a normal electrical rhythm. The result can be heart

failure, or arrhythmias. Problems also arise in heart valves due to a weakened heart. Treatment is

palliative, not curative, and the client needs to deal with numerous lifestyle changes and a

shortened life span.

Causes

■ Exact cause is unknown.

The risk factors may include; drinking too much alcohol, eating foods without proper

vitamins, exposure to toxins, pregnancy, systemic hypertension, infections, heredity etc.

Classifications

■ Dilated cardiomyopathy (DCM): most common type of cardiomyopathy characterized

by ventricular dilation, contractile dysfunction and heart failure.

■ Hypertrophic cardiomyopathy: massive ventricular hypertrophy, leading to

hypercontraction of the left ventricle and rigid walls that causes obstruction of the left

ventricular outflow.

■ Restrictive cardiomyopathy: rigid ventricular wall, restriction of filling of the ventricles

or reduced diastolic compliance of the ventricle.

Pathophysiology

■ The pathophysiology of all cardiomyopathies is a series of events that culminate in

impaired cardiac output.

■ Decreased stroke volume stimulates the sympathetic nervous system and the renin

angiotensin - aldosterone response, resulting in increased systemic vascular resistance

and increased sodium and fluid retention, which places an increased workload on the

heart.

■ These alterations can lead to heart failure.

■ The heart muscle is weakened, becomes unusually enlarged, thickened, or stiffened. As

a result, the heart cannot pump blood to the rest of the body, which causes heart failure.

■ The heart loses its ability to pump blood and, in some instances, heart rhythm is

disturbed, leading to irregular heartbeats, or dysrhythmias.

The condition tends to be progressive and sometimes worsens quickly.

Signs and symptoms__________

Dilated cardiomyopathy

• Shortness of breath

• Palpitations, dysrhythmias, chest pain

• Dizziness or lightheadedness, fainting

• Weakness and fatigue

• Activity intolerance

• Lower extremities swelling, weight gain

• Nausea, bloating, and poor appetite due to fluid retention

• Blood clots in the dilated left ventricle because of pooling of the blood

Hypertrophic myopathy
• Exertional dyspnea, syncope

• Palpitation

• Chest pain that occurs at exercise

• Chest pain is prolonged, unrelated to exertion and not relieved by nitrates dysrhythmias

• Fainting, especially during or just after exercise or exertion

Restrictive myopathy

• Shortness of breath (at first with exercise; but over time it occurs at rest)

• Fatigue, weakness

• Activity intolerance

• Swelling of the legs and feet

• Weight gain

• Palpitations

Diagnosis

■ Medical and family history of heart disease and physical exam- swelling of the ankles,

feet, legs, abdomen or veins in the neck suggests fluid buildup, which is a sign of heart

failure.

■ Chest X Ray, ECG, holter monitoring

■ Echocardiography, cardiac catheterization, coronary angiography

■ Myocardial Biopsy

Treatment includes

■ Symptomatic management to relieve symptoms

■ Diuretics, cardiac glycosides and vasodilators are administered to increase cardiac

output

■ Antidysrhythmics are administered to control dysrhythmias

■ Instruct the patient to report any signs of dizziness of fainting, which may indicate a

dysrhythmia

■ Instruct the patient to avoid ingestion of alcohol because of cardiac depressant effect
■ Beta blockers and calcium antagonists decrease the outflow obstruction and decrease

the heart rate

■ In hypertrophic, vasodilators and cardiac glycosides are contraindicated because

vasodilator and positive inotropic effects augment the obstruction

Pharmacological management remember “ABCDD”

A = ACE inhibitors (which is end in -pril) e.g., Lisinopril, enalapril

B = Beta blocker (end in -lol) e.g., atenolol

C = Calcium channel blocker (end in -dipine, -zem, -amil) e.g., nifidipine, diltizem.

verapamil

D = Digoxin, cardiac glycosides

D = Diuretics loop or thiazide e.g., furosemide, hydrochlorothiazide

Nursing management of cardiomyopathy

Assessment

■ Vital signs, SOB, restlessness, chest pain, ECG, level of anxiety, alertness

■ History of fainting, intake of alcohol, past medical history

Nursing diagnosis

■ Decreased cardiac output may be related to decreased ventricular function and/or

dysrhythmias

■ Activity intolerance may be related to low cardiac output

■ Fluid volume excess may be related to ventricular dysfunction

■ Anxiety related may be related to fear of death and hospitalization

■ Fatigue related may be related to decreased cardiac output, heart failure

Nursing interventions

■ Obtain vital signs every 15 minutes during acute phase.

