Valvular heart disease (VHD) is frequently observed in patients undergoing surgery. As the medical and minimally invasive management of coronary artery disease increases, the number of patients with untreated advanced valvular disease is likely to supersede the number of patients with advanced coronary disease. Similarly, the rapidly expanding use of percutaneous transcatheter aortic valve replacement for high- and intermediate-risk patients with aortic stenosis (AS), as well as the emergence of devices such as the Mitraclip for symptomatic management of high-risk patients with ischemic mitral regurgitation (MR), may increase the pool of patients with significant valvular disease undergoing noncardiac surgery. The association of VHD with other clinical predictors of increased perioperative cardiovascular risk is of prime importance, particularly as it relates to unstable coronary syndromes, decompensated heart failure with left ventricular (LV) dysfunction, and significant arrhythmias. For example, VHD has been reported to be a major predictor of increased perioperative cardiovascular risk, including myocardial infarction, heart failure, and cardiac death. In patients older than 65 years presenting for noncardiac or coronary artery surgery without concomitant valvular surgery, a history of VHD is predictive of lower LV ejection fraction (LVEF), and patients with preoperative symptomatic valvular disease have increased risk of congestive heart failure (CHF) after elective general surgical procedures. Similarly, significant aortic and mitral valvular dysfunction diagnosed by preoperative transthoracic echocardiography is an independent risk factor for perioperative myocardial infarction. Significant AS is one of the major factors adversely affecting the clinical outcome after noncardiac surgery, where it is found to increase the risk of both myocardial infarction and mortality. Thus, although it is important to preoperatively evaluate the presence, type, and severity of VHD, its natural history and relation to other disease states are key factors in determining the clinical management strategy for the perioperative period.
The physician must know the patient’s preoperative history and the results of the physical examination. If a cardiac murmur is present on preoperative evaluation, the anesthesiologist needs to decide whether it represents significant VHD (see later). Current American Heart Association/American College of Cardiology guidelines suggest that valvular intervention before elective noncardiac surgery is effective in reducing perioperative risks, so delaying elective noncardiac surgery if additional diagnostic interventions and treatment are needed is reasonable ( Fig. 14.1 ). Furthermore, while surgery not amenable to delays for definitive treatment can be performed, mapping the valvular lesion and its severity at minimum can usually be performed quickly. This can be helpful to facilitate discussion with the patient about the perioperative risks and to guide the anesthesiology team about anesthetic approaches, increased hemodynamic perioperative monitoring (including invasive hemodynamic catheters and echocardiography), and postoperative disposition of the patient to an appropriate setting (such as the intensive care unit). Patients with severe VHD may be more prone to hemodynamic instability during the operation, coupled with longer times for both anesthesia and surgery when compared with patients without VHD. High-risk surgical procedures (emergent major operations, aortic and peripheral vascular surgery, and prolonged surgical procedures associated with large fluid shifts or blood loss) pose a greater risk of hemodynamic instability and increased perioperative morbidity and mortality. Although no randomized trials have been performed to ascertain the best timing of surgical intervention, the indications for evaluation and treatment of valvular lesions prior to elective noncardiac surgery are the same as in the nonoperative setting. Thus, symptomatic stenotic lesions often require valve replacement or percutaneous valvotomy prior to noncardiac surgery to decrease cardiac risk, while it may be reasonable to perform elevated-risk elective noncardiac surgery in patients with asymptomatic severe stenotic lesions or with regurgitant lesions, as these may be more amenable to medical management in the perioperative setting. However, all of these patients have elevated risk for postoperative morbidity and mortality compared with patients free of VHD.
Transthoracic echocardiography usually provides the most thorough assessment of the significance of a cardiac murmur, although preoperative electrocardiography and chest radiography can provide clues to the severity of VHD and associated cardiac conditions. Echocardiography is an important tool for assessing the significance of cardiac murmurs by imaging cardiac structure, function, and the direction and velocity of blood flow through cardiac valves and chambers. Current guidelines recommend performing preoperative echocardiography for patients with clinically suspected moderate or greater degrees of valvular stenosis or regurgitation, provided there is no echocardiography exam available in the year prior to the procedure. Furthermore, a repeat examination is indicated for patients with a significant change in either clinical status or physical examination since last echocardiography. If the results of transthoracic echocardiography are inconclusive in defining the diagnosis, other tests, including transesophageal echocardiography (TEE) and cardiac catheterization, should be considered. It is important to glean from the echocardiography report not only the severity of the most significant valvular lesion but also other indices of cardiac function, including presence of dilated atriae, the size and thickness of the left and right ventricles, evidence of elevated right ventricular pressures, and presence and severity of diastolic dysfunction. Preoperative knowledge of those parameters is very helpful in the perioperative management of patients with VHD. In determining whether symptoms are present, exercise testing may be helpful, as many patients tend to limit their daily activity.
