Chapter 7. Mitral Valve Disease

• While the aortic valve serves as the gateway to the systemic circulation, the mitral valve is a one-way door to the left ventricle (LV). When intact, the mitral valve makes sure that a stroke volume's (SV) worth of blood is delivered to the LV. Should the valve be too tight as in mitral stenosis (MS), the LV is underloaded reducing the SV (Video 7–1A, 7–1B, 7–1C). Moreover, the narrowed mitral valve prevents adequate drainage of the left atrium (LA) and the pulmonary circulation. With time, the LA dilates and pulmonary arterial (PA) pressures increase leading to the development of atrial fibrillation, pulmonary edema, and right ventricular failure. Consequently, these conditions make the anesthetic management of the MS patient for mitral valve (MV) replacement most challenging.
• When the mitral valve becomes incompetent it no longer functions to ensure the one-way, forward flow of blood during each cardiac cycle. As the LV contracts during systole, blood can be ejected forward through the aortic valve (AV) into the systemic circulation, or the blood can flow retrograde into the LA via the leaky MV. Like aortic regurgitation (AR), mitral regurgitation (MR) can develop both acutely or exist chronically. Patients with chronic MR develop compensatory mechanisms, which permit them to eject a sufficient SV into the systemic circulation to maintain circulatory function. Conversely, the patient with acute MR lacks adequate compensatory mechanisms. Acute MR frequently presents secondary to papillary muscle dysfunction or rupture following myocardial infraction or due to the destruction of the valve during mechanical trauma or by infectious processes. As such, the acute MR patient usually presents in cardiogenic shock as the SV ejected into the systemic circulation is inadequate to meet the patient's metabolic demands.

Mitral Stenosis

The normal area of the MV is 4 to 6 cm2. Isolated narrowing of the MV is frequently associated with rheumatic heart disease.1 MS is more likely to occur in female compared to male patients by a ratio of 2:1. Calcification of the MV independent of rheumatic heart disease occurs infrequently. However, MV calcification can occur in dialysis-dependent chronic renal failure patients. As the rheumatic process progresses the valve area declines leading to an increased pressure gradient between the LA and the LV during diastole. This increased gradient drives diastolic filling of the LV as blood is pushed forcefully through the stenotic MV orifice.

As the gradient progressively increases and mitral valve area falls below 1.5 cm2, patients become increasingly symptomatic. Pressure gradients between the LA and LV can become greater than 25 mm Hg. Patients frequently become dyspneic as the high LA pressure is transmitted to the pulmonary vasculature. Pulmonary arterial pressures increase at times leading to pulmonary edema. Patients with MS may be asymptomatic at rest but when diastolic time is decreased (such as during exercise, stress, or pregnancy) the LA may not have sufficient time to empty and to load the LV—reducing the SV and increasing LA pressure. Increased LA pressure is transmitted to the pulmonary vasculature and the patient becomes dyspneic. Likewise, as the LA becomes distended secondary to MS, the patient can develop atrial fibrillation. Atrial fibrillation, especially when accompanied by rapid ventricular rate, reduces diastolic filling time, which in conjunction with the lack of atrial contraction at the end of diastole, further decreases LV filling and increases LA pressure leading to the patient becoming even more symptomatic.

Chronic Mitral Regurgitation

Many disease processes can acutely or chronically disrupt the integrity of the MV apparatus. For the valve not to leak, the valve annulus, leaflets, chordae, and papillary muscles must function properly (Video 7–2). Should the heart dilate secondary to cardiomyopathy the annulus can become enlarged preventing the coaptation of the anterior and posterior valve leaflets during systole—resulting in regurgitation (Figure 7–1 and Video 7–3). Should the papillary muscles or chordae be dysfunctional, torn, or stretched, the leaflets can prolapse or flail into the LA during systole—again resulting in regurgitation (Figure 7–2 and Videos 7–4A and B). Similarly, should a leaflet be too short or restricted, it will not be able to effectively close during systole (Figure 7–3 and Video 7–5). Finally, any disease process, which destroys or damages the leaflets, will also cause the regurgitation of blood into the LA during ventricular systole.