■ Assess the patient’s condition regularly for example:

 > changes in neurological function every hour and as clinically indicated.

> skin warmth, color, and capillary refill time, chest discomfort because myocardial

ischemia may result from poor perfusion.

> heart and lung sounds to evaluate the degree in heart failure.

■ Continuously monitor the oxygen status with pulse oximetry.

■ Provide oxygen at 2 to 4 L/min to maintain or improve oxygenation.

■ Maintain proper rest to minimize oxygen demand.

■ Obtain BP every hour or more frequently if the patient’s condition is unstable.

■ Monitor:

> Urinary output every hour to evaluate status of cardiac output and effects of

medications.

> The patient’s activities and nursing interventions that may adversely affect

oxygenation.

■ Analyze ECG rhythm strip at least every 4 hours

■ Provide drugs as prescribed.

■ Provide liquid diet on acute phase

■ Monitor serum potassium before and after the administration of loop diuretics.

■ Provide proper skin care to prevent pressure ulcer.

Heart failure

Heart failure or cardiac failure is inability of the heart to pump an adequate supply of blood to

meet the metabolic needs of the body. It is a clinical syndrome, which is developed due to

accumulation of the blood in front of the left or right parts of the heart.

Causes of heart failure

Left sided

• MI

• Hypertension

• Ischemic heart disease

• Aortic valve disease

• Mitral stenosis

Right sided

• Left sided heart failure

• Right ventricular infarction

• Atherosclerotic heart disease

• COPD

• Pulmonic stenosis

• Pulmonary embolism

Classification of heart failure

■ Systolic vs. diastolic

■ High output vs. low output

■ Acute vs. chronic

■ Right sided vs. left sided

■ Forward vs. Backward

Pathophysiology

■ The common pathophysiologic state that perpetuates the progression of heart failure is

extremely complex, regardless of the precipitating event.

■ Compensatory mechanisms exist on every level of organization, from sub-cellular all

the way through organ-to-organ interactions.

■ Only when this network of adaptations becomes overwhelmed does heart failure ensue.
Ventricular dysfunction limits a patient's ability to perform the routine activities.

Signs and symptoms

Left heart failure

• Dyspnea, orthopnea, PND, tiredness, cough, muscle weakness

• Tachycardia

• PMI displaced laterally

• Possible S3

• Bronchial wheezing, rales or crackles

• Cyanosis, pallor

• Decreased PaO2, increased pCO2

Right heart failure

• Anorexia, nausea, weight gain

• Dependent pitting edema

• Jugular venous distension

• Bounding pulses

• Hepatomegaly
• Cool extremities

• Oliguria

New York Heart Association Functional Classification

Class I: No symptoms with ordinary activity

Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical

activity results in fatigue, palpitation, dyspnea, or angina

Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary

physical activity results in fatigue, palpitation, dyspnea, or anginal pain

Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac

insufficiency may be present even at rest

Diagnosis

■ Patient history of clinical manifestations, risk factors, chief complaints etc.

■ Physical examination: vital signs, abnormal heart and lung sounds, swelling, weight gain

■ Laboratory and diagnostic tests

■ ECG

■ Chest x-ray

■ Echocardiography

Management of heart failure

■ Improving myocardial ‘pump’ performance:

> Digitalis

> Dopamine and dobutamine- facilitate myocardial contractility and enhance stroke volume

■ Reducing myocardial workload:

> Diuretics-|preload

> Vasodilators-J,afterload e.g. nitroglycerine, isosorbide dinitrate, hydralazine etc.