Finally, the specific type of surgery and urgency of the operation are important factors in stratifying perioperative risk for VHD surgical patients. High-risk surgical procedures, including emergent major operations, aortic and peripheral vascular surgery, and prolonged surgical procedures associated with large fluid shifts or blood loss, pose a greater threat of hemodynamic instability and portend an increase in perioperative morbidity and mortality.
Surgical procedures may induce bacteremia and thus expose patients to the risk of acquiring infective endocarditis, a potentially lethal disease if not aggressively treated. Valvular abnormalities, particularly those that result in high-velocity jets, can damage the endothelial lining, lead to platelet aggregation and fibrin deposition at those sites, and create a higher risk for bacterial colonization. To date, the efficacy of prophylactic antibiotics is based on laboratory animal models and small-scale clinical studies using primarily surrogate markers of infective endocarditis. Current clinical strategies in endocarditis prevention are based on recommendations from the American Heart Association in 2007 and are outlined in Box 14.1 and Table 14.1 . These recommendations are substantially different from earlier guidelines from 1997. Current guidelines suggest that antibiotic prophylaxis solely for prevention of infective endocarditis is reasonable only for a small subset of patients with valvular disease at a high risk of adverse outcome from endocarditis. These patients include surgical patients with prosthetic valves, patients with previous history of endocarditis, unrepaired cyanotic congenital heart disease, or completely repaired congenital heart defect with prosthetic material or device within 6 months of the procedure. Furthermore, cardiac transplant patients with secondary valvulopathies are at a high risk of endocarditis. Antibiotic prophylaxis for these high-risk patients (see Box 14.1 ) is considered reasonable for dental and oral procedures involving manipulation of gingival tissue, the periapical region of teeth, or perforation of the oral mucosa. In addition, prophylaxis is reasonable for surgical procedures involving the respiratory tract or infected skin, skin structures, or musculoskeletal tissue. In contrast, prophylaxis is not routinely recommended for infective endocarditis prevention in patients undergoing genitourinary or gastrointestinal procedures. In terms of administration, the initial dose of antimicrobials should begin within 1 hour prior to surgical incision.
Endocarditis prophylaxis recommended
Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
Previous infective endocarditis
Congenital heart disease (CHD)
Unrepaired cyanotic CHD, including palliative shunts and conduits
Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
Cardiac transplant recipients who develop cardiac valvulopathies
|Regimen: single dose 30 to 60 min |
Some patients with VHD receive chronic anticoagulation therapy. It is important to understand the indication for anticoagulation to determine the risks associated with holding anticoagulation in the perioperative period as well as options for anticoagulation bridging. In general, anticoagulation should not be held for procedures that do not have elevated bleeding risk. Patients with mechanical valves are currently all chronically anticoagulated with warfarin, as novel oral anticoagulation agents (NOACs) have not been tested or found to have excess risk. Per current guidelines, patients with mechanical mitral valves, mechanical caged-ball or tilting-disc aortic valves, or patients with mechanical valves and recent stroke/transient ischemic attack are considered at high risk for thrombotic complications, and periprocedural bridging is recommended for procedures with elevated bleeding risk. Bridging can either be performed by unfractionated heparin (UFH) infusion or subcutaneous low-molecular-weight heparin. Patients with bileaflet mechanical aortic valves but without atrial fibrillation and other stroke risk factors are considered to be at low risk for thrombotic complications, so no bridging is recommended. Patients with bileaflet mechanical aortic valves and either atrial fibrillation or risk factors for stroke (prior stroke or transient ischemic attack, hypertension, diabetes, CHF, or age over 75 years) are considered at moderate risk for thrombotic complications, so the risk of thrombosis must be weighed carefully against the risk of increased bleeding during the perioperative period. Patients with VHD who have not undergone a surgical replacement but require anticoagulation for atrial fibrillation are generally either considered to be at low or moderate risk of thrombotic complication, with the exception of patients with stroke or transient ischemic attack less than 3 months ago, a high burden of stroke risk factors (indicated by CHADS 2 score of 5 or higher), or rheumatic heart disease. Most of these patients will therefore not require an anticoagulation bridge from warfarin. Furthermore, many of these will be chronically anticoagulated with NOACs that allow patients to relatively quickly reverse anticoagulation by stopping the medication secondary to their short half-life compared with warfarin.
