• Stephen B Smith, Shawn Carr, Stacey Psikula, Anita Das, and Katherine Grichnik.
• From the *Department of Anesthesiology, New Hanover Regional Medical Center, Wilmington, North Carolina; †Inclin, Inc., San Mateo, California; and ‡American Anesthesiology National Medical Group, Sunrise, Florida.
• Anesth. Analg.. 2015 Feb 1;120(2):479-83.

BackgroundDeep sedation of surgical patients may be associated with hypoventilation, airway collapse, and hypercarbia, although the extent of hypercarbia is rarely quantified. In this prospective, randomized, controlled clinical pilot study, we assessed the efficacy of nasal continuous positive airway pressure (nCPAP) for reducing arterial partial pressure of carbon dioxide (PaCO2) among deeply sedated, spontaneously ventilated patients undergoing total knee arthroplasty (TKA) under subarachnoid block (SAB), versus standard airway management in a control group.MethodsForty ASA status I-III patients underwent deep sedation with propofol to level 2 on the Modified Observers Assessment of Alertness/Sedation Scale during TKA performed under SAB. Nasal or oral airways were placed at the discretion of the anesthesia team, but they were not used in conjunction with nCPAP. Baseline arterial blood gas analysis (ABG-1) was performed after Modified Observers Assessment of Alertness/Sedation Scale level 2 was reached. Patients were then randomized to receive nCPAP (nCPAP group, N = 20) or standard oxygen mask management (control group, N = 20). A second ABG (ABG-2) was performed 30 minutes later to assess the effect of nCPAP on PaCO2. The primary efficacy end point was change in PaCO2 from baseline to the 30-minute time point.ResultsBaseline (ABG-1) PaCO2 values were similar between nCPAP and control groups with median values of 54.5 and 56.1 mm Hg, respectively. There was a significant decline in PaCO2 in the nCPAP group (median of -4.6 mm Hg [10th-90th quantile, -14.55 to 3.85]) as compared with the control group (median of 0.95 mm Hg [-4.75 to 9.85]; P = 0.015; 95% confidence interval [CI] for location shift = -9.5 to -1.3). Within the control group, PaCO2 was similar from ABG-1 to ABG-2 (median [10th-90th quantile] = 56.1 mm Hg [47.2-67.0] vs 56.6 mm Hg [46-68.8]; P = 0.52; 95% CI for the median = -3.4 to 3.4). Forty percent of all patients received an airway before ABG-1. The baseline PaCO2 value of patients receiving an airway was not different from that of patients without an airway (median [10th-90th quantile] = 56.0 mm Hg [46.0-68.4] vs 54.1 mm Hg [45.6-65.6], respectively; P = 0.33; 95% CI for location shift = -2.30 to 7.20).ConclusionsDeep sedation of TKA patients during SAB resulted in moderate hypercarbia (mean and median PaCO2 = 55). There was a trend showing that nCPAP treatment reduced PaCO2 versus treatment for control group patients receiving standard airway management; however, estimated treatment difference varied widely, from 1.4 to 12.6 mm Hg. Among control group patients, the initial PaCO2 during deep sedation was similar to the PaCO2 when measured after a 30-minute period of continued deep sedation. Finally, baseline PaCO2 among deeply sedated patients who received an airway was not different from that of patients who did not receive an airway.

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