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Anesthesia for cardiac valve surgery

Anesthesia for cardiac valve surgery
Literature review current through: Aug 2023.
This topic last updated: Oct 28, 2022.

INTRODUCTION — Since the overall prevalence and severity of valvular heart disease increases with age, the need for cardiac valve surgery has increased in aging populations. In developed countries, the most common valve lesions are aortic stenosis (AS) due to calcific disease (affecting a trileaflet or bicuspid valve), and mitral regurgitation (MR) due to primary causes that include degenerative disease or secondary functional causes such as ischemic heart disease or non-ischemic cardiomyopathy (figure 1). Patients often have both stenosis and regurgitation affecting a single cardiac valve, as well as more than one affected valve. (See "Valvular heart disease in older adults".)

This topic will review anesthetic management of patients undergoing cardiac valve surgery. Considerations include the pathophysiology of the predominant valve lesion (ie, stenosis and/or regurgitation) and procedure-specific challenges.

General considerations during the perioperative period for patients undergoing cardiac surgical procedures and cardiopulmonary bypass (CPB) are reviewed separately:

Preoperative considerations. (See "Preoperative evaluation for anesthesia for cardiac surgery".)

Prebypass considerations

(See "Anesthesia for cardiac surgery: General principles", section on 'Monitoring'.)

(See "Anesthesia for cardiac surgery: General principles", section on 'Induction of general anesthesia'.)

(See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance of general anesthesia'.)

(See "Anesthesia for cardiac surgery: General principles", section on 'Preparations for cardiopulmonary bypass'.)

Cardiopulmonary bypass

(See "Initiation of cardiopulmonary bypass".)

(See "Management of cardiopulmonary bypass".)

(See "Weaning from cardiopulmonary bypass".)

Postbypass considerations

(See "Anesthesia for cardiac surgery: General principles", section on 'Management during the postbypass period'.)

(See "Intraoperative problems after cardiopulmonary bypass".)

ANESTHETIC MANAGEMENT: GENERAL CONSIDERATIONS — General anesthesia is often maintained with a volatile inhalation anesthetic agent. However, a total intravenous anesthetic (TIVA) technique, or a combination of inhalation and intravenous (IV) agents are reasonable alternatives. For example, a continuous infusion of a potent synthetic opioid (eg, sufentanil or remifentanil), short to moderate duration sedation (eg, midazolam or propofol) and neuromuscular blocking agent (eg, vecuronium or rocuronium) provide a hemodynamically stable anesthetic before during and after cardiopulmonary bypass (CPB) with rapid clearance after discontinuation of administration of each agent. Low doses of volatile anesthetic agents with a short duration can be added when necessary to smooth out the hemodynamic responses to stimulation. Depth of anesthesia monitoring (eg, bispectral index monitoring) is recommended, especially during bypass, when using this infusion regimen. (See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance of general anesthesia'.)

TRANSESOPHAGEAL ECHOCARDIOGRAPHY: GENERAL CONSIDERATIONS — Intraoperative transesophageal echocardiography (TEE) is typically used to confirm and characterize cardiac valve pathology before cardiac valve procedures, monitor air removal after open cardiotomy, and assess the adequacy of the repaired or replaced valve(s) [1-3]. Observational data suggest that intraoperative TEE for cardiac valve surgery may improve outcomes. A matched cohort study of 872,936 patients undergoing open cardiac valve surgery and/or proximal aortic surgery from the Society of Thoracic Surgeons (STS) database found that intraoperative TEE was associated with lower 30-day mortality (3.81 versus 5.27 percent; odds ratio [OR] 0.69, 95% CI 0.67-0.72) compared with not using TEE [4]. Composite outcomes were also lower in patients who received intraoperative TEE, including stroke or 30-day mortality (5.56 versus 7.01 percent; OR 0.77, 95% CI 0.74-0.79), and reoperation or 30-day mortality (7.18 versus 8.87 percent; OR 0.78, 95% CI 0.76-0.80). Results were similar for within hospital, within surgeon matched analyses. These findings suggest, but do not prove, important clinical benefits from intraoperative TEE in patients undergoing cardiac valve surgery and/or proximal aortic surgery. We employ intraoperative TEE for patients undergoing surgical cardiac valve repair or replacement or proximal aortic surgery.

Preoperative evaluation of valve structure and function, associated lesions, hemodynamics, and ventricular function with transthoracic echocardiography and TEE is discussed in the preoperative sections below, as well as in individual topic reviews. Precautions and contraindications for use of TEE are similar to those for patients undergoing noncardiac surgical procedures. (See "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Contraindications and precautions'.)

Prebypass period – After initial probe insertion, TEE examination enables confirmation of the preoperative diagnoses and refinement of the operative plan (eg, valve repair versus replacement) [5]. Notably, intraoperative assessment of the severity of cardiac valve stenosis and/or regurgitation may differ from preoperative assessments due to hemodynamic changes that occur with induction of general anesthesia [6,7]. For example, reduced systemic blood pressure (BP) decreases severity of aortic regurgitation (AR) and/or mitral regurgitation (MR), while reduced cardiac output (CO) decreases the gradients across stenotic valves.

The structure and function of all other cardiac valves are also assessed. It is critically important to note significant (ie, more than mild) AR since this will limit delivery of adequate antegrade cardioplegia solution into the coronary artery ostia after cross-clamping the ascending aorta, with much of the cardioplegia solution regurgitating back through the incompetent aortic valve into the left ventricle (LV). Consequences include failure to achieve cardioplegia as well as distention of the LV. Management of significant AR during cardiopulmonary bypass (CPB) typically includes use of alternative methods for delivery of cardioplegia (eg, retrograde cardioplegia) as well as insertion of an LV vent to maintain LV decompression (see "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Aortic regurgitation'). In addition, significant AR is a relative contraindication to the placement of an intraaortic balloon pump (IABP) because the degree of regurgitation may be increased by diastolic balloon inflation during counterpulsation. (See "Intraaortic balloon pump counterpulsation", section on 'Contraindications'.)

A comprehensive TEE examination is also performed to identify other pathology (eg, a coexisting patent foramen ovale that will be repaired during planned open cardiotomy) and assessment of global and regional ventricular function (figure 2 and figure 3 and movie 1) [2]. Patients with significant LV or right ventricular (RV) systolic dysfunction may require intraoperative inotropic support (movie 2 and movie 3). This initial assessment of both regional and global biventricular function, as well as intravascular volume status (movie 4), allows comparisons during subsequent continuous TEE monitoring.

Removal of air after open cardiotomy – Air accumulates in the left heart chambers during aortic or mitral valve repair or replacement. TEE is employed to identify air in the cardiac chambers, with ongoing monitoring to guide its removal via surgical venting. In particular, air accumulates in the pulmonary veins, the left atrial appendage, the dome of the left atrium (LA), and the LV apex. Any intracardiac air may embolize to the coronary, cerebral, and other vital organ arteries once the aortic cross-clamp is removed and the heart begins to contract (movie 5 and movie 6 and movie 7 and movie 8). Thus, it is important to remove nearly all air prior to allowing full ventricular ejection during weaning from CPB in order to avoid or minimize arterial embolization. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Arterial air embolization'.)

Retained air may be eliminated via a vent/catheter in the aortic root as well as via an LV vent catheter, just prior to and following removal of the aortic cross-clamp. The right coronary artery is in a superior or nondependent position when a patient is supine; thus, air preferentially enters the right coronary artery, which may cause ischemia of the RV and inferior wall of the LV, as well as arrhythmias (particularly heart block) (movie 5). The de-airing process is monitored with TEE (movie 7). In some centers, the patient is placed in the Trendelenburg position during de-airing to decrease the risk of cerebral air embolization.

