Why do chest compressions aid delayed defibrillation?

doi:10.1016/j.resuscitation.2007.11.010

Resuscitation

Volume 77, Issue 1, April 2008, Pages 10-15

https://doi.org/10.1016/j.resuscitation.2007.11.010 Get rights and content

Summary

The new resuscitation guidelines permit compressions before delayed, defibrillation, a change that has generally been welcomed. The benefits are generally assumed to relate to the immediate provision of limited coronary perfusion with protection or replenishment of myocardial metabolic reserves. In this paper we argue that the concept is inadequate to explain many experimental and clinical observations made during resuscitation attempts. We argue that changes in the size and shape of the ventricles are the most important reason for the narrow window of opportunity for defibrillation alone and for the value of compressions in extending this period. We also draw attention to the implication for clinical resuscitation and to one aspect of the current guidelines of the European Resuscitation Council that we believe to be inconsistent with the evidence that we review.

Introduction

Successful defibrillation provides the best opportunity for recovery from cardiac arrest. In the absence of a shockable rhythm, as with asystole or pulseless ventricular rhythm, the outlook is particularly bleak. But even with ventricular fibrillation, only a minority of cases can be successfully treated. Two principal determinants influence whether or not defibrillation is likely to lead to recovery of spontaneous circulation: the duration of the cardiac arrest before defibrillation can be achieved, and the condition of the heart before the arrhythmic episode that is not generally amenable to treatment during the resuscitation attempt.

The period without an effective cardiac output is critical to the viability of the heart because of the direct effects of ischaemia that include increasing tissue acidosis,¹ the loss of metabolic substrate that reduces calcium flux,² and persisting vascular insufficiency due to the no-reflow phenomenon in small blood vessels.³ These will eventually render cardiac arrest irreversible, with permanent loss of cerebral function occurring within a similar time frame.

The pathophysiology of cardiac arrest is complex, however. Restoration of a spontaneous circulation becomes increasingly unlikely within minutes, even before any permanent myocardial or vascular damage has occurred. The window of opportunity for successful defibrillation is therefore brief but can be extended by effective chest compressions. These considerations led Weisfeldt and Becker⁴ to describe three phases of cardiac arrest: an electrical phase lasting for about 4 min when defibrillation alone may suffice to restore a circulation, a longer circulatory phase when chest compressions may restore the possibility that defibrillation will lead to an effective circulation, and a later metabolic phase that offers no chance of a successful outcome with current therapies. Within 20–30 min without effective treatment, changes in the myocardium become irreversible—manifest sometimes by one final agonal contraction known as ‘stone heart’ in which the ventricles become contracted almost to cavity obliteration.⁵

Section snippets

The new wisdom

Conventional practice had previously called for defibrillation as soon as possible in the presence of any shockable rhythm, followed by compressions and artificial ventilation if spontaneous circulation was not achieved immediately. Recent studies6, 7 have shown, however, that a period of elective compressions given before an attempt at defibrillation can further improve the prospects of restoration of the circulation after the early electrical phase has passed, a practice that is now permitted

Limitations of the metabolic hypothesis

The aortic to right atrial pressure gradient generated by chest compressions falls very rapidly during any interruption, and so coincidentally if not causally, does the likelihood of recovery from cardiac arrest as a result of defibrillation. The time-course is remarkable. In a rat model, even 10 s without compressions reduced survival from 100% to 60%.¹³ Indirect observations in man based on analysis of fibrillatory waveforms suggest that ‘hands-off’ even for a limited period has dire

The complex haemodynamics of cardiac arrest

The profound changes that occur in the volume and shape of the ventricles during the first minutes of cardiac arrest are still not widely known nor are their implications appreciated. As long ago as 1955, Guyton et al. described the equilibration of arterial and venous pressures that were achieved after effective cardiac activity ceased,¹⁹ a concept first proposed more than a century earlier by Weber.²⁰ They predicted that equilibration of pressures would occur within approximately 40 s.

An alternative view

We do not discount the importance of metabolic factors, but propose that haemodynamics factors are at least as important, particularly in the early minutes of a cardiac arrest. This has important practical implications.

