What the Anesthesiologist Should Know before the Operative Procedure
During the past decade, mitral valve repair has become the preferred surgery for mitral valve regurgitation. Some cases of mitral stenosis are also amenable to repair. This increase in caseload is due to significant improvement in survival of these patients and perhaps in part to the widespread use of perioperative transesophageal echocardiography (TEE). Additional advantages of mitral valve repair over mitral valve replacement include preserved left ventricular function, lower rates of endocarditis, and elimination of long-term anticoagulation requirements.
Structure of the mitral valve
Anatomically, the mitral valve apparatus consists of
1. Anterior and posterior mitral leaflets
2. Mitral valve annulus
3. Chordae tendineae
4. Papillary muscles
5. Adjacent myocardium
The mitral annulus is saddle-shaped with the anterior and posterior commissural areas projecting towards the ventricle. The anterior mitral leaflet is continuous with the aortic valve, and the fibrous skeleton of the heart and the margin form one-third of the annular circumference. The posterior leaflet contributes to the remaining two-thirds of the annular circumference, and the annulus is also more muscular posteriorly.
The posterior leaflet is divided into three scallops designated P1, P2. and P3. The corresponding areas on the anterior leaflet are called A1, A2, and A3, although the anterior segments are not as clearly defined as its posterior counterparts (Figure 1).
The chordae tendineae are classified according to their implantation site on the mitral valve. Primary chordae are implanted on the free edge of the valve; secondary chords are on the body and the tertiary chordae implant at the mitral valve base. All the chordae originate from either the anterolateral or posteromedial papillary muscle in the left ventricle. The posteromedial papillary muscle is supplied by the right coronary artery, whereas the anterolateral papillary muscle has dual supply from the left anterior descending and the circumflex coronary arteries.
Mitral valve disease in patiens presenting for mitral valve repair
At present, mitral regurgitation is the most frequently diagnosed valvular heart disease in the US and is the most frequent indication for mitral valve repair.
Mechanism of mitral regurgitation – The Carpentier classification
Type I: Characterized by normal leaflet motion. Since leaflet motion is normal, mitral regurgitation may be caused by either annular dilatation, resulting in an inadequate coaptation surface, or by mitral valve leaflet perforation, as seen in cases of endocarditis or congenital mitral clefts.
Type II:Characterized by increased leaflet motion. The free tip of the leaflet moves above the mitral annular plane during systole (mitral valve prolapse). This typically occurs with chordal rupture or elongation. Rupture may occur with blunt chest trauma, endocarditis, or endocardial biopsies while chordal elongation is caused by myxomatous degeneration.
Type IIIa: Characterized by restricted leaflet motion in both systole and diastole. This is often seen in a rheumatic process, causing fibrosis of the chordae with shortening and stiffening.
Type IIIb: Characterized by restricted leaflet motion in systole only. This type of mitral regurgitation suggests papillary muscle dysfunction due to ischemia or dilated cardiomyopathy. Leaflets are tethered inferiorly and posteriorly by ventricular dilatation, leading to mitral regurgitation. Leaflets open normally during diastole.
These mechanisms are demonstrated in Figure 2.
Etiology of mitral regurgitation
The etiology of mitral regurgitation can be organic or functional.
Mitral valve degenerative disease, which causes 75% of all cases of mitral regurgitation, often leads to mitral valve prolapse in which part of the valve moves beyond the annular plane of the mitral valve. The most common types of degenerative disease include:
Barlow’s disease (mitral valve prolapse syndrome or diffuse myxomatous degeneration) is due to myxomatous degeneration of the mitral valve. On average, it affects 3% of the total population. Mitral regurgitation is caused mainly by a dilated annulus; but the chordae become thickened and elongated, and there is redundant valve tissue. This leads to both type I and type II mitral regurgitation from mitral valve prolapse. Patients typically have a long history of a systolic heart murmur. Women are more likely to have Barlow’s than men. Mitral valve prolapse is demonstrated in Figure 3.
Fibroelastic degeneration usually presents suddenly in patients older than 70 years, in contrast to Barlow’s, which is seen in a younger population. In fibroelastic degeneration the valves are delicate and transparent with chordae that are thin and may be ruptured. The annulus is dilated with variable amounts of calcification. The mechanism of mitral regurgitation is both type I and II.
Marfan syndrome is characterized by a dilated annulus and calcification is rarely seen. No myxomatous degeneration is present.
Other causes of organic mitral regurgitation may include infective endocarditis with leaflet perforation, trauma leading to papillary muscle or chordal rupture, and inflammatory diseases like rheumatoid arthritis. Acute myocardial infarction resulting in papillary muscle necrosis may lead to papillary muscle rupture a flail leaflet.
Functional mitral regurgitation can be either ischemic or nonischemic, as in the case of dilated cardiomyopathy.
Mitral stenosis represents the minority of patients indicated for mitral valve repair. Mitral stenosis is almost exclusively caused by rheumatic fever and is thus rarely seen in industrialized countries. Furthermore, women are two times more likely to be affected by rheumatic fever than are men. Almost half of rheumatic mitral valve patients have both stenosis and regurgitation, and roughly one-third have multivalve involvement. Valves are thickened, calcified, and rigid with fused commissures attached to shortened and fused chordae. Initial damage is rheumatic, but changes in flow patterns cause turbulence and further trauma. Other rare conditions that may present clinically like mitral stenosis include left atrial myxoma, cor triatriatum, parachute mitral valve, and degenerative calcific mitral stenosis.