With regard to pregnancy, the American College of Chest Physicians concluded that it is reasonable to use one of the following three regimens to manage anticoagulation during pregnancy: (1) either LMWH or UFH between 6 and 12 weeks of gestation and close to term, with warfarin administered at all other times; (2) aggressive dose-adjusted UFH throughout pregnancy; or (3) aggressive dose-adjusted LMWH throughout pregnancy. In general, anticoagulation should be resumed postoperatively as quickly as possible from a procedural bleeding standpoint.
Patients with severe VHD are often treated with antiarrhythmic, inotropic, or diuretic therapy (or more than one of these), and it is extremely important that these drugs be continued during the perioperative period. An inability to administer postoperative oral medications in a timely fashion to heart failure patients could be one reason for the occurrence of postoperative CHF. Similarly, cessation of antiarrhythmic drugs may pose a serious risk for the patient with severe AS in whom cardiac output and hemodynamic stability critically depend on normal sinus rhythm. Finally, therapy aimed at minimizing the perioperative cardiac risk has to be considered. Perioperative beta-blockade has been shown to reduce the risk of cardiac events in patients with a risk of myocardial ischemia undergoing noncardiac surgery. Withholding beta-blockers has shown to be a strong risk factor for postoperative atrial fibrillation after coronary bypass surgery, and continuation of beta-blockers after noncardiac surgery is associated with lower operative mortality and lower incidence of myocardial infarction. However, initiating beta-blockade in all-comers in the perioperative setting has been shown to increase mortality and elevate risk of strokes. Thus, the safety and efficacy of beta-blockers in heart failure patients undergoing noncardiac surgery is uncertain and should be evaluated on a case-by-case basis. The benefit has to be balanced against the risk of compromising cardiac inotropic function in unstable VHD patients or those with limited contractile reserve. Furthermore, recent data have cast some doubt on the efficacy of perioperative beta-blocker therapy in patients with intermediate risk factors. There is also growing evidence that alpha-2-agonists and statins reduce the risk of adverse cardiac events in surgical patients ; however, additional large-scale trials are still needed to further delineate the role of these agents. Finally, although an active inflammatory process contributing to calcific AS has been recognized, a prospective randomized clinical trial concluded that intensive lipid-lowering therapy with statin drugs did not halt the progression of stenosis or induce its regression.
Pathophysiology of Disease and Physiologic Principles of Management
The current hemodynamic principles of perioperative management of patients with VHD (see Table 14.2 ) are based on underlying pathophysiology and the natural history of the disease. As such, perioperative management is guided by basic physiologic and pathophysiologic principles.
|AS||Maintain NSR |
tachycardia, severe bradycardia
May not withstand beta-blockade
Consider augmenting prior to anesthetic induction
|Avoid sudden |
|Maintain||Consider preinduction arterial line and external defibrillator Proceed carefully with neuraxial anesthesia|
|MS||Often AF, rate control |
If baseline NSR
and converts to
|Maintain within normal limits||Maintain normovolemia (left atrial pressure) |
Avoid rapid fluid infusion
Caution with Trendelenburg position
|Avoid sudden decreases||Avoid |
|Avoid respiratory depression (cautious premedication) Be aware of left atrial thrombi |
Gentle neuraxial dosing to avoid sudden drops in SVR
Control sympathetic response with adequate analgesia, maintenance of normothermia
|TS||Often AF, rate control |
|Avoid tachycardia |
|Maintain||Maintain without producing venous congestion||Avoid sudden decreases||Maintain||Hepatic dysfunction common |
PA catheter placement can be challenging
|PS||May be in AF||Maintain baseline heart rate||Avoid myocardial depression||Maintain normovolemia Consider gentle augmentation of intravascular volume||Maintain||Avoid |
|Consider hepatic dysfunction |
Be mindful of associated congenital lesions or concomitant tricuspid disease
In general, blood flow through a valve is governed by simple hydraulic principles, where the valve area, the square root of the pressure gradient across the valve, and the duration of transvalvular flow during a specific phase of the cardiac cycle are the principal determinants of this flow. Lowering or raising these determinant factors will decrease or increase the transvalvular flow accordingly. In stenotic lesions, the anesthetic goal is to support transvalvular flow, which is partially “fixed” by an obstructive lesion. In regurgitant lesions, the primary goal is to minimize the fraction of regurgitant flow through the abnormal valve while simultaneously increasing the degree of forward flow. Another consideration in regurgitant lesions is that the regurgitant orifice area can change dynamically because of changes in valvular annulus or ventricular dimensions produced by varying loading conditions. Thus, perioperative management of heart rate, preload, and systemic and pulmonary vascular resistance (PVR) depend on the specific type of valvular abnormality (see Table 14.2 ).
