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?

Patients must have adequate intravascular volume to fill the noncompliant ventricle. Contractility should be maintained to overcome the high pressure gradient across the aortic valve. Reductions in blood pressure or peripheral resistance do not decrease LV afterload because of the fixed valvular resistance, but they do decrease coronary perfusion, with a great risk for development of subendocardial ischemia and sudden death. Extremes of heart rate should be avoided. Bradycardia leads to a decrease in CO in patients with relatively fixed stroke volume. Tachycardia may produce ischemia with a limited diastolic time for coronary perfusion. Maintenance of sinus rhythm is imperative because of the importance of atrial contraction in LV filling.

13 Discuss the management of the patients with aortic stenosis after aortic valve replacement

After surgery, LV end-diastolic pressure decreases and stroke volume increases, but the hypertrophied LV still may require an elevated preload to function adequately. Depressed myocardial function may suggest inadequate myocardial protection during the surgery due to the difficulty perfusing the hypertrophied left ventricle. Inotropic agents (dopamine, dobutamine, and epinephrine) can improve the LV performance in this situation.

14 Discuss the pathophysiology of aortic insufficiency

In chronic aortic insufficiency (AI) there is an LV diastolic volume overload because part of the stroke volume regurgitates across the incompetent aortic valve during diastole. Patients have large end-diastolic and stroke volumes. The volume load generates high wall tension in diastole, initiating eccentric hypertrophy (dilated left ventricle with normal or thickened wall). Increasing regurgitant orifice area, slow heart rate (relatively more time spent in diastole) and increased systemic vascular resistance increase the amount of regurgitant flow. Compliance and stroke volume may be markedly increased in chronic AI, whereas contractility gradually diminishes (Figure 35-3). AI can be caused by diseased valve leaflets or enlargement of the aortic root. In the developing world the most common cause of AI is rheumatic heart disease. In developed countries AI is most often caused by aortic root dilation, congenital bicuspid aortic valve, or infective endocarditis. Causes of acute AI are infective endocarditis, aortic dissection (Marfan syndrome), and AI after aortic balloon valvotomy or a failed surgical valve repair.

Figure 35-3 Pressure-volume loops in aortic regurgitation compared to the normal loop. In acute aortic insufficiency (AI) the end-diastolic and end-systolic volume is increasing. The stroke volume can be increased, normal or decreased, depending on the severity of AI. The left ventricular (LV) volume is increasing during the isovolumic relaxation period (DA segment). The end diastolic pressure (AB segment, B point) is high. Contractility is decreased because the myocardium is overstretched. In chronic AI the end-diastolic, end-systolic, and stroke volumes are enlarged. Cardiac output is normal, and the contractility is decreased. The LV volume is increasing during the isovolumic relaxation period also (DA segment), but the end diastolic pressure (AB segment, B point) is normal; thus the heart has diastolic reserve to accommodate to limited volume or pressure load. LV, Left ventricular.

Ideally patients with chronic AI should have valve replacement surgery before the onset of irreversible myocardial damage. In acute AI the left ventricle is subjected to rapid, massive volume overload with elevated end-diastolic pressure. Hypotension and pulmonary edema may necessitate emergent valvular replacement (see Figure 35-3).

15 What parameters can be used in echocardiography to characterize the severity of aortic insufficiency?

See Table 35-2.

TABLE 35-2 Severity of Aortic Insufficiency

LVOT, Left ventricular outflow tract.

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

Based on the ACC/AHA 2006 guidelines, aortic valve replacement is indicated in the following patients:

Symptomatic patients with severe AI irrespective of LV systolic function

Asymptomatic patients with chronic severe AI and LV systolic dysfunction (ejection fraction 50% or less) at rest

Asymptomatic patients with chronic severe AI while undergoing CABG or surgery on the aorta or other heart valves

It is reasonable for asymptomatic patients with severe AI with normal LV systolic function (ejection fraction greater than 50%) but with severe LV dilation (end-diastolic dimension greater than 75 mm or end-systolic dimension greater than 55 mm).

17 What does the pressure-volume loop look like in acute and chronic aortic insufficiency?

In acute AI the end-diastolic and end-systolic volume is increasing. The stroke volume can be increased, normal, or decreased, depending on the severity of AI. The LV volume is increasing during the isovolumic relaxation period. The end-diastolic pressure is high. End-diastolic pressure >25 to 30 mm Hg manifests as pulmonary edema. Contractility is decreased because the myocardium is overstretched. There is no diastolic reserve, thus the heart cannot increase the stroke volume with increasing preload or afterload (see Figure 35-3).

