Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease

INTRODUCTION — Valvular heart disease (VHD) increases with age, and more than 13 percent of adults ≥75 years old have moderate or severe disease of one or more cardiac valves (table 1). The most common lesions are aortic stenosis (AS) due to degeneration and calcification of the valve in older adults or early calcification of a congenital bicuspid aortic valve, and mitral regurgitation (MR) due to primary causes (eg, intrinsic disease of the mitral leaflets or subvalvular apparatus) or secondary functional causes (eg, cardiomyopathy with left ventricular enlargement and annular dilatation or ischemic [postinfarction] MR) (figure 1). Patients often have a combination of stenosis and regurgitation in a single cardiac valve, or disease of more than one valve. (See "Valvular heart disease in older adults".)

This topic will discuss anesthetic management during elective or urgent noncardiac surgery in patients with cardiac valvular heart disease (VHD). Those with severe valve lesions, particularly those with severe AS, are at greatest risk for adverse perioperative cardiovascular events.

Specific considerations for patients with aortic or mitral valve disease who are undergoing cardiac surgery or labor and delivery are discussed in separate topics.

●(See "Anesthesia for cardiac valve surgery".)

●(See "Anesthesia for labor and delivery in high-risk heart disease: Specific lesions".)

PREANESTHESIA CONSULTATION — The preanesthetic consultation for patients with valvular heart disease (VHD) involves assessing cardiac and overall health risks, identifying issues that may cause perioperative problems, working with the cardiologist and surgeon to optimize medical conditions, and developing an anesthetic care plan to provide appropriate hemodynamic conditions and avoid cardiovascular complications.

The preanesthetic consultation includes assessment of:

●Severity, chronicity, and associated pathophysiologic alterations due to one or more valvular lesions. The 2014 American Heart Association/American College of Cardiology guidelines classify VHD into stages A to D, based on the presence or absence of symptoms, hemodynamic severity of disease, and the impact of the valve lesion on ventricular function [1].

●Effects that the planned surgical procedure and specific anesthetic techniques might have on pre-existing cardiac loading conditions and function.

●Whether invasive hemodynamic monitoring will be beneficial.

●Which vasoactive agents should be selected and prepared.

Other topics discuss preoperative and postoperative considerations for patients with cardiac valve disease:

●(See "Noncardiac surgery in adults with aortic stenosis".)

●(See "Rheumatic mitral stenosis: Overview of management", section on 'Management of noncardiac surgery'.)

●(See "Noncardiac surgery in patients with mitral or aortic regurgitation".)

History and physical examination — The history and physical examination includes assessment of New York Heart Association functional class I to IV status, as an indication of the severity of VHD and associated congestive heart failure (CHF) (table 2). Mild cardiac valve disease does not typically contribute to hemodynamic instability. Patients with moderate VHD can be at significant risk for adverse events if there are combined valve lesions (eg, concomitant aortic stenosis and regurgitation) (see 'Patients with combined valve lesions' below), or concomitant heart failure or ischemic heart disease. (See "Intraoperative management for noncardiac surgery in patients with heart failure" and "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

Most left sided heart valve lesions cause either a left ventricular (LV) pressure overload state (eg, aortic stenosis) or an LV volume overload state (eg, aortic or mitral regurgitation). In contrast, mitral stenosis impairs LV diastolic filling and, if severe enough, can cause pulmonary hypertension with right ventricular (RV) pressure or volume overload and associated tricuspid valve regurgitation [2]. (See "Determining the etiology and severity of heart failure or cardiomyopathy".)

Symptoms of CHF in patients with severe mitral or aortic stenosis include sudden dyspnea in response to increased cardiac demand with exertion, such as stair climbing. Signs of CHF include rales, wheezing, jugular venous distention, hepatomegaly, ascites, and peripheral edema. Symptoms of CHF in patients with severe mitral or aortic regurgitation typically manifest as excessive fatigue with gradual onset of dyspnea during exertion, due to gradual decrease in forward cardiac output and increase in pulmonary congestion. Severe physical deconditioning may be present in patients who limit their physical activity because of symptoms interfering with ability to exercise or even to perform normal daily activities (table 2). (See "Heart failure: Clinical manifestations and diagnosis in adults", section on 'Physical examination'.)

