Matthew M. Townsley and Donald E. Martin
1. Increasing utilization of intraoperative transesophageal echocardiography (TEE) has greatly expanded the role of the cardiac anesthesiologist in operations for valve repair and replacement.
2. Because atrial contraction contributes up to 40% of left ventricular (LV) filling in patients with aortic stenosis (AS) and with hypertrophinc obstructive cardiomyopathy, it is essential to maintain sinus rhythm and treat arrhythmias aggressively in both of these conditions.
3. In patients with AS, the early use of α-adrenergic agonists such as phenylephrine is indicated to prevent drops in blood pressure that can lead quickly to sudden death.
4. Patients with severe acute aortic regurgitation are not capable of maintaining sufficient forward stroke volume (FSV) and often develop sudden and severe dyspnea, cardiovascular collapse, and deteriorate rapidly. Patients with chronic aortic regurgitation may be asymptomatic for many years.
5. In patients with mitral stenosis, particular attention should be paid to avoiding any increases in pulmonary artery pressure (PAP) due to inadequate anesthesia or inadvertent acidosis, hypercapnia, or hypoxemia.
6. Bradycardia is harmful in patients with mitral regurgitation, leading to an increase in LV volume, reduction in forward cardiac output, and an increase in regurgitant fraction (RF). The heart rate should be kept in the normal to elevated range.
7. In patients with tricuspid regurgitation (TR), high airway pressures during pulmonary ventilation and agents that can increase pulmonary arterial (PA) pressure should be avoided. If inotropic support is necessary, dobutamine, isoproterenol, or milrinone, which dilate the pulmonary vasculature, should be used.
8. Hypertrophy and pressure within the right ventricle with pulmonic stenosis limit right ventricular (RV) subendocardial blood flow to diastole. Coronary perfusion pressure (CPP) must be maintained to provide an adequate RV subendocardial coronary blood supply.
9. The hemodynamic requirements for AS and mitral regurgitation are contradictory. Because AS will most frequently lead these patients into deadly intraoperative situations, it should be given priority when managing the hemodynamic variables.
Following the “golden age” of cardiac surgery in the 1980s and 1990s, recent years have seen an overall decline in cardiac surgery volume. Surgery is no longer the preferred option for treating many forms of cardiac disease, especially in the case of coronary artery disease (CAD). The number of coronary artery bypass grafting (CABG) operations has undergone a noticeable decline, in large part due to continuing advances in the field of interventional cardiology. However, the same does not hold true for the surgical treatment of valvular heart disease, as the volume of valve surgery remains steady and now represents 10% to 20% of all cardiac surgical procedures in the United States . In the majority of these cases, surgery remains the best, and often only effective, approach to treatment. Valve surgery should continue to thrive with an aging patient population and continued improvements in surgical techniques, available prosthetic valves, and patient outcomes following these procedures. Approximately 66% of valvular surgery is on the aortic valve, most often because of AS .
The prevalence of valvular heart disease remains relatively constant at about 2.5% of the population in industrialized countries because an increase in the frequency of degenerative valvular disease has balanced the decrease in rheumatic disease. Further, the widespread use of echocardiography improves the detection and may increase the apparent incidence of disease. In Nkomo’s large echo-based series in Minnesota, the two most common valvular lesions were mitral regurgitation and AS, and the prevalence of disease increased markedly with age, ranging from less than 2% before age 65, to 8.5% in patients age 65 to 75, to 13.2% in patients older than 75 yrs . Further, almost one-third of patients presenting for surgical management have had a prior medical or surgical intervention . The mortality of valve surgery ranges from 0% to 3% for isolated mitral valve repair to 6% to 11% in patients undergoing multiple valve replacement, depending on the severity of the patient’s cardiac disease as well as their age and general health .
The anesthetic management of valvular surgical patients is often quite challenging. These lesions may lead to pathophysiologic changes in the heart with profound hemodynamic consequences, particularly in the setting of general anesthesia and surgical stress. A well-planned anesthetic must compensate for these stresses by manipulating several hemodynamic variables. The most important variables to consider include heart rate and rhythm, preload, afterload, and contractility. In addition, it is critical to consider the time course of the disease, as the clinical presentation and management will vary dramatically in the setting of acute versus chronic valvular disorders.
Increasing utilization of intraoperative TEE has greatly expanded the role of the cardiac anesthesiologist in operations for valve repair and replacement. In the setting of valve surgery, the anesthesiologist is frequently consulted by the surgeon to provide diagnostic interpretation of the echo findings to help guide the operative approach. The echo exam is also critical to immediately assess the adequacy of a valve repair or replacement and, if necessary, alert the surgeon to any complications that may require further attention and correction. There are few other settings in which an anesthesiologist’s diagnostic skills play such an integral role in surgical decision making as in the cardiac operating room during valve surgery.
This chapter will review the physiologic implications of the most common types of valvular heart disease and the practical approach to the anesthetic management of these patients. All four cardiac valves will be discussed, focusing on the stenotic and regurgitant lesions of each. A section addressing prosthetic valves will conclude the chapter with a review of each of the different types of prostheses most frequently used for valve replacement.
II. Stenotic versus regurgitant lesions
A. Valvular stenosis. Stenotic lesions lead to pathology associated with pressure overload. Narrowing of the orifice of a cardiac valve will ultimately lead to obstruction of blood flow through the valve. This obstruction translates into an increase in blood flow velocity as it approaches the stenotic valve orifice. The pattern of blood flow is distinctly different in the regions proximal and distal to a stenotic valve. The high-velocity flow proximal to the stenosis is laminar and organized, whereas distal to the stenosis, it becomes turbulent and disorganized. In addition, the increased blood flow velocities observed in valvular stenosis translate into an increase in the pressure gradient across the valve. The simplified Bernoulli equation helps explain this relationship. In this equation, the pressure gradient through the stenotic valve can be estimated by multiplying the velocity squared times four:
Pressure gradient (Δ) = 4 * Blood Flow Velocity (v) squared
(ΔP = 4v2)
The simplified Bernoulli equation allows blood flow velocities measured by Doppler echocardiography to be converted into pressure gradients that can be used to quantify the severity of valvular stenosis . It is also important to understand that valvular obstruction can be of two primary types: Fixed versus dynamic. In fixed obstruction (i.e., true valvulvar AS, subaortic membrane), the degree of obstruction to blood flow remains constant throughout the cardiac cycle and is not affected by the loading conditions of the heart. With dynamic obstruction (i.e., HOCM with dynamic subaortic stenosis), obstruction is only present for part of the cardiac cycle, primarily occurring in mid- to late systole. The degree of obstruction is highly dependent on loading conditions, changing in severity as loading conditions change.
B. Valvular regurgitation. Regurgitant lesions lead to pathology associated with volume overload, resulting in chamber dilatation and eccentric hypertrophy. Clinically, although this chamber remodeling will initially allow the left ventricle to compensate for the increased volume load, it will lead to an eventual decline in LV systolic function that can ultimately lead to irreversible LV failure. Effective perioperative management of valvular regurgitation is facilitated by understanding how preload, afterload, and heart rate each affect the contributions of the FSV (flow reaching the peripheral circulation) and regurgitant stroke volume (retrograde flow back across the valve) to the overall total stroke volume (TSV) of the ventricle . Hemodynamic management of these patients should aim to optimize the FSV while minimizing the amount of regurgitant stroke volume.
III. Structural and functional response to valvular heart disease.
The anesthetic management of patients undergoing valvular heart surgery requires a thorough understanding of the hemodynamic changes associated with valvular heart disease, as well as the cardiac remodeling imposed by abnormal valves.
A. Cardiac remodeling includes changes in the size, shape, and function of the heart in response to an acute or chronic cardiac injury. In valvular heart disease, cardiac injury is usually caused by alterations in ventricular loading conditions. Depending on the nature of the valvular pathology, the ventricle will be subject to either pressure or volume overload, or both. This leads to cardiac remodeling in the form of chamber dilation and ventricular hypertrophy. In addition to mechanical stress, cardiac remodeling results from the activation of neurohumoral factors, enzymes such as angiotensin II, ion channels, and oxidative stress . Intended initially as an adaptive response to maintain cardiac performance, remodeling eventually leads to decompensation and deterioration in ventricular function. Ventricular hypertrophy is defined as increased LV mass. Ventricular hypertrophy can be either concentric or eccentric. Pressure overload usually results in concentric ventricular hypertrophy, which means that ventricular mass is increased by myocardial thickening, whereas ventricular volume is not increased. Its adaptive purpose is to reduce the increased wall stress that results from the chronic pressure overload. Recall the law of LaPlace to understand how this compensatory hypertrophy results in reduced wall stress, where:
LV wall stress = (LV pressure * LV radius)/2 * LV wall thickness
The increased afterload results in an elevated LV pressure, which translates into an increase in LV wall stress. The resulting increase in wall thickness, seen in the denominator of the above equation, will have the beneficial effect of reducing LV wall stress and avoiding a significant decline in LV systolic function. The cost of LV hypertrophy is a reduction in LV compliance, which leads to diastolic dysfunction with an increase in LV end-diastolic pressure (LVEDP) and subendocardial ischemia.
Volume overload, on the other hand, leads to eccentric hypertrophy, which means that ventricular mass is increased by an increase in ventricular volume, whereas myocardial thickness remains unchanged .
B. 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. Systolic function represents the ventricle’s ability to contract and eject blood. Normal systolic function means that ventricular contractility is normal.
a. Contractility can be defined as the intrinsic ability of the myocardium to contract and generate force. Contractility itself is independent of preload and afterload. Normal contractility means that a ventricle of normal size and normal preload can generate sufficient stroke volume at rest and during exercise.
b. Preload can be defined as the load placed on myocardium before the contraction. This load results from a combination of diastolic volume and filling pressure and can be expressed as end-diastolic stress.
c. Afterload is the load placed on the myocardium during contraction. This load results from the combination of systolic volume and generated pressure and can be expressed as end-systolic stress.
2. Diastolic function represents the ventricle’s ability to accept inflowing blood. Diastolic function consists of a combination of relaxation and compliance. In general, normal diastolic function means that the ventricle accepts normal diastolic volume at normal filling pressure. When diastolic dysfunction occurs, maintaining normal ventricular diastolic volume requires elevated ventricular filling pressure. Both systolic and diastolic functions require energy and can be compromised by ventricular ischemia.
IV. Pressure–volume loops may be utilized to illustrate LV function and performance. These loops are constructed by plotting ventricular pressure (y-axis) versus ventricular volume (x-axis) over the course of a complete cardiac cycle (Fig. 12.1). The presence of valvular heart disease alters the normal pressure–volume loop tracing, representing changes in ventricular physiology and loading conditions imposed by valvular pathology. The ventricle adapts differently to each valvular lesion and characteristic patterns of the pressure–volume loop help illustrate these changes.
Figure 12.1 Normal pressure–volume loop. The first segment of the ventricular pressure–volume loop (Phase 1) represents diastolic filling of the left ventricle. The next two segments represent the two stages of ventricular systole: Isovolemic contraction (Phase 2) and ventricular ejection (Phase 3). The final segment of the loop corresponds to isovolemic relaxation of the left ventricle, which precedes ventricular filling and the start of the next cardiac cycle. The isovolemic relaxation and ventricular filling phases constitute the two phases of diastole. Both end-systolic volume at the time of aortic valve closure (AC), and end-diastolic volume at the time of mitral valve closure (MC), are represented as distinct points on the loop. MO, mitral valve opening; AO, aortic valve opening. [Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth. 1982;1:240.]