1. What is the urgency of the surgery?
What is the risk of delay in order to obtain additional preoperative information?
Emergent: Acute left ventricular failure in a patient following acute mitral regurgitation is a surgical emergency. Acute mitral regurgitation may be a manifestation of a chronic condition such as myxomatous degeneration, that presents acutely with chordal rupture, annular dilatation, papillary muscle dysfunction, or rupture.
In a pathophysiological sense, acute mitral regurgitation is an emergency because of the normal compliance of the left atrium. In chronic mitral regurgitation the left atrium dilates to facilitate a higher volume. In acute mitral regurgitation no compensation occurs and this leads to high pulmonary vascular pressures and ultimately pulmonary edema and right ventricular failure. Emergency mitral valve repair carries higher perioperative mortality and morbidity than elective surgery.
Chronic mitral regurgitation
Mitral valve repair for chronic organic mitral regurgitation is generally considered an elective procedure.
Indications for mitral valve repair include patients with severe mitral regurgitation, whether they are symptomatic or asymptomatic. The benefit of mitral valve repair in symptomatic severe mitral regurgitation is evident, but in order to consider surgery in the asymptomatic patient, supporting evidence of left ventricular dysfunction or left ventricular dilatation, or atrial fibrillation is required. Indications for more moderate symptomatic mitral regurgitation are less clear.
Patients undergoing primarily CABG but who have severe concomitant mitral regurgitation should have a simultaneous mitral valve repair.
Elective surgery: mitral regurgitation
Mitral stenosis is a slowly progressive disease, and patients usually present for elective surgery. In the developed world, mitral stenosis now commonly presents in patients who are in their 60s and 70s rather than in their 40s or 50s, as is seen in developing countries. Open valvotomy is indicated for patients with symptomatic (NYHA class III or IV) moderate or severe mitral stenosis if percutaneous balloon valvotomy is contraindicated, or not available, or if the valve morphology is unsuitable. Patients with combined mitral stenosis and mitral regurgitation may also present for mitral valve repair. Furthermore, mitral valve repair is often offered to patients with mild to moderate mitral stenosis but with complications such as recurrent embolic events and severe pulmonary hypertension.
2. Preoperative evaluation
Patients scheduled for mitral valve repair have a continuum of symptoms and clinical signs. Acute severe mitral regurgitation may present with cardiogenic shock, pulmonary edema, dyspnea, orthopnea, and right heart failure. Angina, when present, may point to myocardial infarction with papillary muscle rupture as the cause of mitral regurgitation. Chronic mitral regurgitation symptoms are often attributed to other causes. These patients have fatigue and loss of exercise tolerance, which are related to impaired left ventricular ejection. Pulmonary hypertension is also frequently present and leads to dyspnea.
Patients with mitral valve prolapse syndrome (Barlow’s disease) have increased incidence of supraventricular tachycardia and Wolff-Parkinson-White syndrome. Other rhythm disturbances may be evident including premature atrial and ventricular beats, sinus bradycardia, and atrioventricular node blocks. Atrial fibrillation can develop in any patient with mitral regurgitation with risk directly related to an enlarged left atrium size.
The mitral regurgitation murmur is typically a high-pitched holosystolic murmur best heard at the apex and spreading to the left axilla. In case of acute posterior leaf prolapse, the anteriorly directed jet may sound very similar to an aortic stenosis murmur. Palpating a rapid carotid pulse upstroke in these cases may help to distinguish between these two conditions. Patients with severe mitral regurgitation may have “silent mitral regurgitation” with no murmur because of the low amount of turbulence across the wide-open flail valve. Therefore auscultation alone is not a very good predictor of mitral regurgitation severity. An early diastolic rumble can be due to increased transmitral volume early in diastole and should not be confused with mitral stenosis. An S3 (rapid filling) impulse can often be palpated together with a laterally displaced apex beat.
Mitral stenosis from rheumatic heart disease develops slowly, but once symptoms appear the disease is progressive, and fatal if left untreated. The normal mitral orifice area is 4-5 cm2. Debilitating symptoms usually become evident with an orifice area of around 1.5 cm2. Mitral stenosis patients have decreased left ventricular filling, which leads to decreased cardiac output. Pulmonary venous congestion then develops, and right ventricular afterload increases. Eventually, right ventricular hypertrophy develops with right ventricular failure.
A right ventricular heave may be palpated, and the apical impulse is quiet due to underfilling of the left ventricle. S1 is typically loud and S2 may increase in intensity if pulmonary hypertension is present. An opening snap is typical early in diastole accompanied by a diastolic rumble best heard at the apex. Moderate isometric exercise, like a handgrip may increase the intensity of the diastolic murmur. A diastolic blowing murmur (Graham Steell murmur) may indicate pulmonary incompetence and pulmonary hypertension.
Atrial fibrillation remains the most common complication of mitral stenosis and may lead to abrupt worsening of symptoms. Atrial fibrillation leads to loss of the atrial contribution to filling volume, and the rapid ventricular response may shorten diastolic filling time, compromising filling volume even more. Onset of atrial fibrillation worsens the overall prognosis of mitral stenosis patients. Mitral stenosis is also a risk factor for infective endocarditis.
a. B-type atrial natriuretic peptide (BNP) is often elevated in patients with mitral regurgitation.