Electrocardiogram — We agree with the 2014 American College of Cardiology/American Heart Association (ACC/AHA) guidelines for perioperative cardiovascular evaluation stating that a preoperative resting 12-lead electrocardiogram (ECG) should be obtained in patients with known significant structural heart disease [3]. Many patients with VHD have atrial arrhythmias, and older patients may have ECG evidence of ischemic heart disease. If postoperative ECG abnormalities are present, the baseline ECG is useful for comparison. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Electrocardiogram for some patients'.)

Specialized cardiac testing — Other specialized cardiac tests such as transthoracic or transesophageal echocardiography are not routinely ordered unless there is an indication unrelated to the proposed surgical procedure. (See "Evaluation of cardiac risk prior to noncardiac surgery", section on 'Testing to further define risk'.)

Preoperative medication management — Chronically administered medications for management of cardiac risk are typically continued in the perioperative period. These include:

●Cardiovascular medications (eg, beta blockers, calcium channel blockers, statins, clonidine). Also, angiotensin-converting enzyme [ACE] inhibitors and angiotensin II receptor blockers (ARBs) are generally continued, particularly in patients with heart failure, unless there is evidence of hemodynamic instability, hypovolemia, or acute elevation of creatinine. Some clinicians administer the evening dose of an ACE inhibitor or ARB on the day before surgery (but not on the morning of surgery) if large perioperative fluid shifts are anticipated.

●Antiarrhythmic medications for treatment of chronic atrial fibrillation (AF) or ventricular arrhythmias (eg, amiodarone, calcium channel blockers, digoxin).

●Aspirin.

Details regarding perioperative management of these cardiovascular medications are available elsewhere:

●(See "Management of cardiac risk for noncardiac surgery".)

●(See "Perioperative management of heart failure in patients undergoing noncardiac surgery", section on 'Preoperative management'.)

●(See "Perioperative medication management", section on 'Cardiovascular medications'.)

Medications to minimize pulmonary vascular resistance in patients with pulmonary hypertension are typically continued (eg, epoprostenol, iloprost, sildenafil, tadalafil, or endothelin receptor antagonists, such as bosentan or ambrisentan) [2]. (See "Treatment and prognosis of pulmonary arterial hypertension in adults (group 1)", section on 'Surgical or periprocedural care'.)

Management of chronic anticoagulant therapy in patients with AF balances thromboembolic risk and bleeding risk to determine the optimum timing of anticoagulant interruption and whether to use bridging anticoagulation. Patients undergoing urgent or emergent surgery after recent administration of anticoagulant therapy (other than chronic aspirin therapy) may require urgent anticoagulant reversal to prevent or treat severe bleeding. Such patients are not appropriate candidates for a neuraxial technique. Further discussion is available in separate topics. (See "Perioperative management of patients receiving anticoagulants" and "Neuraxial anesthesia/analgesia techniques in the patient receiving anticoagulant or antiplatelet medication".)

AORTIC STENOSIS — Severe aortic stenosis (AS) causes obstruction of left ventricular (LV) outflow resulting in LV pressure overload, concentric hypertrophy, and diastolic dysfunction that often leads to decreased stroke volume (SV) and cardiac output (CO). Prevalence, etiology, pathophysiology, clinical manifestations, and stages of AS severity are discussed separately (table 3) [1,4]. (See "Clinical manifestations and diagnosis of aortic stenosis in adults" and "Natural history, epidemiology, and prognosis of aortic stenosis".)

Preoperative medical assessment and management considerations before noncardiac surgery for a patient with possible or known AS, including indications for surgical or transcatheter aortic valve replacement (TAVR) [5], are addressed separately. (See "Noncardiac surgery in adults with aortic stenosis" and "Noncardiac surgery in adults with aortic stenosis", section on 'Patients with indications for AVR'.)

Hemodynamic management — Key points for perioperative hemodynamic goals and anesthetic management of patients with AS are summarized in the table (table 4). (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Aortic stenosis'.)

