A Practical Approach to Cardiac Anesthesia

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CHAPTER 12. Anesthetic Management for the Treatment of Valvular Heart Disease

Roger A. Moore and Donald E. Martin

Quick Links to Sections in this Chapter

–Cardiac response to valvular heart disease.

–Aortic stenosis

–Aortic regurgitation

–Mitral stenosis

–Mitral regurgitation

–Tricuspid stenosis

–Tricuspid regurgitation

–Pulmonic stenosis

–Mixed valvular lesions.

–Prosthetic cardiac valves.

–Prophylaxis of subacute bacterial endocarditis.

–Anticoagulation management

See Related Case Study from Yao & Artusio's Anesthesiology

  1. Cardiac response to valvular heart disease. The anesthetic management of patients undergoing valvular heart surgery requires a thorough understanding of the following:

    • Abnormal pressure and volume loads imposed by abnormal valves

    • Structural and functional mechanisms by which the heart attempts to compensate

    • Events that may signal the limits of compensation, such as arrhythmias, ischemia, and cardiac failure

    • Secondary complications, such as endocarditis or emboli

    1. Ventricular function. To anticipate the effect of valvular lesions on ventricular function, it is helpful to separate ventricular function into its two distinct components [1].

      1. Systolic function represents the ventricle's ability to contract and eject blood against an afterload. Systolic function allows the ventricle to respond to a pressure load and is best described by the ratio of end-systolic pressure to end-systolic volume. As end-systolic pressure (afterload) increases, the ventricle cannot empty completely, and end-systolic volume increases. However, the ratio of end-systolic pressure to volume remains almost constant under most circumstances and is directly related to ventricular contractility.

      2. Diastolic function represents the ventricle's ability to relax and accept inflowing blood, or preload. Diastolic function is necessary for the ventricle to respond to a volume load and is best described by the relationship between end-diastolic pressure and end-diastolic volume, or ventricular compliance.

        Both systolic and diastolic function require energy and can be compromised by ventricular ischemia.

    2. Ventricular hypertrophy. Chronic volume and pressure loads each evokes a characteristic ventricular response. Pressure loads usually result in concentric ventricular hypertrophy, with an increase in ventricular wall thickness that allows the heart to maintain its normal, or concentric, position within the chest cavity. Volume loading, on the other hand, leads to eccentric hypertrophy. The word eccentric in this context means that the heart dilates and, because of increased chamber size, assumes an eccentric position in the chest.

    3. Pressure–volume relationship. Both systolic and diastolic components of ventricular function, along with the corresponding pressure and volume loads, can be represented graphically by a pressure–volume loop, which shows the pressure– volume relationship at each instant during a single cardiac cycle [2]. Figure 12.1 shows a representative pressure–volume loop under normal conditions. Diastolic function is represented by a dashed line and includes phase 1, isovolumetric relaxation, and phase 2, ventricular filling. Systolic function is represented by a solid line and includes phase 3, isovolumetric contraction, and phase 4, ventricular ejection. The area inside the loop provides a rough index of the energy used to eject blood, or the stroke work. The shape of this loop changes with variations in ventricular load, ventricular compliance, and ventricular contractility. Each valvular lesion imposes its own unique set of stresses on the left ventricle (LV) and the right ventricle (RV). These variations lead to specific hemodynamic profiles for each lesion that suggest the anesthetic and therapeutic priorities for patients with each type of valvular heart disease.

      FIG. 12.1 Pressure–volume loop for the normal ventricle. AC, aortic valve closure; AO, aortic valve opening; MC, mitral valve closure; MO, mitral valve opening; phase 1, isovolumetric relaxation; phase 2, ventricular filling; phase 3, isovolumetric contraction; phase 4, ventricular ejection. (Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth 1982;1:240.)


  2. Aortic stenosis

    1. Natural history

      1. Etiology. Aortic stenosis is classified as valvular, subvalvular, or supravalvular based on the anatomic location of the stenotic lesion. Pure valvular aortic stenosis is the most common, accounting for more than 75% of patients. In the past, the primary cause of valvular aortic stenosis was rheumatic valvular degeneration. Because of improved recognition and treatment of streptococcal infections, rheumatic carditis has now become less common. Calcific degeneration of a congenitally bicuspid aortic valve currently is the most common etiology. A congenitally bicuspid aortic valve occurs in approximately 1% to 2% of the general population, making it one of the most common congenital malformations. Senile degeneration of normal aortic valves also can occur. Thirty percent of patients older than 85 years are found to have significant degenerative changes of the aortic valve on autopsy. A characteristic finding of senile valvular degeneration is progression of calcification from the base of the valve toward the edge, as opposed to rheumatic degeneration, in which calcification spreads from the edge toward the base.

      2. Symptomatology. Patients with rheumatic aortic stenosis may be asymptomatic for 40 years or more. Patients with congenitally bicuspid aortic valves may develop symptomatic aortic stenosis any time between the ages of 15 and 65 years, but calcification of the valve more often occurs after age 30 and usually in the seventh or eighth decade of life. The onset of any one of a triad of symptoms is an ominous sign and indicates a life expectancy of less than 5 years:

        1. Angina pectoris. Angina is the initial symptom in 50% to 70% of patients with severe aortic stenosis. Angina secondary to aortic stenosis alone most commonly occurs with exertion. In contrast, angina at rest commonly indicates associated coronary artery disease.

        2. Syncope. Syncope is the first symptom in 15% to 30% of patients. Once syncope appears, the average life expectancy is 3 to 4 years.

        3. Congestive heart failure. Once signs of LV failure occur, the average life expectancy is only 1 to 2 years. All patients with aortic stenosis are at increased risk for sudden death. Only 18% of patients are alive 5 years after stenosis has progressed to the point of peak systolic pressure gradient greater than 50 mm Hg or effective aortic valve orifice size less than 0.7 cm2 (aortic valve index less than 0.5 cm2/m2).

    2. Pathophysiology

      1. Natural progression

        1. Stage 1: mild aortic stenosis—asymptomatic with physiologic compensation. The normal adult aortic valve area is 2.6 to 3.5 cm2, representing a normal aortic valve index of 2 cm2/m2. As stenosis progresses, the maintenance of normal stroke volume is associated with an increasing systolic pressure gradient between the LV and the aorta. LV systolic pressure increases to as much as 300 mm Hg, whereas the aortic systolic pressure and stroke volume remain relatively normal. This higher gradient results in a compensatory concentric LV hypertrophy (increased muscle mass in the LV wall without dilation of the ventricular chamber). The resultant increase in LV end-diastolic pressure (LVEDP) is not a sign of systolic dysfunction or failure but rather an indication of the decreased LV diastolic function or reduced compliance.

        2. Stage 2: moderate aortic stenosis—symptomatic impairment. As stenosis progresses toward the critical orifice size of 0.7 to 0.9 cm2 (aortic valve index 0.5 cm2/m2), dilation as well as hypertrophy of the LV may occur, leading to increases in both LV end-diastolic volume (LVEDV) and LVEDP. A decrease in ejection fraction may be noted, indicating compromise of LV contractility. Ventricular contractility decreases more rapidly in some patients than in others but eventually is reduced in all untreated patients.

          The increased LVEDV and LVEDP leads to increased myocardial work and O2 demand. In this situation, two of the primary determinants of myocardial O2 demand (tension developed by the myocardium and duration of systole) are increased. At the same time, myocardial O2 supply is impeded because of the elevated LVEDP, causing a decrease in coronary perfusion pressure. Finally, the Venturi effect of the jet of blood flowing through the aortic valve and past the coronary arteries may lower pressure in the coronary ostia enough to reverse systolic coronary blood flow. These factors produce a heart particularly at risk for ischemia and sudden death, even in the absence of concurrent atherosclerotic coronary disease.

          The initial appearance of symptoms in patients with aortic stenosis often is associated with the development of atrial fibrillation. Normal patients depend on atrial contraction for approximately 20% of the stroke volume. However, with the reduced ventricular compliance and increased LVEDP that is present in patients with aortic stenosis, passive ventricular filling is reduced, and atrial contraction can supply as much as 40% of ventricular filling during diastole. Therefore, loss of sinus rhythm and atrial contribution to cardiac output can lead to rapid clinical deterioration.

        3. Stage 3: critical aortic stenosis—terminal failure. Continuation of the disease process with reduction of the aortic valve index to less than 0.5 cm2/m2 leads to further decreases in ejection fraction and increases in LVEDP. Pressure builds up in the pulmonary venous circuit, leading to pulmonary edema when the left atrial pressure increases to more than 25 to 30 mm Hg. Normally, sudden death will intervene, but if the patient is able to survive, the increasing pulmonary arterial hypertension eventually will produce RV failure.

      2. Pressure–volume relationship (Fig. 12.2). As the pressure gradient across the aortic valve develops, stroke volume is preserved by an increase in LV systolic pressure. During the early stages of LV compensation, LV hypertrophy leads to reduced LV compliance, with elevation of LVEDP, whereas the LV end-systolic volume stays relatively normal. In the later stages of the disease, myocardial ischemia and compromise of LV function can lead first to marked elevations of LVEDP and LVEDV and, finally, to elevation of LV end-systolic volume and depression of stroke volume. Each of these changes, but especially elevated ventricular pressures, increases O2 cost to an already compromised myocardium.

        FIG. 12.2 Pressure–volume loop of a patient with moderate aortic stenosis and left ventricular compensation showing markedly elevated left ventricular systolic pressure, elevated end-systolic and end-diastolic volumes, and increased diastolic pressure. AC, aortic valve closure; AO, aortic valve opening; MC, mitral valve closure; MO, mitral valve opening; phase 1, isovolumetric relaxation; phase 2, ventricular filling; phase 3, isovolumetric contraction; phase 4, ventricular ejection. (Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth 1982;1:241.)


      3. Calculation of stenosis. Determination of the aortic valve area is performed using the Gorlin modification of standard hydraulic formulas [3]. The formula for calculating aortic valve area is summarized as follows:

        where 1 is the aortic orifice constant and HR is heart rate.

        A simplified version of the Gorlin formula that is accurate enough to be clinically useful at normal heart rates is as follows:

        This simplified version of the formula is valid only because the product of the heart rate, systolic ejection period, and the constant approximates unity.

        There is a direct relationship between the aortic valve area and the flow across the aortic valve. A series of relationships can be established between the rate of aortic valve blood flow and the mean systolic pressure gradient for any aortic valve area (Fig. 12.3). Blood flow is not significantly impeded until the aortic valve area falls below a critical level of 0.5 to 0.7 cm2.