V. Aortic stenosis (AS)
A. Natural history
1. Etiology. The normal adult aortic valve has three cusps, with an aortic valve area of 2.6 to 3.5 cm2, representing a normal aortic valve index of 2 cm2/m2. AS may result from congenital or acquired valvular heart disease. Congenital AS is classified as valvular, subvalvular, or supravalvular based on the anatomic location of the stenotic lesion. Subvalvular and supravalvular AS are usually caused by a membrane or muscular band. Congenital valvular AS may occur with a unicuspid, bicuspid, or a tricuspid aortic valve with partial commissural fusion.
A congenitally bicuspid aortic valve occurs in approximately 1% to 2% of the general population, making it the most common congenital valvular malformation. Calcification of a congentially bicuspid valve results in the early onset of AS, and represents the most common cause of AS among patients younger than 70 yrs of age . Currently, bicuspid aortic valve disease accounts for approximately 50% of all valve replacements for AS in the United States and Europe . Commonly associated findings in patients with bicuspid aortic valves include abnormalities of the aorta, including aortic coarctation, aortic root dilatation, and an increased risk of aortic dissection.
Of the acquired aortic stenoses, senile degeneration is the most common cause in the developed world, with 30% patients older than 85 yrs demonstrating significant degenerative aortic valve changes on autopsy. The calcification seen with senile degeneration of the aortic valve also appears to have an inflammatory component as well, similar to that observed in CAD . While rheumatic AS is now rarely seen in the developed world, it remains the most common cause of AS worldwide. Additionally, rheumatic AS is usually associated with some degree of aortic regurgitation and frequently affects the mitral valve as well. Less frequent causes of AS include atherosclerosis, end-stage renal disease, and rheumatoid arthritis.
A characteristic finding of senile valvular degeneration is progression of the 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. Symptoms. Unicuspid AS often presents in infancy. Patients with rheumatic AS may be asymptomatic for 40 yrs or more. Congenital bicuspid aortic valves in the majority of cases must undergo calcific degeneration to become stenotic. The time of onset and speed of progression of calcific degeneration varies from patient to patient. This is why patients with congenitally bicuspid aortic valves may develop symptomatic AS anytime between the ages of 15 and 65, and even later in life. Degenerative stenosis of a tricuspid aortic valve usually develops in the seventh or eighth decade of life. Asymptomatic patients with AS have an excellent prognosis . Patients with even severe AS may stay asymptomatic for many years and carry a small risk of sudden death, which does not exceed the risk of operation. However, the onset of any one of the following triad of symptoms is an ominous sign and indicates a life expectancy of less than 5 yrs:
a. Angina pectoris. Angina is the initial symptom in approximately two-thirds of patients with severe AS. Angina and dyspnea secondary to AS alone initially occur with exertion . Life expectancy when angina develops is about 5 yrs.
b. Syncope. Syncope is the first symptom in 15% to 30% of patients. Once syncope appears, the average life expectancy is 3 to 4 yrs.
c. Congestive heart failure. Once signs of LV failure occur, the average life expectancy is only 1 to 2 yrs.
1. Heart remodeling. As stenosis progresses, the maintenance of normal stroke volume is associated with an increasing systolic pressure gradient between the LV and the aorta. The LV systolic pressure increases to as much as 300 mm Hg, whereas the aortic systolic pressure and stroke volume remain relatively normal. This pressure gradient results in a compensatory concentric LV hypertrophy. As stenosis progresses, eccentric LV hypertrophy may develop. This is usually associated with low LV ejection fraction, indicating a compromise of LV contractility.
2. Hemodynamic changes
a. Arterial pressure. In severe AS, the arterial pulse pressure usually is reduced to less than 50 mm Hg. 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.
b. PA 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. Pressure–Volume Loop in AS. (Fig. 12.2)
Figure 12.2 Pressure–volume loop in AS. In comparison to the normal loop, note the elevated peak systolic pressure necessary to generate a normal stroke volume in the face of the elevated pressure gradient through the aortic valve. Also, end-diastolic pressure is elevated with a steeper diastolic slope, reflecting diastolic dysfunction with altered LV compliance. Phase 1, Diastolic filling; Phase 2, Isovolumetric contraction; Phase 3, Ventricular ejection; Phase 4, Isovolumetric relaxation; MO, Mitral valve opening; MC, Mitral valve closure; AO, Aortic valve opening; AC, Aortic valve closure. [Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth. 1982;1:241.]
C. Assessment of severity (echocardiographic criteria; see Table 12.1)
1. Transthoracic echocardiography. Echocardiography is now the standard modality for quantifying the severity of AS. With the exception of rare cases where echocardiography is non-diagnostic or discrepant with clinical data, cardiac catheterization is no longer recommended for this purpose. The most commonly utilized methods for quantifying AS severity with echocardiography include measurement of the peak blood flow velocity of the AS jet, mean gradient across the aortic valve, and determination of aortic valve area. In AS, the valve area can be measured by the direct planimetry and continuity equation methods. The pressure gradient can be measured using a simplified Bernoulli equation. (Fig. 12.3) Cardiac remodeling is assessed by measurement of left atrial size, LV end-systolic and end-diastolic dimensions, and LV myocardial thickness.
Figure 12.3 Severe AS, showing determination of valve gradient using the Bernoulli equation. This image displays a deep transgastric long-axis TEE view with a continuous wave Doppler beam aligned through the left ventricular outflow tract (LVOT) and aortic valve (AV). Tracing 2 on the spectral display (outer envelope) demonstrates blood flow through the severely stenotic aortic valve, with a maximum velocity (AV Vmax) of 4.95 m/s and peak AV pressure gradient (AV max PG) of 97.9 mmHg. Tracing 1 (inner envelope) demonstrates blood flow through the LVOT, with a maximum velocity (Vmax) of 1.19 m/s and peak LVOT pressure gradient (Pmax) of 5.66 mmHg. Additional parameters: AV Vmean, Mean velocity of blood flow across the aortic valve; AV meanPG, Mean pressure gradient across the aortic valve; AV VTI, Aortic valve velocity-time integral; V mean, Mean velocity of blood flow in LVOT; Pmean, Mean pressure gradient in LVOT; VTI, LVOT velocity-time integral in LVOT; HR, Heart Rate. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2008:246, Figure 12.2.]
2. Transesophageal echocardiography (TEE). TEE is useful in patients with a poor transthoracic window or in patients with complex cardiac pathology (e.g., a combination of subaortic and valvular stenosis). It is also useful when precise planimetry of the aortic valve area is necessary or when infective endocarditis is suspected.
3. Dobutamine stress echocardiography is useful in patients with apparently severe AS on the echocardiogram that is combined with severe LV dysfunction and low cardiac output. Low cardiac output will not allow the generation of elevated blood flow velocities and pressure gradients commonly observed in AS. This combination of findings may be explained either by primary severe valvular AS causing LV dysfunction or by severe LV dysfunction independent of some degree of AS. In this case, the aortic valve does not open to its full extent due to low stroke volume and low generated pressure, which imitates severe AS. If with dobutamine infusion the transvalvular pressure gradient increases and the aortic valve area on the echocardiogram does not change, then AS is probably fixed and has caused the LV dysfunction. In this case, the patient will most likely benefit from surgical intervention . If, however, the apparent aortic valve area increases with dobutamine, then ventricular dysfunction is likely the prime factor and valve replacement would have little benefit.
4. If cardiac catheterization data is utilized, the mean pressure gradient may be measured from a direct transaortic measurement and the aortic valve area may be calculated using the Gorlin formula.
D. Timing and type of intervention
1. Due to the high risk of sudden death and limited life expectancy, symptomatic patients should undergo surgery. Asymptomatic patients with severe AS may be monitored closely until symptoms develop. However, the risk of waiting should be carefully weighted against the risk of surgery. For example, prior to elective noncardiac surgery under general or neuraxial anesthesia, asymptomatic patients with severe AS should be considered for aortic valve surgery.
2. Patients with moderate AS should have aortic valve surgery if they happen to require another cardiac operation, such as CABG, because the rate of progression of AS is approximately 0.1 cm2/yr and the risk of having to redo cardiac surgery is substantially higher than the risk of the primary operation. Similarly, if a patient undergoing aortic valve surgery has significant CAD, CABG should be performed simultaneously. In patients over age 80 yrs, the risk of aortic valve replacement (AVR) alone is approximately the same as the risk of combined AVR and CABG .
3. A commissural incision or balloon aortic valvuloplasty is often the first procedure performed in young patients with severe noncalcific aortc valve stenosis, even if they are asymptomatic . This operation frequently results in some residual AS and aortic regurgitation. Eventually, most patients require a subsequent prosthetic valve replacement. In older adult patients with calcific AS, valve replacement is the primary operation. In young adults, a viable alternative to AVR is the Ross (switch) procedure. In the Ross procedure, the diseased aortic valve is replaced with a patient’s normal pulmonary valve and the pulmonary valve is replaced with a pulmonary homograft. This more complex procedure avoids the need for systemic anticoagulation and extends the time until reoperation is required by several decades.
4. Surgical intervention should not be denied to patients, almost no matter how severe the symptoms, because irreversible LV failure occurs only very late in the disease process.
5. Balloon aortic valvuloplasty in adults with advanced disease often results in significant aortic regurgitation and early restenosis, and is reserved for patients with severe comorbidity. Percutaneous AVR is a treatment modality with potential applications for high-risk patients deemed not suitable candidates for surgery. Transapical AVR, involving a small thoracotomy incision and insertion of the valve via the LV apex, has shown similar promise in this same high-risk patient population. Both techniques require brief cessation of the patient’s cardiac output via rapid pacing during positioning of the device. Hemodynamic instability is common and necessitates prompt recognition and treatment. These techniques have demonstrated improved rates of procedural success and clinical outcomes, with an overall 94% success rate and an 11.3% 30-day mortality .
E. Goals of perioperative management
1. Hemodynamic profile (Table 12.2)
a. LV preload. Due to the decreased LV compliance as well as the increased LVEDP and LV end-diastolic volume (LVEDV), preload augmentation is necessary to maintain a normal stroke volume.
b. 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 these 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 atrial contraction contributes up to 40% of LV filling, due to decreased LV compliance and impaired early filling during diastole, it is essential to maintain a sinus rhythm. Supraventricular dysrhythmias should be treated aggressively, if necessary, with synchronized DC shock, because both tachycardia and the loss of effective atrial contraction can lead to rapid reduction of cardiac output.
c. Contractility. Stroke volume is maintained through preservation of a heightened contractile state. The 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.
d. 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. In addition, patients with hemodynamically significant AS cannot increase cardiac output in response to a drop in systemic vascular resistance. Thus, arterial hypotension may rapidly develop in response to the majority of anesthetics. Finally, when hypotension develops, the hypertrophied myocardium of the patient with AS is at great risk for subendocardial ischemia because coronary perfusion depends on maintenance of an adequate systemic diastolic perfusion pressure. Therefore, the early use of a-adrenergic agonists such as phenylephrine is indicated to prevent drops in blood pressure that can lead quickly to sudden death.
e. Pulmonary vascular resistance (PVR). Except for end-stage AS, PAPs remain relatively normal. Special intervention for stabilizing PVR is not necessary.
