Bakker J, Vincent J L, Gris P, Leon M, Coffernils M, Kahn R J
Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Belgium.
Chest. 1992 Feb;101(2):509-15. doi: 10.1378/chest.101.2.509.
Recent reports have shown that venous hypercarbia, resulting in a widening of the veno-arterial difference in PCO2 (dPCO2), is related to systemic hypoperfusion in various forms of low-flow state. Although septic shock usually is a hyperdynamic state, other factors can influence the CO2 production and elimination, and thus dPCO2 in septic shock This study examined the dPCO2 and acid-base balance together with cardiac output measurements and oxygen-derived variables in 64 adult patients with documented septic shock. For a total of 191 observations, a significant exponential relation between dPCO2 and CO was found. At time of first measurement, 15 patients had an increased dPCO2 (above 6 mm Hg) and a higher mixed venous PCO2 (PvCO2) (47.2 +/- 10.0 vs 35.9 +/- 7.3 mm Hg, p less than 0.001). These patients had a lower cardiac index (2.9 +/- 1.3 vs 3.8 +/- 2.0 L/min.m2, p less than 0.01), a higher oxygen extraction ratio, but a similar VO2 than patients with normal dPCO2. The higher dPCO2 could also be related to an impaired CO2 elimination as indicated by a higher PaCO2 and a lower PaO2/FIO2 in these patients. Nonsurvivors had a significantly higher dPCO2 than survivors (5.9 +/- 3.4 vs 4.4 +/- 2.3 mm Hg, p less than 0.05) in the presence of similar cardiac output. The higher dPCO2 in these patients was probably related to the higher blood lactate levels (7.7 +/- 5.3 mmol/L vs 4.5 +/- 2.8 mmol/L, p less than 0.01) and the more severe pulmonary impairment (SaO2 90 +/- 8 percent vs 95 +/- 4 percent, p less than 0.001). Arteriovenous oxygen content difference (dAVO2) and VO2 were similar in survivors and nonsurvivors. In conclusion, dPCO2 patients with septic shock is related principally to cardiac output but apparently also to the degree of pulmonary impairment. Although dPCO2 is larger in nonsurvivors, its prognostic value is modest.
近期报告显示，静脉血二氧化碳潴留导致动脉血与静脉血二氧化碳分压差（dPCO2）增大，这与各种低流量状态下的全身低灌注有关。虽然感染性休克通常是高动力状态，但其他因素可影响二氧化碳的产生和清除，进而影响感染性休克患者的dPCO2。本研究对64例确诊为感染性休克的成年患者的dPCO2、酸碱平衡、心输出量及氧代谢指标进行了检测。在总共191次观察中，发现dPCO2与心输出量之间存在显著的指数关系。首次测量时，15例患者的dPCO2升高（超过6 mmHg），混合静脉血二氧化碳分压（PvCO2）也较高（47.2±10.0 vs 35.9±7.3 mmHg，p<0.001）。与dPCO2正常的患者相比，这些患者的心指数较低（2.9±1.3 vs 3.8±2.0 L/min·m2，p<0.01），氧摄取率较高，但氧耗量相似。这些患者较高的dPCO2也可能与二氧化碳清除受损有关，表现为动脉血二氧化碳分压（PaCO2）较高，动脉血氧分压与吸入氧分数比值（PaO2/FIO2）较低。在相似的心输出量情况下，非存活患者的dPCO2显著高于存活患者（5.9±3.4 vs 4.4±2.3 mmHg，p<0.05）。这些患者较高的dPCO2可能与较高的血乳酸水平（7.7±5.3 mmol/L vs 4.5±2.8 mmol/L，p<0.01）和更严重的肺功能损害（动脉血氧饱和度[SaO2] 90±8% vs 95±4%，p<0.001）有关。存活患者和非存活患者的动静脉血氧含量差（dAVO2）及氧耗量相似。总之，感染性休克患者的dPCO2主要与心输出量有关，但显然也与肺功能损害程度有关。虽然非存活患者的dPCO2较大，但其预后价值有限。
