HEART FAILURE

Click to edit Master subtitle style

PRESENTER: CHAPIMA F. MSc. CLINICAL PATH - STUDENT

THE HEART

4/16/12

Introduction o The heart is a vitally life-sustaining organ; it is responsible for pumping more than 6000 liters of blood daily through the body. o In its normal, healthy state, the heart perfuses tissues with a steady supply of vital nutrients and facilitates the removal of waste products. o When pathology supervenes, cardiac dysfunction is associated with devastating physiologic consequences.

4/16/12

Heart disease remains the leading cause of morbidity and mortality in industrialized nations. In this chapter we will first review the features of congestive heart failure (CHF), the common end point of many cardiac diseases. This will be followed by a discussion of the major categories of cardiac disease including selected congenital heart dieases, IHD (coronary artery disease), hypertensive heart disease.

4/16/12

heart disease caused by intrinsic pulmonary diseases (cor pulmonale), valvular heart disease, and primary myocardial disease. A few highlights about pericardial disease and cardiac neoplasms are also presented before we conclude with a brief look at cardiac transplantation.

4/16/12

HEART FAILURE

4/16/12

Heart failure o Heart failure (also called congestive heart failure, or CHF) is a frequent end point of many of the conditions of the heart. o Most heart failure is the consequence of systolic dysfunction, the progressive deterioration of myocardial contractile function. o This is most commonly due to ischemic heart. disease or hypertension. o However, in 20% to 50% of patients the heart contracts normally but relaxation is abnormal.
4/16/12

These patients with "diastolic" failure are generally older and more likely to be female with hypertension or diabetes mellitus. Heart failure may be caused by valve failure (e.g., endocarditis) or can also occur in normal hearts suddenly burdened with an abnormal load (e.g., fluid or pressure overload).

4/16/12

o o

In heart failure, the heart is unable to pump blood at a rate that meets the requirements of the metabolizing tissues, or can only do so only with filling pressures that are higher than normal. Onset may be insidious or acute. In most cases of CHF the heart cannot keep pace with basic peripheral demands; in a minority of cases, heart failure results from greatly increased tissue demands for blood (high-output failure).

4/16/12

Excluded from the definition are conditions in which inadequate cardiac output occurs because of blood loss or some other process that impairs blood return to the heart. In a mechanical sense, the failing heart in CHF can no longer pump the blood delivered to it by the venous circulation. Inadequate cardiac output-called forward failureis almost always accompanied by increased congestion of the venous circulation (backward failure), because the failing ventricle is unable to eject the venous blood delivered to it.
4/16/12

This results in an increased end-diastolic ventricular volume, leading to increased enddiastolic pressures and, finally, elevated venous pressures. Although the root problem in CHF is typically abnormal cardiac function, virtually every other organ is eventually affected by some combination of forward and backward failure.

4/16/12

The cardiovascular system can adapt to reduced myocardial contractility or increased hemodynamic burden by a few different pathways. The most important are; o Activation of neurohumoral systems, especially o (1) release of the neurotransmitter norepinephrine by the sympathetic nervous system (increases heart rate and augments myocardial contractility and vascular resistance),
o

4/16/12

o o

(2) activation of the renin-angiotensinaldosterone system, and (3) release of atrial natriuretic peptide (ANP). This is a polypeptide hormone secreted by the atria in the setting of atrial distension. It causes vasodilation, naturiuresis, and diuresis that help alleviate volume or pressure overload states. The Frank-Starling mechanism.

4/16/12

As cardiac failure progresses, end-diastolic pressures increase, causing individual cardiac muscle fibers to stretch; This ultimately increases the volume of the cardiac chamber. In accordance with the Frank-Starling relationship, these lengthened fibers initially contract more forcibly, thereby increasing cardiac output. If the dilated ventricle is able to maintain cardiac output at a level that meets the needs of the body, the patient is said to be in compensated heart failure.
4/16/12

However, increasing dilation increases ventricular wall tension, which increases the oxygen requirements of an already compromised myocardium. With time, the failing myocardium is no longer able to propel sufficient blood to meet the needs of the body, even at rest. At this point, patients enter a phase termed decompensated heart failure. Myocardial structural changes, including hypertrophy, to increase the mass of contractile tissue.
4/16/12

Because adult cardiac myocytes cannot proliferate, adaptation to a chronically increased workload involves hypertrophy of individual muscle cells. In pressure overload states (e.g., hypertension, valvular stenosis), the hypertrophy is characterized by increased diameter of individual muscle fibers. This yields concentric hypertrophy, in which the thickness of the ventricular wall increases without an increase in the size of the chamber.

4/16/12

In volume overload states (e.g., valvular regurgitation or abnormal shunts), it is the length of individual muscle fibers that increases. This results in eccentric hypertrophy, characterized by an increase in heart size as well as an increase in wall thickness.

4/16/12

Initially, these adaptive mechanisms may be adequate to maintain cardiac output in the face of declining cardiac performance. However, with sustained or worsening heart function, pathologic changes may eventually supervene, resulting in structural and functional disturbances; such degenerative changes include myocyte apoptosis, cytoskeletal alterations, and altered extracellular matrix synthesis and remodelling. Even hypertrophy comes at a significant cost to the cell.

