Intraoperative hemodynamic management of aortic or mitral valve disease in adults

INTRODUCTION — Risk for development of 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 perioperative hemodynamic management for patients with aortic or mitral valve lesions. Among patients with VHD, patients with severe valve lesions, particularly those with severe AS, are at greatest risk for adverse perioperative cardiovascular events. 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 AS and aortic regurgitation [AR]), or concomitant heart failure or ischemic heart disease.

Additional anesthetic considerations for noncardiac surgery in patients with these comorbidities are addressed separately. (See "Intraoperative management for noncardiac surgery in patients with heart failure" and "Anesthesia for noncardiac surgery in patients with ischemic heart disease".)

Other anesthetic considerations for patients with aortic or mitral valve disease who are undergoing cardiac or noncardiac surgery are discussed in separate topics.

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

●(See "Anesthesia for noncardiac surgery in patients with aortic or mitral valve disease".)

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

AORTIC STENOSIS — Severe aortic stenosis (AS) poses substantial risks for maintenance of perioperative hemodynamic stability [1]. Key points for perioperative hemodynamic management of patients with AS are described below and summarized in the table (table 2).

Heart rhythm — Maintenance of sinus rhythm (SR) is particularly important in patients with AS because filling of the hypertrophic noncompliant left ventricle (LV) depends significantly on left atrial contraction (atrial "kick") during end-diastole. Loss of atrioventricular (AV) synchrony may result in severe hypotension. Examples include supraventricular tachyarrhythmia (SVT) such as atrial fibrillation (AF) or flutter, or AV dissociation such as junctional rhythm or ventricular pacing. Hypotension occurs due to markedly reduced LV filling, which reduces stroke volume (SV) and cardiac output (CO).

New onset of AF or other SVT is rapidly treated to restore SR, as well as to control ventricular rate. In a hemodynamically stable patient, treatment with short-acting drugs such as esmolol or diltiazem may be adequate. In a hemodynamically unstable patient with severe hypotension or evidence of cardiogenic shock, synchronized cardioversion may be necessary to restore SR. During preparations for urgent cardioversion, systemic blood pressure (BP) is maintained with vasoconstrictors (eg, phenylephrine or norepinephrine). (See "Arrhythmias during anesthesia", section on 'Other narrow QRS complex atrial tachyarrhythmias'.)

A junctional rhythm with loss of atrial kick may occur during administration of a volatile inhalation agent or other anesthetics [2-5]. Attempts to restore SR include decreasing the dose of inhalation anesthetic while maintaining systemic BP with administration of phenylephrine, ephedrine, or norepinephrine.

If severe hypotension persists despite treatment of the arrhythmia in a patient undergoing cardiac surgery, cardiopulmonary bypass is initiated as rapidly as possible. Nonperfusing arrhythmias are particularly dangerous in patients with AS due to limited effectiveness of chest compressions during resuscitation efforts. Perfusion to the brain and other end-organs may be inadequate because the stenotic aortic valve obstructs LV outflow.

Heart rate — Maintain heart rate (HR) in the low to normal range (eg, 60 to 80 beats per minute [bpm]) in patients with AS; the target range may be adjusted based upon the patient's baseline HR. Tachycardia may compromise LV filling or lead to myocardial ischemia, while bradycardia may result in inadequate CO with compromise of vital organ perfusion.

●Prevention and management of tachycardia – Prevent tachycardia by ensuring adequate volume status and adequate depth of anesthesia and perioperative analgesia. A rapid HR results in inadequate oxygen delivery to the hypertrophied myocardium due to the decrease in diastolic filling time (figure 2). Myocardial ischemia can occur, particularly in patients with coexisting coronary artery disease (table 3). (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)

Sinus tachycardia due to noxious surgical stimuli is treated by increasing anesthetic depth (eg, increasing concentration of volatile or intravenous (IV) anesthetic agents or administration of additional opioid). If other causes of tachycardia such as hypovolemia and anemia have been excluded and tachycardia persists, an IV beta blocker (eg, esmolol as a bolus dose of 20 to 30 mg and/or by continuous infusion, or metoprolol in 2.5 to 5 mg increments [or lower incremental doses for small or frail patients]) may be administered to control HR. (See "Arrhythmias during anesthesia", section on 'Sinus tachycardia'.)

