The main function of the lung is gas exchange: the elimination of carbon dioxide (CO2) and the delivery of oxygen (O2) to the tissues. When either function is impaired, the result is respiratory failure. Hypercarbic respiratory failure is a consequence of and is in direct proportion to a reduction of alveolar ventilation. Since the third major alveolar gas, nitrogen (N), is inert, any increase in CO2 is accompanied by a reduction of O2, unless supplemental oxygen is provided. When there is an acute or rapid reduction of alveolar ventilation, the result is acute respiratory acidosis. At other times, chronic respiratory failure can result from chronic lung disease, chest wall disease, or an abnormal respiratory control of ventilation. With such patients, there is often compensation of the hypercarbic respiratory failure and the acidosis may be corrected. This chapter will discuss the physiology of hypercarbic respiratory failure and describe clinical scenarios associated with hypercarbia and their associated management.
PHYSIOLOGY OF HYPERCARBIC RESPIRATORY FAILURE
Ventilation is the process of moving air from the atmosphere to the alveoli for the purpose of exchanging oxygen and carbon dioxide. Room air contains essentially no carbon dioxide. Mixed venous blood has a partial pressure of carbon dioxide (PCO2) of approximately 46 mmHg. Alveolar PCO2 (PaCO2) is approximately 40 mmHg, and there is no significant gradient between alveolar and arterial blood PCO2 (PaCO2). Thus, PaCO2 is a nearly perfect indicator of alveolar PCO2. An elevated PaCO2 indicates hypoventilation or hypercapnic respiratory failure.
Hypercapnic respiratory failure may exist in the presence of or independently of hypoxemia. As stated in Chapter 8, there are 5 mechanisms of hypoxemia: hypoventilation, ventilation/perfusion (V̇/Q̇) mismatch, shunt, diffusion abnormalities, and reduction in oxygen tension. As stated in Chapter 1, the alveolar–arterial (A-a) gradient may help determine which mechanism is involved.
Hypoventilation may be caused by a ventilatory drive problem (“won’t do”) or from a disease of the respiratory system (“can’t do”). The PaCO2 is normally very carefully regulated by the brain, with even small changes resulting in almost immediate changes in ventilation. The normal ventilatory response to elevated PaCO2 is 1.5 to 2 L/min/mmHg. Normal resting minute ventilation is approximately 6 L/min. This indicates that the normal response to an elevated PaCO2 of only 43 mmHg would be to nearly double resting minute ventilation. The increase in ventilatory drive is normally perceived as dyspnea. Clinically, any patient with an elevated PaCO2 who does not appear dyspneic has a blunted ventilatory drive, either from a central nervous system (CNS) problem or from habituation. Hypoxic respiratory drive is much weaker, and patients who are hypoxic may not have symptoms of dyspnea. Hypoventilation due to decreased drive ...