Nonpharmacologic factors may facilitate or interfere with the provision of anesthesia for patients with VHD. For example, the Trendelenburg position may help to support preload in an emergency, but it may also promote pulmonary vascular congestion and decompensation in patients with elevated pulmonary artery pressures (such as in severe mitral stenosis [MS]) or right-sided valvular lesions. Similarly, changing to the upright position increases venous pooling, decreasing preload, cardiac output, and potentially worsening dynamic LV outflow tract obstruction in patients with hypertrophic cardiomyopathy. Positive pressure ventilation and positive end-expiratory pressure may also decrease venous return to the right heart and increase PVR. Other important conditions that increase PVR include hypoxia, hypercapnia, acidosis, and hypothermia. Hypothermia also increases the sympathetic drive and represents an additional risk factor for morbid cardiac events. Additionally, preservation of normothermia has been shown to reduce the incidence of surgical infection.
Premedication may be helpful in preventing perioperative anxiety and stress-induced tachycardia. However, in some patients, acutely withdrawing the sympathetic tone may be undesirable. In patients with severe VHD, premedication should be tailored to preserve myocardial function and to avoid significant reduction in preload and systemic vascular resistance (SVR). In patients with pulmonary hypertension, right-sided valvular disease, or severe mitral disease, hypoventilation leading to hypoxemia or hypercapnia should also be avoided.
Type of Anesthesia: General, Regional, or Local with Monitored Sedation
Many anesthetic regimens are used for patients with VHD who are undergoing noncardiac surgery. Today, there is no strong evidence to support a specific anesthetic technique in providing optimal perioperative outcomes. Monitored anesthesia care with sedation alone may cause less hemodynamic disturbance than general or neuraxial approaches, but it is useful in only a limited number of surgical procedures. The risk of deep venous thrombosis is generally lower with spinal or epidural anesthesia than with general anesthesia. Neuraxial anesthesia may, however, reduce sympathetic tone, SVR, and preload, potentially promoting hemodynamic instability. Although decreases in afterload may help to maintain forward flow in regurgitant valvular lesions, sudden and profound drops in SVR can be detrimental to patients with stenotic lesions. Unfortunately, there is a paucity of high-quality data pertaining to regional anesthesia in stenotic valvular lesions, but case report data indicate that it may be a safe approach. Certain neuraxial techniques, such as continuous spinal and epidural anesthesia, can be tailored to minimize the rapid changes in sympathetic tone. In particular, avoiding the blockade of the thoracic sympathetic nerve fibers by using lower-level block may help to reduce these side effects. Reduction of local anesthetic doses by using them in combination with epidural and intrathecal narcotics also helps to minimize the sympatholytic effects of regional anesthesia.
For patients with normal ventricular function, a balanced general anesthesia with lower concentrations of volatile anesthetics is usually a safe option that minimizes adverse effects on contractility and loading conditions. Patients with compromised ventricular function may be particularly intolerant of the vasodilation accompanying volatile anesthetics. Nitrous oxide should be used carefully in patients with mild or moderate pulmonary hypertension, and possibly avoided when significant disease is present, because of the potential of this gas to increase pulmonary artery pressures. Light anesthesia and poor pain control are other factors that may contribute to the increase in sympathetic drive and PVR. The choice of muscle relaxant is related to the specific hemodynamic effects it may cause. Regardless of the type of anesthesia, there must be prompt response to sudden hemodynamic changes. Intraoperative fluctuations in mean arterial pressure increase the probability of postoperative heart failure in high-risk patients undergoing elective general surgery. Thus, for patients with severe VHD, inotropic and vasoactive drips should be readily available. Additionally, the preoperative placement of defibrillator pads and provision of a defibrillator to facilitate expeditious cardioversion is reasonable for patients with severe valvular disease.
