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Clinical Investigations: CARDIOLOGY |

Effects of Dobutamine on Critical Capillary Po2 and Lactic Acidosis Threshold in Patients With Cardiovascular Disease*

Akira Koike, MD; Kazuo Kobayashi, MD; Hiromasa Adachi, MD; Noritaka Shimizu, MD; Haruki Itoh, MD; Michiaki Hiroe, MD; Karlman Wasserman, MD, PhD, FCCP
Author and Funding Information

*From The Cardiovascular Institute (Drs. Koike and Itoh), Tokyo; Hokushin General Hospital (Drs. Kobayashi and Adachi), Nagano; Second Department of Internal Medicine (Drs. Shimizu and Hiroe), Tokyo Medical and Dental University, Tokyo; and Division of Respiratory and Critical Care Physiology and Medicine (Dr. Wasserman), Harbor-UCLA Medical Center, Torrance, CA.

Correspondence to: Akira Koike, MD, The Cardiovascular Institute, 3–10, Roppongi 7-chome, Minato-ku, Tokyo 106-0032, Japan; e-mail: koike@cepp.ne.jp



Chest. 2001;120(4):1218-1225. doi:10.1378/chest.120.4.1218
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Background: Muscle capillary Po2 has been found to reach a minimal value, ie, a critical capillary Po2, in the midrange of work capacity in patients with cardiovascular disease. However, it is not known if the critical capillary Po2 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 Po2 (as approximated by femoral vein Po2), lactate concentration, oxygen uptake (V̇o2), 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, 6μ g/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 V̇o2 and V̇o2 at the lactic acidosis threshold (LAT) but not peak V̇o2. The femoral vein Po2 rapidly decreased toward a minimal value with increasing work rate (V̇o2) irrespective of the infusion of dobutamine. After reaching its nadir (critical Po2), femoral vein lactate began to increase without further decrease in Po2. Infusion of dobutamine significantly increased femoral vein resting Po2 (27.4 ± 4.9 mm Hg vs 32.5 ± 3.8 mm Hg) and critical Po2 (20.5 ± 1.5 mm Hg vs 21.9 ± 1.7 mm Hg), but not the Po2 at peak V̇o2 (22.1 ± 3.3 mm Hg vs 22.0 ± 2.9 mm Hg).

Conclusions: Infusion of dobutamine was found to raise the critical Po2 and LAT but not peak V̇o2. These findings suggest that some of the acute increase in blood flow induced by dobutamine infusion benefits exercising muscle by increasing capillary Po2, thereby delaying the onset of lactic acidosis.

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