Objective: Cardiac complications (CdCs) have been reported in subarachnoid hemorrhage (SAH). There is an assumption that a positive history of cardiac disease (HxCD) increases one's risk for CdCs, cerebral vasospasm and neurological deterioration (ND). This study tested the hypothesis that a positive HxCD is related to the occurrence of CdCs, angiographic vasospasm, and ND in patients with SAH.
Design: This project was a secondary analysis using a descriptive and comparative design from a prospective, ongoing NIH funded study related to SAH.
Population and Sample: This sample included 81 aneurysmal SAH patients with a Fisher grade of > 2 and or a Hunt and Hess grade of > 3 admitted to the NeuroVascular ICU (NV-ICU). The population was 78% female (n=63) and 94% Caucasian (n=76) and ranged in age from 22 to 75 years (M=54,SD=13). Data collection occurred over a 2 year period from May 1999 through April 2001.
Methods: Data were collected within the first 14 days after SAH. Clinical records were reviewed for a positive HxCD (defined as a history of hypertension, coronary artery disease, coronary artery bypass surgery, arrhythmias, or a permanent pacemaker). CdCs in the NV-ICU were defined as elevation in cardiac enzymes or troponin, abnormal EKG or echocardiagram suggestive of a myocardial infarction, arrhythmias, or pulmonary edema. Cerebral angiograms, read independently by neurosurgeons, verified the presence of cerebral vasospasm (none/mild, moderate, severe) in 25 segments of the cerebral vasculature. ND was assessed every 2 hours and defined as a decline of > 2 Glasgow Coma Score, or a deterioration in pupillary, motor or sensory response. Descriptive and chi square analyses were conducted.
Findings: Of the 81 patients in this study, 31 (38%) had a positive HxCD and 50 (62%) were negative for HxCD.
CdC's occurred in 23 (28%) of the patients in this study. There was no significant relationship between a positive HxCD and CdC. Of the 31 patients (38%) with a positive HxCD, 11 (35%) experienced a CdC. Of the 50 patients (62%) without HxCD, 12 (24%) experienced a CdC (chi square=2.776, p=.735). All CdCs occurred within 5 days of the initial SAH.
The majority of patients were admitted with a Fisher score of 3 (62%, n=50), and Hunt and Hess 2-4 (81%, n=65). There was no significant relationship between HxCD and admission Fisher (Chi square=.239, p=.625), or Hunt and Hess (chi square=.128 and p=.720) scores. However, there was statistical significance between CdC's and Fisher (chi square=3.806, p=.051), as well as Hunt and Hess (chi square=10.658, p=.001) scores.
Thirty-five patients (41%) had no vasospasm [20 patients without HxCD (57%) vs.15 patients with a positive HxCD (43%)]. Forty-one (54%) had moderate vasospasm [25 patients without HxCD (61%) vs.16 patients with a positive HxCD (39%) (chi square=.115, p=.750)]. Seventeen patients (22%) had severe vasospasm [10 patients without HxCD (59%) vs.7 patients with a positive HxCD (41%) (chi square=.001, p=.971)]. Five patients were not included in this analysis because they did not have angiograms.
Of the 81 patients, 74% (n=60) developed ND. There was a tendency for patients with a positive HxCD to have ND but not necessarily from cardiac problems. Thirty-seven percent (n=30) developed vasospasm-related ND [18 patients without HxCD (36.%) vs.12 patients with a positive HxCD (39%)]. An additional 6 patients (7.4%) developed cardiac-related ND [5 patients without HxCD (10%) vs. 1 patient with a positive HxCD (3%) (chi square=2.021, p=.568)].
Conclusions: A positive history of cardiac disease is not a predictive factor of cardiac complication or vasospasm after SAH. Fifty-two percent of patients in this study with cardiac complications did not have a positive history of cardiac disease; and of the patients with cardiac-related neurological deterioration,83% did not have a history of cardiac disease. More significant injury was associated with the development of cardiac complications.
Implications: This study suggests a need to routinely monitor all SAH patients for cardiac complications regardless of their history, in the first days after SAH, especially patients with higher degrees of injury. A SAH may initiate a catecholamine response, increasing the risk for cardiac complications, even in individuals with no history of cardiac disease.
Study supported by the National Institute of Nursing Research Grant #960213 Keyword: cardiac disease, subarachnoid hemorrhage, neurologic deterioration
Back to Rehabilitation: Assessment Continued
Back to The Advancing Nursing Practice Excellence: State of the Science