Anesthetic management — The choice of anesthetic techniques and agents is based on requirements for accomplishing the surgical procedure, as well as hemodynamic goals for AS [6].

Sedation with monitored anesthesia care — For minor procedures requiring only sedation with monitored anesthesia care (MAC), standard American Society of Anesthesiologists (ASA) monitoring is sufficient (table 5) [7]. (See "Monitored anesthesia care in adults".)

Adequate analgesia may avoid sympathetic responses that result in tachycardia and hypertension. In some cases, combining MAC with a peripheral nerve block may provide excellent analgesia to avoid pain-induced tachycardia and hypertension, as well as avoiding the risk of hypotension that may occur during neuraxial or general anesthesia. If necessary, a beta blocker (eg, esmolol 20 to 30 mg or metoprolol 2.5 to 5 mg) may be administered to control HR. (See 'Hemodynamic management' above.)

Neuraxial anesthesia — For appropriate surgical procedures, a very slowly titrated epidural technique can be safely employed in most patients with moderate AS, but is typically avoided in patients with severe AS. Such patients will not tolerate rapid onset of a sympathectomy and the consequent hypotension and critical reduction in coronary perfusion pressure. As an alternative to epidural anesthesia, a continuous spinal anesthetic may be very slowly titrated. If a neuraxial technique is selected, specific precautions to avoid hemodynamic collapse include:

●Insertion of an intra-arterial catheter for continuous monitoring of BP before placement of a neuraxial needle or catheter.

●Fluid administration to maintain optimal intravascular volume. Fluid is administered incrementally (eg, in 100- to 250-mL boluses) to avoid volume overload in patients with congestive heart failure (CHF).

●Very slow titration (eg, 3 to 5 mL every five minutes) of the local anesthetic selected for epidural administration, or small incremental doses of bupivacaine 3 to 5 mg for a continuous spinal technique.

●Prompt treatment of hypotension with IV fluid and phenylephrine administered as bolus doses of 40 to 100 mcg, followed by a phenylephrine infusion if necessary. Norepinephrine and/or vasopressin should also be immediately available in the event that phenylephrine is ineffective (table 6). Epinephrine is a reasonable alternative, particularly if the patient has poor LV function. (See 'Hemodynamic management' above.)

General anesthesia — General anesthesia may be selected because of the type of surgical procedure or patient choice. Combining general anesthesia with a neuraxial technique such as continuous epidural analgesia may provide optimal perioperative pain management in selected patients, thereby avoiding pain-induced tachycardia during and after surgery.

●Monitoring – Pads for a five-lead ECG should be placed for continuous monitoring of both lead II and a precordial lead (V₅ or V₄), for optimal detection of myocardial ischemia [8]. It is also reasonable to place defibrillator pads before anesthetic induction, so that cardioversion or defibrillation may be rapidly accomplished if necessary (figure 2). (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Monitoring for myocardial ischemia'.)

An intra-arterial catheter is inserted for continuous BP monitoring and rapid detection of hypotension.

For procedures with anticipated significant fluid losses or bleeding (eg, major vascular, orthopedic, or abdominal procedures), a central venous catheter (CVC) is typically inserted to provide large-bore venous access for fluid and blood administration, as well as vasoactive drug infusions. Although central venous pressure (CVP) monitoring poorly predicts fluid responsiveness, this provides supplemental data regarding intravascular volume status [9]. (See "Intraoperative fluid management", section on 'Traditional static parameters'.)

If equipment and expertise are available, intraoperative TEE may be helpful for major vascular, orthopedic or abdominal procedures, particularly for urgent or emergent surgery in a patient with known severe AS or if severity is unknown. Significant AS is suggested by heavily calcified or poorly mobile aortic valve leaflets on TEE images (image 1 and image 2). Volume status, vascular resistance, and ventricular function can be continuously monitored during surgery. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Assessment of aortic stenosis'.)