The use of invasive monitoring for patients with VHD is based on the severity of disease, associated cardiac and noncardiac problems, the nature of the surgical procedure, and the practice setting. Asymptomatic patients without concurrent disease going for minimal risk surgery require ASA standard monitoring just as those without VHD do. On the other hand, symptomatic patients undergoing major surgical procedures require invasive monitoring that provides hemodynamic data on an instantaneous basis. Such intensive monitoring has been shown to attenuate risk during noncardiac surgery in some patient groups, such as those with severe AS. Therefore, except for minor surgical procedures (e.g., cataract extraction), direct arterial pressure monitoring should be used for most patients with severe stenotic lesions (i.e., AS, MS) and should be considered in patients with regurgitant lesions accompanied by concomitant ventricular dysfunction or hemodynamic instability.
Right heart catheterization with a pulmonary artery catheter (PAC) is an important technique to assess the adequacy of circulating blood volume (right ventricular [RV] and LV preload), cardiac output, and mixed venous oxygenation. However, the use of the PAC remains controversial in perioperative medicine. In the practice guidelines of the American Society of Anesthesiologists, it is emphasized that with some exceptions, routine pulmonary artery catheterization is generally inappropriate for low- or moderate-risk patients. PAC monitoring is, however, appropriate or necessary in patients undergoing high-risk procedures with large fluid changes or hemodynamic disturbances or with high risk of morbidity and mortality, or in those with severe cardiac disease whose hemodynamic disturbances have a great chance of causing organ dysfunction or death. Additionally, practice settings, particularly catheter use skills and technical support, play an important role in decisions related to PAC use. For patients with VHD, interpretation of PAC data involves understanding that central venous waveforms are altered with significant tricuspid valve lesions, and the pulmonary artery wedge pressures are not reflective of LV end-diastolic pressures in patients with severe mitral disease.
TEE is widely used during cardiac and noncardiac surgery and in the early postoperative period. Because global and regional heart function, loading conditions, and valvular dysfunction can be effectively monitored by this technique, monitoring with TEE is particularly beneficial for patients with severe VHD and those with a significant risk of hemodynamic disturbances during surgery. There is strong evidence supporting the perioperative use of TEE for evaluating acute, persistent, and life-threatening hemodynamic disturbances in which ventricular function and its determinants are uncertain and have not responded to treatment. In situations where invasive monitoring is not required for postoperative care, intraoperative TEE alone may be sufficient for monitoring during periods of changing hemodynamics.
The principles of hemodynamic optimization based on the pathophysiology of specific VHD apply also to the postoperative management of these patients. Both preoperative status and intraoperative course should be taken into consideration as risk factors for postoperative complications. Patients with severe VHD are prone to develop a number of postoperative problems, including myocardial ischemia, arrhythmias, and heart failure. Continuation of invasive monitoring enables prompt and effective management while the patient is stabilizing after surgery. Effective pain management is of paramount importance so that uncontrolled surges in sympathetic activity are prevented. Alleviation of postoperative pain may also help to decrease perioperative morbidity and mortality. Patients who were on beta-blockers preoperatively should have them continued postoperatively to reduce the risk of myocardial ischemia. Antimicrobial agents should be discontinued within 24 hours of the end of surgery. Avoidance of perioperative hyperglycemia reduces the rate of postoperative infections and overall in-hospital mortality among critically ill patients in the surgical intensive care unit. Oral anticoagulants should be reinstituted as soon as possible, with initial administration of heparin if necessary. In patients with tenuous valvular lesions, including severe AS or MS, admission to the intensive care unit for closer monitoring may be warranted.
Specific Valvular Lesions
The type of valvular lesion should be determined prior to the surgical procedure, because the perioperative management of stenotic lesions differs significantly from that of regurgitant lesions. Each type of VHD imposes a unique set of stresses on the LV and RV, leading to specific hemodynamic profiles and recommendations for anesthetic and therapeutic priorities for each lesion (see Tables 14.2 and 14.3 ). Aortic and mitral lesions are the most common and are discussed in greater detail. Tricuspid and pulmonary lesions are less frequent and therefore less studied in the perioperative environment. Management of tricuspid lesions is generally thought to be similar to the matching lesion in the left heart (i.e., a mitral lesion), but high-quality evidence is lacking.