Abstract 265: Deterioration of Hemodynamic Support During Prolonged Mechanical CPR in a Porcine Model of Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Shannon E Allen ◽  
Samantha Ang ◽  
Cody Smith ◽  
George Techiryan ◽  
John M Canty ◽  
...  

Introduction: Although mechanical CPR devices provide automated delivery of fixed depth chest compressions, the consistency of hemodynamic support during prolonged resuscitation efforts is unclear, particularly in the absence of concomitant vasopressor treatment. In light of recent concerns regarding potentially harmful effects of epinephrine, we evaluated the hemodynamic support generated by 20 min of mechanical CPR without concurrent vasopressor administration in a porcine model of cardiac arrest (CA). Methods: Swine (n=10) were subjected to 7-8 min of CA following electrical induction of ventricular fibrillation. CPR was subsequently performed for 20 min using a mechanical compression system (LUCAS 3.1, Stryker) programmed to administer 102 compressions/min at a fixed depth of 2.1 inches. Aortic pressure (Ao), coronary perfusion pressure (CPP), and cerebral oxygen saturation (rSO 2 ; near-infrared spectroscopy) were continuously recorded. Results were compared to a separate group of swine (n=11) that received manual CPR with a compression rate of 100/min and depth necessary to achieve peak Ao of 100 mmHg. Results: Initially, mechanical CPR generated significantly higher peak Ao and CPP vs. manual CPR ( Figure ). However, by 4 min CPR, peak Ao and CPP were no longer different between groups. Both parameters continued to decline in the mechanical CPR group but remained stable in animals receiving manual CPR. Cerebral rSO 2 values fell from 57±2 % at baseline to 42±4 % during CA (p<0.01) but were not significantly improved by mechanical or manual CPR. Conclusion: The superior hemodynamic support initially offered by mechanical CPR deteriorates during prolonged CPR when pharmacologic vasopressor support is absent. These results demonstrate that a fixed compression depth does not necessarily produce consistent hemodynamic support and suggest that concomitant vasopressor administration may be necessary to sustain Ao and CPP during prolonged mechanical CPR.

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Shannon E Allen ◽  
Allison Hubert ◽  
Dorcas Nsumbu ◽  
Samantha Ang ◽  
John M Canty ◽  
...  

Introduction: Mechanical devices offer the ability to provide consistent fixed-depth chest compressions during CPR. Although compression depth is considered a primary determinant of CPR quality, the influence of other device settings has received less attention. Accordingly, we evaluated the combined effect of compression depth and device start position on CPR hemodynamics in a porcine model of cardiac arrest (CA). Methods: Swine (n=119) were subjected to 7-10 min of CA following electrical induction of ventricular fibrillation. CPR was subsequently performed manually (target peak aortic pressure: 100 mmHg; n=73) or with a mechanical compression system (LUCAS 3.1, Stryker; n=46). Within the mechanical CPR group, animals received 102 compressions/min using either factory default settings (“QuickFit” automated suction cup start position; compression depth: 2.1”; n=13) or custom settings (manual suction cup start position; compression depth: 1.8”; n=33). Aortic pressure (Ao), coronary perfusion pressure (CPP), and regional cerebral oxygen saturation (rSO 2 ; via near infrared spectroscopy) were compared between groups after 1 min of CPR. Results: Mechanical CPR with automated suction cup start position and compression depth of 2.1” resulted in significantly higher peak Ao and CPP than mechanical CPR with manual start position and compression depth of 1.8” ( Table ). Compared with manual CPR, only mechanical CPR with automated start position and compression depth of 2.1” led to a higher CPP. However, cerebral rSO 2 values fell from 61±1 % at baseline to 49±1 % during CA (p<0.01) and did not increase during CPR in any group. Conclusion: Compared with a manual start position and compression depth of 1.8”, use of the LUCAS “QuickFit” feature and compression depth of 2.1” led to a significantly higher CPP during mechanical CPR. Future studies are necessary to determine if differences persist during prolonged CPR with and without concomitant vasopressor administration.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Alexander Esibov ◽  
Tyson G Taylor ◽  
Sharon B Melnick ◽  
Fred W Chapman ◽  
Gregory P Walcott

