Question

PROBLEM #3 INTRODUCTION: The contractile performance of heart muscle depends on its inotropic state, preload and afterload. These factors also determine the stroke output of the heart. In vivo, the aortic pressure, the pressure against which the left ventricle must pump, is the main afterload. If the outflow resistance of the aortic valve should increase, however, it too can impose a significant afterload on the ventricle. Use the following websites to understand what preload and afterload are and how they affect the force of contraction in the heart.

http://www.cvphysiology.com/Cardiac%20Function/CF007.htm

http://www.cvphysiology.com/Cardiac%20Function/CF004.htm

http://www.cvphysiology.com/Cardiac%20Function/CF008.htm

PROBLEM #3: Predict the consequences (increase, decrease, no change) of an increase in afterload on heart muscle and the effect of a sudden stenosis of the aortic valve (reduction in the cross-sectional area of the valve) on the heart. Explain your predictions.

            CARDIAC MUSCLE                                   

            1. velocity of shortening

            2. shortening

            HEART

            3. end systolic volume

            4. end diastolic volume

            5. stroke volume

Answer 1

Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. Preload, therefore, is related to muscule sarcomere length. Because sarcomere length cannot be determined in the intact heart, other indices of preload are used such as ventricular end-diastolic volume or pressure.

When venous return to the heart is increased, the end-diastolic pressure and volume of the ventricles are increased, which stretches the sarcomeres, thereby increasing their preload. In contrast, hypovolemia resulting from a loss of blood volume (e.g., hemorrhage) leads to less ventricular filling and therefore shorter sacromere lengths (reduced preload). Changes in ventricular preload dramatically affect ventricular stroke volume by what is called the Frank-Starling mechanism. Increased preload increases stroke volume, whereas decreased preload decreases stroke volume by altering the force of contraction of the cardiac muscle.

The concept of preload can be applied to either the ventricles or atria. Regardless of the chamber, the preload is related to the chamber volume, and therefore sarcomere length, just prior to contraction.

Aortic stenosis. The considerations just reviewed imply that in patients with valvular heart disease knowledge of the effects of altered loading conditions on the left ventricle is highly important in reaching a proper decision concerning the timing of corrective operation. In acquired valvular aortic stenosis in the adult patient, M-mode and two-dimensional echocardiography are helpful in diagnosis but often inconclusive for reaching a decision concerning operation (70), although recent studies (71) indicate that Doppler estimates of aortic valve gradient may be more reliable for determining the severity of stenosis , Nevertheless, cardiac catheterization and coronary arteriography are almost always desirable when the clinical examination and echocardiographic findings suggest the possibility of significant stenosis. Surgical treatment should be recommended in the patient with symptoms in whom hemodynamically significant stenosis is established since the outlook without operation is extremely poor, whereas with surgical treatment it is quite favorable regardless of the preoperative level of left ventricular function. Aortic regurgitation. Among patients with chronic valvular regurgitation. we can now begin to identify by noninvasive means those patients who are developing depression of left ventricularfunction. In chronic aortic regurgitation, postoperative depression of left ventricular function is becoming less of a problem since the current tendency is to operate earlier (54). Recent studies (57) suggest that in many patients with chronic aortic regurgitation, symptoms will occur before or at the time depression of left ventricular function becomes manifest. Moreover, if the patient is asymptomatic and left ventricular size and function are not markedly abnormal, a delay until the onset of symptoms or to verify significant and progressive left ventricular dysfunction can be justified since left ventricular function tends to improve postoperatively even if it is moderately depressed before operation (25.57.72). In those relatively few patients with severe aortic regurgitation and no symptoms who have depressed function and a markedly enlarged ventricle or progressive depression of function, some guidelines have been offered (Table 3) for considering operation whenever left ventricular function and size approach certain limits found to be associated with irreversible myocardial damage. Mitral regurgitation. Chronic mitral regurgitation poses a more difficult problem. It is important that patients with few or no symptoms who have cardiomegaly due to severe mitral regurgitation be studied regularly by echocardiography to detect early depression of left ventricular function. In those patients who exhibit deterioration toward certain limits (Table 4), present information indicates that operation should be recommended even if symptoms are mild because once the ventricle reaches those limits, left ventricular function may seriously deteriorate postoperatively. If left ventricular function has markedly deteriorated, it is possible that the natural history of the patients may be more favorable without operation. As more experience is gained with valve reconstructive procedures for mitral regurgitation (73), which are being performed with increasing frequency in some centers, more enthusiasm may develop for earlier operation in patients with chronic mitral regurgitation and few symptoms. In any case, it appears that we are waiting too long to recommend corrective surgery in some patients with chronic mitral regurgitation.