Abstract 167: Epinephrine Plus Chest Compressions May Be Superior to Epinephrine Alone in a Hypoxia-Induced Porcine Model of Lifeless Shock

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Felipe Teran ◽  
Claire Centeno ◽  
Alex L Lindqwister ◽  
William J Hunckler ◽  
William Landis ◽  
...  

Background: Lifeless shock (LS) (previously called EMD and pseudo-PEA) is a global hypotensive ischemic state with retained coordinated myocardial contractile activity and an organized ECG. We have previously described our hypoxic LS model. The role of standard external chest compressions remains unclear in the setting of LS and its associated intrinsic hemodynamics. Although it is known the patients with LS have better prognosis compared to PEA, it is unclear what is the best treatment strategy. Prior work has shown that chest compressions (CC) when synchronized with native systole results in significant hemodynamic improvement, most notably coronary perfusion pressure (CPP), and hence it is plausible that standard dyssynchronous CC may be detrimental to hemodynamics. Furthermore, retrospective clinical data has shown that LS patients treated with vasopressors and no CC, may have better outcomes. We compared epinephrine only versus epinephrine and chest compression, in a porcine model of LS. Methods: Our porcine model of hypoxic LS has previously been described. We randomized pigs to episodes of LS treated with epinephrine only (control) (0.0015 mg/kg) versus epinephrine plus standard external chest compressions (intervention). Animals were endotracheally intubated and mechanically ventilated, and the fraction of inspired oxygen (FiO 2 ) was gradually lowered from room air (20-30% O 2 ) to a target FiO 2 of 3-7% O 2 . This target FiO 2 was maintained until the systolic blood pressure (SBP) dropped to 30 mmHg for 30 seconds, or the animal became bradycardic (HR less than 40), which was defined as the start of LS. FiO 2 was then raised to 100%, and then animal would receive control or intervention. Return of spontaneous circulation (ROSC) was defined as SBP 60 mmHg, stable after 2 minutes. Results: Twenty-six episodes of LS in 11 animals received epinephrine only control and 21 episodes the epinephrine plus chest compression intervention. The rates of ROSC in two minutes or less were 5/26 (19%) in the control arm vs 14/21 (67%) in the intervention arm (P=0.001;95% CI 19.7 %-67.2%). Conclusions: In a swine model of hypoxia induced LS, epinephrine plus CPR may be superior to epinephrine alone.

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.


2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
S. Eichhorn ◽  
A. Mendoza ◽  
A. Prinzing ◽  
A. Stroh ◽  
L. Xinghai ◽  
...  

According to the European Resuscitation Council guidelines, the use of mechanical chest compression devices is a reasonable alternative in situations where manual chest compression is impractical or compromises provider safety. The aim of this study is to compare the performance of a recently developed chest compression device (Corpuls CPR) with an established system (LUCAS II) in a pig model. Methods. Pigs (n = 5/group) in provoked ventricular fibrillation were left untreated for 5 minutes, after which 15 min of cardiopulmonary resuscitation was performed with chest compressions. After 15 min, defibrillation was performed every 2 min if necessary, and up to 3 doses of adrenaline were given. If there was no return of spontaneous circulation after 25 min, the experiment was terminated. Coronary perfusion pressure, carotid blood flow, end-expiratory CO2, regional oxygen saturation by near infrared spectroscopy, blood gas, and local organ perfusion with fluorescent labelled microspheres were measured at baseline and during resuscitation. Results. Animals treated with Corpuls CPR had significantly higher mean arterial pressures during resuscitation, along with a detectable trend of greater carotid blood flow and organ perfusion. Conclusion. Chest compressions with the Corpuls CPR device generated significantly higher mean arterial pressures than compressions performed with the LUCAS II device.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Norman A Paradis ◽  
Karen L Moodie ◽  
Christopher L Kaufman ◽  
Joshua W Lampe

Introduction: Guidelines for treatment of cardiac arrest recommend minimizing interruptions in chest compressions based on research indicating that interruptions compromise coronary perfusion pressure (CPP) and blood flow and reducing the likelihood of successful defibrillation. We investigated the dynamics of CPP before, during, and after compression interruptions and how they change over time. Methods: CPR was performed on domestic swine (~30 Kg) using standard physiological monitoring. Blood flow was measured in the abdominal aorta (AAo), the inferior vena cava, the right common carotid and external jugular. Ventricular fibrillation (VF) was electrically induced. Mechanical chest compressions (CC) were started after four minutes of VF. CC were delivered at a rate of 100 compressions per minute (cpm) and at a depth of 2” for a total of 12 min. CPP was calculated as the difference between aortic and right atrial pressure at end-diastole per Utstein guidelines. CPP was determined for 5 compressions prior to the interruption, every 2 seconds during the CC interruption, and for 7 compressions after the interruption. Per protocol, 12 interruptions occurred at randomized time points. Results: Across 12 minutes of CPR, averaged CPP prior to interruption was significantly greater than the averaged CPP after the interruption (22.4±1.0 vs. 15.5±0.73 mmHg). As CPR continued throughout the 12 minutes, CPP during compressions decreased (First 6 min = 24.1±1.4 vs. Last 6 min = 20.1±1.3 mmHg, p=0.05), but the effect of interruptions remained constant resulting in a 20% drop in CPP for every 2 seconds irrespective of the prior CPP. The increase (slope) of CPP after resumption of compressions was significantly reduced over time (First 6 min = 1.47±0.18 vs. Last 6 min = 0.82±0.13 mmHg/compression). Conclusions: Chest compression interruptions have a detrimental effect on coronary perfusion and blood flow. The magnitude of this effect increases over time as a resuscitation effort continues. These data confirm the importance of providing uninterrupted CPR particularly in long duration resuscitations.


