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38 Cards in this Set

  • Front
  • Back

Heart Failure

common chronic health problem.

most common reason for hospital stay in persons over 65.

Diseased heart can not pump (perfuse) the vital organs.

Also called pump failure.

Types of heart failure

Left sided heart failure.

Right sided heart failure.

High output failure

left sided heart failure

typical causes:

HTN / coronary artery disease, and valvular disease involving the mitral or aortic valve. Decreased tissure perfusion from poor cardiac output and pulmonary congestion from increased pressure in the pulmonary vessels indicate LVF (left ventricular failure)

May be: acute / chonic : mild / severe

Formerly called : CHF (congestive heart failure)

Systolic Heart Failure (SVD: systolic ventricular dysfunction)

when the heart cannot contract forcefully enough during systole to effect adequate amounts of blood into the circulation. Preload increases with decreased contractility and afterload increases as a result of increased peripheral resistance

ejection fraction

the percentage of blood ejected from the heart during systole.

normal 50% to 70%.

diastolic heart failure

heart failure with preserved left ventricular function: occurs when the left ventricle cannot relax adequately during diastole. Inadequate relaxation or "stiffening" prevents the ventricle from filling with sufficient blood to ensure an adequate cardiac output

Right sided heart failure (Ventricular failure)

may be caused by left ventricular failure, right ventricular myocardial infarction (MI), or pulmonary hypertension. In this type of heart failure the right ventricle cannot empty completely. Increased volume and pressure develop in the venous system, and peripheral edema results

High output heart failure

can occur when cardiac output remains normal or above normal, unlike left and right sided heart failure, which are typically low output states. High output failure is caused by increased metabolic needs or hyperkinetic conditions, such as septicemia, high fever, anemia, and hyperthyroidism. Not as common as other types of HF.

NYHA (New York Heart Association) staging categories

Class 1: high risk of developing HF

Class 1: cardiac structural abnormalities but NO HF symptoms

Class 2 or 3: patients with current or prior symptoms of HF

Class 4: patients with refractory end-stage HF

Compensatory Mechanisms

when cardiac output is insufficient to meet the demands of the body, compensatory mechanisms work to improve cardiac output. Initially increasing cardiac output, but eventually have a damaging effect on pump function.

1. sympathetic nervous system stimulation

2. RAS : Renin Angiotensin system activation

3. Other chemical responses

4. myocardial hypertrophy


Heart rate "times" stroke volume = cardiac output


the resistance against which the heart must pump.

This is the major determinant of myocardial oxygen requirements.

Africans affected more often than


Common Causes and Risk Factors for HF

HTN / coronary artery disease / cardiomyopathy / substance abuse / valvular disease / congenital defects / cardiac infections and inflammations / dysrhythmias / diabetes mellitus / smoking : tobacco / family history / obesity / severe lung disease / sleep apnea / hyperkinetic conditions ie: hyperthyroidism

Key Features: Left sided Heart Failure

Decreased Cardiac Output:

fatigue / weakness / oliguria and nocturia / angina / confusion, restlesness / dizziness / tachycardia, palpitations / pallor / weak peripheral pulses / cool extremities

Pulmonary Congestion:

hacking cough : worse at night / dyspnea: breathlessness / crackles or wheezes in lungs / frothy, pink tinged sputum / tachypnea / S3/S4 summation gallop

Key Features: Right sided Heart Failure

System Congestion:

Jugular Vein Distention / Enlarged liver and spleen / Anorexia and nausea / Dependent edema (legs and sacrum) / swollen hands and fingers / polyuria at night / weight gain / increased blood pressure (from excess volume) or decreased blood pressure (from failure)

S 3 Gallop

Third heart sound / an early diastolic filling sound indicating an increase in left ventricular pressure. This sound is often the first sign of HF. Increased heart size is common with a displacement of the apical impulse to the left.

Thyroxine (T4) and TSH levels should be assessed in patients

over 65.

/ have A-fibrillation or evidence of thyroid disease. HF may be caused by hypothyroidism or hyperthyroidism.

ABG values (arterial blood gases)

often reveal hypoxemia (low blood oxygen)

/ Respiratory alkalosis may occur because of hyperventilation / respiratory acidosis may occur because of carbon dioxide retention / metabolic acidosis may indicate an accumulation of lactic acid.


respiratory alkalosis

carbon dioxide retention

respiratory acidosis

accumulation of lactic acid

metabolic acidosis

Intervention: Reduce Preload

Preload reduction is appropriate for HF accompanied by congestion with total body sodium and water overload.

Nutrition Therapy

Aimed at reducing sodium and water retention decreasing the workload on the heart. Restrict sodium to decrease fluid retention.

