Cerebral cardiovascular and respiratory variables after an experimental brain missile wound

Brain missile wounding (BMW) affects brainstem and medullary cadiorespiratory functions leading to immediate systemic hypertension, bradycardia, and apnea. Secondary complications may also occur because of subsequent changes in systemic and intracranial physiological variables. To delineate the immediate and secondary effects of BMW, we monitored changes in several cerebral and cardiorespiratory parameters in pentobarbital-anesthetized spontaneously breathing cats before wounding and up to 90 min afterward. Total and regional cerebral blood flow (rCBF) and cardiac output (CO) were measured (microsphere technique) and arterial blood was sampled for pH, PO2 and PCO2 once before BMW and one to four times afterward. Mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP = MABP - ICP), electrocardiogram (ECG), heart rate (HR), and electroencephalogram (EEG) were continuously recorded. Respiratory frequency (f), tidal volume (Vt), and ventilation (V) were recorded during each flow measurement and periodically throughout the experiment. Four unwounded cats served as controls and 15 cats were wounded at 1.4 J fronto-occipitally through an intact cranium. Unwounded cats showed no significant changes in any physiological variable measured during a 100 min experimentation period. Four wounded cats survived a 90 min post-BMW period and had only a transient brainstem effect including a 50% increase in MABP concurrently with 50% reductions in the f and HR. Nonsurvivors (11 of 15) lived from 1 to 41 min after wounding. These cats initially demonstrated similar changes in MABP, f, and HR to survivors, but these variables remained unstable, possibly indicating a persisting brainstem damage. Apnea accounted for death in 10 of 11 nonsurvivors. Although the primary brainstem effect might have existed in all nonsurvivors, it appears that only one cat died from reduced respiration alone. Others had one or several postwounding secondary complications: abruptly increased ICP producing a negative CPP, extreme reductions in CO or CBF and ventilation. Cardiac arrest occurred once. Thus, post-BMW mortality cannot be consistently ascribed to the impairment of a single physiological variable.