2015 ◽  
Author(s):  
Charles N. Pozner ◽  
Jennifer L Martindale

The most effective treatment for cardiac arrest is the administration of high-quality chest compressions and early defibrillation; once spontaneous circulation is restored, post–cardiac arrest care is essential to support full return of neurologic function. This review summarizes the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of cardiac arrest and resuscitation. Figures show the foundations of cardiac resuscitation, ventricular arrhythmias, coronary perfusion pressure as a function of time, an algorithm for initial treatment of cardiac arrest, sample capnographs, and the electrocardiographic appearance of varying degrees of hyperkalemia. Tables include components of suboptimal cardiac resuscitation and corrective actions, recommended doses of medications commonly used in cardiac resuscitation, causes of pulseless electrical activity/asystolic arrest to consider, immediate post–return of spontaneous circulation checklist, and resuscitation goals during post–cardiac arrest care. This review contains 6 highly rendered figures, 5 tables, and 142 references.


Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
James J Menegazzi ◽  
David D Salcido ◽  
Allison C Koller ◽  
Cornelia Genbrugge ◽  
Ericka L Fink ◽  
...  

Background: Current guidelines recommend that chest compressions for children be done at either 1.5 inches depth and 100 per minute, or one-third the chest A-P diameter depth and 100 per minute. Neither of these recommendations is based on scientific evidence. Objective: As part of an ongoing efficacy trial, we sought to compare the safety of three different chest compression strategies in a porcine model of pediatric cardiac arrest. Methods: Following anesthesia, instrumentation, and induction of asphyxial cardiac arrest, we randomly assigned 48 domestic swine to one of three groups (n=16 per group). The mean mass of 25.7 kg approximates the 50 th percentile for a 7 year old. Group 1 had fixed chest compression depth of 1.5 inches/rate 100; group 2 had fixed proportional depth of one-third the A-P diameter/rate 100; group 3 used an adaptive algorithm that incrementally increased chest compression rate and/or depth from baseline 1.5in (max: 2.13in) and 100/min (max; 130/min) every 25s while coronary perfusion pressure was below 25mmHg. Necropsies were independently performed by a veterinarian and veterinary technologist who were blinded to group assignment. The primary safety outcome was unrecoverable injury (i.e. toxicity), which we defined as either a total lung injury score ≥16 (score can range from 0 to 20) plus presence of hemothorax, or disruption of either the aorta or vena cava. Data were analyzed with the Bayesian Beta Binomial to determine if within-group toxicity exceeded an unacceptable level (30%) with a pre-selected posterior predictive threshold of 0.75(ptox). Lung injury scores between groups were compared with Kruskal-Wallis tests. Results: Median total lung injury scores were: 12 for group 1; 18 for group 2; 14 for group 3. Group 2 was significantly different from both groups 1 and 3 (p<0.001). Groups 1 and 3 did not differ (p=0.24). Toxicity occurred in zero animals in group 1 (ptox=0.0001); 7 animals in group 2 (ptox=0.8180); and 1 animal in group 3 (ptox=0.0076). The posterior probability threshold was exceeded in group 2 which warranted termination of the treatment arm for safety. Conclusions: Chest compressions performed at a depth of one-third the A-P diameter are unsafe. The safety of this approach in children should be carefully evaluated.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Tao Yu ◽  
Giuseppe Ritagno ◽  
Jun H Cho ◽  
Shijie Sun ◽  
Max H Weil ◽  
...  