        FIG. 12.3 Comparison between rate of blood flow and mean systolic pressure gradient across the aortic valve in individuals with different aortic valve areas, as determined by the Gorlin formula. (From Schlant RC. Altered cardiovascular function of rheumatic heart disease and other acquired valvular disease. In: Hurst JW, Logue RB, Schlant RC, et al., eds. The heart, 4th ed. New York: McGraw-Hill, 1978:968, with permission.)


      4. Pressure wave disturbances

        1. Arterial pressure. Arterial pulse pressure usually is reduced to less than 50 mm Hg in severe aortic stenosis. The systolic pressure rise is delayed with a late peak and a prominent anacrotic notch. As stenosis increases in severity, the anacrotic notch occurs lower in the ascending arterial pressure trace. The dicrotic notch is relatively small or absent.

        2. Pulmonary arterial wedge pressure. Because of the elevated LVEDP, which stretches the mitral valve annulus, a prominent V wave can be observed but, with progression of the disease and the development of left atrial hypertrophy, a prominent A wave becomes the dominant feature.

    3. Goals of perioperative management

      1. Hemodynamic profile

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Aortic stenosis↓ (sinus)Maintain constantMaintain constant
        1. LV preload. Because of the decreased LV compliance as well as the increased LVEDP and LVEDV, preload augmentation is necessary to maintain a normal stroke volume. Use of nitroglycerin may dangerously reduce cardiac output.

        2. Heart rate. Extremes of heart rate are not tolerated well. A high heart rate can lead to decreased coronary perfusion. A low heart rate can limit cardiac output in patients with a fixed stroke volume. If a choice must be made, however, low heart rates (50 to 70 beats/min) are preferred to rapid heart rates (greater than 90 beats/min) to allow time for systolic ejection across a stenotic aortic valve. Because of the importance of atrial contraction for LV filling, it is essential to maintain a sinus rhythm.

        3. Contractility. Stroke volume is maintained through preservation of a heightened contractile state. β-Blockade is not well tolerated and can lead to an increase in LVEDV and a decrease in cardiac output significant enough to induce clinical deterioration.

        4. Systemic vascular resistance. Most of the afterload to LV ejection is caused by the stenotic aortic valve itself and thus is fixed. Systemic blood pressure reduction does little to decrease LV afterload. However, the hypertrophied myocardium of the patient with aortic stenosis is at great risk for development of subendocardial ischemia. Coronary perfusion depends on maintenance of an adequate systemic diastolic perfusion pressure. Therefore, early use of α-adrenergic agonists is indicated to prevent drops in blood pressure that can lead quickly to sudden death [4]. Because the primary impedance to ventricular ejection occurs at the aortic valve, blood pressure augmentation using α-adrenergic agonists does little to reduce total forward flow.

        5. Pulmonary vascular resistance. Except for end-stage aortic stenosis, pulmonary artery pressures remain relatively normal. Special intervention for stabilizing pulmonary vascular resistance is not necessary.

      2. Anesthetic techniques

        1. Light premedication is necessary to provide a calm patient without tachycardia. However, the use of a heavy premedicant with agents that markedly reduce either preload or afterload should be avoided. A combination of morphine, 0.05 to 0.10 mg/kg intramuscularly (IM), and scopolamine, 0.2 to 0.3 mg IM; lorazepam, 1 to 2 mg by mouth (PO), alone; or midazolam, 1 to 3 mg PO or IM, can be used with little adverse hemodynamic effect. Dosage of premedication should be adjusted for each patient based on individual considerations, including the patient's age and physical status.

        2. Thermodilution cardiac output pulmonary artery catheters are helpful for evaluating the cardiac output of patients before repair of the aortic valve. Pulmonary capillary wedge pressure, however, may underestimate the true end-diastolic pressure of a noncompliant LV. There is also a small dysrhythmogenic risk during transventricular passage of a pulmonary artery catheter. If a patient shows dysrhythmias during advancement of a pulmonary artery catheter, the catheter tip should be left in a central venous position until repair of the aortic valve is completed. Mixed venous oxygen saturation monitoring via an oximetric pulmonary artery catheter may be used to provide a continuous index of cardiac output. However, because postbypass management is not likely to be marked by myocardial failure or low-output states, this technique may be best reserved for patients with other valve lesions.

        3. Any anesthetic agent that causes myocardial depression, blood pressure reduction, tachycardia, or other dysrhythmias should be used with caution. Each of these physiologic changes can lead to rapid deterioration. A narcotic-based anesthetic usually is chosen for this reason.

        4. During the induction and maintenance of anesthesia, a potent α-adrenergic agent such as phenylephrine should be readily available for early and aggressive treatment of reductions in systemic systolic or diastolic pressure.

        5. If the patient develops signs or symptoms of ischemia, nitroglycerin should be used with caution because its effect on preload or arterial pressure may worsen the patient's condition.

        6. Supraventricular dysrhythmias should be treated aggressively with synchronized direct-current shock because both tachycardia and the loss of effective atrial contraction can lead to rapid reduction of cardiac output and hemodynamic deterioration. Ventricular ectopy also should be treated aggressively because patients whose rhythm deteriorates into ventricular fibrillation often cannot be successfully resuscitated.

        7. An experienced cardiac surgeon should be present, and the perfusionist should be prepared before induction of anesthesia, in the event that rapid cardiovascular deterioration necessitates emergency use of cardiopulmonary bypass.

        8. In the presence of myocardial hypertrophy, adequate myocardial preservation with cardioplegic solution during bypass is essential to avoid myocardial "contracture" or "stone heart." The traditional cold potassium cardioplegia, which must be administered via coronary ostial catheters during valve replacement, may be inadequate. Retrograde administration of warm blood cardioplegia via the coronary sinus may have an important role in preserving myocardial integrity.

        9. In the absence of preoperative ventricular dysfunction and associated coronary disease, inotropic support often is not required after cardiopulmonary bypass because valve replacement decreases ventricular afterload.

        10. Omniplanar transesophageal echocardiography (TEE) is suggested for intraoperative monitoring of LV function and detection of intracavitary thrombi. If commissurotomy is performed rather than valve replacement, TEE is a highly effective method for quantitating residual aortic regurgitation. With total valve replacement, TEE will readily identify perivalvular leaks.

      3. Surgical intervention. Because of the high risk of sudden death, all symptomatic patients should undergo surgery. Asymptomatic patients with a transvalvular gradient greater than 50 mm Hg or valve index less than 0.5 cm2/m2 should undergo surgery. The initial surgical procedure often is a valvular commissurotomy performed under direct vision, which frequently results in some residual aortic stenosis and aortic regurgitation. Eventually, most patients require prosthetic valve replacement. Surgical intervention should not be denied to patients no matter how severe the symptomatology because irreparable LV failure occurs only very late in the disease process. After isolated aortic valve replacement, hospital mortality is 3% to 5%. Of the patients leaving the hospital, 85% can expect to survive for at least 5 years.

      4. Postoperative care. After aortic commissurotomy or valve replacement, pulmonary capillary wedge pressure and LVEDP immediately decrease and stroke volume rises. Myocardial function improves rapidly, although the hypertrophied ventricle still may require an elevated preload to function normally. Over a period of several months, LV hypertrophy regresses. It must be remembered that if a prosthetic valve has been used, a residual gradient of 7 to 19 mm Hg may be present and, if a commissurotomy has been performed, concurrent aortic regurgitation may be present. Most patients do very well after surgery for aortic stenosis, provided intraoperative myocardial preservation is adequate.

    4. Idiopathic hypertrophic subaortic stenosis (hypertrophic cardiomyopathy). This disease process represents a dynamic stenosis of the aortic outflow tract, unlike valvular aortic stenosis, which is fixed. The response of the myocardium to this disease process is similar to that seen in valvular aortic stenosis; however, the increased muscle mass in the subaortic region eventually leads to severe obstruction of LV outflow. In this special situation, β-blockade may be beneficial. These patients also benefit from preload augmentation for maintaining LV volume, from afterload augmentation for increasing diastolic perfusion through the hypertrophied muscle mass and from slow heart rates. Patients with hypertrophic cardiomyopathy are at increased risk from arrhythmias, particularly tachyarrhythmias, during surgery.

  3. Aortic regurgitation

    1. Natural history

      1. Etiology. Rheumatic fever and syphilitic aortitis were the primary causes of aortic regurgitation in the past. However, with early identification and successful treatment of these diseases, they now are seen infrequently as causes of aortic regurgitation. Increasingly, bacterial endocarditis, trauma, aortic dissection, and a variety of congenital diseases leading to abnormal collagen formation, such as Marfan syndrome or cystic medionecrosis, are becoming the primary etiologies.

      2. Symptomatology. Patients with chronic aortic regurgitation may be asymptomatic for up to 20 years. The 10-year mortality for asymptomatic aortic regurgitation varies between 5% and 15%. However, once symptoms develop, patients progressively deteriorate and have an expected survival rate of 5 to 10 years. Early symptoms include dyspnea, fatigue, and palpitations. Angina pectoris normally is a late symptom and is an ominous sign. Patients with acute aortic regurgitation, on the other hand, may deteriorate rapidly, and the prognosis is guarded.

    2. Pathophysiology

      1. Natural progression

        1. Acute aortic regurgitation. The sudden occurrence of acute aortic regurgitation places a major volume load on the LV. An immediate compensatory mechanism for maintenance of adequate forward flow is increased sympathetic tone, producing tachycardia and an increased contractile state. Fluid retention increases preload. However, the combination of increased LVEDV and increased total stroke volume and heart rate may not be sufficient to maintain normal cardiac output. Rapid deterioration of LV function can occur, necessitating emergency surgical intervention.

        2. Chronic aortic regurgitation

          1. Stage 1: mild aortic regurgitation—asymptomatic with physiologic compensation. The onset of aortic regurgitation leads to LV systolic and diastolic volume overload. The increased volume load leads to eccentric hypertrophy of the LV, with increases in both the thickness of the LV wall and the size of the ventricular cavity. Because the LVEDV increases slowly, the LVEDP remains relatively normal. Because volume work is less expensive metabolically than pressure work, no major increase in myocardial O2 demand occurs, despite an increased ejection fraction. Forward flow is aided by the presence of chronic peripheral vasodilation, which occurs along with a large stroke volume in patients with mild aortic regurgitation. There is minimal symptomatology as long as the regurgitant fraction remains less than 40% of the stroke volume.

