A Therapeutic Commentary.
ABSTRACT: Thirty-one million patients in the United States undergo surgical procedures every year. Approximately 10%-the majority of these with hypertension-are at an increased risk for perioperative and postoperative cardiovascular morbidity and mortality. Thus, hypertensive patients requiring surgery, especially the 2.1 million undergoing noncardiac procedures, should be evaluated carefully for the magnitude, and if severe, the cause of the hypertension. Additionally, their associated metabolic and cardiovascular status should be characterized and corrected with aggressive therapy. Hypertensive patients with known ischemic heart disease, those with multiple risk factors for ischemic heart disease (IHD), some with valvular heart disease, and those with congestive heart failure should be evaluated for their ability to perform the physical and social activities of everyday life, and, when necessary, have formal stress testing. Most studies suggest that blood pressures of 180/110 mm Hg or greater are associated with a greater risk for perioperative ischemic events. Therefore, the goals of blood pressure control should be to reduce the blood pressure without jeopardizing organ function. Antihypertensive medication should be administered until the time of surgery. beta-Receptor blockers should be instituted or continued in patients with angina and in some patients with congestive heart failure. Those without prior antihypertensive therapy might be best treated with beta-blocker therapy perioperatively as evidenced by the Multicenter Study of Perioperative Research Group with atenolol and those earlier studies with metoprolol. The risks of the surgery should be discussed with the patient so the risks can be weighed against the expected benefit. Studies suggest that perioperative risk for any patient, and especially patients with hypertension, are in part related to the adrenergic arousal before, during, and after the procedure as evidenced by the rise in heart rate and blood pressure, along with the liberation of clotting facators and increased risk for plaque rupture, coronary vasoplasm, and consequent myocardial infarction and fibrosis.
DeQuattro
V
Division of Cardiology, University of Southern California School of medicine, Los Angeles, California, USA
Li
D