The Heart

The heart is located in the mediastinum, the cavity between the lungs. The heart is tilted so that its pointed end, the apex, points downward toward the left hip, while the broad end, the base, faces upward toward the right shoulder.

As blood travels through the heart, it enters a total of four chambers and passes through four valves. The two upper chambers, the right and left atria, are separated longitudinally by the interatrial septum. The two lower chambers, the right and left ventricles, are the pumping machines of the heart and are separated longitudinally by the interventricular septum. A valve follows each chamber and prevents the blood from flowing backward into the chamber from which the blood originated.

The right atrium, located in the upper right side of the heart, and a small appendage, the right auricle, act as a temporary storage chamber so that blood will be readily available for the right ventricle. Deoxygenated blood from the systemic circulation enters the right atrium through three veins, the superior vena cava, the inferior vena cava, and the coronary sinus. During the interval when the ventricles are not contracting, blood passes down through the right atrioventricular (AV) valve into the next chamber, the right ventricle. The AV valve is also called the tricuspid valve because it consists of three flexible cusps (flaps).

The right ventricle is the pumping chamber for the pulmonary circulation. The ventricle, with walls thicker and more muscular than those of the atrium, contracts and pumps deoxygenated blood through the three-cusped pulmonary semilunar valve and into a large artery, the pulmonary trunk. The pulmonary trunk immediately divides into two pulmonary arteries, which lead to the left and right lungs, respectively. The following events occur in the right ventricle.

When the right ventricle contracts, the right AV valve closes and prevents blood from moving back into the right atrium. Small tendonlike cords, the chordae tendineae, are attached to papillary muscles at the opposite, bottom side of the ventricle. These cords limit the extent to which the AV valve can be forced closed, preventing it from being pushed through and into the atrium.

When the right ventricle relaxes, the initial backflow of blood in the pulmonary artery closes the pulmonary semilunar valve and prevents the return of blood to the right ventricle.

The left atrium and its auricle appendage receive oxygenated blood from the lungs though four pulmonary veins (two from each lung). The left atrium, like the right atrium, is a holding chamber for blood in readiness for its flow into the left ventricle. When the ventricles relax, blood leaves the left atrium and passes through the left AV valve into the left ventricle. The left AV valve is also called the mitral or bicuspid valve, the only heart valve with two cusps. The left ventricle is the pumping chamber for the systemic circulation. Because a greater blood pressure is required to pump blood through the much more extensive systemic circulation than through the pulmonary circulation, the left ventricle is larger and its walls are thicker than those of the right ventricle. When the left ventricle contracts, it pumps oxygenated blood through the aortic semilunar valve, into a large artery, the aorta, and throughout the body. The following events occur in the left ventricle, simultaneously and analogously with those of the right ventricle.

When the left ventricle contracts, the left AV valve closes and prevents blood from moving back into the right atrium. As in the right AV valve, the chordae tendineae prevent overextension of the left AV valve.

When the left ventricle relaxes, the initial backflow of blood in the aorta closes the aortic semilunar valve and prevents the return of blood to the left ventricle.

Figure 1 The pathway of blood through the chambers and valves of the heart.

A diverse range of conditions that promote cardiomyocyte injury or loss may cause dilated cardiomyopathy. Dilated cardiomyopathy is characterized by ventricular chamber enlargement and systolic dysfunction with normal left ventricle (LV) wall thickness. Ventricular enlargement and dysfunction generally leads to progressive heart failure with further decline in LV contractile function. Sequelae include ventricular and supraventricular Compensatory mechanisms associated with low cardiac output induce arrhythmias, conduction system abnormalities, thromboembolism, and sudden or heart failurerelated death.reflex upregulation of sympathetic tone and the renin-angiotensin axis, causing increased release of vasopressin, aldosterone, and atrial natriuretic peptide. Stimulation of these hormonal tracts results in volume expansion, which induces vasoconstriction. Vasoconstriction increases afterload that, in turn, decreases stroke volume. As cardiac output depends on stroke volume and heart rate, vasoconstriction ultimately can contribute to decreased cardiac output. Treatment of dilated cardiomyopathy is directed at interrupting this negative cycle.