          2. Stage 2: moderate aortic regurgitation—symptomatic impairment. As the amount of aortic regurgitation progresses to more than 60% of stroke volume, continued LV dilation and hypertrophy occur, finally leading to irreversible LV myocardial tissue damage. An early sign of these changes is an increase in LVEDP to greater than 20 mm Hg, indicating LV dysfunction. The onset of LV dysfunction is followed by an increase in pulmonary arterial pressure with symptoms of dyspnea and congestive heart failure.

          3. Stage 3: severe aortic regurgitation—terminal failure. After the onset of symptomatology, LV dysfunction continues to progress and eventually becomes irreversible. Symptomatology is rapidly progressive, and surgical intervention at this point is not always successful. Angina pectoris may occur because of the reduction in diastolic aortic pressure with decreased diastolic coronary perfusion, ventricular dilation with increased wall tension, and the presence of a hypertrophied LV. As a compensatory mechanism for poor cardiac output and poor coronary perfusion, sympathetic constriction of the periphery occurs, leading to further decreases in cardiac output.

      2. Pressure–volume relationship (Fig. 12.4). In acute aortic regurgitation, a sudden volume load is placed on a normally compliant LV. This leads to increases in both LV end-diastolic and end-systolic volumes. Because the LV does not have time to compensate through eccentric hypertrophy, the result is a sudden increase in LVEDP. The compensatory mechanism of sympathetic stimulation may not be sufficient to maintain adequate stroke volume.

        FIG. 12.4 Pressure–volume loops, aortic insufficiency. Loop A, from a patient with acute aortic insufficiency, shows moderately elevated left ventricular systolic and diastolic volumes as well as an increase in ventricular volume during ventricular relaxation. Loop C, from a patient with chronic aortic insufficiency, shows markedly increased systolic and diastolic volumes but lower end-diastolic pressure. (Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth 1982;1:247.)


        In chronic aortic regurgitation, eccentric hypertrophy occurs, leading to massive increases in LV end-diastolic and end-systolic volumes. An increase in LV compliance over time allows the LVEDP to remain only mildly elevated. With this compensatory mechanism, stroke volume can be maintained for some time. Ejection fraction is an unreliable index of LV function in patients with aortic regurgitation.

      3. Determination of severity

        1. Qualitative estimate. The amount of aortic regurgitation usually is estimated based on angiocardiographic clearance of injected dye into the aortic root [5].

           
          +1 Slight reflux of dye into the LV during LV diastole with opacification limited to the LV outflow tract; dye is completely cleared with next systole
          +2 Moderate reflux of dye into the LV during diastole; dye is not completely cleared with the next systole
          +3 Complete opacification of the LV for several systoles
          +4 Complete opacification of the LV by the end of the first diastole, with maintenance of opacification for several systoles; density of the dye in the LV is greater than that in the aorta
        2. Calculation of regurgitant fraction. A more quantitative estimate of the severity of aortic regurgitation can be obtained by comparing forward flow (thermodilution cardiac output) with total volume of blood ejected by the LV (angiographic cardiac output). The regurgitant fraction, or fraction of each stroke volume flowing back into the LV, can be calculated using the following equation:

          where EDV is end-diastolic volume, ESV is end-systolic volume, HR is heart rate, and CO is thermodilution cardiac output (forward flow).

      4. Pressure wave disturbances

        1. Arterial pressure. Patients with aortic regurgitation show a wide pulse pressure with a rapid rate of rise, a high systolic peak, and the presence of a low diastolic pressure. The pulse pressure may be as high as 80 to 100 mm Hg. The rapid upstroke is due to the large stroke volume, and the rapid downstroke is due to the rapid flow of blood from the aorta back into the ventricle and into the dilated peripheral vessels. The occurrence of a double peaked or bisferiens pulse trace is not unusual owing to the occurrence of a "tidal" or back wave.

        2. Pulmonary capillary wedge trace. Normally, stretching of the mitral valve annulus leads to functional mitral regurgitation, a prominent V wave, and a rapid Y descent. The V wave is more prominent in acute regurgitation and with the onset of LV failure.

    3. Goals of perioperative management

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Aortic regurgitationMaintainMaintain
        1. LV preload. Because of the increased LV volumes, maintenance of forward flow depends on preload augmentation. Pharmacologic intervention that produces venous dilation may significantly impair cardiac output in these patients by reducing preload.

        2. Heart rate. Patients with aortic regurgitation show a significant increase in forward cardiac output with an increase in heart rate. The decreased time spent in diastole during tachycardia leads to a decreased regurgitant fraction. Actual improvement in subendocardial blood flow is observed with tachycardia due to a higher systemic diastolic pressure and a lower LVEDP. This explains why a patient who is symptomatic at rest may show improvement in symptomatology with exercise. A heart rate of 90 beats/min seems to be optimal, improving cardiac output while not inducing ischemia. Maintenance of sinus rhythm is not as important as it is in patients with stenotic lesions, and the presence of atrial fibrillation is common.

        3. Contractility. LV contractility must be maintained. In patients with impaired LV function, use of pure β-agents can increase stroke volume through a combination of peripheral dilation and increased contractility.

        4. Systemic vascular resistance. Normally, patients with chronic aortic insufficiency initially compensate for the limitation in cardiac output by dilation of the peripheral arterioles. The forward flow can be improved further with afterload reduction. Increases in afterload result in increased stroke work and can significantly increase the LVEDP. The patient in end-stage aortic regurgitation with LV impairment benefits most from therapy with afterload-reducing agents.

        5. Pulmonary vascular resistance. Pulmonary vascular pressure remains relatively normal except in patients with end-stage aortic regurgitation associated with severe LV dysfunction.

      2. Anesthetic technique

        1. Premedication that dilates the capacitance vessels should be avoided. Light premedication is recommended to maintain myocardial contractility and heart rate because tachycardia actually can be helpful for these patients. Increases in systemic vascular resistance that may arise from anxiety, however, may be detrimental.

        2. A pulmonary artery catheter is essential for maintaining cardiac output and LV filling pressures, particularly when vasodilators are required to maintain forward flow.

        3. The agent of choice for induction and maintenance of anesthesia should be directed at preserving the patient's preload, maintaining the peripheral arterial dilation, improving contractility, and keeping the heart rate near 90 beats/min. Use of isoflurane and pancuronium in combination with fluid augmentation is acceptable, except in patients with end-stage disease with reduced ventricular function in whom a synthetic narcotic in combination with pancuronium is better tolerated.

        4. In patients with acute aortic regurgitation associated with poor ventricular compliance, LV pressure may increase fast enough to close the mitral valve before end diastole. In this situation, the continued regurgitation of blood raises LVEDP above left atrial pressure, and pulmonary capillary wedge pressure can significantly underestimate the true LVEDP.

        5. Use of an intraaortic balloon pump is contraindicated in the presence of aortic regurgitation because augmentation of diastolic pressure will increase the amount of regurgitant flow.

        6. Omniplanar TEE is beneficial for monitoring LV function and quantitating regurgitation before valve repair. If annuloplasty or plication is performed, TEE is valuable for providing immediate feedback concerning the integrity of valvular function. In total valve replacement, TEE allows assessment of perivalvular leaks.

      3. Surgical intervention. Surgical repair can be performed with an annuloplasty or valvular plication but most frequently is provided through the use of valvular replacement with a prosthetic valve. Surgery is indicated if the patient is symptomatic or preferably as soon as echocardiographic evidence of LV dysfunction exists in the asymptomatic patient. It is important to intervene surgically before LV dysfunction progresses.

      4. Postoperative care. Immediately after aortic valve replacement, LVEDP and LVEDV decrease. However, LV hypertrophy and dilation persist. In the immediate postbypass period, preload augmentation must be continued to maintain filling of the dilated LV. In the early postoperative period, a decline in LV function may necessitate inotropic or intraaortic balloon pump support. If surgical intervention is delayed until major LV dysfunction has occurred, the prognosis for long-term survival is not good. The 5-year survival rate for patients whose hearts do not return to a relatively normal size within 6 months after surgical repair is only 43%. If surgery is performed early enough, the heart will return to relatively normal dimensions, and a long-term survival rate of 85% to 90% after 6 years can be expected.

  4. Mitral stenosis

    1. Natural history

      1. Etiology. In adults, mitral stenosis almost always is secondary to rheumatic heart disease, which leads to scarring and fibrosis of the free edges of the mitral valve leaflets. Fusion of the valvular commissures, progressive scarring of the leaflets, and contraction of the chordae tendineae lead to the development of a funnel-shaped mitral apparatus that can become secondarily calcified. Women are affected twice as frequently as men. Mitral stenosis, of rheumatic origin, often occurs along with mitral regurgitation or aortic regurgitation.

      2. Symptomatology. Patients are normally asymptomatic for 20 years or more after an acute episode of rheumatic fever. However, as stenosis develops, symptoms appear, associated at first with exercise or high cardiac output states. Twenty percent of patients in whom the diagnosis of symptomatic mitral stenosis is made die within 1 year, and 50% die within 10 years after diagnosis, without surgical intervention. The natural history is a slow progressive downhill course with repeated episodes of pulmonary edema, dyspnea, paroxysmal nocturnal dyspnea, fatigue, chest pains, palpitations, and hemoptysis, as well as hoarseness due to compression of the left recurrent laryngeal nerve by a distended left atrium and enlarged pulmonary artery. Symptoms often become apparent with the onset of atrial fibrillation, and patients in atrial fibrillation are at increased risk for formation of left atrial thrombi and subsequent cerebral or systemic emboli. Medical management can be successful if it is initiated early. Chest pain may occur in 10% to 20% of patients with mitral stenosis, but it is a poor predictor of the coexistence of coronary disease, which may be present in approximately 25% of patients.

    2. Pathophysiology

      1. Natural progression

        1. Stage 1: mild mitral stenosis—asymptomatic with physiologic compensation. The normal mitral valve area is 4 to 6 cm2 (mitral valve index, 4.0 to 4.5 cm2/m2). The patient can remain essentially symptom-free during the 20- to 30-year period of slow progression of stenosis until a valve area of 1.5 to 2.5 cm2 (or valve index of 1.0–2.0 cm2/m2) is reached. At this point, moderate exercise may induce dyspnea. Exercise testing in the cardiac catheterization laboratory, by detecting increased filling pressures with exercise, can identify this stage of the disease. Further progression of mitral stenosis leads to increases in left atrial pressure and volume that are reflected back into the pulmonary circuit.

