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Potassium and magnesium depletion might lead to cardiac arrhythmias and cardiac arrest. The usage of thiazide diuretics is often related to loss of electrolytes, most considerably potassium but additionally sodium, chloride, bicarbonate, and magnesium. Use warning when using these brokers collectively and monitor serum potassium periodically. CNS stimulants enhance blood stress and heart rate; using some agents may be contraindicated in patients with severe/uncontrolled hypertension. Therapy with thiazide diuretics needs to be administered cautiously in patients with impaired hepatic perform or progressive liver disease, and discontinued promptly if indicators of impending hepatic coma appear (e.g., tremors, confusion, and elevated jaundice). Therapy with thiazide diuretics should be administered cautiously in patients with a historical past or threat of SLE. Therapy with carvedilol should be administered cautiously in patients with peripheral vascular illness. The beta-adrenergic receptor blocking effects of carvedilol could precipitate or aggravate signs of arterial insufficiency in patients with peripheral vascular disease. Systemic beta-adrenergic receptor blocking brokers (aka beta-blockers) may decrease intraocular stress. Increases in serum VLDL and LDL cholesterol and triglycerides, as well as decreases in HDL cholesterol, have been reported with some beta-blockers. As well as, the nonselective beta-blockers (e.g., propranolol, pindolol, timolol) may attenuate catecholamine-mediated vasodilation during exercise by blocking beta-2 receptors in peripheral vessels. Carvedilol may also attenuate catecholamine-mediated vasodilation throughout train by blocking beta-2 receptors in peripheral vessels.
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