As noted above, if tachycardia is due to AF with rapid ventricular response, ventricular rate control should be achieved, whether or not SR is restored. (See 'Heart rhythm' above and "Arrhythmias during anesthesia", section on 'Other narrow QRS complex atrial tachyarrhythmias'.)

●Management of bradycardia – Treat bradycardia by administering IV bolus doses of ephedrine 5 to 10 mg and/or small doses of epinephrine (eg, 4 to 10 mcg). Use of anticholinergic agent (glycopyrrolate 0.2 mg or atropine 0.4 mg) can be ineffective and/or have inconsistent responses in patients with AS since patients with AS are at risk for conduction disease below the AV node [6]. Causes should be identified and treated (table 4). (See "Arrhythmias during anesthesia", section on 'Bradyarrhythmias' and "Arrhythmias during anesthesia", section on 'Pharmacologic treatment of bradycardia'.)

Severe bradycardia typically results in inadequate CO with hypotension in patients with severe AS because they cannot compensate for low HR by increasing SV through the stenotic aortic valve. For hemodynamically unstable patients, temporizing measures include continuous infusion of an adrenergic agonist (eg, epinephrine, dopamine, or dobutamine) or temporary transcutaneous pacing. Patients with recurrent or severe bradycardia causing hemodynamic instability may require transvenous pacing via insertion of a pacing catheter inserted into a central venous catheter or a pulmonary artery catheter with pacing capability. (See "Arrhythmias during anesthesia", section on 'Pharmacologic treatment of bradycardia' and "Arrhythmias during anesthesia", section on 'Temporary pacing options'.)

Expert cardiology (ie, electrophysiology) consultation is sought to assist with management of persistent or recurrent severe bradycardia and the potential need for permanent pacing.

Preload (intravascular volume) — Maintain adequate intravascular volume (ie, preload) to preserve adequate SV and CO, while avoiding volume overload.

Hypovolemia should be promptly identified and treated. Fluid boluses are titrated according to clinical assessment of volume status and the patient's hemodynamic response. If an intra-arterial catheter and/or transesophageal echocardiography (TEE) probe have been inserted, we employ a goal-directed approach to fluid therapy, using dynamic parameters to assess intravascular volume status, guide fluid administration during treatment of hypovolemia, and avoid hypervolemia and pulmonary edema (figure 3 and movie 1). As a temporary measure, changing patient position to mild Trendelenburg may augment preload in patients with hypotension. (See "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)

Afterload (systemic vascular resistance) — Maintain systolic BP at >100 mmHg, mean arterial pressure (MAP) >70 mmHg, or both within 20 percent of baseline. Although afterload is chronically increased in patients with AS, sudden reductions in systemic vascular resistance (SVR) may result in decreased diastolic BP, with decreased coronary perfusion and consequent myocardial ischemia.

Hypotension should be prevented and/or treated promptly. An alpha-adrenergic vasoconstrictor such as phenylephrine may be administered as bolus doses of 40 to 100 mcg or by continuous infusion. If phenylephrine is ineffective, norepinephrine or vasopressin may be administered (table 5). These vasoconstrictors increase SVR without the chronotropic side effects associated with sympathomimetic vasoactive agents such as epinephrine, dopamine, or dobutamine. If hypovolemia is suspected, fluids are also administered as described above. (See 'Preload (intravascular volume)' above.)