        2. Stage 2: moderate mitral stenosis—symptomatic impairment. Between a valve area of 1.0 and 1.5 cm2, increasing symptomatology appears with only mild-to-moderate exertion. Severe congestive failure can be induced either by the onset of atrial fibrillation or by a variety of disease processes leading to high cardiac output states, such as thyrotoxicosis, pregnancy, anemia, or fever. In all these conditions, the left atrial and pulmonary artery pressures suddenly rise as a result of the increased cardiac demand. The increase in pulmonary vascular resistance in response to high left atrial pressure eventually can lead to RV failure. Pulmonary arterial constriction, pulmonary intimal hyperplasia, and pulmonary medial hypertrophy eventually result in a picture of chronic pulmonary arterial hypertension associated with restrictive lung disease. Because atrial contraction contributes 30% of LV filling in mitral stenosis, the onset of atrial fibrillation can lead to significant impairment in cardiac output.

        3. Stage 3: critical mitral stenosis—terminal failure. With a valve area less than 1.0 cm2, a patient is considered to have critical mitral stenosis, and symptoms are present even at rest. Not only are left atrial pressures on the border of producing congestive failure, but cardiac output also may be reduced. Chronic pulmonary hypertension eventually leads to RV dilation. The dilated RV can cause a leftward shift of the intraventricular septum, thereby limiting the already reduced LV size and further impairing LV ejection. With further RV dilation, tricuspid regurgitation results, leading to signs of peripheral congestion. A mitral valve area of 0.3 to 0.4 cm2 is the smallest area compatible with life.

      2. Pressure–volume relationship (Fig. 12.5). Due to the restriction of flow from the left atrium to the ventricle, patients with significant mitral stenosis have reduced LVEDV and LVEDP. Stroke volume also is reduced. The actual LV performance is relatively normal. The limitation of stroke volume in these patients is entirely due to inadequate filling of the LV.

        FIG. 12.5 Pressure–volume loop, mitral stenosis, showing decreased left ventricular systolic and diastolic volumes, reduced stroke volume, and decreased systolic and end-diastolic pressures. AC, aortic valve closure; AO, aortic valve opening; MC, mitral valve closure; MO, mitral valve opening; phase 1, isovolumetric relaxation; phase 2, ventricular filling; phase 3, isovolumetric contraction; phase 4, ventricular ejection. (Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth 1982;1:244.)


      3. Calculation of mitral valve area. Quantitative evaluation of mitral stenosis based only on the diastolic pressure gradient across the mitral valve is inaccurate, as with the aortic valve, because it does not take into consideration the important factor, flow. The Gorlin formula for determination of the mitral valve area is as follows:

        where 0.85 is the mitral orifice constant and mitral valve flow (mL/s) is cardiac output (mL/min)/diastolic filling period (s/beat) × HR (beats/min).

        Because tachycardia shortens the diastolic filling period, it compromises LV filling and leads to clinical deterioration. Comparisons of the rate of blood flow and the mean diastolic pressure can be graphically represented (Fig. 12.6). It is apparent that when the mitral valve area is 1.0 cm2 or less, little additional flow can be obtained by increasing the pressure gradient across the valve.

        FIG. 12.6 Comparison between rate of blood flow across the mitral valve and mean diastolic pressure gradient across the mitral valve in individuals with different mitral valve areas, as determined by the Gorlin formula. Below a critical mitral valve area of 1.0 cm2, a large increase in mean diastolic pressure gradient across the mitral valve produces a minimal increase in blood flow. The point at which pulmonary capillary pressure exceeds normal plasma oncotic pressure leading to the transudation of fluid and the development of pulmonary edema is indicated on the graph. (From Schlant RC. Altered cardiovascular function of rheumatic heart disease and other acquired valvular disease. In: Hurst JW, Logue RB, Schlant RC, et al., eds. The heart, 4th ed. New York: McGraw-Hill, 1978:972, with permission.)


      4. Pressure wave disturbances

        1. Pulmonary capillary wedge pressure. Mitral stenosis produces a large A wave and, if it is associated with an element of mitral regurgitation, a prominent V wave. With increased impairment of left atrial contractility secondary to severe mitral obstruction, the A wave may become small. In the presence of atrial fibrillation, the A wave is obviously absent.

    3. Goals of perioperative management

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Mitral stenosisMaintainMaintain
        1. LV preload. Forward flow across the stenotic mitral valve is dependent on adequate preload. On the other hand, patients with mitral stenosis already have elevated left atrial pressures so that overly aggressive use of fluids can easily send a patient who is in borderline congestive failure into florid pulmonary edema.

        2. Heart rate. Blood flow across the mitral valve occurs during ventricular diastole. Tachycardia shortens the diastolic period so that at increased heart rates, the flow across the stenotic mitral valve must be increased to maintain the same level of cardiac output. Based on Poiseuille's law, the atrial–ventricular pressure gradient is proportional to the fourth power of the instantaneous flow across the mitral valve; hence, any increase in instantaneous flow requires a large increase in left atrial pressure. At the same time, excessive bradycardia can be dangerous because stroke volume is relatively fixed.

          Atrial contraction in patients with mitral stenosis contributes approximately 30% of the LV stroke volume. If atrioventricular pacing is initiated in these patients, a long PR interval of 0.15 to 0.20 ms is optimal to allow blood adequate time, after atrial contraction, to cross the stenotic mitral valve. Decreases in the PR interval will drop diastolic flow and result in a reduced cardiac output. In patients with atrial fibrillation, the contribution of atrial contraction is lost.

        3. Contractility. Adequate forward flow depends on adequate RV and LV contractility. Chronic underfilling of the LV, however, leads to cardiomyopathy with depressed ventricular contractility even in the face of restored filling. In end-stage mitral stenosis, depression of LV contractility may lead to severe congestive heart failure. Depression of RV contractility limits left atrial filling and, eventually, cardiac output. Many patients will require inotropic support before and especially after cardiopulmonary bypass.

        4. Systemic vascular resistance. To maintain blood pressure in the presence of limited cardiac output, patients with mitral stenosis normally develop increased systemic vascular resistance. Afterload reduction is not helpful in improving forward flow because the limiting factor for cardiac output is the stenotic mitral valve. It is recommended that the afterload be kept in the normal range for these patients.

        5. Pulmonary vascular resistance. These patients frequently have elevated pulmonary vascular resistances and are prone to exaggerated pulmonary vasoconstriction in the presence of hypoxia. Particular attention should be paid to avoiding any increases in pulmonary artery pressure due to injudicious use of anesthetic agents, particularly nitrous oxide, or to inadvertent acidosis, hypercapnia, or hypoxemia.

      2. Anesthetic technique

        1. Premedication should be light to avoid an acute decrease in preload or the possibility of sedation with resultant hypoxemia and hypercapnia. Avoidance of an anticholinergic should be considered to minimize tachycardia.

        2. Continue digitalis for heart rate control right up to the morning of surgery.

        3. Avoid pharmacologic agents or conditions that produce tachycardia, increased pulmonary vascular resistance, decreased preload, or decreased contractility. In particular tachycardia, whether it is due to a sinus mechanism or atrial fibrillation, must be treated aggressively. An attempt should be made to maintain sinus rhythm at all times with immediate use of cardioversion if new atrial fibrillation should occur. A narcotic anesthetic technique with high inspired O2 concentration usually is chosen for these patients [6].

        4. Pulmonary artery catheters almost always are indicated for perioperative management. However, the catheters often must be inserted further than usual because of the dilated pulmonary arteries. Special care should be taken when placing the catheters because of the increased risk of pulmonary artery rupture. Further, the pressure data obtained from the catheters must be interpreted carefully. Pulmonary artery diastolic pressure often is not an accurate estimate of left atrial pressure because of significant pulmonary hypertension. Even pulmonary capillary wedge pressure that does reflect left atrial pressure overestimates LV filling pressure because of the stenotic mitral valve.

          Because of the risk of pulmonary artery rupture and the questionable information obtained from a wedge pressure, final placement of the pulmonary artery catheter in a wedge position usually is not necessary.

        5. TEE evaluation is particularly helpful for monitoring the adequacy of mitral valve repair. Mitral commissurotomy may result in significant mitral regurgitation, which can be identified in the immediate postbypass period so that further surgical intervention can be provided promptly. In addition, complications associated with mitral valve replacement, such as paravalvular leak, which otherwise would require a repeat procedure, can be identified rapidly and repaired while still in the operating room.

      3. Surgical intervention. Surgical intervention should occur before the development of severe symptomatology because irreversible ventricular dysfunction may result if surgery is delayed too long. Surgery is not recommended for the asymptomatic patient unless there is evidence of systemic embolization or progressive pulmonary hypertension. Mitral commissurotomy is the operation of choice if the valve is not significantly calcified or severely fibrotic. Commissurotomy does not totally relieve the stenosis but rather makes it less severe. Restenosis of the mitral valve will occur in as many as 30% of patients within 5 years after commissurotomy and in 60% after 9 years. Nevertheless, during this time the patient does not require anticoagulation and is at risk for less morbidity than with an indwelling prosthetic valve. If the valve is not amenable to commissurotomy, mitral valve replacement should be performed. After isolated mitral valve replacement, 95% of patients survive to leave the hospital and, of these hospital survivors, 80% survive 5 years. A balloon-dilating technique at catheterization can be used to delay the necessity for open heart surgery by effectively relieving the mitral obstruction but with the risk of significant postdilation mitral regurgitation.

      4. Postoperative care. Successful surgical intervention leads to a drop in pulmonary vascular resistance, pulmonary arterial pressure, and left atrial pressure while increasing cardiac output in the first postoperative day. However, immediately after bypass, even patients with seemingly normal preoperative LV function may have major depression of myocardial contractility owing to their underlying cardiomyopathy exacerbated by ischemic arrest during cardiopulmonary bypass. These patients frequently require inotropic and intraaortic balloon pump support.

        Pulmonary vascular resistance in most patients will continue to decrease with time after surgery. Failure of the pulmonary artery pressure to decrease usually is indicative of irreversible pulmonary hypertension and probably irreversible LV dysfunction. This places the patient in a prognostically poor group.

        Preload augmentation as well as afterload reduction should be undertaken in the immediate postbypass period to improve forward blood flow. Patients previously in chronic atrial fibrillation occasionally can be converted to sinus rhythm by prophylactic treatment with a bolus of procainamide (500 mg to 1 g) or amiodarone (150 mg) during bypass. If the patient does convert to a sinus rhythm, this rhythm can be maintained, at least for short periods of time, with continuous infusion of procainamide (2 mg/min) or amiodarone (33 mg/min) and overdrive atrial pacing at a rate of approximately 110 beats/ min. It must be remembered that after prosthetic valve placement, a residual 4 to 7 mm Hg gradient across the mitral valve will still be present.

