Chest
Effects of Hypercapnia on Hemodynamic, Inotropic, Lusitropic, and Electrophysiologic Indices in Humans
Section snippets
Subjects
Eight healthy male volunteers, mean age 24 years (range, 21 to 34 years), were studied. There was no abnormality present on clinical history, examination, 12-lead ECG, echocardiography, biochemical screening, or hematologic screening. Informed written consent to the study protocol, previously approved by the Tayside Committee for Medical Research Ethics, was obtained.
Study Protocol
Subjects attended the clinical laboratory and were studied in a supine position, rolled slightly on the left side. An IV cannula
Oxygenation and ETco2
Breathing the CO2/air mixture compared to air significantly increased respiratory rate 21 ±1 vs 13 ±1 breaths/min, ETCO2 7.0±0.2 vs 5.0±0.3 kPa, and oxygen saturation 98±0.2 vs 97±0.2%, respectively. There was no significant difference between T2 (30 min posthypercapnia) and baseline.
Pulmonary Hemodynamics
Hypercapnia (T1) was associated with a significant (p<0.05) increase in both MPAP and PVR compared with baseline (To) (Fig 1). There was no significant difference between T2 (30 min posthypereapnia) and baseline.
Systemic Hemodynamics
DISCUSSION
We have shown that acute hypercapnia causes true pulmonaiy vasoconstriction in vivo in normal volunteers as reflected by a significant increase in both MPAP and PVR. Although acute hypercapnia had no significant inotropic or lusitropic effects, it significantly increased QT dispersion, suggesting that hypercapnia may cause abnormalities in myocardial repolarization.
The effect of CO2 on the pulmonary circulation in man remains controversial, although the evidence appears to suggest a
ACKNOWLEDGMENTS
We would like to thank Lesley McFarlane and Wendy Coutie for their expert technical assistance.
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