To the Editor,
As a nonanesthesia team that has administered independent propofol for endoscopic procedural sedation over the last 9 years in more than 5,000 cases with no adverse outcomes, we found Rozario, Sloper, and Sheridan's (2008) recent article very timely. Even though several of these points have been mentioned and referenced in the article, we feel several highlighted below need to be emphasized upon. We believe that this will improve the understanding of the pathophysiology of the sedation and enhance patient safety.
1. During moderate (nonintubated) procedural sedation, hypoxia (desaturation on pulse oximetry) is due to impaired ventilation, either from partial obstruction of airways or due to expected reduced ventilatory drive from sedation. It is not due to lack of inspired oxygen. Supplemental oxygen does not improve ventilation per se.
2. Pulse oximetry in room air is consistently very sensitive in detecting hypoventilation within a few seconds (Fu, Downs, Schweiger, Miguel, & Smith, 2004; Stemp & Ramsay, 2006). This alerts the monitoring nurse to take measures to correct the etiology (i.e., chin lift and encouraging the patient to breathe). It should certainly indicate caution in giving more sedative medications that suppress ventilation.When supplemental oxygen has already been applied, pulse oximetry no longer correlates with the onset of hypoventilation (Fu et al., 2004; Stemp & Ramsay, 2006). In this setting, as much as 6 minutes or more may pass before the saturation drops below 90% because it is being propped up by extra oxygen. It is counterintuitive, but turning on supplemental oxygen has the same consequence and implication as having no pulse oximeter during early stages of hypoventilation. Actually, supplemental oxygen may be a detriment, because an acceptable oxygen saturation reading fosters a false sense of security that the patient is breathing adequately, when, in fact, severe and prolonged hypoventilation may be present.
3. Prolonged hypoventilation has its own consequences beyond hypoxia. The most immediate and direct change is a rise in CO2 (hypercarbia). Hypercarbia is detrimental in multiple ways. First, it leads to acute respiratory acidosis that can progress to acute metabolic acidosis. Second, it may lead to CO2 narcosis (a condition in which alertness is reduced by high levels of CO2 in the blood). This acts as a confounding unknown factor when sedatives are used, where further hypoventilation creates a vicious cycle of hypercarbia. Supplemental oxygen does nothing to correct it and could make the hypercarbia worse. Only ventilation can reverse these changes.
4. Implications of desaturation to 90% in room air are greatly different from those of desaturation to a similar level on supplemental oxygen. It is like jumping from 3 ft off the ground compared with a fall from a second-floor window. More prolonged and more severe hypoventilation is needed to cause the same desaturation if the patient is on supplemental oxygen. In this study as well as in our own clinical observation, we note that the incidence of desaturation below 90% is not zero in supplemental oxygen. This subset of patients is at much greater risk in the supplemental oxygen group, because they have been hypopneic much longer.
5. Transient desaturation while the person is under close watch has not been shown to result in clinically detectable worse outcomes (Pedersen, Dyrlund Pederson, & Moller, 2003). The first study to show this fact was published in 1993, when more than 20,000 cases were analyzed (Moller et al., 1993). Even though the detection of hypoxia was dramatically more frequent, clinical outcomes were similar.
The clinical impact and understanding of the etiology is critical in realizing what is primary and clinically significant. Parallels exist in medicine: use of many antiarrhythmics was associated with higher cardiovascular mortality (Epstein et al., 1993). Similarly, not all antidiabetic medications produce similar survival advantage (Garratt et al., 1993). In our context, ventilation is primary and significant, whereas mild transient desaturation is not, especially if corrective measures are applied when such hypoventilation is promptly detected. The focus should therefore be on prompt detection of the hypoventilation, and measures that delay or mask it should be avoided.
A middle ground can be reached where the sedation should be started in room air if the patient is not already oxygen dependent. When the oxygen saturation begins to drop from 99% or 100% to 95% or 96%, then further sedative medication administration should be dramatically curtailed and the patient should be advised to take a couple of deep breaths. If the patient is already somnolent, then a chin lift should be done. If these measures do not stabilize the saturation, then supplemental oxygen may be started. In our experience, within 20-30 seconds, the saturation rises to baseline and at that time the supplemental oxygen may be continued or stopped. If the oxygen saturation continues to drop, and the patient is not able to respond, then reversal agents and positive pressure ventilation should be given. In our experience, it is rarely needed.
The last sentence in the Limitation section of the Rozario et al. (2008) article states, "Measuring end tidal CO2 would yield richer data about hypoxemia and indicate whether the use of supplemental oxygen masked hypoxemia"(p. 285). Perhaps the authors meant "masked hypercarbia" instead of "masked hypoxemia." We know that it does (Freeman, Hennessy, Cass, & Pheley, 1993).
In conclusion, pulse oximetry is very accurate (but only in room air) in detecting ventilatory status and transient desaturation into the upper 80s has not been found to be associated with clinically significant adverse outcomes. Focus should be on ventilation and not on mild, transient desaturation. The desaturation in room air should be used as a cautionary flag to refrain from giving more sedation and institute corrective measures. This increases the margin of safety and leads to a quicker recovery from lower sedative amounts.
Acknowledgments
The author thanks Betsy Kruel, RN, and Barbara Acita, LPN, the gastrointestinal endoscopy nurse team at Lowry Surgicenter.
Sincerely,
Pradeep Kumar, MD
Gastroenterologist, Board Certified in Internal Medicine, Clinical Nutrition, and Gastroenterology/Hepatology, Lowry Surgicenter, 1117 Lowry Avenue, Jeannette, PA 15644, [email protected]
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