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Cerebral blood flow and oxygen consumption during isoflurane and halothane anesthesia in man
Author(s) -
Algotsson L.,
Messeter K.,
Nordstrom C. H.,
Ryding E.
Publication year - 1988
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1988.tb02678.x
Subject(s) - halothane , isoflurane , medicine , anesthesia , cerebral blood flow , fentanyl , anesthetic , nitrous oxide , hyperventilation , ventilation (architecture) , engineering , mechanical engineering
In 13 patients, the effects on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMR02) of isoflurane and halothane administered in a clinically relevant situation were studied. Measurements were performed during fentanyl/nitrous oxide (65%) anesthesia together with moderate hyperventilation (Pac02 approx 4.5 kPa), and repeated after addition of 0.65 MAC of isoflurane (n = 6) or halothane (n=7). CBF was measured after intravenous administration of 133 xenon and CMR02 was calculated from the arterial venous differences of oxygen content (AVD02) determined in arterial and jugular venous bulb blood. CBF and CMR02 (means ± s.e. mean) determined prior to administration of volatile agents were 28 ± 5 ml × 100 ‐1 × min ‐1 and 2.0 ± 0.3 ml × 100 g ‐1 × min ‐1 , respectively, in the isoflurane group. In the halothane group, CBF was 25 ± 0.4 ml × 100 g ‐1 × min ‐1 and CMR0 2 was 2.0±0.4 ml × 100 g ‐1 × ml ‐1 . There were no significant intergroup differences. Isoflurane did not change CBF, whereas halothane produced an increase of 36% (P<0.05) compared to values obtained during fentanyl/N20 anesthesia. In addition, isoflurane caused a further decrease in CMRo 2 of 12% ( P <0.01) as compared to a 20% increase ( P <0.05) with halothane. The cerebral metabolic depression caused by the short‐acting anesthetic induction agents would be expected to decrease with time, and could partly explain the observed increase in CMR02 produced by halothane. The study suggests that the cerebrovascular and metabolic properties of isoflurane differ from those of halothane, also in man.

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