Suresh, Mithun

Background: The efficacy of different conventional ventilation during automated head-up (AHUP) CPR using active decompression and impedance threshold device with head and torso elevation is unknown. We sought to determine the central and peripheral hemodynamics while using the 10:1 versus the 30:2 positive pressure ventilation (PPV). Research Question: Does the PPV delivery method affect the hemodynamics during AHUP-CPR? Methods: Ventricular fibrillation was induced in anesthetized pigs (n=5), followed by AHUP-CPR initiation with positive pressure ventilations applied using an automated bag compressor to deliver 10ml/kg of tidal volume over 1 sec at a rate of 10 breaths/min. After 15 minutes of CPR using a 10:1 ratio, ventilation was changed to a 30:2 ratio for 2 minutes with 2 PPV delivered consecutively. Thereafter 10:1 ratio was resumed followed by another 2-minute round of 30:2 PPV mode. Intraventricular pressures and volumes using conductance catheters placed in the right ventricle (RV), along with other hemodynamic parameters were recorded continuously, during the 2-minute intervals between PPV delivery. A mixed-effects model was used to evaluate the effects of PPV mode on pressure-volume (PV) loop parameters while using a Spearman correlation to explore the relationship between PV loop indices. Results: There was no statistically significant difference between RV stroke volume (SV) with 10:1 versus 30:2 PPV mode (Table 1). Throughout 2 minutes, 30:2 ventilation mode resulted in a significantly higher end-tidal CO2 (ETCO2), and higher pressures with a higher pulmonary elastance (Ea) imposed on RV (p<0.05). Higher Ea was strongly correlated with lower SV and ETCO2 (Spearman's rho correlation confidence of -0.97 and -0.83, respectively). No significant differences were observed between the two ventilation modes in any other hemodynamic parameters, including intrathoracic, aortic and right atrial pressures, as well as coronary and cerebral perfusion pressures. Conclusion: No significant difference was found for right ventricular stroke volume when comparing one breath after 10 chest compressions to two breaths after 30 compressions during automated head-up CPR. Delivering two consecutive breaths after 30 continuous compressions led to an overall higher ETCO2, but it also imposed greater ventricular pressure and afterload, which were significantly correlated with reduced SV and ETCO2.

Background: Active compression-decompression (ACD) cardiopulmonary resuscitation (CPR), an impedance threshold device (ITD) and controlled, gradual, automated head and thorax elevation, collectively termed automated Head Up Position (AHUP) CPR, increases cerebral perfusion pressure (CerPP), brain blood flow, coronary perfusion pressure (CorPP), end tidal CO2 (ETCO2) and cerebral oximetry (rSO2) in animal models when compared with conventional (C) CPR. AHUP-CPR in patients is associated with increased neurologically favorable survival versus C-CPR. This study tested the hypothesis that AHUP CPR will increase cardiac stroke volume (SV) and other hemodynamics compared with C-CPR in a porcine model of cardiac arrest. Methods: Farm pigs (n=15) were sedated, anesthetized, and ventilated. Hemodynamics, including intracardiac conductance catheter based biventricular (BiV) pressure-volume (PV) loops, were continuously measured and recorded. After 10 minutes of untreated ventricular fibrillation, C-CPR was performed for 2 minutes in the supine position using an automated CPR device designed for pigs at a rate of 100 compressions/minute, depth of 21% of the chest antero-postero diameter, a 50% duty cycle, and no active decompression. ACD+ITD was then performed with 3 cm of active decompression for 2 minutes, followed by AHUP-CPR, where the head and thorax were initially raised to 10 cm and 8 cm for a 2-minute priming phase, followed by elevation over the next 2 minutes to 24 cm and 9 cm. A linear mixed-effects model with a random intercept for individual pigs was used for statistical analysis. Results: CerPP, CorPP, ETCO2, and rSO2, as well as BiV SV and cardiac output, increased progressively and significantly with implementation of AHUP-CPR (p<0.05). C-CPR generated a right ventricular (RV) SV of 25.0 mL (48% of baseline pre-VF) and left ventricular (LV) SV of 17.5 mL (39% of baseline). ACD+ITD significantly increased RV and LV SV by an average of ~ 48% versus C-CPR; AHUP-CPR further increased BiV SV by an average of ~ 83%, reaching 85% and 75% of RV and LV pre-VF values, respectively. (Figure 1) Conclusion: This study demonstrated biventricular stroke volume is significantly augmented with AHUP-CPR versus C-CPR or ACD+ITD in the flat position. These findings, together with AHUP-enhanced higher ETCO2, rSO2, and CerPP values versus C-CPR or ACD-CPR in the flat position, help explain the improved clinical outcomes associated with early use of AHUP-CPR.