3. What are the implications of co-existing disease on perioperative care?
b. Cardiovascular system
Patients with chronic functional mitral regurgitation may have a biventricular pacing device as part of their therapy. Anesthesia management of patients with a biventricular pacing device is similar to the approach used with other cardiac rhythm management devices. For surgery, the pacemaker should be programmed to an asynchronous mode above the intrinsic rate to ensure ventricular pacing. Many of these devices will not change to asynchronous pacing mode with magnet placement. The defibrillation or cardioversion therapy should be disabled for the duration of the surgery. Special precautions must also be taken to place the defibrillator pads away from the device.
Often, intra-aortic balloon counterpulsation may be employed for stabilization prior to surgical repair of the mitral regurgitation.
Chest x-rays show signs of left atrial and ventricular enlargement with a double atrial shadow and the enlarged atrium forming the right heart border. The clinician will more likely find these x-ray signs in patients with long standing mitral regurgitation. Calcification of the mitral valve and mitral valve annulus may be seen on a lateral chest x-ray. Patients with acute mitral regurgitation are also likely to show x-ray signs of acute pulmonary edema with kerley-B lines, and peri-hilar infiltrates (the so-called “bat wing” appearance). Asymmetric pulmonary edema may be seen with eccentric jets.
Hemoptysis is associated with mitral stenosis, due to rupture of bronchial-pulmonary anastomosis from chronic venous engorgement, which also predisposes patients to recurrent pulmonary infections. The chronic venous engorgement leads to pulmonary hypertension by several mechanisms including pulmonary arterial constriction and interstitial edema in the pulmonary vasculature. Pulmonary compliance is low due to fibrosis of the alveoli and arteriolar walls.
With spirometric testing, vital capacity, maximum minute ventilation and diffusion capacity are all decreased. Compliance may further reduce with exercise and patients have overall increased work of breathing. Ortner syndrome is hoarseness resulting from compression or stretch of the recurrent laryngeal nerve by an enlarged atrium or pulmonary artery. Pulmonary embolism is responsible for 10% of the mortality of untreated mitral stenosis. Chest x-ray will show signs of chronic left atrial volume and pressure overload, evidenced by straightening of the left heart border.
Systemic embolization is more common in mitral stenosis. Left atrial thrombus formation is responsible for most emboli even in patients who are in sinus rhythm. Spontaneous echo contrast is seen in 45% of patients with mitral stenosis. Risk factors for thrombus formation are related to left atrial size, increasing age, and atrial fibrillation. Patients with long-standing mitral valve prolapse may have higher risk of systemic embolization, probably related to an enlarged left atrium.
g. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (eg. musculoskeletal in orthopedic procedures, hematologic in a cancer patient)
Liver enzymes may also be elevated in cases of right heart failure.
4. What are the patient’s medications and how should they be managed in the perioperative period?
Management of chronic severe mitral regurgitation consists of beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and diuretics. Generally, no benefit is seen in treating patients with chronic mitral regurgitation with vasodilators. There is good evidence for continuing perioperative beta-blockade in this patient population. Continuation of ACE inhibitors, however, is associated with high incidence of intraoperative hypotension; therefore, they are generally withheld prior to cardiac surgery.
h. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern?
Patients who had previous transient ischemic attacks will be taking aspirin (75-325 mg). Aspirin should be stopped for 3-6 days before elective mitral valve repair. However, if the patient is at high risk for coronary artery thrombosis (a recent myocardial infarction, for instance), aspirin should be continued up to the day of surgery.
Warfarin (Coumadin) is indicated in patients with mitral regurgitation who have atrial fibrillation. Warfarin should be discontinued for at least 4 doses prior to surgery. Due to a particularly high thrombotic risk; however, bridging therapy should be instituted. Low molecular weight heparin 1 mg/kg SC q12h or unfractionated heparin infusion, adjusted to laboratory results for partial thrombin time, is usually recommended. The International Normalized ratios (INR) should be monitored daily. If the INR level is above 1.5 at the time of surgery, vitamin K 1-2 mg IV may be given to decrease the INR.
Patients presenting for mitral valve repair who have acute mitral regurgitation may be receiving arterial vasodilator medication, usually in the form of a nitroprusside infusion with or without concomitant inotropic agents like dopamine or epinephrine.
Mitral stenosis patients may be on aspirin or warfarin and an anticoagulant for stroke prophylaxis. Perioperative management of anticoagulation is discussed in the section above. Symptomatic patients often take oral diuretics for symptom relief and are prescribed beta-blockers, calcium channel blockers, or digoxin for ventricular rate control in cases of atrial fibrillation. All of these drugs should be continued in the perioperative period.
i. What should be recommended with regard to continuation of medications taken chronically?
j. How To modify care for patients with known allergies –
Patients who have heparin-induced thrombocytopenia (HIT) or history of HIT represent a special management challenge in mitral valve repair on cardiopulmonary bypass. This is due to antibodies against platelet factor 4 (PF4), which activate platelets causing hypercoagulability, thrombosis, and thrombocytopenia. One treatment option is to delay surgery until antibody titers become undetectable. Bivalirudin, Lepirudin, and Danaparoid are alternative anticoagulants, but none have FDA approval for use during cardiopulmonary bypass.
Patients who have had previous heparin therapy or have taken low doses of antithrombin-III preoperatively may have heparin resistance. These cases may be managed with additional doses of heparin, 1-2 units of fresh frozen plasma (FFP), or antithrombin III concentrate.
