Chest
Volume 109, Issue 5, May 1996, Pages 1215-1221
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Effects of Hypercapnia on Hemodynamic, Inotropic, Lusitropic, and Electrophysiologic Indices in Humans

https://doi.org/10.1378/chest.109.5.1215Get rights and content

Study objective

The inotropic, lusitropic, and electrophysiologic effects of acute hypercapnia in humans are not known. Although the effects of hypercapnia on the systemic circulation have been well documented, there is still some debate as to whether hypercapnia causes true pulmonary vasoconstriction in vivo. We have therefore evaluated the effects of acute hypercapnia on these cardiac indices and the interaction of hypercapnia with the systemic and pulmonary vascular beds in humans.

Participants and interventions

Eight healthy male volunteers were studied using Doppler echocardiography. After resting for at least 30 min to achieve baseline hemodynamic parameters (To), they were rendered hypercapnic to aeheive an end-tidal carbon dioxide (CO2) of 7 kPa for 30 min by breathing a variable mixture of CO2/air (T1). They were restudied after 30 min recovery breathing air (T2). Hemodynamic, diastolic, and systolic flow parameters, QT dispersion (maximum-minimum QT interval measured in a 12-lead ECG), and venous blood samples for plasma renin activity (PRA), angiotensin II (ANG II), and aldosterone (ALDO) were measured at each time point.

Results

Hypercapnia compared with placebo significantly increased mean pulmonary artery pressure 14±1 vs 9±1 mm Hg and pulmonary vascular resistance 171 ±17 vs 129±17 dyne±cm−5, respectively. Heart rate, stroke volume, cardiac output, and mean arterial BP were increased by hypercapnia. Indexes of systolic function, namely peak aortic velocity and aortic mean and peak acceleration, were unaffected by hypercapnia. Similarly, hypercapnia had no effect on lusitropic indexes reflected by its lack of effect on isovolumic relaxation time, mitral E-wave deceleration time, and mitral E/A wave ratio. Hypercapnia was found to significantly increase both QTc interval and QT dispersion: 428±8 vs 411 ±3 ms and 48±2 vs 33±4 ms, respectively. There was no significant effect of hypercapnia on PRA, ANG II, or ALDO.

Conclusion

Thus, acute hypercapnia appears to have no adverse inotropic or lusitropic effects on cardiac function, although repolarization abnormalities, reflected by an increase in QT dispersion, and its effects on pulmonary vasoconstriction may have important sequelae in man.

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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