> ACE inhibitors- suppress RAAS-frenal blood flow &|renal vascular resistance-dieresis

■ Diet- |Na (2-4gm/day), limit fluid

■ Cardiac resynchronization therapy increases the patient’s (heart) efficiency by changing

lifestyle e.g. rest, exercise, reduce weight, quit smoking, goal setting etc

> Create realistic goal: Have patients set their own goals of what they would like to

do e.g. grocery shopping, walking to the mailbox without stopping

> Encourage them to participate in activities e.g. daily weight check, regular

follow up

Treatment approach for the patient with heart failure

Nursing management

Assessment

■ Vital signs, fatigue, dyspnea, exertional dyspnes, swelling, restlessness, dietary pattern,

anxiety, support system, level of knowledge, practice of health maintenance etc

■ CBC, electrolytes, RFT, LFT etc

■ ECG, echocardiogram, chest-xray

Nursing diagnosis

■ Cardiac output decreases may be related to heart failure, dysrhythmia

■ Fluid volume excess may be related to reduced GFR, decreased cardiac output,

increased ADH, and water and sodium retention

■ Impaired gas exchange may be related to fluid in alveoli, or pulmonary congestion

■ High risk for decreased peripheral tissue perfusion may be related to decreased cardiac

output and vasoconstriction

■ High risk for activity intolerance may be related to reduced cardiac output

■ High risk for impaired skin integrity may be related to immobility, swelling

■ Anxiety may be related to unknown outcome, decrease functional ability

■ Risk for injury may be related to drug toxicity, hypoxia

Nursing interventions

■ Monitor respiratory status and provide adequate ventilation (when progress to

pulmonary edema):

> Administer 02 therapy

> Maintain the patient in semi or high Fowler’s position

> Monitor ABGs

> Assess for breath sounds, noting any changes

■ Provide physical and emotional rest:

> Consequently, assess level of anxiety

> Maintain bed rest with limited activity

> Maintain quiet, relaxed environment

> Organize nursing care around rest periods

■ Increase cardiac output

> Administer digitalis, vasodilators, diuretics, as prescribed and monitor effects

> Monitor ECG, vital signs, daily weight, CVP, electrolyte, peripheral edema,

> Maintain accurate 1 & O and measure abdominal girth daily

> Provide sodium restricted diet as prescribed

 > Provide meticulous skin care

■ Provide teaching

> Need to monitor self daily weight and S &S of CHF

> Medical regimen including name, purpose, dosage, frequency, and side effects

> Prescribed dietary plan

> Need to avoid fatigue and schedule the rest period

Shock

Shock is an abnormal physiologic state where an imbalance between the amount of circulating

blood volume and the size of vascular bed results in circulatory failure and oxygen and nutrient

deprivation of the tissues. It is a life-threatening condition of circulatory failure resulting in severe

dysfunction of organs vital to survival. The effects of shock are initially reversible, but rapidly

become irreversible, resulting in multi-organ failure and death.

Classification of shock

■ Hypovolemic: loss of blood or body fluids or water; decreased circulatory blood

volume lead to decrease in diastolic filling pressure and volume which results in

adequate cardiac output hypotension and shock e.g., hemorrhage, severe diarrhea or

vomiting etc

■ Cardiogenic: failure of the heart to pump properly; marked by the reduced cardiac

function resulting from direct myocardial damage or mechanical abnormality leading to

decrease in cardiac output and BP e.g. MI, CHF, arrhythmias etc

• Distributive: distributive shock is characterized by vasodilatation leading to a decrease

in preload that leads to hypotension with a normal or increased cardiac output such as

neurogenic, anaphylactic, septic shock

> Neurogenic: failure of arteriolar resistance, leading to massive vasodilation and

pooling of blood. It is caused by interruption of sympathetic impulses from

exposure to unpleasant circumstances, extreme pain, spinal cord injury, head

injury etc.
 > Anaphylactic: massive vasodilatation resulting from allergic reaction due to

release of histamine and related substances e.g. allergic reaction to medications,

insect venom etc.

