Abstract 299: Effect of Start Position and Compression Depth on Mechanical CPR Hemodynamics in Swine

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Shannon E Allen ◽  
Allison Hubert ◽  
Dorcas Nsumbu ◽  
Samantha Ang ◽  
John M Canty ◽  
...  
Keyword(s):  
Near Infrared ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Compression Depth ◽  
Start Position ◽  
Suction Cup ◽  
Mechanical Devices ◽  
Electrical Induction ◽  
Mechanical Cpr

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.

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 ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Near Infrared ◽  
Porcine Model ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Hemodynamic Support ◽  
Electrical Induction ◽  
Automated Delivery ◽  
Mechanical Cpr

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.

Abstract 306: Similar Hemodynamic Efficacy Between 30 mm and 50 mm Compression Depth During Mechanical Chest Compression with Weil Mini Chest Compressor

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Zhengfei Yang ◽  
Ping Gong ◽  
Xiaobo Wu ◽  
Jie Qian ◽  
Shen Zhao ◽  
...  
Keyword(s):  
Chest Compression ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Compression Depth ◽  
Successful Resuscitation ◽  
Mechanical Chest Compression ◽  
Significant Difference ◽  
Manual Chest Compression ◽  
End Tidal ◽  
Mechanical Cpr

Introduction: Current guidelines require a 50 mm compression depth for manual chest compression. During mechanical chest compression, however, because of the design of each device, whether this depth yields the most optimal hemodynamic efficacy remains to be tested. In this study, we investigated the effects of compression depth on hemodynamics efficacy during mechanical CPR with the Weil Mini Chest Compressor in a porcine model. Hypothesis: There is no significant difference in hemodynamic efficacy between compression depth of 30 mm and 50 mm during mechanical CPR with the Weil Mini Chest Compressor. Methods: Ten male domestic pigs weighing 34±2 kg were utilized. Ventricular fibrillation was electrically induced and untreated for 7 min. The animals were then randomized to receive compression depth of 30 mm or 50 mm. Coincident with the start of precordial compression, the animals were mechanically ventilated at a rate of 10 breaths per minute. Defibrillation was attempted by a single 150 J shock. If resuscitation was not successful, CPR was resumed for 2 mins prior to the next defibrillation until either successful resuscitation or for a total of 15 mins. Results: All animals were successfully resuscitated. There were no differences in coronary perfusion pressure (CPP), end-tidal carbon dioxide (ETCO2) and carotid blood flow (CBF) between the two groups (Table). A significantly less rib fracture was observed in the 30 mm group [0 (0-0) vs 1.2 (0-2), p<0.05]. Conclusion: Similar hemodynamic efficacy was observed between 30 and 50 mm compression depth during mechanical CPR with the Weil Mini Chest Compressor.

Abstract 289: Effect of Elevated Legs on Hemodynamic Performance During Cardiopulmonary Resuscitation in a Porcine Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eric Qvigstad ◽  
Andres Neset ◽  
Theresa M Olasveengen ◽  
øystein Tømte ◽  
Morten Eriksen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Supine Position ◽  
Life Support ◽  
Advanced Life Support ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Positive Pressure ◽  
Coronary Perfusion ◽  
End Tidal

