Background Decreased arterial partial pressure of oxygen (Pa-O2) during vol
atile anesthesia is well-known. Halothane has been examined with the multip
le inert gas elimination technique and has been shown to alter the distribu
tion of pulmonary blood flow and thus Pa-O2. The effects of isoflurane and
sevoflurane on pulmonary gas exchange remain unknown. The authors hypothesi
zed that sevoflurane with a relatively high minimum alveolar concentration
(MAC) would result in significantly more gas exchange disturbances in compa
rison with isoflurane or control.
Methods: This study was performed in a porcine model with an air pneumoperi
toneum that generates a reproducible gas exchange defect. After a baseline
measurement of pulmonary gas exchange (multiple inert gas elimination techn
ique) during propofol anesthesia, 21 pigs were randomly assigned to three g
roups of seven animals each. One group received isoflurane anesthesia, one
group received sevoflurane anesthesia, and one group was continued on propo
fol anesthesia (control). After 30 min of volatile anesthesia at 1 MAC or p
ropofol anesthesia, a second measurement (multiple inert gas elimiiation te
chnique) was performed.
Results: At the second measurement, inert gas shunt was 15 +/-3% (mean +/-
SD) during sevoflurane anesthesia versus 9 +/-1% during propofol anesthesia
(P = 0.02). Blood flow to normal ventilation/perfusion (<(V) overdot>(A)/<
(Q) overdot>) lung areas was 83 +/-5% during sevoflurane anesthesia versus
89 +/-1% during propofol anesthesia (P = 0.04). This resulted in a Pa-O2 of
88 +/- 11 mmHg during sevoflurane anesthesia versus 102 +/- 15 mmHg during
propofol anesthesia (P = 0.04). inert gas and blood gas variables during i
soflurane anesthesia did not differ significantly from those obtained durin
g propofol anesthesia.
Conclusions: In pigs with an already existent gas exchange defect, sevoflur
ane anesthesia but not isoflurane anesthesia causes significantly more gas
exchange disturbances than propofol anesthesia does.