Postbypass period – During and immediately after weaning from CPB, TEE is used to assess function of the repaired or replaced valve (including identification of any paravalvular leaks) and identify complications such as myocardial ischemia, evidenced by development of new or worsening regional wall motion abnormalities. Communication with the surgeon regarding complications noted on the TEE examination facilitates decisions to reinstitute CPB for surgical correction, if necessary. These assessments are ideally performed when hemodynamic variables are similar to the patient's baseline values obtained after induction of general anesthesia and before initiation of CPB.

After the initial postbypass TEE examination, TEE is employed to continuously monitor LV and RV function, as well as intravascular volume status, for the remainder of the intraoperative period. After aortic decannulation, the ascending aorta is evaluated to exclude aortic dissection.

Additional considerations for use of TEE before and after CPB during cardiac surgical procedures are discussed in a separate topic. (See "Anesthesia for cardiac surgery: General principles", section on 'Prebypass transesophageal echocardiography' and "Anesthesia for cardiac surgery: General principles", section on 'Postbypass transesophageal echocardiography'.)

SURGERY FOR AORTIC STENOSIS

Overview of the valve lesion — Severe aortic stenosis (AS) causes obstruction of left ventricular (LV) outflow, resulting in LV pressure overload, concentric hypertrophy, diastolic LV dysfunction with decreased stroke volume and cardiac output (CO). Etiology, pathophysiology, stages of AS severity, and indications for aortic valve replacement (AVR), either surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI), are discussed in separate topics (table 1) [8]:

(See "Clinical manifestations and diagnosis of aortic stenosis in adults".)

(See "Clinical manifestations and diagnosis of low gradient severe aortic stenosis".)

(See "Natural history, epidemiology, and prognosis of aortic stenosis".)

(See "Indications for valve replacement for high gradient aortic stenosis in adults".)

(See "Management and prognosis of low gradient aortic stenosis".)

(See "Choice of intervention for severe calcific aortic stenosis".)

Anesthetic management considerations for percutaneous interventions involving the aortic valve (TAVI or aortic balloon valvotomy) are discussed separately. (See "Anesthesia for percutaneous cardiac valve interventions", section on 'Aortic valve interventions'.)

Preoperative considerations — During the preanesthetic consultation and examination of results of cardiac diagnostic studies, particular attention is paid to the severity of AS, presence of associated aortic regurgitation (AR), other cardiac valve pathology, LV and right ventricular (RV) dysfunction, and coexisting coronary artery disease. Patients with AS who have a high pulmonary-systemic ratio (mean pulmonary arterial pressure/mean systemic arterial pressure) are at greater risk for perioperative morbidity and mortality [9-11]. (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Assessment of patient and procedural risk factors' and "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Preoperative tests'.)

In the immediate preoperative period when the patient is being continuously monitored by the anesthesiologist, small incremental doses of a short-acting agents such as intravenous benzodiazepine (eg, midazolam 0.5 to 1 mg) and/or an opioid (eg, fentanyl 25 to 50 mcg) may be administered according to individualized needs to reduce the stress response (eg, during central venous catheter placement). Extra caution is warranted for patients with critical AS, severe ventricular dysfunction, or age >75 years. (See "Anesthesia for cardiac surgery: General principles", section on 'Premedication' and "Anesthesia for cardiac surgery: General principles", section on 'Intravascular cardiac monitors'.)

Prebypass hemodynamic management — Key points for hemodynamic goals and anesthetic management during the prebypass period for patients with AS are summarized in the tables (table 2), and are described in detail in a separate topic. (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Aortic stenosis'.)

Prebypass TEE assessment — Prior to cardiopulmonary bypass (CPB), the transesophageal echocardiography (TEE) examination focuses on confirmation of the presence of AS (eg, heavily calcified or poorly mobile aortic valve leaflets (image 1)), precise measurement of aortic annulus, aortic root, and sinotubular junction diameters, and quantification of AS severity (table 3). Continuous-wave Doppler measurement of the transvalvular gradient can usually be obtained from the deep transgastric or transgastric long-axis views (image 2). Notably, the transvalvular gradient is frequently underestimated by suboptimal alignment of the ultrasound beam with the stenotic jet (as beam alignment is frequently more limited with TEE than with transthoracic echocardiography). Since the transvalvular gradient may be underestimated, severe AS is not excluded if the valve appearance suggests this diagnosis, but the mean aortic valve gradient is <40 mm Hg. Calculation of aortic valve area employing the continuity equation also requires beam alignment with maximum left ventricular outflow tract (LVOT) and aortic jet velocities. Planimetry of the aortic valve orifice during systolic opening provides a potential alternative estimate of effective aortic valve area but should be interpreted with caution due to technical limitations such as artifact caused by calcification [12]. Significant ventricular septal hypertrophy and systolic anterior motion (SAM) of the mitral valve should be assessed, as dynamic LVOT obstruction may persist or worsen following AVR; ventricular septal myectomy at the time of surgery may prevent this postoperative problem from occurring. (See "Aortic valve area in aortic stenosis in adults", section on 'Echocardiography' and "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Assessment of aortic stenosis' and "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction".)

It is also important to identify coexisting hemodynamically significant AR, which will impact decisions regarding administration of cardioplegia (see 'Transesophageal echocardiography: General considerations' above and 'Prebypass TEE assessment' below). In particular, a congenital bicuspid aortic valve may cause both severe aortic valve stenosis and/or regurgitation by the fourth decade of life (image 1), and may also be associated with dilation of the ascending aorta, (which may require repair). (See "Bicuspid aortic valve: Intervention for valve disease or aortopathy in adults", section on 'Intervention for aortic stenosis' and "Bicuspid aortic valve: Intervention for valve disease or aortopathy in adults", section on 'Aortic surgery'.)

Surgical aortic valve replacement — SAVR is performed using a bioprosthetic or mechanical valve (see "Choice of prosthetic heart valve for surgical aortic or mitral valve replacement"). This is achieved through a midline sternotomy, followed by aortic cannulation and initiating CPB. Following administration of cardioplegia to establish diastolic cardiac arrest, the aorta is opened, and the aortic valve is excised with care to remove all calcific debris from the diseased valve and from the surgical field, since risk of cerebral infarction due to particulate embolization is high after AVR for AS [13]. The aortic annulus is then measured, and the prosthetic valve implanted. After closure of the aorta, residual air is fastidiously removed from the ascending aorta and left heart chambers.

After the cross-clamp is removed, the heart is reperfused, and the patient is weaned from CPB (see "Weaning from cardiopulmonary bypass"). Minimizing residual air is ensured with continued TEE monitoring (see 'Transesophageal echocardiography: General considerations' above). Epicardial pacing wires are attached to the right atrium and RV in most patients to maintain a stable postbypass rhythm given the risk of postoperative atrioventricular block. (See 'Postbypass period' below.)

Postbypass TEE assessment — Shortly after removal of the aortic cross clamp, with the heart beating and systemic blood pressure (BP) restored to the prebypass range, initial transesophageal echocardiography (TEE) examination is performed to allow early identification of unacceptable surgical problems such as stuck leaflets and/or significant paravalvular leaks. Upon termination of bypass, normal function of the prosthetic valve is confirmed (ie, symmetrical movement of all leaflets and normal closure). Since paravalvular leaks can develop with time and increases in systemic pressure, TEE examination should be repeated several times after termination of CPB. Leaflet dysfunction or greater than trace paravalvular leak will generally trigger a decision to return to CPB in order to fix the problem.

Structures adjacent to the prosthetic valve are also examined to detect unintentional collateral damage. For example, the base of the anterior leaflet of the mitral valve may become damaged as a result of a suture being placed too deeply in the posterior aspect of the aortic annulus. This will appear as a high-velocity jet of MR originating at the base of the anterior portion of the mitral valve annulus. Alternatively, MR may occur following valve replacement owing to dynamic LVOT obstruction and SAM of the mitral leaflets. Patients with hypovolemia, severe LV hypertrophy, and increased contractility are at increased risk [14,15].

