1 Discuss the basic pathophysiology of valvular heart diseases

Valvular heart diseases cause chronic volume or pressure overload, and each evokes a characteristic ventricular response called ventricular hypertrophy. Ventricular hypertrophy is defined as increased left ventricular (LV) mass. Pressure overload produces concentric ventricular hypertrophy with an increase in ventricular wall thickness with a cardiac chamber of normal size. Volume overload leads to eccentric hypertrophy with normal wall thickness and dilated cardiac chamber.

2 Describe common findings of the history and physical examination in patients with valvular heart disease

Most systolic heart murmurs do not signify cardiac disease, and many are related to physiologic increases in blood flow velocity. Diastolic murmurs virtually always represent pathologic conditions and require further cardiac evaluation, as do most continuous murmurs.

A history of rheumatic fever, intravenous drug abuse, embolization in different organs, genetic diseases such as Marfan syndrome, heart surgery in childhood, or heart murmur should alert the examiner to the possibility of valvular heart disease. Exercise tolerance is frequently decreased; patients may exhibit signs and symptoms of heart failure, including dyspnea, orthopnea, fatigue, pulmonary rales, jugular venous congestion, hepatic congestion, and dependent edema. Angina may occur in patients with a hypertrophied left ventricle, and atrial fibrillation frequently accompanies enlargement of the atria.

3 Which tests are useful in the evaluation of valvular heart disease?

Echocardiography with Doppler technology is a fundamental diagnostic method in evaluation of valvular heart diseases. The size and function of heart chambers and the pressure gradients at the valves and the valve areas can be measured, and the severity of the diseases can be determined.

Echocardiography is recommended for:

Asymptomatic patients with diastolic murmurs, continuous murmurs, holosystolic murmurs, grade 3 or louder mid-peaking systolic murmurs, late systolic murmurs, murmurs associated with ejection clicks, or murmurs that radiate to the neck or back.

Patients with heart murmurs and symptoms or signs of heart failure, myocardial ischemia/infarction, syncope, thromboembolism, infective endocarditis, or other clinical evidence of structural heart disease.

An electrocardiogram should be examined for evidence of ischemia, arrhythmias, atrial enlargement, and ventricular hypertrophy. Chest radiograph may show enlargement of cardiac chambers, suggest pulmonary hypertension, or reveal pulmonary edema and pleural effusions. Cardiac catheterization is used in the evaluation of such patients before surgery, mostly for diagnosing coronary artery disease. This method allows measurement of pressures in various heart chambers and pressure gradients across different valves.

4 How is echocardiography helpful in anesthesia management?

Transesophageal echocardiography can be used in the operating room during the surgical management of valvular diseases. The severity of the valvular disease and accompanying structural or functional changes can be reevaluated. Evaluation of valve repair or function of artificial valves is an important part of the patient management. Systolic and diastolic function of the left and right ventricle before and after cardiopulmonary bypass can be assessed, and appropriate management can be planned and followed.

5 Which other monitors aid the anesthesiologist in the perioperative period?

Besides standard American Society of Anesthesiologists (ASA) monitors, an arterial catheter provides beat-to-beat blood pressure measurement and continuous access to the bloodstream for sampling. Pulmonary artery catheters enable the anesthetist to measure cardiac output (CO), mixed venous saturation, central venous and pulmonary artery pressures, and pulmonary capillary wedge pressure, which are important indexes of right and LV function and filling and are useful for guiding intravenous fluid and inotropic therapy.

6 What is a pressure-volume loop?

A pressure-volume loop plots LV pressure against volume through one complete cardiac cycle. Each valvular lesion has a unique profile that suggests compensatory physiologic changes by the left ventricle.