Protamine reactions result in bronchospasm, pulmonary hypertension, right heart failure, and hypotension. Volume infusion together with small doses of vasoconstrictors or inotropes is usually enough to manage the brief hemodynamic instability, but severe reactions may require a return to CPB. Management options for those with a prior history of protamine reactions include not reversing heparin at all, using a non-protamine heparin reversal agent (PF4 or heparinase) or using a heparin alternative in the first place (not FDA approved).
k. Latex allergy- If the patient has a sensitivity to latex (eg. rash from gloves, underwear, etc.) versus anaphylactic reaction, prepare the operating room with latex-free products.
If the patient has a sensitivity to latex (eg. rash from gloves, underwear, etc.) versus anaphylactic reaction, prepare the operating room with latex-free products.
l. Does the patient have any antibiotic allergies?
Known penicillin allergy: Recommendations for patients with penicillin allergy are vancomycin with additional gram negative coverage by an aminoglycocide antibiotic (gentamicin). Gentamicin elimination is retarded by CPB which cause otorenal toxicity. A single dose of 4 mg/kg is recommended.
m. Does the patient have a history of allergy to anesthesia?
5. What laboratory tests should be obtained and has everything been reviewed?
Preoperative echocardiographic evaluation of the mitral valve in mitral regurgitation
Patients with mitral regurgitation should have a complete echocardiographic evaluation preoperatively. TEE is not required but adds incremental information about the feasibility of mitral valve repair. An overview of the qualitative and quantitative parameters used for grading mitral regurgitation severity can be found in Table 1. The left ventricular ejection fraction and loading conditions should be noted as the severity of mitral regurgitation may be dependent on these variables.
Echocardiography is the most accurate noninvasive measure to diagnose and quantify mitral stenosis. The most common method for quantifying mitral stenosis is to measure the transmitral gradient (using the modified Bernoulli equation). The mitral valve area can be determined by a variety of methods including planimetry (calculated by measuring the proximal isovelocity surface area), using the continuity equation, or using the pressure half-time method. (An overview of the parameters used for grading mitral stenosis severity are shown in Table 2.) Echocardiographic scoring systems from Wilkens et al. (PUBMED:3190958) may help determine the potential success of repair vs. balloon angioplasty.
Intraoperative Management: What are the options for anesthetic management and how to determine the best technique?
Mitral valve repair is performed under general anesthesia and requires CPB. Newer percutaneous techniques for mitral valve repair do not require CPB and are often performed in interventional rooms with fluoroscopy and TEE. These procedures also require general anesthesia in order to control the airway and ventilation, and to ensure patient comfort.
External defibrillator pads should be placed for all re-operations and minimally invasive procedures. Lung isolation is also mandatory for minimally invasive approaches. This can be achieved by either a double-lumen endotracheal tube or a single-lumen tube in combination with a bronchial blocker. Peripheral CPB cannulation is often used and must be considered when placing an arterial catheter. (For instance, right axillary cannulation makes a right radial arterial catheter undesirable.).
Cardiovascular active drugs should be readily available. These include epinephrine, vasopressin, phenylephrine, milrinone, nitroprusside, nitroglycerin, amiodarone, potassium chloride, and calcium chloride. Blood and blood products should be available immediately in the room before skin incision. Extra blood products should be ordered and immediately available in the case of repeat “re-do” surgery.
Invasive hemodynamic monitoring is standard of care for mitral valve repair. An arterial catheter is placed before induction of anesthesia, usually in a radial artery. A central venous catheter aids in monitoring fluid response. In acute mitral regurgitation, a large V wave is often seen in the pulmonary capillary wedge pressure tracing (PCWP) and may lead to overestimation of the left ventricular filling pressure. In chronic mitral regurgitation, however, the left atrial compliance change results in loss of the V wave.
Heart rate and rhythm are monitored with a 5-lead ECG and ST-segment analysis software. Depth of anesthesia monitoring with a BIS-monitor is helpful.
A urinary catheter with an integrated thermistor tip is inserted after induction. Temperature should be monitored at more than one site. Bladder and nasopharyngeal temperature monitoring is commonly recommended.
The use of intraoperative TEE is standard of care for mitral valve repair and will be discussed separately.
b. General Anesthesia
Anesthesia goals before instituting CPB for mitral valve repair for mitral regurgitation can be summarized as:
1. Increasing effective forward cardiac output.
2. Minimizing the regurgitant volume into the left atrium.
3. Preventing pulmonary hypertension and pulmonary vascular congestion.
4. Managing right heart failure.
The preferred anesthesia technique uses an opioid in combination with a low dose inhaled anesthetic agent.
Because mitral regurgitation is a dynamic condition, changes in intraoperative loading conditions can dramatically alter its extent. A gentle decrease in afterload with inhaled anesthetics or nitroprusside improves systemic perfusion by decreasing the regurgitant volume to the left atrium. Dopamine, low-dose epinephrine, or milrinone can be used to support contractility. Inotropic agents help to minimize regurgitation by reducing annular size especially in functional regurgitation in patients with depressed left ventricular function.
Preload should be maintained or even augmented before induction of anesthesia. Care should be taken with fluid administration, however, because mitral regurgitation patients may have associated pulmonary hypertension with pulmonary venous congestion. Left ventricular overfilling may easily lead to frank pulmonary edema or mitral annular dilatation. Care, as always, should be taken to avoid hypercapnia, acidosis, uncontrolled pain, hypothermia, and hypoxia since all of these conditions increase pulmonary arterial pressures.
