TY - JOUR
T1 - Effect of oxygen inhalation on systemic, central, and splanchnic haemodynamics in cirrhosis
AU - Møller, S
AU - Becker, U
AU - Schifter, S
AU - Abrahamsen, J
AU - Henriksen, Jens Henrik Sahl
N1 - Keywords: Administration, Inhalation; Adult; Aged; Amines; Gases; Hemodynamics; Humans; Liver Cirrhosis; Lung; Lung Volume Measurements; Middle Aged; Oxygen; Peptides; Splanchnic Circulation
PY - 1996
Y1 - 1996
N2 - BACKGROUND/AIMS: Patients with cirrhosis exhibit a hyperdynamic circulation with increased cardiac output and low arterial blood pressure. The aim of the present study was to assess the effects of oxygen inhalation on systemic, central, and splanchnic haemodynamics and vasoactive systems in patients with cirrhosis (n = 19). RESULTS: Spirometry was normal, but the carbon monoxide diffusing capacity (transfer factor) was significantly decreased, 18.8 ml.min-1.mmHg-1 (-32% of that predicted, p < 0.0001), and correlated significantly with the cardiac output (r = 0.78, p < 0.0005), plasma volume (r = 0.72, p < 0.001) and the central and arterial blood volume (r = 0.67, p < 0.005). After inhalation of 100% oxygen over a period of 20 min, the cardiac output decreased from 7.4 to 6.6 l/min (p < 0.0005), and the systemic vascular resistance increased from 980 to 1124 dyn.s.cm-5 (p < 0.005). The change in systemic vascular resistance was significantly greater in patients with mild liver dysfunction than in those with severe liver dysfunction (p < 0.02). In contrast, no significant changes were seen in the arterial or portal venous pressures during inhalation of oxygen. Arterial concentrations of catecholamines, renin, endothelin-1, and calcitonin gene-related peptide were all increased in patients with cirrhosis, but only the catecholamine concentrations decreased significantly (noradrenaline -13%, p < 0.02 and adrenaline -16%, p < 0.01) in response to oxygen. CONCLUSION: During oxygen inhalation cardiac output decreases and systemic vascular resistance increases in association with a decrease in arterial concentrations of catecholamine, but oxygen supply in patients with cirrhosis does not normalise the hyperdynamic circulation or the low arterial blood pressure.
AB - BACKGROUND/AIMS: Patients with cirrhosis exhibit a hyperdynamic circulation with increased cardiac output and low arterial blood pressure. The aim of the present study was to assess the effects of oxygen inhalation on systemic, central, and splanchnic haemodynamics and vasoactive systems in patients with cirrhosis (n = 19). RESULTS: Spirometry was normal, but the carbon monoxide diffusing capacity (transfer factor) was significantly decreased, 18.8 ml.min-1.mmHg-1 (-32% of that predicted, p < 0.0001), and correlated significantly with the cardiac output (r = 0.78, p < 0.0005), plasma volume (r = 0.72, p < 0.001) and the central and arterial blood volume (r = 0.67, p < 0.005). After inhalation of 100% oxygen over a period of 20 min, the cardiac output decreased from 7.4 to 6.6 l/min (p < 0.0005), and the systemic vascular resistance increased from 980 to 1124 dyn.s.cm-5 (p < 0.005). The change in systemic vascular resistance was significantly greater in patients with mild liver dysfunction than in those with severe liver dysfunction (p < 0.02). In contrast, no significant changes were seen in the arterial or portal venous pressures during inhalation of oxygen. Arterial concentrations of catecholamines, renin, endothelin-1, and calcitonin gene-related peptide were all increased in patients with cirrhosis, but only the catecholamine concentrations decreased significantly (noradrenaline -13%, p < 0.02 and adrenaline -16%, p < 0.01) in response to oxygen. CONCLUSION: During oxygen inhalation cardiac output decreases and systemic vascular resistance increases in association with a decrease in arterial concentrations of catecholamine, but oxygen supply in patients with cirrhosis does not normalise the hyperdynamic circulation or the low arterial blood pressure.
M3 - Journal article
C2 - 8895011
SN - 0168-8278
VL - 25
SP - 316
EP - 328
JO - Journal of Hepatology
JF - Journal of Hepatology
IS - 3
ER -