Bitar Zouheir Ibrahim, Maadarani Ossama Sajeh, El-Shably AlAsmar Mohammed, Elshabasy Ragab Desouky, Zaalouk Tamer Mohamed
Critical Care Unit, Ahmadi Hospital, Kuwait Oil Company, P.O. Box 46468, Postal Code 64015, Ahmadi, Kuwait.
Crit Care Res Pract. 2020 Jan 7;2020:9281623. doi: 10.1155/2020/9281623. eCollection 2020.
Central venous-arterial carbon dioxide difference (PCO2 gap) can be a marker of cardiac output adequacy in global metabolic conditions that are less affected by the impairment of oxygen extraction capacity. We investigated the relation between the PCO2 gap, serum lactate, and cardiac index (CI) and prognostic value on admission in relation to fluid administration in the early phases of resuscitation in sepsis. We also investigated the chest ultrasound pattern A or B.
We performed a prospective observational study and recruited 28 patients with severe sepsis and septic shock in a mixed ICU. We determined central venous PO2, PCO2, PCO2 gap, lactate, and CI at 0 and 6 hours after critical care unit (CCU) admission. The population was divided into two groups based on the PCO2 gap (cutoff value 0.8 kPa).
The CI was significantly lower in the high PCO2 gap group (=0.001). The high PCO2 gap group, on admission, required more administered fluid and vasopressors (=0.01 and =0.009, respectively). There was also a significant difference between the two groups for low mean pressure (=0.01), central venous O2 (=0.01), and lactate level (=0.003). The mean arterial pressure was lower in the high PCO2 gap group, and the lactate level was higher, indicating global hypoperfusion. The hospital mortality rate for all patients was 24.5% (7/28). The in-hospital mortality rate was 20% (2/12) for the low gap group and 30% (5/16) for the high gap group; the odds ratio was 1.6 (95% CI 0.5-5.5; =0.53). Patients with a persistent or rising PCO2 gap larger than 0.8 kPa at = 6 and 12 hours had a higher mortality change ( = 6; in-hospital mortality was 21.4%) than patients with a PCO2 gap of less than 0.8 kPa at = 6 ( = 1; in-hospital mortality was 3%); this odds ratio was 5.3 (95% CI 0.9-30.7; =0.08). The PCO2 gap had no relation with the chest ultrasound pattern.
The PCO2 gap is an important hemodynamic variable in the management of sepsis-induced circulatory failure. The PCO2 gap can be a marker of the adequacy of the cardiac output status in severe sepsis. A high PCO2 gap value (>0.8 kPa) can identify situations in which increasing CO can be attempted with fluid resuscitation in severe sepsis. The PCO2 gap carries an important prognostic value in severe sepsis.
在受氧摄取能力损害影响较小的整体代谢状况下，中心静脉 - 动脉二氧化碳差值（PCO₂ 差值）可作为心输出量充足的标志物。我们研究了 PCO₂ 差值、血清乳酸和心脏指数（CI）之间的关系，以及在脓毒症复苏早期与液体输注相关的入院时的预后价值。我们还研究了胸部超声模式A或B。
我们进行了一项前瞻性观察研究，在一个混合重症监护病房招募了28例严重脓毒症和脓毒性休克患者。在重症监护病房（CCU）入院后0小时和6小时测定中心静脉血氧分压、二氧化碳分压、PCO₂ 差值、乳酸和CI。根据PCO₂ 差值（临界值0.8 kPa）将研究人群分为两组。
高PCO₂ 差值组的CI显著更低（P = 0.001）。高PCO₂ 差值组在入院时需要更多的输注液体和血管升压药（分别为P = 0.01和P = 0.009）。两组在低平均压力（P = 0.01）、中心静脉血氧含量（P = 0.01）和乳酸水平（P = 0.003）方面也存在显著差异。高PCO₂ 差值组的平均动脉压更低，乳酸水平更高，表明存在整体灌注不足。所有患者的医院死亡率为24.5%（7/28）。低差值组的院内死亡率为20%（2/12），高差值组为30%（5/16）；比值比为1.6（95%可信区间0.5 - 5.5；P = 0.53）。在6小时和12小时时PCO₂ 差值持续或升高且大于0.8 kPa的患者，其死亡率变化更高（6小时时；院内死亡率为21.4%），高于6小时时PCO₂ 差值小于0.8 kPa的患者（1小时时；院内死亡率为3%）；该比值比为5.3（95%可信区间0.9 - 30.7；P = 0.08）。PCO₂ 差值与胸部超声模式无关。
PCO₂ 差值是脓毒症诱导的循环衰竭管理中的一个重要血流动力学变量。PCO₂ 差值可作为严重脓毒症中心输出量状态充足的标志物。高PCO₂ 差值（>0.8 kPa）可识别在严重脓毒症中可尝试通过液体复苏增加心输出量的情况。PCO₂ 差值在严重脓毒症中具有重要的预后价值。
