Carbon dioxide (CO2) is produced by the body's metabolism at approximately the same rate as O2 consumption, about 3 mL/kg/minute at rest, increasing dramatically with heavy exercise. CO2 diffuses readily from the cells into the bloodstream, where it is carried partly as bicarbonate ion (HCO3-), partly in chemical combination with hemoglobin and plasma proteins, and partly in solution at a partial pressure of -6 kPa (46 mm Hg) in mixed venous blood. CO2is transported to the lung, where it is normally exhaled at the same rate at which it is produced, leaving a partial pressure of -5.2 kPa (40 mm Hg) in the alveoli and in arterial blood. An increase in Pco2 results in a respiratory acidosis and may be due to decreased ventilation or the inhalation of CO2, whereas an increase in ventilation results in decreased Pco2 and a respiratory alkalosis. Since CO2is freely diffusible, changes in blood Pco2 and pH soon are reflected by intracellular changes in Pco2 and pH.
Carbon dioxide is a rapid, potent stimulus to ventilation. Inhalation of 10% CO2 can produce minute volumes of 75 L/min in normal individuals. Carbon dioxide acts at multiple sites to stimulate ventilation. Elevated PCO2 causes bronchodilation, whereas hypocarbia causes constriction of airway smooth muscle; these responses may play a role in matching pulmonary ventilation and perfusion. Circulatory effects of CO2 result from the combination of direct local effects and centrally mediated effects on the autonomic nervous system. The direct effects are diminished contractility of the heart and vascular smooth muscle (vasodilation). The indirect effects result from the capacity of CO2 to activate the sympathetic nervous system; these indirect effects generally oppose the local effects of CO2 . Thus, the balance of opposing local and sympathetic effects determines the total circulatory response to CO2. The net effect of CO2 inhalation is an increase in cardiac output, heart rate, and blood pressure. In blood vessels, however, the direct vasodilating actions of carbon dioxide appear more important, and total peripheral resistance decreases when the PCO2 is increased. CO2 also is a potent coronary vasodilator. Cardiac arrhythmias associated with increased PCO2 are due to the release of catecholamines.
Hypocarbia results in opposite effects: decreased blood pressure and vasoconstriction in skin, intestine, brain, kidney, and heart. These actions are exploited clinically in the use of hyperventilation to diminish intracranial hypertension.
Hypercarbia depresses the excitability of the cerebral cortex and increases the cutaneous pain threshold through a central action. In patients who are hypoventilating from narcotics or anesthetics, increasing Pco2 may result in further CNS depression, which in turn may worsen the respiratory depression. This positive-feedback cycle can be deadly.
Inhalation of CO2 is used less commonly today than in the past because there are now more effective treatments for most indications. Inhalation of carbon dioxide has been used during anesthesia to increase the speed of induction and emergence from inhalational anesthesia by increasing minute ventilation and cerebral blood flow. However, this technique results in some degree of respiratory acidosis. Hypocarbia, with its attendant respiratory alkalosis, still has some uses in anesthesia. It constricts cerebral vessels, decreasing brain size slightly, and thus may facilitate the performance of neurosurgical operations. Although CO2 stimulates respiration, CO2 is not useful in situations where respiratory depression has resulted in hypercarbia or acidosis because further depression results.
CO2 is commonly used for insufflation during endoscopic procedures (e.g., laparoscopic surgery) because CO2 is highly soluble and does not support combustion. Any inadvertent gas emboli thus are dissolved and eliminated more easily via the respiratory system. CO2 can be helpful during open cardiac surgery, where the gas is used to flood the surgical field and, because of its density, displaces the air surrounding the open heart, assuring that any gas bubbles trapped are CO2 rather than insoluble nitrogen. For the same reasons, CO2 is used to debubble cardiopul-monary bypass and extracorporeal membrane oxygenation (ECMO) circuits. It also can be used to adjust pH during bypass procedures when a patient is cooled.
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