Explorative study on lower inflection point dynamics during cardiopulmonary resuscitation: Potential implications for airway management.

INTRODUCTION: In patients undergoing cardiopulmonary resuscitation (CPR) after an Out-of-Hospital Cardiac Arrest (OHCA), intrathoracic airway closure can impede ventilation, adversely affecting patient outcomes. This explorative study investigates the evolution of intrathoracic airway closure by analyzing the lower inflection point (LIP) during the inspiration phase of CPR, aiming to identify the potential thresholds for alveolar recruitment. METHODS AND MATERIALS: Eleven OHCA patients undergoing CPR with endotracheal intubation and manual bag ventilation were included. Flow and pressure measurements were obtained using Sensirion SFM3200AW and Wika CPT2500 sensors attached to the endotracheal tube, connected to a Surface Go Tablet for data collection. Flow data was analyzed in Microsoft Excel, while pressure data was processed using the Wika USBsoft2500 application. Analysis focused on the inspiration phase of the first 6-8 breaths, with an additional 2 breaths recorded and analyzed at the end of CPR. RESULTS: Across the cohort, the median tidal volume was 870.00 milliliter (mL), average flow was 31.90 standard liters per minute (slm), and average pressure was 17.21 cmH2O. The calculated average LIP was 31.47 cmH2O. Most cases (72.7%) exhibited a negative trajectory in LIP evolution during CPR, with 2 cases (18.2%) showing a positive trajectory and 1 case remaining inconclusive. The average LIP in the first 8 breaths was significantly higher than in the last 2 breaths (p = 0.018). No significant correlation was found between average LIP and return of spontaneous circulation (ROSC), compression depth, frequency, or end-tidal CO2 (EtCO2). However, a significant negative correlation was observed between the average LIP of the last 2 breaths and CPR duration (p = 0.023). VALIDATION: LIP calculation in low-flow ventilations using the novel mathematical method yielded values consistent with those reported in the literature. DISCUSSION/CONCLUSION: These explorative data demonstrate a predominantly negative trajectory in LIP evolution during CPR, suggesting potential challenges in maintaining airway patency. Limitations include a small sample size and sensor recording issues. Further research is warranted to explore the evolution of LIP and its implications for personalized ventilation strategies in CPR.

Is the occurrence of reversed airflow in manual ventilation during cardiopulmonary resuscitation associated with reduced net tidal volumes?

Background: During cardiopulmonary resuscitation, following advanced airway placement, chest compressions and ventilations are performed simultaneously. During inspiration, chest compressions and positive pressure ventilation exert opposite forces on the respiratory system, frequently resulting in reversed airflow. Methods: Following endotracheal intubation, a flow sensor was connected to the respiratory circuit of intubated, adult out-of-hospital cardiac arrest patients receiving manual chest compressions and manual ventilations. Chest compression parameters were measured using an accelerometer. Inspiratory and expiratory volumes during the inspiratory phase of positive pressure ventilations were quantified. Duration of the inspiratory and expiratory phases was calculated. Results: In this study, 25 patients were included, 682 ventilations were analyzed. Reversed airflow was observed in 23 patients, occurring 389 times during 270 ventilations. Median volume of reversed airflow was 2 mL (IQR 1.4-7 mL). There was no difference between net tidal volumes of ventilations during which reversed airflow did (median 420 mL, IQR 315-549) or did not occur (median 406 mL, IQR 308-530). When reversed airflow occurred, the duration of the inspiratory phase was longer (median 1.2 sec, IQR 0.9-1.4) compared to ventilations without reversed airflow (median 0.9 sec, IQR 0.9-1.4). Univariate analysis showed a weak correlation between chest compression depth and volume of reversed airflow. Conclusion: Reversed airflow frequently occurs during cardiopulmonary resuscitation. Volumes of reversed airflow were small, showing a weak correlation with chest compression depth. The occurrence of reversed airflow was not associated with reduced net tidal volumes.

Chest compression release velocity: An independent determinant of end-tidal carbon dioxide in out-of-hospital cardiac arrest.

BACKGROUND: Chest compression (CC) depth, CC rate and ventilatory rate (VR) are known to have an impact on end-tidal carbon dioxide (ETCO2) values. Chest compression release velocity (CCRV) is increasingly acknowledged as a novel metric in cardiopulmonary resuscitation (CPR). The objective of this study was to analyze whether CCRV would have any effect on ETCO2 values. METHODS: In out-of-hospital cardiac arrests (OHCA), effects of CC depth, CC rate, CCRV and VR on ETCO2 were analyzed through linear mixed effect models. A stratification was made on a CCRV of 300, 400 and 500 mm/s. In these categories, mean ETCO2 values were corrected for CC depth and compared through a one-way ANOVA. RESULTS: A 10 mm increase in CC depth was associated with a 1.5 mmHg increase in ETCO2 (p < 0.001), a 100 mm/s increase in CCRV with a 0.8 mmHg increase (p = 0.010) and a 5 breaths per minute increase in VR with a 2.0 mmHg decrease (p < 0.001). CC depth was strongly correlated with CCRV (Pearson's r = 0.709, p < 0.001). After adjusting for CC depth, ETCO2 was on average 6.5 mmHg higher at a CCRV of 500 than at 400 mm/s (p = 0.005) and 5.3 mmHg higher than at 300 mm/s (p = 0.033). CONCLUSIONS: In OHCA patients, higher CCRV values resulted in higher ETCO2 values. This effect is independent of CC depth, despite the strong correlation between CCRV and CC depth.

