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We were surprised to read the poor results described in the article by Sharon et al. (1)comparing bilevel positive airway pressure (BiPAP) ventilation with intravenous isosorbide-dinitrate in patients with severe pulmonary edema. These findings are in marked contrast to our own research and experience with this modality (2–4). We routinely use BiPAP ventilatory support in those patients with severe pulmonary edema with acute respiratory failure and imminent need of endotracheal intubation (ETI). Our success rate at avoiding ETI is generally >90% in patients more severely ill than those described in the study by Sharon et al. Our patients receive sublingual nitroglycerin (0.25 mg) along with sublingual captopril (25 mg) to supplement their respiratory support. Although intravenous nitrates may be ideal, we find use of the sublingual route can frequently reverse a patient’s respiratory distress before intravenous access is even established.
The fact that two dramatically different outcomes are described for the same intervention may be explained by variations in the overall treatment of the two populations. Our research has shown that an independent predictor of BiPAP failure and subsequent ETI is the use of morphine sulfate. Even moderate amounts such as those used in the study of Sharon et al. seem to be enough to interfere with a patient’s abilities to successfully use the BiPAP system.
In treating acute pulmonary edema, high expiratory positive airway pressures (EPAPs) are required, and we routinely begin our BiPAP treatments with EPAPs of 8 to 10 cm H2O. Patients begun on regimens of any lower pressures are titrated up to a level of ≥10 cm within 1 min of placement of the nasal mask. In the study of Sharon et al., patients were begun with EPAPs of 3 cm H2O and increased by 1 cm every 3 to 4 min to a maximum of 5 cm H2O. Given these parameters, we are surprised that the authors experienced any success at all. These pressures are far too low and titration is far too slow for patients with acute respiratory distress. When applied at the higher pressures, BiPAP-treated patients demonstrate marked improvements within a few breaths and are clinically out of danger for ETI within 2 to 3 min.
The presence of positive creatine phosphokinase (CK) markers in BiPAP-treated patients is an artifact of the rapid drop in left ventricular wall pressures that occurs when the BiPAP is applied. There is a washout effect that produces a narrow spike in CK that exceeds normal thresholds for acute myocardial infarctions, although the total amount of CK is the same as that which is slowly washed out over an extended period of time with conventional therapy.
In summary, we believe that the poor outcomes described in the study of Sharon et al. reflect more problems with the manner in which the BiPAP was utilized than a failure of the therapy itself.
- American College of Cardiology