Perioperative hypertension is primarily due to increased systemic vascular resistance (SVR). Therefore, the major therapeutic approaches are directed at reducing vasoconstriction, using drugs that increase cyclic nucleotides or block calcium entry into vascular smooth muscle. Nitroprusside and other nitric oxide–derived vasodilators affect both the resistance vessels and the vascular capacitance bed. Antihypertensive drugs that affect venous return can have unpredictable effects on blood pressure and calculated SVR. The new intravenous dihydropyridine calcium antagonists have arterial vasodilating actions and are especially promising as new therapeutic approaches for perioperative hypertension. Following coronary bypass–grafting, patients have undergone direct mechanical manipulation of their native grafts, coronary arteries, and internal mammary artery, creating a potential risk for coronary or internal mammary spasm. Calcium antagonists may be an important therapy for perioperative hypertension in such patients. Experimental models have demonstrated that calcium antagonists can attenuate the production of inflammatory mediators and thereby reduce cellular damage following reperfusion. These potential anti–inflammatory drugs may prove to offer additional benefits in the therapy of perioperative hypertension. The potential anti–inflammatory and cytoprotective effects of calcium antagonists may make them the ideal agents for the treatment of acute perioperative hypertension.

We report the case of a patient with Crohn's disease receiving short-term postoperative parenteral nutrition supplemented with trace elements who nevertheless became selenium deficient with evidence of a cardiomyopathy. This was fully reversible with oral selenium supplementation. Current parenteral feeding regimes may not contain enough selenium for malnourished patients.

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