2. Anesthetic techniques
a. Light premedication is necessary to provide a calm patient without tachycardia. An experienced cardiac surgeon should be present, and perfusionists should be prepared, before induction of anesthesia should rapid cardiovascular deterioration necessitate emergency use of cardiopulmonary bypass.
b. Placement of external defibrillator pads should be considered to allow for rapid defibrillation if cardiovascular collapse occurs on induction or prior to sternotomy.
c. Preinduction arterial line placement is standard practice at most institutions and is generally well tolerated with light premedication and local anesthetic infiltration. Invasive blood pressure monitoring facilitates early recognition and intervention if any hemodynamic instability occurs during induction.
d. During induction of anesthesia, in order to maintain hemodynamic stability, medications should be carefully titrated to a fine line between a reasonable depth of anesthesia and hemodynamic stability.
e. During the maintenance stage of anesthesia, anesthetic agents causing myocardial depression, blood pressure reduction, tachycardia, or dysrhythmias can lead to rapid deterioration. A narcotic-based anesthetic is usually chosen for this reason. Low concentrations of volatile anesthetics are usually safe.
f. If the patient develops signs or symptoms of ischemia, nitroglycerin should be used with caution because its effect on preload or arterial pressure may actually make things worse.
g. Thermodilution cardiac output. Pulmonary artery catheters are helpful in evaluating the cardiac output of patients prior to repair of the aortic valve. The pulmonary capillary wedge pressure (PCWP), however, may overestimate preload of a noncompliant LV. Mixed venous oxygen saturation monitoring via an oximetric PA catheter may be used to provide a continuous index of cardiac output. However, because the postbypass management is not likely to be marked by myocardial failure or low output states, this technique may be best reserved for other patients who may be at higher risk of postbypass hemodynamic complications.
There is also a small risk of life-threatening arrhythmias leading to drug-resistant hypotension during passage of a pulmonary artery catheter through the right atrium and ventricle. In the absence of pre-existing left bundle branch block (LBBB) or tachyarrhythmias, a pulmonary artery catheter may be placed under continuous rhythm monitoring, perhaps after placement of transcutaneous pacing electrodes. In the presence of pre-existing abnormal rhythms or conduction disturbances, however, the most conservative approach dictates leaving the catheter tip in a central venous position until the chest is open, when internal defibrillator pads can be easily applied and cardiopulmonary bypass can be initiated within a few minutes if necessary.
h. Omniplane TEE is useful for intraoperative monitoring of LV function, preload, and afterload. TEE can predict prosthetic aortic valve size based on the LV outflow tract width. It is also very helpful in the detection of air and facilitating deairing prior to weaning from cardiopulmonary bypass. TEE is the method of choice for the postbypass assessment of a prosthetic valve for paravalvular regurgitation and prosthetic valve stenosis. It is important to remember that Doppler-derived blood flow velocities and pressure gradient must be interpreted in light of the altered loading conditions seen in the dynamic operating room setting.
i. In the presence of myocardial hypertrophy, adequate myocardial preservation with cardioplegic solution during bypass is a challenging task. A combination of antegrade cardioplegia administered via coronary ostia and retrograde cardioplegia via the coronary sinus has an important role in preserving myocardial integrity.
j. 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.
F. Postoperative care. After a sharp drop in the aortic valve gradient, PCWP and LVEDP immediately decrease and stroke volume rises. Myocardial function improves rapidly, although the hypertrophied ventricle may still require an elevated preload to function normally. Over a period of several months, LV hypertrophy regresses. It must be remembered that a prosthetic aortic valve may cause a mean pressure gradient of 7 to 19 mm Hg.
VI. Hypertrophic cardiomyopathy
A. Natural history
1. Etiology and classification. Hypertrophic cardiomyopathy (HCM) is a relatively uncommon genetic disorder affecting approximately 0.2% of the general population. The inheritance pattern is autosomal dominant with variable penetrance, making it a heterogeneous condition with a highly variable presentation. Historically, several names have been given to this disorder, such as idiopathic hypertrophic subaortic stenosis (IHSS) and asymmetric septal hypertrophy. Since ventricular hypertrophy may occur in multiple patterns, not just confined to the septum, the term HCM is now used to describe this disorder. Additionally, despite the classic association of HCM with obstruction to systolic outflow through the left ventricular outflow tract (LVOT), only 25% of patients with HCM exhibit this subvalvular obstruction. The term HOCM is used to refer to this subset of HCM patients.
2. Symptoms. Patients with HCM may present with a wide range of symptoms, with many having no symptoms at all. The most common presenting symptom is dyspnea on exertion with poor exercise tolerance. Patients may also experience syncope, presyncope, chest pains, fatigue, and palpitations. Though LVOT obstruction may cause symptoms, there is no clear relationship between the degree of LVOT obstruction and the occurrence or severity of the symptoms. Other equally important causes of symptoms include diastolic dysfunction, dysrhythmias, mitral regurgitation, and an imbalance of myocardial oxygen supply and demand. Unfortunately, the initial presenting symptom in many patients is sudden cardiac death, usually due to ventricular fibrillation. Though all patients with HCM are at risk for sudden death, the highest-risk groups include those with a family history of HCM and young patients undergoing significant physical exertion. This has led to increased and improved measures to screen for HCM in young athletes and patients with a family history of the disorder.
B. Pathophysiology. By definitition, HCM involves an abnormal thickening of the myocardium without an identifiable cause of hypertrophy. There is an absence of chamber dilation and, in most cases, normal to hyperdynamic LV systolic function. In addition, there are important histological derangements, including abnormal cellular architecture and disarray of the cardiac myocytes, interstitial fibrosis, increased connective tissue, and patchy myocardial scarring. These cellular abnormalities contribute significantly to the common, and potentially catastrophic, dysrhythmias seen in these patients. HCM patients are prone to both atrial and ventricular dysrhythmias, with ventricular fibrillation as the most common cause of sudden death.
In the subset of patients with HOCM, hypertrophy occurs disproportionately in the ventricular septum. As the septum enlarges, it extends into and narrows the LVOT, whose borders are formed by the ventricular septum and the anterior leaflet of the mitral valve. During systole, there is further narrowing of the LVOT due to inward septal movement with ventricular contraction, leading to increased blood flow velocities and pressure gradients through the narrowed outflow tract. Rapid blood flow creates hydraulic forces (Venturi effect) capable of pulling the anterior mitral leaflet into the LVOT, causing further narrowing and obstruction. This abnormal systolic anterior motion (SAM) of the mitral valve leads to dynamic obstruction, in which the degree of obstruction varies based upon cardiac loading conditions and contractility. The obstruction occurs proximal to the aortic valve (subaortic) and occurs only in mid- to late systole. The degree of obstruction is directly proportional to LV contractility and inversely proportional to LV preload and afterload.
While dynamic LVOT obstruction is seen in only a subset of HCM patients, most of them exhibit diastolic dysfunction secondary to ventricular hypertrophy, as well as hypertrophy and disarray of the myocytes. Early diastolic filling is impaired secondary to this poor diastolic compliance, making atrial contraction, and thus maintenance of sinus rhythm, critical for adequate diastolic filling. Mitral regurgitation can be significant, as SAM does not allow for normal coaptation of the mitral valve, creating a regurgitant orifice as the anterior mitral valve leaflet is pulled into the LVOT. Mismatch of oxygen supply and demand is a frequent occurrence in HCM that predisposes to ischemia. The hypertrophied myocardium represents a large muscle mass and there is increased oxygen demand associated with elevated ventricular pressures and wall tension .
C. Preoperative evaluation and assessment of severity. Echocardiography allows for assessment of the location and severity of hypertrophy and helps determine the necessity and feasibility of potential surgical intervention. It demonstrates the degree of LVOT narrowing, as well as the presence or absence of SAM. Doppler measurements in the LVOT help determine the presence and severity of subaortic obstruction, with outflow gradients of >30 mm Hg representing significant obstruction. In addition to the mitral coaptation defect associated with SAM, the mitral apparatus itself may be abnormal in HCM patients and should be thoroughly examined. LV systolic function is typically normal or hyperdynamic and diastolic function is almost always abnormal.
D. Timing and type of intervention. The mainstay of medical therapy for HCM involves treatment with β-blockers, which help reduce LVOT obstruction due to their negative inotropic effects and reduction in heart rate. Calcium channel blockers are also frequently utilized for their favorable effect on diastolic compliance. The most critical intervention in patients identified as high risk for malignant dysrthythmias is placement of an automated implantable cardioverter-defibrillator. Other non-surgical approaches to decrease outflow obstruction include dual-chamber pacing and ethanol ablation of the ventricular septum. Surgical treatment involves removal of septal muscle tissue to widen the LVOT via septal myomectomy and may occasionally involve modification of the mitral valve apparatus or mitral valve repair/replacement.
E. Goals of perioperative management
1. Hemodynamic profile (Table 12.3)
a. LV preload. Any condition that leads to a decrease in LV cavity size can potentially exacerbate dynamic LVOT obstruction, as this places the septum and anterior mitral leaflet in closer proximity, narrowing the outflow tract and increasing the potential for SAM and obstruction. In this regard, preload augmentation is essential to help maintain ventricular volume. Additionally, like in AS, diastolic dysfunction will lead to decreased LV compliance with increased LVEDP, which will necessitate adequate preload to maintain a normal stroke volume. Treatment with nitroglycerin, or other vasodilators, should be avoided as it may dangerously reduce cardiac output.
b. Heart rate. It is essential to avoid tachycardia in patients with HCM because it leads to a reduction in ventricular volume, exacerbation of dynamic LVOT obstruction, and increased oxygen demand. Decreased heart rates are beneficial as this prolongs diastole and allows more time for ventricular filling. Maintenance of sinus rhythm is essential, as the atrial contraction component of ventricular filling is critical due to reduced early diastolic filling because of reduced LV compliance.
c. Contractility. Decreases in myocardial contractility help reduce outflow obstruction. The β-blockade, volatile anesthetics, and avoidance of sympathetic stimulation are all beneficial. The use of intraoperative inotropic agents can increase contractility, worsen LVOT, lead to severe hemodynamic instability, and must be avoided.
d. Systemic vascular resistance. Decreases in afterload must be promptly and aggressively treated with vasopressors such as phenylephrine or vasopressin. Hypotension can be especially detrimental in this population because diastolic dysfunction leads to increased LVEDP, requiring an increased blood pressure to provide adequate CPP:
CPP = Diastolic blood pressure (aorta) − LVEDP
e. PVR. PAPs remain relatively normal in this patient population. Special intervention for stabilizing PVR is not necessary.
2. Anesthetic technique
a. Premedication. Many of these patients are on maintenance therapy with β-blockers or calcium channel blockers, which should be given on the day of surgery and continued throughout the perioperative period.
b. Induction and maintenance of anesthesia. During induction and laryngoscopy, careful attention is required to avoid decreases in afterload, as well as sympathetic stimulation leading to increases in heart rate and contractility. Adequate preload must be maintained and all blood or fluid losses must be aggressively replaced. The direct myocardial depression of volatile anesthetics is advantageous.
c. Patients with HCM are at risk for atrial and ventricular tachyarrythmias during surgery. Preparation must be in place for immediate cardioversion or defibrillation.
d. Intraoperative TEE, like preoperative echocardiography, allows visualization of the location and extent of hypertrophy in the septum, the degree SAM, the degree of obstruction, and quantification of the degree of mitral regurgitation. Since CVP and PCWP measurements will overestimate true volume status, TEE is the most reliable means of accurately assessing volume. The ability to monitor LV systolic function and wall motion is useful, as the oxygen supply–demand relationship is tenuous in these patients, making them prone to ischemia. The adequacy of surgical repair and any post-repair complications can be immediately assessed.
e. Postoperative care. Potential complications in the immediate postoperative period following septal myomectomy include residual LVOT obstruction, residual SAM, residual mitral regurgitation, complete heart block, and the creation of a ventricular septal defect.
VII. Aortic regurgitation
A. Natural history
1. Etiology. Aortic insufficiency can be caused by aortic valve disease, aortic root dilation, or a combination of both . Examples of causes of chronic aortic valve insufficiency include rheumatic fever, infective endocarditis, congenital bicuspid valve, and rheumatoid arthritis. Aortic root dilation can be caused by degenerative aortic dilation, syphilitic aortitis, Marfan’s syndrome, and aortic dissection. Acute aortic insufficiency is usually caused by aortic dissection, trauma, or aortic valve endocarditis.
