Anesthesia for Severe Mitral and Tricuspid Regurgitation

Anesthesia for Severe Mitral and Tricuspid Regurgitation

ANESTHETIC PROTOCOLS FOR SPECIFIC CONDITIONS 465 minimize increases in heart rate and stress-related catecholamine release are desirable. Patients w...

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ANESTHETIC PROTOCOLS FOR SPECIFIC CONDITIONS

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minimize increases in heart rate and stress-related catecholamine release are desirable. Patients with dilative cardiomyopathy can present asymptomatic or in.congestive heart failure. The overall myocardial defect is a depression of systolic function. An anesthetic regimen that minimizes myocardial depression is essential. References 1. Fox PR: Feline and canine myocardial disease. In Fox PR, ed: Canine and Feline Cardiology. New York, Churchill Livingstone, 1988, pp 435-493 2. Thomas SJ: Noncoronary heart disease. Int Anesth Res Soc review course lectures, Las Vegas, 1986, pp 80-83

Anesthesia for Severe Mitral and Tricuspid Regurgitation A. Thomas Evans, DVM, MS From the Department of Small Animal Clinical Sciences, Veterinary Medical Center, Michigan State University College of Veterinary Medicine, East Lansing, Michigan

MITRAL REGURGITATION

Mitral regurgitation is common and is found in dilated cardiomyopathy, as a sequela to patent ductus arteriosis, and as a result of endocardiosis of the mitral valve in geriatric patients. There is a decrease in forward left ventricular stroke volume as a result of regurgitated volume through the incompetent mitral valve. Regurgitant fraction is directly related to the size of the mitral valve orifice, the heart rate (determines duration of ventricular ejection), and the pressure gradient across the mitral valve. A mild increase in heart rate can increase forward left ventricular stroke volume. Conversely, bradycardia could result in an acute volume overload of the left atrium. The pressure gradient depends on the compliance of the left ventricle and the impedance to left ventricular ejection into the aorta. A reduction in systemic vascular resistance greatly improves left ventricular stroke volume. The anesthetic protocol should minimize the likelihood of bradycardia or an increase in systemic vascular resistance. A modest increase in heart rate and a small decrease in systemic vascular resistance are

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ANESTHETIC PROTOCOLS FOR SPECIFIC CONDITIONS

desirable. Because epidural anesthesia may decrease systemic vascular resistance to dangerous levels, it is not advisable for these patients. Opioidlbenzodiazepine administration with appropriate anticholinergic to prevent bradycardia is a recommended induction technique. A slow, smooth induction is preferable, to prevent excitement-induced increases in systemic vascular resistance. Maintenance is best accomplished with nitrous oxide plus volatile anesthetic. If severe cardiovascular disease is present, nitrous oxide plus opioid analgesic induction is preferred. Atracurium or pancuronium is recommended as the choice of muscle relaxants. Pancuronium produces a slight increase in heart rate. Ventilation should be controlled so that normal carbon dioxide levels are maintained. Any fluids lost should be replaced, volume overloading should be avoided. TRICUSPID REGURGITATION

Tricuspid regurgitation occurs as an acquired disease in small breeds and as a congenital disease in large breeds (Ebstein's anomaly). The goals for anesthesia are to maintain high fluid administration to ensure filling of the right ventricle. Be careful of intermittent positivepressure ventilation and drug-induced vasodilation because of the potential for decreased venous return. It is also wise to avoid arterial hypoxemia and hypercarbia because these increase pulmonary vascular resistance. Choices for inhalational anesthetic include halothane or isoflurane because of minimal effects on the pulmonary vasculature. Nitrous oxide is a weak pulmonary vasoconstrictor when used with opioids and so would be contraindicated. Monitoring should include central venous pressure to check right atrial filling pressure. SUMMARY

Anesthesia for mitral or tricuspid regurgitation should be designed to maintain cardiac output by decreasing systemic and pulmonary vascular resistance to aortic and pulmonCJ.ry outflow, respectively, and by carefully preserving venous return. A moderate increase in heart rate may be helpful with mitral regurgitation; bradycardia should be avoided. Isoflurane, halothane, or opioid anesthesia is preferred.