Chest compressions during ventilation in out-of-hospital cardiopulmonary resuscitation cause fragmentation of the airflow.

INTRODUCTION: When a patient suffers an out-of-hospital cardiac arrest, ventilation and chest compressions are often given simultaneously during cardiopulmonary resuscitation. These simultaneous chest compressions may cause a fragmentation of the airflow, which may lead to an ineffective ventilation. This study focusses on the occurrence and quantification of this fragmentation and its effect on ventilation. MATERIALS AND METHODS: This study is a single-center observational study, held at Ghent University Hospital. A custom-built bidirectional flow sensor was used to quantify the volumes of ventilation. Adult cardiac arrest patients who were prehospitally intubated and resuscitated by the medical emergency team were eligible for inclusion. Data of the patients who were ventilated and received simultaneous chest compressions, was used to calculate the volumes of ventilation and the amount and volumes of fragmentation. All data in this study is reported as mean (standard deviation; range). RESULTS: Data of 10 patients (7 male) with a mean age of 71 years (14;51-87) was used in this study. The mean ventilation frequency was 12/min (2;9-16), the mean minute volume and tidal volume were respectively 6.21 L (1.51;3.79-8.15) and 514 mL (99;422-682). Fragmentation of the airflow was observed in all patients, with an average of 3 (1;2-5) fragments per inspiration and a mean volume of 214 mL (65;112-341) per fragment. DISCUSSION AND CONCLUSION: Chest compressions during ventilation caused fragmentation of the airflow in all patients. There was wide variation in the number and volume of the fragments between patients. The importance of quantification of airflow volumes and the effect fragmentation of the airflow on the efficacy of ventilation can be essential in improving cardiopulmonary resuscitation techniques and therefore needs further investigation.

Do manual chest compressions provide substantial ventilation during prehospital cardiopulmonary resuscitation?

INTRODUCTION: Chest compressions have been suggested to provide passive ventilation during cardiopulmonary resuscitation. Measurements of this passive ventilatory mechanism have only been performed upon arrival of out-of-hospital cardiac arrest patients in the emergency department. Lung and thoracic characteristics rapidly change following cardiac arrest, possibly limiting the effectiveness of this mechanism after prolonged resuscitation efforts. Goal of this study was to quantify passive inspiratory tidal volumes generated by manual chest compression during prehospital cardiopulmonary resuscitation. MATERIALS AND METHODS: A flowsensor was used during adult out-of-hospital cardiac arrest cases attended by a prehospital medical team. Adult, endotracheally intubated, non-traumatic cardiac arrest patients were eligible for inclusion. Immediately following intubation, the sensor was connected to the endotracheal tube. The passive inspiratory tidal volumes generated by the first thirty manual chest compressions performed following intubation (without simultaneous manual ventilation) were calculated. RESULTS: 10 patients (5 female) were included, median age was 64 years (IQR 56, 77 years). The median compression frequency was 111 compression per minute (IQR 107, 116 compressions per minute). The median compression depth was 5.6 cm (IQR 5.4 cm, 6.1 cm). The median inspiratory tidal volume generated by manual chest compressions was 20 mL (IQR 13, 28 mL). CONCLUSION: Using a flowsensor, passive inspiratory tidal volumes generated by manual chest compressions during prehospital cardiopulmonary resuscitation, were quantified. Chest compressions alone appear unable to provide adequate alveolar ventilation during prehospital treatment of cardiac arrest.

Detection and quantification of gasping during resuscitation for out-of-hospital cardiac arrest.

AIM: To detect and quantify gasping during cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrest (OHCA) patients and to investigate whether gasping is associated with increased return of spontaneous circulation (ROSC). MATERIALS AND METHODS: A prospective observational study in patients resuscitated and mechanically or manually ventilated for OHCA by emergency physicians of Ghent University Hospital. After intubation, pressure catheters were inserted in the endotracheal tube (ETT) and pressures were measured at the proximal and distal ends of the ETT. Gasping was analysed with custom-developed software and volumes were calculated based on pressure differences between the catheters. Data are expressed as median (interquartile range). RESULTS: Data were collected in 292 resuscitated patients of whom 36.2% achieved ROSC. Seventy-six of 292 (26.0%) patients showed gasping on the pressure curves during resuscitation. The median gasping volume was 274ml (196-434). The median gasping rate was 3.7 gasps/min (1.5-7.3). Gasping occurred significantly more in patients displaying ventricular fibrillation as the initial rhythm compared to patients with pulseless electrical activity, pulseless ventricular tachycardia or asystole. The median gasping rate was significantly higher in the ROSC group compared to the non-ROSC group (11.8 gasps/min (95% CI [4.2, 13.9]) and 2.8 gasps/min (95% CI [1.7, 3.9]) respectively (P<0.001)). A gasping rate of >7.3 gasps/min appeared to be the optimal criterion value to herald ROSC. Deeper negative pressures were associated with an increased incidence of ROSC (P=0.011). There was no significant difference in ROSC between patients with gasping and those without. CONCLUSION: The occurrence of gasping during CPR was high. Significant gasping volumes were measured. The presence or absence of gasping was not associated with ROSC, but higher gasping rate and deeper negative pressures were.