Chapter 8 The Heart
Heart failure is a condition in which the heart cannot meet the functional needs of the body. It may be of sudden onset (acute) or chronic. It elicits a number of hemodynamic, neural, hormonal, and renal responses, and it is clinically assessed as compensated or decompensated.
This subset of heart failure is characterized by a high cardiac output (high systolic ejection fraction) caused by increased demand. It is typically encountered in conditions such as anemia, thyrotoxicosis, beriberi, and pregnancy. Prolonged ventricular overload leads ultimately to overexhaustion of the heart and heart failure.
Cyanosis is bluish discoloration of the skin, mucosa or both due to reduced oxygenation of the blood. Clinically, it becomes evident when the oxygenation of hemoglobin falls below 85%. Two forms of cyanosis are recognized:
Dyspnea, or shortness of breath, results from pulmonary congestion and edema caused by left ventricle failure. Stagnant blood cannot be adequately oxygenated and does not reach the periphery to meet the oxygen demands. The edema fluid inside the alveoli forms a barrier that further impedes the gas exchange. To compensate for the resultant hypoxia followed by hypercapnia, the respiratory centers increase the rate of respiration (tachypnea). Orthopnea refers to dyspnea that occurs in the lying position and is relieved by sitting up or raising the head and chest with pillows. Dyspnea so severe that it would wake up the patient from sleep is called paroxysmal nocturnal dyspnea.
IHD is a consequence of atherosclerosis and develops when the coronary blood flow is inadequate to meet the needs of the myocardium. Ischemia that results from narrowing or obstruction of coronary arteries may be relative or absolute and will present itself in several clinical conditions:
Risk factors can be divided into two groups: those that cannot be modified (e.g., age, male sex, and familial predisposition [usually multifactorial]) and those that can be modified or avoided (e.g., hypertension, smoking, obesity, diabetes, and sedentary lifestyle).
Stable angina and Prinzmetal angina do not cause any significant myocardial cell necrosis, and accordingly there are no microscopic changes in the heart. Unstable angina may be accompanied by focal myocyte necrosis, which is repaired by foci of fibrosis.
Most myocardial infarcts involve the left ventricle. The left coronary artery is more often occluded than the right coronary artery. The anatomic distribution of transmural infarcts depends on the site of occlusion.
However, the patient may die before the infarct heals. These patients most often die because of electrical disturbances, and the examination of the heart at autopsy will reveal the typical macroscopic and microscopic features of an infarct at various stages of evolution or healing.
Dressler syndrome is a complication of transmural myocardial infarcts clinically presenting with pericardial pain associated with pericardial friction rub. Although the pathogenesis of this complication is not known, it is thought to be immunologically mediated. Pericarditis is presumably caused by the development of antibodies to proteins released from the necrotic myocardial cells. These patients have fever, pleural effusion, and joint pains (i.e., symptoms suggestive of serum sickness), all of which may also be caused by autoantibodies. Cortisone treatment is beneficial, also supporting an immunologic explanation.
Myocardial infarctions typically develop in people who usually have generalized atherosclerosis. Accordingly, one can expect that the occluded coronary artery is not the only abnormal vessel and that other coronary arteries are also narrowed to some extent. Loss of myocardium in the infarcted area is accompanied by increased demand for work by the remaining uninfarcted myocardium. Because the blood to this normal myocardium flows through narrowed and calcified arteries, which cannot dilatate, the increased demand generates relative ischemia. Chronic pump failure develops over time.
The most common finding is thrombosis of coronary arteries. Typically, it develops over a ruptured “soft” atheroma—that is, an atheroma that has a soft central core (composed of semiliquid lipid-rich debris) covered with a fibrous cap. The rupture of the fibrous cap will release the atheromatous material into the coronary vessel. Because this material acts as thromboplastin, it will initiate local coagulation of the blood and result in the formation of thrombus. Other causes of sudden cardiac death are coronary diseases (e.g., vasculitis and coronary artery aneurysm), cardiac diseases not clinically recognized (e.g., cardiomyopathies and myocarditis), and valvular disease (e.g., mitral valve prolapse and aortic stenosis).
The hypertrophic heart appears enlarged. At autopsy, such hearts weigh 500 g or more. The walls of the left and the right ventricle is thickened. Extremely enlarged hearts weighing more than 600 g are colloquially called “cor bovinum” because they resemble bovine hearts.