Quantification of ventilation volumes produced by compressions during emergency department cardiopulmonary resuscitation

McDannold, Robyn; Bobrow, Bentley J.; Chikani, Vatsal; Silver, Annemarie; Spaite, Daniel W; Vadeboncoeur, Tyler

doi:10.1016/j.ajem.2018.06.057

Cited by 32 publications

(23 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar results have also been indirectly suggested by other groups, but the exact mechanism has not been explicated and may be partially misinterpreted. 12,19 These findings are consistent, however, with classical physiological descriptions, which report that airways are likely to collapse as end-expiratory lung volume falls below the closing capacity. 20 Hence, intrathoracic airway closure is also documented during ARDS, which is characterized by lung volume loss, reduced functional residual capacity (FRC) due to alveolar flooding, and inflammatory edema.…”

Section: Thoracic Airway Closure and Lung Volume Reductionsupporting

confidence: 88%

“…Since the first report, other authors have demonstrated that chest compressions could generate variable tidal volumes that were often lower than dead space. 11,12 The mechanisms regulating the capability of chest compressions to produce alveolar ventilation had never been thoroughly investigated until recent observations. It is of great interest because animal models have shown that progressive hypoxemia, hypercapnia, and acidemia develop if adequate ventilation is not provided during prolonged CPR.…”

Section: Chest Compression-related Ventilationmentioning

confidence: 99%

“…As discussed at the beginning of this article, the tidal volume produced by chest compressions is extremely variable and is often lower than dead space, including after endotracheal intubation. 11,12 It is known that CPR yields significant alveolar de-recruitment and a reduction in compliance. 18,36,39 According to classic physiology, when lung volume decreases below a threshold value (ie, the closing capacity), small distal airways are likely to collapse; this could also be due to gas-liquid interfacing in small airways.…”

Section: Alveolar Ventilation Produced By Chest Compressionsmentioning

confidence: 99%

See 2 more Smart Citations

Ventilation During Cardiopulmonary Resuscitation: What Have We Learned From Models?

Charbonney

Grieco²,

Cordioli

et al. 2019

Respir Care

View full text Add to dashboard Cite

The optimization of ventilation during cardiopulmonary resuscitation (CPR) is a broad field of research. Recent physiological observations in this field challenge the current understanding of respiratory and circulatory interactions. Thanks to different models available (bench, animal, human), the understanding of physiological phenomena occurring during CPR has progressed. In this review, we describe the clinical observations that have led to the emerging concept of lung volume reduction and associated thoracic airway closure. We summarize the clinical and animal observations supporting these concepts. We then discuss the different contributions of bench, animal, and human models to the understanding of airway closure and their impact on intrathoracic pressure, airway closure, and hemodynamics generated by chest compression. The limitation of airway pressure and ventilation, resulting from airway closure reproducible in models, may play a major role in ventilation and gas exchange impairment observed during prolonged resuscitation.

show abstract

Section: Thoracic Airway Closure and Lung Volume Reductionsupporting

confidence: 88%

Section: Chest Compression-related Ventilationmentioning

confidence: 99%

Section: Alveolar Ventilation Produced By Chest Compressionsmentioning

confidence: 99%

See 1 more Smart Citation

Ventilation During Cardiopulmonary Resuscitation: What Have We Learned From Models?

Charbonney

Grieco²,

Cordioli

et al. 2019

Respir Care

View full text Add to dashboard Cite

show abstract

“…Chest compressions themselves can result in gas movement into the airway through the generation of subatmospheric pressures in the airway during the recoil phase of chest compressions as previously reported [ 10 – 12 , 25 ]. However, the volume of air mobilized through chest compressions alone is less than the physiologic dead space, and is therefore inadequate for effective alveolar ventilation and carbon dioxide removal, most importantly after a few minutes of compressions [ 9 – 12 ]. Cordioli et al demonstrate in five hospital cardiac arrest subjects that using zero PEEP, chest compressions produced extremely low ventilation that was flow limited, as depicted by end-tidal carbon dioxide tracings during CPR.…”

Section: Discussionmentioning

confidence: 82%

Effect of positive end-expiratory pressure on additional passive ventilation generated by CPR compressions in a porcine model

