In Response: We appreciate the thoughtful commentary provided by Overdyk et al. (1) and the opportunity to clarify our recommendations for improved monitoring of patients (2). Joint Commission on Accreditation of Healthcare Organizations (JCAHO)-mandated pain management standards have increased the need for accurate monitoring to detect clinically significant hypoventilation and increase patient safety. It is likely that all patients who receive narcotic analgesics will have some degree of respiratory depression. As noted by Overdyk et al., respiratory rate is woefully inadequate as a monitor of ventilatory adequacy. Studies cited by Cashman and Dolin (3) reported decreased respiratory rate in only 1.1% of patients receiving narcotic analgesics. Yet respiratory depression was indicated by decreased oxygen saturation in 37% of patients receiving narcotics IM even when Fio2 was not specified. Witting et al. (4) were able to detect 88 of 92 cases of narcotic-induced hypercapnia with a pulse oximeter, as long as patients inhaled room air, indicating the sensitivity of Spo2 for detecting hypoventilation. Although we agree that high-risk patients need close monitoring for opioid-induced respiratory depression, Overdyk et al. disagree with our recommendation that pulse oximetry be used to monitor such patients. The basis for their disagreement is the observation that most high-risk patients receive supplemental inspired oxygen. Such therapy is based on the unproven, yet widely accepted, premise that moderate arterial hypoxemia is associated with increased morbidity and/or mortality. It is our contention that this premise is absolutely unfounded (5). When patients breathe room air, without supplemental oxygen, the pulse oximeter has been demonstrated to be a sensitive monitor of ventilation (4,6). Capnography has been offered as a means of monitoring ventilatory adequacy (7). However, this technique has failed to demonstrate efficacy in clinical practice (8,9). It is possible that the pulse oximeter is the only clinically useful monitor of ventilation, as long as the inspired oxygen concentration is 0.21. An increase in Fio2 will increase the arterial partial pressure of oxygen but will do nothing to correct the pathological condition causing arterial hypoxemia (7,8). Should patients demonstrate a decrease in oxygen saturation while breathing room air, the clinician, when alerted, may investigate to determine if arterial hypoxemia is secondary to hypoventilation, low, but finite, ventilation-to-perfusion ratio, or right-to-left intrapulmonary shunting of blood. Contrary to concerns expressed by Overdyk et al., we feel that patients at risk for developing, but not yet manifesting, arterial hypoxemia are best monitored while breathing room air, which will allow detection and correction of pulmonary dysfunction sooner than will occur with an Fio2 >0.21 (10). Timely detection of inadequate ventilation is essential so that appropriate therapy may be instituted before dangerously high levels of carbon dioxide result in even more profound respiratory depression. It is physiologically not possible for a patient breathing room air to develop a Paco2 >75 mm Hg while maintaining an Spo2 >90%. However, it is possible for a patient to breathe as little as 25% inspired oxygen to maintain Spo2 >90%, with a Paco2 > 100 mm Hg! At this level, CO2 narcosis may further impair ventilation. Respiratory arrest and rapid, profound arterial hypoxemia will likely then occur. Weighing the risks (if there are any) of mild arterial hypoxemia (Spo2 > 80%) against the hazard of undetected profound hypoventilation, leads us to the conclusion that the pulse oximeter should be viewed as an effective means of monitoring adequacy of ventilation but only if inspired air is not supplemented with additional oxygen. Hector Vila Jr, MD John B. Downs, MD Anesthesiology Division Department of Interdisciplinary Oncology H. Lee Moffitt Cancer Center and Research Institute University of South Florida College of Medicine Tampa, FL [email protected]
Read full abstract
Dec 27, 2024
I A Kozlov 
Open Access