This document discusses heart failure, including its causes, types, signs and symptoms, diagnosis, and treatment. Heart failure occurs when the heart cannot pump effectively to meet the body's needs. It can be caused by problems with the heart muscle itself or with the heart's workload. Treatment focuses on improving heart function through medications like diuretics, ACE inhibitors, and beta blockers to manage symptoms and prevent worsening of the condition.
2. Heart failure
Introduction:
• When the myocardium can’t pump effectively enough to meet the
body’s metabolic needs, heart failure occurs.
• Pump failure usually occurs in a damaged left ventricle, but it may
also happen in the right ventricle. Usually, left-sided heart failure
develops first.
Heart failure is classified as:
• high-output or low-output
• acute or chronic
• left-sided or right-sided
• forward or backward.
3. How it happens( pathophysiology):
• Heart failure may result from a primary abnormality of the heart
muscle—for example, an infarction that impairs ventricular function and
prevents the heart from pumping enough blood.
• Heart failure may also be caused by problems unrelated to MI:
• Mechanical disturbances in ventricular filling during diastole, due to
blood volume that’s too low for the ventricle to pump, occur in mitral
stenosis secondary to rheumatic heart disease or constrictive pericarditis
and in atrial fibrillation.
• Systolic hemodynamic disturbances—such as excessive cardiac workload
caused by volume overload or pressure overload—limit the heart’s
pumping ability. This problem can result from mitral or aortic insufficiency,
which leads to volume overload. It can also result from aortic stenosis or
systemic hypertension, which causes increased resistance to ventricular
emptying and decreased cardiac output.
4. Factors favorable to failure
• Certain conditions can predispose a patient to heart failure, especially if he has
underlying heart disease.
These include:
• arrhythmias, such as tachyarrhythmias, which can reduce ventricular filling time;
arrhythmias that disrupt the normal atrial and ventricular filling synchrony; and
bradycardia, which can reduce cardiac output
• pregnancy, which increases circulatory blood volume
• thyrotoxicosis, which increases the force of myocardial contractions
• pulmonary embolism, which elevates PAP, causing right-sided heart failure
• infections, which increase metabolic demands and further burden the heart
• anemia, in which less oxygen is delivered to the heart muscle by the coronary
arteries; severe anemia results in decreased cardiac output as the heart muscle is
deprived of oxygen
• increased physical activity, increased salt or water intake, emotional stress, or
failure to comply with the prescribed treatment regimen for the underlying heart
disease
5. Left-sided heart failure
1. Increased workload and end-diastolic volume enlarge the left ventricle .
Because of lack of oxygen, the ventricle enlarges with stretched tissue rather
than functional tissue. The patient may experience increased heart rate, pale
and cool skin, tingling in the extremities, decreased cardiac output, and
arrhythmias.
2. Diminished left ventricular function allows blood to pool in the ventricle
and the atrium and eventually back up into the pulmonary veins and
capillaries, as shown below. At this stage, the patient may experience
dyspnea on exertion, confusion, dizziness, orthostatic hypotension,
decreased peripheral pulses and pulse pressure, cyanosis, and an S3 gallop.
3. As the pulmonary circulation becomes engorged, rising capillary pressure
pushes sodium and water into the interstitial space, causing pulmonary
edema. You’ll note coughing, subclavian retractions, crackles, tachypnea,
elevated pulmonary artery pressure, diminished pulmonary compliance, and
increased partial pressure of carbon dioxide.
6. 4. When the patient lies down, fluid in the extremities moves into the
systemic circulation. Because the left ventricle can’t handle the
increased venous return, fluid pools in the pulmonary circulation,
worsening pulmonary edema. You may note decreased breath sounds,
dullness on percussion, crackles, and orthopnea.
5. The right ventricle may now become stressed because it’s pumping
against greater pulmonary vascular resistance and left ventricular
pressure. When this occurs, the patient’s symptoms worsen.
8. Right-sided heart failure
6. The stressed right ventricle enlarges with the formation of stretched tissue.
Increasing conduction time and deviation of the heart from its normal axis can
cause arrhythmias. If the patient doesn’t already have left-sided heart failure, He
may experience increased heart rate, cool skin, cyanosis, decreased cardiac output,
palpitations, and dyspnea.
7. Blood pools in the right ventricle and right atrium. The backed-up blood causes
pressure and congestion in the vena cava and systemic circulation (see illustration
below). The patient will have elevated central venous pressure, jugular vein
distention, and hepatojugular reflux.
8. Backed-up blood also distends the visceral veins, especially the hepatic vein. As
the liver and spleen become engorged (see illustration below), their function is
impaired. The patient may develop anorexia, nausea, abdominal pain, palpable
liver and spleen, weakness, and dyspnea secondary to abdominal distention.
9. Rising capillary pressure forces excess fluid from the capillaries into the
interstitial space (see illustration below). This causes tissue edema, especially in the
lower extremities and abdomen. The patient may experience weight gain, pitting
edema, and nocturia.
9. Getting complicated
• Eventually, sodium and water may enter the lungs, causing pulmonary
edema, a life-threatening condition. Decreased perfusion to the brain,
kidneys, and other major organs can cause them to fail.
• MI can occur because the oxygen demands of the overworked heart
can’t be met.
10. Classifying heart failure
• Heart failure may be classified different ways according to its pathophysiology.
