TY - JOUR
T1 - The PaCO2 rate of rise in anesthetized patients with airway obstruction
AU - Stock, M. Christine
AU - Schisler, John Q.
AU - McSweeney, Thomas D.
PY - 1989
Y1 - 1989
N2 - Apneic, anesthetized patients frequently develop airway obstruction or may be disconnected from ventilatory support. The rate of PaCO2 rise is usually assumed to be equal to that of anesthetized humans who are receiving apneic oxygenation. Apneic oxygenation may eliminate CO, because it requires a continuous O2 flow. The CO2 rate of rise in anesthetized humans with airway obstruction was measured. Fourteen consenting healthy adults were monitored continuously with pulse oximetry and EKG. Enflurane-O2 anesthesia was established for at least 10 minutes with normal PaCO2 without neuromuscular blockade so that anesthesia was deep enough to prevent spontaneous ventilation. Then, patients' tracheal tubes were clamped. Arterial blood samples were obtained before and after 0, 20, 40, 60, 120, 180, 240, and 300 seconds after clamping, provided that oxyhemoglobin saturation exceeded 0.92. The equation that best described the PaC02 rise was a logarithmic function. Piecewise linear approximation yielded a PaC02 increase of 12 mmHg during the first minute of apnea, and 3.4 mmHg/minute thereafter. These values should be employed when estimating the duration of apnea from PaC02 change for anesthetized patients who lack ventilatory support. In addition, it appears that the flows of O2 that most earlier investigators used when delivering apneic oxygenation probably did not eliminate significant C02 quantities.
AB - Apneic, anesthetized patients frequently develop airway obstruction or may be disconnected from ventilatory support. The rate of PaCO2 rise is usually assumed to be equal to that of anesthetized humans who are receiving apneic oxygenation. Apneic oxygenation may eliminate CO, because it requires a continuous O2 flow. The CO2 rate of rise in anesthetized humans with airway obstruction was measured. Fourteen consenting healthy adults were monitored continuously with pulse oximetry and EKG. Enflurane-O2 anesthesia was established for at least 10 minutes with normal PaCO2 without neuromuscular blockade so that anesthesia was deep enough to prevent spontaneous ventilation. Then, patients' tracheal tubes were clamped. Arterial blood samples were obtained before and after 0, 20, 40, 60, 120, 180, 240, and 300 seconds after clamping, provided that oxyhemoglobin saturation exceeded 0.92. The equation that best described the PaC02 rise was a logarithmic function. Piecewise linear approximation yielded a PaC02 increase of 12 mmHg during the first minute of apnea, and 3.4 mmHg/minute thereafter. These values should be employed when estimating the duration of apnea from PaC02 change for anesthetized patients who lack ventilatory support. In addition, it appears that the flows of O2 that most earlier investigators used when delivering apneic oxygenation probably did not eliminate significant C02 quantities.
KW - Apnea
KW - airway obstruction
KW - anesthesia
KW - carbon dioxide
KW - oxygen
KW - respiratory acidosis
KW - respiratory failure
KW - ventilation
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U2 - 10.1016/0952-8180(89)90070-6
DO - 10.1016/0952-8180(89)90070-6
M3 - Article
C2 - 2516732
AN - SCOPUS:0024809559
VL - 1
SP - 328
EP - 332
JO - Journal of Clinical Anesthesia
JF - Journal of Clinical Anesthesia
SN - 0952-8180
IS - 5
ER -