C.1. Outline the hemodynamic management goals for each of the four valvular lesions. What are the anesthetic goals with respect to heart rate and rhythm, preload, afterload, and contractility?
Answer:
Table 7.3 summarizes the hemodynamic goals with respect to heart rate and rhythm, preload, afterload, and contractility.
Table 7.3: Hemodynamic Goals for Various Valvular Lesions
| Lesion | HR and Rhythm | Hemodynamic Goals | ||
|---|---|---|---|---|
| Preload | Afterload | Contractility | ||
| Aortic stenosis | 60-70, sinus | Full | Maintain | - |
| Aortic insufficiency | 80-90 | Maintain | Lower | May need support |
| Mitral stenosis | 60-70 | Full | - | - |
| Mitral regurgitation | 80-90, sinus if possible | Maintain | Lower | May need support |
Patients with AS depend on left ventricular filling through adequate preload and well-timed atrial contraction. The stenotic AV is a fixed lesion that will not respond to pharmacologic intervention or decreased afterload. Reducing vascular tone will only lower diastolic coronary perfusion gradients and should be avoided. Patients with AS experiencing angina may require the administration of an α-agonist such as phenylephrine rather than nitroglycerin to increase coronary perfusion pressure.
The severity of AI is determined by the size of the regurgitant orifice, the diastolic pressure gradient between the aorta and LV, and the duration of diastole. Elevated heart rates reduce the time spent in diastole and can lead to a decrease in heart size and regurgitation. Afterload reduction can lessen the regurgitant driving pressure but is limited by resulting systemic hypotension.
Slower heart rates permit adequate time for flow of blood from the LA to the LV across the stenotic MV. Left atrial emptying reduces left atrial pressure, thereby decreasing the pressure gradient across the MV and diminishing pulmonary congestion. Patients with MS can rapidly deteriorate in the setting of rapid heart rates. The reduced filling time exacerbates the marked elevation of left atrial pressures, and pulmonary edema can ensue. Whereas left ventricular contractility is generally preserved in MS, use of β-blockade can result in decreased RV contractility, which in the setting of pulmonary hypertension can further compromise cardiac output and systemic blood pressure. However, the loss in RV contractility is typically offset by the beneficial effects of heart rate reduction. Because an adverse response could be catastrophic, short-acting β-blockers, such as esmolol, should be used if necessary.
Patients with MR can rapidly deteriorate with marked increases in systemic blood pressure, so afterload reduction is recommended. As with AI, slightly increased heart rates (80-90 beats per minute) should result in smaller left ventricular volumes. However, tachycardia should be avoided in patients with ischemic (functional) MR.
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