In chronic AI the end-diastolic, end-systolic and stroke volumes are enlarged. Cardiac output is normal, although the contractility is decreased. Despite the enlarged LV end-diastolic volume, the end-diastolic pressure is normal; thus the heart has diastolic reserve to increase the stroke volume with increasing preload or afterload (see Figure 35-3).

18 What are the hemodynamic goals in the anesthetic management of patients with aortic insufficiency?

In acute AI the goal is to achieve the lowest tolerable systemic blood pressure to increase the stroke volume and CO. Appropriate preload is necessary for maintenance of forward flow. Modest tachycardia reduces ventricular volumes and limits the time available for regurgitation. Contractility must be maintained; β-adrenergic agonists may be used if necessary. Dobutamine can be ideal because it does not increase the afterload. Afterload reduction augments forward flow, but additional intravascular volume may be necessary to maintain preload. Increases in afterload result in increasing LV end-diastolic pressure and pulmonary hypertension.

19 Discuss the hemodynamic changes in patients with aortic insufficiency after aortic valve replacement

After surgery LV end-diastolic volume and pressure decrease. Preload should be increased by volume administration to maintain filling of the dilated left ventricle. The decreased myocardial contractility may necessitate inotropic or intra-aortic balloon pump support.

20 What is the pathophysiology of mitral stenosis?

As the orifice of the MV narrows, the left atrium experiences pressure overload. In contrast to other valvular lesions, the left ventricle shows relative volume underload because of the obstruction of forward blood flow from the atrium. The elevated atrial pressure may be transmitted to the pulmonary circuit and thus lead to pulmonary hypertension and right heart failure. The overdistended atrium is susceptible to fibrillation with resultant loss of atrial systole, leading to reduced ventricular filling and CO. Symptoms (fatigue, dyspnea on exertion, hemoptysis) may be worsened when increased CO is needed (e.g., with pregnancy, illness, anemia, and exercise). Blood stasis in the left atrium is a risk for thrombus formation and systemic embolization. MS is usually secondary to rheumatic disease (80% to 90%), infective endocarditis (3.3%), and mitral annular calcification (2.7%). Critical stenosis of the valve occurs 10 to 20 years after the initial rheumatic disease.

21 What parameters can be used in echocardiography to characterize the severity of mitral stenosis?

See Table 35-3.

TABLE 35-3 Severity of Mitral Stenosis

22 What is the indication for mitral valve replacement in mitral stenosis?

Based on the ACC/AHA 2006 guidelines, MV surgery is indicated in the following patients:

MV surgery (repair if possible) is indicated in patients with symptomatic moderate or severe MS (NYHA functional class III–IV) when:

Percutaneous mitral balloon valvotomy is unavailable.

Percutaneous mitral balloon valvotomy is contraindicated because of left atrial thrombus despite anticoagulation or because concomitant moderate-to-severe mitral regurgitation (MR) is present.

The valve morphology is not favorable for percutaneous mitral balloon valvotomy in a patient with acceptable operative risk.

Symptomatic patients with moderate-to-severe MS who also have moderate-to-severe MR should receive MV replacement unless valve repair is possible at the time of surgery.

MV replacement is reasonable for patients with severe MS and severe pulmonary hypertension (pulmonary artery systolic pressure greater than 60 mm Hg) with NYHA functional class I–II symptoms who are not considered candidates for percutaneous mitral balloon valvotomy or surgical MV repair.

23 How is the pressure-volume loop changed from normal in mitral stenosis?

The end-diastolic, end-systolic, and stroke volume are small because of the limited flow into the LV. The LV generates low blood pressure. The contractility is decreased because of chronic underfilling of the left ventricle (Figure 35-4).

Figure 35-4 Pressure-volume loop in mitral stenosis compared to the normal loop. In mitral stenosis (MS) the end-diastolic, end-systolic, and stroke volume is small. The left ventricle (LV) generates low blood pressure. The contractility is decreasing due to the chronic underfilling of the LV.

24 What are the anesthetic considerations in mitral stenosis?

The intravascular volume must be adequate to maintain flow across the stenotic valve. A slower heart rate allows more time for the blood to flow across the valve, increasing ventricular filling. Sinus rhythm should be maintained because atrial contraction contributes about 30% of the stroke volume. Afterload should be kept in the normal range. Chronic underfilling of the left ventricle leads to depressed ventricular contractility even after the restoration of normal filling. Negative inotropic agents should be avoided. Increases in pulmonary vascular resistance may exacerbate right ventricular failure; thus hypoxemia, hypercarbia, and acidosis should be avoided. For this reason the respiratory depressant effects of preoperative medications may be particularly deleterious.