        One catastrophic complication that can occur within the first few days after valve replacement is atrioventricular disruption. One method suggested to help avoid this complication is to reduce LVEDP to as low a level as possible while maintaining adequate cardiac output. Atrioventricular disruption is a particular risk for the elderly patient with a relatively noncompliant LV who experiences increased diastolic tension on the LV wall after surgery. Thus, inotropes in the postbypass period can serve two functions by (a) increasing contractility and (b) reducing LV size and wall tension.

  5. Mitral regurgitation

    1. Natural history. The spectrum of mitral regurgitation varies from acute forms, in which rapid deterioration of myocardial function can occur, to chronic forms, which have slow indolent courses. Mitral regurgitation can be either primary or secondary to LV dilation or ischemia.

      1. Etiology—chronic mitral regurgitation. In the United States, the most common cause of mitral regurgitation probably is mitral valve prolapse, a common disorder that leads to significant regurgitation in 10% to 15% of cases. Rheumatic disease is an uncommon cause of mitral regurgitation. When it does occur, it is rarely pure. Usually it exists in combination with mitral stenosis. Rheumatic mitral regurgitation is a slow indolent process with an asymptomatic period that lasts 20 to 40 years. There is a gradual onset of fatigue and increasing dyspnea. Although mitral regurgitation can be tolerated for many years without ill effect, the onset of significant symptomatology (fatigue, dyspnea, or orthopnea) usually heralds a relatively rapid downhill course, with death occurring within 5 years. A sequela such as bacterial endocarditis, atrial fibrillation, reactive pulmonary hypertension, or systemic embolization leads to rapid clinical deterioration. Atrial fibrillation occurs in nearly 75% of cases. Survival rates are better in patients when surgery is performed before the development of irreversible LV dysfunction.

      2. Etiology—acute mitral regurgitation. Acute mitral regurgitation is being seen more frequently, especially mitral regurgitation on the basis of papillary muscle dysfunction due to myocardial ischemia. Papillary muscle dysfunction occurs in approximately 40% of patients who sustain a posterior septal myocardial infarction and in 20% of patients with an anterior septal infarction. Bacterial endocarditis is another frequent cause of nonrheumatic mitral regurgitation.

    2. Pathophysiology

      1. Natural progression

        1. Acute. Sudden development of mitral regurgitation leads to marked left atrial volume overload. Because of the normal compliance of the left atrium, the sudden volume overload leads to significant increases in left atrial pressure that are passed on to the pulmonary circuit. As immediate compensation for decreased cardiac output, sympathetic stimulation increases contractility and produces tachycardia. In addition, the LV functions on a higher portion of the Frank–Starling curve because of increased LV volumes. The acute increases in left atrial and pulmonary artery pressures can lead to pulmonary congestion and edema. Of concern, the compensatory sympathetic stimulation can lead to increased myocardial O2 consumption in myocardium already rendered ischemic by increased LVEDP and decreased subendocardial blood flow, and to peripheral constriction, further compromising systemic blood flow. Because LV ischemia is a common cause, acute mitral regurgitation often presents as biventricular failure.

        2. Chronic

          1. Stage 1: mild mitral regurgitation—asymptomatic with physiologic compensation. During the slow development of chronic mitral regurgitation, eccentric hypertrophy of the LV occurs, with the heart shifting eccentrically into the left side of the chest. Both LV dilation and hypertrophy occur. The dilation of the LV allows preservation of a relatively normal LVEDP despite a markedly increased LVEDV. The forward cardiac output is preserved by an overall increase in total LV stroke volume (combined forward stroke volume and regurgitant stroke volume). In addition, the left atrium enlarges and becomes distensible. A large distensible left atrium can maintain near-normal left atrial pressures despite large regurgitant volumes, which helps to protect the pulmonary vascular bed. Most of these patients eventually develop atrial fibrillation.

          2. Stage 2: moderate mitral regurgitation—symptomatic impairment. LV dilation and hypertrophy continue to compensate for increasing regurgitation until eventually the forward stroke volume is compromised. Continued left atrial dilation may lead to further increases in regurgitation owing to stretching of the mitral annulus. At this point, the symptoms of forward heart failure, including increased fatigability and generalized weakness, may intervene. Once the regurgitant fraction is greater than 60%, congestive heart failure occurs. LV ejection fraction usually is elevated in patients with mitral regurgitation because of the ease of ejecting blood backward into the low-pressure pulmonary circuit. An ejection fraction of 50% or less indicates the presence of significant ventricular dysfunction in these patients.

          3. Stage 3: severe mitral regurgitation—terminal failure. Continued severe compromise of forward cardiac output leads to increases in pulmonary artery pressure and eventually RV failure. In addition, LV function continues to deteriorate, and the depression of ventricular function becomes irreversible even after cardiac valve replacement.

      2. Pressure–volume relationship (Fig. 12.7). In chronic mitral regurgitation, LVEDP may remain relatively normal until the disease is far advanced despite major increases in LV end-diastolic and end-systolic volumes. The eccentric hypertrophy of the ventricle allows preservation of forward stroke volume by increasing total stroke volume. Blunting of the LV pressure increase during LV contraction occurs secondary to rapid early runoff of LV volume into the low-pressure left atrium. In contrast, in acute mitral regurgitation the compensatory increases in LV end-diastolic and end-systolic volumes are attenuated by acute increases in LVEDP until compensatory dilation can intervene.

        FIG. 12.7 Pressure–volume loop, moderate mitral insufficiency, showing markedly increased left ventricular end-systolic and end-diastolic volumes, along with some increase in left ventricular end-diastolic pressure. AC, aortic valve closure; AO, aortic valve opening; MC, mitral valve closure; MO, mitral valve opening; phase 1, isovolumetric relaxation; phase 2, ventricular filling; phase 3, isovolumetric contraction; phase 4, ventricular ejection. (Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth 1982;1:248.)


      3. Calculation of severity. The regurgitant fraction, which indicates the severity of mitral regurgitation, can be calculated quantitatively in the same way as in patients with aortic regurgitation (see Section III.B.3.b).

        Mitral regurgitation consisting of less than 30% of total LV stroke volume is considered mild, 30% to 60% is considered moderate, and greater than 60% is considered severe.

        Normally, determination of regurgitant volume is made only qualitatively through the use of angiographic dye injection into the LV:

         
        1+Minimal opacification of the left atrium is rapidly cleared
        2+Moderate opacification of left atrium is rapidly cleared
        3+Left atrial opacification is as intense as LV and aortic opacification
        4+Left atrial opacification is more intense than LV and aortic opacification
        Severe mitral regurgitation can be detected perioperatively on Doppler TEE by noting sustained reversal in the direction of pulmonary venous blood flow during systole and quantitated by the area of the regurgitant plume.

      4. Pressure wave disturbances

        1. Pulmonary capillary wedge tracing. The size of the regurgitant wave is not directly related to the severity of mitral regurgitation. The size of the regurgitant wave or "giant V wave" depends on the compliance of the left atrium, the compliance of the pulmonary vasculature, the amount of pulmonary venous return, and the regurgitant volume. In patients with sudden onset of mitral regurgitation, a relatively noncompliant left atrium leads to large V waves. Patients with chronic mitral regurgitation have a large compliant left atrium that can accept the regurgitant volume without passing the pressure wave on to the pulmonary circuit [7].

          In patients with giant V waves or regurgitant waves, differentiation between the pulmonary arterial pressure trace and the pulmonary capillary wedge pressure trace can be difficult (Fig. 12.8). One easy way to make this differentiation, however, is by superimposition of the pulmonary arterial trace and the arterial pressure trace. Normally, the pulmonary arterial upstroke occurs slightly before the systemic arterial upstroke but, when a wedge position is achieved, an immediate rightward shift is observed in the position of the upstroke and peak to the position of the giant V wave, which occurs later than the arterial pressure upstroke. Therefore, when placing pulmonary artery catheters in patients with mitral regurgitation or patients at risk for having giant V waves, it is imperative to perform simultaneous observation of pulmonary arterial and systemic arterial traces [8].

          FIG. 12.8 Electrocardiogram, radial arterial trace, and pulmonary arterial trace in the unwedged and wedged positions for a patient with severe mitral regurgitation. The amplitude of the "giant V wave" or regurgitant wave is greater than the peak pulmonary artery pressure. (From Moore RA, Neary MJ, Gallagher JD, et al. Determination of the pulmonary capillary wedge position in patients with giant left atrial V waves. J Cardiothorac Anesth 1987;1:110, with permission.)


    3. Goals of perioperative management

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Mitral regurgitation↑,↓↑MaintainMaintain
        1. LV preload. Augmentation and maintenance of preload frequently are helpful for ensuring adequate forward stroke volume. Unfortunately, a universal recommendation for preload augmentation cannot be made because in some patients dilation of the left atrial and LV compartments dilates the mitral valve annulus and increases the regurgitant fraction. A decision about the best level of preload augmentation for an individual patient must be based on that patient's clinical response to a fluid load.

        2. Heart rate. Bradycardia is harmful in patients with mitral regurgitation because it leads to an increase in LV volume, reduction in forward cardiac output, and increase in regurgitant fraction. The heart rate should be kept in the normal to elevated range in these patients. Atrial contribution to preload is not as important in patients with mitral regurgitation as in those with stenotic lesions, and many of these patients, particularly those with chronic mitral regurgitation, come to the operating room in atrial fibrillation.

        3. Contractility. Maintenance of forward stroke volume is dependent on maximal function of the eccentrically hypertrophied LV. Depression of myocardial contractility can lead to major LV dysfunction and clinical deterioration. Inotropic agents that increase contractility have a tendency to provide increased forward flow and actually can decrease regurgitation due to constriction of the mitral annulus.

        4. Systemic vascular resistance. An increase in afterload leads to an increase in regurgitant fraction and reduction in systemic cardiac output. For this reason, afterload reduction normally is desired, and α-adrenergic agents should be avoided. Typically, sodium nitroprusside will decrease LV filling pressure and cause a significant increase in forward cardiac index. However, in patients with acute mitral regurgitation secondary to ischemic papillary muscle dysfunction, nitroglycerin might be a more logical choice for use as a dilating agent.

