Cardiomegaly denotes an enlarged heart muscle. The most critical pathophysiological changes leading to cardiomegaly include dilated hypertrophy, fibrosis, and contractile malfunction. Contractile dysfunction and abnormal myocardial remodeling can lead to hypertrophic cardiomyopathy or dilated cardiomyopathy. Mechanical stretching, circulating neurohormones, and oxidative stress are significant stimuli for the signal transduction of inflammatory cytokines and MAP kinase in cardiomyocytes. Signal transduction leads to changes in structural proteins and proteins that regulate excitation-contraction. Dilated cardiomyopathy mutations result in a reduced force of the sarcomere contraction and a reduction in sarcomere content. Hypertrophic cardiomyopathy mutations result in a molecular phenotype of hyperdynamic contractility, poor relaxation, and increased energy consumption.

Option B: Cardiomyopathy is a heart muscle disease of unknown origin. In cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid. In rare cases, the muscle tissue in the heart is replaced with scar tissue.
Option C: Myocarditis refers to inflammation of the heart muscle. It is an inflammatory disease of the myocardium with a wide range of clinical presentations, from subtle to devastating.
Option D: Pericarditis is an inflammation of the pericardium. Pericarditis is usually acute – it develops suddenly and may last up to several months. The condition usually clears up after 3 months, but sometimes attacks can come and go for years. When a client has pericarditis, the membrane around the heart is red and swollen, like the skin around a cut that becomes inflamed. Sometimes there is extra fluid in the space between the pericardial layers, which is called pericardial effusion.

These are the classic symptoms of heart failure. Heart failure is the pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure.

Option A: Pericarditis is exhibited by a feeling of fullness in the chest and auscultation of a pericardial friction rub.
Option B: Hypertension is usually exhibited by headaches, visual disturbances, and a flushed face. Myocardial infarction causes heart failure but isn’t related to these symptoms.
Option C: Obliterative cardiomyopathy is very rare. It may result from the end stage of eosinophilic syndromes, in which intracavitary thrombus fills the left ventricular apex and hampers the filling of the ventricles.

Cardiac output isn’t affected by hypertrophic cardiomyopathy because the size of the ventricle remains relatively unchanged. Three explanations for the systolic anterior motion of the mitral valve have been offered, as follows: (1) the mitral valve is pulled against the septum by contraction of the papillary muscles, which occurs because of the valve’s abnormal location and septal hypertrophy altering the orientation of the papillary muscles; (2) the mitral valve is pushed against the septum because of its abnormal position in the outflow tract; (3) the mitral valve is drawn toward the septum because of the lower pressure that occurs as blood is ejected at high velocity through a narrowed outflow tract (Venturi effect).

Option A: Dilated cardiomyopathy causes a decrease in cardiac output. Progressive dilation can lead to significant mitral and tricuspid regurgitation, which may further diminish the cardiac output and increase end-systolic volumes and ventricular wall stress. In turn, this leads to further dilation and myocardial dysfunction.
Option C: Restrictive cardiomyopathy causes decreased cardiac output. Reduced LV filling leads to reduced stroke volume resulting in low cardiac output symptoms such as fatigue and lethargy. Increased filling pressures cause pulmonary and systemic congestion and symptomatic dyspnea.
Option D: Obliterative cardiomyopathy may affect cardiac output because a thrombus hampers ventricular filling, which may decrease the cardiac output.

An S4 occurs as a result of increased resistance to ventricular filling after atrial contraction. This increased resistance is related to decreased compliance of the ventricle.

Option A: A dilated aorta doesn’t cause an extra heart sound, though it does cause a murmur. The aorta is considered pathologically dilated if the diameters of the ascending aorta and the aortic root exceed the norms for a given age and body size. A 50% increase over the normal diameter is considered aneurysmal dilatation.
Option C: Decreased myocardial contractility is heard as a third heart sound. Optimal myocardial contractility is dependent on an optimal filling pressure, afterload, and the presence and availability of inotropic substances (eg, epinephrine, norepinephrine, or calcium). Calcium influx and binding to troponin C is essential for cardiac contraction.
Option B: An S4 isn’t heard in a normally functioning heart. The fourth heart sound is a low-pitched sound coincident with the late diastolic filling of the ventricle due to atrial contraction. It thus occurs shortly before the first heart sound. Although it is also called the atrial sound, and its production requires an effective atrial contraction, the fourth heart sound is the result of vibrations generated within the ventricle.

By decreasing the heart rate and contractility, beta-adrenergic blockers improve myocardial filling and cardiac output, which are primary goals in the treatment of cardiomyopathy.

Option A: Antihypertensives aren’t usually indicated because they would decrease cardiac output in clients who are often already hypotensive. Many antihypertensive drugs have their primary action on systemic vascular resistance. Some of these drugs produce vasodilation by interfering with sympathetic adrenergic vascular tone (sympatholytics) or by blocking the formation of angiotensin II or its vascular receptors.
Option C: Calcium channel blockers are sometimes used for the same reasons as beta-adrenergic blockers; however, they aren’t as effective as beta-adrenergic blockers and cause increased hypotension. These channels are responsible for regulating the influx of calcium into muscle cells, which in turn stimulates smooth muscle contraction and cardiac myocyte contraction. In cardiac nodal tissue, L-type calcium channels play an important role in pacemaker currents, and in phase 0 of the action potentials.
Option D: Nitrates aren’t’ used because of their dilating effects, which would further compromise the myocardium. Nitrates exert their effects by dilating venous vessels, coronary arteries, and small arterioles; its maximal vasodilation is in the venous vessels.