Furthermore, function of the LV and RV is carefully assessed. Regional wall motion abnormalities may be detected in the right coronary or other coronary arterial territories following air embolism (movie 5), or as a result of calcific emboli from the native valve (figure 3), or malposition of the aortic valve prosthesis such that a coronary ostium is partially blocked.

Postbypass management — Since LV contractility is typically well-preserved in most patients with severe AS, inotropes are not typically necessary during weaning from CPB after AVR. (See "Weaning from cardiopulmonary bypass".)

Conversely, it may be necessary to manage hypertension due to the hypertrophied hyperdynamic LV that no longer must eject across a stenotic valve. The most common complication immediately after AVR is bleeding (see "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Achieving hemostasis and management of bleeding'). Hypertension increases risk of arterial bleeding and also increases the potential for aortic dissection at the aortic cannulation site. Management includes increasing anesthetic depth with volatile inhalation agents and use of vasodilator drugs. Infusion of a short-acting beta-blocking agent such as esmolol may also be necessary.

AV conduction abnormalities are common after AVR; thus, epicardial pacing is usually necessary in the immediate postoperative period. (See "Weaning from cardiopulmonary bypass", section on 'Maintenance of optimal pacemaker function'.)

SURGERY FOR AORTIC REGURGITATION

Overview of the valve lesion

Chronic aortic regurgitation – Severe chronic aortic regurgitation (AR) causes volume overload of the left ventricle (LV) with gradually developing LV dilation and eccentric hypertrophy. Although biventricular function typically remains intact in patients with moderate to severe AR, dilated cardiomyopathy may be present in advanced stages, with ultimate LV failure manifested by a progressive decrease in ejection fraction and cardiac output (CO), as well as increased left atrial (LA) and pulmonary artery pressures [16]. Notably, severe chronic AR results in a low diastolic blood pressure (BP) and a wide pulse pressure; this is well tolerated unless concomitant coronary artery disease is present.

Etiology, pathophysiology, stages of chronic AR severity, and indications for surgery are discussed separately (table 4) [8]:

(See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

(See "Natural history and management of chronic aortic regurgitation in adults".)

Acute aortic regurgitation – In acutely developing AR (eg, due to aortic dissection or endocarditis), rapid volume overload of the relatively noncompliant LV develops. This increases LV end-diastolic and LA pressures and decreases coronary perfusion pressure. Sudden onset of severe heart failure and progression to cardiogenic shock may occur. Treatment requires initial intensive medical management and emergency cardiac surgical repair. Perioperative risk is high. Use of an intraaortic balloon pump (IABP) is contraindicated since this would increase regurgitation across the aortic valve and exacerbate LV dilation. (See "Acute aortic regurgitation in adults" and 'High-risk emergency procedures' below.)

Preoperative considerations — During the preanesthetic consultation and examination of results of cardiac diagnostic studies, particular attention is paid to the severity of AR, presence and severity of heart failure, and whether there is associated aortic root dilation, aortic stenosis (AS), or pathology of other cardiac valves. Patients should be medically optimized before proceeding with elective aortic valve surgery for chronic AR. (See "Natural history and management of chronic aortic regurgitation in adults", section on 'Treatment'.)

Patients with acute severe AR require emergency aortic valve surgery. If there is a delay in surgery, temporary stabilization may be attempted using intravenous (IV) vasodilators (eg, nitroprusside) and possibly an inotropic agent (eg, dobutamine). (See "Acute aortic regurgitation in adults", section on 'Treatment'.)

Heavy premedication is avoided in patients with severe AR, although small incremental doses of a short-acting IV benzodiazepine (eg, midazolam 1 to 2 mg) may be administered in the immediate preoperative period if necessary for anxiolysis. (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Alleviation of patient anxiety'.)

Prebypass hemodynamic management — Key points for hemodynamic goals and anesthetic management during the prebypass period for patients with AR are summarized in the tables (table 5), and are described in detail in a separate topic. (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Aortic regurgitation'.)

Prebypass TEE assessment

Chronic aortic regurgitation – Prior to cardiopulmonary bypass (CPB), the transesophageal echocardiography (TEE) examination is focused on confirmation of the presence of AR and quantification of its severity (table 6). Severity of AR is qualitatively estimated with color-flow Doppler to measure the largest jet width in the left ventricular outflow tract (LVOT) within 1 cm of the aortic valve. This jet width is expressed as a percentage of the width of the LVOT (mild regurgitation is a jet width ≤30 percent of the LVOT (movie 9); severe regurgitation is a jet width ≥65 percent of the LVOT (image 3 and table 6). We also measure the narrowest neck of the regurgitant jet (ie, the vena contracta) in the midesophageal aortic valve long-axis view (image 4). Also, continuous-wave Doppler imaging of the regurgitant jet is performed to determine the pressure half-time, as well as pulsed-wave Doppler imaging of the descending aorta to identify holodiastolic flow reversal (image 5). (See "Transesophageal echocardiography in the evaluation of aortic valve disease", section on 'Aortic regurgitation' and "Echocardiographic evaluation of the aortic valve", section on 'Severity of aortic regurgitation'.)

In addition, the likely etiology of the lesion, measurements of the annulus and sinotubular junction, and geometry of the aortic root are assessed. When aortic valve repair is contemplated, echocardiographic features of the aortic valve and root that suggest a high likelihood of successful repair include isolated cusp prolapse or aortic root dilation with normal aortic valve cusp motion. An eccentric jet of regurgitation may be a clue to the presence of leaflet prolapse. In patients with obvious restrictive movement of the aortic valve cusps, replacement rather than repair is usually necessary [17].

The other cardiac valves are also examined. In addition, the LV is examined for global dysfunction, although most patients are advised to undergo surgical repair of severe AR before development of LV decompensation [18,19]. (See "Natural history and management of chronic aortic regurgitation in adults", section on 'Indications for aortic valve surgery'.)

Acute aortic regurgitation – For patients presenting with acute AR, intraoperative TEE facilitates confirmation of etiology (eg, endocarditis, aortic dissection, traumatic rupture of the valve leaflets). In these patients, there is early closure of the mitral valve (before the R wave), and flow reversal in the proximal descending aorta may not be holodiastolic even if AR is severe (table 6) [20]. (See "Acute aortic regurgitation in adults", section on 'Etiology' and "Acute aortic regurgitation in adults", section on 'Echocardiography'.)

Procedure-specific considerations — Aortic valve surgery (replacement or repair) is the mainstay of treatment for symptomatic severe AR. Transcatheter valve implantation for native aortic valve regurgitation is an investigational procedure that is discussed separately. (See "Natural history and management of chronic aortic regurgitation in adults", section on 'Treatment'.)

Surgical aortic valve replacement — Surgical aortic valve replacement (SAVR) with a bioprosthetic or mechanical aortic valve is the predominant treatment for symptomatic severe AR (see "Natural history and management of chronic aortic regurgitation in adults"). This is achieved through a midline sternotomy or an upper ministernotomy, followed by establishment of CPB. After application of the aortic cross-clamp, cardioplegia solution delivered into the aortic root is unlikely to lead to adequate diastolic arrest of the heart, due to reflux of cardioplegia into the LV and inadequate flow into the coronary arteries. Therefore, either the aortic root is immediately opened so that cardioplegia can be delivered directly into the coronary ostia, or retrograde cardioplegia is delivered via the coronary sinus. (See "Management of special populations during cardiac surgery with cardiopulmonary bypass", section on 'Aortic regurgitation'.)

Once cardiac arrest has been successfully achieved with these techniques, the native valve leaflets are excised, the aortic annulus is measured, and the prosthetic valve is implanted. Similar to SAVR procedures for severe AS, air must be removed from both the ascending aorta and the left heart chambers prior to weaning from CPB. (See 'Transesophageal echocardiography: General considerations' above.)

