TY - JOUR
T1 - Oxygen-induced hypercarbia in obstructive pulmonary disease
AU - Dunn, W. F.
AU - Nelson, S. B.
AU - Hubmayr, R. D.
PY - 1991
Y1 - 1991
N2 - We investigated the mechanisms responsible for oxygen-induced hypercarbia in ventilator-dependent patients with advanced chronic obstructive pulmonary disease (COPD). To quantitate the effects of oxygen (O2) on respiratory drive, we determined the CO2 recruitment threshold (P(CO2) RT) in 10 mechanically ventilated patients under normoxic (Pa(O2) = 67 ± 7 mm Hg) and hyperoxic (Pa(O2) = 370 ± 67 mm Hg) conditions. P(CO2) RT is a measure of the CO2 responsiveness of the mechanically unloaded respiratory system and, as such, is independent of mechanical impedance and respiratory muscle strength. After O2 supplementation, P(CO2) RT increased from 42 ± 6 to 45 ± 6 mm Hg (p ≤ 0.05), indicating a suppression of so-called hypoxic respiratory drive. The effect of hyperoxia on the dead space to tidal volume ratio (VD/VT) and CO2 elimination (V̇(CO2)) was studied in 6 patients. Measurements were made at identical ventilator settings, thus eliminating breathing pattern- and respiratory work-related effects on these variables. VD/VT rose from 0.49 ± 0.09 to 0.55 ± 0.06 (p ≤ 0.05), but V̇(CO2) remained constant at 0.21 L/min. We discuss why measuring O2-induced changes in minute ventilation, V̇(CO2), Pa(O2), and VD/VT in spontaneously breathing patients is insufficient to distinguish between gas exchange- and respiratory drive-related mechanisms for hypercarbia. Based on the O2-induced increase in P(CO2) RT, we conclude that so-called suppression of hypoxic drive plays an important role in the pathogenesis of this disorder.
AB - We investigated the mechanisms responsible for oxygen-induced hypercarbia in ventilator-dependent patients with advanced chronic obstructive pulmonary disease (COPD). To quantitate the effects of oxygen (O2) on respiratory drive, we determined the CO2 recruitment threshold (P(CO2) RT) in 10 mechanically ventilated patients under normoxic (Pa(O2) = 67 ± 7 mm Hg) and hyperoxic (Pa(O2) = 370 ± 67 mm Hg) conditions. P(CO2) RT is a measure of the CO2 responsiveness of the mechanically unloaded respiratory system and, as such, is independent of mechanical impedance and respiratory muscle strength. After O2 supplementation, P(CO2) RT increased from 42 ± 6 to 45 ± 6 mm Hg (p ≤ 0.05), indicating a suppression of so-called hypoxic respiratory drive. The effect of hyperoxia on the dead space to tidal volume ratio (VD/VT) and CO2 elimination (V̇(CO2)) was studied in 6 patients. Measurements were made at identical ventilator settings, thus eliminating breathing pattern- and respiratory work-related effects on these variables. VD/VT rose from 0.49 ± 0.09 to 0.55 ± 0.06 (p ≤ 0.05), but V̇(CO2) remained constant at 0.21 L/min. We discuss why measuring O2-induced changes in minute ventilation, V̇(CO2), Pa(O2), and VD/VT in spontaneously breathing patients is insufficient to distinguish between gas exchange- and respiratory drive-related mechanisms for hypercarbia. Based on the O2-induced increase in P(CO2) RT, we conclude that so-called suppression of hypoxic drive plays an important role in the pathogenesis of this disorder.
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U2 - 10.1164/ajrccm/144.3_pt_1.526
DO - 10.1164/ajrccm/144.3_pt_1.526
M3 - Article
C2 - 1909846
AN - SCOPUS:0025949110
SN - 0003-0805
VL - 144
SP - 526
EP - 530
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 3 I
ER -