Aortic Stenosis

Critical to the management of a patient with AS is avoidance of hypotension, which can initiate a cascade of events leading to cardiac arrest. Hypotension decreases the gradient for coronary perfusion with resultant ischemia. Ischemia leads to diminished cardiac output and decreased blood pressure further compromising coronary perfusion. The occurrence of cardiac arrest in a patient with AS can be catastrophic because closed-chest cardiac massage will provide little gradient for blood flow across a stenotic AV.

Patients with AS are particularly dependent on their atrial "kick" for adequate ventricular filling volume and can rapidly become hypotensive and ischemic following onset of supraventricular tachycardia or atrial fibrillation. These rhythms are not uncommon during atrial cannulation. Therefore, all preparations for the initiation of CPB should be made before atrial manipulation.

The increased muscle mass of the hypertrophied LV can be more difficult to adequately protect with cardioplegia. Careful attention to surface cooling, myocardial temperature measurement, and the use of retrograde cardioplegia can be helpful. Following AV replacement, hypertension from LV output now unopposed by the stenotic valvular lesion can result in stress on suture lines and excessive bleeding. The compliance of the LV is unchanged by surgery and still critically dependent on adequate preload and sinus rhythm. Hypertension is best managed with an afterload-reducing agent, such as nicardipine, rather than a preload-reducing agent, such as nitroglycerin.

Aortic Insufficiency

Patients undergoing AV replacement for AI often present difficult management decisions. The usual treatment measures for hypotension (α-agonist) can have deleterious effects by increasing regurgitant volume. Use of combined α- and β-agonists (ephedrine, epinephrine, or infusions of dopamine or dobutamine) might be required. Although it can lessen regurgitant volume, afterload reduction is beneficial in only a subset of patients with AI. Those patients with elevated LVEDP, reduced ejection fraction, diminished cardiac output, and systemic hypertension usually benefit from afterload reduction. In contrast, those patients without this constellation can experience a decrease in cardiac output secondary to diminished preload from reduced atrial filling. Systemic hypotension usually limits the utility of targeted afterload reduction in the acute setting. The presence of AI makes initiation of CPB a critical period. Periods of bradycardia or ventricular fibrillation can lead to rapid volume overload of the LV through the incompetent AV. Pacing, electrical defibrillation, and/or cross-clamping should be performed to prevent ventricular distention. Similarly, myocardial protection is compromised by AI. Adequate root pressures are usually not obtainable; hence, delivery of cardioplegia requires aortotomy and cannulation of the coronary ostia. Use of retrograde cardioplegia is advantageous. Following AV replacement, the ventricle no longer has the lower pressure/impedance outflow afforded by the low aortic diastolic pressure, and inotropic support is often required. As with AS, the presence of an aortic suture line necessitates rapid response to hypertension to avoid bleeding and dissection.

Mitral Stenosis

Patients undergoing MV replacement for MS are particularly challenging to manage. Marked elevations in pulmonary vascular resistance can be present with associated right-sided heart failure. Stasis in the LA necessitates careful echocardiographic examination for the presence of atrial and atrial appendage thrombi. Manipulation of the heart before cross-clamping should be avoided due to risk of acute decreases in preload. Following replacement, the chronically underfilled, underworked LV might be unable to accommodate the new volume load. Inotropic support is often required for RV failure and occasionally to improve LV function. Afterload reduction and improved systemic perfusion using an IABP can be beneficial.

Mitral Regurgitation

Similarly, patients with MR can have pulmonary hypertension and right-sided heart failure. In contrast to AI, almost all patients with MR greatly benefit from afterload reduction, both pharmacologically and through an IABP. Diminution of LV systolic pressure through afterload reduction decreases the pressure gradient from the LV to the LA during systole, with a resultant decrease in regurgitant volume.

Pre-bypass assessment of LV function can be misleading. Preserved ejection fraction and elevated stroke volume can mask marked LV systolic dysfunction. In MR much of the LV volume is ejected into the low-pressure/impedance outflow path of the LA. This route is no longer available after valve replacement. Following MV replacement, a dysfunctional LV might be unable to provide adequate cardiac output into the systemic circulation with its higher vascular resistance, which usually necessitates inotropic support.

Patients previously in atrial fibrillation without marked atrial enlargement often revert to or can be converted to sinus rhythm following valve replacement. When the diameter of the atrium is significantly enlarged; however, the likelihood of maintaining sinus rhythm dramatically decreases.

References

• Gaudino M, Di Franco A, Rong LQ, Piccini J, Mack M. Postoperative atrial fibrillation: from mechanisms to treatment. Eur Heart J. 2023;44:1020-1039.
• Ramakrishan H, Craner RC, Devaleria PA, Cook DJ, Housmans PR, Rehfeldt KH. Valvular heart disease: replacement and repair. In: Kaplan JA, Augustides J, Maneck GR, Maus T, eds. Kaplan's Cardiac Anesthesia. 7th ed. Elsevier; 2017:770-817.