        5. Pulmonary vascular resistance. Most patients with extensive mitral regurgitation will develop increased pulmonary vascular pressure and even can present in right-sided heart failure. Extreme caution must be taken to avoid hypercapnia, hypoxia, nitrous oxide, and pharmacologic or other interventions that might lead to pulmonary constrictive responses.

      2. Anesthetic management

        1. Premedication should be used judiciously because oversedation can lead to hypercapnia and marked increases in pulmonary vascular resistance.

        2. Pulmonary artery catheters are extremely helpful in guiding fluid management. They also help in evaluating the changing clinical state and significance of regurgitation for any particular patient as judged by changes in the height of the giant V wave.

        3. Anesthetic agents that lead to decreased contractility should be avoided. High-dose narcotic relaxant anesthetics are used most commonly.

        4. Patients with papillary muscle dysfunction secondary to ischemia frequently are helped by preoperative insertion of an intraaortic balloon pump. Inotropic support frequently is required in the postbypass period [9].

        5. Evaluation of the patient's regurgitant fraction is aided by the use of TEE. In addition, TEE can be invaluable for assessing the adequacy of valvular repair should annuloplasty or plication be chosen. When the valve is completely replaced, TEE is important for detecting the presence of a perivalvular leak in the immediate postbypass period so that repairs can be undertaken immediately.

        6. Nitric oxide, as a specific pulmonary artery dilator, may have an important role in the management of patients with reversible pulmonary hypertension. Hyperventilation is a second therapeutic modality available for selectively dilating the pulmonary vasculature without affecting the patient's systemic blood pressure. Prostaglandin E1 also has been used but is accompanied by a decrease in systemic pressure.

      3. Surgical intervention is not recommended if the patient can be treated medically with adequate relief of symptoms. However, once significant LV dysfunction occurs, surgery should be performed as soon as possible before the LV failure becomes irreversible. The surgical procedure usually performed is valve replacement using a mechanical or biologic valve, although occasionally annuloplasty can be performed with good results.

      4. Postoperative care. A primary concern after valve replacement is the need to maintain LV performance. Once the valve is in place, the LV has to eject a full-stroke volume into the aorta without the protection of a low-pressure popoff into the left atrium. The result is an increase in LV wall tension that can compromise ejection fraction. Therefore, in the postbypass period, LV performance frequently must be augmented using intraaortic balloon counterpulsation or inotropic support until the LV can adjust to the new hemodynamic state. After valve replacement, left atrial and pulmonary arterial pressures should decrease. Patients with long-standing mitral regurgitation will continue to need elevated left atrial pressure for maintenance of adequate forward flow. Immediately after weaning from cardiopulmonary bypass, patients who have been in chronic atrial fibrillation occasionally may revert to a sinus rhythm for a short period. An attempt should be made to keep the patient in sinus rhythm by using overdrive atrial pacing and treatment with procainamide or amiodarone.

  6. Tricuspid stenosis

    1. Natural history

      1. Etiology. The primary cause of acquired tricuspid stenosis is rheumatic valvulitis. Other causes of tricuspid stenosis include systemic lupus erythematosus, endomyocardial fibroelastosis, and carcinoid syndrome.

      2. Symptomatology. Isolated tricuspid stenosis is manifest by the signs and symptoms of right-sided heart failure, including hepatomegaly, hepatic dysfunction, ascites, edema, and jugular venous distention with giant A waves visible on the central venous pressure recording. As stenosis progresses, cardiac output may be limited, at least during exercise. However, patients with tricuspid stenosis frequently have associated mitral stenosis, which is the primary cause of symptomatology and clinical deterioration.

    2. Pathophysiology

      1. Natural progression. The tricuspid valve area normally is 7 to 9 cm2 in the typical adult. Significant impairment to forward blood flow does not occur until the valve orifice decreases to less than 1.5 cm2. Therefore, there is a long asymptomatic period as stenosis develops. With progression of the stenosis, right atrial pressure increases and forward blood flow decreases. Preservation of sinus rhythm is important for maintaining flow across the tricuspid valve, and rapid clinical deterioration can occur if the sinus rhythm is lost.

      2. Calculation of severity. Normally the gradient across the tricuspid valve is only 1 mm Hg. A mean gradient of 3 mm Hg across the tricuspid valve indicates significant tricuspid stenosis and usually corresponds to a valve area of 1.5 cm2. A gradient of 5 mm Hg across the tricuspid valve indicates severe stenosis and corresponds to a valve area of 1.0 cm2.

    3. Goals of perioperative management

      1. Hemodynamic management

         
          RV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Tricuspid stenosis↓ MaintainMaintainMaintain
        1. RV preload. Adequate forward flow of blood across the stenotic tricuspid valve depends on maintenance of adequate preload.

        2. Heart rate. Patients with tricuspid stenosis depend on maintenance of sinus rhythm. Supraventricular tachyarrhythmias can cause rapid clinical deterioration and should be controlled with either immediate cardioversion or pharmacologic intervention. At the same time, bradycardia can be harmful because it reduces total forward flow.

        3. Contractility. RV filling is impeded by tricuspid stenosis. Adequate cardiac output is maintained by an increase in RV contractility. A sudden depression in ventricular contractility can severely limit cardiac output and elevate right atrial pressure.

        4. Systemic vascular resistance. Changes in systemic afterload have little effect on the hemodynamic state of patients with tricuspid stenosis unless there is associated mitral valve involvement, particularly mitral regurgitation. However, systemic vasodilatation may lead to hypotension in patients with limited blood flow across the tricuspid valve.

        5. Pulmonary vascular resistance. Because the limitation to forward flow is at the tricuspid valve, reducing pulmonary vascular resistance has little positive effect on improving forward flow. Keeping pulmonary vascular resistance in the normal range is adequate.

      2. Anesthetic technique

        1. Extensive preoperative preparation—including salt restriction, digitalization, and diuretics—may reduce hepatic congestion, improve hepatic function, and reduce surgical risks.

        2. In patients with coexisting mitral valve disease, anesthetic technique is determined by the mitral valve lesion, as previously described. In patients with isolated tricuspid stenosis, the need to maintain high preload, high afterload, and adequate contractility favors the use of a narcotic-based anesthetic technique.

        3. Passage of a pulmonary artery catheter through the stenotic tricuspid valve may be impossible, and the catheter will have to be removed during bypass even if it can be placed. Therefore, use of a central venous pressure catheter, with surgical placement of a left atrial catheter and possibly a surgically placed pulmonary artery thermistor for cardiac output determination, may represent the best possible monitoring in this setting. Alternatively, a Swan–Ganz catheter placed into the superior vena cava until after bypass and then floated into the pulmonary artery is another approach.

      3. Surgical intervention. Commissurotomy of the tricuspid valve is commonly the procedure of choice. However, in cases of extensive calcification, valve replacement with a low-profile prosthetic valve may be necessary. In the postcardiopulmonary bypass period, preload augmentation must be continued.

  7. Tricuspid regurgitation

    1. Natural history. Isolated tricuspid regurgitation most frequently is seen in association with drug abuse, endocarditis, or chest trauma. More commonly, tricuspid regurgitation is associated with other cardiac abnormalities, such as end-stage aortic or mitral valve disease, most often mitral stenosis. With severe aortic or mitral valve disease, elevated pulmonary artery pressure leads to RV strain and, eventually, RV failure with tricuspid regurgitation. Carcinoid syndrome may produce isolated tricuspid regurgitation. The primary congenital cause of tricuspid regurgitation is Ebstein anomaly.

    2. Pathophysiology

      1. Natural progression. Isolated tricuspid regurgitation is well tolerated because the RV can compensate for volume overload. On the other hand, a pressure load is not well tolerated by the RV. Most symptoms associated with tricuspid regurgitation are directly related to an increased RV afterload. Therefore, when tricuspid regurgitation is associated with pulmonary vascular hypertension, the impedance to RV ejection produces significant clinical deterioration from decreased cardiac output. Most patients with tricuspid regurgitation have associated atrial fibrillation due to distention of the right atrium.

      2. Pressure wave abnormalities. Central venous pressure tracings may show the presence of giant V waves. However, as with mitral regurgitation, the compliance of the right atrium, filling of the right atrium, and regurgitant volume each helps to determine the size of the regurgitant wave.

    3. Goals of perioperative management

      1. Hemodynamic management

         
          RV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Tricuspid Regurgitation↑ MaintainMaintainMaintain
        1. RV preload. To provide adequate forward flow, preload augmentation is desirable. A drop in central venous pressure can severely limit RV stroke volume.

        2. Heart rate. Normal to high heart rates are beneficial in these patients to sustain forward flow and prevent peripheral congestion. Most of these patients are in chronic atrial fibrillation, so maintenance of a sinus mechanism is rarely possible.

        3. Contractility. RV failure is the primary cause of clinical deterioration in patients with tricuspid regurgitation. Because the RV is designed geometrically to accommodate volume but not pressure loads, it may require perioperative inotropic support, especially in the setting of positive-pressure ventilation or elevated pulmonary vascular resistance. Any suppression of contractility with myocardial depressants may induce severe RV failure.

        4. Systemic vascular resistance. Variations in systemic afterload have little effect on tricuspid regurgitation unless there is concurrent aortic or mitral valve dysfunction.

        5. Pulmonary vascular resistance. Because the RV does not tolerate pressure loads, RV function and forward blood flow are improved with decreases in pulmonary vascular resistance. Hyperventilation is helpful in reducing pulmonary vascular resistance by producing hypocapnia. However, high airway pressures during pulmonary ventilation and agents such as nitrous oxide that can increase pulmonary arterial pressure should be avoided. If inotropic support is necessary, dobutamine, isoproterenol, or milrinone, which dilate the pulmonary vasculature, should be used. Inhalation of nitric oxide may have an important role in selectively reducing pulmonary vascular resistance in these patients.

      2. Surgical intervention. Many patients can be treated successfully with tricuspid valvular plication or annuloplasty. If the valve has deteriorated, valve replacement may be necessary. If a prosthetic valve is placed, residual tricuspid stenosis will occur because the valve prosthesis is smaller than the native valve, and postbypass preload augmentation will be necessary. In addition, in the immediate postbypass period, the RV will be under increased strain because the entire stroke volume will have to be ejected against the higher pulmonary vascular resistance, with no popoff pressure lowering back into the right atrium. Therefore, RV failure requiring inotropic support may occur.