An ideal heart rate for mitral valve regurgitation patients is at the higher end of normal (80-100 bpm). Bradycardia increases ejection time, giving rise to an increased regurgitant fraction. Sinus rhythm, although desirable, is of less critical importance than in patients with mitral stenosis.
De-airing of the heart is facilitated by a head-down position and gentle ventilation of the lungs after the cardiac chambers have been surgically closed. Inadequate de-airing may lead to air embolism to the right coronary artery, which may complicate separation from CPB. TEE is an excellent way to look for any residual intracardiac air.
Inotropic support when weaning from CPB should be used if known predictors of low cardiac output syndrome are present. CPB separation in patients for mitral valve repair often presents challenges in managing right ventricular failure. Inhaled nitric oxide is a good choice for managing elevated right ventricular pressures. Milrinone and dobutamine are alternative pulmonary vasodilators, but their use often leads to unwanted systemic hypotension.
Left ventricular function often declines by about 10%-20% following mitral valve repair for mitral regurgitation. This is due to the sudden increase in afterload (wall stress) of the dilated left ventricle and decreased preload following the mitral valve repair. Cardiac index should be above 2 L/min/m2 and mean arterial pressures of 65-85 mm Hg are acceptable. Epicardial pacing wires should be placed after mitral valve repair and may be used to augment cardiac output in patients whose underlying rhythm or rate is temporarily inadequate.
Goals of anesthesia in mitral stenosis patients include:
1. Maintaining left ventricular preload.
2. Keeping heart rate low normal to maximize diastolic filling time.
3. Managing right heart failure.
4. Avoid aggravating the pulmonary hypertension.
Managing the preload in mitral stenosis patients generally represents the most challenging aspect of the anesthesia care. The flow across the stenosed valve is dependent on the pressure gradient and any decrease in the filling pressure from fluid shifts or vasodilatation results in a profoundly low cardiac output. The normal physiologic response to vasodilation is tachycardia, but in MS, tachycardia only serves to lower the cardiac output further. Sinus rhythm is highly desirable since loss of the atrial kick or a fast ventricular response rate is both catastrophic in mitral stenosis. Target heart rates are at the lower end of normal (60-80 bpm).
Contractility and left ventricular function are preserved in most patients with isolated mitral stenosis, although up to 30% of mitral stenosis patients may suffer from left ventricular dysfunction related to the rheumatic process, ie, chronic myocardial inflammation, fibrosis, and dysfunction of the subvalvular apparatus. The right ventricle often needs support since long-standing pulmonary hypertension causes a dilated and hypertrophied right ventricle with minimal contractile reserve. Inhaled nitric oxide is often used to treat high pulmonary artery pressures, but dobutamine or milrinone are other choices while low dose epinephrine supports the right ventricle in the face of high pulmonary pressures.
A combination of inhaled anesthetic agent and opioid is the preferred technique. Any drop in blood pressure is aggressively treated with vasoconstrictor drugs like phenylephrine. Patients may have increased work of breathing due to pulmonary changes, and early ventilatory support is indicated with induction.
The intraoperative transesophageal echocardiographic evaluation
Mitral valve repair is a class I indication for the use of intraoperative TEE. Surgeons may make repair decisions based on precise intraoperative TEE findings. Of the 20 standard views, 6 are used specifically to evaluate the mitral valve:
- Midesophageal views:
1. Four-chamber view.
2. Commissural view.
3. Two-chamber view.
4. Long-axis view.
- Transgastric views:
1. Basal short-axis view.
2. Transgastric two-chamber view.
The reader should refer to a standard echocardiographic textbook for a detailed discussion of the different views and echocardiographic examination of the mitral valve. The preoperative diagnosis of mitral regurgitation or mitral stenosis should be confirmed with intraoperative TEE at the start of the case. Structural parameters, Doppler parameters, and quantitative parameters should all be considered when grading the severity of mitral regurgitation or mitral stenosis.
The structural aspects evaluated with TEE that are specifically important in mitral valve repair include the leaflets which may have perforations, clefts, thickening, calcium deposits, or impaired mobility. A mitral annulus diameter greater than 4 cm is an indication of annular dilatation. Mitral annular calcification complicates mitral valve repair and should be reported when present. Left ventricular dilatation may tether mitral valve leaflets causing restricted valve movements and functional mitral regurgitation. A dilated LV may also be as consequence of structural mitral regurgitation. The subvalvular apparatus is evaluated for chordal fusion, shortening, or rupture. Spontaneous echo contrast in the left atrial appendage suggests a high risk for thrombosis.
TEE is also useful for examining the aorta for atherosclerotic plaque, which is especially important if retrograde arterial perfusion is employed, or in case if an intra-aortic balloon pump will be placed to support the circulation after CPB. TEE is required to confirm position of the venous cannula in the superior vena cava when port access is used for mitral valve repair.
Post-repair systolic anterior motion (SAM) with dynamic outflow tract obstruction is associated with mitral valve repair. Pre-repair TEE may be used to quantify the risk factors of SAM. If the C-sept distance (the distance measured from the mitral valve coaptation point to the septum) is less than 2.5 cm, the patient may be at risk for SAM. Similarly, a ratio less than 1.3 of the anterior mitral valve leaflet length to the posterior mitral valve leaflet length (AL/PL) is also associated with an increased risk for SAM after the repair.
