We studied the hemodynamic events that followed abrupt withdrawal of nitroprusside in 20 patients with severe chronic heart failure. With nitroprusside, cardiac index increased from 1.96 to 2.87 liters per minute per square meter of body-surface area, but it decreased to 1.66 (P<0.001) after withdrawal of nitroprusside. Left ventricular filling pressure and systemic vascular resistance decreased from 23.9 to 15.3 mm Hg and from 1642 to 921 dyn·sec·cm-5, respectively, with nitroprusside, but increased to 30.4 mm Hg and 2109 dyn·sec·cm-5 (both P<0.001) upon its discontinuation. These rebound changes were maximal 10 to 30 minutes after nitroprusside withdrawal and returned to control levels one to three hours later. Although in 17 of 20 patients, these rebound changes caused no or minimal exacerbation of symptoms, pulmonary edema, which resolved with readministration of nitroprusside, developed in three patients. Activation of reflex vasoconstrictive forces during vasodilator therapy may explain these effects of withdrawal. (N Engl J Med 301:1193–1197, 1979) THE administration of nitroprusside produces rapid hemodynamic and clinical improvement in patients with severe chronic congestive heart failure.1 2 3 4 5 6 By producing arteriolar dilatation and thus reducing impedance to left ventricular ejection, nitroprusside increases cardiac output; by producing venodilatation and thus decreasing left ventricular filling, the drug reduces ventricular filling pressures.7 Nitroprusside can only be administered intravenously and has a brief duration of action; since it is unstable in solution, frequent changes in infusing solutions are needed to maintain pharmacologic effectiveness.8 As a result, abrupt termination of nitroprusside therapy is likely to be a frequently encountered clinical event. Since adverse clinical reactions.
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