Supraglottic airway devices variably develop negative intrathoracic pressures: A prospective cross-over study of cardiopulmonary resuscitation in human cadavers.

AIM OF THE STUDY: Negative intrathoracic pressure (ITP) during the decompression phase of cardiopulmonary resuscitation (CPR) is essential to refill the heart, increase cardiac output, maintain cerebral and coronary perfusion pressures, and improve survival. In order to generate negative ITP, an airway seal is necessary. We tested the hypothesis that some supraglottic airway (SGA) devices do not seal the airway as well the standard endotracheal tube (ETT). METHODS: Airway pressures (AP) were measured as a surrogate for ITP in seven recently deceased human cadavers of varying body habitus. Conventional manual, automated, and active compression-decompression CPR were performed with and without an impedance threshold device (ITD) in supine and Head Up positions. Positive pressure ventilation was delivered by an ETT and 5 SGA devices tested in a randomized order in this prospective cross-over designed study. The primary outcome was comparisons of decompression AP between all groups. RESULTS: An ITD was required to generate significantly lower negative ITP during the decompression phase of all methods of CPR. SGAs varied in their ability to support negative ITP. CONCLUSION: In a human cadaver model, the ability to generate negative intrathoracic pressures varied with different SGAs and an ITD regardless of the body position or CPR method. Differences in SGAs devices should be strongly considered when trying to optimize cardiac arrest outcomes, as some SGAs do not consistently develop a seal or negative intrathoracic pressure with multiple different CPR methods and devices.

Consistent head up cardiopulmonary resuscitation haemodynamics are observed across porcine and human cadaver translational models.

AIM: The objectives were: 1) replicate key elements of Head Up (HUP) cardiopulmonary resuscitation (CPR) physiology in a traditional swine model of ventricular fibrillation (VF), 2) compare HUP CPR physiology in pig cadavers (PC) to the VF model 3) develop a new human cadaver (HC) CPR model, and 4) assess HUP CPR in HC. METHODS: Nine female pigs were intubated, and anesthetized. Venous, arterial, and intracranial access were obtained. After 6 min of VF, CPR was performed for 2 min epochs as follows: Standard (S)-CPR supine (SUP), Active compression decompression (ACD) CPR + impedance threshold device (ITD-16) CPR SUP, then ACD + ITD HUP CPR. The same sequence was performed in PC 3 h later. In 9 HC, similar vascular and intracranial access were obtained and CPR performed for 1 min epochs using the same sequence as above. RESULTS: The mean cerebral perfusion pressure (CerPP, mmHg) was 14.5 ±â€¯6 for ACD + ITD SUP and 28.7 ±â€¯10 for ACD + ITD HUP (p = .007) in VF, -3.6 ±â€¯5 for ACD + ITD SUP and 7.8 ±â€¯9 for ACD + ITD HUP (p = .007) in PC, and 1.3 ±â€¯4 for ACD + ITD SUP and 11.3 ±â€¯5 for ACD + ITD HUP (p = .007) in HC. Mean systolic and diastolic intracranial pressures (ICP) (mmHg) were significantly lower in the ACD + ITD HUP group versus the ACD + ITD SUP group in all three CPR models. CONCLUSION: HUP CPR decreased ICP while increasing CerPP in pigs in VF as well as in PC and HC CPR models. This first-time demonstration of HUP CPR physiology in humans provides important implications for future resuscitation research and treatment.

Correlation of end tidal carbon dioxide, amplitude spectrum area, and coronary perfusion pressure in a porcine model of cardiac arrest.

Amplitude Spectrum Area (AMSA) values during ventricular fibrillation (VF) correlate with myocardial energy stores and predict defibrillation success. By contrast, end tidal CO2 (ETCO2) values provide a noninvasive assessment of coronary perfusion pressure and myocardial perfusion during cardiopulmonary resuscitation (CPR). Given the importance of the timing of defibrillation shock delivery on clinical outcome, we tested the hypothesis that AMSA and ETCO2 correlate with each other and can be used interchangably to correlate with myocardial perfusion in an animal laboratory preclinical, randomized, prospective investigation. After 6 min of untreated VF, 12 female pigs (32 ± 1 Kg), isoflurane anesthetized pigs received sequentially 3 min periods of standard (S) CPR, S-CPR+ an impedance threshold device (ITD), and then active compression decompression (ACD) + ITD CPR Hemodynamic, AMSA, and ETCO2 measurements were made with each method of CPR The Spearman correlation and Friedman tests were used to compare hemodynamic parameters. ETCO2, AMSA, coronary perfusion pressure, cerebral perfusion pressure were lowest with STD CPR, increased with STD CPR + ITD and highest with ACD CPR + ITD Further analysis demonstrated a positive correlation between AMSA and ETCO2 (r = 0.37, P = 0.025) and between AMSA and key hemodynamic parameters (P < 0.05). This study established a moderate positive correlation between ETCO2 and AMSA These findings provide the physiological basis for developing and testing a novel noninvasive method that utilizes either ETCO2 alone or the combination of ETCO2 and AMSA to predict when defibrillation might be successful.

