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Bicarbonate therapy in severely acidotic trauma patients increases mortality

机译:重碳酸中毒创伤患者的碳酸氢盐治疗可增加死亡率

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BACKGROUND: Normally, end-tidal CO2 is within 2 mm Hg of arterial PO2 (PaCO2). However, if dead space in the lungs increases owing to shock with poor lung perfusion, the arterial-end tidal PCO2 difference [P(a-ET)CO2] increases. We have found that in severely injured patients, P(a-ET)CO2 of less than 10 mm Hg is associated with survival and P(a-ET)CO2 of greater than 16 mm Hg is usually fatal. Our initial studies suggested that intravenously administered bicarbonate increases P(a-ET)CO2. METHODS: This retrospective therapeutic study evaluated the effects of intravenously administered bicarbonate in a cohort of 225 severely acidotic (arterial pH ≤ 7.10) trauma patients who underwent emergency surgery from 1989 through 2011. Patients were divided into groups: early deaths (<48 hours), deaths in the operating room, deaths within 48 hours, and survivors. Winter's formula was defined as PaCO2 = (HCO3) (1.5) + 8 ± 4. RESULTS: Of the 225 patients, the mean (SD) initial arterial pH was 6.92 (0.16) with HCO3 of 11.0 (3.5) mEq/L. According to the Winter's formula, PaCO2 should have been 24 (4) mm Hg but actually was 50 (14) mm Hg. In 73 patients, the effect of an average of two to eight vials of bicarbonate increased HCO3 from 10.5 (3.1) mEq/L to 16.8 (4.0) mEq/L. In addition, PaCO2 increased from 44 (9) mm Hg to 51 (11) mm Hg and end-tidal CO2 stayed relatively constant (26 [6] to 25 [5]). This resulted in a increase in P(a-ET)CO2 from 17 (9) mm Hg to 24 (13) mm Hg, affecting survival. In the final values after resuscitation, the P(a-ET)CO2 in the 75 patients who survived was 10 (6) mm Hg, while the 103 patients who died in the operating room or within 48 hours of surgery had a P(a-ET)CO2 of 23 (10) mm Hg (p < 0.001). CONCLUSION: In severely acidotic, critically injured patients, reducing the PaCO2 to less than 40 mm Hg and decreasing the P(a-ET)CO2 to 10 (6) mm Hg should be attempted, using as little HCO3 therapy as possible. Bicarbonate should be given only if severe acidosis persists despite resuscitation and if PaCO2 levels near those which are appropriate can be obtained. LEVEL OF EVIDENCE: Therapeutic study, level IV.
机译:背景:通常,潮气末的CO2在动脉PO2(PaCO2)的2 mm Hg之内。但是,如果由于肺灌注不良导致的休克导致肺死腔增加,则动脉端潮气PCO2差异[P(a-ET)CO2]会增加。我们发现,在严重受伤的患者中,小于10 mm Hg的P(a-ET)CO2与生存有关,大于16 mm Hg的P(a-ET)CO2通常是致命的。我们的初步研究表明,静脉内施用碳酸氢盐会增加P(a-ET)CO2。方法:这项回顾性治疗研究评估了1989年至2011年接受急诊手术的225例严重酸中毒(动脉pH≤7.10)创伤患者的静脉注射碳酸氢盐的效果。患者分为两组:早期死亡(<48小时) ,手术室死亡,48小时内死亡以及幸存者。 Winter的公式定义为PaCO2 =(HCO3)(1.5)+ 8±4。结果:在225例患者中,平均(SD)初始动脉pH为6.92(0.16),HCO3为11.0(3.5)mEq / L。根据Winter的公式,PaCO2应该为24(4)mm Hg,但实际上为50(14)mm Hg。在73例患者中,平均2到8瓶碳酸氢盐的作用使HCO3从10.5(3.1)mEq / L增加到16.8(4.0)mEq / L。此外,PaCO2从44(9)mm Hg增加到51(11)mm Hg,潮气末CO2保持相对恒定(26 [6]至25 [5])。这导致P(a-ET)CO2从17(9)mm Hg增加到24(13)mm Hg,影响生存。在复苏后的最终值中,幸存的75例患者的P(a-ET)CO2为10(6)mm Hg,而在手术室或手术后48小时内死亡的103例患者的P(a) -ET)CO2为23(10)毫米汞柱(p <0.001)。结论:在严重酸中毒,重症患者中,应尝试使用尽可能少的HCO3疗法,将PaCO2降至40 mm Hg以下,将P(a-ET)CO2降至10(6)mm Hg。仅在复苏时严重酸中毒持续且PaCO2水平接近适当水平时,才应使用碳酸氢盐。证据级别:治疗研究,四级。

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