7 How does a normal pressure-volume loop appear?

The AB segment is ventricular filling, BC is isovolumic contraction, CD is ejection, and DA is isovolumic relaxation. D point represents the aortic valve closing, A the mitral valve (MV) opening, B the MV closing, and C the aortic valve opening. Stroke volume through the aortic valve is the distance between C and D points. End-systolic volume can be measured at the D point, and end-diastolic volume can be measured at the B point. The end-systolic pressure–volume relationship slope is a measure of contractility. A horizontal-clockwise shift of the slope represents a decrease in contractility (Figure 35-1).

Figure 35-1 Pressure-volume loop in normal heart performance. AB, Diastolic filling; BC, isovolumic contraction; CD, ejection; DA, isovolumic relaxation. A, Mitral valve opening; B, mitral valve closing; C, aortic valve opening; D, aortic valve closing. The end-systolic pressure volume relationship curve (ESPVR) is a load-independent index of myocardial contractility. If the contractility is increasing, the ESPVR curve is moving counterclockwise. The pressure-volume loop is an excellent tool to characterize the performance of the heart in different pathologic conditions. LV, Left ventricular.

8 Discuss the pathophysiology of aortic stenosis

Aortic stenosis (AS) is classified as valvular, subvalvular, or supravalvular obstruction of the LV outflow tract. Concentric hypertrophy (thickened ventricular wall with normal chamber size) develops in response to the increased intraventricular systolic pressure and wall tension necessary to maintain forward flow. Ventricular relaxation decreases, causing diastolic dysfunction. Decreasing LV compliance accompanies elevated LV end-diastolic pressure. Contractility and ejection fraction are usually maintained until late in the disease process. Atrial contraction may account for up to 40% of ventricular filling (normally 20%). In developing countries rheumatic valve disease is still the most common cause of AS. In North America and Europe AS is primarily caused by calcification of a native trileaflet or a congenital bicuspid valve. Patients often present with angina, syncope, or congestive heart failure. Angina with exertion can occur in the absence of coronary artery disease because the thickened myocardium is susceptible to ischemia and the elevated LV end-diastolic pressure reduces coronary perfusion pressure. Life expectancy with symptoms of angina is about 5 years. Once syncope appears, the average life expectancy is 3 to 4 years. Once congestive heart failure occurs, the average life expectancy is 1 to 2 years.

9 How can be the severity of aortic stenosis characterized by echocardiography?

AS severity is graded on the basis of a variety of hemodynamic and natural history data using definitions of valve area, mean pressure gradient, and aortic jet velocity (Table 35-1).

TABLE 35-1 Severity of Aortic Stenosis

10 What is the indication for aortic valve replacement in aortic stenosis?

Based on the 2006 guidelines from the American College of Cardiology/American Heart Association (ACC/AHA), aortic valve replacement is indicated in the following patients:

Symptomatic patients with severe AS

Patients with severe AS undergoing coronary artery bypass graft surgery (CABG)

Patients with severe AS undergoing surgery on the aorta or other heart valves

Patients with severe AS and LV systolic dysfunction (ejection fraction less than 50%)

It is reasonable for patients with moderate AS undergoing CABG or surgery on the aorta or other heart valves.

11 How are the compensatory changes in the left ventricle represented by a pressure-volume loop?

Because of the AS, the left ventricle is working with higher intraventricular pressures to generate a normal stroke volume. The higher systolic wall tension initiates myocardial thickening and LV hypertrophy (LVH). The hypertrophied left ventricle has increased contractility to accomplish the pressure work (Figure 35-2). LVH decreases the wall tension during systole, improving the relationship of systolic work to oxygen demand. As the AS increases, LV systolic pressure increases to the level at which LVH cannot normalize the wall tension. At this point the heart starts dilating, resulting in systolic dysfunction and decreasing CO.

Figure 35-2 Pressure-volume loop in aortic stenosis (AS) compared to the normal loop. To generate normal stroke volume the intraventricular pressure is high because of the pressure gradient at the aortic valve level. The end-diastolic pressure is higher than normal in cases when left ventricular (LV) hypertrophy alters LV compliance. Myocardial contractility is higher than normal.

12 What are the hemodynamic goals in the anesthetic management of patients with aortic stenosis?