After separation from CPB, TEE is used to assess the quality of the repair. Any residual mitral regurgitation leads to a slightly worse prognosis, but generally, only moderate and severe mitral regurgitation is an indication for returning to CPB. TEE is also an excellent tool to ensure proper de-airing of the heart before CPB separation.
Complications of mitral valve repair may be diagnosed by TEE. Injury of the circumflex artery during the repair is diagnosed by visualizing new lateral and posterolateral wall motion abnormalities. In the rare case of ventricular perforation, continuous entrainment of air will be present in the ventricle. Evidence of SAM should be reported and treated.
3D TEE evaluation of the mitral valve
Because of the complex 3D saddle shape of the mitral valve, real-time 3D TEE has been advocated for investigating the complex mitral valve and its apparatus in patients receiving mitral valve repair. Using 2D echo to evaluate the mitral valve requires the user to integrate several 2D images in order to understand valve structure or pathology. This may lead to interobserver variability and errors. Real-time 3D TEE of the mitral valve can overcome many of the traditional limitations, especially in patients with bi-leaflet pathology, clefts of the valve surface, or commissural disease.
Comprehensive real-time 3D TEE examination of the mitral valve includes the following images:
- The “en face” view, which is similar to the surgeon’s view of the mitral valve
- Color 3D Doppler that can be used to measure the vena contracta (VC)
- Full-volume acquisition of the left ventricle to evaluate the interrelationship of the mitral valve with the subvalvular apparatus
Real-time 3D TEE has shown promise in evaluating the post-repair mitral valve. It may improve the diagnosis of paravalvular leaks and also aids in understanding the implications of edge-to-edge stitches that might have been placed. In addition it is useful in evaluating the left ventricular outflow tract for any SAM that may occur after the mitral valve repair. Real-time 3D TEE is a promising technology, although its place in routine clinical practice has not yet been established.
Median sternotomy is the most common surgical incision for mitral valve repair. Alternative techniques, such as port access and robotic mitral valve repair, are on the increase. Surgical incision for these techniques is a 6-cm mini thoracotomy in the fourth intercostal space with additional incisions for multiport access. Peripheral CPB cannulation is mandatory. Mini-incision direct vision mitral valve repair is performed occasionally and requires an upper or lower hemisternotomy. The minimally invasive approaches result in decreased perioperative blood loss, better cosmetic results and shorter hospital stays.
Lateral tilt of the operating table is used often, and the care team must ensure that the patient is well secured. Myocardial protection is based on the use of moderate hypothermia (28-30°C) with intermittent cold-blood high-potassium cardioplegia infusion. The surgeon insufflates carbon dioxide in the field while specialized instruments and vacuum-assisted venous drainage are used to facilitate minimally invasive procedures.
The ultimate goal of mitral valve reconstruction is to reestablish normal leaflet motion, stabilize and correct annular dilatation, and create a large surface area for coaptation.
Specific surgical repair techniques
Remodeling ring annuloplasty
This ring restores the normal physiological anterolateral-to-transverse diameter of the mitral annulus during systole. Annuloplasty rings are either rigid or flexible. The annuloplasty increases the coaptation surface without causing mitral stenosis. Using a prosthetic ring greatly increases the durability of the repair by decreasing the tension on the sutures. Therefore, prosthetic rings are used in most mitral valve repair procedures except in cases of infective endocarditis. The surgeon chooses the correct ring size by measuring the annulus with an obturator. (Figure 4)
Quadrangular resection of the posterior leaflet
A prolapsing posterior leaflet is often seen in degenerative conditions. The excess tissue is first removed by resecting in a perpendicular direction from the free edge toward the annulus. The valve is then reconstructed with plication sutures. Alternatively, a sliding leaflet technique can also be used along with quadrangular resection. With this technique, the bases of P1 and P3 segments are detached, moved inward, and reattached to the annulus. Posterior leaflet height should be reduced to less than 1.5 cm to decrease the risk for post-repair SAM. (Figure 5 and Figure 6)
Anterior leaflet prolapse
A small anterior leaf prolapse can be treated with a triangular resection of the anterior mitral valve leaflet. This resection should be less than 10% of the anterior valve area since resecting more of the valve may cause unacceptable distortion of the anterior valvular geometry. Various chordal reconstruction techniques can also be employed with anterior leaflet prolapse. Chords can be transpositioned from the posterior to anterior leaflets, and secondary chords can be transferred to the free edge. When reconstruction with native chords is not possible, artificial chords can be attached using a polytetrafluoroethylene expandable suture. Papillary muscle sliding plasty and papillary muscle shortening are techniques used to correct anterior leaflet prolapse that is due to elongated papillary muscles or elongated chords. Splitting the papillary muscle can, however, compromise the blood supply of the papillary muscle and is therefore not advocated by all surgeons.(Figure 7)
Patch closure of leaflet perforation
Defects on the anterior mitral valve leaflet, usually from perforations, can be closed with autologous pericardium or segments of homograft. (Figure 8)
This technique involves approximating and suturing the free edges of the anterior and posterior leaflets together, thereby creating a double orifice mitral valve. Sutures are most commonly placed central in the A2 and P2 segments but may also be placed closer to the commissures. Edge-to-edge repair can now be done with percutaneous, transseptal technique (E-clip). (Figure 9)
This technique is used to enlarge the opening of fused mitral valve leaflet and it is performed by open repair or by percutaneous balloon procedure in patients who meet criteria for open balloon valvuloplasty.
