title: Cardiac injury associated with neurogenic pulmonary edema following subarachnoid hemorrhage.
abstract: 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 echocardiographic 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.
authors.affiliation: Department of Neurology, Columbia-Presbyterian Medical Center, New York, NY.
authors.forename: S A
authors.initials: SA
authors.lastname: Mayer
authors.forename: M E
authors.initials: ME
authors.lastname: Fink
authors.forename: S
authors.initials: S
authors.lastname: Homma
authors.forename: D
authors.initials: D
authors.lastname: Sherman
authors.forename: G
authors.initials: G
authors.lastname: LiMandri
authors.forename: L
authors.initials: L
authors.lastname: Lennihan
authors.forename: R A
authors.initials: RA
authors.lastname: Solomon
authors.forename: L M
authors.initials: LM
authors.lastname: Klebanoff
authors.forename: A
authors.initials: A
authors.lastname: Beckford
authors.forename: E C
authors.initials: EC
authors.lastname: Raps
mesh_terms: D000328:Adult; D005260:Female; D006335:Heart Injuries / Q000209:etiology* / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D008875:Middle Aged; D011654:Pulmonary Edema / Q000150:complications* / Q000209:etiology / Q000503:physiopathology; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D016277:Ventricular Function, Left