2. Symptoms. Patients with severe acute aortic regurgitation are not capable of maintaining sufficient FSV and often develop sudden and severe dyspnea, cardiovascular collapse, and deteriorate rapidly. Patients with chronic aortic regurgitation may be asymptomatic for many years. Symptoms such as shortness of breath, palpitations, fatigue, and angina usually develop after significant dilatation and dysfunction of the LV myocardium. The 10-yr mortality for asymptomatic aortic regurgitation varies between 5% and 15%. However, once symptoms develop, patients progressively deteriorate and have an expected survival of only 5 to 10 yrs.
1. Pathophysiology and natural progression
a. Acute aortic regurgitation. The sudden occurrence of acute aortic regurgitation places a major volume load on the LV. The immediate compensatory mechanism for the 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 stroke volume and heart rate may not be sufficient to maintain a normal cardiac output. Rapid deterioration of LV function can occur, necessitating emergency surgical intervention.
b. Chronic aortic regurgitation. The onset of aortic regurgitation leads to LV systolic and diastolic volume overload. The increased volume load causes an increase in the size of the ventricular cavity, or eccentric ventricular hypertrophy. Because the LVEDV increases slowly, the LVEDP remains relatively normal. 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. As the LV dilation and hypertrophy progresses, coronary perfusion finally decreases leading to irreversible LV myocardial tissue damage and dysfunction. The onset of LV dysfunction is followed by an increase in PAP with symptoms of dyspnea and congestive heart failure. As a compensatory mechanism for the poor cardiac output and poor coronary perfusion, sympathetic constriction of the periphery occurs to maintain blood pressure, which in turn leads to further decreases in cardiac output.
2. Pressure wave disturbances
a. Arterial pressure. Incompetence of the aortic valve leads to regurgitant blood flow from the aorta back into the LV during diastole. This causes a pronounced decline in aortic diastolic blood pressure, translating into a wide pulse pressure. Patients with aortic regurgitation, therefore, show a wide pulse pressure with a rapid rate of rise, a high systolic peak, and a low diastolic pressure. The pulse pressure may be as great 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 due to the occurrence of a “tidal” or backwave.
b. Pulmonary capillary wedge trace. Stretching of the mitral valve annulus may lead to functional mitral regurgitation, a prominent V wave, and a rapid Y descent. 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 the LVEDP above left atrial pressure, and the PCWP can significantly underestimate the true LVEDP.
3. Pressure–volume loop in aortic regurgitation (Fig. 12.4)
Figure 12.4 Pressure–volume loop in acute and chronic aortic regurgitation. Note the rightward shift of the loop in chronic aortic regurgitation (C), reflecting elevated LV volume without a dramatic elevation in filling pressure. In acute aortic regurgitation (A), LV volumes are also increased; however, the ventricle has not adapted to accommodate the increased volumes without elevation of filling pressures. [Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth.1982;1:247.]
C. Assessment of severity
1. Traditionally, the amount of aortic regurgitation is estimated based on angiocardiographic clearance of dye injected into the aortic root. Currently, echocardiography is the method of choice for qualitative, semiquantitative, and quantitative assessment of aortic regurgitation.
a. Echocardiographic assessment of aortic regurgitation
The severity of aortic regurgitation can be assessed with echocardiography by several qualitative, quantitative, and semiquantitative techniques (Table 12.4). Qualitative assessment includes the two-dimensional analysis of the aortic valve anatomy, with particular attention to any structural abnormalities of the leaflets. The aortic root and LV cavity should be closely examined for evidence of dilation. Color flow Doppler allows visualization of the regurgitant jet, originating at the aortic valve and extending back into the LVOT in diastole. An experienced echocardiographer can often accurately estimate the degree of regurgitation with this initial observation; however, quantitative measurements can be made to assess the severity more accurately. The vena contracta is perhaps the most widely utilized measurement. It represents the narrowest point of the regurgitant jet and corresponds to the size of the regurgitant orifice. It is a relatively easy measurement to obtain and is also not affected by changes in preload or afterload (Fig. 12.5). Severity of regurgitation can also be estimated by determining the extent to which the regurgitant jet occupies the LVOT. The ratio of jet width to LVOT width, or jet area to LVOT area, has been found to correlate well with angiocardiographic assessment. (Fig. 12.6) Continuous-wave Doppler can be used to measure the deceleration rate of the regurgitant jet and the pressure half-time (PHT). These measurements are based on the rate of equilibration between aortic and LV pressures. As regurgitant severity increases (i.e., regurgitant orifice becomes larger), these pressures will equilibrate more quickly. Thus, significant aortic regurgitation corresponds to a steep slope of the jet deceleration rate and a short PHT. Severe aortic regurgitation may also be associated with holodiastolic flow reversal in the descending thoracic aorta seen on a pulsed-wave Doppler exam.
Figure 12.5 Vena Contracta. Caliper measurement of the narrowest portion of the aortic regurgitant jet, which corresponds to an approximation of the regurgitant orifice area. LA, Left atrium; LV, Left ventricle; Ao, aorta. [ECHO image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:232, Figure 11.4.]
Figure 12.6 Color M-mode assessment of aortic regurgitation. Utilizing a midesophageal aortic long-axis view, the width of the regurgitant jet and the LVOT are measured. The ratio of jet width:LVOT width can be used to estimate the severity of the aortic regurgitation. [ECHO image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:229, Figure 11.2.]
b. Quantitative assessment of aortic regurgitation—calculation of regurgitant volume and RF. A quantitative estimate of the severity of aortic regurgitation may be obtained by calculating the regurgitant volume and RF. The TSV in a patient with aortic regurgitation is the regurgitant volume plus the FSV actually ejected into the circulation. The regurgitant volume is the amount of blood that flows back through the incompetent aortic valve during each cardiac cycle. It is quantified as the difference between the TSV flowing through the aortic valve and the total FSV through a different valve. This reference valve is most commonly the mitral valve, with Doppler echocardiography being used to calculate the transmitral stoke volume. Total LV stroke volume can be determined with either Doppler echocardiography measurement of flow through the LV outflow tract or derived from left ventriculogram on cardiac catheterization. The RF, or fraction of each stroke volume flowing back into the LV, equals the ratio of the regurgitant volume to the TSV through the regurgitant aortic valve. These relationships can be summarized using the following equations:
TSV = Regurgitant Volume + FSV
Regurgitant Volume = TSV − FSV
RF = Regurgitant Volume/TSV
D. Timing and type of intervention
1. Acute aortic regurgitation. Urgent surgical intervention is often indicated in acute aortic regurgitation due to a high incidence of hemodynamic instability. Inotropic support is frequently needed to maintain cardiac output.
2. Chronic aortic regurgitation. Symptomatic patients with severe and moderately severe chronic aortic regurgitation should have surgery. Asymptomatic patients with severe and moderately severe chronic aortic regurgitation and normal LV function should be examined clinically and echocardiographically every 6 months. These patients should have surgical intervention at the earliest sign of LV dysfunction, as overall outcomes are significantly improved when surgery is performed prior to deterioration of ventricular function. Additionally, evidence of ventricular dilatation should prompt consideration for surgery, even in the presence of normal LV function. Patients with mild and moderate aortic regurgitation should be followed on a 12- to 24-month basis.
3. Surgical intervention. Surgical treatment of aortic regurgitation is most frequently provided through the use of valvular replacement with a prosthetic valve. However, techniques for surgical repair are becoming more widely accepted, with reports of an in-hospital mortality of 1%, late mortality rate of 4%, and the development of functional classifications of valve lesions to guide selection of surgical technique. Techniques include annuloplasty or commissural plication in the case of annular dilation, and leaflet resuspension or patch. . Aortic valve repair may also be particularly beneficial in patients with aortic regurgitation secondary to bicuspid aortic valve disease, especially considering the younger age at which these patients typically present for surgical intervention. This avoids the need for anticoagulation following mechanical valve placement and may potentially provide more long-term valve integrity than a prosthetic valve. The long-term results of some of the more experimental techniques of aortic valve repair are still not known.
E. Goals of perioperative management
1. Hemodynamic management (Table 12.5)
a. LV preload. Due to 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.
b. 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 RF. Actual improvement in subendocardial blood flow is observed with tachycardia owing to a higher systemic diastolic pressure and a lower LVEDP. This explains why a patient who is symptomatic at rest may show an improvement in symptoms with exercise. A heart rate of 90 beats/min seems to be optimal, improving cardiac output while not inducing ischemia.
c. Contractility. LV contractility must be maintained. In patients with impaired LV function, use of pure β-agonists or phosphodiesterase inhibitors can increase stroke volume through a combination of peripheral dilation and increased contractility.
d. Systemic vascular resistance. The forward flow can be improved with afterload reduction. Increases in afterload result in increased stroke work and can significantly increase the LVEDP.
e. PVR. Pulmonary vascular pressure remains relatively normal except in patients with end-stage aortic regurgitation associated with severe LV dysfunction.
2. Anesthetic technique
a. Premedication. Light premedication is recommended.
b. Induction and maintenance. Serious hemodynamic instability during induction of general anesthesia is less likely with severe aortic insufficiency than with severe AS because arterial vasodilation, which is a major effect of most of the induction drugs, is beneficial in aortic insufficiency and transient hypotension is well tolerated. However, the importance of careful titration of induction agents in combination with adequate hydration should not be underestimated. Particular caution is warranted with acute aortic insufficiency where ventricular decompensation is more likely to occur. The hemodynamic goals for induction and maintenance of anesthesia should be directed at preserving the patient’s preload and contractility, maintaining the peripheral arterial dilation, and keeping the heart rate near 90 beats/min.
c. A pulmonary artery catheter is helpful in evaluating the cardiac output of patients prior to repair of the aortic valve and especially in the postbypass period for monitoring and optimizing preload and myocardial function.
d. Omniplane TEE is beneficial for monitoring LV function and assessment of the severity of regurgitation prior to valve repair. Specific pathology of the aortic valve leaflets and aortic root can be easily assessed. It is also useful in predicting the appropriate size of a prosthetic valve based on the diameters of the aortic annulus and LV outflow tract. If aortic valve repair is performed, TEE is valuable for providing immediate feedback concerning the integrity of valvular function. In AVR, TEE allows assessment of perivalvular regurgitation and the pressure gradient across the prosthetic valve (Fig. 12.7).
Figure 12.7 Color flow Doppler image of a mechanical bileaflet prosthetic valve in the mitral position with a paravalvular leak. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:271, Figure 13.14.]
e. Use of an intra-aortic balloon pump is contraindicated in the presence of aortic regurgitation because augmentation of the diastolic pressure will increase the amount of regurgitant flow.
f. Weaning from cardiopulmonary bypass may be complicated by LV dysfunction secondary to suboptimal myocardial protection and coronary air embolism. AVR leads to a mild transvalvular gradient because a majority of prosthetic valves are intrinsically stenotic. Mild AS in combination with a significantly dilated LV may result in increased afterload, low cardiac output, and may contribute to the LV dysfunction. Inotropic support may be indicated in order to maintain cardiac output and avoid further LV dilation and dysfunction. Preload augmentation must be continued to maintain filling of the dilated LV.
3. Postoperative care. Immediately following AVR, the LVEDP and LVEDV decrease. However, the LV dilation and eccentric hypertrophy persist. In the early postoperative period, a decline in LV function may necessitate inotropic or intra-aortic 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-yr survival rate for patients whose hearts do not return to a relatively normal size within 6 months following 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 yrs can be expected .
VIII. Mitral stenosis
A. Natural history
1. Etiology. In adults, mitral stenosis is predominately secondary to rheumatic heart disease, which leads to scarring and fibrosis of the free edges of the mitral valve leaflets. Rheumatic changes are present in 99% of surgically excised stenotic mitral valves . Women are affected twice as frequently as men. Rheumatic heart disease commonly affects multiple cardiac valves and is often associated with both valvular stenosis and regurgitation.
