Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.

<h4>Aims</h4>To assess the impact of two different respiratory rates in hemodynamic, perfusion and ventilation parameters in a pediatric animal model of cardiac arrest (CA).<h4>Methods</h4>An experimental randomized controlled trial was carried out in 50 piglets under asphyxi...

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Main Authors: Jorge López, Patricia Arias, Beatriz Domenech, Daniel Horcajo, Juan Pablo Nocete, Laura Zamora, Sarah Nicole Fernández, Jesús López-Herce
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2020-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0237736
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spelling doaj-af344c2aee2b43999badd79a3b7f03f12021-03-04T11:14:51ZengPublic Library of Science (PLoS)PLoS ONE1932-62032020-01-01158e023773610.1371/journal.pone.0237736Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.Jorge LópezPatricia AriasBeatriz DomenechDaniel HorcajoJuan Pablo NoceteLaura ZamoraSarah Nicole FernándezJesús López-Herce<h4>Aims</h4>To assess the impact of two different respiratory rates in hemodynamic, perfusion and ventilation parameters in a pediatric animal model of cardiac arrest (CA).<h4>Methods</h4>An experimental randomized controlled trial was carried out in 50 piglets under asphyxial CA. After ROSC, they were randomized into two groups: 20 and 30 respirations per minute (rpm). Hemodynamic, perfusion and ventilation parameters were measured 10 minutes after asphyxia, just before ROSC and at 5, 15, 30 and 60 minutes after ROSC. Independent medians test, Kruskal-Wallis test and χ2 test, were used to compare continuous and categorical variables, respectively. Spearman's Rho was used to assess correlation between continuous variables. A p-value <0.05 was considered significant.<h4>Results</h4>Arterial partial pressure of carbon dioxide (PaCO2) was significantly lower in the 30 rpm group after 15 minutes (41 vs. 54.5 mmHg, p <0.01), 30 minutes (39.5 vs. 51 mmHg, p < 0.01) and 60 minutes (36.5 vs. 48 mmHg, p = 0.02) of ROSC. The percentage of normoventilated subjects (PaCO2 30-50 mmHg) was significantly higher in the 30 rpm group throughout the experiment. pH normalization occurred faster in the 30 rpm group with significant differences at 60 minutes (7.40 vs. 7.34, p = 0.02). Lactic acid levels were high immediately after ROSC in both groups, but were significantly lower in the 20 rpm group at 30 (3.7 vs. 4.7 p = 0.04) and 60 minutes (2.6 vs. 3.6 p = 0.03).<h4>Conclusions</h4>This animal model of asphyxial CA shows that a respiratory rate of 30 rpm is more effective to reach normoventilation than 20 rpm in piglets after ROSC. This ventilation strategy seems to be safe, as it does not cause hyperventilation and does not affect hemodynamics or cerebral tissue perfusion.https://doi.org/10.1371/journal.pone.0237736
collection DOAJ
language English
format Article
sources DOAJ
author Jorge López
Patricia Arias
Beatriz Domenech
Daniel Horcajo
Juan Pablo Nocete
Laura Zamora
Sarah Nicole Fernández
Jesús López-Herce
spellingShingle Jorge López
Patricia Arias
Beatriz Domenech
Daniel Horcajo
Juan Pablo Nocete
Laura Zamora
Sarah Nicole Fernández
Jesús López-Herce
Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
PLoS ONE
author_facet Jorge López
Patricia Arias
Beatriz Domenech
Daniel Horcajo
Juan Pablo Nocete
Laura Zamora
Sarah Nicole Fernández
Jesús López-Herce
author_sort Jorge López
title Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
title_short Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
title_full Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
title_fullStr Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
title_full_unstemmed Effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
title_sort effect of ventilation rate on recovery after cardiac arrest in a pediatric animal model.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2020-01-01
description <h4>Aims</h4>To assess the impact of two different respiratory rates in hemodynamic, perfusion and ventilation parameters in a pediatric animal model of cardiac arrest (CA).<h4>Methods</h4>An experimental randomized controlled trial was carried out in 50 piglets under asphyxial CA. After ROSC, they were randomized into two groups: 20 and 30 respirations per minute (rpm). Hemodynamic, perfusion and ventilation parameters were measured 10 minutes after asphyxia, just before ROSC and at 5, 15, 30 and 60 minutes after ROSC. Independent medians test, Kruskal-Wallis test and χ2 test, were used to compare continuous and categorical variables, respectively. Spearman's Rho was used to assess correlation between continuous variables. A p-value <0.05 was considered significant.<h4>Results</h4>Arterial partial pressure of carbon dioxide (PaCO2) was significantly lower in the 30 rpm group after 15 minutes (41 vs. 54.5 mmHg, p <0.01), 30 minutes (39.5 vs. 51 mmHg, p < 0.01) and 60 minutes (36.5 vs. 48 mmHg, p = 0.02) of ROSC. The percentage of normoventilated subjects (PaCO2 30-50 mmHg) was significantly higher in the 30 rpm group throughout the experiment. pH normalization occurred faster in the 30 rpm group with significant differences at 60 minutes (7.40 vs. 7.34, p = 0.02). Lactic acid levels were high immediately after ROSC in both groups, but were significantly lower in the 20 rpm group at 30 (3.7 vs. 4.7 p = 0.04) and 60 minutes (2.6 vs. 3.6 p = 0.03).<h4>Conclusions</h4>This animal model of asphyxial CA shows that a respiratory rate of 30 rpm is more effective to reach normoventilation than 20 rpm in piglets after ROSC. This ventilation strategy seems to be safe, as it does not cause hyperventilation and does not affect hemodynamics or cerebral tissue perfusion.
url https://doi.org/10.1371/journal.pone.0237736
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