Resection of chordae in rheumatic disease
In patients with contracted and fused chordae due to rheumatic disease, this technique is used to achieve better valve mobility. Because of the low incidence of rheumatic heart disease in the developed world, however, it is performed in a minority of cases presenting for mitral valve repair.
Residual mitral regurgitation
The quality of the repair should be evaluated after the repair. The surgeon generally injects saline into the ventricle and looks for a linear lineof coaptation parallel to the annulus. If the posterior leaflet occupies more than 50% of the mitral orifice area, its height should be reduced to minimize the risk of SAM. After separation from CPB, TEE examination is used to evaluate the repaired valve for incompetence orfunctional problems. Mild post-repair mitral regurgitation is acceptable but moderate mitral regurgitation may warrant a return to CPB tocorrect residual regurgitation or even convert to a valve replacement procedure.
Mitralstenosis can occur after mitral valve repair especially when an Alfieristitch or an undersized annular ring is used. A mean gradient of morethan 5 mm Hg or peak gradient of more than 15 mm Hg with continuous wave Doppler is suggestive of stenosis. Compliance changes post repair makes the pressure half-time measure unreliable for assessing mitral stenosis but proximal isovelocity area measurements may be used reliably.
Dynamic left ventricular outflow tract obstruction and SAM
Dynamic left ventricular outflow tract obstruction may be observed in up to 8%of patients following mitral valve repair. In almost all cases this is due to SAM of the anterior mitral valve leaflet, which occurs when the annular ring displaces the posterior ventricular wall closer to the outflow tract causing the filling compartment of the LV to be in-line with the subaortic region. This positions the mitral valve in the outflow tract and causes SAM during the ejection phase. High velocity causes a Venturi effect and pulls the anterior mitral valve leaflet into the left ventricular outflow tract although other factors may play a role.
SAM can usually be treated conservatively with volume loading, discontinuation of inotropes and vasodilators, or by starting alpha-agents and beta-blockers. In rare cases, valve re-repair or mitral valve replacement may be necessary.
Annuloplasty ring placement may compromise the integrity of the noncoronary and left coronary cusps of the aortic valve causing aortic incompetence.
6. What is the author’s preferred method of anesthesia technique and why?
What prophylactic antibiotics should be administered? The most common surgical site infection in cardiac surgery is from Staphylococcus species. Administering prophylactic antibiotic has been proved to lower infection.
Current antibiotic prophylaxis recommendations are based on the STS guidelines of 2006. Cephalosporins are often the drug of choice. Newer generations of cephalosporins have more gram negative than gram positive coverage; therefore the older generation drugs provide better protection. Evidence shows no difference between cefazolin and cefuroxime, and either can be recommended as an antibiotic prophylaxis. Vancomycin is suggested as an adjuvant drug in patients with high risk for MRSA. This includes patients who have been hospitalized for more than 3 days, patients who are already receiving antibiotic treatment, or patients who have prosthetic cardiac valves, or patients who will be in an environment with high incidence of MRSA postoperatively.
Cephalosporin should be given within 60 minutes of skin incision. Additional doses are indicated every 3-4 hours during surgery, preferably after conclusion of CPB, since cephalosporin is sequestered in the CPB circuit. Vancomycin is given by slow IV infusion, which should be completed within 1 hour of skin incision. Dosage is based on weight (15 mg/kg) with a maximum dose of 1.5 g. The utility of a second dose of vancomycin after the conclusion of CPB has not been established.
b. If the patient is intubated, are there any special criteria for extubation?
c. Postoperative management
After completion of the repair, patients generally remain intubated for 4-6 hours in the ICU to ensure a period of hemodynamic stability and to confirm hemostasis.
Atrial fibrillation is now recognized as an important postoperative complication.
Glucose control reduces the rate of postoperative infections, although “tight glucose control” is controversial and not recommended.
Atrial fibrillation is common after cardiac surgery and typically occurs on postoperative days 2-5. Specifically, it is associated with higher incidence of postoperative neurologic, renal, and infectious complications. Multivariate predictors of postoperative atrial fibrillation includes increasing age, medical history of chronic obstructive pulmonary disease, or history of prior atrial fibrillation, valve surgery, and withdrawal of ACE inhibitor or beta-blocker therapy.
Therefore, patients at high risk for postoperative atrial fibrillation should receive prophylaxis. Beta-blockers are known to be effective and should be restarted as soon as they can be tolerated. Amiodarone is also an effective prophylaxis and should be considered when beta-blockers are contraindicated.
Bi-atrial pacing decreases the incidence of post cardiac surgery atrial fibrillation and should be considered but is not commonly used. As with all dysrhythmias, electrolyte levels should be normalized, with potassium and magnesium concentrations being of particular importance. Heart blocks due to edema of the conduction tissue are treated with atrioventicular pacing. Patients may be atrial-paced or AV paced at 80-90 bpm in the post-CPB period to maintain cardiac output
Coronary artery injury
The circumflex coronary artery is located in the atrioventricular groove close to the posterior mitral annulus. Inadvertent suturing of the circumflex artery may compromise flow and cause myocardial ischemia. This complication may be suggested by new lateral wall abnormalities seen on TEE or by ST segment changes on ECG.
Other rare cardiac complications include ventricular rupture through the atrioventricular groove or papillary muscles that may require patch repair.
Long-term repair failure
Mitral valve repair is most successful when applied to degenerative mitral valves, and 15-year followup suggests that up to 93% of patients do not require re-operation. Failure of repair is related to progression of the disease or procedural problems such as suture dehiscence or chordal rupture. Specifically, shortening of chordae seems to increase the risk for re-operation as does failure to place an annuloplasty ring.