Background: Active compression-decompression cardiopulmonary resuscitation (ACD-CPR) combined with an impedance threshold device (ITD) and controlled head-up positioning, collectively termed AHUP-CPR, is associated with improved outcomes compared with conventional CPR (C-CPR). Active decompression (AD) forcibly lifts the anterior chest wall with suction after each compression, while the ITD simultaneously impedes airflow into the lungs. AD and ITD synergistically lower intrathoracic pressure during decompression, improving venous return, ventricular refilling and cardiac output. Concurrently, head-up positioning lowers intracranial pressures and improves cardiac preload. This pig study focused on the physiological role of AD during AHUP-CPR, simulating real clinical scenarios. Methods: Ten male and female farm pigs (~40 kg) were anesthetized, intubated and ventilated. Hemodynamic parameters, end-tidal CO2 (ETCO2), and biventricular pressure-volume loops were recorded continuously. Ventricular fibrillation was induced and left untreated for 10 mins. Then, after 2 min of automated C-CPR in the flat position, AHUP-CPR with a 3 cm lift above the neutral position of the chest was performed for 13 min. AD was then abruptly discontinued, restarted 1 min later, and increased incrementally every min to up to 4 cm of active lift. Data were analyzed with a linear mixed-effects model, using random intercepts for individual pigs. Results: Upon cessation of AD, coronary and cerebral perfusion pressures, compression and decompression aortic pressures, compression right atrial pressure, ETCO2, right and left ventricular preload, compliance, stroke volume and cardiac output all decreased immediately and significantly (p<0.01), whereas decompression right atrial and biventricular pressures increased. With restoration of AD, physiological parameters returned to ≥ 90% of pre-AD discontinuation values (Figures 1 and 2). Conclusion: Full chest wall lift, achieved with > 3 cm of AD, was needed to maintain and optimize hemodynamics during AHUP-CPR in pigs. After pausing AD, incremental restoration of AD resulted in nearly complete restoration of peripheral and central hemodynamic measures. These observations support the benefit of and need for ≥3 cm of AD to optimize AHUP-CPR. Effective means to generate ≥3 cm of AD should be considered when implementing and developing AHUP-CPR devices to optimize outcomes.

Background: Addition of resuscitative endovascular balloon occlusion of the aorta (REBOA) to automated head-up position (AHUP) cardiopulmonary resuscitation (CPR), the combination of active compression decompression CPR, an impedance threshold device, and controlled gradual elevation of the head and thorax, increases cerebral perfusion pressure. Optimal management of REBOA deflation after prolonged AHUP-CPR and ROSC is unknown. Hypothesis: We hypothesized that partial deflation of REBOA, rather than full deflation after ROSC, would result in better hemodynamic parameters. Aims: To compare hemodynamic parameters 1 minute before and 1 minute after complete (100%) versus partial (50%) REBOA deflation after prolonged AHUP-CPR and ROSC. Methods: Yorkshire pigs weighing ∼40 kg were anesthetized and ventilated. After 10 minutes of untreated ventricular fibrillation, AHUP-CPR was started and continued for a median time of 44 minutes. After ROSC, REBOA deflation was initiated in two ways: complete (100%) or partial (50%) deflation over 5 seconds. The following hemodynamic parameters were measured 1 minute before and 1 minute after deflation: mean aortic pressure (MAP), cerebral perfusion pressure (CerPP), and coronary perfusion pressure (CorPP). Data, in mmHg, are presented as mean ± SD, and compared using a paired t-test. Results: 13 pigs were included, with 8 pigs in the 100% deflation group and 5 in the 50% deflation group. After ROSC in the 100% deflation group, MAP was 81.5±36.0 before deflation vs. 43.0±14.4 after (p=0.01), whereas in the 50% deflation group, MAP was 90.5±33.0 vs. 83.4±33.3 (p=0.02). CerPP was 72.3±34.4 before deflation vs. 35.9±14.6 (p=0.01) in the 100% deflation group, and 84.6±31.2 vs. 77.6±31.8 (p=0.02) with 50% deflation. Similarly, CorPP was 74.1±37.3 before deflation vs. 36.1±15.8 (p=0.01) after in the 100% deflation group, and 83.0±32.7 vs. 76.1±33.0 (p=0.02) in the 50% deflation group. The differences from before to after deflation were markedly less in the 50% deflation group versus the 100% deflation group: MAP (7.0±4.3 vs. 38.5±25.7, p=0.02), CerPP (7.1±4.4 vs. 36.3±24.4, p=0.02), and CorPP (6.0±4.2 vs. 39.8±25.2, p=0.02), respectively. Conclusion: In this porcine model of prolonged cardiac arrest, partial deflation of the REBOA balloon post ROSC resulted in strikingly higher hemodynamics compared with complete deflation. These findings highlight the need to develop a post-ROSC REBOA deflation strategy when used during AHUP-CPR.