2. Symptoms. In rheumatic mitral stenosis, patients are frequently asymptomatic for 20 yrs or more following an acute episode of rheumatic fever. However, as stenosis develops, symptoms appear, associated at first with exercise or high cardiac output states. Without surgical intervention, 20% of the patients, in whom the diagnosis of mitral stenosis is made, die within 1 yr and 50% die within 10 yrs following the diagnosis. The natural history is a slow, progressive downhill course with repeated episodes of fatigue, chest pains, palpitations, shortness of breath, paroxysmal nocturnal dyspnea, pulmonary edema, 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 an increased risk of forming left atrial thrombi and subsequent cerebral or systemic emboli. Chest pain may occur in 10% to 20% of patients with mitral stenosis. However, it is a poor predictor of the coexistence of CAD, probably because symptoms also may be caused by coronary thromboembolism or pulmonary hypertension.
1. Natural progression. The normal mitral valve is composed of anterior and posterior leaflet, with an area of 4 to 6 cm2 (mitral valve index: 4 to 4.5 cm2/m2). When the valve area decreases to <2.5 cm2 (or valve index to less than 2 cm2/m2), moderate exercise may induce dyspnea. Further progression of mitral stenosis leads to increases in left atrial pressure and volume that are reflected back into the pulmonary circuit. Increased left atrial pressure results in atrial enlargement, which predisposes these patients to atrial fibrillation. Between a valve area of 1 to 1.5 cm2, increasing symptoms appear with 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 PAPs suddenly rise as a result of the increased cardiac demand. Because atrial contraction contributes about 30% of LV filling in mitral stenosis, the onset of atrial fibrillation can lead to significant impairment in cardiac output. With a valve area below 1 cm2, a patient is considered to have severe mitral stenosis, and symptoms are present even at rest. Not only are left atrial pressures sufficient to produce congestive heart failure, but cardiac output may also be reduced. The increase in PVR in response to a high left atrial pressure can eventually lead to RV dilation and failure. PA constriction, pulmonary intimal hyperplasia, and pulmonary medial hypertrophy eventually result in chronic PA hypertension associated with restrictive lung disease. The dilated RV can cause a leftward shift of the interventricular septum, thereby limiting the already reduced LV size and further impairing stroke volume. With further RV dilation, TR 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. Intracardiac hemodynamics and cardiac remodeling. Due to the restriction of flow from the left atrium to the left ventricle, patients with significant mitral stenosis have a reduced LVEDV and LVEDP. Stroke volume is also reduced. The actual LV contractility is usually normal, but may be reduced due to chronic LV deconditioning. The limitation of stroke volume in these patients is due to inadequate filling of the LV. Patients with severe mitral stenosis typically have a dilated left atrium, normal or diminished LV size, and a dilated RV and right atrium.
3. Pressure wave disturbances. Mitral stenosis produces a large A wave on the PCWP tracing in patients with preserved sinus rhythm. If the mitral stenosis is associated with mitral regurgitation, a prominent V wave is also present. 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.
4. Pressure–volume loop in mitral stenosis (Fig. 12.8).
Figure 12.8 Pressure–volume loop in mitral stenosis. Both end-diastolic and end-systolic volumes, as well as LV filling pressures, are reduced, resulting in a decreased stroke volume. AO, aortic valve opening; MC, mitral valve closure; MO, mitral valve opening. Phase 1, Ventricular filling; Phase 2, Isovolumetric contraction; Phase 3, Ventricular ejection; Phase 4, Isovolumetric relaxation. [Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth. 1982;1:244.]
5. TEE findings. Patients with rheumatic mitral stenosis exhibit several characteristic echocardiographic findings. The valve leaflets appear thickened, calcified, and have limited mobility (Fig. 12.9). In particular, the body of the anterior mitral valve leaflet exhibits diastolic doming and is often described as having a “hockey-stick” appearance. Additional findings may include mitral regurgitation and left atrial enlargement. Spontaneous echo contrast, indicating a low flow state in the enlarged left atrium, is frequently seen and should prompt examination for thrombus formation (Fig. 12.10). The most likely location for atrial thrombus is the left atrial appendage.
Figure 12.9 Classic echocardiographic appearance of rheumatic mitral stenosis, including thickened mitral leaflets with diastolic doming of the anterior leaflet. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:192, Figure 9.3.]
Figure 12.10 Mitral stenosis. The left atrium is significantly enlarged, with spontaneous echo contrast (“smoke”) demonstrating low flow state. LA, Left atrium; LV, Left ventricle; AL, Anterior leaflet; PL, Posterior leaflet. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:217, Figure 10.10.]
C. Assessment of severity of mitral stenosis can be done by the calculation of mitral valve area or a diastolic pressure gradient across the mitral valve using echocardiography or, infrequently, cardiac catheterization. Assessment of mitral stenosis by the pressure gradient is less accurate than the area method because pressure gradient depends on transmitral flow (Table 12.6).
Mitral stenosis severity can also be graded by the PHT method, in which prolongation of the PHT correlates with a reduction in mitral valve orifice area. A normal PHT, measured with continuous wave Doppler, is relatively short, corresponding to rapid early diastolic filling of the LV and the associated rapid decline in the LA to LV pressure gradient during this early filling phase. Since this LA to LV pressure gradient remains elevated for a longer period in mitral stenosis, the PHT will become more prolonged as the degree of stenosis worsens . A PHT greater than 220 ms corresponds to severe mitral stenosis, as the valve area will be less than 1.0 cm2 as seen by the following equation:
Mitral valve area = 220/PHT
D. Timing and type of intervention. Surgical intervention should occur prior to the development of severe symptoms because irreversible ventricular dysfunction may result if surgery is delayed too long. Surgery is not recommended for the asymptomatic patient. In patients with mild symptoms, the decision about surgical intervention should be individualized and based on the lifestyle desired, mitral valve orifice size, evidence of systemic embolization, and risk of the procedure. The presence and severity of pulmonary hypertension should also guide the decision-making process. Surgical intervention is likely warranted once the pulmonary artery systolic pressure exceeds 50 mm Hg . Four types of interventions are available for rheumatic mitral stenosis: (i) Mitral valve replacement, (ii) open mitral commissurotomy, (iii) closed commisurotomy, and (iv) balloon mitral valvuloplasty. Closed mitral comissurotomy can be performed without cardiopulmonary bypass in a carefully selected group of patients without atrial thrombosis, significant valvular calcification, or chordal fusion. It is rarely done in the United States, being almost completely replaced by the balloon mitral valvuloplasty. Balloon mitral valvuloplasty is performed by interventional cardiologists in the cardiac catheterization laboratory. It consists of the advancement of a balloon catheter through the interatrial septum and its inflation at the mitral orifice. This procedure may be complicated by severe mitral regurgitation, systemic embolism, and residual atrial septal defect. Commissurotomy and balloon mitral valvuloplasty do not totally relieve the stenosis, but rather make it less severe. In addition, they carry significant risk of restenosis. Nevertheless, they can delay the ultimate procedure. 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 balloon mitral valvuloplasty or commissurotomy, mitral valve replacement should be performed. When chronic atrial fibrillation is present, scar tissue can be created surgically in the left atrium during open heart surgery in order to disrupt re-entry circuits of atrial fibrillation in what is called maze procedure.
E. Goals of perioperative management
1. Hemodynamic management (Table 12.7)
a. 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 and are prone to pulmonary vascular congestion, so that overly aggressive use of fluids can easily send a patient who is in borderline congestive heart failure into florid pulmonary edema. Intraoperative TEE is often the best method to assess volume status. However, other invasive monitoring techniques (i.e., the pulmonary artery catheter) can also be used.
b. Heart rate. Blood flow across the mitral valve occurs during ventricular diastole, so slower heart rates are hemodynamically beneficial. At the same time, excessive bradycardia can be dangerous because stroke volume is relatively fixed.
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 reduced cardiac output.
c. Contractility. Adequate forward flow depends on adequate RV and LV contractility. Chronic underfilling of the LV, however, may lead to a deconditioning 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.
d. Systemic vascular resistance. To maintain blood pressure in the presence of a limited cardiac output, patients with mitral stenosis usually develop an 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.
e. PVR. These patients frequently have elevated PVR and are prone to exaggerated pulmonary vasoconstriction in the presence of hypoxia. Particular attention should be paid to avoiding any increases in PAP due to inadequate anesthesia or inadvertent acidosis, hypercapnia, or hypoxemia.
2. Anesthetic technique
a. Premedication should be light to avoid either an acute decrease in preload or the possibility of oversedation with resultant hypoxemia and hypercapnia, with subsequent exacerbation of any preexisting pulmonary hypertension. Use of cardioversion is recommended if new atrial fibrillation should occur.
b. Pulmonary artery catheters are useful for perioperative management. However, because of dilated pulmonary arteries, special care should be taken in the placement of these catheters due to the increased risk of pulmonary artery rupture. Because of the risk of pulmonary artery rupture and the questionable information obtained from a wedge pressure, placement of the pulmonary artery catheter in a wedge position is usually not necessary.
c. TEE evaluation is particularly helpful in monitoring the adequacy of mitral valve repair. Mitral commissurotomy may result in significant mitral regurgitation, which can be identified in the immediate postbypass period in order to provide further surgical intervention for the patient. In addition, complications associated with mitral valve replacement, such as paravalvular regurgitation and SAM of the anterior mitral valve leaflet, may also be rapidly identified and repaired while still in the operating room. TEE is also helpful for the assessment of the RV and LV loading conditions and contractility.
d. Immediately following cardiopulmonary bypass, even patients with seemingly normal preoperative LV function may have major depression of myocardial contractility due to their underlying myocardial dysfunction exacerbated by ischemic arrest. Subsequently, volume therapy should be used carefully to avoid LV and RV failures. Inotropes and pressors may be required to maintain cardiac output and to avoid volume overload. In patients previously in chronic atrial fibrillation, especially after the maze procedure, prophylactic use of amiodarone is indicated.
3. Postoperative course. In spite of the fact that following prosthetic valve placement, a mean pressure gradient of 4 to 7 mm Hg across the mitral valve persists, successful surgical intervention leads to a drop in PVR, PAP, and left atrial pressure while increasing cardiac output in the first postoperative day. PVR in most patients will continue to decrease with time following surgery. Failure of the PAP to decrease is usually indicative of irreversible pulmonary hypertension and/or irreversible LV dysfunction, either of which places the patient in a prognostically poor group.
IX. Mitral regurgitation
A. Natural history. The spectrum of mitral regurgitation varies from acute forms, in which rapid deterioration of myocardial function can occur, to chronic forms that have slow indolent courses. Mitral regurgitation may result from mitral valve leaflet abnormalities, mitral annulus dilation, chordate rupture, papillary muscle disorder, global LV dysfunction, or disproportional LV enlargement .
1. Acute mitral regurgitation. Acute mitral regurgitation may result from papillary muscle dysfunction due to myocardial ischemia, or papillary muscle rupture due to myocardial infarction or blunt chest trauma. Chordae tendineae rupture can be caused by myxomatous disease of the mitral valve or acute rheumatic fever. A mitral valve leaflet can acutely deteriorate as a result of infective endocarditits, balloon valvuloplasty, or a penetrating chest injury.
