The association between the degree of neurological deficit and cardiopulmonary dysfunction in patients with spontaneous subarachnoid hemorrhage (SAH) is poorly understood. Method: A systematic search (MEDLINE, bibliographies, to 9.2004) was performed for prospective studies (any architecture; =10 patients with SAH), reporting on neurological deficit and cardiopulmonary dysfunction. Neurological deficit was graded according to the Hunt-Hess or Botterell scores as minimal (1 or 2 points), moderate (3), or severe (4 or 5), and tested for an association with cardiopulmonary dysfunction (chisquare test). Results: Relevant data came from two randomized trials, four case-control studies, and 31 uncontrolled series. In eight studies (386 patients), ECG abnormalities were found in 32% of patients with minimal, 55% with moderate, and 58% with severe neurological deficit (P<0.0001). In six studies (135), echocardiographic abnormalities were found in 4% of patients with minimal, 30% with moderate, and 52% with severe neurological deficit (P=0.0001). In two trials (63), reatinine phosphoskinase was increased in 18% of patients with minimal, 71% with moderate, and 100% with severe neurological deficit (P<0.0001). In three trials (309), troponin-I was increased in 10% of patients with minimal, 20% of patients with moderate, and 46% with severe neurological deficit (P<0.0001). In five trials (163), pulmonary edema was found in 4% of patients with minimal, 12% with moderate, and 35% with severe neurological deficit (P<0.0001). Seventeen studies reported on mortality; 26% of the patients died, 80% of deaths were directly related to SAH. Conclusions: In patients with spontaneous SAH, cardiopulmonary dysfunction is more likely to occur with increasing neurological deficit.