●Induction – Induction agents and doses are selected to reduce the likelihood of hypotension, while establishing anesthetic depth adequate to minimize sympathetic stimulation and avoid tachycardia during laryngoscopy and endotracheal intubation. For patients with moderate to severe AS with or without systolic LV dysfunction, etomidate 0.2 to 0.3 mg/kg is typically selected to maintain hemodynamic stability. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate'.)

Propofol is a reasonable alternative in patients with preserved ventricular function (LV ejection fraction ≥50 percent); an initial low dose of 0.5 to 1 mg/kg is administered, and additional propofol may be titrated to effect. Administration of a high initial dose of propofol (eg, >1.5) is avoided as this may decrease systemic vascular resistance (SVR). (See "General anesthesia: Intravenous induction agents", section on 'Propofol'.)

Ketamine is avoided for induction of anesthesia since bolus administration typically causes tachycardia. (See "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

Synthetic opioids such as fentanyl provide hemodynamic stability during induction. For cases expected to last more than three hours, administration of a relatively large dose of an opioid is an option during induction (eg, fentanyl 5 to 10 mcg/kg). For cases of short duration, an option is administration of the ultrashort-acting opioid remifentanil as a supplemental agent during and after induction in a dose of 1 to 2 mcg/kg (or ≤1 mcg/kg in older patients). Remifentanil reduces the risk of tachycardia without risk of prolonged respiratory depression. (See "General anesthesia: Intravenous induction agents", section on 'Opioids'.)

●Maintenance – We prefer a combined inhalational and IV opioid anesthetic technique for maintenance of anesthesia, with administration of a neuromuscular blocking agent (NMBA) if necessary to facilitate the surgical procedure.

Any of the volatile anesthetic agents may be used and titrated to the desired effect. Advantages of volatile anesthetics include possible cardioprotective effects [10-12], although these are unlikely to be clinically significant during noncardiac surgery [13]. High doses of volatile anesthetic agents are avoided due to the potential for vasodilation, myocardial depression, and hypotension. (See "Maintenance of general anesthesia: Overview", section on 'Volatile inhalation agents'.)

Fentanyl is a reasonable choice for the opioid component of a combined technique, and can be administered either as bolus doses of 50 to 100 mcg, or as a continuous infusion at 1 to 2 mcg/kg/hour. An alternative is remifentanil administered as a continuous infusion at 0.2 to 1 mcg/kg/minute (typically after a 1 mcg/kg loading dose). If remifentanil is selected, a longer-acting opioid should be administered shortly before or after extubation to ensure adequate analgesia during recovery from anesthesia.

●Emergence – Weaning of mechanical ventilation and emergence from anesthesia should be controlled to avoid deleterious hemodynamic changes. Tachycardia due to pain or reflex airway responses to the endotracheal tube may result in hemodynamic deterioration. Thus, tachycardia is avoided or treated during emergence by planning analgesic techniques and administering additional titrated doses of fentanyl 25 to 50 mcg IV. Small IV doses of esmolol 20 to 30 mg, labetalol 2.5 to 5 mg, or metoprolol 2.5 to 5 mg may also be administered if necessary to control tachycardia.

MITRAL STENOSIS — Severe mitral stenosis (MS) causes impaired left ventricular (LV) filling due to obstruction of left atrial (LA) outflow. LA pressure, pulmonary artery pressure (PAP), and pulmonary artery wedge pressure (PAWP) are increased. Patients with chronic MS typically have increased pulmonary vascular resistance (PVR) and [2]. Prevalence, etiology, pathophysiology, clinical manifestations, and stages of chronic MS severity are discussed separately (table 7) [1]. (See "Pathophysiology and natural history of mitral stenosis" and "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

Patients with unrepaired MS should be medically optimized before proceeding with elective noncardiac surgery. This includes adequate control of heart rate (HR) and management of volume overload. Details regarding preoperative medical assessment and management of a patient with MS before noncardiac surgery are discussed separately. (See "Rheumatic mitral stenosis: Overview of management", section on 'Management of noncardiac surgery'.)

Hemodynamic management — Key points for perioperative hemodynamic goals and anesthetic management of patients with MS are summarized in the table (table 8). (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Mitral stenosis'.)

