Abrupt withdrawal of nitroprusside in severe chronic heart failure caused significant rebound hemodynamic worsening, including decreased cardiac index and increased filling pressures (P<0.001).
Observational (n=20)
Does abrupt withdrawal of nitroprusside cause rebound hemodynamic events in patients with severe chronic heart failure?
Abrupt withdrawal of nitroprusside in patients with severe heart failure causes significant rebound hemodynamic deterioration, which can lead to pulmonary edema.
p-value: p=<0.001
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 less than 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 less than 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 in three patients. Activation of reflex vasoconstrictive forces during vasodilator therapy may explain these effects of withdrawal.
Packer et al. (Thu,) conducted a observational in severe chronic heart failure (n=20). Abrupt withdrawal of nitroprusside vs. Nitroprusside therapy was evaluated on Hemodynamic changes (cardiac index, left ventricular filling pressure, systemic vascular resistance) (p=<0.001). Abrupt withdrawal of nitroprusside in severe chronic heart failure caused significant rebound hemodynamic worsening, including decreased cardiac index and increased filling pressures (P<0.001).