Purpose of the study: During advanced life support (ALS) end-tidal carbon dioxide (EtCO 2 ) reflects cardiac output (CO). A recent clinical study found an association between passive leg raising (PLR) and increased EtCO 2 during ALS. This may reflect a transient increase in pulmonary blood flow and CO, but might cause a detrimental decrease in coronary perfusion pressure (CPP). We evaluated the effect of PLR during experimental ALS in a randomized, factorial design. Materials and methods: In nine anesthetized domestic pigs (30±1.8 kg) ventricular fibrillation was induced electrically. After 3 minutes of no-flow, mechanical chest compressions (5cm @ 100 min -1 ) were started. During four 5-minute segments of CPR we measured CO, EtCO 2 , perfusion pressures, carotid and cerebral cortical microcirculatory blood flow (MBF) and CPP (the average of the positive pressure difference between decompression aortic pressure (AP) and right atrial pressure (RAP)) at minute 2 and 4. Interventions were provided in a randomized sequence with PLR vs supine position, with or without epinephrine (0.5mg iv). Values are given as mean±standard deviation. Results: PLR did not increase EtCO2 compared to supine position (3.1±0.7 vs 3.0±0.8 kPa), but CO was minimally increased from 1.1±0.3 to 1.2±0.3 Lmin -1 ,(p=0.003). PLR did not significantly increase AP (57±15 vs. 48±18 mmHg, p=0.3), but RAP was higher (43±10 vs. 31±7, p=0.003). However, no difference was found in CPP due to marked variation in both groups (median(range): PLR 20 (9,43) and supine 17(9,58)). The effect of epinephrine during this experimental setup was minimal. Conclusion: We did not find a positive effect of PLR during experimental ALS, but there were no obviously detrimental effects either.

Abstract 149: Role of Pre and Intra-Arrest Hemodynamics in Evolution of the Ventricular Fibrillation Electrocardiogram Waveform

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Caelie E Kern ◽  
David D Salcido
Keyword(s):  
Ventricular Fibrillation ◽  
Trajectory Analysis ◽  
Venous Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Pressure Transducers ◽  
Surface Ecg ◽  
Electrical Induction

Purpose: Quantitative waveform measures (QWM) of the ventricular fibrillation (VF) waveform have been shown in laboratory and clinical studies to be predictive of return of spontaneous circulation (ROSC) and survival to hospital discharge. During resuscitation, QWM are responsive to hemodynamic changes resulting from CPR. It is not known whether the trajectory of QWM are affected by pre-arrest hemodynamics or intra-arrest arterio-venous pressure equilibration. We sought to investigate the role of hemodynamics on the evolution of VF before and during prolonged VF. Methods: We pooled data from six previous porcine experiments. Each modeled prolonged VF and included electrical induction of VF which was left untreated for up to 10 minutes, followed by attempted resuscitation. All animals were instrumented with pressure transducers (Millar, MikroTip) placed via femoral cutdown in the aorta and right atrium, as well as Lead II surface ECG. Signals were recorded continuously at 1000Hz with a data acquisition unit (PowerLab, ADInstruments). Mean baseline central arterial (CAP) and central venous pressure (CVP) were calculated from 1- minute of immediate pre-VF pressure traces. Coronary perfusion pressure (CPP) during untreated VF was calculated as the continuous difference between the CAP and CVP channels. Median slope (MS), a QWM, was calculated in 1-second windows and interpolated to the full length of the intra-arrest ECG. For trajectory analysis, CPP and MS traces were normalized on a 0-1 scale and grouped by morphological similarity. Pearson’s Correlation coefficient was calculated between corresponding CPP and MS traces. Results: A total of 141 experiments were included in the analysis. Overall mean (SD) correlation between CPP and MS was 0.56 (0.29). CPP-MS correlation strength did not correlate with baseline pressures. However, trajectory analysis revealed multiple patterns of hemodynamic and QWM evolution through untreated VF, with the most well-defined (mean coeff. = 0.58) indicating a shared bimodality temporally offset between CPP and MS. Conclusions: Hemodynamics during untreated VF show some correlation with the trajectory of QWM of the VF signal. More work is needed to understand the mechanism of this relationship.

Cardiopulmonary resuscitation in the rat

1988 ◽  
Vol 65 (6) ◽  
pp. 2641-2647 ◽  
Author(s):  
I. von Planta ◽  
M. H. Weil ◽  
M. von Planta ◽  
J. Bisera ◽  
S. Bruno ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Cardiopulmonary Resuscitation ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Low Flow ◽  
Coronary Perfusion ◽  
Flow State ◽  
Successful Resuscitation ◽  
End Tidal ◽  
The Right

A standardized method of cardiopulmonary resuscitation in rodents has been developed for anesthetized, mechanically ventilated rats. Ventricular fibrillation was induced and maintained by an alternating current delivered to the right ventricular endocardium. After 4 min of ventricular fibrillation, the chest was compressed with a pneumatic piston device. Eight of 14 animals were successfully resuscitated with DC countershock after 6 min of cardiac arrest. In confirmation of earlier studies from our laboratories in dogs, pigs, and human patients, this rodent model of cardiopulmonary resuscitation demonstrated large venoarterial [H+] and PCO2 gradients associated with reduced pulmonary excretion of CO2 during the low-flow state. Mean aortic pressure, coronary perfusion pressure, and end-tidal CO2 during chest compression were predictive of successful resuscitation.