> Septic: release of bacterial toxins that act directly on the blood vessels producing

massive vasodilation and pooling of blood results usually occurs in gram negative

septicemia.

■ Extra cardiac obstructive: results secondary to obstruction to flow in the

cardiovascular circuit e. g. tension pneumothorax or cardiac tamponade

Body response to shock

■ Hyperventilation leading to respiratory alkalosis

■ Vasoconstriction: shunts blood to heart and brain

■ Tachycardia to meet the demand of tissues and organs

■ Fluid shifts: intracellular to extracellular to maintain circulating blood volume.

■ Impaired metabolism: tissue anoxia leads to anaerobic metabolism causing lactic acid

buildup, resulting in metabolic acidosis.

■ Impaired organ function e.g. renal failure (decreased perfusion in kidneys), shock lung

(ARDS)

Signs and symptoms of shock

■ Cool, pale moist skin (in hypovolemic and cardiogenic shock); warm, dry and pink skin

(in septic and neurogenic shock)

■ Tachycardia with weak and thready pulse

■ BP may be normal in the early stage due to compensatory mechanisms and BP drops in

the later stage.

■ Rapid and shallow respiration due to tissue anoxia

■ Altered LOC: restlessness and apprehension, progressing to coma

■ Decreased urinary output

■ Decreased temperature
Nursing interventions

■ Maintain patent airway and adequate ventilation

> Establish and maintain airway

> Administer oxygen as prescribed

> Monitor respiratory status, ABGs

> Start resuscitation procedures as required

■ Promote restoration of blood volume; administer fluids (crystalloid solutions. RL, NS;

colloid solutions: albumin, dextran, plasmanate) and blood products as prescribed.

■ Administer drugs as prescribed

■ Minimize factors contributing to shock

> Elevate lower extremities to 45° to promote venous return to heart, thereby

improving cardiac output.

> Avoid Trendelenburg’s position because it increases respiratory impairment.

> Promote rest by using energy conservation measures and maintain quiet

environment as possible

> Relieve pain by cautious use of narcotics

❖ Narcotics interfere with vasoconstriction, give only if absolutely necessary

through IV and in small doses

❖ If given IM or SC, vasoconstriction may cause incomplete absorption; when

the circulation improves, the patient may get overdose.

> Keep the patient warm

■ Continue assessment of the patient

> Check vital signs frequently

> Monitor urine output, CVP, ECG and report significant changes e.g., decrease

urine less than 30 ml /hr.

> Check laboratory reports: CBC, electrolytes, BUN, creatinine, blood gases

■ Provide psychological support to the patient and family; reassure the patient to relieve
apprehension
Drugs used to treat shock

Drugs Actions of the drugs

Dopamine Low dosage: dilates renal, mesenteric and splanchnic vessels, that
increase kidney perfusion and urine output
High dosage: increase cardiac contractility; causes vasoconstriction
Dobutamine (dobutrex) Increase myocardial contractility, vasodilator
Norepinephrine Improves cardiac contractility and cardiac output; potent vasoconstrictor
Sodium nitroprusside Vasodilator, decreased peripheral resistance and workload of the heart,
(Nipride) thereby increasing cardiac output, used in cardiogenic shock and
hypertensive emergencies
Isoproterenol (Isuprel) Increased myocardial contractility. Decreased peripheral resistance by
dilating peripheral vascular bed
Digitalis preparation Improves cardiac performance
Corticosteroids Help to protect cell membranes and decrease the inflammatory response,
used specially in septic shock
Antibiotics Used in treating infection

Cardiac arrest

Cardiac arrest is the condition where the heart’s pumping function is “arrested,” or stopped. It is a

sudden, sometimes temporary, cessation of the heart's functioning due to malfunction of the

electrical function of the heart.