Surgical aortic valve repair — Only selected patients with severe AR are candidates for surgical aortic valve repair (see "Natural history and management of chronic aortic regurgitation in adults", section on 'Choice of procedure'). Similar to SAVR, surgical aortic valve repair procedures require establishment of standard CPB with cardiac arrest. Once achieved, the surgeon can examine the native aortic valve to determine if it is reparable. Examples of repair procedures include resuspension of a prolapsing aortic valve leaflet or remodeling of the aortic root (including the sinotubular junction) [21]. Other aspects of de-airing and weaning from CPB are the same as for aortic valve replacement (AVR) procedures. (See 'Surgical aortic valve replacement' above.)

Postbypass TEE assessment — The postbypass TEE examination after SAVR focuses on whether there is normal function of the prosthetic valve, as described above for an AVR procedure for AS (see 'Postbypass TEE assessment' above). Abnormal function or significant paravalvular leak(s) necessitate a return to CPB to fix the problem.

For TEE assessment of an aortic valve repair, the three most important indicators of the risk of recurrent postoperative AR are postbypass persistence of a residual AR jet, leaflet coaptation length <4 mm, or a coaptation point of the tip of the aortic valve leaflets that is below the level of the aortic annulus [22,23].

Postbypass management — Contractility is typically well-preserved in patients with severe AR, but inotropic agent(s) may be necessary during weaning from CPB in patients with severe LV dilation and documented preexisting impairment of LV function. We typically administer an inodilator (eg, milrinone) and/or a beta adrenergic inotropic agent (eg, dobutamine) that has inodilator properties (table 7). Notably, excessive vasodilation due to inodilator administration may be counteracted with small bolus doses and/or an infusion of an alpha-adrenergic agent such as phenylephrine or norepinephrine.

Other aspects of postbypass management are similar to an AVR procedure for AS. (See 'Postbypass management' above.)

SURGERY FOR MITRAL REGURGITATION

Overview of the valve lesion — Mitral regurgitation (MR) can be chronic or acute, and also primary or secondary in nature.

Chronic mitral regurgitation – Chronic MR causes volume overload of the left atrium (LA) and left ventricle (LV), accompanied by LA and LV enlargement, elevated LA pressure, and atrial dysrhythmias (typically, atrial fibrillation [AF]). Pulmonary vascular resistance (PVR) and pulmonary artery pressure may be significantly increased in patients with chronic severe MR [11].

Primary chronic MR is a disease of the mitral leaflets and intrinsic supporting structures. Failure of leaflet coaptation results from annular dilatation, leaflet prolapse, or leaflet flail, occurring as a consequence of degenerative and/or rheumatic valve disease. If preoperative LV ejection fraction (LVEF) is reduced in a patient with chronic primary MR, it is likely that significant LV systolic dysfunction is present, and the patient is at risk for worse long-term outcomes. (See "Chronic primary mitral regurgitation: Indications for intervention", section on 'Approach to identifying candidates for intervention'.)

Secondary chronic or functional MR results from underlying LV dysfunction that may be either ischemic or non-ischemic in origin. With these conditions, there is tethering or tenting of mitral leaflets, impaired valve closing as a result of impaired or dyssynchronous LV function, and annular enlargement. Occasionally, surgical mitral valve replacement or repair for severe chronic secondary MR is performed during a cardiac surgical procedure to repair other pathology (eg, coronary artery bypass grafting [CABG] for ischemic heart disease) [18,19,24-26]. In these patients, anesthetic considerations include management of the underlying ischemic heart disease or cardiomyopathy with significant LV dysfunction, as well as management of MR. (See "Chronic secondary mitral regurgitation: Intervention", section on 'Introduction'.)

Details regarding etiology and pathophysiology of primary or secondary MR, stages of chronic MR severity, indications for surgical intervention, and decisions regarding selection of the optimal surgical procedure are discussed separately (table 8) [8]:

(See "Clinical manifestations and diagnosis of chronic mitral regurgitation".)

(See "Chronic primary mitral regurgitation: General management".)

(See "Chronic primary mitral regurgitation: Indications for intervention".)

(See "Chronic secondary mitral regurgitation: General management and prognosis".)

(See "Surgical procedures for severe chronic mitral regurgitation".)

Dynamic MR may occur secondary to hypertrophic cardiomyopathy with systolic anterior motion (SAM) of the mitral valve leaflets with mitral-ventricular septal contact. In some patients, ventricular septal myectomy is performed to relieve left ventricular outflow tract (LVOT) obstruction. Any abnormalities of the mitral valve and papillary muscles are also addressed at the time of septal myectomy. Anesthetic and surgical management of patients with hypertrophic cardiomyopathy are discussed in other topics. (See "Anesthesia for patients with hypertrophic cardiomyopathy undergoing noncardiac surgery", section on 'Hemodynamic goals and management' and "Hypertrophic cardiomyopathy: Management of patients with outflow tract obstruction", section on 'Septal reduction therapy'.)

Acute mitral regurgitation – Acute MR may be caused by ruptured chordae (due to causes including degenerative mitral valve disease and infective endocarditis), papillary muscle rupture (due to causes including myocardial infarction) or papillary muscle displacement due to myocardial infarction or ischemia or rapid onset of cardiomyopathy. The presentation and pathophysiology of acute MR differs from chronic MR. The suddenly increased LA pressure may cause "flash" pulmonary edema, acute right heart failure, or cardiogenic shock. Treatment of acute MR typically requires intensive medical stabilization and generally requires urgent or emergency cardiac surgical repair with a high perioperative risk. However, for patients with acute ischemic MR, percutaneous coronary revascularization may lead to resolution of the MR without mitral valve intervention. In patients with acute MR, insertion of an intraaortic balloon pump (IABP) preoperatively (or prior to coronary intervention) may be beneficial by reducing LV afterload and increasing diastolic coronary arterial blood flow. (See 'High-risk emergency procedures' below and "Acute mitral regurgitation in adults", section on 'Etiology' and "Acute mitral regurgitation in adults", section on 'Treatment'.)

Preoperative considerations — During the preanesthetic consultation and examination of results of cardiac diagnostic studies, particular attention is paid to the severity of MR, presence and severity of heart failure, and whether there is associated mitral stenosis (MS), pathology of other cardiac valves, or regional or global LV dysfunction indicating myocardial ischemia or cardiomyopathy. The chest radiograph (CXR) may reveal signs of pulmonary edema and right heart enlargement in advanced cases. Patients should be medically optimized before proceeding with elective mitral valve surgery for chronic MR.

Many patients with severe MR have AF and are receiving chronic anticoagulation therapy. Management of medications affecting hemostasis is discussed separately. (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Medications affecting hemostasis'.)

Prebypass hemodynamic management — Key points for hemodynamic goals and anesthetic management during the prebypass period for patients with MR are similar to those for patients with aortic regurgitation (AR), and summarized in the tables (table 5). Additional considerations apply to patients with secondary MR due to ischemic heart disease (table 9). These considerations are described in detail in a separate topic. (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Mitral regurgitation'.)

Prebypass TEE assessment — Prebypass transesophageal echocardiography (TEE) assessment is similar for chronic and acute MR. (See "Transesophageal echocardiography in the evaluation of mitral valve disease", section on 'Role of intraoperative transesophageal echocardiography'.)

Chronic mitral regurgitation — Prior to cardiopulmonary bypass (CPB), the TEE examination is focused on the mechanism causing MR and whether the valve can be repaired, quantification of MR severity, and status of LV and right ventricular (RV) function (table 10). (See "Chronic secondary mitral regurgitation: Intervention", section on 'Concurrent mitral valve surgery and CABG'.)

