eISSN: 1731-2515
ISSN: 0209-1712
Anestezjologia Intensywna Terapia
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3/2021
vol. 53
 
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abstract:
Original paper

Artificial hyperventilation normalizes haemodynamics and arterial oxygen content in hypoxic rats

Diego de Villalobos
1
,
Andres Laserna
2
,
Cosmo Fowler
3
,
John A. Cuenca
1
,
Peyton Martin
1
,
Michele Guindani
4
,
Wenli Dong
5
,
Howard B. Gutstein
6
,
Kristen J. Price
1
,
Joseph L. Nates
1

  1. Department of Critical Care Medicine, Division of Anesthesiology, Critical Care & Pain Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA
  2. Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, NY, USA
  3. Department of Medicine, Case Western Reserve University – MetroHealth, Cleveland, OH, USA
  4. Department of Statistics, University of California, Irvine, CA, USA
  5. Department of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, TX
  6. Department of Anesthesiology and Perioperative Medicine, University of Pittsburgh, Pittsburgh, PA
Anestezjologia Intensywna Terapia 2021; 53, 3: 223–231
Online publish date: 2021/10/27
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Introduction
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.

Material and methods
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.

Results
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.

Conclusions
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.

keywords:

respiratory insufficiency, hypocapnia, critical illness, hypoxia, artificial respiration, hyperventilation
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