scholarly journals Corpuls CPR Generates Higher Mean Arterial Pressure Than LUCAS II in a Pig Model of Cardiac Arrest

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
S. Eichhorn ◽  
A. Mendoza ◽  
A. Prinzing ◽  
A. Stroh ◽  
L. Xinghai ◽  
...  
Keyword(s):  
Blood Flow ◽  
Chest Compression ◽  
Near Infrared ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Pig Model ◽  
Coronary Perfusion ◽  
Organ Perfusion ◽  
Chest Compressions ◽  
Carotid Blood Flow

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.

Abstract 17334: The Detrimental Effect of Chest Compression Interruptions on Coronary Perfusion Pressure Dynamics

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Norman A Paradis ◽  
Karen L Moodie ◽  
Christopher L Kaufman ◽  
Joshua W Lampe
Keyword(s):  
Blood Flow ◽  
Chest Compression ◽  
Detrimental Effect ◽  
Perfusion Pressure ◽  
Vena Cava ◽  
Coronary Perfusion Pressure ◽  
Right Atrial ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Over Time

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.

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 ◽  
...  
Keyword(s):  
Chest Compression ◽  
Porcine Model ◽  
Contractile Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Swine Model ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Fraction Of Inspired Oxygen ◽  
External Chest Compressions

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.

Cardiac Arrest and Resuscitation

2015 ◽  
Author(s):  
Charles N. Pozner ◽  
Jennifer L Martindale
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Arrhythmias ◽  
Perfusion Pressure ◽  
Pulseless Electrical Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Cardiac Resuscitation ◽  
Neurologic Function

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.

Abstract 2043: Even Minimal Interruptions in Chest Compression for Ventilation Significantly Decreases Coronary Perfusion Pressure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Tao Yu ◽  
Giuseppe Ritagno ◽  
Jun H Cho ◽  
Shijie Sun ◽  
Max H Weil ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Chest Compression ◽  
Left Atrial ◽  
Perfusion Pressure ◽  
Experimental Studies ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Significant Delay ◽  
Chest Compressions ◽  
The Difference

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.

Cardiac massage and blood flow management during cardiac arrest

2016 ◽  
Author(s):  
Gavin D. Perkins
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Essential Element ◽  
Coronary Perfusion Pressure ◽  
Cardiac Massage ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Term Survival

When cardiac arrest occurs, blood flow to the vital organs diminishes rapidly. Chest compressions are an essential element of cardiopulmonary resuscitation (CPR), yet they achieve, at best, one-third of the normal cardiac output. The speed of initiating CPR, as well as its quality is critical to patient outcomes. Optimal chest characteristics of compressions are defined as pushing hard (depth > 5 cm) and fast (compression rate 100–120/min). Pressure should be released fully between sequential chest compressions and interruptions in chest compressions should be minimized. Even short interruptions in CPR around the time of attempted defibrillation can be harmful. CPR feedback and prompt devices can be used to monitor the quality of CPR. Studies have shown these devices can improve the quality of CPR, but do not improve overall survival. Mechanical chest compression devices may be usefully deployed when it is difficult or unsafe to perform manual CPR, but there is no evidence that the routine deployment of these devices improves outcome. Vasoactive drugs improve coronary perfusion pressure and increase the chances of return of spontaneous circulation. However, there is no definitive evidence that they improve long-term survival. Recent data have raised the possibility that adrenaline may worsen long-term outcomes.

scholarly journals Even Four Minutes of Poor Quality of CPR Compromises Outcome in a Porcine Model of Prolonged Cardiac Arrest

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Heng Li ◽  
Lei Zhang ◽  
Zhengfei Yang ◽  
Zitong Huang ◽  
Bihua Chen ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Porcine Model ◽  
Coronary Perfusion Pressure ◽  
Poor Quality ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Yorkshire Pigs ◽  
Anterior Posterior

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.

Abstract 254: Synchronized Chest Compressions for Pseudo-PEA: Proof of Concept and Synching Algorithm

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Keith Marill ◽  
James J Menegazzi ◽  
Allison C Koller ◽  
Matthew Sundermann ◽  
David D Salcido
Keyword(s):  
Cardiac Arrest ◽  
Chest Compression ◽  
Porcine Model ◽  
Pulseless Electrical Activity ◽  
Compression Therapy ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Compression Rate ◽  
Proof Of Concept ◽  
Chest Compressions

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.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

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