Introduction: Ischemic post-conditioning (IPC) has shown promise in mitigating ischemia-reperfusion injury. Controlled pauses during CPR (CP-CPR) following cardiac arrest (CA) and prolonged downtime may help invoke IPC mechanisms and have been shown to improve neurological outcome in swine. We tested whether CP-CPR would improve return of spontaneous circulation (ROSC) and/or 4-hr survival rates, compared with standard CPR from a mechanical chest compression device (M-CPR), following prolonged downtime in a porcine model of ventricular fibrillation (VF)-induced CA. Methods: Twenty anesthetized and instrumented pigs were block randomized to two protocols. Following 10 min of VF, mechanical CPR was initiated (100 comp/min, 50% duty cycle, 2 inch depth). Over the first 5 minutes of CPR, the M-CPR protocol group received continuous chest compressions, while the CP-CPR protocol included four 20-sec pauses in compressions starting at 40, 100, 160, and 220 sec. All other interventions were the same in the two groups. After 5 minutes, a first shock was delivered during a pause. If the shock failed to convert to a perfusing rhythm for ≥ 30 s with a systolic aortic pressure (sAoP) ≥ 50 mmHg for at least the first three contiguous sAoP values, CPR was continued in 2 min cycles, followed by a shock (if indicated) at the end of each cycle, for up to 10 cycles. As soon as these criteria were met between two CPR cycles, ROSC was documented and a post-resuscitation protocol was initiated. During the post-resuscitation protocol, inotropic agents were provided as needed to maintain sAoP ≥ 50 mmHg. Survival was declared if the sAoP was maintained above threshold for 4 hrs following ROSC. Results: Nineteen animals were successfully instrumented for data gathering (9 CP-CPR, 10 M-CPR). In the CP-CPR and M-CPR groups respectively, 3/9 (33%) vs. 5/10 (50%) achieved ROSC (p = 0.46); when ROSC was achieved, time to ROSC was 7.7±1.2 min vs. 5.8±1.1 min (p = 0.08). All animals that achieved ROSC survived to 4 hours. Conclusions: In a porcine model of CA following prolonged VF, CP-CPR did not improve ROSC or 4-hr survival. The trend towards delayed time to ROSC suggests controlled pauses may impair initial resuscitation, even if they ultimately improve neurological outcome. Further studies are warranted.


Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Mohamad H Tiba ◽  
Brendan M McCracken ◽  
Brandon C Cummings ◽  
Carmen I Colmenero ◽  
Chandler J Rygalski ◽  
...  

Introduction: Despite advancements in CPR, survival to hospital discharge remains low for in- and out-of-hospital cardiac arrest (CA). Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is an evolving tool for temporary control of non-compressible truncal hemorrhage. In this investigation, we examined whether REBOA use during non-traumatic CA would produce favorable hemodynamic changes associated with return of spontaneous circulation (ROSC). Hypothesis: We hypothesized that REBOA use during CPR would result in higher coronary perfusion pressure (CPP) and common carotid artery blood flow (C-Flow) in a prolonged model of CA. Methods: Six male swine were anesthetized and instrumented to measure and monitor CPP, and C-Flow. A REBOA catheter (Prytime Medical Devices) was advanced into zone 1 of the aorta through the femoral artery. Ventricular fibrillation was electrically induced and untreated for 8 minutes. CPR was started manually at minute-8, then changed to mechanical CPR at minute-12 for the duration of the experiment. Continuous infusion of epinephrine (0.0024mg/kg/min) was simultaneously started with mechanical CPR. The REBOA balloon was inflated beginning at minute-16 for 3 minutes then deflated for 3 minutes for a total of 6 cycles. At the end of the final cycle (REBOA inflation), CPR was stopped (after 33 minutes of total arrest time) and animals were defibrillated using 200 J biphasic shocks, repeated up to 6 times. Animals achieving ROSC were monitored for an additional 25 minutes. Results: Analysis using repeated measure ANOVA showed significant differences between balloon deflation and inflation periods for CPP (p<0.0001) with mean difference(SD) of 14(2.6) (Range: 17 to 42) mmHg and for C-Flow (p<0.0001) with mean difference(SD) 16(23) (Range: 115 to 269) mL/min across all animals. Three animals achieved ROSC and had significantly higher CPP (48 vs. 24mmHg, p<0.0001) and C-Flow (249 vs. 168mL/min) by t-test (p<0.0001). Post-mortem aortic histology did not reveal any changes produced by balloon inflation. Conclusion: REBOA significantly increased CPP and C-Flow in this swine model of prolonged CA. These increases may have contributed to the ability to achieve ROSC after greater than 30 min of CA.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Joshua C Reynolds ◽  
David D Salcido ◽  
James J Menegazzi

Introduction: The amount of myocardial perfusion required for successful defibrillation after prolonged cardiac arrest is not known. Coronary perfusion pressure (CPP) is a surrogate for myocardial perfusion. One limited clinical study reported that a threshold of 15mmHg was necessary for return of spontaneous circulation (ROSC), and that CPP was predictive of ROSC. A distinction between threshold and dose of CPP has not been reported. Hypothesis: Animals that achieve ROSC will have higher mean CPP and higher area under the CPP curve (AUC) than no-ROSC swine. Methods: Data from 4 similar swine cardiac arrest studies were retrospectively pooled. Animals had undergone 8 –11 minutes of untreated ventricular fibrillation, 2 minutes of mechanical CPR, administration of drugs, and 3 more minutes of CPR prior to the first shock. Mean CPP ± standard error was derived from the last 20 compressions of each 30 second epoch of CPR and compared between ROSC/no-ROSC groups by RM-ANOVA. AUC for all compressions delivered over the 5 minutes was calculated by direct summation and compared by Kruskal-Wallis test. Prediction of ROSC was assessed by logistic regression. Results : During 5 minutes of CPR (n=80), mean CPP ± SEM was higher in animals with ROSC (n=63) (p < 0.001). Animals with ROSC received more total flow than animals without ROSC (p < 0.001). Two regression models identified CPP (OR 1.11; 95% CI 1.05, 1.18) and AUC (OR 1.10; 95% CI 1.05, 1.16) as predictors of ROSC. Experimental protocol also predicted ROSC in each model (OR 1.70; 95% CI 1.15, 2.50) and (OR 1.59; 95% CI 1.12, 2.25), respectively. Conclusion : Higher CPP threshold and dose are associated with and predictive of ROSC.