Anesthetic management — The choice of anesthetic techniques and agents is based on requirements for accomplishing the surgical procedure, as well as hemodynamic goals for MS [6].

Sedation with monitored anesthesia care — Management of monitored anesthesia care (MAC) with or without a peripheral nerve block is similar to that for patients with AS. (See 'Sedation with monitored anesthesia care' above.)

It is particularly important to avoid oversedation with consequent hypoventilation. In a patient with pre-existing pulmonary hypertension, hypoxemia and/or hypercapnia may acutely increase PVR, with resultant exacerbation of RV dysfunction and rapid progression to hemodynamic collapse [2].

Neuraxial anesthesia — For appropriate surgical procedures, a very slowly titrated epidural technique can be safely employed in most patients with moderate MS. Management of a neuraxial technique is similar to that for patients with AS, including insertion of an intra-arterial catheter to monitor BP during and after placement of a neuraxial needle or catheter. (See 'Neuraxial anesthesia' above.)

General anesthesia — Management of general anesthesia is similar to that for patients with AS (see 'General anesthesia' above), with the following specific points:

●Monitoring – An intra-arterial catheter is inserted before induction for continuous monitoring of BP.

During major surgical procedures, central venous pressure (CVP) is typically monitored to provide an estimate of right-sided heart pressures, as an aid to avoiding excessive fluid administration and consequent pulmonary edema. Awake patients with severe MS and dyspnea at rest may not tolerate a Trendelenburg position or even lying flat during attempts to insert a central venous catheter (CVC). For this reason, we typically insert the CVC after general anesthesia has been induced, with endotracheal intubation and controlled mechanical ventilation established.

If equipment and expertise are available, intraoperative TEE may be helpful in a patient with known MS when a major vascular, orthopedic or abdominal procedure is planned, particularly if surgery is urgent or emergent and the severity of MS is uncertain. Significant MS is suggested by a thickened valve with reduced leaflet opening (movie 1), as well as a high-velocity aliased LV inflow on color-flow Doppler imaging (image 3 and image 4). During surgery, volume status, vascular resistance, and both LV and RV function are continuously monitored. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Assessment of mitral stenosis'.)

●Induction – Similar to patients with AS, it is reasonable to use etomidate 0.2 to 0.3 mg/kg for induction in patients with severe MS to maintain hemodynamic stability while avoiding tachycardia. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate'.)

If necessary, an opioid or other supplemental agents may be administered just before and during laryngoscopy and endotracheal intubation to avoid or treat tachycardia. Examples include fentanyl 1 to 2 mcg/kg, or the ultra-short-acting opioid remifentanil in a dose of 1 to 2 mcg/kg (or ≤1 mcg/kg in an older patient) may be selected to avoid risk of prolonged respiratory depression. A beta blocker (eg, esmolol 20 to 30 mg IV, labetalol 2.5 to 5 mg, or metoprolol 2.5 to 5 mg) is administered if necessary to control increases in HR. (See "General anesthesia: Intravenous induction agents", section on 'Opioids'.)

Propofol is a reasonable alternative. An initial dose of 0.5 to 1 mg/kg is administered, and additional propofol is titrated to effect. However, high doses of propofol that may decrease systemic vascular resistance (SVR) are avoided. (See "General anesthesia: Intravenous induction agents", section on 'Propofol'.)

Ketamine is avoided because an induction dose typically causes tachycardia. (See "General anesthesia: Intravenous induction agents", section on 'Ketamine'.)

●Maintenance – Similar to patient with AS, we prefer a technique that combines a volatile inhalational anesthetic and an intravenous opioid for maintenance of anesthesia. We avoid nitrous oxide since this agent may further increase PVR [14]. A neuromuscular blocking agent (NMBA) is administered to facilitate the surgical procedure and/or mechanical ventilation if necessary.

●Emergence – Hypoxemia and hypercarbia are minimized during emergence to avoid exacerbating pulmonary hypertension. Emergence techniques are discussed separately. (See "Maintenance of general anesthesia: Overview", section on 'Transition to the emergence phase'.)

