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The primary function of the lungs is to exchange gases. Specifically, this involves the transport of oxygen (O2) into the blood, and the elimination of carbon dioxide (CO2) from the blood. In addition, the lungs serve as minor organs of metabolism and elimination for a number of xenobiotics, a source of insensible water loss, and a means of temperature regulation.

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Cellular oxygen use is dependent on many factors, including respiratory drive; percent of oxygen in inspired air; airway patency; chest wall and pulmonary compliance; diffusing capacity; ventilation–perfusion mismatch; hemoglobin content; hemoglobin oxygen loading and unloading; cellular oxygen uptake; and cardiac output. Xenobiotics have the unique ability to inhibit or impair each of these factors necessary for oxygen use and result in respiratory dysfunction. This chapter illustrates how xenobiotics interact acutely with the mechanisms of gas exchange and oxygen use. Discussion of chronic occupational lung injury is beyond the scope of this text; the reader is referred to a number of reviews for further information.5,14,18,91

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Respiratory Drive

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Respiratory rate and depth are regulated by the need to maintain a normal PCO2 and pH. Most of the control for ventilation occurs at the level of the medulla, although it is modulated both by involuntary input from the pons and voluntary input from the higher cortices. Changes in PCO2 are measured primarily by a central chemoreceptor which measures cerebral spinal fluid (CSF) pH, and secondarily by peripheral chemoreceptors in the carotid and aortic bodies, which measure PCO2. Input with regard to PO2 is obtained from carotid and aortic chemoreceptors. Stretch receptors in the chest relay information about pulmonary dynamics, such as the volume and pressure.

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Xenobiotics can affect respiratory drive in one of several ways: direct suppression of the respiratory center; alteration in the response of chemoreceptors to changes in PCO2; direct stimulation of the respiratory center; increase in metabolic demands such as result from agitation or fever, which, in turn, increases total body oxygen consumption; or indirectly, as a result of the creation of acid–base disorders. For example, opioids (Chap. 38) depress respiration by decreasing the responsiveness of chemoreceptors to CO2 and by direct suppression of the pontine and medullary respiratory centers.34,78,104 Any xenobiotic that causes a decreased respiratory drive or a decreased level of consciousness can produce bradypnea (a decreased respiratory rate), hypopnea (a decreased tidal volume), or both, resulting in hypoventilation (Chap. 3).

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Methylxanthines, cocaine, and other sympathomimetics may cause an increase in respiratory drive as well as an increase in oxygen consumption. Salicylates produce hyperventilation by both central and peripheral effects via respiratory alkalosis and metabolic acidosis. The net consequence of increased respiratory drive, increased oxygen consumption, or metabolic acidosis is the generation of either tachypnea (an elevated respiratory rate), hyperpnea (an ...

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