2. Chronic mitral regurgitation
a. Mitral annulus dilatation may result from LV dilatation due to dilated or ischemic cardiomyopathy or aortic insufficiency. It can also develop from left atrial enlargement in patients with diastolic dysfunction, e.g., AS or systemic hypertension. Finally, mitral annulus dilatation will eventually exacerbate mitral regurgitation of any other cause secondary to left atrial and LV enlargement and stretching of the annulus.
b. Disorders of mitral leaflets include mitral valve prolapse that may be idiopathic or caused by rheumatic fever or myxomatous degeneration; mitral leaflet damage by infective endocarditis; and restrictive changes due to thickening or calcification from any inflammatory or degenerative processes. Restriction can also be caused by disproportional enlargement of the LV in relation to papillary muscles and chordae tendineae causing incomplete mitral valve closure. This occurs in a majority of cases of ischemic mitral regurgitation.
c. Disorders of subvalvular apparatus. Rupture or elongation of chordae tendineae may occur in myxomatous degeneration. Rheumatic heart disease may lead to chordae tendineae rupture, thickening, and calcium deposition in subvalvular apparatus. Depending on the type and number of chordae ruptured, subsequent mitral regurgitation may range from acute to chronic and from mild to severe.
d. Functional mitral regurgitation. Mitral regurgitation that occurs in the setting of normal leaflets and chordal structures is frequently due to functional mitral regurgitation. This phenomenon is not fully understood, but is most likely the result of global LV dysfunction, which results in disruption of the normal geometric relationship between the mitral valve leaflets, papillary muscles, and LV. The LV dysfunction results in ventricular dilatation and a more spherical appearance of the LV, which ultimately disrupts the normal structure and function of the entire mitral apparatus . Ischemic mitral regurgitation is a type of functional mitral regurgitation that is caused by ischemic heart disease.
3. Carpentier classification. This widely recognized classification scheme is used to describe differing mechanisms of mitral regurgitation based upon the leaflet motion of the valve (Table 12.8) .
1. Natural progression
a. 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 a decreased cardiac output, sympathetic stimulation increases ventricular contractility and produces tachycardia. In addition, the LV functions on a higher portion of the Frank–Starling curve owing to increased LV volume. Increased LV volume leads to increased LVEDP, which in combination with tachycardia can cause ischemia and LV dysfunction. The acute increases in left atrial and PAPs can lead to pulmonary congestion, pulmonary edema, and RV failure. Thus, acute mitral regurgitation often presents as biventricular failure.
b. Chronic. During the slow development of chronic mitral regurgitation, left atrial dilatation and eccentric hypertrophy of the LV develops. At early stages, the dilation of the LV allows the 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 FSV and regurgitant stroke volume). Left atrial enlargement, however, may lead to the development of atrial fibrillation. In addition, continued left atrial dilation may lead to further increases in regurgitation due to stretching of the mitral annulus. Continued worsening of regurgitation results in an increase in PAP, pulmonary congestion, and eventually RV failure. When LV dilation and hypertrophy can no longer compensate for increasing regurgitation, the FSV is eventually compromised. At this point, the symptoms of forward heart failure, including increased fatigability and generalized weakness, may appear. LV ejection fraction 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. The depression of ventricular function may become irreversible even after mitral valve replacement.
2. Intracardiac hemodynamics and remodeling. In acute mitral regurgitation, LVEDP increases rapidly to dilate the left atrium and maintain stroke volume. In contrast, in chronic mitral regurgitation, compensatory dilation occurs slowly and the LVEDP may remain relatively normal until the disease is far advanced. The eccentric hypertrophy of the ventricle allows preservation of FSV by increasing TSV.
3. Pressure wave disturbances. On pulmonary capillary wedge tracing, 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.
4. Pressure–volume loop in mitral regurgitation (Fig. 12.11).
Figure 12.11 Pressure–volume loop in acute and chronic mitral regurgitation. With chronic mitral regurgitation, end-diastolic volume is elevated without significant elevation of LV filling pressures. In contrast, with acute mitral regurgitation LVEDV is increased, but is accompanied by an increase in LV filling pressure. AC, aortic valve closure; AO, aortic valve opening; MC, mitral valve closure; MO, mitral valve opening. Phase 1, ventricular filling; Phase 2, isovolumetric contraction; Phase 3, ventricular ejection; Phase 4, isovolumetric relaxation. [Modified from Jackson JM, Thomas SJ, Lowenstein E. Anesthetic management of patients with valvular heart disease. Semin Anesth. 1982;1:248.]
5. TEE. The baseline TEE exam in the operating room should focus on identifying the specific underlying pathology. A thorough examination of the structure and function of the leaflets is critical, as is a close examination of the subvalvular apparatus and LV function and shape (Fig. 12.12). This initial intraoperative assessment is often needed by the surgeon to help formulate the ultimate surgical plan (i.e., in determining whether the mitral valve is suitable for an attempt at valve repair). If mitral repair is to be attempted, the baseline TEE exam should focus on identifying any predictors of post-repair SAM, which is a noted complication of this procedure. The ratio of the anterior leaflet to posterior mitral leaflet, expressed as the AL:PL ratio, should be assessed. A longer posterior leaflet will push the normal leaflet coaptation point toward the LVOT and increase the risk of post-repair SAM. This distance between the coaptation point and the LVOT, at the border of the anterior ventricular septum, is called C-sept distance and should also be measured.
Figure 12.12 The 2D images of excessive mitral valve motion. A: billowing. B: prolapse. C: Flail. [Echo Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:175, Figure 8.4.]
Assessing the severity of mitral regurgitation is not always reliable in the operating room setting, as the severity of mitral regurgitation may be significantly underestimated under the altered loading conditions of general anesthesia. In this regard, it is more appropriate to grade the severity of mitral regurgitation using the preoperative echo exam as opposed to an exam performed under general anesthesia .
C. Assessment of severity. As with aortic regurgitation, estimation of mitral regurgitation by angiocardiographic dye clearance has been almost completely replaced by echocardiography.
1. Echocardiographic assessment of mitral regurgitation (Table 12.9)
2. Quantitative assessment of mitral regurgitation—calculation of RF (Fig. 12.13). A quantitative estimate of the severity of mitral regurgitation may be obtained by calculation of the regurgitant volume and RF. As for patients with aortic regurgitation, RF is defined as a fraction of regurgitant volume in relation to TSV. FSV can be obtained by thermodilution from a PA catheter or by measurement of stroke volume in the LV outflow tract by echocardiogram with Doppler (in the absence of aortic regurgitation). Total LV stroke volume can be derived from the LV angiogram or measured by echocardiogram with Doppler as the diastolic volume of blood flowing through the mitral valve, and the regurgitant volume and RF calculated as for aortic regurgitation.
Figure 12.13 Vena contracta. Measurement of the narrowest portion of the color flow Doppler jet (arrow) corresponds to the severity of mitral regurgitation. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:176, Figure 8.5.]
Mitral regurgitation consisting of less than 30% of the total LV stroke volume is considered mild, 30% to 39% is considered moderate, 40% to 49% is considered moderately severe, and greater than 50% is considered severe.
D. Surgical intervention for mitral regurgitation involves either mitral valve repair or replacement, with many now recommending an attempt at mitral valve repair whenever feasible, assuming the surgeon has appropriate expertise in valve repair surgery and that the mitral valve appears suitable for repair. Benefits of mitral valve repair over replacement include avoidance of chronic anticoagulation (with mechanical valves) and future reoperation for prosthetic valve failure (with bioprosthetic valves). Perhaps more importantly, LV function is better preserved following valve repair. The mitral valve support apparatus is a critical structural and functional component to the left ventricle and any disruption of this apparatus, as can occur during mitral valve replacement, can lead to LV dysfunction. Since mitral repair leaves the mitral apparatus intact, this cause of LV failure can be avoided.
Surgery should be strongly considered in symptomatic patients with New York Heart Association (NYHA) Class II heart failure and/or chronic or recurrent atrial fibrillation resulting from mitral regurgitation. In asymptomatic patients, the benefits of surgery must be weighed carefully against the benefits of waiting. The decision is made based on the presence of LV enlargement, dysfunction, and pulmonary hypertension, with the onset of LV dysfunction being the most important indicator for surgery in asymptomatic patients . When in doubt, stress echo can be done to search for latent LV dysfunction. If chances of repair are good, early surgery is recommended because good long-term results are likely and anticoagulation is not needed. If CABG is indicated and at least moderate ischemic mitral regurgitation is present, mitral valve repair/replacement at the same time as CABG is beneficial. In this scenario, successful mitral valve repair is often straightforward, requiring only placement of an annuloplasty ring .
1. Mitral valve repairability. In general, mitral valve lesions that are relatively easy to repair include leaflet perforation, mitral valve annulus dilatation, and excessive motion of mitral valve leaflets. Among difficult-to-repair conditions are restricted leaflet motion, severe calcification, and active infection. The greatest likelihood for successful repair involves isolated lesions of the posterior mitral valve leaflet. Pathology of the anterior leaflet only or both mitral leaflets presents a significantly greater challenge to the surgeon and minimizes the chances for successful repair (Table 12.10).
Table 12.10 Mitral valve repair techniques for specific lesions
E. Goals of perioperative management
1. Hemodynamic management (Table 12.11)
a. LV preload. Augmentation and maintenance of preload is frequently helpful to ensure adequate FSV. 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 RF. A decision about the best level of preload augmentation for an individual patient should be based on that patient’s hemodynamic and clinical response to a fluid load.
b. 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 an increase in RF. The heart rate should be kept in the normal to elevated range in these patients. Atrial contribution to preload is important in patients with mitral regurgitation, but not as critical as in those with stenotic lesions. Many of these patients, particularly those with chronic mitral regurgitation, will come to the operating room in atrial fibrillation.
c. Contractility. Maintenance of FSV is dependent on systolic 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 can actually decrease regurgitation due to constriction of the mitral annulus.
d. Systemic vascular resistance. An increase in afterload leads to an increase in RF and reduction in systemic cardiac output. For this reason, careful afterload reduction is normally desired.
e. PVR. Patients with severe mitral regurgitation develop elevated pulmonary pressure secondary to increased PVR, as well as elevated left atrial pressure. The importance of each component in elevating PAP can be determined by calculating PVR using the following formula:
If elevated PVR is present, caution must be taken to avoid hypercapnia, hypoxia, nitrous oxide, and light anesthesia that might lead to pulmonary constrictive responses.
2. Anesthetic management
a. Premedication. Light premedication is indicated.
b. Induction and maintenance of general anesthesia. As with aortic insufficiency, the hemodynamic goals for induction and maintenance of anesthesia should be directed to maintaining peripheral arterial dilation, ventricular contractility, and keeping the heart rate close to 90 beats/min. Careful titration of narcotics, hypnotics, and volatile anesthetics are usually well tolerated. Tracheal intubation in inadequately anesthetized patients may lead to a sudden rise in arterial blood pressure followed by a dramatic increase in RF and, subsequently, pulmonary edema.
c. Pulmonary artery catheters are helpful in guiding fluid management and in the timely detection and treatment of hemodynamic conditions associated with elevated PAP. These conditions include (a) sudden increase in RF (e.g., from LV ischemia or vasoconstriction resulting from inadequate depth of anesthesia) as well as (b) PA vasoconstriction. Nitric oxide, as a specific pulmonary artery dilator, may have an important role in the management of patients with reversible pulmonary hypertension. Hyperventilation, but with minimum increases in intrathoracic pressure, is a second therapeutic modality available for selectively dilating the pulmonary vasculature without affecting the patient’s systemic blood pressure. Prostaglandin E1 has also been used but is accompanied by a decrease in systemic pressure as well. Inhaled milrinone may represent a promising alternative, as it avoids the significant systemic hypotension frequently seen with the intravenous form of the drug .
d. TEE. Post-bypass, TEE is invaluable for the assessment of the adequacy of valvular repair. When valve replacement is performed, TEE is important in detecting the presence of a paravalvular leak or a hemodynamically significant pressure gradient in the immediate postbypass period. If a large paravalvular leak, significant residual regurgitation, or a hemodynamically significant pressure gradient are seen at this point, it is critical to communicate with the surgical team and discuss the potential need to return to cardiopulmonary bypass to address these issues.
e. Weaning from cardiopulmonary bypass. A primary concern following mitral valve repair or 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 pop-off into the left atrium. The result is an increase in LV wall tension that can compromise ejection fraction. Patients who had mitral valve repair less often require inotropic support than patients after mitral valve replacement. This is because mitral valve replacement introduces more changes in LV structure, particularly when extensive resection of the subvalvular apparatus is performed. Severity of regurgitation, LV ejection fraction, presence of pulmonary hypertension, and aortic cross-clamp time are other factors to consider in determining the postbypass use of inotropes. In some cases, insertion of an intra-aortic balloon pump may be needed to prevent LV dilatation and failure. Immediately following the patient’s weaning from cardiopulmonary bypass, an attempt should be made to keep the patient in sinus rhythm, often by treatment with amiodarone. Amiodarone is routinely used if mitral valve surgery was combined with a maze procedure.