Hypertension may also aggravate ischemia should also be prevented by ensuring adequate depth of anesthesia and perioperative analgesia. Severe or persistent hypertension should be controlled. For hypertension accompanied by an increased HR, a beta blocker may be administered (eg, esmolol in small bolus doses of 20 to 30 mg and/or by continuous infusion, or metoprolol in 2.5 to 5 mg increments [or lower incremental doses for small or frail patients]) (table 6). Other antihypertensive agents should be administered with caution (ie, titrated slowly in incremental doses) as need for adequate BP control. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)

Contractility — Avoid doses of anesthetic agents that might cause significant depression of myocardial contractility (eg, high doses of propofol or volatile inhalation anesthetic agents). Although biventricular function is typically preserved in patients with moderate to severe AS, LV ejection fraction may be lower than normal (due to the afterload excess imposed by the stenotic valve rather than intrinsic LV contractile dysfunction) [7-9]. If inotropic support is needed, norepinephrine is preferred unless there is coexisting bradycardia (table 5). Other agents with stronger inotropy and chronotropy (eg, epinephrine) may cause tachycardia and increase myocardial oxygen demand leading to myocardial ischemia.

MITRAL STENOSIS — Key points for perioperative hemodynamic management of patients with mitral stenosis (MS) are described below and summarized in the table (table 7).

Heart rate — Maintain a slow to normal heart rate (HR) at 50 to 70 beats per minute (bpm).

Avoid tachycardia. Any tachyarrhythmia (eg, sinus tachycardia or atrial fibrillation [AF] with rapid ventricular response) can result in severe hypotension and pulmonary edema due to shortening of the diastolic period (figure 2), with inadequate time for blood to flow from the left atrium (LA) into the left ventricle (LV) through the stenotic mitral valve. This decrease in LV filling, stroke volume (SV), and cardiac output (CO) leads to hypotension, while the increase in LA pressure leads to pulmonary edema.

Although a relatively slow HR is optimal, CO is partially dependent on maintenance of an adequate HR. Severe bradycardia should be avoided as the limited flow across the stenotic mitral valve limits LV filling and SV. Pharmacologic agents for severe bradycardia associated with hypotension include atropine, glycopyrrolate or ephedrine. (See "Arrhythmias during anesthesia", section on 'Pharmacologic treatment of bradycardia'.)

Heart rhythm — Although sinus rhythm (SR) is preferred, many patients with MS have chronic AF because of left atrial dilation. The presence of AF is less important for patients with MS than those with aortic stenosis (AS) because there is less dependence on end-diastolic LA contraction (atrial "kick") to achieve adequate LV filling. However, regardless of rhythm, the ventricular rate must remain well controlled. Thus, onset of AF with rapid ventricular response warrants urgent rate control. Clinical settings in which urgent or emergency cardioversion to SR may be required include evidence of acute myocardial ischemia, evidence of organ hypoperfusion or shock, severe heart failure, and severe refractory hypotension despite therapies including volume repletion and attempted rate control. The risks and benefits of cardioversion should be weighed since patients with significant MS who are cardioverted to SR may soon revert to AF. Also, patients with MS and AF are at risk for thromboembolism. Thus, evaluation with transesophageal echocardiography (TEE) to exclude left atrial thrombus is generally necessary prior to urgent intraoperative cardioversion, even if anticoagulants have been chronically administered. (See "Anesthesia for cardiac valve surgery", section on 'Prebypass TEE assessment' and "Atrial fibrillation in patients undergoing noncardiac surgery", section on 'Intraoperative atrial fibrillation' and "Rheumatic mitral stenosis: Overview of management", section on 'Prevention of thromboembolism' and "Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation" and "Atrial fibrillation: Cardioversion" and "Rheumatic mitral stenosis: Overview of management", section on 'Management of atrial fibrillation'.)

Preload (intravascular volume) — Maintain intravascular volume (ie, preload) to preserve adequate SV and CO.

Fluid boluses are titrated according to clinical assessment of intravascular volume status, and the hemodynamic response to each incremental bolus of 100 to 250 mL is assessed. Because of obstructed flow from the LA to the LV, aggressive fluid administration may result in increased LA pressure and pulmonary congestion. If an intra-arterial catheter and/or TEE probe have been inserted, we employ a goal-directed approach to fluid therapy (figure 3 and movie 1), similar to management of AS. (See 'Preload (intravascular volume)' above and "Intraoperative fluid management", section on 'Dynamic parameters to assess volume responsiveness'.)