Abstract 359: Use of Resuscitative Balloon Occlusion of the Aorta in a Swine Model of Prolonged Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Mohamad H Tiba ◽  
Brendan M McCracken ◽  
Brandon C Cummings ◽  
Carmen I Colmenero ◽  
Chandler J Rygalski ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Balloon Occlusion ◽  
Mean Difference ◽  
Repeated Measure ◽  
Swine Model ◽  
Coronary Perfusion ◽  
Temporary Control ◽  
Mechanical Cpr

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.

Abstract P115: Higher Threshold and Dose of Coronary Perfusion Pressure are Associated with ROSC in Prolonged Swine Cardiac Arrest

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Joshua C Reynolds ◽  
David D Salcido ◽  
James J Menegazzi
Keyword(s):  
Cardiac Arrest ◽  
Myocardial Perfusion ◽  
Regression Models ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Experimental Protocol ◽  
Total Flow ◽  
Mechanical Cpr

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.

Cardiopulmonary resuscitation in the mouse

2002 ◽  
Vol 93 (4) ◽  
pp. 1222-1226 ◽  
Author(s):  
Lei Song ◽  
Max Harry Weil ◽  
Wanchun Tang ◽  
Shijie Sun ◽  
Tommaso Pellis
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Cardiopulmonary Arrest ◽  
Threshold Level ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Successful Resuscitation ◽  
Threshold Levels ◽  
The Right

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.

Coronary endothelium-derived vasodilation during cooling and rewarming of the in situ heart

1999 ◽  
Vol 77 (1) ◽  
pp. 56-63 ◽  
Author(s):  
Torkjel Tveita ◽  
Olav Hevrøy ◽  
Helge Refsum ◽  
Kirsti Ytrehus
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Aortic Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Rate ◽  
Rate Pressure Product ◽  
Coronary Perfusion ◽  
The One ◽  
Core Cooling

The integrity of coronary vascular endothelial vasodilator function during core cooling and rewarming was investigated in a pentobarbital-anesthetized open-chest dog model. Vasodilator response was assessed as the change from baseline blood flow by injecting the endothelial-dependent vasodilator acetylcholine (ACh) (1.0 µg) or the endothelial-independent vasodilator nitroglycerin (NTG) (50 µg) into the left anterior descending (LAD) coronary artery. Change in blood flow was measured using a transit time ultrasonic volume flowmeter technique. During cooling and rewarming LAD blood flow was significantly decreased. After rewarming, aortic pressure was artificially elevated to reach control. This procedure restored heart work (LV-RPP, left ventricular rate pressure product) and coronary perfusion pressure, but LAD blood flow remained lowered. Ability to dilate the vascular bed supplied by LAD, after injections of ACh or NTG, was present both during cooling and rewarming. At 25°C coronary blood flow (LAD) increased from 3 ± 1 to 9 ± 1 mL·min-1 in response to both ACh and NTG. Posthypothermic blood flow increased from 7 ± 1 to 19 ± 2 and 20 ± 3 mL·min-1 in response to ACh and NTG, respectively. Measured as the percent change from baseline LAD blood flow, the response was not significantly different from the one obtained in prehypothermic hearts. In conclusion, coronary vasodilator function, both endothelium dependent and endothelium independent, is present but not maintained at the same level during cooling to 25°C and rewarming. In spite of the deterioration of cardiac function, no selective defect in the endothelium-dependent response was detected, either during hypothermia or after rewarming.Key words: rewarming shock, cold, temperature, coronary blood flow, acetylcholine, nitroglycerin.

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