It is a condition of sudden, unexpected cessation of breathing and adequate circulation of blood by the
heart. Cardiac arrest, also known as cardiopulmonary arrest or circulatory arrest, is the cessation of
normal circulation of the blood due to failure of the heart to contract effectively.

Arrested blood circulation prevents delivery of oxygen to the body. Lack of oxygen to the brain causes
loss of consciousness, which then results in abnormal or absent breathing. Brain injury is likely to
happen if cardiac arrest goes untreated for more than five minutes. For the best chance of survival and
neurological recovery, immediate and decisive treatment is imperative.

Causes

■ Cardiac causes

> Arrhythmias: ventricular fibrillation, ventricular tachycardia

 > Ischemic heart disease, cardiomyopathy, myocarditis, congestive heart failure, cardiac
tamponade, trauma

■ Non cardiac causes: drug overdose, pulmonary embolism, poisoning, hypo/hyperkalemia, hypoxia etc.

Pathophysiology

Heart stop contraction or failure to contract effectively

Cessation of normal blood circulation

Lack of oxygen to the brain

Loss of consciousness; abnormal breathing

If untreated within five minute

Brain death

Signs and symptoms

■ Unresponsiveness, cessation of respiration

■ Pallor, cyanosis

■ Absence of heart sounds/blood pressure/palpable pulses

■ Dilation of pupils

■ Ventricular fibrillation then asystole is seen if the patient is on a cardiac monitor

Management

■ Assess level of consciousness, pulse and respiration to find out cardiac arrest

(unresponsiveness, no/abnormal breathing and pulse)

■ Ask for help and activate emergency response system according to agency policy or

protocol

■ Start cardiopulmonary resuscitation as soon as possible at the rate of 100 to 120

compress/minute

■ Defibrillation

■ Drug therapy:

> Adrenaline (ephinephrine): the first drug given in all causes of cardiac arrest to

enhance myocardial automaticity, excitability, conductivity and contractility that

increase the heart rate and blood pressure.

> Amiodarone: antiarrhythmic drugs used in tachycardia, ventricular tachycardia,

ventricular fibrillation

> Lidocaine if amiodarone is ineffective or unavailable in cardiac arrest from

VT/VF

> Atropine sulfate to reduce vagus nerve’s control over the heart, thus increasing the

heart rate

> Sodium bicarbonate: administered during the first few moments of a cardiac arrest

to correct respiratory and metabolic acidosis

> Calcium chloride: calcium ion helps the heart beat more effectively by enhancing

the myocardium’s contractile force

■ If a patient has a Return of Spontaneous Circulation (ROSC) such as breathing,

coughing, or movement and a palpable pulse or a measurable blood pressure

> Maintain oxygen saturation (>94%), fluid volume (systolic pressure > 90 mmHg),

body temperature (>36°C), ICU service

> For a low blood pressure, consider one or more of these treatments:

❖ Give 1 to 2 liters of saline or Ringer’s lactate IV fluid.

❖ Start an epinephrine IV infusion to keep the systolic pressure > 90 mmHg.

❖ Start a dopamine IV infusion

❖ Consider norepinephrine for extremely low systolic blood pressure.

According to American Heart Association the Chain of Survival are:

■ Immediate recognition of cardiac arrest and activation of the emergency response

system

■ Early CPR with an emphasis on chest compressions

■ Rapid defibrillation

■ Effective advanced life support

■ Integrated post-cardiac arrest care

Nursing management

■ Monitor arrest caused by ventricular fibrillation

> Begin precordial thump and if successful administer drugs

> If unsuccessful, defibrillation

> If defibrillation is unsuccessful, initiate CPR immediately

> Assist with administration of and monitor effects of additional emergency drugs

■ Provide post cardiac arrest care according to organizational policy

> Manage the airway, provide oxygen and maintain oxygen saturation >94%.

> Keep IV line open and administered IV fluids and medication as prescribed.

> Monitor the effects of drugs

> Assess vital signs and level of consciousness of the patient

> Obtain a 12-lead ECG and action according to protocol

> Provide emotional support to the patient and patient party