Effects of hypercapnia on myocardial blood flow in healthy human subjects

Abstract

Elevation of the end-tidal partial pressure of CO 2 (P ET CO 2 ) increases cerebral and myocardial blood flow (MBF), suggesting that it may be a suitable alternative to pharmacologic stress or exercise for myocardial perfusion imaging. The purpose of this study was to document the pharmacodynamics of CO 2 for MBF using prospective end-tidal targeting to precisely control arterial PCO 2 and PET to measure the outcome variable, MBF. Methods: Ten healthy men underwent serial 82 Rb PET/CT imaging. Imaging was performed at rest and during 6-min hypercapnic plateaus (baseline; P ET CO 2 at 50, 55, and 60 mm Hg; repeat of P ET CO 2 at 60 mm Hg; and repeat of baseline). MBF was measured using 82 Rb injected 3 min after the beginning of hypercapnia and a 1-tissue-compartment model with flow-dependent extraction correction. Results were compared with those obtained during an adenosine stress test (140 µg/kg/min). Results: Baseline P ET CO 2 was 38.9 6 0.8 (mean 6 SD) mm Hg (range, 35–43 mm Hg). All P ET CO 2 targets were sustained, with SDs of less than 1.5 mm Hg. Heart rate, systolic blood pressure, rate · pressure product, and respiratory frequency increased with progressive hypercapnia. MBF increased significantly at each level of hypercapnia to 1.92-fold over baseline (0.86 6 0.24 vs. 0.45 6 0.08 mL/min/g; P 5 0.002) at a P ET CO 2 of 60 mm Hg. MBF after the administration of adenosine was significantly greater than that with the maximal hypercapnic stimulus (2.00 vs. 0.86 mL/min/g; P, 0.0001). Conclusion: To our knowledge, this study is the first to assess the response of MBF to different levels of hypercapnia in healthy humans with PET. MBF increased with increasing levels of hypercapnia; MBF at a P ET CO 2 of 60 mm Hg was double that at baseline.