Head and thorax elevation during active compression decompression cardiopulmonary resuscitation with an impedance threshold device improves cerebral perfusion in a swine model of prolonged cardiac arrest.

AIM OF THE STUDY: As most cardiopulmonary resuscitation (CPR) efforts last longer than 15min, the aim of this study was to compare brain blood flow between the Head Up (HUP) and supine (SUP) body positions during a prolonged CPR effort of 15min, using active compression-decompression (ACD) CPR and impedance threshold device (ITD) in a swine model of cardiac arrest. METHODS: Ventricular fibrillation (VF) was induced in anesthetized pigs. After 8min of untreated VF followed by 2min of ACD-CPR+ITD in the SUP position, pigs were randomized to 18min of continuous ACD-CPR+ITD in either a 30° HUP or SUP position. Microspheres were injected before VF and then 5 and 15min after start of CPR. RESULTS: The mean blood flow (ml/min/g, mean±SD) to the brain after 15min of CPR was 0.42±0.05 in the HUP group (n=8) and 0.21±0.04 SUP (n=10), respectively, (p<0.01). The HUP group also had statistically significantly lower intracranial pressures and higher calculated cerebral perfusion pressures after 5, 15, 19 (before adrenaline) and 20 (after adrenaline) minutes of HUT versus SUP CPR. CONCLUSIONS: After prolonged ACD-CPR+ITD in the HUP position, brain blood flow was 2-fold higher versus the SUP position. These positive findings provide strong pre-clinical support to proceed with a clinical evaluation of elevation of the head and thorax during ACD-CPR+ITD in humans in cardiac arrest.

Evaluation of the Boussignac Cardiac arrest device (B-card) during cardiopulmonary resuscitation in an animal model.

AIM OF THE STUDY: The purpose of this study was to examine continuous oxygen insufflation (COI) in a swine model of cardiac arrest. The primary hypothesis was COI during standard CPR (S-CPR) should result in higher intrathoracic pressure (ITP) during chest compression and lower ITP during decompression versus S-CPR alone. These changes with COI were hypothesized to improve hemodynamics. The second hypothesis was that changes in ITP with S-CPR+COI would result in superior hemodynamics compared with active compression decompression (ACD) + impedance threshold device (ITD) CPR, as this method primarily lowers ITP during chest decompression. METHODS: After 6min of untreated ventricular fibrillation, S-CPR was initiated in 8 female swine for 4min, then 3min of S-CPR+COI, then 3min of ACD+ITD CPR, then 3min of S-CPR+COI. ITP and hemodynamics were continuously monitored. RESULTS: During S-CPR+COI, ITP was always positive during the CPR compression and decompression phases. ITP compression values with S-CPR+COI versus S-CPR alone were 5.5±3 versus 0.2±2 (p<0.001) and decompression values were 2.8±2 versus -1.3±2 (p<0.001), respectively. With S-CPR+COI versus ACD+ITD the ITP compression values were 5.5±3 versus 1.5±2 (p<0.01) and decompression values were 2.8±2 versus -4.7±3 (p<0.001), respectively. CONCLUSION: COI during S-CPR created a continuous positive pressure in the airway during both the compression and decompression phase of CPR. At no point in time did COI generate a negative intrathoracic pressures during CPR in this swine model of cardiac arrest.

Chest compliance is altered by static compression and decompression as revealed by changes in anteroposterior chest height during CPR using the ResQPUMP in a human cadaver model.

INTRODUCTION: Chest compliance plays a fundamental role in the generation of circulation during cardiopulmonary resuscitation (CPR). To study potential changes in chest compliance over time, anterior posterior (AP) chest height measurements were performed on newly deceased (never frozen) human cadavers during CPR before and after 5min of automated CPR. We tested the hypothesis that after 5min of CPR chest compliance would be significantly increased. METHODS: Static compression (30, 40, and 50kg) and decompression forces (-10, -15kg) were applied with a manual ACD-CPR device (ResQPUMP, ZOLL) before and after 5min of automated CPR. Lateral chest x-rays were obtained with multiple reference markers to assess changes in AP distance. RESULTS: In 9 cadavers, changes (mean±SD) in the AP distance (cm) during the applied forces were 2.1±1.2 for a compression force of 30kg, 2.9±1.3 for 40kg, 4.3±1.0 for 50kg, 1.0±0.8 for a decompression force of -10kg and 1.8±0.6 for -15kg. After 5min of automated CPR, AP excursion distances were significantly greater (p<0.05). AP distance increased to 3.7±1.4 for a compression force of 30kg, 4.9±1.6 for 40kg, 6.3±1.9 for 50kg, 2.3±0.9 for -10kg of lift and 2.7±1.1 for -15kg of lift. CONCLUSIONS: These data demonstrate chest compliance increases significantly over time as demonstrated by the significant increase in the measured AP distance after 5min of CPR. These findings suggest that adjustments in compression and decompression forces may be needed to optimize CPR over time.