Severity of chronic MR is semiquantitatively estimated with color-flow Doppler to assess regurgitant jet size (ie, the length, area, and eccentricity of the regurgitant jet in the LA) (image 6 and table 10) [27]. Proximal isovelocity surface area (PISA) method can be helpful in quantitation of effective regurgitant orifice area (EROA) or regurgitant volume. However, ventricular loading conditions and jet eccentricity can result in incorrect estimation of severity with color-Doppler assessment. Systolic reversal of flow in the pulmonary veins can be seen in severe MR. In addition, the width of the vena contracta should be measured because it is easy to acquire, reproducible, and relatively independent of ventricular loading conditions (movie 10). This measurement is made at the narrowest neck of the MR jet, obtained in a midesophageal four-chamber view [27]. Other echocardiographic signs of severe MR include a peak E velocity >1.2 m/second or a dense continuous wave Doppler MR jet signal. Of clinical note, however, all these intraoperative echocardiographic methods have pitfalls [28]. For example, MR severity is typically underestimated after induction of general anesthesia due to decreases in sympathetic tone and LV afterload, and MR severity can vary considerably during surgery [27,29]. Thus, if intraoperative confirmation of severity is critically important, assessment should be performed during hemodynamic conditions approximating the patient's preoperative baseline. Transient use of a vasopressor agent such as phenylephrine may be necessary to restore the blood pressure (BP) to baseline levels [29]. (See "Transesophageal echocardiography in the evaluation of mitral valve disease", section on 'Severity of mitral regurgitation'.)

TEE examination of mitral valve structure includes assessment of the anterior leaflet, posterior leaflet, papillary muscles, chordae tendineae, and mitral valve annulus (figure 4) [27]. For patients with primary MR, intraoperative three dimensional (3D) TEE has been used to enable detailed study of valve morphology and quantitative analysis of annular size and leaflet dimensions important to the repair of degenerative mitral valves (resulting in mitral valve prolapse, partial flail, or flail leaflet). Carpentier's classification of mitral valve regurgitation is often used to facilitate a common language between the echocardiographer and surgeon, and permit an assessment of the etiology of MR and the likelihood of successful repair. Type 1 lesions (with normal leaflet motion) and type 2 lesions (excessive leaflet motion) are typically more amenable to operative repair than type 3 lesions (restricted leaflet motion) [27,30]. Other assessments to determine whether the mitral valve can be repaired include the estimated risk of post-repair SAM of the mitral valve, precise location of the left circumflex coronary artery relative to the location of annular sutures, prediction of the correct annuloplasty device size, and prediction of the largest size mitral valve prosthesis that will fit in the patient (based on intertrigonal distance in case the repair fails). Repair is less likely to be successful if there is extensive calcification or degeneration of a leaflet or annulus, prolapse of more than one-third of the leaflet tissue, or extensive chordal fusion, calcification, or papillary muscle rupture [27]. Further information is available in other topics:

(See "Transesophageal echocardiography in the evaluation of mitral valve disease", section on 'Role of intraoperative transesophageal echocardiography'.)

The other cardiac valves are also examined, with particular attention to whether significant aortic regurgitation (AR) is present (see 'Prebypass TEE assessment' above). In addition, the LV is examined for regional wall motion abnormalities that may be associated with ischemic MR, or global LV dysfunction or dilatation due to ischemia or chronic volume overload [18,19]. The RV is also examined for possible dilation and dysfunction due to chronic pulmonary hypertension. In some patients, severe tricuspid regurgitation (TR) is noted, and may be an indication for concomitant tricuspid valve repair [11]. (See "Management and prognosis of tricuspid regurgitation", section on 'At the time of left-sided valve surgery'.)

Acute mitral regurgitation — Prior to CPB, the TEE examination is focused on the mechanism causing MR and whether the valve can be repaired, hemodynamics (including Doppler estimation of cardiac output (CO) through the left ventricular outflow tract), and status of LV and RV function; quantitation of MR severity is also attempted although indicators of chronic severe MR may not apply to acute MR. In acute MR the jet velocity may be lower, the jet area may not be large, and the jet is often markedly eccentric, all of which may contribute to underestimating the degree of regurgitation (table 10). Mitral valve structure and other valve lesions are also evaluated as described above. (See "Acute mitral regurgitation in adults", section on 'Echocardiography'.)

Presence of the combination of a flail leaflet or ruptured papillary muscle, pulmonary vein systolic flow reversal, and a hyperdynamic LV with low systemic output by Doppler suggest acute severe MR, even in the absence of large regurgitant jet [20]. Since patients with acute MR frequently present with hypotension (even prior to induction of general anesthesia), high LA pressure, and an eccentric MR jet, color-flow Doppler imaging may not detect a large regurgitant jet in the LA despite the presence of pulmonary vein systolic flow reversal [20]. Thus, the above described methods for detecting chronic severe MR may not apply to acute MR.

Procedure-specific considerations

Surgical mitral valve repair or replacement — For patients with an indication for mitral valve surgery, the choice between surgical mitral valve repair and replacement is discussed separately. (See "Chronic secondary mitral regurgitation: Intervention", section on 'Choice of mitral surgical procedure'.)

Open mitral valve repair or replacement is usually achieved through a midline sternotomy, followed by the establishment of CPB and opening of the LA to repair or replace the valve. The left atriotomy may be made directly behind the right atrium (RA), or the LA can be entered across the atrial septum via a right atriotomy. In all instances, however, bicaval venous cannulation is recommended to facilitate adequate venous drainage for CPB.

If mitral valve replacement is necessary, either a bioprosthetic or mechanical mitral valve may be implanted (see "Choice of prosthetic heart valve for surgical aortic or mitral valve replacement"). After completion of the procedure, the LA is closed and air is removed from the left heart prior to removal of the aortic cross-clamp. After the cross-clamp is removed, the heart is reperfused, and the patient is weaned from CPB. Removal of residual air is guided by TEE monitoring. (See 'Transesophageal echocardiography: General considerations' above.)

Minimally invasive mitral valve repair — Minimally invasive mitral valve repair can be performed via a small right thoracotomy with or without the aid of CPB and with or without the aid of robotic technology [31-35]. Immediate access to the heart is not possible in such cases; thus, placement of external defibrillator pads is particularly important. (See "Minimally invasive aortic and mitral valve surgery", section on 'Minimally invasive mitral valve surgery (MI-MVR)'.)

Anesthetic techniques for such minimally invasive procedures should facilitate early extubation and mobilization [35]. Thus, short-acting anesthetic agents are selected and normothermia is maintained so that tracheal extubation may be accomplished shortly after completion of surgery (eg, one to two hours). Postoperative pain control can often be achieved with multimodal anesthetic techniques (eg, regional blocks such as paravertebral, serratus anterior plane, intercostal, or pectoral nerves I and II blocks) [35]. (See "Thoracic nerve block techniques".)

Anesthetic management considerations for transcatheter mitral valve repair (performed without CPB) such as a mitral clip procedure (figure 5) are discussed separately. (See "Anesthesia for percutaneous cardiac valve interventions", section on 'Transcatheter mitral valve repair'.)

Postbypass TEE assessment — Specific highlights for postbypass transesophageal echocardiography (TEE) after mitral valve repair or replacement are described below.

In addition, following any mitral valve procedure, it is important to assess LV and RV function and check for incidental injury to adjacent cardiac structures (eg, damage to the aortic valve causing AR or to the circumflex artery causing inferolateral LV regional wall motion abnormalities) [27].

Finally, removal of residual air is guided by TEE monitoring. (See 'Transesophageal echocardiography: General considerations' above.)

After mitral valve repair — A repaired mitral valve is interrogated for residual MR immediately after weaning from CPB. If significant residual MR is present, the mechanism causing it is identified (eg, inadequate repair or a paravalvular leak around an annuloplasty ring) [27]. With the aid of TEE interrogation of the repaired valve, the surgeon and cardiac anesthesiologist must jointly decide whether further attempts to repair the mitral valve are feasible, or whether replacement of the mitral valve will be necessary. Postbypass hemodynamics must be considered in evaluating the adequacy of the repair, since hypotension may lead to erroneous underestimation of MR severity. Thus, BP should be normalized before final surgical decisions are made.

