[Cardiovascular and pulmonary changes in patients with an isolated cerebral lesion. I. Hemodynamics].

This study included 44 patients with a severe isolated cerebral lesion (decerebrate posturing on admission) with the purpose of examining the hemodynamic changes caused by cerebral trauma to see whether these changes might give additional information as to the prognosis of these patients. Patients with a previous myocardial infarction, pulmonary edema or embolism, chronic obstructive or restrictive pulmonary disease, proven or suspected aspiration, and polytrauma patients with an accompanying cerebral lesion were excluded. The study started on the day of admission to the intensive care unit and lasted for up to 6 days maximally. Both on admission and throughout the observation period, survivors (S) showed a higher neurological status score on the Innsbruck Coma Scale than non-survivors (NS). The hemodynamic profile was characterized by a hyperdynamic reaction with an increase in cardiac index and systemic arterial pressure. The hyperdynamic state was much more pronounced in S than in NS, who tended to show a normo-or even hypodynamic state. On admission to the intensive care unit 13 of 31 NS (41.9%) had a cardiac index less than 3.01/min.m2 as compared to only 1 of the 13 S (7.7%). With regard to pulmonary artery pressure, there was no difference between S and NS, while the pulmonary vascular resistance was significantly higher in NS than in S. In addition, S showed a kind of circadian rhythm of systemic arterial pressure, that was absent in NS. Rather than one single hemodynamic parameter being of prognostic relevance it is the complex parameter "left-ventricular work index" (LVWI) includes all the relevant parameters of left-ventricular mechanical work. Throughout the observation period, this parameter was consistently higher in S than in NS, although the left ventricular filling pressure (represented by the diastolic pulmonary artery pressure) was equal in both groups. While an inverse relationship between age and LVWI could be shown in S, this could not be demonstrated for NS, indicating that the differences in hemodynamic patterns between S and NS should be due to other reasons, such as the degree of the cerebral lesion affecting the trauma-adaptive regulation of the cardiovascular reaction to a severe isolated cerebral lesion.