Afterload (systemic vascular resistance) — Maintain systolic blood pressure (BP) >100 mmHg, mean arterial pressure (MAP) >70 mmHg, or both within 20 percent of baseline. Maintenance of systemic vascular resistance (SVR) is important since the presence of MS interferes with normal compensatory responses to hypotension (ie, SV cannot be substantially increased and a slow HR must be maintained).

When hypotension is presumed to be caused by decreased SVR, it should be treated with an alpha-adrenergic vasoconstrictor such as phenylephrine, administered as bolus doses of 40 to 100 mcg or as an infusion (table 5). If phenylephrine is ineffective, a norepinephrine or vasopressin infusion may be administered.

It is rarely necessary to treat hypertension, since the obstruction to transmitral flow limits CO and usually prevents development of high BP.

Contractility — Avoid doses of drugs that might cause significant depression of LV or right ventricular (RV) contractility (eg, high doses of propofol or volatile inhalation anesthetic agents).

Although most patients with advanced MS have preserved LV systolic function, RV function is often impaired. Avoiding further RV depression is particularly important in patients with significant pulmonary hypertension (PH). If inotropic support is necessary, the inodilator milrinone is typically selected because it increases SV via a combination of peripheral dilation and enhanced contractility and has pulmonary vasodilating effects (table 5). However, a low-dose epinephrine infusion is a reasonable alternative for hypotensive patients.

Pulmonary vascular resistance — Avoid hypoxemia, hypercarbia, and metabolic acidosis, which increase PVR. These are particularly detrimental in patients with severe MS because exacerbation of pre-existing PH may cause acute RV failure.

AORTIC REGURGITATION — Key points for perioperative hemodynamic management of patients with aortic regurgitation (AR) are described below and summarized in the table (table 8).

Heart rate — In contrast to the management of patients with aortic or mitral stenosis (MS), maintain a normal to fast heart rate (HR) of 80 to 95 beats per minute (bpm) in patients with AR. A faster HR limits the duration of diastole when aortic valvular regurgitation is occurring; thus, regurgitant volume is reduced.

Avoid bradycardia because this increases the regurgitant fraction. A slow HR associated with hypotension is treated with bolus doses of ephedrine 5 to 10 mg. Atropine 0.4 mg may also be administered and/or a low-dose infusion of epinephrine, dopamine, or dobutamine may be initiated (table 5).

Heart rhythm — Although sinus rhythm (SR) is preferred, supraventricular tachyarrhythmia (SVT) will be better tolerated in patients with AR than in those with aortic stenosis (AS) or MS. However, if hemodynamic instability develops and HR cannot be controlled pharmacologically, synchronized cardioversion is used to restore SR.

Afterload (systemic vascular resistance) — Prevent significant increases in systemic vascular resistance (SVR) by maintaining a low to normal systolic blood pressure (BP) of approximately 100 to 120 mmHg, or within 20 percent of baseline. Maintaining a low SVR enhances forward flow during systole and may reduce the regurgitant fraction.

Mild hypotension is typically well tolerated in patients with AR. However, the pulse pressure may be large and diastolic BP may be very low; therefore, we typically follow mean arterial pressure (MAP) as well as systolic BP. Significant hypotension or a very low diastolic BP in patients with concomitant coronary artery disease is treated with bolus doses of an agent that increases contractility (eg, ephedrine).

Avoid and promptly treat hypertension since increased SVR increases regurgitant flow and decreases forward flow. Elevations in MAP are prevented by ensuring continuation of chronically administered antihypertensive medications, adequate depth of intraoperative anesthesia, and effective postoperative analgesia. If necessary, a vasodilator (eg, calcium channel blocker, nitroprusside) may be infused to decrease MAP and SVR (table 5 and table 6).

Preload (intravascular volume) — Maintain preload while attempting to avoid excessive volume administration. The goal is to maintain adequate intravascular volume without precipitating fluid overload and pulmonary congestion. In patients with preexisting heart failure, a restrictive (zero balance) fluid strategy is typically employed. (See "Intraoperative fluid management", section on 'Restrictive (zero-balance) strategy'.)