AORTIC REGURGITATION — Severe chronic aortic regurgitation (AR) causes ongoing volume overload of the left ventricle (LV) with eccentric LV dilation. Although biventricular function typically remains intact in patients with moderate to severe AR, dilated cardiomyopathy may be present in advanced stages, with decreased myocardial contractility and cardiac output (CO) and increased left atrial (LA) and pulmonary artery pressures (PAP) [15]. Prevalence, etiology, pathophysiology, clinical manifestations, and stages of chronic AR severity are discussed separately (table 9) [1]. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

Preoperative medical assessment and management considerations for a patient with chronic AR before noncardiac surgery are addressed separately. (See "Noncardiac surgery in patients with mitral or aortic regurgitation", section on 'Chronic aortic regurgitation'.)

Hemodynamic management — Key points for perioperative hemodynamic goals and anesthetic management of patients with AR are summarized in the table (table 10). (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Aortic regurgitation'.)

Anesthetic management — The choice of anesthetic techniques and agents is based on requirements for accomplishing the surgical procedure, as well as hemodynamic goals for AR [6].

Sedation with monitored anesthesia care — Management of monitored anesthesia care (MAC) with or without a peripheral nerve block is similar to that for patients with aortic stenosis (AS). (See 'Sedation with monitored anesthesia care' above.)

Neuraxial anesthesia — Gradual afterload reduction that occurs with standard dosing of neuraxial anesthesia is beneficial to decrease the regurgitant volume through the aortic valve. Both epidural and spinal anesthesia are generally well tolerated. Invasive blood pressure monitoring with an intra-arterial catheter is not typically necessary.

General anesthesia — General anesthesia may be selected because of the type of surgical procedure or patient choice. Combining general anesthesia with a neuraxial technique may be beneficial to avoid sympathetic stimulation and hypertension due to intraoperative and/or postoperative pain.

●Monitoring – An intra-arterial catheter is not typically inserted, unless the patient has dilated cardiomyopathy with reduced LV systolic function or moderate to severe pulmonary hypertension [2].

A central venous catheter (CVC) is not typically inserted to monitor volume status, but may be employed for administration of vasoactive drug infusions or to provide access for fluid and blood administration during major surgery with large fluid shifts or potential for significant bleeding.

If equipment and expertise are available, intraoperative transesophageal echocardiography (TEE) may be helpful in a patient with known AR when a major vascular, orthopedic, or abdominal procedure is planned, particularly if surgery is urgent or emergent and the severity of AR is uncertain. Severity of AR is estimated with color-flow Doppler by examination of the largest jet width in the left ventricular outflow tract (LVOT) (movie 2 and movie 3). Volume status, vascular resistance, degree of regurgitation, and both left and right ventricular function can be continuously monitored during surgery. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Assessment of aortic regurgitation'.)

●Induction – Induction agents and doses are selected to reduce or maintain a low normal systemic vascular resistance (SVR) to minimize regurgitant flow, while maintaining adequate cardiac output and myocardial oxygen delivery. We prefer induction with slowly titrated propofol 1 to 2 mg/kg because of its ability to reduce SVR. Propofol may be combined with adjuvant agents to minimize sympathetic stimulation and resultant hypertension during laryngoscopy and endotracheal intubation. (See "General anesthesia: Intravenous induction agents", section on 'Propofol' and "General anesthesia: Intravenous induction agents", section on 'Adjuvant agents'.)

For patients with significant stage C2 or stage D cardiomyopathy (see 'Preanesthesia consultation' above), induction with etomidate 0.2 to 0.3 mg/kg is a reasonable alternative to maintain hemodynamic stability. (See "General anesthesia: Intravenous induction agents", section on 'Etomidate'.)

●Maintenance – We prefer a potent volatile inhalation agent to maintain anesthesia because of beneficial vasodilatory effects that reduce afterload and decrease aortic regurgitant volume. Any of the volatile agents may be used as the primary anesthetic and titrated to the desired effect. High doses of volatile agents are avoided due to the potential for myocardial depression and resultant hypotension. Opioids and/or other adjuvant agents may be administered as needed. (See "Maintenance of general anesthesia: Overview", section on 'Volatile inhalation agents'.)