Various diseases including coronary artery disease, cardiomyopathies, rheumatic heart disease can lead to chronic MR. Patients can tolerate mild to moderate chronic MR for many years until they become increasingly dyspneic with exertion. As chronic MR is often secondary to other cardiac diseases such as coronary artery disease, it is difficult to differentiate between the symptoms of the chronic MR and those of the underlying cardiac disease.

Acute Mitral Regurgitation

Acute MR occurs when the mitral apparatus becomes acutely dysfunctional. Patients may present in shock in the setting of an acute myocardial infarction with papillary muscle ischemia. Similarly, endocarditis can lead to loss of MV integrity resulting in acute MR and cardiogenic shock (Video 7–6). Patients are often dyspneic and in congestive heart failure. Such cases usually require emergent surgery if they are to be salvaged. Intra-aortic balloon pump (IABP) placement may be temporarily needed to reduce LV afterload so to minimize regurgitation until surgery can be commenced.

The heart of the patient with MV disease attempts to compensate for the inability of the MV to ensure efficacious loading of the LV and ejection of an adequate SV into the systemic circulation. The LV of the patient with MS is chronically underloaded while that of the patient with MR is either acutely or chronically volume overloaded.

MR can occur either from a primary defect in the structure of the MV or secondary to abnormalities in the structure or geometry of the LV. As the LV dilates secondary to cardiomyopathy or ischemia, the papillary muscles shift caudally to the valve and can prevent the leaflets from effectively closing. Moreover, annular dilatation is also contributory.

The heart of the MR patient must respond to the increased volume load presented to it during each diastolic filling period.2-5 In the patient with an incompetent MV, during ventricular systole the SV is not fully ejected out through the AV into the systemic circulation. Rather, a good percentage of the SV enters the LA. To compensate, the LV hypertrophies eccentrically and dilates allowing for a greater left ventricular end-diastolic volume (LVEDV). This dilatation can further worsen MR. Concurrently, the LA dilates to accommodate the regurgitant volume. The increase in LVEDV is often accomplished without an increase in left ventricular end-diastolic pressure (LVEDP). Consequently, patients can tolerate chronic MR for many years because they maintain the forward SV by increasing the size of the LV.

Unfortunately, as with all of these compensatory mechanisms there are limits to their ability to maintain near-normal physiologic function in the setting of abnormal structural function. As the disease progresses, the heart increasingly dilates and contractile function deteriorates. LV compliance becomes decreased, thereby reducing the ability of the heart to accommodate increased LVEDV with only minimal changes in LVEDP. Additionally, ventricular remodeling increases the ratio of ventricular radius to ventricular wall thickness.4 This increased ratio together with an increase in LVEDP will result in an increase in wall stress according to the LaPlace law:

LV wall stress = (LV pressure × LV radius)/LV thickness

This increase in wall stress ultimately leads to an increase in myocardial oxygen demand.

The increased LVEDP is transmitted to the left atrium raising the left atrial pressure (LAP). Patients become progressively dyspneic and fatigued, as the heart can no longer eject a near normal SV into the systemic circulation.

The patient with acute MR does not have time to develop compensatory mechanisms for the reduction in forward flowing SV. When the MV becomes acutely incompetent, a part of the total SV is ejected in a retrograde manner in to the LA during systole.

Total SV = Forward Flowing SV + Retrograde Flowing SV

In the chronic MR patient, the total SV is increased secondary to dilation of the LV to compensate for that part of the total SV, which flows retrograde (retrograde flowing SV). Consequently, the forward flowing SV remains largely unchanged until the compensatory mechanisms are overwhelmed and the heart fails.

The patient with acute MR cannot increase the total SV since there is no time for such compensatory mechanisms to develop. Therefore, the forward flowing SV is reduced. The patient often presents in cardiogenic shock secondary to a reduced forward cardiac output. Concurrently, the LA cannot accommodate the regurgitant volume resulting in increased pulmonary pressures and pulmonary congestion.

The heart of the patient with MS must compensate for the chronic underloading of the LV and a reduced SV. Additionally, the pulmonary vasculature must mitigate the effects of increased LAP to prevent pulmonary congestion.

