Effects of dobutamine on critical capillary PO(2) and lactic acidosis threshold in patients with cardiovascular disease.

Koike, A; Kobayashi, K; Adachi, H; Shimizu, N; Itoh, H; Hiroe, M; Wasserman, K · Chest · 2001

prospective_cohort · Level II

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Abstract

BACKGROUND: Muscle capillary PO(2) has been found to reach a minimal value, ie, a critical capillary PO(2), in the midrange of work capacity in patients with cardiovascular disease. However, it is not known if the critical capillary PO(2) can be influenced by a change in blood flow response to exercise. This study was carried out to determine the effect of changing the blood flow response to exercise, using low-dose infusion of dobutamine, on muscle end-capillary PO(2) (as approximated by femoral vein PO(2)), lactate concentration, oxygen uptake (O(2)), and the relation among these variables. METHODS: Eleven male patients with coronary artery disease performed an incremental exercise test on a cycle ergometer with and without continuous infusion of dobutamine, 6 microg/kg/min. Respiratory gas analysis was performed on a breath-by-breath basis; femoral vein blood was sampled every minute through a percutaneous catheter. RESULTS: Dobutamine increased resting O(2) and O(2) at the lactic acidosis threshold (LAT) but not peak O(2). The femoral vein PO(2) rapidly decreased toward a minimal value with increasing work rate (O(2)) irrespective of the infusion of dobutamine. After reaching its nadir (critical PO(2)), femoral vein lactate began to increase without further decrease in PO(2). Infusion of dobutamine significantly increased femoral vein resting PO(2) (27.4 +/- 4.9 mm Hg vs 32.5 +/- 3.8 mm Hg) and critical PO(2) (20.5 +/- 1.5 mm Hg vs 21.9 +/- 1.7 mm Hg), but not the PO(2) at peak O(2) (22.1 +/- 3.3 mm Hg vs 22.0 +/- 2.9 mm Hg). CONCLUSIONS: Infusion of dobutamine was found to raise the critical PO(2) and LAT but not peak O(2). These findings suggest that some of the acute increase in blood flow induced by dobutamine infusion benefits exercising muscle by increasing capillary PO(2), thereby delaying the onset of lactic acidosis.

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