25 Discuss the postoperative management of patients with mitral stenosis after mitral valve replacement

Decreases in left atrial pressure result in declines in pulmonary artery resistance and pulmonary artery pressure and increased CO. However, the LV performance can be depressed because of the chronic underfilling of the left ventricle, especially after cardiopulmonary bypass. Preload augmentation and afterload reduction should be applied to improve forward blood flow. Inotropic or intraaortic balloon pump support may be necessary to improve the systolic performance of the left ventricle.

26 Describe the pathophysiology of mitral regurgitation

The causes of primary valve disease and chronic mitral regurgitation (MR) include MV prolapse, infective endocarditis, trauma, rheumatic heart disease, drugs (ergotamine, pergolide), and congenital valve cleft. The secondary causes of MR include ischemic heart disease, LV systolic dysfunction, and hypertrophic cardiomyopathy.

In chronic mitral regurgitation the left ventricle and atrium show volume overload, leading to increased LV end-diastolic volume with normal end-diastolic pressure. Left ventricular end-systolic volume is normal; thus the stroke volume is high, but part of the stroke volume escapes through the incompetent valve into the left atrium. Ejection fraction is usually high because of the low resistance against the regurgitation. An ejection fraction of 50% may indicate significant LV dysfunction. A large distensible left atrium can maintain near-normal left atrial pressure despite large regurgitant volumes. Regurgitant flow depends on regurgitant orifice size, time available for regurgitant flow (bradycardia), and transvalvular pressure gradient.

In acute MR end-diastolic volume and pressure increase; and the pulmonary circuit and right heart are subjected to sudden increases in pressure and volume, which may precipitate acute pulmonary hypertension, pulmonary edema, and right heart failure. Acute MR may occur in the setting of flailed leaflet caused by MV prolapse, infective endocarditis, or trauma. Chordae tendineae may rupture spontaneously or from trauma, infective endocarditis, or rheumatic fever. Papillary muscles may rupture because of acute myocardial infarction or trauma.

27 What parameters can be used in echocardiography to characterize the severity of mitral regurgitation?

See Table 35-4.

TABLE 35-4 Severity of Mitral Regurgitation

28 What is the indication for mitral valve replacement in mitral regurgitation?

Based on the ACC/AHA 2006 guidelines, MV surgery is indicated in the following patients:

Symptomatic patients with acute severe MR

Symptomatic patients (NYHA functional classes II, III, or IV) with chronic severe MR

Asymptomatic patients with chronic severe MR and mild-to-moderate LV dysfunction (ejection fraction 30% to 60%, and/or end-systolic dimension ≥40 mm but ≤55 mm)

MV repair is recommended over MV replacement in the majority of patients with severe chronic MR who require surgery

29 How is the pressure-volume loop in mitral regurgitation changed from normal?

In acute MR the end-diastolic volume increases with high end-diastolic pressure. End-systolic volume is normal or decreased, stroke volume is increased, but the ejected volume into the aorta is relatively small, depending on the regurgitant volume (Figure 35-5).

Figure 35-5 Pressure-volume loop in mitral regurgitation compared to the normal loop. In acute mitral regurgitation (MR) the end-diastolic volume is increasing with higher end-diastolic pressure. The end-systolic volume is either normal or less than normal because part of the stroke volume is flowing back the low-pressure left atrium during the isovolumic contraction period (BC segment). In chronic MR the end-diastolic volume is high with normal or slightly elevated end-diastolic pressure. The end-systolic volume is normal or bigger than normal, depending on the severity of the MR and the systolic function of the left ventricle (LV). The ejected stroke volume is sufficient to maintain adequate cardiac output. The contractility is decreased.

In chronic MR the end-diastolic volume is increased with normal end-diastolic pressure resulting from the chronic myocardial remodeling process. The end-systolic volume is normal. The markedly increased stroke volume preserves the forward CO despite the significant regurgitation. The contractility is decreased (see Figure 35-5).

30 What are the hemodynamic goals in anesthetic management of mitral regurgitation?

The intravascular volume should remain full to supply the dilated left ventricle. The best level of preload augmentation for a patient must be based on the clinical response to a fluid load. Bradycardia increases the regurgitant volume, decreasing the ejected volume into the aorta. Normal or slightly elevated heart rate helps to decrease the regurgitant flow volume. Dobutamine or milrinone can be administered to enhance contractility while reducing afterload. Afterload reduction augments forward flow and decreases regurgitation. As in MS, drugs and maneuvers that increase pulmonary vascular resistance must be avoided.

31 Discuss the hemodynamic management after mitral valve repair or replacement in patient with mitral regurgitation

Once the valve is in place, the LV has to eject the full stroke volume into the aorta. This immediate pressure load increases LV tension and may compromise the ejection fraction. Therefore inotropic or intraaortic balloon pump support can be necessary until the left ventricle can adjust to the new hemodynamic condition. Preload should be augmented to fill up the dilated left ventricle.