In patients with MS, a pressure gradient develops between the LA and LV during diastole. Recall, the SV is loaded into the LV during diastole. The stenotic MV impedes the delivery of blood to the LV. As the MV area decreases an increased LAP develops as blood is forced to flow through the narrowed MV orifice. This increased LAP is transmitted to the pulmonary veins. Should atrial fibrillation develop or the patient become tachycardic for any reason the patient will have a decrease in diastolic time—further reducing the time that the SV can pass through the narrowed orifice of the MV into the LV. Left atrial pressure further increases leading to pulmonary congestion. At the same time, the SV is progressively reduced as the LV is inadequately loaded. Patients become increasingly inactive, as the SV cannot meet the needs of the patient to conduct normal life activities.

The pulmonary vasculature tries to mitigate the increase in LAP in order to protect against the development of pulmonary edema. Pulmonary arteriolar changes may protect the pulmonary capillary bed by making it less leaky in the setting of high pulmonary venous pressures.1 Although such compensatory mechanisms may retard the development of pulmonary edema, they produce over time profound pulmonary hypertension (Chapter 8). Increasing resistance in the pulmonary arteries requires the right ventricle (RV) to do increased pressure work to pump the SV through the pulmonary vasculature. Although the RV responds with compensatory mechanisms to this pressure challenge, in time, RV failure ensues leading to peripheral edema, ascites, and hepatic failure. Consequently, the compensatory responses of the heart and pulmonary vasculature to MS can produce profound pulmonary hypertension and RV failure. Additionally, the chronically underloaded LV may itself have impaired contractility. Following relief of MS, the patient's chronically underloaded LV may not be able to accommodate the additional volume load presented to it in diastole through an open mitral valve without becoming distended with a very high LVEDP.

Transthoracic echocardiography (TTE) is an initial step in the cardiologist's diagnosis of the MV patient. Perioperatively TEE is most likely to be employed to assist the surgeon performing MV repair or replacement.6 Three-dimensional TEE is becoming more commonly available and is used increasingly to examine the mitral valve perioperatively (Video 7–7). The basic TEE views of the normal mitral valve were discussed in the introduction to echocardiography and should be briefly reviewed before proceeding with this section (Figure 7–4).

Mitral Stenosis

The anterior and posterior leaflets of the MV appear thickened and poorly mobile in patients with mitral stenosis. As the patient's valve becomes stenotic, the orifice narrows obstructing diastolic filling of the LV.

When performing a perioperative TEE examination in the MS patient it is also critical to look for additional echo findings associated with mitral stenosis such as a dilated left atrium with stagnant blood (Video 7–8). The smoky appearance or spontaneous echo contrast is indicative of decreased blood velocities in the LA. The two-chamber view demonstrates both the MV and the beak-like left atrial appendage (LAA). The LAA is often the site of clot formation; the clot can be removed at the time of surgery and the LAA subsequently ligated. Left and right ventricular function is often impaired in the MS patient secondary to LV underloading, pulmonary hypertension, and RV failure.

Cardiologists employ both TTE and TEE to examine and quantify the mitral valve.7,8 Perioperatively the valve area and pressure gradient across the MV will have already been determined before the patient is referred for surgery. Nonetheless, it is important to be able to assess the pressure gradient and estimate valve area in the operating room. Doppler measurements and the Bernoulli equation are used perioperatively to determine the transmitral pressure gradient between the LV and the LA.

LAP − LVEDP = 4V2

where V is the velocity of flow between the LA and the LV across the stenotic MV. Recall, that in areas of stenosis, blood flows faster (the rapids!!) indicating a greater pressure gradient between the two heart chambers. Mean pressure gradients greater than 10 mm Hg are associated with severe MS and a valve area less than 1.0 cm2.

There are several techniques, which can estimate the valve area of the stenotic MV. Although the cardiologist will have performed these prior to surgery it is useful to understand the concepts especially when MS is detected unexpectedly during a perioperative TEE examination.

The pressure half-time (PHT) method can estimate the degree of mitral stenosis (Figure 7–5). Using continuous wave Doppler, as discussed in the introductory chapter, we can measure the blood velocity across the stenotic mitral valve, and by using the Bernoulli equation we can calculate the atrioventricular pressure gradient. PHT is the time required for the atrioventricular pressure gradient to decrease from the initial maximal value to one-half of that value. It is calculated by the software incorporated in the TEE machine as 0.7 × maximal velocity of the blood across the mitral valve. PHT is obtained from the spectral Doppler display of the blood flow across the mitral valve by tracing the slope from the maximal to the minimal velocity in the Doppler envelope.

