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Effects of oxygen inhalation in ascitic cirrhotic patients: Therapeutic implications?
Author(s) -
Henriksen Jens H.
Publication year - 1990
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840120428
Subject(s) - medicine , cardiac output , anesthesia , inhalation , baroreceptor , vascular resistance , cirrhosis , blood pressure , cardiology , vasoconstriction , arterial blood , portal venous pressure , reflex , heart rate , portal hypertension
Abstract In patients with cirrhosis, O 2 uptake, i.e., O 2 consumption, is abnormally deceased. We administered 50% O 2 for 30 min in eight patients with alcoholic cirrhosis to determine whether the subsequent increase in arterial O 2 content may correct the low O 2 consumption. In addition, we studied in these patients the reflex control of cardiac output and blood pressure by arterial baroreceptors, as O 2 inhalation induces a systemic vasoconstriction. Arterial O 2 tension, oxyhaemoglobin saturation and arterial O 2 content significantly increased as well as systemic vascular resistance and arterial pressure. In contrast, O 2 consumption (which was below normal values) under basal conditions, O 2 transport, O 2 extraction ratio, heart rate, right atrial and pulmonary wedged pressures, cardiac output, hepatic venous pressures, hepatic and azygos blood flows were unaffected by O 2 administration. In three patients receiving air, no significant change was observed. Our results show that, in patients with cirrhosis, inhalation of 50% O 2 does not correct O 2 consumption. We may conclude that reflex control of cardiac output and arterial pressure by arterial baroreceptors is impaired in these patients.