Porth's Essentials of Pathophysiology, 4e

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Circulatory Function

U N I T 5

persons with advanced aortic stenosis and is similar to that observed in CAD. Dyspnea, marked fatigability, peripheral cyanosis, and other signs of heart failure usually are not prominent until late in the course of the disease. Syncope (fainting) is most commonly due to the reduced cerebral circulation that occurs during exertion when the arterial pressure declines conse- quent to vasodilation in the presence of a fixed cardiac output. AorticValve Regurgitation. Aortic valve regurgitation or aortic insufficiency is the result of an incompetent aortic valve that allows blood to flow back to the left ventricle during diastole (see Fig. 19-15). As a result, the left ventricle increases its stroke volume to accom- modate blood entering from the pulmonary veins in addition to the volume of blood leaking back through the regurgitant valve. This defect may result from con- ditions that cause scarring of the valve leaflets or from enlargement of the valve orifice to the extent that the valve leaflets no longer meet. There are various causes of aortic regurgitation, including rheumatic fever, idio- pathic dilation of the aorta, congenital abnormalities, infective endocarditis, and Marfan syndrome. Other causes include hypertension, trauma, and failure of a prosthetic valve. Acute aortic regurgitation is characterized by a sudden, large regurgitant volume to a left ventricle of normal size that has not had time to adapt to the vol- ume overload. It is caused by disorders such as infec- tive endocarditis, trauma, or aortic dissection. Using the Frank-Starling mechanism, the heart responds by increasing heart rate, but the compensatory mechanisms fail to maintain the cardiac output. As a result, there is severe elevation in left ventricular end-diastolic pres- sure, which is transmitted to the left atrium and pulmo- nary veins, culminating in pulmonary edema. A decrease in cardiac output leads to sympathetic activation and a resultant increase in heart rate and peripheral vascular resistance that cause the regurgitation to worsen. Death from pulmonary edema, ventricular arrhythmias, or circulatory collapse is common in severe acute aortic regurgitation. Chronic aortic regurgitation, which usually has a gradual onset, represents a condition of combined left ventricular volume and pressure overload. As the valve deformity increases, regurgitant flow into the left ventri- cle increases, diastolic blood pressure falls, and the left ventricle progressively enlarges or eccentrically hyper- trophies. Hemodynamically, the increase in left ven- tricular volume results in the ejection of a large stroke volume that usually is adequate to maintain the forward cardiac output until late in the course of the disease. Most persons remain asymptomatic during this com- pensated phase, which may last decades. The only sign for many years may be a soft systolic aortic murmur. As the disease progresses, signs and symptoms of left ventricular failure begin to appear. These include exertional dyspnea, orthopnea, and paroxysmal noc- turnal dyspnea. In aortic regurgitation, failure of aortic valve closure during diastole causes an abnormal drop

in diastolic pressure. Because coronary blood flow is greatest during diastole, the drop in diastolic pressure produces a decrease in coronary perfusion. Although angina is rare, it may occur when the heart rate and diastolic pressure fall to low levels. Persons with severe aortic regurgitation often complain of an uncomfort- able awareness of heartbeat, particularly when lying down, and chest discomfort due to pounding of the heart against the chest wall. Tachycardia, occurring with emotional stress or exertion, may produce pal- pitations, head pounding, and premature ventricular contractions. The major physical findings relate to the widening of the arterial pulse pressure, a hallmark of chronic aortic regurgitation. The pulse has a rapid rise and fall (Corrigan pulse), with an elevated systolic pressure and low diastolic pressure owing to the large stroke volume and rapid diastolic runoff of blood back into the left ventricle. Korotkoff sounds may persist to zero, even though intra-arterial pressure rarely falls below 30 mm Hg. 37 The large stroke volume and wide pulse pres- sure may result in prominent carotid pulsations in the neck, throbbing peripheral pulses, and a left ventricular impulse that causes the chest to move with each beat. The hyperkinetic pulse of more severe aortic regurgita- tion, called a water-hammer pulse, is characterized by distention and quick collapse of the artery. On ausculta- tion, the turbulence of flow across the aortic valve dur- ing diastole produces a high-pitched or blowing sound. Diagnosis andTreatment Valvular defects usually are detected through cardiac auscultation (i.e., heart sounds). Echocardiography provides a means of visualizing valvular motion, pat- terns of flow, and closure patterns. Pulsed Doppler ultrasonography provides a semiquantitative or quali- tative estimation of the severity of transvalvular gra- dients, right ventricular systolic pressure, and valvular regurgitation. Color flow Doppler provides a visual pattern of flow velocities over the anatomic 2-D echo- cardiographic image. This allows for demonstration of turbulence from stenotic and regurgitant valves. Transesophageal echocardiography with Doppler ultra- sonography is used to obtain echocardiographic data when surface sound transmission is poor, particularly of the AV valves and prosthetic heart valves. Cardiac cath- eterization may be used to further describe the effects of the defect. The treatment of valvular defects consists of medical management of heart failure and associated problems and surgical valve repair or replacement, if warranted by the extent of deformity. Valvular replacement with a prosthetic device or a homograft usually is reserved for severe disease because the ideal substitute valve has not as yet been developed. Percutaneous balloon valvu- loplasty involves the opening of a stenotic valve by guid- ing an inflated balloon through the valve orifice. The procedure is done in the cardiac catheterization labora- tory and involves the insertion of a balloon catheter into the heart through a peripheral blood vessel.