[The effects of increased intracranial pressure on respiratory functions in clinical setting]

Respiratory insufficiency following acutely elevated intracranial pressure (ICP) may occur as a result of pulmonary edema which is supposed to be caused by increased sympathetic discharge from the central nervous system. Supporting experimental studies have been reported concerning this immediate respiratory consequence, while delayed respiratory consequences with an elevated ICP remain poorly characterized clinically. We studied delayed effects of an increased ICP on respiratory functions (pulmonary shunt ratio (Qs/Qt), respiratory index (A-aDO2/PaO2), oxygenation index (PaO2/FIO2) ), extravascular lung water (EVLW), and hemodynamics [cardiac index (CI), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), systemic vascular resistance (SVR), pulmonary vascular resistance (PVR)] in 15 cases with head injury, 4 with cerebrovascular diseases, and one with hypoxic brain damage. Ten cases had either aspiration, long bone fractures (the syndrome of fat embolism), or pneumonia, and the 10 cases without these pulmonary insults were defined as the cases without pulmonary complications and studied further. Pulmonary functions deteriorated as the ICP rose in the total cases, but in the cases without pulmonary complications, the correlations between the pulmonary functions and the ICP were not significant. None of the hemodynamic parameters correlated with the ICP in both the total cases and the cases without pulmonary complications.(ABSTRACT TRUNCATED AT 250 WORDS)