Right-sided or left-sided
• Right-sided heart failure is a result of ineffective right ventricular contractile function. It may be caused by an acute right
ventricular infarction or pulmonary embolus. However, the most common cause is profound backward flow due to left-sided heart
failure.
• Left-sided heart failure is the result of ineffective left ventricular contractile function. It may lead to pulmonary congestion or
pulmonary edema and decreased cardiac output. Left ventricular myocardial infarction (MI), hypertension, and aortic and mitral
valve stenosis or insufficiency are common causes.
• As the decreased pumping ability of the left ventricle persists, fluid accumulates, backing up into the left atrium and then into the
lungs. If this worsens, pulmonary edema and right-sided heart failure may also result.
Systolic or diastolic
• In systolic heart failure, the left ventricle can’t pump enough blood out to the systemic circulation during systole and the ejection
fraction falls. Consequently, blood backs up into the pulmonary circulation, pressure rises in the pulmonary venous system, and
cardiac output falls.
• In diastolic heart failure, the left ventricle can’t relax and fill properly during diastole and the stroke volume falls. Therefore, larger
ventricular volumes are needed to maintain cardiac output.
Acute or chronic
• “Acute” refers to the timing of the onset of symptoms and whether compensatory mechanisms kick in. Typically, fluid status is
normal or low, and sodium and water retention don’t occur.
• In chronic heart failure, signs and symptoms have been present for some time, compensatory mechanisms have taken effect, and
fluid volume overload persists. Drugs, diet changes, and activity restrictions usually control symptoms.
11. Acute or insidious
• The patient’s underlying condition determines whether heart failure is
acute or insidious.
• Heart failure is commonly associated with systolic or diastolic overloading
and myocardial weakness. As stress on the heart muscle reaches a critical
level, the muscle’s contractility is reduced and cardiac output declines.
Venous input to the ventricle remains the same, however.
The body’s responses to decreased cardiac output include:
• reflex increase in sympathetic activity
• release of renin from the juxtaglomerular cells of the kidney
• anaerobic metabolism by affected cells
• increased extraction of oxygen by the peripheral cells.
12. Signs and symptoms (What to look for):
The early signs and symptoms of heart failure include:
• fatigue
• exertional, paroxysmal, and nocturnal dyspnea
• neck vein engorgement
• hepatomegaly.
Later signs and symptoms include:
• tachypnea
• palpitations
• dependent edema
• unexplained, steady weight gain
• nausea
14. Diagnosis(What tests tell you)
These tests help diagnose heart failure:
• ECG reveals ischemia, tachycardia, and extra systole.
• Echocardiogram identifies the underlying cause as well as the type and
severity of the heart failure.
• Laboratory studies, such as B-type natriuretic peptide, confirm the
presence of heart failure.
• Chest X-ray shows increased pulmonary vascular markings, interstitial
edema, or pleural effusion and cardiomegaly.
• PAP monitoring shows elevated PAP, and left ventricular end-diastolic
pressure in left-sided heart failure and elevated right atrial pressure or CVP
in right-sided heart failure.
15. Treatment:
• The goal of treatment for heart failure is to improve pump function, thereby reversing
the compensatory mechanisms that produce or intensify the clinical effects.
• Heart failure can usually be controlled quickly with treatment, including:
• administration of diuretics (such as furosemide [Lasix], metolazone,
hydrochlorothiazide, ethacrynic acid [Edecrin], bumetanide,
• spironolactone [Aldactone] combined with a loop or thiazide diuretic, or triamterene
[Dyrenium]) to reduce total blood volume and circulatory congestion
• bed rest
• oxygen administration to increase oxygen delivery to the myocardium and other vital
organs
• administration of inotropic drugs (such as digoxin) to strengthen myocardial
contractility; sympathomimetic (such as dopamine and dobutamine) in acute
situations; or inamrinone or milrinone to increase contractility and cause arterial
vasodilation
• administration of vasodilators to increase cardiac output or angiotensin-converting
enzyme inhibitors to decrease afterload
• Anti embolism stockings to prevent veno stasis and thromboembolism formation.
16. Acute pulmonary edema
• As a result of decreased contractility and elevated fluid volume and pressure, fluid may be driven from the
pulmonary capillary beds into the alveoli, causing pulmonary edema. Treatment for acute pulmonary
edema includes:
• administration of morphine.
• administration of nitroglycerin or nitroprusside to diminish blood return to the heart
• administration of dobutamine, dopamine, inamrinone, or milrinone to increase myocardial contractility and
cardiac output
• administration of diuretics to reduce fluid volume
• administration of supplemental oxygen
• placement of the patient in high Fowler’s position.
Continued care
• After recovery, the patient must continue medical care and usually must continue taking digoxin,
angiotensin converting enzyme inhibitors, beta-adrenergic blockers, diuretics, and potassium supplements.
The patient with valve dysfunction who has recurrent, acute heart failure may need surgical valve
replacement.
What’s left?
• Left ventricular remodeling surgery may also be performed. This surgical procedure involves cutting a
wedge about the size of a small slice of pie out of the left ventricle of an enlarged heart.
• The left ventricle is repaired. The result is a smaller ventricle that can pump blood more efficiently. The only
option for some patients is heart transplantation. A left ventricular assist device may be necessary until a
heart is available for transplantation.