Drug Therapy:

reduce preload : diuretic and venous vasodilators. Morphine sulfate given in acute HF to reduce anxiety, decrease preload and afterload, slow respirations, and reduce the apin associated with a myocardial infarction (MI)

Drugs that enhance contractility

Digoxin: for chronic HF. // Digoxin is a cardio glycoside / provides symptomatic benefits for patients in chronic HF with sinus rhythm and Atrial fibrillation. Dig reduces worsening HF. But may increase mortality due to drug toxicity.

Potential benefits of DIG: increased contractility / reduced heart rate / slowing conduction through AV node / Inhibits sympathetic activity / enhances parasympathetic activity

Dobutamine (beta-adrenergic agonists)

used for short term treatment of acute episodes of HF. Improves cardiac contractility / and thus cardiac output and myocardial systemic perfusion. given IV

milrinone (primacor)

more potent drug used for acute HF, functions as a vasodilator / inotropic medication with phosphodiesterase activity. This drug increases cyclic adenosine monophosphate (cAMP), which enhances the entry of calcium into myocardial cells to increase contractile function. given IV

Levosimendan (Simdax)

a calcium sensitizing medication and a positive inotropic drug. Appears to bind to troponin C in the heart muscle and therefore increases the contraction of the heart. Simdax is used most often in patients who have had or are at high risk for MI.

Beta Adrenergic BLOCKERS

Carvedilol (Coreg), metoprolol succinate (Toprol XL), bisoprolol (Zebeta) CHRONIC HF ONLY ///

Improve condition of some paitens in HF. Prolonged exposure to increased levels of sympathetic stimulation and catecholamines worsens cardiac function. Geta blocakde reverses this effect, improving morbidity, mortality,a nd qualityof life for patients in HF. Beta blockers must be started slowly for HF. patients in acute HF must NOT be started on beta blockers

Pulmonary Edema

crackles // dyspnea at rest / disorientation or acute confusion (esp: elderly) / tachycardia / Hypertension or hypotension / reduced urinary output / cough with frothy, pink tinged sputum / premature ventricular contractions and other dysrhythmias / anxiety / restlessness / lethargy

Heart Failure Self Management


M: medications

take meds as prescribed and do not run out.

know the purpose and side effects of each drug.

avoid NSAIDS to prevent sodium and fluid retention.

A: Activity

stay active / don't over do it

know your limits

be able to carry on a conversation while exercising

W: Weight

weigh each day at the same time / same scale to monitor fluid retention

D: Diet

limit daily sodium intake to 2 to 3 grams as prescribed. Limit daily fluid intake to 2 liters

S: Symptoms

note any new or worsening symptoms and notify the health care provider immediately

Beta Blocker / Digoxin Therapy

1. same time every day

2. continue unless doctor tells you to stop

3. Do not take at same time as antacids or laxatives

4. take pulse before each dose

5. if you forget a dose take it quick or skip it completely

6. do all scheduled lab tests (potassium and dig levels)

7. if potassium supplements are prescribed do not stop taking them until doctor tells you to stop.

mitral stenosis

usually results from rheumatic carditis, which can cause valve thickening by fibrosis and calcification. (rheumatic fever).


valve leaflets fuse and become stiff and the chordae tendineae contract and shorten.

mitral regurgitation

fibrotic and calcific changes occurring prevent the mitral valve from closing completely during systole. Incomplete closure of the valve allows the backflow of blood into the left atrium when the left ventricle contracts. During diastole, the regurgitant output again flows from the left atrium to the left ventricle along with the normal blood flow. The increased volume must be ejected during the next systole. To compensate for the increased volume and pressure, the left atrium and ventricle dilate and hypertrophy.

Mitral Valve Prolapse (MVP)

occurs because the valbular leaflets enlarge and prolapse into the left atrium during systole. This abnormality is usually benign but amy progress to pronounced mitral regurgiatation in some patients. most patients with mvp are asymptomatic but some report chest pain, palpitations or exercise intolerance. A midsystolic click and a late systolic murmur may be heard at the apex of the heart.

Aortic Stenosis

the most common cardiac valve dysfunction in the United States and is often considered a disease of "wear and tear". the aortic valve orifice narrows and obstructs left ventricular outflow during systole. this increased resistance to ejection or afterload results in ventricular hypertrophy. as stenosis worsens, cardiac output becomes fixed and cannot increase to meet the demands of the body during exertion.

Aortic regurgitation (insufficiency)

the aortic valve leaflets do not close properly during diastole and the annulus (the valve ring that attaches to the leaflets) may be dilated, loose, or deformed. This allows flow of blood from the aorta back into the left ventricle during diastole. The left ventricle, in compensation, dilates to accommodate the greater blood volume and eventually hypertrophies.


Usually results from NON rheumatic conditions such as infective endocarditis, congenital anatomic aortic valvular abnormalities, hypertension and marfan syndrome ( a rare, generalized, system disease of connective tissue)