In patients with greater degree of stenosis, it takes longer for the pressures between the left atrium and left ventricle to equilibrate resulting in a longer pressure half-time. The stenotic valve area can be estimated from the PHT calculation as follows:

MV valve area = 220/PHT

Hence, any PHT greater than 220 milliseconds is associated with a mitral valve area of less than 1 cm2 area and as such with severe mitral stenosis.

The proximal isovelocity surface area (PISA) method can likewise be used to estimate valve area in mitral stenosis (Figure 7–6).

The blood flow across the mitral valve can be visualized by using color flow Doppler. As blood rushes toward the narrowed orifice of the stenotic mitral valve, it accelerates, with the formation of multiple shells of hemispheric shape. The area of a flow convergence hemisphere is known as proximal isovelocity surface area and the velocity on the surface of this hemisphere is the same. According to the conservation of mass principle, the flow rate at the surface of a hemispheric shell is the same with the flow rate through the stenotic mitral valve. Generally, the Nyquist limit determines the velocity on the color flow map where the blood flow appears to change direction known as "aliasing." By adjusting the Nyquist limit of the color flow Doppler map, the flow velocity at the hemispheric surface where the flow is "aliasing" can be known. The radius of the hemisphere where the flow is "aliasing" can be measured. The maximum velocity of the blood at the level of the stenotic valve can be also measured. Thus, it is possible to estimate valve area by knowing the velocity of blood flow at the point of the stenosis, the area of the PISA hemisphere, and the velocity of flow at the hemisphere.

PISA area = 2πR2 where R is the radius of the PISA (cm) The PISA velocity = the Nyquist limit (cm/s)

The velocity of blood flow through the stenotic valve is measured with continuous wave Doppler at the level of the mitral valve in diastole.

So,

MV area = (PISA area × Nyquist limit/maximal MV flow velocity) × α/180

The angle correction α/180 is added to the calculation to adjust for the reality that the PISA is not a complete hemisphere. The alpha (α) angle reflects the reality that the mitral valve leaflets do not sit as a straight line but are angled from the baseline.

Mitral Regurgitation

Both acute and chronic MR can be diagnosed with the aid of either TTE or TEE. Knowledge of MV anatomy is necessary in determining the mechanism and significance of MR in the perioperative period.

The anterior and posterior mitral leaflets are joined at both the anterolateral and posteromedial commissures. The posterior leaflet has been described as consisting of three scallops: anterolateral (P1), medial (P2), and posteromedial (P3). These three posterior leaflet scallops coapt with their respective areas of the anterior leaflet of the MV (A1, A2, and A3). The various TEE views of the MV allow the visualization of these scallops. As such, it is possible to identify areas of valvular prolapse or restriction and use the TEE to identify the mechanism of regurgitation. The mitral valve fails to coapt during systole secondary to one of the following possible mechanisms:

1. The mitral annulus is dilated such that the leaflets do not come together sufficiently to fully close. In this instance, the color flow Doppler jet of MR is usually centrally directed.

2. The leaflets of the mitral valve move too much and prolapse or flail above the point of coaptation. This results in an eccentric color flow Doppler jet directed away from the prolapsing/flail valve leaflet.

3. The mitral valve leaflets do not move enough. Restriction of movement of one or more of the leaflets prevents the valve from coapting resulting similarly in an eccentric regurgitant jet.

Often disease processes of the papillary muscles and chordae can lead to the development of acute MR secondary to ruptured chordae and/or ischemic papillary muscles resulting in a "flail" mitral leaflet (Video 7–9).

TEE allows the determination of both the location and cause of MR as well as an estimation of its severity. Using the Carpentier nomenclature of the mitral valve leaflets as outlined above, it is possible to identify the source of leaflet pathology. Mastery of this takes some time and only those with the appropriate training and certification in perioperative TEE should undertake to guide surgery by the identification of MV pathology. Still, it is quite possible to readily discern if leaflets are restricted, flail, prolapsed, intact, or unable to coapt secondary to annular dilatation.