As with any CPB procedure, patients coming for mitral valve repair are at risk for developing postprocedure renal dysfunction. Renal failure requiring dialysis is associated with mortality in excess of 60% compared to 1% for those not having renal failure. Prolonged hospitalizations and intensive care unit (ICU) stays are the norm these patients. Preexisting renal dysfunction, diabetes mellitus, low cardiac output syndromes, emergency surgery, and nephrotoxic agents like NSAIDs and iodinated radiocontrast agents are all renal risk factors.
Patients undergoing mitral valve surgery have higher risk for cerebral complications. Open-chamber cardiac surgery predisposes the patient to embolism of thrombi, gas bubbles, or debris. Neurologic injury is divided into type I and type II injury with a combined incidence of around 6% after cardiac surgery. Type I injury includes postoperative nonfatal stroke and coma. Type II injury includes memory deficit and seizures. More subtle changes in cognitive performance, i.e., postoperative cognitive decline, may occur in up to 50% of patients 6 weeks after surgery.
Mitral valve repair has become the preferred surgical therapy for mitral regurgitation. Patients with degenerative mitral valve disease represent the majority of mitral regurgitation cases, and fortunately, degenerative valves are the most suitable for mitral valve reconstructive surgery. The durability of contemporary repair techniques is excellent, and survival of patients with preserved left ventricular function is now similar to age-matched controls. Intraoperative TEE is indispensable for the whole team and its skilled use of this tool by anesthesiologists provides an excellent opportunity for improving overall outcome. A thorough understanding of the underlying pathophysiology helps to guide the anesthesia approach, which contributes greatly to the success of modern mitral valve repair.
What’s the Evidence?
Enriquez-Sarano. “Mitral regurgitation”. Lancet . vol. 373. 2009. pp. 1382-94.
“Augoustides and Atluri. Progress in mitral valve disease: understanding the revolution”. YJCAN . vol. 23. 2010. pp. 916-923.
Bonow. “Focused Update Incorporated Into the ACC/AHA 2006 Guidelines for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons”. Circulation . vol. 118. 2008. pp. e523-e661.
Filsoufi and Carpentier. “Principles of reconstructive surgery in degenerative mitral valve disease”. Semin Thorac Cardiovasc Surg . vol. 19. 2007. pp. 103-10.
Engelman. “The Society of Thoracic Surgeons Practice Guideline Series: antibiotic prophylaxis in cardiac surgery, part II: antibiotic choice”. Ann Thorac Surg . vol. 83. 2007. pp. 1569-1576.
Fischer. “Intraoperative classification of mitral valve dysfunction: The role of the anesthesiologist in mitral valve reconstruction”. YJCAN . vol. 23. 2011. pp. 531-543.
Jungwirth, B, Mackensen, GB. “Real-time 3-dimensional echocardiography in the operating room”. Semin Cardiothorac Vasc Anesth. vol. 12. 2008. pp. 248
Mathew, JP, Swaminathan, M, Ayoub, CM. Clinical manual and review of transesophageal echocardiography. 2010.
Mathew. “A multicenter risk index for atrial fibrillation after cardiac surgery”. JAMA . vol. 291. 2004. pp. 1720-9.
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- What the Anesthesiologist Should Know before the Operative Procedure
- 1. What is the urgency of the surgery?
- What is the risk of delay in order to obtain additional preoperative information?
- 2. Preoperative evaluation
- 3. What are the implications of co-existing disease on perioperative care?
- b. Cardiovascular system
- c. Pulmonary
- d. Renal-GI:
- e. Neurologic:
- f. Endocrine:
- g. Additional systems/conditions which may be of concern in a patient undergoing this procedure and are relevant for the anesthetic plan (eg. musculoskeletal in orthopedic procedures, hematologic in a cancer patient)
- 4. What are the patient's medications and how should they be managed in the perioperative period?
- h. Are there medications commonly seen in patients undergoing this procedure and for which should there be greater concern?
- i. What should be recommended with regard to continuation of medications taken chronically?
- j. How To modify care for patients with known allergies -
- k. Latex allergy- If the patient has a sensitivity to latex (eg. rash from gloves, underwear, etc.) versus anaphylactic reaction, prepare the operating room with latex-free products.
- l. Does the patient have any antibiotic allergies?
- m. Does the patient have a history of allergy to anesthesia?
- 5. What laboratory tests should be obtained and has everything been reviewed?
- Intraoperative Management: What are the options for anesthetic management and how to determine the best technique?
- Intraoperative management
- Mitral regurgitation
- Mitral stenosis
- The intraoperative transesophageal echocardiographic evaluation
- 3D TEE evaluation of the mitral valve
- Surgical approach
- Specific surgical repair techniques
- Remodeling ring annuloplasty
- Quadrangular resection of the posterior leaflet
- Anterior leaflet prolapse
- Patch closure of leaflet perforation
- Alfieri stitch
- Open commissurotomy
- Resection of chordae in rheumatic disease
- Residual mitral regurgitation
- Mitral stenosis
- Dynamic left ventricular outflow tract obstruction and SAM
- Aortic incompetence
- 6. What is the author's preferred method of anesthesia technique and why?
- a. Neurologic:
- b. If the patient is intubated, are there any special criteria for extubation?
- c. Postoperative management