BACKGROUND: Medical treatment of arterial vasospasm following aneurysmal subarachnoid hemorrhage (SAH) generally consists of triple H therapy, which frequently relies on inotropic agents in order to increase cardiac output (CO). Patients with concurrent left ventricular outflow tract (LVOT) obstruction may have paradoxical decreases in CO following administration of inotropic pressors, placing them at significant risk for cerebral ischemia and stroke. METHODS: The clinical courses of two patients with SAH-induced arterial vasospasm and underlying left ventricular outflow obstruction are reported. Both patients had hypotension and low cardiac output that were refractory to medical management with triple H therapy. Echocardiography in both patients demonstrated LVOT obstruction secondary to hypertrophic obstructive cardiomyopathy (HOCM). RESULTS: Intervention in both patients included discontinuation of inotropic agents and maintenance of hypervolemia to a target pulmonary capillary wedge pressure range, resulting in improved cardiac output and mean arterial pressure. CONCLUSION: Medical treatment for cerebral vasospasm with inotropic pressor agents may result in paradoxical decreases in hemodynamic parameters and cerebral perfusion in patients with LVOT obstruction. While HOCM is the most likely structural abnormality to cause this phenomenon, it can be induced by several physiological conditions encountered in the neurocritical care setting. Modifications in triple H therapy regimens may be required in order to optimize cerebral perfusion and prevent cerebral ischemia and stroke in these patients.
BACKGROUND: Medical treatment of arterial vasospasm following aneurysmal subarachnoid hemorrhage (SAH) generally consists of triple H therapy, which frequently relies on inotropic agents in order to increase cardiac output (CO). Patients with concurrent left ventricular outflow tract (LVOT) obstruction may have paradoxical decreases in CO following administration of inotropic pressors, placing them at significant risk for cerebral ischemia and stroke. METHODS: The clinical courses of two patients with SAH-induced arterial vasospasm and underlying left ventricular outflow obstruction are reported. Both patients had hypotension and low cardiac output that were refractory to medical management with triple H therapy. Echocardiography in both patients demonstrated LVOT obstruction secondary to hypertrophic obstructive cardiomyopathy (HOCM). RESULTS: Intervention in both patients included discontinuation of inotropic agents and maintenance of hypervolemia to a target pulmonary capillary wedge pressure range, resulting in improved cardiac output and mean arterial pressure. CONCLUSION: Medical treatment for cerebral vasospasm with inotropic pressor agents may result in paradoxical decreases in hemodynamic parameters and cerebral perfusion in patients with LVOT obstruction. While HOCM is the most likely structural abnormality to cause this phenomenon, it can be induced by several physiological conditions encountered in the neurocritical care setting. Modifications in triple H therapy regimens may be required in order to optimize cerebral perfusion and prevent cerebral ischemia and stroke in these patients.
Authors: K Okeie; M Shimizu; H Yoshio; H Ino; M Yamaguchi; T Matsuyama; T Yasuda; J Taki; H Mabuchi Journal: J Am Coll Cardiol Date: 2000-09 Impact factor: 24.094