2002 ◽  
Vol 93 (4) ◽  
pp. 1222-1226 ◽  
Author(s):  
Lei Song ◽  
Max Harry Weil ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Tommaso Pellis

We sought to develop a model of cardiac arrest and resuscitation on mice that would be comparable to that of large mammals and would allow for more fundamental investigations on cardiopulmonary arrest and cardiac resuscitation. A model of cardiopulmonary resuscitation previously developed by our group on rats was adapted to anesthetized, mechanically ventilated adult male Institute of Cancer Research mice that weighed 46 ± 3 g. The trachea was intubated through the mouth, and end-tidal Pco 2(Pet CO2 ) was measured with a microcapnometer. Catheters were advanced into the aorta and into the right atrium, and coronary perfusion pressure (CPP) was computed. A 1.5-mA alternating current was delivered to the right ventricular endocardium, which produced ventricular fibrillation or a pulseless rhythm. Precordial compression was begun 4 min later. Ten sequential studies were performed, during which five animals were successfully resuscitated and five failed resuscitation efforts. Successful resuscitation was contingent on the restoration of threshold levels of CPP and Pet CO2 during chest compression. As in rats, swine, and human patients, threshold levels of mean aortic pressure, CPP, and Pet CO2 were critical determinates of resuscitability in this murine model of threshold level of cardiac arrest and resuscitation.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Heng Li ◽  
Lei Zhang ◽  
Zhengfei Yang ◽  
Zitong Huang ◽  
Bihua Chen ◽  
...  

Objective. Untrained bystanders usually delivered suboptimal chest compression to victims who suffered from cardiac arrest in out-of-hospital settings. We therefore investigated the hemodynamics and resuscitation outcome of initial suboptimal quality of chest compressions compared to the optimal ones in a porcine model of cardiac arrest.Methods. Fourteen Yorkshire pigs weighted 30 ± 2 kg were randomized into good and poor cardiopulmonary resuscitation (CPR) groups. Ventricular fibrillation was electrically induced and untreated for 6 mins. In good CPR group, animals received high quality manual chest compressions according to the Guidelines (25% of animal’s anterior-posterior thoracic diameter) during first two minutes of CPR compared with poor (70% of the optimal depth) compressions. After that, a 120-J biphasic shock was delivered. If the animal did not acquire return of spontaneous circulation, another 2 mins of CPR and shock followed. Four minutes later, both groups received optimal CPR until total 10 mins of CPR has been finished.Results. All seven animals in good CPR group were resuscitated compared with only two in poor CPR group (P<0.05). The delayed optimal compressions which followed 4 mins of suboptimal compressions failed to increase the lower coronary perfusion pressure of five non-survival animals in poor CPR group.Conclusions. In a porcine model of prolonged cardiac arrest, even four minutes of initial poor quality of CPR compromises the hemodynamics and survival outcome.


Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Keith Marill ◽  
James J Menegazzi ◽  
Allison C Koller ◽  
Matthew Sundermann ◽  
David D Salcido

Introduction: Pulseless electrical activity (PEA) is a common rhythm in cardiac arrest with a persistently poor outcome. This report describes our successful development of a synchronized compression device and algorithm to treat PEA with or without intrinsic myocardial contractions. Methods: We adapted our previously developed signal-guided CPR system to provide synchronized compressions in a porcine model of cardiac arrest. We describe the first comparison of unsynchronized to synchronized compressions in a single animal as a proof-of-concept. We developed an algorithm to provide optimal synchronized chest compressions regardless of intrinsic heartrate while simultaneously maintaining the chest compression rate within a desired range. We tested the algorithm with computer simulations measuring the proportion of intrinsic and compression beats that were synchronized, and the compression rate and its standard deviation, as a function of intrinsic heartrate and heartrate jitter. Results: We demonstrate and compare unsynchronized versus synchronized chest compressions in a single porcine model with an intrinsic rhythm and hypotension. Synchronized, but not unsynchronized, chest compressions were associated with increased blood pressure and coronary perfusion pressure (Figure). Our synchronized chest compression algorithm is able to provide synchronized chest compressions to over 90% of intrinsic beats for most heartrates while maintaining an average compression rate between 95 and 135 BPM with relatively low variability. Conclusion: Synchronized chest compression therapy for pulseless electrical rhythms is feasible. A high degree of synchronization can be maintained over a broad range of intrinsic heart rates while maintaining the compression rate within a satisfactory range. Further investigation to assess benefit for treatment of PEA is warranted.


CHEST Journal ◽  
2015 ◽  
Vol 148 (4) ◽  
pp. 55A
Author(s):  
Steven Keller ◽  
Sarah Fink ◽  
Henry Halperin ◽  
Muz Zviman

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