Mechanism of hyperventilation in acute cerebrovascular accidents.
Lumbar cerebrospinal fluid and arterial blood acid-base state were assessed in 19 patients within 24 hours of an acute cerebrovascular accident. Those with haemorrhage into the C.S.F. showed a lower C.S.F. pH and higher C.S.F. lactate than those without haemorrhage but the Pco(2), was similar in the two groups, suggesting that this greater C.S.F. acidity was not responsible for a greater degree of hyperventilation. In those without haemorrhage an inverse relation was found between C.S.F. pH and arterial Pco(2), suggesting that a non-chemical ventilatory drive-for example, due to central neurological damage-was responsible for the acid-base changes observed.
D000138:Acidosis / Q000134:cerebrospinal fluid; D001158:Arteries; D002245:Carbon Dioxide / Q000134:cerebrospinal fluid; D002543:Cerebral Hemorrhage / Q000134:cerebrospinal fluid; D002561:Cerebrovascular Disorders / Q000503:physiopathology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D006985:Hyperventilation / Q000503:physiopathology*; D007773:Lactates / Q000134:cerebrospinal fluid; D010101:Oxygen Consumption; D011773:Pyruvates / Q000134:cerebrospinal fluid; D013129:Spinal Puncture
D007773:Lactates; D011773:Pyruvates; D002245:Carbon Dioxide