Contractility — Avoid doses of drugs that might cause significant depression of myocardial contractility (eg, high doses of propofol or volatile anesthetic agents).

If necessary to treat hypotension in a patient with severe chronic AR and heart failure, continuous infusion of an inodilator that increase stroke volume (SV) via a combination of peripheral dilation and enhanced contractility is typically selected (eg, a phosphodiesterase inhibitor such as milrinone and/or a beta adrenergic inotropic agent such as dobutamine) (table 5). In some patients, addition or substitution of a low-dose epinephrine infusion may be necessary to maintain adequate BP.

MITRAL REGURGITATION — Key points for perioperative hemodynamic management of patients with primary mitral regurgitation (MR) are similar to those for aortic regurgitation (AR) (table 8).

Hemodynamic considerations are somewhat different for patients with secondary MR due to ischemic heart disease or nonischemic heart disease (dilated cardiomyopathy), as described below and in the table (table 9).

Hemodynamic considerations for patients with MR secondary to hypertrophic cardiomyopathy with systolic anterior motion of the mitral valve leaflets are discussed in a separate topic (table 10). (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery", section on 'Hemodynamic goals and management'.)

Heart rate

●Primary MR – For patients with primary MR, maintain a normal to fast heart rate (HR) of 80 to 95 beats per minute (bpm) to reduce regurgitation into the left atrium (LA) during systole. However, excessive tachycardia (eg, due to poorly controlled ventricular rate in a patient with atrial fibrillation [AF]) is avoided.

Avoid bradycardia. Bradycardia associated with hypotension is treated with bolus doses of ephedrine 5 to 10 mg. If ineffective, atropine 0.4 mg may be administered, and a low-dose infusion of epinephrine, dopamine, or dobutamine may be initiated (table 5). (See "Arrhythmias during anesthesia", section on 'Sinus bradycardia'.)

●Secondary MR – For patients with secondary MR due to ischemic heart disease, a slower HR of 55 to 80 bpm is generally optimal to reduce the risk of provoking ischemia (table 3), while those with secondary MR due to heart failure with reduced ejection fraction may have a lower HR due to preoperative treatment with a beta blocker and/or renin-angiotensin system blocker (table 9).

Dynamic secondary MR associated with hypertrophic cardiomyopathy accompanied by left ventricular (LV) outflow tract obstruction is summarized in the table (table 10), and is discussed in a separate topic. (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery".)

Heart rhythm — Although sinus rhythm (SR) is preferred, many patients with chronic primary MR have AF because of dilation of the LA. A supraventricular tachyarrhythmia (SVT) such as AF will be better tolerated in patients with primary MR than in those with aortic stenosis (AS) or mitral stenosis (MS). However, sudden onset of SVT with a rapid ventricular response may result in hemodynamic instability requiring pharmacologic rate control or cardioversion.

Afterload (systemic vascular resistance) — Control of hypertension is important in patients with MR as elevated blood pressure (BP) may worsen regurgitant flow into the LA and decrease cardiac output (CO). Prevention and treatment of hypertension are similar to management of patients with AR. (See 'Afterload (systemic vascular resistance)' above.)

●Primary MR – Prevent significant increases in systemic vascular resistance (SVR) by maintaining a low to normal systolic BP of approximately 100 to 120 mmHg, or within 20 percent of baseline.

●Secondary MR – For patients with secondary MR, management of BP is particularly challenging. Adequate BP is necessary to maintain adequate coronary perfusion pressure and myocardial oxygen supply during diastole (table 3). However, acute increases in systolic BP are avoided or treated since these may increase regurgitant flow into the LA and decrease forward flow, and may also increase myocardial oxygen demand. A reasonable approach is to maintain systemic BP close to preoperative values throughout the perioperative period. (See "Anesthesia for noncardiac surgery in patients with ischemic heart disease", section on 'Prevention of ischemia'.)

