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. 2021;12(4):303-308.
doi: 10.5847/wjem.j.1920-8642.2021.04.009.

Protective effect of extracorporeal membrane pulmonary oxygenation combined with cardiopulmonary resuscitation on post-resuscitation lung injury

Ji-Yang Ling  1 , Chun-Sheng Li  2 , Yun Zhang  1 , Xiao-Li Yuan  1 , Bo Liu  3 , Yong Liang  3 , Qiang Zhang  3
Affiliations

Protective effect of extracorporeal membrane pulmonary oxygenation combined with cardiopulmonary resuscitation on post-resuscitation lung injury

Ji-Yang Ling et al. World J Emerg Med. 2021.

Abstract

Background: Cardiac arrest (CA) is a critical condition that is a concern to healthcare workers. Comparative studies on extracorporeal cardiopulmonary resuscitation (ECPR) and conventional cardiopulmonary resuscitation (CCPR) technologies have shown that ECPR is superior to CCPR. However, there is a lack of studies that compare the protective effects of these two resuscitative methods on organs. Therefore, we aim to perform experiments in swine models of ventricular fibrillation-induced CA to study whether the early application of ECPR has advantages over CCPR in the lung injury and to explore the protective mechanism of ECPR on the post-resuscitation pulmonary injury.

Methods: Sixteen male swine were randomized to CCPR (CCPR; n=8; CCPR alone) and ECPR (ECPR; n=8; extracorporeal membrane oxygenation with CCPR) groups, with the restoration of spontaneous circulation at 6 hours as an endpoint.

Results: For the two groups, the survival rates between the two groups were not statistically significant (P>0.05), the blood and lung biomarkers were statistically significant (P<0.05), and the extravascular lung water and pulmonary vascular permeability index were statistically significant (P<0.01). Compared with the ECPR group, electron microscopy revealed mostly vacuolated intracellular alveolar type II lamellar bodies and a fuzzy lamellar structure with widening and blurring of the blood-gas barrier in the CCPR group.

Conclusions: ECPR may have pulmonary protective effects, possibly related to the regulation of alveolar surface-active proteins and mitigated oxidative stress response post-resuscitation.

Keywords: Alveolar surface-active protein; Cardiac arrest; Oxidative stress injury; Pulmonary edema; Swine.

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Conflict of interest statement

Conflicts of interests: The authors declare that they have no conflicts of interest regarding this article.

Figures

Figure 1
Figure 1
Comparison of serum markers at each time point between the two groups. Data were expressed as mean±standard deviation (n=8); CCPR: conventional cardiopulmonary resuscitation; ECPR: extracorporeal cardiopulmonary resuscitation; SP-A: surfactant protein A; SP-D: surfactant protein D; CC16: Clara cell protein 16; MDA: malondialdehyde; SOD: superoxide dismutase; ROSC: return of spontaneous circulation; ROSC1h/2h/4h/6h: 1, 2, 4, and 6 hours after ROSC; compared with baseline, *P<0.01, **P <0.05.
Figure 2
Figure 2
Organizational structure on electron microscopy. Red arrow: type II lamellar (×2,500); blue arrow: blood-gas barrier (×12,000); A, B: CCPR group; C, D: ECPR group; CCPR: conventional cardiopulmonary resuscitation; ECPR: extracorporeal cardiopulmonary resuscitation.
See this image and copyright information in PMC

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