Diseases of the heart fit into several general categories: congenital heart disease, ischemic heart disease, valvular diseases, and diseases of the myocardium (i.e., cardiomyopathies). Pericardial diseases and cardiac tumors are an additional small subset of conditions affecting the heart. A common manifestation of many different forms of heart disease is congestive heart failure (CHF). In general terms, congestive heart failure is the inability of the heart to pump enough blood to supply the body's oxygen requirements. It can represent failure of cellular adaptation (e.g., decompensated hypertrophy due to hypertension or chamber dilation due to regurgitant valves) or the outcome of myocardial damage caused by other diseases (e.g., scarring due to ischemic injury, inflammation, or accumulation of iron in hemochromatosis).
Classic symptoms of heart disease are chest pain or discomfort, dyspnea (including orthopnea and paroxysmal nocturnal dyspnea), palpitations, syncope, and edema. Dyspnea is an uncomfortable awareness of breathing. Orthopnea is dyspnea when in the recumbent position due to increased venous return and increased pulmonary venous pressure. Patients with orthopnea sleep upright on pillows to avoid becoming short of breath. Paroxysmal nocturnal dyspnea is when patients awaken with dyspnea 2–4 hours after falling asleep (due to central redistribution of peripheral edema).
An understanding of heart sounds is important in the clinical evaluation of heart disease. The S1 sound is caused by closing of the mitral and tricuspid valves, and the S2 sound is caused by closing of the aortic and pulmonary valves. In a patient with hypertension (systemic or pulmonary), closing of the associated valve (aortic or pulmonic) is accentuated (louder); in a patient with stenosis, the closing is diminished in strength (softer sound). S2 is physiologically split during inspiration (aortic, A2, first and pulmonic, P2 second)—increased venous return to the right side of the heart delays closure of the pulmonic valve and decreased return to the left side speeds closure of the aortic valve. Wide splitting of S2 is caused by a greater than normal delay in pulmonic closure (e.g., right bundle branch block, pulmonic stenosis) or earlier aortic valve closure due to decreased left ventricular volume (e.g., mitral regurgitation, ventricular septal defect). Paradoxical splitting (P2 first and A2 second) occurs with delayed closure of the aortic valve (e.g., left bundle branch block, aortic stenosis). A pathologic S3 occurs with ventricular systolic dysfunction during the rapid filling phase of diastole or from impact of the left ventricle against the chest wall. It is particularly common in the setting of CHF. S4 is from ejection of blood from the atrium into a noncompliant ventricle, as might be encountered in the setting of ventricular hypertrophy related to systemic hypertension, or in the setting of an acute myocardial infarct.
This chapter will discuss congenital heart disease, ischemic heart disease, hypertensive cardiovascular disease, congestive heart failure, valvular heart disease, cardiomyopathies, myocarditis, pericardial disease, and cardiac tumors.