After a mitral valve repair procedure that includes preservation of the anterior leaflet, it is also important to assess and document presence of SAM or LVOT obstruction [27,36]. On TEE examination, SAM is identified when the mitral leaflets are drawn anteriorly into the LVOT during systole, causing LVOT obstruction and concomitant MR. The LVOT obstruction can be identified by Doppler color flow mapping and the resulting gradient can be quantified with spectral Doppler interrogation. Notably, LVOT obstruction is exacerbated by LV "underfilling" (ie, hypovolemia) and by positive inotropic agents. If SAM does not resolve after volume loading and withdrawal of inotropic agents, then revision of the mitral valve repair or mitral valve replacement is likely necessary [27]. If further surgical revisions to repair the native valve are unsuccessful, then mitral valve replacement is usually required.

The transmitral gradient should also be assessed after mitral valve repair [36]. If the transmitral gradient is significantly elevated (eg, mean gradient >6 mmHg) and the elevation is not caused by a high output state, then re-repair or replacement of the valve may be necessary [37].

After mitral valve replacement — After mitral valve replacement, TEE is used to rule out paravalvular leak, abnormal prosthetic leaflet mobility, or a high gradient across the mitral prosthesis indicating a stuck leaflet.

Postbypass management — Following separation from CPB, hemodynamic parameters are typically corrected to baseline levels prior to completing assessment of valve function, thereby reducing risk for underestimating any residual MR.

Typically, patients with preoperative LV impairment will require inotropic support during the immediate postbypass period. In some cases, acute LV failure occurs with attempts to terminate CPB. Inodilator agents such as milrinone may be employed, particularly in patients with elevated PVR, often with concomitant use of norepinephrine to avoid excessive systemic vasodilatation. An IABP may be inserted to improve coronary perfusion to the left heart and provide afterload reduction in selected patients with significant LV dysfunction. (See "Intraaortic balloon pump counterpulsation".)

Acute refractory right heart failure with a high PVR may occur in some patients during attempted weaning from CPB [11]. Treatment is described separately. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Right ventricular dysfunction'.)

Arrhythmias, particularly AF, are common in the postbypass and postoperative periods. Treatment includes synchronized cardioversion (especially if sinus rhythm was present before CPB) and administration of amiodarone if cardioversion is unsuccessful [38], as well as correction of potassium and magnesium levels to high-normal values. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Arrhythmias' and "Intraoperative problems after cardiopulmonary bypass", section on 'Metabolic abnormalities'.)

Similar to surgical procedures involving the aortic valve, bleeding is a common complication (see "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Achieving hemostasis and management of bleeding'). Very rarely, intractable bleeding occurs due to disruption of atrioventricular continuity after mitral valve replacement, particularly in the setting of severe mitral annular calcification. This complication is associated with high mortality (see "Management and prognosis of mitral annular calcification", section on 'Mitral valve surgery').

SURGERY FOR MITRAL STENOSIS

Overview of the valve lesion — Severe chronic mitral stenosis (MS) causes impaired left ventricular (LV) filling due to a fixed obstruction to left atrial (LA) outflow. LA pressure, pulmonary artery pressure, and pulmonary vascular resistance (PVR) are increased, and atrial fibrillation (AF) is common. Patients often have chronic pulmonary hypertension and ultimately develop right ventricular (RV) failure [11]. Conversely, the LV is chronically "underloaded," but may exhibit myocardial fibrosis with some impairment of LV systolic and diastolic function.

Rheumatic heart disease is the most common cause of MS, affecting the leaflet edges (thickening and rolling), the commissures (fusion), and subvalvular apparatus (with chordal shortening and valve thickening). An increasingly recognized cause is severe mitral annular calcification, with calcification involving the leaflets. Other causes include infiltrative diseases, and congenital abnormalities. Details regarding etiology and pathophysiology of MS, stages of chronic MS severity, indications for surgical intervention, and decisions regarding selection of the optimal surgical procedure are discussed separately (table 11) [8]:

(See "Rheumatic mitral stenosis: Clinical manifestations and diagnosis".)

(See "Pathophysiology and natural history of mitral stenosis".)

(See "Clinical manifestations and diagnosis of rheumatic heart disease", section on 'Mitral stenosis'.)

(See "Clinical manifestations and diagnosis of mitral annular calcification", section on 'Mitral stenosis'.)

(See "Rheumatic mitral stenosis: Overview of management".)

(See "Surgical and investigational approaches to management of mitral stenosis".)

Anesthetic management considerations for percutaneous mitral valve balloon valvotomy are discussed separately. (See "Anesthesia for percutaneous cardiac valve interventions", section on 'Percutaneous mitral balloon valvotomy'.)

Preoperative considerations — During the preanesthetic consultation and examination of results of cardiac diagnostic studies, particular attention is paid to the severity of MS and associated mitral regurgitation (MR), other cardiac valve pathology, presence of LA or left atrial appendage (LAA) thrombus, or severity of RV dysfunction. In addition, the chest radiograph (CXR) may reveal signs of pulmonary edema and right heart enlargement in advanced cases.

Patients should receive optimized medical therapy before proceeding with elective mitral valve surgery, but indicated surgery should not be delayed in symptomatic patients. Control of heart rate (HR) with avoidance of tachycardia is particularly important; thus, antiarrhythmic and antitachycardia drugs are maintained up to and including the day of surgery. Also, small incremental doses of a short-acting intravenous benzodiazepine premedication (eg, midazolam 1 to 2 mg) may be administered in the immediate preoperative period or pre-induction to avoid tachycardia due to anxiety.

Many patients with severe MS have AF and are receiving chronic anticoagulation therapy. Management of medications affecting hemostasis is discussed separately. (See "Preoperative evaluation for anesthesia for cardiac surgery", section on 'Medications affecting hemostasis'.)

Prebypass hemodynamic management — Key points for hemodynamic goals and anesthetic management during the prebypass period for patients with MS are summarized in the tables (table 12), and are described in detail in a separate topic. (See "Intraoperative hemodynamic management of aortic or mitral valve disease in adults", section on 'Mitral stenosis'.)

Prebypass TEE assessment — Prior to CPB, the transesophageal echocardiography (TEE) examination focuses on confirmation of the presence of mitral valve stenosis and quantification of its severity (eg, a thickened valve with reduced leaflet opening (movie 11), as well as a high-velocity aliased mitral inflow on color-flow Doppler imaging (image 7)) (table 13). Continuous-wave Doppler interrogation of the mitral inflow can be used to measure the transvalvular gradient (image 8); the mean mitral valve gradient is usually >5 to 10 mmHg with severe MS but is variable depending upon heart rate and stroke volume (table 13). The degree of concomitant MR is also assessed. (See "Transesophageal echocardiography in the evaluation of mitral valve disease", section on 'Role of intraoperative transesophageal echocardiography'.)

Furthermore, the LA and LAA are carefully interrogated for the presence of spontaneous echo contrast or thrombus (movie 12) [39]. Administration of an echocardiography contrast agent may be necessary to distinguish spontaneous echo contrast from thrombus. (See "Transesophageal echocardiography in the evaluation of mitral valve disease", section on 'Left atrial appendage' and "Transesophageal echocardiography in the evaluation of mitral valve disease", section on 'Spontaneous echo contrast'.)

In addition, the RV is assessed for evidence of dysfunction or dilatation due to chronic pulmonary hypertension. In some patients, tricuspid annular dilation with severe tricuspid regurgitation (TR) is present; this is an indication for concomitant tricuspid valve repair [18,19]. (See 'Surgery for tricuspid valve disease' below and "Management and prognosis of tricuspid regurgitation", section on 'At the time of left-sided valve surgery'.)

Surgical mitral valve repair, commissurotomy, or replacement — Mitral valve surgery for MS includes repair, commissurotomy, or replacement, with valve replacement most common in patients with rheumatic MS who are not candidates for or who have failed percutaneous mitral balloon valvotomy. The surgical approach is similar to that described above for mitral valve surgery for MR.