  8. Pulmonic stenosis

    1. Natural history

      1. Etiology. Pulmonic stenosis may be valvular, infundibular, or located in a pulmonary arterial branch (distal pulmonary artery). Nearly all cases of pulmonic stenosis are congenital, although rarely rheumatic heart disease can lead to pulmonic stenosis.

      2. Symptomatology. Patients with pulmonic stenosis may live for extended periods completely without symptoms and frequently survive past the age of 70 years without surgical intervention. Symptoms, when they do occur, include tachypnea, syncope, angina, or hepatomegaly and peripheral edema. Intervening bacterial endocarditis or RV failure due to severe stenosis may lead to death.

    2. Pathophysiology

      1. Natural progression. The normal pressure gradient across the pulmonic valve orifice usually is between 5 and 10 mm Hg. The diagnosis of pulmonic stenosis can be made when the gradient across the pulmonic valve reaches 15 mm Hg and RV systolic pressure reaches 30 mm Hg in the absence of an intracardiac shunt. Stenosis of the valve of more than 60% can occur before any significant obstruction to flow is generated. A peak systolic gradient of 50 mm Hg or less is considered mild pulmonic stenosis, between 50 and 100 mm Hg is considered moderate stenosis, and more than 100 mm Hg is considered severe pulmonic stenosis. As the pulmonic stenosis progresses from mild to moderate, concentric hypertrophy of the RV occurs. The increased hypertrophy and pressure within the RV lead to a situation in which RV subendocardial blood flow no longer occurs throughout the cardiac cycle but only during diastole, similar to the LV. Coronary perfusion pressure must be maintained to provide an adequate RV subendocardial coronary blood supply.

      2. Pressure wave abnormalities

        1. Pulmonary arterial pressure trace. The pulmonary artery pressure upstroke is delayed, and there is a late systolic peak owing to impedance of blood flow through the stenotic pulmonary valve.

        2. Central venous pressure trace. A prominent A wave frequently is found in the central venous pressure trace.

    3. Goals of perioperative management

      1. Hemodynamic management

         
          RV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Pulmonic stenosisMaintainMaintain↓ Maintain
        1. RV preload. RV performance depends on adequate preload for the RV. Decreases in central venous pressure will lead to inadequate filling of the RV and decreased RV stroke volume.

        2. Heart rate. As pulmonic stenosis progresses, the patient becomes increasingly dependent on atrial contraction to provide adequate RV filling. Unfortunately, in severe pulmonic stenosis, tricuspid regurgitation can develop, leading to right atrial distention and atrial fibrillation. Because blood flow across the stenotic pulmonary valve occurs primarily during ventricular systole, increases in heart rate usually provide increased flow. Rarely, RV hypertrophy in combination with angina symptoms dictates the need for a slower heart rate to allow adequate time in diastole for subendocardial coronary blood flow.

        3. Contractility. With severe pulmonic stenosis, the RV hypertrophies in response to the pressure load. Depression of the contractile state can lead to RV failure and clinical deterioration. Pharmacologic intervention that depresses RV function should be avoided.

        4. Systemic vascular resistance. Afterload should be maintained to provide adequate coronary perfusion to the hypertrophied RV.

        5. Pulmonary vascular resistance. Because the primary impedance to forward flow is the pulmonic valve, reducing pulmonary vascular resistance will do little to enhance forward blood flow. However, especially in patients with mild or moderate pulmonary stenosis, major increases in pulmonary vascular resistance potentially can harm forward blood flow and lead to RV dysfunction. Therefore, pulmonary vascular resistance should be kept in the low-to-normal range.

      2. Surgical intervention. Any patient who develops significant symptomatology, a peak systolic gradient across the pulmonic valve of more than 80 mm Hg, or a peak systolic RV pressure of 100 mm Hg should have surgical intervention. Normally, valvulotomy is all that is necessary. Rarely, the pulmonic valve must be replaced. An attractive alternative to open heart surgery is the use of transluminal balloon angioplasty, which frequently is used for congenital pulmonic valvular stenosis.

  9. Mixed valvular lesions. For all mixed valvular lesions, management decisions emphasize the most severe or the most hemodynamically significant lesion.

    1. Aortic stenosis and mitral stenosis. Pathophysiologically, the progression of the disease follows a course similar to that seen in patients with pure mitral stenosis with development of pulmonary hypertension and, eventually, RV failure. Symptomatology is primarily referable to the pulmonary circuit, including dyspnea, hemoptysis, and atrial fibrillation. This combination of valvular heart disease may lead to underestimation of the severity of the aortic stenosis because the aortic valve gradient may be relatively low because of low aortic valvular flow. Such a combination of lesions can be extremely serious because of the limitations of blood flow at two points.

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Mitral stenosis aloneMaintain
        Aortic stenosis aloneMaintainMaintain
        Typical management for combined lesionMaintain
        1. The best hemodynamic management for a patient with both aortic and mitral stenosis includes preload augmentation, normal-to-low heart rates, and preservation of contractility. Due to the high risk of decreased coronary perfusion, systemic vascular resistance must be increased whenever the diastolic perfusion pressure falls. All agents or conditions that might augment pulmonary vascular resistance must be aggressively avoided. Pco2 should be maintained in the low-to-normal range, and a high inspired O2 concentration should be supplied to minimize pulmonary vasoconstriction.

    2. Aortic stenosis and mitral regurgitation. This combination is relatively rare but should be suspected in patients with aortic stenosis who also have left atrial enlargement with atrial fibrillation. Mitral regurgitation can be exacerbated by LV dysfunction due to severe aortic stenosis. In this situation, the mitral valve does not require replacement, and the mitral regurgitation regresses after the aortic valve is replaced.

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Aortic stenosis aloneMaintainMaintain
        Mitral regurgitation alone↑,↓Maintain
        Typical management for combined lesionMaintainMaintainMaintain
        In managing these patients, the hemodynamic requirements for aortic stenosis and mitral regurgitation are contradictory. Because aortic stenosis most frequently will lead these patients into deadly intraoperative situations, it should be given priority when managing the hemodynamic variables.

        Preload augmentation normally is beneficial and, for coronary perfusion, maintenance of at least normal afterload is desirable. Obviously, increased systemic vascular resistance may hurt forward flow, but the stenotic aortic valve provides the primary impedance to forward flow no matter what the systemic vascular resistance is. Heart rate should be kept at least in the normal range, and tachycardia should be avoided at all costs. Contractility should not be depressed, and conditions or pharmacologic agents that increase pulmonary vascular resistance should be avoided.

    3. Aortic stenosis and aortic regurgitation. The combination of aortic regurgitation and aortic stenosis is not well tolerated because it provides the LV with both severe pressure and volume overloading. These stresses lead to major increases in myocardial O2 consumption (Mvo2) and, as might be expected, angina pectoris is an early symptom with this combination. Once symptomatology develops, the prognosis is similar to that of pure aortic stenosis.

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Aortic stenosis aloneMaintainMaintain
        Aortic regurgitation aloneMaintainMaintain
        Typical management for combined lesionMaintainMaintainMaintainMaintain
        Normally, augmentation of preload is beneficial for both aortic stenosis and aortic regurgitation. However, the hemodynamic requirements for afterload and heart rate for these two lesions are contradictory. Generally, maintaining a hemodynamic profile consistent with aortic stenosis is logical because compromise of this lesion intraoperatively is potentially more deadly than increasing the aortic regurgitation. Despite the risk of decreasing cardiac output, systemic vascular resistance should be augmented whenver systemic pressures begin falling to preserve coronary blood flow. Maintaining a normal heart rate, contractility, and pulmonary vascular resistance will help stabilize the patient.

    4. Aortic regurgitation and mitral regurgitation. The combination of aortic and mitral regurgitation occurs frequently, and this combination can cause rapid clinical deterioration.

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Mitral regurgitation alone↑,↓Maintain
        Aortic regurgitation aloneMaintainMaintain
        Typical management for combined lesionMaintainMaintain
        The hemodynamic requirements of aortic regurgitation and mitral regurgitation are similar. The primary problem is providing adequate forward flow and peripheral circulation. The development of acidosis leading to peripheral vasoconstriction and an increased impedance to LV outflow can lead to rapid clinical deterioration. Therefore, keeping the systemic vascular resistance relatively low while maintaining adequate perfusion pressure is the fine clinical balance needed until cardiopulmonary bypass can be initiated.

    5. Mitral stenosis and mitral regurgitation. Rheumatic mitral stenosis rarely is pure and commonly exists in conjunction with mitral regurgitation. When dealing with patients with combined mitral stenosis and mitral regurgitation, decisions concerning hemodynamic management must consider which lesion is predominant. As a rule of thumb, normalization of afterload, heart rate, and contractility, while avoiding agents or conditions that lead to reactive pulmonary constriction and providing adequate preload, leads to optimal hemodynamic stabilization.

      1. Hemodynamic management

         
          LV preload Heart rate Contractile state Systemic vascular resistance Pulmonary vascular resistance
        Mitral stenosis aloneMaintainMaintain
        Mitral regurgitation alone↑,↓Maintain
        Typical management for combined lesionMaintainMaintain↓ Maintain
  10. Prosthetic cardiac valves. The first successful prosthetic cardiac valve was placed in the descending thoracic aorta in 1952 by Charles Hufnagel in a patient with severe aortic regurgitation. Over the past 50 years, the available prosthetic valves have expanded to include stentless porcine bioprostheses, stented porcine and pericardial bioprostheses, allografts, and a wide range of mechanical prostheses. The decision regarding which prosthetic valve should be used for a particular patient is based upon a variety of factors, including the life expectancy of the patient (mechanical prostheses last longer), the ability of the patient to comply with anticoagulation therapy (mechanical prostheses require ongoing anticoagulation), the anatomy and pathology of the existing valvular disease, and the experience of the operating surgeon [10,11].

    1. Essential characteristics of prosthetic heart valves

      An ideal prosthetic heart valve is nonthrombogenic, chemically inert, preserves blood elements, and allows physiologic blood flow. The large number of different prosthetic valves that have been developed indicates that no ideal valve has yet been found.

    2. Types of prosthetic valves

      1. Mechanical. Current mechanical prosthetic valves are durable but thrombogenic. At present, all patients with mechanical prosthetic valves require anticoagulation therapy for the remainder of their lives. Normally, anticoagulation is provided with warfarin sodium, administered at a dose that will elevate the prothrombin time to 1.5 to 2.0 times control. There are four basic types of mechanical prosthetic valves.

