EFFECTS OF HYPERCAPNIA ON HEMODYNAMIC, INOTROPIC, LUSITROPIC, AND ELECTROPHYSIOLOGIC INDEXES IN HUMANS

Study objective: The inotropic, lusitropic, and electrophysiologic eff ects of acute hypercapnia in humans are not known. Although the effect s of hypercapnia on the systemic circulation have been well documented , there is still some debate as to whether hypercapnia causes true pul monary vasoconstriction in vivo. We have therefore evaluated the effec ts of acute hypercapnia on these cardiac indices and the interaction o f hypercapnia with the systemic and pulmonary vascular beds in humans. Participants and interventions: Eight healthy male volunteers were st udied using Doppler echocardiography. . After resting for at least 30 min to achieve baseline hemodynamic parameters (T-0), they were render ed hypercapnic to acheive an end-tidal carbon dioxide (CO2) of 7 kPa f or 30 min by breathing a variable mixture of CO2/air (T-1). They were restudied after 30 min recovery breathing air (T-2). Hemodynamic, dias tolic, and systolic flow parameters, QT dispersion (maximum-minimum QT interval measured in a 12-lead EGG), and venous blood samples for pla sma renin activity (PRA), angiotensin II (ANG II), and aldosterone (AL DO) were measured at each time point. Results: Hypercapnia compared wi th placebo significantly increased mean pulmonary artery pressure 14+/ -1 vs 9+/-1 mm Hg and pulmonary vascular resistance 171+/-17 vs 129+/- 17 dyne . s . cm(-5), respectively. Heart rate, stroke volume, cardiac output, and mean arterial BP were increased by hypercapnia. Indexes o f systolic function, namely peak aortic velocity and aortic mean and p eak acceleration, were unaffected by hypercapnia. Similarly, hypercapn ia had no effect on lusitropic indexes reflected by its lack of effect on isovolumic relaxation time, mitral E-wave deceleration time, and m itral 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 hyperca pnia on PRA, ANG II, or ALDO. Conclusion: Thus, acute hypercapnia appe ars to have no adverse inotropic or lusitropic effects on cardiac func tion, although repolarization abnormalities, reflected by an increase in QT dispersion, and its effects on pulmonary vasoconstriction may ha ve important sequelae in man.