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Departments of Neurology, Columbia-Presbyterian Medical Center, New York, NY (Drs. Mayer, Fink, Lennihan, Klebanoff, and Raps)
Departments of Cardiology, Columbia-Presbyterian Medical Center, New York, NY. (Drs. Homma, Sherman, and LiMandri)
Departments of Neuro-surgery, Columbia-Presbyterian Medical Center, New York, NY (Drs. Fink and Solomon and Ms. Beckford).
Objective: To describe the clinical features of cardiac injury associated with neurogenic pulmonary edema (NPE) in patients with acute subarachnoid hemorrhage (SAH).
Background: NPE is generally viewed as a form of noncardiogenic pulmonary edema related to massive sympathetic discharge.
Methods: Case series.
Results: We found echocardiography evidence of reduced global and segmental left ventricular (LV) systolic function in five women (mean age, 44; range, 36 to 57) with SAH and NPE. None had a history of heart disease. Four patients were Hunt/Hess grade III and one was grade IV. All five patients experienced (1) sudden hypotension (systolic blood pressure <110 mm Hg) following initially elevated blood pressures, (2) transient lactic acidosis, (3) borderline (2 to 4%) creatine kinase MB elevations, and (4) varied acute (< 24 hours) electrocardiographic changes followed by widespread and persistent T wave inversions. Pulmonary artery wedge pressures were normal in 3/3 patients at the onset of pulmonary edema but reached high levels (>16 mm Hg) in all four patients studied beyond this period. Reduced cardiac output and LV stroke volume were identified in three patients; the fourth patient demonstrated normal values on high doses of intravenous pressors. Cerebral infarction due to vasospasm occurred in four patients and resulted in two deaths. Follow-up echocardiography performed 2 to 6 weeks after SAH revealed normal LV function in all three survivors.
Conclusions: A reversible form of cardiac injury may occur in patients with NPE following SAH and is associated with characteristic clinical findings. Impaired LV hemodynamic performance in this setting may contribute to cardiovascular instability, pulmonary edema formation, and complications from cerebral ischemia.
Address correspondence and reprint requests to Dr. Stephan A. Mayer, Division of Critical Care Neurology, Neurological Institute, 710 West 168th Street, Box 39, New York, NY 10032.
Supported in part by a grant (ROl-NS27325) from the National Institutes of Health, and by a National Stroke Association Research Fellowship Award (Dr. Mayer).
Presented in part at the 45th annual meeting of the American Academy of Neurology, New York, NY, April 1993.
Received August 19, 1993. Accepted for publication in final form October 22, 1993.
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