Callaham M, Barton C, Matthay M
Department of Medicine, University of California, San Francisco.
Crit Care Med. 1992 Mar;20(3):337-43. doi: 10.1097/00003246-199203000-00008.
To determine if the administration of epinephrine changes the partial pressure of end-tidal CO2 during cardiac arrest, as previously reported. Such a change could diminish the demonstrated ability of end-tidal CO2 measurements to predict resuscitation from cardiac arrest.
The partial pressures of end-tidal CO2 of adult cardiac arrest patients who received i.v. epinephrine in doses from 1 to 15 mg were monitored throughout arrest.
Emergency department of a university hospital.
Adults (n = 64) in cardiac arrest with a mean age of 70 +/- 12 yrs, of whom 35 were males and 15 had a mean time of return of spontaneous circulation of 6.5 +/- 11 hrs.
End-tidal CO2 (in torr) was analyzed on arrival, before the first dose of epinephrine, and 4 mins after epinephrine was administered in varying doses chosen by the supervising physician.
The end-tidal CO2 decreased an average of 0.3 torr (0.04 kPa) after epinephrine was administered. Patients with a return of pulse had a decrease of -2 torr (-0.3 kPa) vs. an increase of 0.3 torr (0.04 kPa) for those patients with no return of pulse (p = .07). In 33% of patients, there was no change; in 28%, the partial pressure of end-tidal CO2 increased, and in 39%, it decreased. There was no correlation between the change in end-tidal CO2 after epinephrine and whether or not patients regained a pulse (r2 = .08, p = .07), although a decrease in end-tidal CO2 was most often associated with return of pulse. At a threshold of 10 torr (1.3 kPa), the first end-tidal CO2 had a positive predictive value for return of pulse of 50% and a negative predictive value of 82%. Just before epinephrine administration, the positive predictive value was 71% and the negative predictive value was 83%; 4 mins after epinephrine administration, the positive predictive value was 64% and the negative predictive value was 86%. A decrease in end-tidal CO2 after epinephrine had a positive predictive value of 53% and a negative predictive value of 92%. End-tidal CO2 readings predicted resuscitation most accurately when taken after initial stabilization and before administration of epinephrine.
Although epinephrine administration may decrease end-tidal CO2 tensions in cardiac arrest, it does so unpredictably in individual patients, and it does not eliminate the predictive value of this measurement.
如先前报道，确定在心脏骤停期间给予肾上腺素是否会改变呼气末二氧化碳分压。这样的变化可能会削弱呼气末二氧化碳测量对预测心脏骤停复苏的已证实能力。
对接受静脉注射剂量为1至15毫克肾上腺素的成年心脏骤停患者在整个骤停过程中监测呼气末二氧化碳分压。
大学医院急诊科。
64名成年心脏骤停患者，平均年龄70±12岁，其中35名男性，15名患者自主循环恢复的平均时间为6.5±11小时。
在到达时、首次给予肾上腺素之前以及在监督医生选择的不同剂量肾上腺素给药后4分钟分析呼气末二氧化碳（以托为单位）。
给予肾上腺素后，呼气末二氧化碳平均下降0.3托（0.04千帕）。有脉搏恢复的患者下降-2托（-0.3千帕），而无脉搏恢复的患者上升0.3托（0.04千帕）（p = 0.07）。33%的患者没有变化；28%的患者呼气末二氧化碳分压升高，39%的患者降低。肾上腺素给药后呼气末二氧化碳的变化与患者是否恢复脉搏之间没有相关性（r2 = 0.08，p = 0.07），尽管呼气末二氧化碳降低最常与脉搏恢复相关。在阈值为10托（1.3千帕）时，首次呼气末二氧化碳对脉搏恢复的阳性预测值为50%，阴性预测值为82%。就在给予肾上腺素之前，阳性预测值为71%，阴性预测值为83%；肾上腺素给药后4分钟，阳性预测值为64%，阴性预测值为86%。肾上腺素给药后呼气末二氧化碳降低的阳性预测值为53%，阴性预测值为92%。在初始稳定后且在给予肾上腺素之前进行呼气末二氧化碳读数时，对复苏的预测最准确。
尽管在心脏骤停时给予肾上腺素可能会降低呼气末二氧化碳张力，但在个体患者中其降低情况不可预测，并且它并没有消除该测量的预测价值。