Levenbrown

Hossain

Keith

et al. 2021

ICMx

View full text Add to dashboard Cite

Background Compressions given during cardiopulmonary resuscitation generate small, ineffective passive ventilations through oscillating waves. Positive end-expiratory pressure increases the volume of these passive ventilations; however, its effect on passive ventilation is unknown. Our objective was to determine if increasing positive end-expiratory pressure during cardiopulmonary resuscitation increases passive ventilation generated by compressions to a clinically significant point. This study was conducted on 13 Landrace-Yorkshire pigs. After inducing cardiac arrest with bupivacaine, cardiopulmonary resuscitation was performed with a LUCAS 3.1. During cardiopulmonary resuscitation, pigs were ventilated at a positive end-expiratory pressure of 0, 5, 10, 15, 20 cmH2O (randomly determined) for 9 min. Using the NM3 respiratory monitoring device, expired minute ventilation and volumetric capnography were measured. Arterial blood gas was obtained for each positive end-expiratory pressure level to compare the effects of positive end-expiratory pressure on carbon dioxide. Results Increasing positive end-expiratory pressure from 0 to 20 cmH2O increased the mean (SEM) expired minute ventilation from 6.33 (0.04) to 7.33 (0.04) mL/min. With the 5-cmH2O incremental increases in positive end-expiratory pressure from 0 to 20 cmH2O, volumetric capnography increased from a mean (SEM) of 94.19 (0.78) to 115.18 (0.8) mL/min, except for 15 cmH2O, which showed greater carbon dioxide exhalation with volumetric capnography compared with 20 cmH2O. PCO2 declined significantly as positive end-expiratory pressure was increased from 0 to 20 cmH2O. Conclusions When increasing positive end-expiratory pressure from 0 to 20, the contribution to overall ventilation from gas oscillations generated by the compressions became more significant, and may even lead to hypocapnia, especially when using positive end-expiratory pressures between 15 and 20.

show abstract

“…Chest compressions with a depth compliant with current guidelines produce measurable and substantial ventilation volumes [35], with 81% of the passive tidal volumes recorded during chest compressions being lower than 20 ml. Chest compressions alone do not provide physiologically significant tidal volumes but may produce alterations in the capnogram.…”

Section: Limitationsmentioning

confidence: 97%

Modeling the impact of ventilations on the capnogram in out-of-hospital cardiac arrest

et al. 2020

View full text Add to dashboard Cite

Aim Current resuscitation guidelines recommend waveform capnography as an indirect indicator of perfusion during cardiopulmonary resuscitation (CPR). Chest compressions (CCs) and ventilations during CPR have opposing effects on the exhaled carbon dioxide (CO 2) concentration, which need to be better characterized. The purpose of this study was to model the impact of ventilations in the exhaled CO 2 measured from capnograms collected during outof-hospital cardiac arrest (OHCA) resuscitation. Methods We retrospectively analyzed OHCA monitor-defibrillator files with concurrent capnogram, compression depth, transthoracic impedance and ECG signals. Segments with CC pauses, two or more ventilations, and with no pulse-generating rhythm were selected. Thus, only ventilations should have caused the decrease in CO 2 concentration. The variation in the exhaled CO 2 concentration with each ventilation was modeled with an exponential decay function using non-linear-least-squares curve fitting. Results Out of the original 1002 OHCA dataset (one per patient), 377 episodes had the required signals, and 196 segments from 96 patients met the inclusion criteria. Airway type was endotracheal tube in 64.8% of the segments, supraglottic King LT-D™ in 30.1%, and unknown in 5.1%. Median (IQR) decay factor of the exhaled CO 2 concentration was 10.0% (7.8 − 12.9) with R 2 = 0.98(0.95 − 0.99). Differences in decay factor with airway type were not statistically significant (p = 0.17). From these results, we propose a model for estimating the contribution of CCs to the end-tidal CO 2 level between consecutive ventilations and for estimating the end-tidal CO 2 variation as a function of ventilation rate.

show abstract

Quantification of ventilation volumes produced by compressions during emergency department cardiopulmonary resuscitation

Cited by 32 publications

References 25 publications

Ventilation During Cardiopulmonary Resuscitation: What Have We Learned From Models?

Ventilation During Cardiopulmonary Resuscitation: What Have We Learned From Models?

Effect of positive end-expiratory pressure on additional passive ventilation generated by CPR compressions in a porcine model

Modeling the impact of ventilations on the capnogram in out-of-hospital cardiac arrest

Contact Info

Product

Resources

About