3. Postoperative course. Following valve replacement, left atrial and PAPs should decrease. Patients with long-standing mitral regurgitation, however, will continue to need an elevated left atrial pressure for maintenance of adequate forward flow.
X. Tricuspid stenosis
A. Natural history
1. Etiology. The primary cause of acquired tricuspid stenosis is rheumatic valvulitis . Rheumatic tricuspid stenosis is rare, almost never exists in isolation, and is often associated with concomitant TR. In the majority of cases, the mitral valve is also involved. Other causes for tricuspid stenosis include systemic lupus erythematosus, endomyocardial fibroelastosis, right atrial tumor, and carcinoid syndrome.
2. Symptoms. Tricuspid stenosis is manifested by the signs and symptoms of right-sided heart failure, including hepatomegaly, hepatic dysfunction, ascites, peripheral edema, and jugular venous distension.
1. Natural progression. The tricuspid valve is the largest cardiac valve with a normal area of 7 to 9 cm2 in the typical adult. It is composed of three leaflets: Anterior, posterior, and septal. The normal gradient across the tricuspid valve is only 1 mm Hg. 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. A valve area of 1.5 cm2 usually corresponds to a mean gradient of 3 mm Hg across the tricuspid valve. With progression of the stenosis, the right atrial pressure increases, right atrium dilates, and forward blood flow decreases.
2. Calculation of severity. As with left-sided stenotic lesions, the severity of tricuspid stenosis can be determined with cardiac catheterization or echocardiography by the measurement and calculation of orifice area and pressure gradient. A gradient of 5 mm Hg across the tricuspid valve and tricuspid valve area of 1 cm2 indicate severe stenosis.
3. TEE. Patients with rheumatic tricuspid stenosis will demonstrate thickened leaflets with restricted motion and diastolic doming. Fusion of the commissures is also frequently seen. If the cause of tricuspid stenosis is functional stenosis, a right atrial mass responsible for the RV inflow obstruction will be seen (Fig. 12.14). Continuous wave Doppler will allow for the assessment of the previously discussed pressure gradients used to grade stenosis severity.
Figure 12.14 Right atrial tumor. The tumor occupies the majority of the right atrium (A) and obstructs the tricuspid valve (B). *Tumor; LA, Left atrium; RA, Right atrium; RVOT, Right ventricular outflow tract; SVC, Superior vena cava. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:405, Figure 19.8.]
C. Surgical intervention. Salt restriction, digitalization, and diuretics may reduce hepatic congestion, improve hepatic function, delay the surgery, and reduce surgical risks in patients with severe tricuspid stenosis. A majority of patients with tricuspid stenosis have other valvular lesions that require operation. Tricuspid valve intervention is indicated if pressure gradients exceed 5 mm Hg or valvular area is less than 2 cm2. 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.
D. Goals of perioperative management
1. Hemodynamic management (Table 12.12)
a. RV preload. Adequate forward flow of blood across the stenotic tricuspid valve depends on maintenance of adequate preload.
b. 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.
c. 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.
d. Systemic vascular resistance. Systemic vasodilation may lead to hypotension in patients with limited blood flow across the tricuspid valve.
e. PVR. Because the limitation to forward flow is at the tricuspid valve, reducing PVR has little positive effect on improving forward flow. Keeping PVR in the normal range is adequate.
2. Anesthetic technique
a. Light premedication is indicated.
b. In patients with coexisting mitral valve disease, the anesthetic technique is determined by the mitral valve lesion. In patients with isolated tricuspid stenosis, the primary requirements are to maintain high preload, high afterload, and adequate contractility.
c. Passage of a pulmonary artery catheter through the stenotic tricuspid valve may be difficult and not always justified. In many cases, the catheter can be left in the superior vena cava (SVC) until after bypass and then advanced by a surgeon upon completion of tricuspid valve repair/replacement or floated after weaning from cardiopulmonary bypass. Detailed discussion with the surgeon prior to the beginning of the operation is needed.
d. During cardiopulmonary bypass, because no flow into the right atrium is allowed and SVC pressure completely depends on the adequate drainage of the SVC by the SCV cannula, attention must be paid to the SVC drainage in order to avoid elevated SVC pressure, reduced cerebral perfusion pressure, and irreversible brain damage. Central venous pressure monitoring above the SVC tie, as well as intermittent assessment of the patient’s head for any signs of edema, is indicated. No drug infusions may be given through any pulmonary artery accessory port since it is isolated from the blood flow during cardiopulmonary bypass.
e. In the postcardiopulmonary bypass period, preload augmentation must be continued. Inotropic support may be necessary if RV failure develops.
XI. Tricuspid Regurgitation
A. Natural history. Isolated TR is most frequently seen in association with drug abuse-related endocarditis, carcinoid syndrome, Ebstein’s anomaly, connective tissue disorders leading to valve prolapse, or chest trauma. More commonly, however, functional TR develops secondary to RV failure, pulmonary hypertension, or left-sided cardiac abnormalities, such as end-stage aortic or mitral stenosis . With severe aortic or mitral valve disease, elevated PAP leads to RV strain and, eventually, RV failure with TR. The primary mechanism of this functional TR results from dilatation of the tricuspid valve annulus. It may is also often seen with RV dilatation leading to tethering of the tricuspid valve leaflets that restricts their mobility.
1. Natural progression. Isolated TR is well tolerated because the RV can compensate for volume overload. Most symptoms associated with TR are directly related to an increased RV afterload. Therefore, when TR is associated with pulmonary hypertension, the impedance to RV ejection produces significant deterioration secondary to decreased cardiac output. Most patients with TR have associated atrial fibrillation due to distension of the right atrium.
2. TEE evaluation and grading of severity of TR (Table 12.13).
With functional TR, the TEE exam will often demonstrate RV dysfunction and dilatation, along with dilatation of the tricuspid valve annulus. The valve leaflets may appear tethered with restricted motion. In the setting of endocarditis, vegetations and valvular perforation are common. With rheumatic disease, findings will include leaflet thickening and restriction, along with commissural fusion and probable mitral and/or aortic valve involvement. Carcinoid heart disease results in diffuse leaflet thickening and restriction. It may frequently lead to both stenosis and regurgitation, and almost always involves both the tricuspid and pulmonic valves. With Ebstein’s anomaly, one or more tricuspid leafltes are positioned abnormally into the RV cavity. The RV is reduced in size and is said to be “atrialized” due to this displacement of the tricuspid leaflets toward the RV apex.
Color flow Doppler, assessing the size of the regurgitant jet, is the primary modality used to grade severity of TR (Fig. 12.15). However, similar to mitral regurgitation, the altered loading conditions induced by general anesthesia may underestimate the true severity of the lesion. Alterations in hepatic vein flow, as seen with pulsed wave Doppler, can also be utilized to assist in grading the severity of regurgitation.
Figure 12.15 Color flow Doppler image of severe tricuspid regurgitation. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:288, Figure 14.8.]
3. 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 determine the size of the regurgitant wave.
C. Goals of perioperative management
1. Hemodynamic management (Table 12.14)
a. RV preload. To provide adequate forward flow, preload augmentation is desirable. A drop in central venous pressure can severely limit RV stroke volume.
b. Heart rate. Normal to high heart rates are beneficial in these patients to sustain forward flow and prevent peripheral congestion.
c. Contractility. RV failure is the primary cause of clinical deterioration in patients with TR. Because the RV is designed geometrically to accommodate volume but not pressure loads, positive-pressure ventilation or elevated PVR may lead to RV failure. Suppression of contractility with myocardial depressants may also induce RV failure.
d. Systemic vascular resistance. Variations in systemic afterload have little effect on TR unless there is concurrent aortic or mitral valve dysfunction.
e. PVR. RV function and forward blood flow are improved with decreases in PVR. Hyperventilation is helpful in reducing PVR by producing hypocapnia. However, high airway pressures during pulmonary ventilation and agents that can increase PAP 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 PVR in these patients.
2. Anesthetic technique
a. Light premedication is indicated.
b. As with tricuspid stenosis, in patients with coexisting mitral valve disease, anesthetic technique is determined by the mitral valve lesion.
c. Passage of a pulmonary artery catheter through the regurgitant tricuspid valve may be difficult due to the tendency of the regurgitant wave to push the catheter in the opposite direction. Determination of cardiac output in the presence of TR is inaccurate because some of the cold injectate is ejected retrograde into the atrium rather than into the pulmonary artery.
d. As with tricuspid stenosis, during cardiopulmonary bypass, attention must be paid to the SVC drainage.
e. If a prosthetic valve is placed, residual tricuspid stenosis may occur because the valve prosthesis is smaller than the native valve, and postbypass preload augmentation may 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 PVR with no pop-off pressure lowering back into the right atrium. Therefore, RV failure requiring inotropic support may occur.
XII. Pulmonary stenosis
A. Natural history
1. Etiology. The majority of pulmonary stenoses are congenital. Rarely, rheumatic heart disease, malignant carcinoid, or extrinsic compression by a tumor or sinus of Valsalva aneurysm may lead to pulmonary stenosis. With both rheumatic heart disease and carcinoid syndrome, there is almost always involvement of other cardiac valves in addition to the pulmonic valve.
2. Symptoms. Patients with pulmonary stenosis may live for extended periods completely without symptoms and frequently survive past the age of 70 yrs 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.
1. Natural progression. The normal pressure gradient across the pulmonary valve orifice is usually under 5 mm Hg. The diagnosis of pulmonary stenosis can be made when the gradient across the pulmonary valve reaches 15 mm Hg. A peak systolic gradient of 36 mm Hg or less is considered mild pulmonary stenosis, between 36 and 64 mm Hg is considered moderate stenosis, and more than 64 mm Hg is considered severe pulmonary stenosis. As the pulmonary stenosis progresses from mild to moderate, concentric hypertrophy of the RV occurs. The increased hypertrophy and pressure within the RV leads 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
a. PAP trace. The PAP upstroke is delayed, and there is a late systolic peak owing to impedance to blood flow through the stenotic pulmonary valve.
b. Central venous pressure trace. A prominent A wave is frequently found in the central venous pressure trace.
3. TEE. The pulmonic valve is not always visualized with TEE based on its anterior location far from the TEE probe, making 2D imaging and Doppler analysis of the pulmonic valve difficult. When adequate visualization of the valve is obtained, continuous wave Doppler allows for estimation of transvalvular gradients used to grade stenosis severity. The degree of RV dilatation and dysfunction may provide some indirect estimation of the degree of stenosis and obstruction to RV outflow (Fig. 12.16).
