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

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.

Download Full-text

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

Circulation ◽

10.1161/circ.118.suppl_18.s_661-a ◽

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.

Download Full-text

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

BioMed Research International ◽

10.1155/2017/5470406 ◽

2017 ◽

Vol 2017 ◽

pp. 1-9 ◽

Cited By ~ 1

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.

Download Full-text

Contribution of extravascular compression to reduction of maximal coronary blood flow

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.262.1.h68 ◽

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.

Download Full-text

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

Circulation ◽

10.1161/circ.140.suppl_2.167 ◽

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.

Download Full-text

Abstract 262: Hemodynamically-Guided Optimum Chest Compression Point in a Rat Model of Cardiopulmonary Resuscitation

Circulation ◽

10.1161/circ.138.suppl_2.262 ◽

2018 ◽

Vol 138 (Suppl_2) ◽

Author(s):

Davide Olivari ◽

Daria De Giorgio ◽

Deborah Novelli ◽

Aurora Magliocca ◽

Laura Ruggeri ◽

...

Keyword(s):

Chest Compression ◽

Rat Model ◽

Coronary Perfusion Pressure ◽

Male Rats ◽

Right Atrial ◽

Maximum Diameter ◽

Coronary Perfusion ◽

Successful Resuscitation ◽

The One

Introduction: CPR aims to re-establish blood flow by chest compression (CC), achieving threshold levels of coronary perfusion pressure (CPP). For this, current guidelines recommend the lower sternal half as optimum CC point. However, this point might be not optimal for every individual. We investigated the hemodynamics generated by CC performed on different chest points in a rat model of CPR. We hypothesized that a CC point hemodynamically-identified would be a better approach compared to the lower sternal half. Methods: Ten male rats were anesthetized and arterial and right atrial pressures monitored. Ventricular fibrillation was induced and untreated for 8 min. CPR, including mechanical CC, ventilation, and epinephrine, was then performed for 8 min. Animals were divided to receive CC performed either on the lower sternal half (standard (STD), n=5) or on an optimum point identified as the one able to generate the maximum CPP (MaxCPP group, n=5). Cardiac districts involved in CC were subsequently identified by computed tomography (CT). Results: STD CC produced a CPP that was constantly below the threshold for successful resuscitation and trended to decrease over time. When the optimum CC point was identified hemodynamically, the CPP generated was constantly > 20 mmHg. Indeed, CPP was significantly higher in the MaxCPP group compared to the STD one for the whole 8 min of CPR (p<0.01, Fig). Moreover, administration of epi rapidly further improved CPP (p<0.01 vs. pre-epi) in the group with an optimized CC point, while no drug effect was observed in the STD one. CT scan showed that the lower sternal half did not correspond to the LV maximum diameter, known to account for a maximum stroke volume generation during CC (Fig). Conclusion: Standard lower sternal half CC point is not able to maximize hemodynamics during CPR, making ineffective CC efforts and vasopressor administration. The quality of CPR may improve if the optimum CC point is identified as a reflection of CPP generated.

Download Full-text

Cardiac Arrest and Resuscitation

10.2310/im.4155 ◽

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.

Download Full-text

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

Circulation ◽

10.1161/circ.130.suppl_2.289 ◽

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.

Download Full-text