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. 2023 May 1;207(9):1183-1193.
doi: 10.1164/rccm.202212-2194OC.

High- versus Low-Flow Extracorporeal Respiratory Support in Experimental Hypoxemic Acute Lung Injury

Serena Brusatori  1 , Carmelo Zinnato  1 , Mattia Busana  1 , Federica Romitti  1 , Simone Gattarello  2 , Maria Michela Palumbo  1 , Tommaso Pozzi  1 , Irene Steinberg  1 , Paola Palermo  2 , Stefano Lazzari  2 , Roberta Maj  1 , Mara Velati  1 , Rosanna D'Albo  1 , Jona Wassong  1 , Killian Meissner  1 , Fabio Lombardo  1 , Peter Herrmann  1 , Michael Quintel  3 , Onnen Moerer  1 , Luigi Camporota  4 , John J Marini  5 , Konrad Meissner  1 , Luciano Gattinoni  1
Affiliations

High- versus Low-Flow Extracorporeal Respiratory Support in Experimental Hypoxemic Acute Lung Injury

Serena Brusatori et al. Am J Respir Crit Care Med. .

Abstract

Rationale: In the EOLIA (ECMO to Rescue Lung Injury in Severe ARDS) trial, oxygenation was similar between intervention and conventional groups, whereas [Formula: see text]e was reduced in the intervention group. Comparable reductions in ventilation intensity are theoretically possible with low-flow extracorporeal CO2 removal (ECCO2R), provided oxygenation remains acceptable. Objectives: To compare the effects of ECCO2R and extracorporeal membrane oxygenation (ECMO) on gas exchange, respiratory mechanics, and hemodynamics in animal models of pulmonary (intratracheal hydrochloric acid) and extrapulmonary (intravenous oleic acid) lung injury. Methods: Twenty-four pigs with moderate to severe hypoxemia (PaO2:FiO2 ⩽ 150 mm Hg) were randomized to ECMO (blood flow 50-60 ml/kg/min), ECCO2R (0.4 L/min), or mechanical ventilation alone. Measurements and Main Results: [Formula: see text]o2, [Formula: see text]co2, gas exchange, hemodynamics, and respiratory mechanics were measured and are presented as 24-hour averages. Oleic acid versus hydrochloric acid showed higher extravascular lung water (1,424 ± 419 vs. 574 ± 195 ml; P < 0.001), worse oxygenation (PaO2:FiO2 = 125 ± 14 vs. 151 ± 11 mm Hg; P < 0.001), but better respiratory mechanics (plateau pressure 27 ± 4 vs. 30 ± 3 cm H2O; P = 0.017). Both models led to acute severe pulmonary hypertension. In both models, ECMO (3.7 ± 0.5 L/min), compared with ECCO2R (0.4 L/min), increased mixed venous oxygen saturation and oxygenation, and improved hemodynamics (cardiac output = 6.0 ± 1.4 vs. 5.2 ± 1.4 L/min; P = 0.003). [Formula: see text]o2 and [Formula: see text]co2, irrespective of lung injury model, were lower during ECMO, resulting in lower PaCO2 and [Formula: see text]e but worse respiratory elastance compared with ECCO2R (64 ± 27 vs. 40 ± 8 cm H2O/L; P < 0.001). Conclusions: ECMO was associated with better oxygenation, lower [Formula: see text]o2, and better hemodynamics. ECCO2R may offer a potential alternative to ECMO, but there are concerns regarding its effects on hemodynamics and pulmonary hypertension.

Keywords: [Formula: see text]O2; [Formula: see text]co2; acute respiratory distress syndrome; high-flow extracorporeal membrane oxygenation; low-flow extracorporeal CO2 removal.

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Figures

Figure 1.
Figure 1.
(A–C) Time courses of SaO2 (A), PaO2 (B), and pulmonary venous admixture fraction (C) in hydrochloric acid (HCl)–treated and oleic acid (OA)-treated animals according to support method (ECMO in red, ECCO2R in blue, no treatment in gray). Values are represented as mean ± SE. “Baseline” refers to values measured before lung injury (light blue background), “After Injury” refers to values after HCl or OA administration before extracorporeal treatment (light blue background), “1h” to “23h” refer to values recorded during treatment (light pink background), and “End” refers to values measured 1 hour after extracorporeal treatment withdrawal while ventilating the pig with the same setting applied after injury (light blue background). ECCO2R = extracorporeal CO2 removal; ECMO = extracorporeal membrane oxygenation.
Figure 2.
Figure 2.
(A and B) Time courses of total pulmonary vascular resistance (A) and respiratory system elastance (B) in hydrochloric acid (HCl)–treated and oleic acid (OA)-treated animals according to method of support (ECMO in red, ECCO2R in blue, no treatment in gray). Values are represented as mean ± SE. “Baseline” refers to values measured before lung injury (light blue background), “After Injury” refers to values after HCl or OA administration before extracorporeal treatment (light blue background), “1h” to “23h” refer to values recorded during treatment (light pink background), and “End” refers to values measured 1 hour after extracorporeal treatment withdrawal while ventilating the pig with the same setting applied after injury (light blue background). ECCO2R = extracorporeal CO2 removal; ECMO = extracorporeal membrane oxygenation.
Figure 3.
Figure 3.
(A and B) Time courses of total V˙o2 (A) and total V˙co2 (B) in hydrochloric acid (HCl)–treated and oleic acid (OA)-treated animals according to support method (ECMO in red, ECCO2R in blue, no treatment in gray). Values are represented as mean ± SE. “Baseline” refers to values measured before lung injury (light blue background), “After Injury” refers to values after HCl or OA administration before extracorporeal treatment (light blue background), “1h” to “23h” refer to values recorded during treatment (light pink background), and “End” refers to values measured 1 hour after extracorporeal treatment withdrawal while ventilating the pig with the same setting applied after injury (light blue background). ECCO2R = extracorporeal CO2 removal; ECMO = extracorporeal membrane oxygenation.
Figure 4.
Figure 4.
Trends of physiological variable alterations according to model, technique, and operator. “Model” refers to HCl or oleic acid injury, “Technique” refers to ECMO or ECCO2R application, and “Operator” refers to mechanical ventilator settings chosen by the physicians. ECCO2R = extracorporeal CO2 removal; ECMO = extracorporeal membrane oxygenation; EVLW = extravascular lung water; HCl = hydrochloric acid; MV = mechanical ventilation; SvO2 = mixed venous oxygen saturation.
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