The Changes of Cerebrospinal Acid - Base Balance during Prolonged Hyperventilation.
10.4097/kjae.1990.23.5.698
- Author:
Sun Ok SONG
1
;
Hee Ju KANG
Author Information
1. Department of Anesthesiology, College of Medicine, Yeungnam University, Daegu, Korea.
- Publication Type:Original Article
- Keywords:
Prolonged hyperventilation;
Cerebrospinal fluid;
Acid-base balance
- MeSH:
Acid-Base Equilibrium;
Acidosis;
Anesthesia;
Carbon Dioxide;
Cerebrospinal Fluid;
Fentanyl;
Humans;
Hydrogen-Ion Concentration;
Hyperventilation*;
Hypocapnia;
Intracranial Aneurysm;
Intracranial Pressure;
Intubation;
Thiopental;
Vecuronium Bromide;
Ventilation
- From:Korean Journal of Anesthesiology
1990;23(5):698-703
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Hyperventilation is a common form of anesthetic management in neurosurgical patients with increased intracranial pressure. Acute hypocapnia through hyperventilation causes an increase in cerebrovascular resistance which decreases the cerebral blood flow within one minute. When the hyperventilation is sustained, the cerebral blood flow gradually rises toward normal. We performed this study for evaluation of the changes of acid-base balance in cerebrospinal fluid (CSF) according to duration of acute hyperventilation. We have studied 12 patients for elective surgery for cerebral aneurysm with a relatively clear mental state. The patients underwent induction of anesthesia with thiopental, fentanyl and vecuronium. After intubation, their ventilation was controlled and maintained at a PaCO2 of about 30 mmHg. Samples in arterial and lumbar CSF were obtained at hourly intervals for 6 hours after the onset of hyperventilation. The results were as follows: 1) The PaCO2 was low 30s mmHg and all arterial blood values were not changed throughout the period of observation. 2) The values of CSF were changed; the pH of CSF was increased for 3 hours and then gradually decreased after 4 hours, carbon dioxide tension was a steady state after an initial fall for 2 hours, HCO3-, was decreased from 2 hours and more significantly decreased after 5 hours, and the base excess was more significantly negative after 5 hours of hyperventilation. From the above data, we conclude that prolonged hyperventilation produces first a rise in CSF pH by decreased CSF PCO2 and then gradually a fall in CSF pH by decreasing CSF HCO3-, concentration, and measurable compensated acidosis in CSF was initiated within 5 hours after onset of hyperventilation.