4/16/12

Oxygen requirements of the hypertrophic myocardium are increased as a result of increased myocardial cell mass and increased tension of the ventricular wall. Because the myocardial capillary bed does not always increase in step with the increased oxygen demands of the hypertrophic muscle fibers, the myocardium becomes vulnerable to ischemic injury. Heart failure can affect predominantly the left side or the right side, or both sides of the heart.

4/16/12

LEFT-SIDED HEART FAILURE

4/16/12

1. 1. 2. 3.

The most common causes of left-sided cardiac failure are; IHD, Systemic hypertension, Mitral or aortic valve disease, and Primary diseases of the myocardium.

4/16/12

Morphology o Findings in the heart depend on the underlying disease process; for example, myocardial infarction or valvular deformities may be present. o Except in cases of mitral valve stenosis (or other processes that restrict left ventricular size), the left ventricle is usually hypertrophied and often dilated, sometimes quite massively. o There are usually nonspecific changes of hypertrophy and fibrosis in the myocardium.
4/16/12

Secondary enlargement of the left atrium with resultant atrial fibrillation (i.e. uncoordinated, chaotic contraction of the atrium) can reduce stroke volume or lead to blood stasis and thrombus formation (particularly in the atrial appendage); a fibrillating left atrium carries a substantially increased risk of embolic stroke. The extracardiac effects of left-sided heart failure are manifested most prominently in the lungs.

4/16/12

Rising pressure in the pulmonary veins is ultimately transmitted retrogradely to the capillaries, resulting in pulmonary congestion and edema. The lungs are heavy and boggy, and histologically there are perivascular and interstitial transudate, alveolar septal edema, and intra-alveolar edema.

4/16/12

Moreover, capillary leakiness leads to the accumulation of erythrocytes (containing hemoglobin) that are phagocytosed by macrophages. Within macrophages, hemoglobin is converted to hemosiderin and hence hemosiderin-containing macrophages in the alveoli (called heart failure cells) are evidence of prior of pulmonary edema.

4/16/12

Clinical Features o Dyspnea usually the earliest and most significant complaint of patients in left-sided heart failure; o Cough is also a common accompaniment of left heart failure due to fluid transudation into airspaces. o Orthopnea; this occurs because of increased venous return from the lower extremities and by elevation of the diaphragm when in the supine position.

4/16/12

o o o o

Cardiomegaly Tachycardia A third heart sound (S3), Fine rales at the lung bases, produced by respirations through edematous pulmonary alveoli. With progressive ventricular dilation, the papillary muscles are displaced laterally, causing mitral regurgitation and a systolic murmur.

4/16/12

Subsequent chronic dilation of the left atrium is often associated with atrial fibrillation, manifested by an "irregularly irregular" heartbeat.

4/16/12

RIGHT-SIDED HEART FAILURE

4/16/12

The most common cause of right-sided heart failure is left ventricular failure, with its associated pulmonary congestion and elevation in pulmonary arterial pressure. Right-sided failure can also occur in the absence of left-sided heart failure in patients with intrinsic diseases of the lung parenchyma and/or pulmonary vasculature (cor pulmonale) and in patients with primary pulmonic or tricuspid valve disease. It sometimes follows congenital heart diseases, i.e. in the setting of left-to-right shunts with chronic volume and pressure overloads.
4/16/12

Morphology o The major morphologic and clinical effects of pure right-sided heart failure differ from those of left-sided heart failure in that pulmonary congestion is minimal, whereas engorgement of the systemic and portal venous systems is typically pronounced. Liver and Portal System. o The liver is usually increased in size and weight (congestive hepatomegaly), and a cut section displays prominent passive congestion, a pattern referred to as nutmeg liver
4/16/12

Congested red centers of the liver lobules are surrounded by paler, sometimes fatty, peripheral regions. In some instances, especially when left-sided heart failure is also present, severe central hypoxia produces centrilobular necrosis along with the sinusoidal congestion. With long-standing severe right-sided heart failure, the central areas can become fibrotic, creating so-called cardiac cirrhosis

4/16/12

Right-sided heart failure also leads to elevated pressure in the portal vein and its tributaries. Congestion produces a tense, enlarged spleen (congestive splenomegaly). With long-standing congestion, the enlarged spleen can achieve weights of 300 to 500 gm (normal <150 gm). Microscopically, there can be marked sinusoidal dilation. Chronic edema of the bowel wall may interfere with absorption of nutrients.

4/16/12

Accumulations of transudate in the peritoneal cavity can cause ascites. Pleural and Pericardial Spaces. o Fluid may accumulate in the pleural space (particularly right) and pericardial space (effusions). o Thus, while pulmonary edema indicates leftsided heart failure, pleural effusions accompany both right-sided and left-sided heart failure. o Pleural effusions (typically serous) can range from 100 mL to well over 1 L and can cause partial atelectasis of the affected lung.
o

4/16/12

Unlike inflammatory edema, the edema fluid in CHF has a low protein content. Subcutaneous Tissues. o Peripheral edema of dependent portions of the body, especially ankle (pedal) and pretibial edema, is a hallmark of right-sided heart failure. o In chronically bedridden patients, the edema may be primarily presacral. o Anasarca
o

4/16/12

Clinical Features o Hepatic and splenic enlargement o Peripheral oedema o Pleural effusion o Ascites o As CHF progresses, patients can become frankly cyanotic and acidotic, as a result of decreased tissue perfusion.

4/16/12

END OF PRESETANTION

4/16/12