The purposes of our study were (1) to investigate whether a 3-min short-term hyperventilation leads to posthyperventilatory hypoxemia and (2) to assess the role of transcutaneous blood gas measurements for monitoring oxygen and carbon dioxide changes during and after the test. In 10 male volunteers arterial and transcutaneous blood gases were measured simultaneously before, during and after a 3-min voluntary hyperventilation maneuver. Baseline arterial PO₂ increased from 13.7 ± 0.4 kPa (103 ± 3 mm Hg) to 18.6 ± 0.3 kPa (139 ± 2.3 mm Hg; p < 0.005 compared to baseline) during hyperventilation. After the provocation test posthyperventilatory hypoxemia occurred with a minimal mean value of 7.8 ± 1.3 kPa (58.5 ± 9.8 mm Hg; p < 0.05 compared to baseline). Whereas close agreement between arterial and transcutaneous measurements was obtained for carbon dioxide values before hyperventilation, transcutaneous O₂ consistently underestimated arterial O₂. A short-term over-breathing of 3 min causes a significant posthyperventilatory hypoxemia. We hypothesize that posthyperventilatory hypoxemia is caused by hypopnea as a result of depleted CO₂ body stores. Noninvasive transcutaneous blood gas measurements are not reliable for monitoring blood gas changes during and after hyperventilation, most probably because of the slow response time of the electrodes and the reflex vasoconstriction of the skin vessels.

Despite higher costs, expenditure, and the necessity of repeatedly reprogramming of dual chamber pacemakers, they are increasingly implanted to achieve an optimal work capacity. The influence of an individually programmed atrioventricular (AV) delay between 100-250 msec on physical work capacity in 12 patients (68 +/- 16 years) with dual chamber pacemakers implanted for high degree AV block was studied. During radionuclide ventriculography at rest the "optimal AV delay" with the maximal achieved left ventricular ejection fraction and the "most unfavorable AV delay" with the least achieved ejection fraction were determined. The ejection fraction at rest with the "optimal AV delay" was 51 +/- 14% and with the "most unfavorable AV delay" 45 +/- 15% (P < 0.001). In random order each patient was assigned to either AV delay and a spiroergometry was performed to determine maximum oxygen uptake (max VO2), which correlates best with work capacity, at a respiratory quotient of 1.1. The results show neither a difference in maximum oxygen uptake (1,262 +/- 446 mL/min with the optimal AV delay, 1,248 +/- 400 mL/min with the most unfavorable AV delay, respectively) nor in heart rate, blood pressure, exercise duration, maximal workload, and minute ventilation. Thus, an individually programmed AV delay affects left ventricular ejection fraction at rest. In contrast, an individually programmed AV delay has no influence on physical work capacity in patients with a dual chamber pacemaker.

No abstract