        1. Caged-ball valve prosthesis (Fig. 12.9). The initial Starr–Edwards caged-ball valve prosthesis had a high rate of thromboembolic phenomena. However, improvements were made to this valve, including covering all metal parts with cloth, to stimulate the growth of surrounding tissue and allow the valve to develop a neointima that decreases thrombus formation. The Starr–Edwards valve has been used in the aortic, mitral, and tricuspid positions. Other valves of this type include the Smeloff–Cutter, Braunwald– Cutter, Magovern–Cromie, and DeBakey–Surgitool. Because these valves are bulky and the most thrombogenic of all current valves, and because the ball tends to interfere with central laminar blood flow, they currently are used very rarely.

          FIG. 12.9 Caged-ball valve prosthesis showing the movement of the ball in the open (A) and closed (B) positions.


        2. Caged-disk valve prostheses (Fig. 12.10). In an attempt to overcome the obstruction to blood flow presented by a bulky caged-ball valve, especially during cardiac tachyarrhythmias, a caged-disk valve was developed. Because of rapid disk breakdown, which included notching of the disk and even embolization, caged-disk valve prostheses are no longer used clinically. However, the widespread use of these valves in the 1970s has produced a reservoir of patients with these valves in place who still may be encountered. Other caged-disk valve prostheses once used include the Starr–Edwards 6500 series, Kay–Shiley, Cross–Jones, Harken, and Cooley–Bloodwell–Cutter valves.

          FIG. 12.10 Caged-disk valve prosthesis showing the disk in the open (A) and closed (B) positions.


        3. Monocuspid tilting-disk valve prosthesis (Fig. 12.11). In an attempt to decrease the postoperative pressure gradient across valves in which a ball or disk occludes the center of the path of blood flow (i.e., caged-ball, caged-disk), the monocuspid, central flow, tilting-disk valve was developed. Although flow characteristics were better than those associated with central occluding valves, thromboembolic complications still occurred even with adequate anticoagulation. Monocuspid tilting-disk valves that may be seen in clinical use at this time are the Sorin Allcarbon (pyrolytic carbon-coated chromium alloy housing with a pyrolytic carbon monoleaflet), Medtronic Hall (titanium housing with pyrolytic carbon leaflet), Omnicarbon (titanium housing with pyrolytic carbon monoleaflet), and Bjork–Shiley Monostrut (cobalt-chromium alloy housing with Pyrolyte carbon monoleaflet).

          FIG. 12.11 Monocuspid tilting-disk valve prosthesis showing the disk in the open (A) and closed (B) positions.


        4. Bileaflet tilting-disk valve prosthesis (Fig. 12.12). In 1977, a bileaflet St. Jude cardiac valve was introduced as a low-profile device to allow central blood flow through two semicircular disks that pivot on supporting struts. The St. Jude valve can be placed in the aortic, mitral, or tricuspid positions. These valves produce low resistance to blood flow and have a lower incidence of thromboembolic complications, although anticoagulation still is necessary. Studies indicate little difference in the hemodynamic profiles or outcome after implantation of either the monocuspid Medtronic–Hall or bicuspid St. Jude prosthesis. Bileaflet mechanical valve prostheses that may be seen in clinical use include the St. Jude Medical (pyrolytic carbon-coated graphite housing and Pyrolyte leaflets with tungsten for radiopacity), CarboMedics (solid Pyrolyte housing with pyrolytic carbon-coated graphite and tungsten substrate leaflets), Edwards Tekna (solid pyrolyte housing with pyrolytic carbon-coated graphite and tungsten leaflets), Bicarbon (Pyrolyte-coated titanium alloy housing with pyrolytic carbon-coated graphite and tungsten substrate leaflets), and Advancing the Standard (Pyrolyte housing with pyrolytic carbon-coated graphite substrate leaflets).

          FIG. 12.12 Bileaflet tilting-disk valve prosthesis showing disks in the open (A) and closed (B) positions.


      2. Bioprosthetic valves. Bioprosthetic valves fall into two classifications: stented and nonstented. The Hancock porcine aortic bioprosthesis was introduced in 1970, followed by the Ionescu–Shiley bovine pericardial prosthesis in 1974 and the Carpentier–Edwards porcine aortic valve bioprosthesis in 1975. In contrast to modern mechanical prostheses, current bioprostheses are less durable but much less thrombogenic. Long-term anticoagulation for a bioprosthesis placed in the aortic position usually is unnecessary, although aspirin, dipyridamole, or other antiplatelet drugs often are used. Unfortunately, bioprostheses placed in the mitral position still place patients at risk for thromboembolism and require warfarin anticoagulation.

        The overall 11-year outcomes for patients receiving mechanical prostheses and bioprostheses were found to be similar, leading to the recommendation that bioprostheses be used in patients older than 60 years who are undergoing aortic valve replacement because of the higher risk of bleeding and lower risk of mechanical valve failure during the remaining life span of these patients. In contrast, mechanical prostheses should be used in patients from ages 35 to 60 years and in those undergoing mitral valve replacement because of the greater risk of structural failure of the bioprosthesis in the mitral position and the higher likelihood that younger patients will outlive their bioprostheses. Because of the teratogenic effects of warfarin, young women who desire to become pregnant should receive a bioprosthesis.

        1. Stented bioprostheses. Bioprostheses constructed from porcine aortic valves or bovine pericardium are placed on a polypropylene stent attached to a silicone sewing ring covered with Dacron. These valves allow for improved central annular flow and less turbulence, but the stent does cause some obstruction to forward flow, thereby leading to a residual pressure gradient across the valve.

          Calcification of the bioprosthesis is a major long-term problem with porcine valves, which appear to calcify at the commissures, whereas bovine pericardial valves calcify at the regions of flexion.

          Stented valves that can be found in clinical use today include the Carpentier–Edwards Supra-annular Porcine, the Hancock II Porcine, Medtronic Intact Porcine, Medtronic Mosaic Porcine, Hancock Modified Orifice Porcine, Biocor Porcine, St. Jude Medical Bioimplant Porcine, St. Jude Medical X-Cell Porcine, Carpentier–Edwards Pericardial, Mitroflow Pericardial, Sorin Pericarbon Pericardial, and Pericarbon Pericardial.

        2. Stentless bioprostheses. Porcine valves fixed in a pressure-free glutaraldehyde solution but without the use of a stent make up the category of stentless bioprostheses. The primary types of valves clinically encountered in this category include the St. Jude Medical–Toronto SPV Stentless Porcine, Medtronic Freestyle Stentless Porcine, Cryolife Bravo Stentless Porcine, Baxter Prima Stentless Porcine, and Biocor Stentless Porcine.

      3. Human valves. The first use of a bioprosthesis taken from a cadaver occurred in 1962. However, techniques such as irradiation or chemical treatment used to sterilize and preserve the early homografts for implantation led to a shortened life span. More recently, antibiotic solutions have been used to sterilize human valves, which then are frozen in liquid nitrogen until implantation. Using these techniques, weakness of the prosthesis leading to cusp rupture occurs infrequently, with more than 75% of prostheses lasting for more than 10 years regardless of patient age. The incidence of prosthetic valve endocarditis and hemolysis resulting from blood flow through the homograft is very low. When homografts are used in the aortic position, anticoagulation is not required. However, in the mitral position a somewhat higher incidence of thromboembolism makes the use of anticoagulation somewhat more controversial.

        Homografts may be most useful for aortic valve replacement in patients younger than 35 years and in patients with native valve endocarditis. Homografts are contraindicated in diseases associated with progressive dilation of the aortic root, which would stretch the valve prosthesis and lead to early regurgitation, and in patients with poorly controlled hypertension, which would place increased stress on valve leaflets.

  11. Prophylaxis of subacute bacterial endocarditis. Prosthetic heart valves, as well as abnormal native valves, provide a nidus for infection. They are not as well protected by the body's immune defenses as are normal heart valves. When any invasive procedure puts the patient with valvular heart disease at risk for bacteremia, precautions should be taken to prevent seeding of an abnormal or artificial valve with bacteria that, once present, are very hard to eradicate. Practically, this concern translates into

    1. Strict aseptic technique for all procedures performed in patients with valvular heart disease

    2. Elimination of existing sources of infection before implantation of a prosthetic valve

    3. Antibiotic prophylaxis before, during, and after invasive proceduress

    Guidelines for antibiotic prophylaxis of patients with valvular heart disease are listed in Table 12.1.

  12. Anticoagulation management

    1. Chronic management

      Because prosthetic heart valves are constructed of foreign materials, they pose the risk of thrombosis and systemic embolization. The extent of this risk depends on the type of prosthetic valve, its location within the heart, and any other coexisting risk factors for thrombosis. In general, mechanical valves are much more thrombogenic than bioprostheses, and valves in the mitral position are at more risk than those in the aortic position.

      Warfarin sodium (Coumadin) is the agent most commonly used to prevent thrombus formation on prosthetic valves on a chronic basis. However, unfractionated heparin, low-molecular-weight heparin, and/or platelet inhibitors such as aspirin are used in special situations.

      Controversy still exists regarding the optimal coumadin dose, and the subsequent target international normalized ratio (INR), to use in many situations and the place that antiplatelet agents should have in therapy. The most recent guidelines proposed by the American College of Chest Physicians are listed in Table 12.2.

    2. Perioperative management

      Although there is universal agreement that the presence of a mechanical heart valve requires systemic anticoagulation chronically, there is less agreement about anticoagulation management immediately before and after surgery [12,13]. Kearon and Hirsh [14] reported that the rate of thromboembolism associated with mechanical heart valve, even without therapy, is only an average of eight events per year, or 0.02 events per day. Based on these statistics, and the expense and complications associated with intravenous heparin use, these authors recommend that warfarin be stopped several days before elective surgery in order to allow the INR to drop to 1.5 or lower and then resumed as soon as possible postoperatively, but with no intervening heparin therapy. Other authors suggest the use of heparin therapy when the INR is less then 2.0, at least for patients with prosthetic mitral valves or other risk factors. Recommendations for perioperative management of anticoagulants for patients with mechanical heart valves who are undergoing noncardiac surgery are listed in Table 12.3.

References

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  9. Butterworth JF, Legault C, Royster RL, et al. Factors that predict the use of positive inotropic drug support after cardiac valve surgery. Anesth Analg 1998;86:461–467.
  10. Edmunds L. Evolution of prosthetic heart valves.Am Heart J2001;141:849–855.
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  13. Stein PD, Alpert JS, Bussey HI, et al. Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves.Chest2001;119:220S–227S.
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