There are a number of TEE techniques, which can be employed to assess the severity of MR including9:

• Jet Area: The area of the regurgitant color flow jet is compared with that of the area of the left atrium. If the area is greater than 40% the MR is thought severe. However, if the jet hugs the wall of the LA this method will underestimate the severity of MR (Video 7–10).
• Vena Contracta: The vena contracta is the narrowest part of the regurgitant jet as it passes through the valve. A vena contracta greater than 6 mm in diameter is thought to be associated with significant MR (Video 7–11).
• PISA: The concept of PISA has been described in the earlier section. As the LV contracts during systole, blood accelerates toward the incompetent mitral valve forming multiple shells of hemispheric shape (Figure 7–7). Using the same formula as above, the area of the regurgitant orifice can be calculated by knowing the Nyquist limit or velocity where the regurgitant flow is aliasing, the radius of the hemisphere where the flow is aliasing, and the maximal velocity of the regurgitant flow at the level of the regurgitant orifice. In a simpler manner, it can be estimated that if the Nyquist limit is set at 40 cm/s a PISA hemisphere radius of >1cm is associated with severe MR.
• Pulmonary Vein Doppler: Blood flows from the pulmonary veins into the LA both in systole and in diastole. The systolic flow in the pulmonary vein is normally greater than that of diastolic flow (Figure 7–8A). When severe mitral regurgitation is present, because of greatly increased LA pressure the systolic pulmonary vein flow is often blunted or reversed (Figure 7–8B).

Decisions of repair or replacement of the MV is dependent upon discussions between the patient, surgeon, and cardiologist. Anesthesiologists are unlikely to participate in any discussion as to which surgical or catheter-mediated approach will be employed. However, anesthesiologists using TEE are likely to be very closely involved not only in providing for perioperative management but also in guiding and assessing the immediate results of surgical manipulations.

MS patients with appropriate valve morphology may be candidates for percutaneous mitral balloon valvotomy.1 Other patients are likely to be referred for MV replacement. Valvotomy is not indicated if there is concomitant MR or LA thrombus or the valve morphology does not appear favorable for that technique.

Patient survivability after MV replacement due to MS is dependent upon patient age, ventricular function, presence of pulmonary hypertension, and the absence of coronary artery disease. Preservation of the mitral apparatus during MVR has been shown to improve LV function and patient survival.10

Patients presenting with mitral regurgitation will frequently undergo mitral valve repair. MV repair offers the advantage of eliminating the need for systemic long-term anticoagulation and additionally spares the mitral apparatus leading to improved ventricular function (Videos 7–12 and 7–13). When complete, the repaired MV should not leak (Videos 7–14, 7–15, and 7–16). Residual regurgitation must be reported to the surgical team so that they can determine if the repair is inadequate and MV replacement warranted.

Various catheter-mediated approaches to mitral regurgitation have also been proposed.10-12 Regurgitation secondary to annular dilatation is surgically corrected by placement of an annuloplasty ring to restore competency of the valve. Catheter-based devices have been introduced into the coronary sinus to "cinch" the mitral annulus and improve valve competency. Patients with redundant or flail mitral valve leaflets are surgically managed with MV repair (if possible) or replacement. Perioperatively anesthesiologists skilled in TEE are asked to assess the competency of these repairs and to rule out systolic anterior motion (SAM) of the mitral valve, which can lead to obstruction of the flow in the left ventricular outflow tract during systole and hemodynamic instability (Chapter 10). Catheter-based techniques can repair the MV by clipping together the anterior and posterior leaflets of the valve to restore valve coaptation creating a double orifice mitral valve (Figure 7–9). Development of catheter delivered prosthetic mitral valves similar to those found in the aortic position have lagged due to the complex interactions between the valve leaflets, chords, annulus, and ventricle. Still, it is possible that anesthesiologists of the future will, with increasing frequency, be called to care for patients in the catheterization laboratory for valvular repair.13,14

