Unless a patient has limited pulmonary reserve, increased CO 2 production does not result in clinically important hypercapnia. It has been estimated that intrinsic lung diseases that increase dead space are responsible for the majority of cases of hypercapnic respiratory failure, while a smaller proportion are due to extra-pulmonary conditions (eg, sedatives, neuromuscular or thoracic cage disorders). MECHANISMS AND ETIOLOGIES OF HYPERCAPNIA - Based upon the formula for the partial pressure of arterial carbon dioxide (PaCO 2) (see 'Formula for arterial carbon dioxide tension' above), factors that increase carbon dioxide (CO 2) production (eg, fever), reduce minute ventilation (eg, sedative-induced hypoventilation), and/or increase dead space (eg, chronic obstructive pulmonary disease exacerbation) may elevate the PaCO 2. Where k is a proportionality constant and V A = V E(1 - V D/V T), ie, alveolar ventilation is total ventilation minus the dead space ventilation. The following calculation is used to determine the PaCO 2: Alveolar ventilation is the component of the expired minute volume that reaches perfused alveoli, and is in turn determined by minute ventilation (V E) and the ratio of dead space (V D) to tidal volume (V T) or V D/V T. (See "The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure".)įORMULA FOR ARTERIAL CARBON DIOXIDE TENSION - The partial pressure of carbon dioxide in arterial blood (PaCO 2) is directly proportional to the rate of carbon dioxide (CO 2) production (VCO 2) by oxidative metabolism and indirectly proportional to the rate of CO 2 elimination by the lung (alveolar ventilation V A). The evaluation and treatment of patients with acute hypercapnia are presented separately. The relevant physiology of ventilatory control, mechanisms, causes, and effects of hypercapnia are presented in this topic review. Understanding the mechanisms, causes, and effects of hypercapnia is critical to its management. INTRODUCTION - Hypercapnia, defined as an elevation in the arterial carbon dioxide tension, is commonly encountered during the evaluation of patients with dyspnea and/or altered sensorium.
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