For patients with severe mitral annular calcification, only surgical or transcatheter mitral valve replacement can relieve the obstruction, since percutaneous balloon valvuloplasty or surgical valve repair are not effective options. However, the presence of severe mitral annular calcification complicates MV surgery and is associated with technical challenges and high operative mortality and morbidity rates, as discussed separately. (See 'Postbypass TEE assessment' below and "Management and prognosis of mitral annular calcification", section on 'Mitral valve surgery'.)

Postbypass TEE assessment — After mitral valve replacement, TEE is used to assess for the presence of paravalvular leak or a high gradient across the mitral prosthesis indicating iatrogenic mitral stenosis (eg, due to a stuck mechanical prosthetic leaflet or an undersized prosthetic valve or annuloplasty ring). If the LAA was ligated to reduce the risk of future thromboembolic events, residual communication between the LAA and LA should be identified and corrected. Also, possible damage to adjacent structures such as the aortic valve or the circumflex coronary artery is ruled out. As with other cardiac valve procedures, removal of residual air is guided by continued TEE monitoring. (See 'Transesophageal echocardiography: General considerations' above.)

Postbypass management — Since the LV has been exposed to chronic "underloading" in severe MS, it is at risk for acute failure following separation from CPB. Inodilator agents such as a milrinone infusion may be employed, particularly in patients with elevated PVR and coexisting RV dysfunction [40]. Concomitant administration of a low-dose dopamine or norepinephrine infusion may be necessary to avoid excessive systemic vasodilation (table 7). A high PVR and acute refractory right heart failure may occur during weaning from CPB [11]. Treatment is described separately. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Right ventricular dysfunction'.)

Arrhythmias, particularly AF, are common in the postbypass and postoperative periods. Treatment is described separately. (See "Intraoperative problems after cardiopulmonary bypass", section on 'Arrhythmias' and "Intraoperative problems after cardiopulmonary bypass", section on 'Metabolic abnormalities'.)

Bleeding is a common complication (see "Achieving hemostasis after cardiac surgery with cardiopulmonary bypass", section on 'Achieving hemostasis and management of bleeding'). Very rarely, intractable bleeding occurs due to disruption of atrioventricular continuity after mitral valve replacement for MS particularly in the setting of severe mitral annular calcification; this complication is associated with high mortality. (See "Management and prognosis of mitral annular calcification", section on 'Mitral valve surgery'.)

SURGERY FOR TRICUSPID VALVE DISEASE — Patients requiring surgery for acquired tricuspid valve disease include those with:

Tricuspid regurgitation – Significant tricuspid regurgitation (TR) is common in patients undergoing mitral valve surgery [18,19,41] but can also be a complication of right ventricular (RV) biopsy, device lead impingement, carcinoid, endocarditis, or other conditions. Concurrent tricuspid valve surgery may be performed at the time of left-sided valve surgery, as discussed separately (see "Management and prognosis of tricuspid regurgitation", section on 'Tricuspid valve surgery'). Etiology and pathophysiology of TR, stages of severity, indications for surgical intervention, and decisions regarding selection of the optimal surgical procedure are discussed in other topics. (See "Etiology, clinical features, and evaluation of tricuspid regurgitation" and "Management and prognosis of tricuspid regurgitation".)

In patients with tricuspid endocarditis, the placement of a pulmonary artery catheter (PAC) has the potential to dislodge a vegetation. This risk must be considered when manipulating guidewires for central venous cannulation and deciding whether to use PAC monitoring.

Intraoperative assessment of TR is accomplished using both two dimensional and three dimensional transesophageal echocardiography (TEE) to determine the severity of regurgitation and the annular dimensions of the tricuspid valve [5,41-43] (see "Echocardiographic evaluation of the tricuspid valve"). Hemodynamic goals for patients with TR include maintaining a normal to fast heart rate (HR) at 80 to 100 beats per minute (bpm) because a faster HR minimizes regurgitant volume. Maintenance of a normal to low pulmonary vascular resistance (PVR) facilitates forward flow in the pulmonary arterial circulation. Avoidance of hypoxia, hypercarbia, and acidosis is particularly important to prevent increases in PVR which may exacerbate RV dysfunction. Systemic vascular resistance (SVR) is maintained in the normal range.

Tricuspid stenosis – Tricuspid stenosis (TS) is most commonly rheumatic in etiology and usually associated with TR. Pathophysiology, stages of severity, indications for surgical intervention, and decisions regarding selection of the optimal surgical procedure are discussed in a separate topic. (See "Tricuspid stenosis".)

Hemodynamic goals for patients with TS include maintaining a normal to slow HR at 60 to 80 bpm, a normal to low PVR, and a normal SVR.

Maintenance of RV function with appropriate inotropic and/or vasopressor infusions (eg, epinephrine plus vasopressin if hypotension is present, or milrinone if hypotension is absent (table 7)) may be necessary in patients with either TR or TS. Such vasoactive support is usually necessary to achieve separation from CPB.

Further details regarding anesthetic management for repair of Ebstein anomaly and other congenital tricuspid valve abnormalities are discussed in a separate topic. (See "Anesthesia for surgical repair of congenital heart defects in adults: Management of specific lesions and reoperation", section on 'Ebstein anomaly' and "Anesthesia for surgical repair of congenital heart defects in adults: Management of specific lesions and reoperation", section on 'Tricuspid valve surgery'.)

Anesthetic management considerations for transcatheter tricuspid valve interventions are discussed separately. (See "Anesthesia for percutaneous cardiac valve interventions", section on 'Transcatheter tricuspid valve repair' and "Anesthesia for percutaneous cardiac valve interventions", section on 'Percutaneous tricuspid balloon valvotomy'.)

SURGERY FOR PULMONIC VALVE DISEASE — Causes of acquired pulmonic valve disease include endocarditis, carcinoid syndrome, and rheumatic fever. Clinical features and management are discussed separately. (See "Pulmonic regurgitation" and "Clinical manifestations and diagnosis of pulmonic stenosis in adults" and "Natural history and treatment of pulmonic stenosis in adults".)

Hemodynamic goals for patients who have pulmonic regurgitation or stenosis include:

Pulmonic regurgitation – For pulmonic regurgitation, a normal to fast heart rate (HR) at 80 to 100 beats per minute (bpm) is maintained because a faster HR minimizes regurgitant volume. Also, a normal to low pulmonary vascular resistance (PVR) is maintained by increasing fraction of inspired oxygen concentration (FiO2), maintaining mild hyperventilation to a partial arterial pressure of carbon dioxide (PaCO2) of approximately 30 to 35 mmHg, and thus avoiding hypoxia, hypercarbia, and acidosis. Systemic vascular resistance (SVR) is kept in the normal range.

Pulmonic stenosis – For pulmonic stenosis, a normal to slow HR at 60 to 80 bpm is maintained. This optimizes RV stroke volume and cardiac output, particularly if associated dynamic right ventricular outflow tract (RVOT) obstruction is present. Tachycardia may increase dynamic RVOT obstruction and reduce time in diastole, which reduces coronary perfusion and lead to myocardial ischemia. A normal to low PVR and a normal SVR are maintained.

Further details regarding anesthetic management for pulmonic regurgitation or pulmonic stenosis are discussed separately. (See "Anesthesia for surgical repair of congenital heart defects in adults: Management of specific lesions and reoperation", section on 'Pulmonic valve intervention'.)

Anesthetic management considerations for transcatheter pulmonic valve interventions are discussed separately. (See "Anesthesia for percutaneous cardiac valve interventions", section on 'Percutaneous pulmonic valve implantation' and "Anesthesia for percutaneous cardiac valve interventions", section on 'Percutaneous pulmonic balloon valvotomy'.)