Figure 12.16 The 2D image of the pulmonic valve, seen in a transgastric pulmonic valve view. PV, pulmonic valve; RA, right atrium; RV, right ventricle. [ECHO Image from Perrino AC, Reeves ST, eds. A Practical Approach to Transesophageal Echocardiography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:292, Figure 14.2.]
C. Surgical intervention. Any patient developing significant symptoms, a peak systolic gradient across the pulmonary 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. Balloon valvuloplasty is a viable alternative to valvulotomy. Rarely, the pulmonary valve actually has to be replaced. An attractive alternative to open heart surgery is transluminal balloon angioplasty, which is frequently used for congenital pulmonary valve stenosis.
D. Goals of perioperative management
1. Hemodynamic management (Table 12.15)
2. 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.
3. Heart rate. As pulmonary stenosis progresses, the patient becomes increasingly dependent on the atrial contraction to provide adequate RV filling. Unfortunately, in severe pulmonary stenosis, TR can develop, leading to right atrial distension and the occurrence of 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.
4. Contractility. With severe pulmonary 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.
5. Systemic vascular resistance should be maintained to provide adequate coronary perfusion to the hypertrophied RV.
6. PVR. Because the primary impedance to forward flow is the pulmonary valve, reducing PVR will do little to enhance forward blood flow. However, especially in patients with mild or moderate pulmonary stenosis, major increases in PVR can potentially harm forward blood flow and lead to RV dysfunction. Therefore, PVR should be kept in the low-normal range.
XIII. Pulmonary regurgitation
A. Natural history
1. Etiology. The majority of patients with acquired pulmonary regurgitation have annular dilatation secondary to pulmonary hypertension of various etiologies . Pulmonary regurgitation also can be associated with congenital valve deformities or primary surgical procedures to correct these deformities. Less commonly, pulmonary regurgitation is caused by connective tissue disorders, trauma, carcinoid syndrome, infective endocarditis, and rheumatic fever.
2. Symptoms. Patients without pulmonary hypertension usually are asymptomatic. Patients with pulmonary hypertension and pulmonary regurgitation usually present with RV failure.
B. Surgical intervention consists of pulmonary valve replacement and is rarely performed in patients with acquired pulmonary regurgitation.
XIV. Mixed valvular lesions.
For all mixed valvular lesions, management decisions emphasize the most severe or the most hemodynamically significant lesion.
A. 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. Symptoms are 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 AS because the aortic valve gradient may be relatively low owing to low aortic valvular flow. Such a combination of lesions can be extremely serious because of the limitation of blood flow at two points.
B. Aortic stenosis and mitral regurgitation. This combination is relatively rare, but should be expected in patients with AS who also have left atrial enlargement with atrial fibrillation. Mitral regurgitation can be exacerbated by LV dysfunction due to severe AS. In this situation, the mitral valve does not require replacement, and the mitral regurgitation usually regresses after the aortic valve is replaced.
In managing these patients, the hemodynamic requirements for AS and mitral regurgitation are contradictory. Because AS will most frequently lead these patients into deadly intraoperative situations, it should be given priority when managing the hemodynamic variables.
C. Aortic stenosis and aortic regurgitation. The combination of aortic regurgitation and AS is not well tolerated because it provides the LV with both severe pressure and volume overloading. These stresses lead to major increases in myocardial oxygen consumption (MVO2) and, as might be expected, angina pectoris is an early symptom with this combination. Once symptoms develop, the prognosis is similar to that of pure AS.
D. Aortic regurgitation and mitral regurgitation. The combination of aortic and mitral regurgitation occurs frequently, and this combination can cause rapid clinical deterioration.
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 increased impedance to LV outflow can lead to rapid clinical deterioration. Therefore, a low systemic vascular resistance with an adequate perfusion pressure is needed until cardiopulmonary bypass can be initiated.
E. Mitral stenosis and mitral regurgitation. Rheumatic mitral stenosis is rarely 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 leading to reactive pulmonary constriction and providing adequate preload, leads to optimal hemodynamic stabilization.
F. Multi-valve surgical procedures. While the surgical management of multi-valve disease has continued to improve, these patients still represent a significantly higher-risk group than patients presenting for surgery on a single valve.
XV. Prosthetic valves
The decision regarding which prosthetic valve should be used for a particular patient is based upon a variety of factors, including the expected longevity 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 .
A. 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 means that no ideal valve has yet been found.
B. 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 times control. There are four basic types of mechanical prosthetic valves, the caged ball, caged disc, monocuspid tilting disc, and bicuspid tilting disc valves. Of these, the bicuspid tilting disc valves are in common use to today. This valve design is less bulky than its predecessors, and provides improved central laminar blood flow.
a. Bileaflet tilting-disk valve prosthesis (Fig. 12.17). 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, though anticoagulation is still necessary. The most popular bileaflet tilting disc is still the St. Jude Medical. Other bileaflet tilting-disk valve prostheses include the CarboMedics, Edwards Tekna, Sorin Bicarbon, and Advancing the Standard (ATS).
Figure 12.17 Bileaflet valve prosthesis showing disks in open (A) and closed (B) positions.
2. Bioprosthetic valves. The Hancock porcine aortic bioprosthesis (now the Medtronic Hancock II stented porcine 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, and also less thrombogenic. Long-term anticoagulation for a bioprosthetic valve is usually unnecessary. Bioprosthetic valves in the aortic position last longer than in the mitral position. Because durability is an issue, and because their lifespan is longer in older patients, bioprosthetic valves are usually used for patients older than 60 yrs and when anticoagulation is not a desirable option (e.g., when pregnancy is anticipated).
a. Bioprosthetic valves fall into two types: Stented and nonstented. Stented bioprosthetic valves 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. Stented valves that can be found in clinical use today include the Carpentier–Edwards perimount (Fig. 12.18), Medtronic Mosaic, Carpentier–Edwards porcine, Hancock porcine, and Medtronic intact porcine.
Figure 12.18 Carpentier–Edwards perimount RSR stented pericardial bioprosthetic aortic valve (Courtesy of Edwards Lifesciences, Irvine, California).
b. Stentless bioprostheses. Porcine valves fixed in a pressure-free glutaraldehyde solution and 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, Edwards Prima Plus stentless bioprosthesis (Fig. 12.19), and Medtronic Freestyle stentless porcine. Stentless bioprosthetic valves are used almost exclusively in the aortic position. They have excellent hemodynamic characteristics, but technically are more difficult to place. Modern stentless bioprosthetic valves are often used when aortic root replacement is also necessary.
Figure 12.19 Edwards Prima Plus stentless bioprosthetic aortic valve (Courtesy of Edwards Lifesciences, Irvine, California).
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 longer than 10 yrs regardless of patient age. The incidence of prosthetic valve endocarditis and hemolysis resulting from blood flow through the homograft is very low. Anticoagulation is usually not required. Homografts are predominately used in the aortic position, especially when aortic root replacement is necessary, and for pulmonary valve replacement in the Ross procedure. Homografts may be most useful in patients younger than 35 and in patients with native valve endocarditis.
XVI. Prophylaxis of bacterial endocarditis
When an invasive procedure puts the patient with valvular heart disease at risk of 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 (a) a strict aseptic technique for all procedures performed in patients with valvular heart disease, (b) elimination of existing sources of infection before implantation of a prosthetic valve, and (c) in selected cases, antibiotic prophylaxis. Guidelines from the American Heart Association on prevention of infective endocarditis limit antibiotic prophylaxis to cardiac conditions associated with the highest risk of infective endocarditis. These conditions include prosthetic cardiac valves or material used in heart valve repair, complex congenital heart diseases, prior infective endocarditis, and transplanted hearts with valvulopathy. Endocarditis prophylaxis is recommended only for “dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.” Endocarditis prophylaxis may be considered for invasive procedures of the respiratory tract involving incision or biopsy of respiratory mucosa, but not for simple bronchoscopy. Guidelines no longer recommend antibiotics solely for endocarditis prophylaxis for any gastrointestinal and genitourinary procedures. However, administration of antibiotics to prevent wound or urinary tract infection is reasonable . Guidelines for antibiotic prophylaxis, to be begun 1 h prior to a procedure, are shown in Table 12.16.
1. Otto CM, Bonow RO. Valvular heart disease. In: Bonow RO, Mann DL, Zipes DP, et al., eds. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. St. Louis, MO: Elsevier; 2011:1468–1530.
2. Nikomo VT, Gardin JM, Skelton TN, et al. Burden of valvular heart disease: a population-based study. Lancet. 2006;368:1005–1011.
3. Cook DJ, Housmans PR, Rehfeldt KH. Valvular heart disease: replacement and repair. In: Kaplan JA, Reich DL, Savino JS, eds. Kaplan’s Cardiac Anesthesia: The Echo Era. 6th ed. St Louis, MO: Elsevier Saunders; 2011:570–614.
4. Iung B, Baron G, Butchard EG, et al. A prospective survey of patients with valvular heart disease in Europe: the euro heart survey on valvular heart disease. Eur Heart J. 2003;24:1231–1243.
5. Otto CM. Textbook of Clinical Echocardiography. 4th ed. Philadelphia, PA: Elsevier Saunders; 2009:259–325.
6. Galderisi M, de Divitiis O. Risk factor induced cardiovascular remodeling and the effects of angiotensin-converting enzyme inhibitors. J Cardiovasc Pharmacol. 2008;51:523–531.
7. Roberts WC, Jong M, Ok BA. Frequency by decades of unicuspid, bicuspid, and tricuspid aortic valves in adults having isolated aortic valve replacement for aortic stenosis, with or without associated aortic regurgitation. Circulation. 2005;111:920–925.
8. Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22:1–23.
9. Agricola E, Oppizzi M, Pisani M. Stress echocardiography in heart failure. Cardiovasc Ultrasound. 2004;2:11.
10. Maslow A, Casey P, Poppas A, et al. Aortic valve replacement with or without coronary bypass graft surgery: the risk of surgery in patients ≥80 years old. J Cardiothorac Vasc Anesth. 2010;24:18–24.
11. Webb JG, Altwegg L, Boone RH, et al. Transcatheter aortic valve implantation: Impact on clinical and valve-related outcomes. Circulation. 2009;119:3009–3016.
12. Boodhwani M, de Kerchove L, Glineure D. Repair oriented classification of aortic insufficiency: impact on surgical techniques and clinical outcomes. J Thoracic Cardiovasc Surg. 2009;137:286–294.
13. Sidebotham D, Legget ME, Sutton T. The mitral valve. In: Sidebotham D, Merry A, Legget M, et al., eds. Practical Perioperative Transesophageal Echocardiography: With Critical Care Echocardiography. 2nd ed. Philadelphia, PA: Elsevier Saunders; 2011:142–147.
14. Stewart WJ, Currie PJ, Salcedo EE, et al. Evaluation of mitral leaflet motion by echocardiography and jet direction by Doppler color flow mapping to determine the mechanisms of mitral regurgitation. J Am Coll Cardiol.1992;20:1353–1361.
15. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2006;48(3):e1–e148.
16. Fattouch K, Guccione F, Sampognaro R, et al. POINT: Efficacy of adding mitral valve restrictive annuloplasty to coronary artery bypass grafting in patients with moderate ischemic mitral valve regurgitation: a randomized trial. J Thorac Cardiovasc Surg. 2009;138:278–285.
17. Denault AY, Lamarche Y, Couture P, et al. Inhaled milrinone: a new alternative in cardiac surgery? Semin Cardiothorac Vasc Anesth. 2006;10:346–360.
18. Rahimtoola SH. Choice of prosthetic heart valve in adults: an update. J Amer Coll Cardiol. 2010;55:2413–2426.
19. Nishimura RA, Carabello BA, Faxon DP, et al. ACC/AHA 2008 Guideline update on valvular heart disease: focused update on infective endocarditis. Circulation. 2008;118:887–896.