Intraoperative hypertension due to sympathetic responses to noxious surgical stimuli is initially treated by increasing anesthetic depth (eg, increasing concentration of the volatile anesthetic, administration of additional opioid boluses such as fentanyl 1 to 2 mcg/kg, small boluses of propofol 0.25 to 0.5 mg/kg). In addition to ensuring adequate anesthetic depth, an infusion of an intravenous inodilator or vasodilator agent may be administered if necessary (eg, milrinone, calcium channel blocker, nitroglycerin, nitroprusside) (table 11).

●Emergence – Weaning from controlled mechanical ventilation and emergence from anesthesia are gradual. Adequate analgesia should be ensured. Sympathetic stimulation caused by pain or airway responses to the endotracheal tube during emergence increase SVR and may cause hemodynamic deterioration. If necessary, hypertension is treated with small IV bolus doses of labetalol, hydralazine, nitroglycerin, nicardipine, or clevidipine (table 11).

MITRAL REGURGITATION

Primary MR versus secondary MR

Primary MR — Primary mitral regurgitation (MR) causes chronic volume overload of the left atrium (LA) accompanied by elevated LA pressure, LA enlargement, and atrial dysrhythmias (typically, atrial fibrillation [AF]). Pulmonary vascular resistance (PVR) and pulmonary artery pressure (PAP) may be significantly increased if MR is severe. Similar to chronic aortic regurgitation (AR), the left ventricle (LV) experiences chronic volume overload. LV ejection fraction typically overestimates actual LV contractile state because a portion of each ejection volume flows into the low-pressure LA chamber rather than against the high impedance of the aorta [15]. Thus, if preoperative estimates of LV ejection fraction are reduced, it is likely that significant ventricular dysfunction is present.

Prevalence, etiology, pathophysiology, clinical manifestations, and stages of chronic mitral regurgitation (MR) severity are discussed separately (table 12) [1]. (See "Clinical manifestations and diagnosis of chronic mitral regurgitation".)

Preoperative medical assessment and management considerations for a patient with possible or known MR before noncardiac surgery are addressed separately. (See "Noncardiac surgery in patients with mitral or aortic regurgitation", section on 'Chronic mitral regurgitation'.)

Secondary MR associated with ischemic heart disease — Secondary functional mitral regurgitation (MR) may be due to chronic postinfarction MR or reversible MR caused by acute ischemia in patients with coronary artery disease. Thus, anesthetic considerations include management of the underlying ischemic heart disease, as well as considerations for MR. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Anesthetic goals'.)

Secondary MR associated with hypertrophic cardiomyopathy — Dynamic mitral regurgitation (MR) may occur in a patient with hypertrophic cardiomyopathy (HCM) accompanied by LV outflow tract (LVOT) obstruction [16]. Hemodynamic goals and anesthetic management are substantially different for these patients compared with those with primary MR or secondary functional MR. Details are available in the table and in a separate topic (table 13). (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery".)

Hemodynamic management — Key points for hemodynamic goals and anesthetic management of patients with primary MR are similar to those for AR (see 'Aortic regurgitation' above), as summarized above and in the table (table 10). In contrast, hemodynamic goals are distinctly different for management of secondary MR associated with ischemic heart disease, as summarized below and in the tables (table 14 and table 15). (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Mitral regurgitation'.)

Anesthetic management — The choice of anesthetic techniques and agents is based on requirements for accomplishing the surgical procedure, as well as the hemodynamic goals for primary MR or similar goals for secondary MR associated with ischemic heart disease. Pain-induced tachycardia and hypertension are avoided. Hypertension with increased systemic vascular resistance (SVR) exacerbates both MR and myocardial ischemia, and tachycardia also exacerbates ischemia (table 10 and table 14).

Sedation with monitored anesthesia care — Management of monitored anesthesia care (MAC) with or without a peripheral nerve block for patients with primary MR due to any etiology is similar to that for patients with AS, MS, or ischemic heart disease. It is particularly important to avoid oversedation with consequent hypoventilation, hypoxemia, and hypercapnia, in order to prevent increases in PVR or exacerbation of ischemia. (See 'Sedation with monitored anesthesia care' above and "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Local anesthesia with monitored anesthesia care'.)

