Department of Critical Care Medicine, Division of Anesthesiology, Critical Care & Pain Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Anaesthesiol Intensive Ther. 2021;53(3):223-231. doi: 10.5114/ait.2021.106562.
Although humans are capable of enduring critically low levels of oxygen, many hypoxaemic patients die despite aggressive therapies. Mimicking the physiological hyperventilation necessary to survive extreme hypoxic conditions could minimize the derangements caused by acute hypoxic-hypoxia. The objective of this study was to measure the haemodynamic-biochemical response to artificially induced hyperventilation in hypoxic rats.
Twenty-four deeply anaesthetized and mechanically ventilated rats were allocated to 3 groups: control (n = 5, FiO2 = 1); hypoxic spontaneously hyperventilating (n = 10, FiO2 = 0.08); and hypoxic artificially induced hyperventilation (n = 9, targeting PaCO2 = 10 mm Hg, FiO2 = 0.08). We compared the spontaneously and artificially hyperventilating groups. P-values < 0.01 were considered statistically significant. Mean arterial pressure (MAP) and serum chemistry were measured for 180 minutes.
The control group remained stable throughout the experiment. The hypoxic groups developed profound hypotension after the decrease in FiO2. However, the artificially induced hyperventilated rats recovered their MAP to levels higher than the spontaneously hyperventilating group (117.1 ± 17.2 vs. 68.1 ± 16.0, P = 0.0048). In regard to the biochemical derangements, even though the serum lactate and PaO2 were not different among the hypoxic groups, the artificially hyperventilated group achieved significantly higher SaO2 (94.3 ± 3.6 vs. 58.6 ± 9.6, P = 0.005), pH (7.87 ± 0.04 vs. 7.50 ± 0.13, P = 0.005), and CaO2 (17.7 ± 2.6 vs. 10.2 ± 1.3, P = 0.005) at 180 minutes.
Artificially induced hyperventilation led to the correction of arterial oxygen content, severe serum chemistry, and haemodynamic derangements. These findings may represent a novel rescue manoeuvre and serve as a bridge to a permanent form of support, but should be further studied before being translated to the clinical setting.
尽管人类能够忍受极低水平的氧气,但许多低氧血症患者尽管接受了积极的治疗仍死亡。模拟生存极端低氧条件下所需的生理性过度通气,可能会最小化急性低氧-缺氧引起的紊乱。本研究的目的是测量人工诱导过度通气对缺氧大鼠的血液动力学-生化反应。
24 只深度麻醉并机械通气的大鼠分为 3 组:对照组(n = 5,FiO2 = 1);低氧自主过度通气组(n = 10,FiO2 = 0.08);低氧人工诱导过度通气组(n = 9,目标 PaCO2 = 10mmHg,FiO2 = 0.08)。我们比较了自主和人工过度通气组。P 值 < 0.01 被认为具有统计学意义。测量平均动脉压(MAP)和血清化学指标 180 分钟。
对照组在整个实验过程中保持稳定。低氧组在 FiO2 降低后出现严重低血压。然而,人工诱导过度通气组 MAP 恢复到高于自主过度通气组的水平(117.1 ± 17.2 比 68.1 ± 16.0,P = 0.0048)。关于生化紊乱,尽管低氧组的血清乳酸和 PaO2 没有差异,但人工过度通气组的 SaO2(94.3 ± 3.6 比 58.6 ± 9.6,P = 0.005)、pH(7.87 ± 0.04 比 7.50 ± 0.13,P = 0.005)和 CaO2(17.7 ± 2.6 比 10.2 ± 1.3,P = 0.005)在 180 分钟时显著更高。
人工诱导过度通气导致动脉氧含量、严重的血清化学和血液动力学紊乱得到纠正。这些发现可能代表一种新的抢救手段,并可作为永久性支持的桥梁,但在转化为临床应用之前,还需要进一步研究。