COMBINED SURGICAL PROCEDURES — Many patients with cardiac valve disease have a combination of stenosis and regurgitation in a single cardiac valve, disease of more than one valve, or coexisting coronary disease. In such cases, optimal prebypass hemodynamic management depends on which of the lesions is predominant and which hemodynamic changes are likely to be most deleterious (table 9 and table 14). A reasonable approach for a patient who is hemodynamically stable and compensated in the preoperative period is to target intraoperative heart rate (HR) and blood pressure (BP) values to approximate the preoperative values.

Common combinations of 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'). For those with both moderate to severe AS and AR, a general hemodynamic goal is to maintain the patient's preanesthetic baseline HR and cardiac loading condition in order to maintain cardiac output (CO) and limit myocardial oxygen consumption (table 2 and table 5). 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 [44]. Hemodynamic targets for such patients take the opposing requirements for each lesion into consideration (table 12 and table 5). Typically, a normal HR (eg, 70 to 80 bpm), normal or low-to-normal SVR, and normal contractility are optimal [45,46].

Valve and coronary artery disease – Many patients with valve disease (particularly patients with AS or ischemic MR) also have coexisting coronary artery disease; these patients are particularly prone to develop myocardial ischemia. Prebypass hemodynamic management involves ensuring adequate systemic BP to optimize oxygen delivery to the myocardium while limiting myocardial oxygen demand (table 9 and table 14). The patient's baseline hemodynamic profile should dictate the targets for prebypass anesthetic management, which may include use of vasopressors, low-doses of inotropic agents, and/or pacing.

Tricuspid regurgitation with mitral valve regurgitation or stenosis – Some adults with severe left-sided cardiac valve disease, usually MR or MS, also have severe tricuspid regurgitation (TR). Prebypass hemodynamic management emphasizes the predominant lesion. Also, patients with severe TR may be receiving chronic therapy for right-sided heart failure and pulmonary hypertension. Hypoxemia and/or hypercarbia are avoided, and chronically administered pulmonary vasodilator agents are continued during the perioperative period.

During the prebypass transesophageal echocardiography (TEE) examination, each cardiac valve is assessed individually to confirm final surgical decisions for repair or replacement. In some patients undergoing cardiac surgery, a decision may be made to leave a valve with moderate regurgitation or stenosis intact since evidence of benefit from valve surgery is lacking. As an example, for patients undergoing aortic valve replacement (AVR) for AS, the available limited evidence has not established a benefit from valve surgery for moderate functional MR [47]. Another example is a patient with moderate MR undergoing coronary artery bypass grafting (CABG) surgery [24,25]. Clinical benefit from mitral valve surgery has not been established in this setting.

HIGH-RISK EMERGENCY PROCEDURES — Selected patients undergoing cardiac valve surgery are unstable upon presentation to the operating room and have extremely high risk for morbidity or mortality (eg, critical aortic stenosis [AS] with coexisting unstable coronary artery disease, acute severe aortic regurgitation [AR] with pulmonary edema, acute mitral regurgitation [MR] with left ventricular [LV] dysfunction, one or more large mobile vegetations due to endocarditis [48]). Such patients are prone to cardiac arrest in the preoperative period and after anesthetic induction before establishment of cardiopulmonary bypass (CPB). In such cases, standard resuscitation methods may not be successful. Considerations for urgent and emergency cardiac surgical procedures in such patients are discussed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Emergency cardiac surgical procedures'.)

POSTBYPASS PERIOD — Recognition and management of common cardiovascular and other intraoperative problems that may occur during the postbypass period are discussed separately. (See "Intraoperative problems after cardiopulmonary bypass".)

Since patients undergoing valve surgery (particularly aortic valve replacement [AVR]) are at increased risk for postoperative atrioventricular block, epicardial (bipolar or unipolar) pacing wires are routinely attached to the right atrium and right ventricle (RV) to maintain a stable postbypass rhythm. These pacing wires are typically placed prior to weaning from CPB (as single or duplicate sets). We ensure that pacing thresholds are adequate and perform regular checks to determine whether there is an adequate underlying cardiac rhythm (see "Weaning from cardiopulmonary bypass", section on 'Maintenance of optimal pacemaker function'). If the underlying rhythm remains inadequate following bypass, an additional temporary (backup) transvenous right RV lead (generally bipolar or quadripolar) may be inserted prior to chest closure. Another option is placement of a lead sewn to the chest wall (skin lead) in the left subclavicular area to allow unipolar RV pacing between the skin and endocardium, if bipolar pacing is not effective. Patients with persistent conduction abnormalities after the third postoperative day are referred for consideration of permanent pacemaker implantation. (See "Postoperative complications among patients undergoing cardiac surgery", section on 'Dysrhythmias' and "Temporary cardiac pacing", section on 'Pacing techniques' and "Permanent cardiac pacing: Overview of devices and indications".)

Transport of the patient and handoff in the intensive care unit are discussed separately. (See "Anesthesia for cardiac surgery: General principles", section on 'Transport and handoff in the intensive care unit'.)

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

Intraoperative transesophageal echocardiography (TEE) TEE is used for cardiac valve procedures in most centers for the following reasons (see 'Transesophageal echocardiography: General considerations' above):

Before cardiopulmonary bypass (CPB), TEE examination allows confirmation of the diagnosis, refinement of the operative plan, and identification of previously unrecognized pathology affecting patient management. After an initial complete examination, TEE is employed to continuously monitor biventricular global and regional function, as well as intravascular volume status.

During weaning from CPB, TEE is used to monitor air removal from the left heart chambers prior to allowing full ventricular ejection in order to avoid arterial air embolism.

After weaning from CPB, TEE is used to assess adequacy of the surgical intervention(s), including evaluation of the function and structure of the repaired or replaced valve and identification of complications such as impaired prosthetic leaflet mobility, paravalvular regurgitation, evidence of damage to adjacent structures such as coronary arteries (eg, regional wall motion abnormalities), or aortic dissection after aortic decannulation. Subsequently, biventricular global and regional function and intravascular volume status are continuously monitored.

Anesthetic management

General considerations General anesthesia is often maintained with a volatile inhalation anesthetic agent. However, a total intravenous anesthetic (TIVA) technique, or a combination of inhalation and intravenous (IV) agents are reasonable alternatives. (See "Anesthesia for cardiac surgery: General principles", section on 'Maintenance of general anesthesia'.)

Considerations for specific lesions – Anesthetic and hemodynamic goals as well as procedure-specific aspects of TEE examination for specific cardiac valve lesions are discussed above:

-Aortic stenosis (AS) (table 2 and table 3) (see 'Surgery for aortic stenosis' above)

-Aortic regurgitation (AR) (table 5 and table 6) (see 'Surgery for aortic regurgitation' above)

-Mitral regurgitation (MR) (table 5 and table 10) (see 'Surgery for mitral regurgitation' above)

-Mitral stenosis (MS) (table 12 and table 13) (see 'Surgery for mitral stenosis' above)

-Tricuspid valve disease (see 'Surgery for tricuspid valve disease' above)

-Pulmonic valve disease (see 'Surgery for pulmonic valve disease' above)

Combined cardiac valve procedures Many patients with cardiac valve disease have a combination of stenosis and regurgitation in a single cardiac valve, disease of more than one valve, or coexisting coronary disease. In such cases, optimal prebypass hemodynamic management depends on which of the valvular lesions is predominant and which hemodynamic changes are likely to be most deleterious (table 9 and table 14). (See 'Combined surgical procedures' above.)

Emergency surgery Some patients presenting for emergency cardiac valve surgery are hemodynamically unstable with high perioperative risk (eg, critical AS with coexisting unstable coronary artery disease, acute severe AR with pulmonary edema, acute MR with left ventricular [LV] dysfunction). Anesthetic considerations are discussed separately. (See 'High-risk emergency procedures' above and "Anesthesia for cardiac surgery: General principles", section on 'Emergency cardiac surgical procedures'.)

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Topic 91483 Version 25.0

References

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