Thorens J B, Jolliet P, Ritz M, Chevrolet J C
Medical ICU, University Hospital, Geneva, Switzerland.
Intensive Care Med. 1996 Mar;22(3):182-91. doi: 10.1007/BF01712235.
To measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS).
Prospective study.
18-bed, medical intensive care unit, university hospital.
11 mechanically ventilated ARDS patients.
Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30-60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h.
Minute ventilation was reduced from 13.5 +/- 6.1 to 8.2 +/- 4.1 l/min (mean +/- SD), PaCO2 increased (40.3 +/- 6.6 to 59.3 +/- 7.2 mmHg), pH decreased (7.40 +/- 0.05 to 7.26 +/- 0.05), and P50 increased (26.3 +/- 2.02 to 31.1 +/- 2.2 mmHg) (p < 0.05). Systemic vascular resistance decreased (865 +/- 454 to 648 +/- 265 dyne.s.cm-5, and cardiac index (CI) increased (4 +/- 2.4 to 4.7 +/- 2.4 l/min/m2) (p < 0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29 +/- 5 to 32 +/- 6 mmHg, p < 0.05). PaO2 remained unchanged, while saturation decreased (93 +/- 3 to 90 +/- 3%, p < 0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2 > 90%. PvO2 increased (36.5 +/- 5.7 to 43.2 +/- 6.1 mmHg, p < 0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545 +/- 240 to 621 +/- 274 ml/min/m2, p < 0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3 +/- 12.3 to 32.8 +/- 13.2, p < 0.05).
These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.
测量急性呼吸窘迫综合征(ARDS)患者快速允许性高碳酸血症对血流动力学和气体交换的影响。
前瞻性研究。
大学医院拥有18张床位的内科重症监护病房。
11例接受机械通气的ARDS患者。
患者在控制模式下进行镇静和通气。在30 - 60分钟内通过降低潮气量诱导高碳酸血症,直至pH值降至7.2和/或P50升高7.5 mmHg。然后维持该设置2小时。
分钟通气量从13.5±6.1降至8.2±4.1升/分钟(均值±标准差),PaCO2升高(40.3±6.6至59.3±7.2 mmHg),pH值降低(7.40±0.05至7.26±0.05),P50升高(26.3±2.02至31.1±2.2 mmHg)(p<0.05)。全身血管阻力降低(865±454至648±265达因·秒·厘米⁻⁵),心脏指数(CI)升高(4±2.4至4.7±2.4升/分钟/平方米)(p<0.05)。平均体动脉压未改变。肺血管阻力未改变,平均肺动脉压(MPAP)升高(29±5至32±6 mmHg,p<0.05)。PaO2保持不变,而血氧饱和度降低(93±3至90±3%,p<0.05),为维持SaO2>90%,需将FIO2从0.56提高至0.64。PvO2升高(36.5±5.7至43.2±6.1 mmHg,p<0.05),而血氧饱和度未改变。动静脉氧含量差未改变。氧输送(DO2)增加(545±240至621±274毫升/分钟/平方米,p<0.05),而氧消耗和提取率无显著变化。静脉混合血(Qva/Qt)增加(26.3±12.3至32.8±13.2,p<0.05)。
这些数据表明,急性高碳酸血症可增加血浆乳酸正常的ARDS患者的DO2和氧卸载能力,而不增加氧提取。对于乳酸水平升高提示组织缺氧的患者,这是否有益仍有待确定。此外,尽管高碳酸血症耐受性良好,但Qva/Qt、CI和MPAP的增加应促使对严重低氧血症患者以及心功能不全和/或严重肺动脉高压患者谨慎行事。