The MV disease patient is at risk for the development of atrial fibrillation (AF). Patients with MS are particularly stressed by the development of a rapid ventricular response to AF. Reduced diastolic time results in less than adequate loading of the LV and an increase in left atrial pressure (LAP). MS patients can quickly develop pulmonary edema and cardiogenic shock. Up to 40% of patients with symptomatic MS will develop AF.1 Medical therapy is aimed at controlling the ventricular response through the use of beta-blockers, calcium antagonists, or amiodarone. Additionally, heparin is administered to prevent thrombus development. In the setting of acute hemodynamic decompensation, synchronized cardioversion is indicated. However, patients who have been in AF for a period of hours may develop left atrial thrombus. The presence of LA thrombus should be ruled out by TEE examination before proceeding with elective cardioversion as restoration of sinus rhythm might provoke systemic thromboembolism.

At the time of MV repair or replacement, surgeons may also undertake the Cox Maze procedure.15 The Maze procedure interrupts pathways of electrical conduction in the atria to reduce the incidence of atrial fibrillation postoperatively. Numerous interruptions in the atrial conduction pathways are performed sometimes using radio frequency or cryoablation. (TEE probes are disconnected from the machine and withdrawn at the time of the maze to avoid the potential for aberrant conduction through the probe and possible esophageal injury.) Patients are often placed on amiodarone therapy intraoperatively following the maze procedure.

Mitral stenosis patients can be amongst the most challenging faced by anesthesiologists for either cardiac or noncardiac surgery. The stenotic valve prevents adequate loading of the LV. A slow heart rate and sufficient diastolic time are needed to accomplish diastolic filling. Tachycardia reduces diastolic time and hence results in increased LAP and decreased SV. Since cardiac output (CO) = SV × HR, the low SV will result in a low CO. Since BP = CO × SVR, maintenance ofBP is predicated upon sufficient systemic resistance. Unfortunately, surgery and anesthesia can both result in tachycardia, hypovolemia, and reduction in vascular tone rendering the patient potentially hemodynamically unstable during anesthetic induction. Moreover, the MS patient may have a degree of pulmonary hypertension and RV failure. Inadequate ventilation and hypercarbia can further increase PA pressures and exacerbate RV failure. The failing RV may inadequately load the LV additionally contributing to inadequate systemic CO. The mere institution of positive pressure ventilation can reduce RV output with concomitant LV failure. Rhythm disturbances associated with anesthetics (eg, nodal rhythm etc) can similarly impair LV filling further worsening the patient's hemodynamic performance.

Ideally for the MS patient, anesthetic management is adjusted to mitigate the various perturbations as described above. In practice, this may be more complicated than might be initially apparent. As always, the choice of anesthetic agents employed is less significant than managing the hemodynamic consequences of those choices. Patients for noncardiac surgery with significant MS should at the least have arterial line monitoring if possible. Patients coming for MVR will of course be fully monitored with TEE included. TEE can also be employed in the patient for noncardiac surgery in lieu of placement of a PA catheter. Additionally, should a PA catheter be included in the plans for hemodynamic management the wedge position is best avoided in patients with pulmonary hypertension in order to avoid PA rupture.

Vasodilatation encountered at the time of anesthetic induction can be managed through the administration of vasopressors (eg, vasopressin, norepinephrine, phenylephrine). RV failure as a consequence of increased PA pressure can be treated by administering inotropic agents. Inotropes such as dobutamine and milrinone may improve myocardial contractility with the caveat that they can also produce tachycardias further decreasing diastolic filling and SV. Nitric oxide (NO) can be very useful in the patient who has pulmonary hypertension and RV dysfunction. Reduced pulmonary vascular resistance can improve RV function and consequently the SV.

Using echocardiography and invasive pressure monitoring, the anesthesiologist must adjust volume delivery, pulmonary vascular resistance, systemic vascular tone, and myocardial contractility to the degree possible up to the initiation of CBP in cardiac surgery or through the end of the case in noncardiac surgery. Management of the pregnant patient with severe MS is particularly challenging due to the volume shifts associated with delivery.16

The patient with acute mitral regurgitation often presents to the OR in the setting of myocardial infarction in cardiogenic shock. These patients are frequently hypotensive requiring multiple vasoactive infusions and are often supported with an intra-aortic balloon pump. Management is largely resuscitative in nature until the patient can be placed on CPB. Anesthetics other than muscle relaxants are administered as hemodynamically tolerated. Bispectral index (BIS) monitoring, although subject to much debate, is suggested for use in this and all cardiac patients as hemodynamic instability frequently requires the use of small amounts of anesthetic agents. Consequently, these patients are at increased risk of awareness intraoperatively and should be assessed for awareness postoperatively so that psychologic interventions can be made.