We have previously reported, on the basis of experimental studies, that interruptions of CPR as little as 10 seconds adversely affect the outcomes of CPR. We therefore investigated interruptions of only 5 seconds for delivering ventilation, which corresponds to the current AHA algorithm in which of 30 compressions followed by 2 ventilations are mandated. We hypothesized that even 5 seconds interruption significantly reduces CPP and with significant delay prior to restoring pre-interruption levels. Ventricular fibrillation (VF) was induced and untreated for 15 minutes in 33 male domestic pigs weighting 40±3 Kg. Chest compressions delivered with the aid of mechanical compressor (Thumper, 1000, MI Instruments) with a rate of 100/min. Ventilations were administrated with a compression / ventilation ratio of 30:2 such that 2 ventilations were delivered over a 5 seconds interval. CPP was continuously measured as the difference between comparison diastolic and simultaneous left atrial pressure. CPP significantly decreased during interruptions for ventilation from 20.5±12.8 mmHg to 9.8±6.7 mmHg( P <0.001). After chest compressions were restarted, the CPP increased to 12.5±7.6 mmHg after first compression( P <0.001). A total of 12±7 compressions over a mean interval of 7.2±4.3 seconds was required prior to restoration of CPP to levels corresponding to those that preceded the interruption. As little as the five seconds of interruption in chest compression currently mandated for 30 to 2 ventilations during CPR significantly reduced CPP and delayed restoration of CPP to its pre-interruption level.


1997 ◽  
Vol 86 (6) ◽  
pp. 1375-1381 ◽  
Author(s):  
Volker Wenzel ◽  
Karl H. Lindner ◽  
Andreas W. Prengel ◽  
Keith G. Lurie ◽  
Hans U. Strohmenger

Background Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to be more effective than optimal doses of epinephrine. This study evaluated the effect of endobronchial vasopressin during CPR. Methods After 4 min of untreated ventricular fibrillation and 3 min of CPR, 21 pigs were randomized to be treated with 0.8 U/kg intravenous vasopressin (n = 7), 0.8 U/kg endobronchial vasopressin (n = 9), or an endobronchial placebo of normal saline (n = 5). Defibrillation was performed 5 min after drug administration to attempt return of spontaneous circulation. Results All animals in the intravenous and endobronchial vasopressin group were resuscitated successfully, but only two of five animals in the placebo group were. At 2 and 5 min after drug administration, coronary perfusion pressure in the intravenous and endobronchial vasopressin group was significantly higher than in the placebo group (50 +/- 10, 34 +/- 5 vs. 16 +/- 6 mmHg, respectively; and 35 +/- 10, 39 +/- 10 vs. 19 +/- 5 mmHg, respectively; P &lt; 0.05). Conclusions Endobronchial vasopressin is absorbed during CPR, coronary perfusion pressure is increased significantly within a short period, and the chance of successful resuscitation is increased in this porcine model of CPR. Endobronchial vasopressin may be an alternative for vasopressor administration during CPR, when intravenous access is delayed or not available.


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 ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Salvatore Aiello ◽  
Jenna Mendelson ◽  
Alvin Baetiong ◽  
Jeejabai Radhakrishnan ◽  
Raul J Gazmuri

Introduction: VF accounts for ~30% of all sudden cardiac arrest episodes. VF signal analysis in the frequency domain - calculating the amplitude spectral area (AMSA) - can inform on the probability that an electrical shock could terminate VF followed by return of spontaneous circulation (ROSC). BLS guidelines require delivery of shocks every 2 min and epinephrine every 4 min. Yet, shocks often do not terminate VF and may injure the myocardium. We have previously reported that guiding the timing of shock delivery based on AMSA reduces myocardial injury and improves outcome. Epinephrine is given to increase the coronary perfusion pressure (CPP) and therefore myocardial blood flow but has detrimental effects on post-resuscitation myocardial function and possibly on neurological outcome. Hypothesis: Monitoring AMSA during CPR could be used not only to guide shock delivery but also to avoid administering epinephrine when AMSA predicts a high probability of shock success, reserving epinephrine when AMSA predicts a low probability of shock success and additional CPP increase might be helpful. Methods: In a swine model of electrically induced VF and mechanical chest compressions, two resuscitation protocols were compared in 8 pigs each: (1) A guidelines-driven (GD), delivering shocks and epinephrine guided by the current BLS protocol and (2) An AMSA-driven, delivering shocks and epinephrine guided by AMSA (ADSE). VF was untreated for 10 min and pigs that achieved ROSC were monitored for 240 min. Results: Compared to GD, ADSE was associated with a shorter time to ROSC (400±80 vs 569±16 sec, p=0.034) and higher survival rate at 240 minutes with borderline statistical significance (7/8 vs 3/8, p=0.059). ADSE required fewer shocks (3±2 vs 5±2, p=0.026) and received fewer doses of epinephrine (median [interquartile range], 1[1-1] vs 2[1.3-3], p=0.038). Conclusions: Resuscitation with the ADSE protocol was superior to the GD protocol resulting in a shorter time to ROSC with improved survival requiring fewer shocks and fewer epinephrine doses. The ADSE protocol represents a more tailored approach to resuscitation enabling delivery of resuscitation interventions with higher precision and consequently minimizing their associated adverse effects.


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