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Diagnostic Errors↗
Biomedical subjects
D J Cionni
Publications and source records attributed to D J Cionni.
Utility of the peak expiratory flow rate in the differentiation of acute dyspnea. Cardiac vs pulmonary origin.
This study examined the utility of a peak expiratory flow rate (PEFR) measurement in the differentiation of acute moderate to severe dyspnea secondary to congestive heart failure or chronic lung disease. A PEFR was determined in 41 episodes of acute respiratory distress in 40 patients prior to emergency department therapy. The mean PEFR +/- SD for the congestive heart failure group (n = 18) was 224 +/- 82 L/min, which was significantly higher (p less than 0.001) than that of the chronic lung disease group (n = 23), which had a mean PEFR of 108 +/- 49 L/min. No single cutoff value allowed 100 percent accurate classification, but the results suggest that the PEFR may be a useful adjunctive tool in the differentiation of acute dyspnea of cardiac vs pulmonary origin.
Acute Disease↗
Oxygen saturation as a marker for admission or relapse with acute bronchospasm.
Oxygen saturation (SaO2) as measured by pulse oximetry was evaluated as a means of complementing or supplementing peak expiratory flow rate (PEFR) for early identification of the adult patient needing prolonged therapy for acute bronchospasm. SaO2 was recorded at baseline and at the time of peak drop after initial bronchodilator therapy for 28 patient visits. PEFR was recorded at baseline and at 15 minutes after initial bronchodilator therapy. Potential admission criteria based on these parameters were compared to patients actually admitted or returned within 72 hours (prematurely discharged). Mean patient age was 36 +/- 16.8 years. Mean baseline SaO2 was 95.4 +/- 2.3% (92 to 100%) and SaO2 at the peak drop after the first bronchodilator therapy was 91.9 +/- 3.0% (86 to 97%). Of the criteria evaluated, the following had a significant correlation with admission or premature discharge: baseline PEFR less than or equal to 100 L/min (P = .017); PEFR after first bronchodilator therapy less than or equal to 160 L/min (P less than .0004); the combination of a baseline PEFR less than or equal to 100 L/min with an improvement in PEFR less than or equal to 100 L/min (P less than .0003); and the combination of baseline SaO2 less than or equal to 95% with an improvement in PEFR less than or equal to 100 L/min (P = .0017). As isolated variables, SaO2 at baseline and SaO2 at peak drop following bronchodilator therapy were not useful predictors of outcome, although patients severely hypoxemic at presentation were not evaluated.
Acute Disease↗
Oxygen desaturation in adults following inhaled metaproterenol therapy.
Following bronchodilator therapy in asthmatic patients, a fall in arterial oxygen tension (PaO2) has been attributed to increased perfusion of persistently underventilated alveoli. We used continuous noninvasive pulse oximetry to evaluate the extent and timing of oxygen saturation (SaO2) decrease in adults following metaproterenol inhalation for acute bronchospasm. We also examined the effect of supplemental oxygen upon these factors. Baseline and peak drop in SaO2 after completion of the first bronchodilator therapy were measured and the percent change in SaO2 was calculated. A total of 47 patient visits were studied; 10 patients received supplemental oxygen. Mean age was 38 +/- 17.9 years. Baseline was SaO2 = 94.6 +/- 2.9%, peak drop SaO2 = 91.4 +/- 3.4%, and percent change in SaO2 = -3.4 +/- 2.5%. The mean time to peak drop was 24.4 +/- 15.4 minutes in the 40 patients, with an observed drop after initial treatment. The absolute change in SaO2 from baseline was significant both with and without oxygen (P less than .05 and less than .01, respectively). The group receiving oxygen had a significantly smaller percent drop and a larger proportion of patients showing no drop in SaO2 (P less than 0.01 and less than 0.03, respectively). Clinically significant oxygen desaturation can occur within 30 minutes of inhaled bronchodilator therapy. Supplemental oxygen (2-3 L/min) helps blunt the metaproterenol-induced drop in SaO2.
Acute Disease↗