Neuraxial anesthesia — For patients with primary or ischemic MR, gradual afterload reduction with neuraxial anesthesia is beneficial to decrease MR severity. However, some patients with MR undergo aggressive diuresis in the preoperative period and may develop hypotension immediately after placement of a neuraxial block. This is managed with incremental fluid boluses of 100 to 250 mL, and with small bolus doses of ephedrine 5 to 10 mg and/or phenylephrine 40 to 100 mcg. Other aspects of management of a neuraxial technique are similar to those for patients with AR. (See 'Neuraxial anesthesia' above.)

General anesthesia — Management of general anesthesia is generally similar to that for patients with AR or ischemic heart disease, including considerations for monitoring, induction, maintenance, and emergence. (See 'General anesthesia' above and "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'General anesthesia'.)

An intra-arterial catheter may be placed for major procedures in patients with fluid overload and pulmonary congestion. Monitoring with TEE may be helpful in a patient with known MR if a major vascular, orthopedic or abdominal procedure is planned, particularly if unstable myocardial ischemia is present or if the severity of MR is uncertain. MR severity is qualitatively estimated with color-flow Doppler to assess regurgitant jet size and eccentricity of the jet (image 5). Volume status, vascular resistance, degree of regurgitation, and both right and left regional and global ventricular function can be continuously monitored during surgery. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Regional LV systolic function' and "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Assessment of mitral regurgitation'.)

PATIENTS WITH COMBINED VALVE LESIONS — Although each cardiac valve lesion is assessed individually, patients may have a combination of stenosis and regurgitation in a single cardiac valve, or disease of more than one valve. Optimal management depends on which of the valvular lesions is predominant and which hemodynamic changes are likely to be most deleterious (table 16). Anesthetic techniques, agents, and vasoactive drugs are selected to achieve appropriate hemodynamic goals. A reasonable approach for a patient who is hemodynamically stable and compensated in the preoperative period is to target preoperative heart rate (HR) and blood pressure (BP) values as a goal during surgery. (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

SUMMARY AND RECOMMENDATIONS

●Preanesthetic consultation – The preanesthetic consultation for patients with valvular heart disease (VHD) includes working with the cardiologist and surgeon to optimize medical conditions and developing an anesthetic care plan to provide appropriate hemodynamic conditions (eg, selection of anesthetic techniques, monitors, vasoactive agents). (See 'Preanesthesia consultation' above.)

●Preoperative medication management – Chronically administered cardiovascular and antiarrhythmic agents, as well as medications that minimize pulmonary vascular resistance, are typically continued in the perioperative period. Patients with chronic atrial fibrillation may be receiving anticoagulant therapy; management balances thromboembolic risk and bleeding risk to determine optimal timing of anticoagulant interruption. (See 'Preoperative medication management' above.)

●Anesthetic management for specific valve lesions – Anesthetic considerations and hemodynamic management goals for the following VHD lesions are shown in tables:

•Aortic stenosis (AS) (table 4) (see 'Aortic stenosis' above)

•Mitral stenosis (MS) (table 8) (see 'Mitral stenosis' above)

•Aortic regurgitation (AR) (table 10) (see 'Aortic regurgitation' above)

•Mitral regurgitation (MR) (see 'Mitral regurgitation' above):

-Primary mitral regurgitation (table 10) (see 'Primary MR' above)

-Secondary mitral regurgitation associated with ischemic heart disease (table 10 and table 14) (see 'Secondary MR associated with ischemic heart disease' above)

-Secondary mitral regurgitation associated with hypertrophic cardiomyopathy (table 13) (see "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery")

●Considerations for combined valve lesions – Although each cardiac valve lesion is assessed individually, patients may have a combination of stenosis and regurgitation in a single cardiac valve, or disease of more than one valve. Optimal management of anesthetic techniques, agents, and vasoactive drugs depends on which of the valvular lesions is predominant and which hemodynamic changes are likely to be most deleterious. (See 'Patients with combined valve lesions' above.)