• George J Crystal.
• From the Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Chicago, Illinois; and Departments of Anesthesiology and of Physiology and Biophysics, University of Illinois College of Medicine, Chicago, Illinois.
• Anesth. Analg. 2015 Sep 1; 121 (3): 610-623.

AbstractCarbon dioxide (CO2) is an end product of aerobic cellular respiration. In healthy persons, PaCO2 is maintained by physiologic mechanisms within a narrow range (35-45 mm Hg). Both hypercapnia and hypocapnia are encountered in myriad clinical situations. In recent years, the number of hypercapnic patients has increased by the use of smaller tidal volumes to limit lung stretch and injury during mechanical ventilation, so-called permissive hypercapnia. A knowledge and appreciation of the effects of CO2 in the heart are necessary for optimal clinical management in the perioperative and critical care settings. This article reviews, from a historical perspective: (1) the effects of CO2 on coronary blood flow and the mechanisms underlying these effects; (2) the role of endogenously produced CO2 in metabolic control of coronary blood flow and the matching of myocardial oxygen supply to demand; and (3) the direct and reflexogenic actions of CO2 on myocardial contractile function. Clinically relevant issues are addressed, including the role of increased myocardial tissue PCO2 (PmCO2) in the decline in myocardial contractility during coronary hypoperfusion and the increased vulnerability to CO2-induced cardiac depression in patients receiving a β-adrenergic receptor antagonist or with otherwise compromised inotropic reserve. The potential use of real-time measurements of PmO2 to monitor the adequacy of myocardial perfusion in the perioperative period is discussed.

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