Abstract Sa201: Effect of Spontaneous Gasping on Intraventricular Volume and Pressure during Untreated Ventricular Fibrillation

Background: Spontaneous gasping or agonal respiration during cardiac arrest is an auto-resuscitative reflex. Patients who gasp during cardiac arrest have better outcomes, regardless of the presenting rhythm. The physiological effects of gasping are similar to taking a deep breath: intrathoracic and intracranial pressure decrease, respiratory gas enters the lungs, venous blood refills the right ventricle (RV). Impedance threshold device (ITD) resistance to inspiration, with or without CPR, further reduces intrathoracic pressure. This study tested the hypothesis that gasping during untreated ventricular fibrillation (VF) would increase left ventricular (LV) and RV pressure and volume, and that ITD use would accentuate these effects. Method: 13 male and female pigs were anesthetized, intubated and mechanically ventilated. VF was induced and left untreated for 10 minutes. Hemodynamics, including biventricular pressure and volume loops using intracardiac conductance catheters were recorded during spontaneous gasping. An ITD, attached to the endotracheal tube, was used intermittently in each pig. Values (mean ± SE) were compared using the mixed-effects model, accounting for animal-to-animal variability and repeated measurements. Results: Baseline RV and LV stroke volumes (ml) were 52.2 ± 4.0 and 49.7 ± 6.9, respectively, before VF. A total of 84 gasps were recorded during untreated VF in all animals: 56 without and 28 with an ITD. There were 11.7 ± 1.0 gasps per pig starting 116.5 ± 6.4 seconds after VF. Gasping intensity followed a crescendo/decrescendo pattern with an initial negative inspiratory phase and a positive expiratory phase. ITD use during gasping significantly decreased in airway pressure (-11.0 ± 0.5 vs -1.8 ± 0.5, p<0.01) versus no ITD. The intraventricular volumes and pressures (mmHg) generated during gasping increased significantly from no ITD to ITD use: RV volume 27.8 ± 3.5 vs 41.4 ± 3.8, p<0.01; RV pressure 14.7 ± 2.2. vs 18.7 ± 2.3, p<0.01, and LV volume 15.0 ± 2.5 vs 19.6 ± 2.8 p=0.053; LV pressure 19.3 ± 3.2 vs 25.8 ± 3.5, p<0.01. Conclusion: Gasping during untreated VF generated RV and LV volumes and pressures of ~ 55% and 27% of pre-VF diastolic values, respectively, while using an ITD increased generated RV and LV volumes and pressures to ~ 85% and 36% of pre-VF diastolic values, respectively. These findings demonstrate the mechanism by which gasping enhances circulation and the clinical importance of this fundamental auto-reflex.

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Journal
Circulation
Published
2024-11-12
DOI
https://doi.org/10.1161/circ.150.suppl_1.sa201
Primary Topic
Cardiac Arrest and Resuscitation
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article
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article

Abstract Sa201: Effect of Spontaneous Gasping on Intraventricular Volume and Pressure during Untreated Ventricular Fibrillation

Anja Metzger, Johanna Moore, Mithun Suresh, Kent R. Bailey et al.
Circulation
Cardiac Arrest and Resuscitation
article

Abstract Sa201: Effect of Spontaneous Gasping on Intraventricular Volume and Pressure during Untreated Ventricular Fibrillation

Anja Metzger, Johanna Moore, Mithun Suresh, Kent R. Bailey, Nicolas Segond, Bayert Salverda, Guillaume Debaty, Keith G. Lurie, Pouria Pourzand, Hamza Hai
article en

Abstract

Background: Spontaneous gasping or agonal respiration during cardiac arrest is an auto-resuscitative reflex. Patients who gasp during cardiac arrest have better outcomes, regardless of the presenting rhythm. The physiological effects of gasping are similar to taking a deep breath: intrathoracic and intracranial pressure decrease, respiratory gas enters the lungs, venous blood refills the right ventricle (RV). Impedance threshold device (ITD) resistance to inspiration, with or without CPR, further reduces intrathoracic pressure. This study tested the hypothesis that gasping during untreated ventricular fibrillation (VF) would increase left ventricular (LV) and RV pressure and volume, and that ITD use would accentuate these effects. Method: 13 male and female pigs were anesthetized, intubated and mechanically ventilated. VF was induced and left untreated for 10 minutes. Hemodynamics, including biventricular pressure and volume loops using intracardiac conductance catheters were recorded during spontaneous gasping. An ITD, attached to the endotracheal tube, was used intermittently in each pig. Values (mean ± SE) were compared using the mixed-effects model, accounting for animal-to-animal variability and repeated measurements. Results: Baseline RV and LV stroke volumes (ml) were 52.2 ± 4.0 and 49.7 ± 6.9, respectively, before VF. A total of 84 gasps were recorded during untreated VF in all animals: 56 without and 28 with an ITD. There were 11.7 ± 1.0 gasps per pig starting 116.5 ± 6.4 seconds after VF. Gasping intensity followed a crescendo/decrescendo pattern with an initial negative inspiratory phase and a positive expiratory phase. ITD use during gasping significantly decreased in airway pressure (-11.0 ± 0.5 vs -1.8 ± 0.5, p<0.01) versus no ITD. The intraventricular volumes and pressures (mmHg) generated during gasping increased significantly from no ITD to ITD use: RV volume 27.8 ± 3.5 vs 41.4 ± 3.8, p<0.01; RV pressure 14.7 ± 2.2. vs 18.7 ± 2.3, p<0.01, and LV volume 15.0 ± 2.5 vs 19.6 ± 2.8 p=0.053; LV pressure 19.3 ± 3.2 vs 25.8 ± 3.5, p<0.01. Conclusion: Gasping during untreated VF generated RV and LV volumes and pressures of ~ 55% and 27% of pre-VF diastolic values, respectively, while using an ITD increased generated RV and LV volumes and pressures to ~ 85% and 36% of pre-VF diastolic values, respectively. These findings demonstrate the mechanism by which gasping enhances circulation and the clinical importance of this fundamental auto-reflex.

CirculationVol. 150(Suppl_1)
University of Minnesota (US), Fairview Health Services (US), University of Minnesota System (US), Hennepin County Medical Center (US), Hennepin Healthcare Research Institute (US), Université Grenoble Alpes (FR)
Good health and well-being
Openalex Percentile: Top 63%
Cardiac Arrest and Resuscitation
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