Patients with chronic MR generally have time to compensate for their leaky MV and routine anesthetic management is aimed at promoting forward blood flow by avoiding bradycardia and by lowering systemic resistance. Induction of anesthesia often results in both vasodilatation and tachycardia making the chronic MR patient somewhat more manageable perioperatively up to a point. However, over time compensatory mechanisms fail and the patients develop ventricular dysfunction, increased ventricular wall stress, dysrhythmias, pulmonary hypertension, and RV failure. These patients can be as hemodynamically unstable as the patients with severe MS during anesthesia.

In those patients with severely impaired LV ventricular function, RV failure, and pulmonary hypertension coming for valve repair or replacement, anesthetic management up to the initiation of CPB can be stormy. The anesthesiologist might need to manipulate volume administration, inotropes, vasoconstrictors, pulmonary vasodilators, and anesthetic agents in order to make the patient as hemodynamically "stable" as possible. It is important to understand that hemodynamic stability might be an elusive goal in the prebypass period and some patients will need emergent institution of CPB.

Patients following valve repair may be challenging to wean from CPB. The patient following MV replacement or repair may be dysfunctional secondary to left, right or biventricular failure.

Briefly, the RV failure patient often requires the use of milrinone or dobutamine to improve RV contractile function and decrease pulmonary vascular resistance. NO and inhaled prostaglandins can be used to further decrease PA pressures and improve RV outflow. LV dysfunction is likewise approached with the use of inotropic agents and/or vasoconstrictors (vasopressin) in order to maintain vascular tone in the presence of vasodilating inotropic agents such as milrinone. Similar to prebypass manipulations, combinations of inotropes, vasoconstrictors must be tried in each patient until the most effective recipe of agents is discerned. In few instances, no combination of hemodynamic and anesthetic agents will permit the heart to generate a sufficient CO to maintain an acceptable BP. In those instances, mechanical assistance of the heart may be required including the use of an intra-aortic balloon pump (IABP) or various ventricular assist devices.

Mitral Valve Disease

A 61-year-old woman presents to her cardiologist with a complaint of dyspnea and irregular rhythm. She is found to be in atrial fibrillation and a TEE examination is performed.

Case Questions

What lesion is present in the Video 7–1A?

Mitral stenosis.

How can the severity of MS be determined by echocardiography?

The severity of MS can be determined intraoperatively by determining a pressure gradient across the mitral valve. Additionally, the valve's area can be estimated using both the PISA and pressure half-time methods.

A pressure gradient of 15 mm Hg is determined and a valve area of 1 cm2 is noted.

What other findings should be considered upon reviewing the echo examination?

RV and LV function are assessed and the atrium is examined for the presence of LAA thrombus.

No thrombus is found; however, her RV function appears reduced.

After uneventful surgery, her MV is replaced.

A bileaflet mechanical valve is placed in the mitral position (Video 7–14). There are no peri-valvular leaks around the valve and the normal washing jets, which prevent the buildup of clot on the valve surface, are present.

The patient is weaned from CPB using milrinone. Her BP is 60/40 mm Hg, PA 40/22, HR 100 bpm, CI 2.2 L/min/m2. What can be done to improvesystemic BP?

Vasopressin 1 to 2 U/h by infusion is administered with improvement of the BP to 90/60 mm Hg.

However, her pulmonary arterial pressures rise to 70/50 mm Hg and she develops right ventricular dysfunction. What can be done?

Nitric oxide (NO) is administered by inhalation and her PA pressures somewhat decrease to 60/40 mm Hg. Her systemic blood pressure is 75/45 mm Hg and her LV is poorly contractile as well despite increasing inotropic support.

How can her function be improved?

An IABP is placed and effective counterpulsation decreases PA pressures to 45/29 mm Hg. Her systemic pressure improves as does her CI. She is safely transported to the ICU.