Abstract
Study objective: This two-part study was designed to determine the effect of supplemental oxygen on the detection of hypoventilation, evidenced by a decline in oxygen saturation (SpO2) with pulse oximetry. Design: Phase 1 was a prospective, patient-controlled, clinical trial. Phase 2 was a prospective, randomized, clinical trial. Setting: Phase 1 took place in the operating room. Phase 2 took place in the postanesthesia care unit (PACU). Patients: In phase 1, 45 patients underwent abdominal, gynecologic, urologie, and lower-extremity vascular operations. In phase 2, 288 patients were recovering from anesthesia. Intervention: In phase 1, modeling of deliberate hypoventilation entailed decreasing by 50% the minute ventilation of patients receiving general anesthesia. Patients breathing a fraction of inspired oxygen (FIO2) of 0.21 (n = 25) underwent hypoventilation for up to 5 min. Patients with an FIO2 of 0.25 (n = 10) or 0.30 (n = 10) underwent hypoventilation for 10 min. In phase 2, spontaneously breathing patients were randomized to breathe room air (n = 155) or to receive supplemental oxygen (n = 133) on arrival in the PACU. Measurements and results: In phase 1, end-tidal carbon dioxide and SpO2 were measured during deliberate hypoventilation. A decrease in SpO2 occurred only in patients who breathed room air. No decline occurred in patients with FIO2 levels of 0.25 and 0.30. In phase 2, SpO2 was recorded every min for up to 40 min in the PACU. Arterial desataration (SpO2 < 90%) was fourfold higher in patients who breathed room air than in patients who breathed supplemental oxygen (9.0% vs 2.3%, p = 0.02). Conclusion: Hypoventilation can be detected reliably by pulse oximetry only when patients breathe room air. In patients with spontaneous ventilation, supplemental oxygen often masked the ability to detect abnormalities in respiratory function in the PACU. Without the need for capnograpliy and arterial blood gas analysis, pulse oximetry is a useful tool to assess ventilatory abnormalities, but only in the absence of supplemental inspired oxygen.
| Original language | English |
|---|---|
| Pages (from-to) | 1552-1558 |
| Number of pages | 7 |
| Journal | Chest |
| Volume | 126 |
| Issue number | 5 |
| DOIs | |
| State | Published - Nov 1 2004 |
| Externally published | Yes |
Fingerprint
Keywords
- Hypoventilation
- Pulse oximetry
- Supplemental oxygen
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
Cite this
Supplement oxygen impairs detection of hypoventilation by pulse oximetry. / Fu, Eugene; Downs, John B.; Schweiger, John W.; Miguel, Rafael V.; Smith, Robert A.
In: Chest, Vol. 126, No. 5, 01.11.2004, p. 1552-1558.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Supplement oxygen impairs detection of hypoventilation by pulse oximetry
AU - Fu, Eugene
AU - Downs, John B.
AU - Schweiger, John W.
AU - Miguel, Rafael V.
AU - Smith, Robert A.
PY - 2004/11/1
Y1 - 2004/11/1
N2 - Study objective: This two-part study was designed to determine the effect of supplemental oxygen on the detection of hypoventilation, evidenced by a decline in oxygen saturation (SpO2) with pulse oximetry. Design: Phase 1 was a prospective, patient-controlled, clinical trial. Phase 2 was a prospective, randomized, clinical trial. Setting: Phase 1 took place in the operating room. Phase 2 took place in the postanesthesia care unit (PACU). Patients: In phase 1, 45 patients underwent abdominal, gynecologic, urologie, and lower-extremity vascular operations. In phase 2, 288 patients were recovering from anesthesia. Intervention: In phase 1, modeling of deliberate hypoventilation entailed decreasing by 50% the minute ventilation of patients receiving general anesthesia. Patients breathing a fraction of inspired oxygen (FIO2) of 0.21 (n = 25) underwent hypoventilation for up to 5 min. Patients with an FIO2 of 0.25 (n = 10) or 0.30 (n = 10) underwent hypoventilation for 10 min. In phase 2, spontaneously breathing patients were randomized to breathe room air (n = 155) or to receive supplemental oxygen (n = 133) on arrival in the PACU. Measurements and results: In phase 1, end-tidal carbon dioxide and SpO2 were measured during deliberate hypoventilation. A decrease in SpO2 occurred only in patients who breathed room air. No decline occurred in patients with FIO2 levels of 0.25 and 0.30. In phase 2, SpO2 was recorded every min for up to 40 min in the PACU. Arterial desataration (SpO2 < 90%) was fourfold higher in patients who breathed room air than in patients who breathed supplemental oxygen (9.0% vs 2.3%, p = 0.02). Conclusion: Hypoventilation can be detected reliably by pulse oximetry only when patients breathe room air. In patients with spontaneous ventilation, supplemental oxygen often masked the ability to detect abnormalities in respiratory function in the PACU. Without the need for capnograpliy and arterial blood gas analysis, pulse oximetry is a useful tool to assess ventilatory abnormalities, but only in the absence of supplemental inspired oxygen.
AB - Study objective: This two-part study was designed to determine the effect of supplemental oxygen on the detection of hypoventilation, evidenced by a decline in oxygen saturation (SpO2) with pulse oximetry. Design: Phase 1 was a prospective, patient-controlled, clinical trial. Phase 2 was a prospective, randomized, clinical trial. Setting: Phase 1 took place in the operating room. Phase 2 took place in the postanesthesia care unit (PACU). Patients: In phase 1, 45 patients underwent abdominal, gynecologic, urologie, and lower-extremity vascular operations. In phase 2, 288 patients were recovering from anesthesia. Intervention: In phase 1, modeling of deliberate hypoventilation entailed decreasing by 50% the minute ventilation of patients receiving general anesthesia. Patients breathing a fraction of inspired oxygen (FIO2) of 0.21 (n = 25) underwent hypoventilation for up to 5 min. Patients with an FIO2 of 0.25 (n = 10) or 0.30 (n = 10) underwent hypoventilation for 10 min. In phase 2, spontaneously breathing patients were randomized to breathe room air (n = 155) or to receive supplemental oxygen (n = 133) on arrival in the PACU. Measurements and results: In phase 1, end-tidal carbon dioxide and SpO2 were measured during deliberate hypoventilation. A decrease in SpO2 occurred only in patients who breathed room air. No decline occurred in patients with FIO2 levels of 0.25 and 0.30. In phase 2, SpO2 was recorded every min for up to 40 min in the PACU. Arterial desataration (SpO2 < 90%) was fourfold higher in patients who breathed room air than in patients who breathed supplemental oxygen (9.0% vs 2.3%, p = 0.02). Conclusion: Hypoventilation can be detected reliably by pulse oximetry only when patients breathe room air. In patients with spontaneous ventilation, supplemental oxygen often masked the ability to detect abnormalities in respiratory function in the PACU. Without the need for capnograpliy and arterial blood gas analysis, pulse oximetry is a useful tool to assess ventilatory abnormalities, but only in the absence of supplemental inspired oxygen.
KW - Hypoventilation
KW - Pulse oximetry
KW - Supplemental oxygen
UR - http://www.scopus.com/inward/record.url?scp=8744243235&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=8744243235&partnerID=8YFLogxK
U2 - 10.1378/chest.126.5.1552
DO - 10.1378/chest.126.5.1552
M3 - Article
C2 - 15539726
AN - SCOPUS:8744243235
VL - 126
SP - 1552
EP - 1558
JO - Chest
JF - Chest
SN - 0012-3692
IS - 5
ER -