If necessary to treat hypotension in a patient with chronic severe MR and associated reduced LV ejection fraction, continuous infusion of an inodilator such as milrinone and/or a beta adrenergic inotropic agent such as dobutamine is reasonable (table 5). Addition or substitution of a low-dose epinephrine infusion may be necessary to maintain adequate BP in some patients. Pure alpha agonists (eg, phenylephrine) are generally avoided. Administration of any vasopressor agents is cautious (ie, in small doses or with incremental adjustments), with close monitoring to avoid a sudden increase in afterload and/or bradycardia, which may worsen MR and further reduce CO.

Preload (intravascular volume) — Maintain preload while attempting to avoid excess volume administration, similar to management of patients with AR. (See 'Preload (intravascular volume)' above.)

Most patients with primary or secondary MR are receiving chronic diuretic therapy, and may present to the operating room with hypovolemia. Fluid is administered in 100 to 250 mL increments to restore and maintain optimal intravascular volume, with assessment of the hemodynamic response after each increment. Aggressive fluid administration is avoided in order to avoid fluid overload and pulmonary congestion.

Conversely, some patients with primary or secondary MR present to the operating room with hypervolemia and pulmonary congestion. In these cases, an intravenous (IV) nitroglycerin infusion (table 6) and/or diuretic administration (eg, furosemide 10 to 20 mg) may be beneficial to reduce preload. Nitroglycerin may be particularly useful in patients with ischemic MR and evidence of hypervolemia and pulmonary congestion.

Contractility — Avoid doses of drugs that might cause significant depression of myocardial contractility (eg, high doses of propofol or volatile anesthetic agents).

Similar to patients with AR, if continuous infusion of an inotropic agent is necessary for a patient with MR and severe ventricular systolic dysfunction, an inodilator such as milrinone or dobutamine is typically selected (table 5) (see 'Contractility' above). Occasionally, infusion of low-dose epinephrine may be necessary to treat hypotension in patients with primary or secondary MR .

Pulmonary vascular resistance — Avoid hypoxemia, hypercarbia, and metabolic acidosis, which further increase pulmonary vascular resistance (PVR), and exacerbate pre-existing pulmonary hypertension (PH).

COMBINATIONS OF 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 stenosis or regurgitation of two separate valves [10]. Optimal management depends on which of the valvular lesions is predominant and which hemodynamic changes are likely to be most deleterious (table 11). 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.

Common combinations of valvular lesions include:

●Aortic stenosis with aortic regurgitation – Concurrent aortic regurgitation (AR) is present in many patients with aortic stenosis (AS), but is usually mild (see "Clinical manifestations and diagnosis of aortic stenosis in adults", section on 'Diagnostic echocardiography'). Typically, a HR target in the normal range of 70 to 80 beats per minute (bpm) is optimal for such patients, rather than a relatively fast or slow HR. Preload, afterload (systemic vascular resistance [SVR]), and contractility are also maintained within normal ranges.

●Mitral stenosis with mitral regurgitation – The combination of mitral stenosis (MS) and mitral regurgitation (MR) is common [11]. Hemodynamic targets for such patients take the differing requirements for each lesion into consideration (table 7 and table 8). Typically, a normal HR (eg, 70 to 80 bpm), normal or low to normal SVR, and normal contractility are optimal [12,13].

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

●Key points for selected valve lesions – Key points for perioperative hemodynamic management of patients with aortic or mitral valve disease are summarized in the tables (figure 1):

•Aortic stenosis (AS) (table 2)

•Mitral stenosis (MS) (table 7)

•Aortic regurgitation (AR) (table 8)

•Mitral regurgitation (MR)

-Primary MR (table 8)

-Secondary MR

Secondary MR associated with ischemic heart disease (table 3)

Secondary MR associated with dilated cardiomyopathy (table 9)

Secondary MR associated with hypertrophic cardiomyopathy (table 10) (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery", section on 'Hemodynamic goals and management'.)

●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 (table 11). (See 'Combinations of valve lesions' above.)