The external compression of the left ventricle by the right ventricle and pericardial constraint prevent any fibre stretch over baseline values in response to venous inflow to the heart. The force of myocardial contraction is related to the degree of its stretch, a relationship

Implications for resuscitation

For reasons already adduced, the progressive change from an effective contraction to a twitch in response to a shock is not due principally to depletion of energy substrate but more to the inhibiting effects of progressive tissue acidosis.¹ During the first minutes of cardiac arrest (the electrical phase), defibrillation may enable the heart to decompress itself sufficiently to reverse the cycle of unfavourable factors; but as minutes pass this can happen only as a result of external

Relevance to the ERC guidelines

Whilst we accept that myocardial acidosis and metabolic depletion are important factors during cardiac arrest that reduce myocardial contractility³⁰ and eventually render it irreversible, we affirm that it is the changes in the ventricular configuration and interaction (together with cerebral protection) that are the most important reasons why compressions aid delayed resuscitation whilst there is still a reasonable window of opportunity for a successful outcome. Loss of left ventricular volume

Conflict of interest

DAC is in receipt of a Laerdal Foundation Grant to support his work in Cardiff (expenses only).

Acknowledgements

The authors are grateful to Prof. Sir Bruce Keogh for permission to use a valuable transoesophageal echocardiogram, and to Dr. Ken Morallee and to Dr. Gavin Perkins for helpful discussions.

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Cited by (24)

The need for hands-on defibrillation during the late downstroke phase of ongoing abdominal compressions only CPR
2017, American Journal of Emergency Medicine
The impact of airway management on quality of cardiopulmonary resuscitation: An observational study in patients during cardiac arrest
2014, Resuscitation
Citation Excerpt :
There is evidence supporting avoidance of interruptions in CPR particularly during the early phases of resuscitation.6,7,33,34 Interruptions in CPR are linked to reductions in coronary perfusion pressure35 and development of ventricular fibrillation.36 Clinical studies have produced conflicting results with Shy identifying early intubation (within 12 min) as linked to improved survival in out-of-hospital cardiac arrest (RR late intubation 0.42, 95% CI 0.26, 0.69).37
Minimising interruptions in chest compressions is associated with improved survival from cardiac arrest. Current in-hospital guidelines recommend continuous chest compressions after the airway is secured on the premise that this will reduce no flow time. The aim of this study was to determine the effect of advanced airway use on the no flow ratio and other measures of CPR quality.
Consecutive adult patients who sustained an in-hospital cardiac arrest were enrolled in this prospective observational study. The quality of CPR was measured using the Q-CPR device (Phillips, UK) before and after an advanced airway device (endotracheal tube [ET] or laryngeal mask airway [LMA]) was inserted. Patients receiving only bag-mask ventilation were used as the control cohort. The primary outcome was no flow ratio (NFR). Secondary outcomes were chest compression rate, depth, compressions too shallow, compressions with leaning, ventilation rate, inflation time, change in impedance and time required to successfully insert airway device.
One hundred patients were enrolled in the study (2008–2011). Endotracheal tube and LMA placement took similar durations (median 15.8 s (IQR 6.8–19.4) vs LMA median 8.0 s (IQR 5.5–15.9), p = 0.1). The use of an advanced airway was associated with improved no flow ratios (endotracheal tube placement (n = 50) improved NFR from baseline median 0.24 IQR 0.17–0.40) to 0.15 to (IQR 0.09–0.28), p = 0.012; LMA (n = 25) from median 0.28 (IQR 0.23–0.40) to 0.13 (IQR 0.11– 0.19), p = 0.0001). There was no change in NFR in patients managed solely with bag valve mask (BVM) (n = 25) (median 0.29 (IQR 0.18–0.59) vs median 0.26 (IQR 0.12–0.37), p = 0.888). There was no significant difference in time taken to successfully insert the airway device between the two groups.
The use of an advanced airway (ETT or LMA) during in-hospital cardiac arrest was associated with improved no flow ratio. Further studies are required to determine the effect of airway devices on overall patient outcomes.
Hemodynamic rescue and ECG stability during chest compressions using adenosine and lidocaine after 8-minute asphyxial hypoxia in the rat
2013, American Journal of Emergency Medicine
Citation Excerpt :
Another standout feature of the present study was the significantly higher DAPs in the AL group of 12 to 19 mm Hg during seven of the twelve 30-second chest compression intervals for 60 minutes of CPR (Figs. 2B and 4). A higher DAP with AL bolus treatment is potentially important in CPR for 2 reasons: (1) it may improve blood flow to the globally ischemic heart because coronary perfusion pressure gradient is the difference between aortic diastolic and right atrial pressures [27,28] and, (2) it may reflect a higher peripheral vascular tone with improved forward flow to vital organs [27,32]. In the 1990s, Paradis and colleagues [33] showed that a coronary perfusion pressure gradient of 15 mm Hg or more was associated with improved ROSC [34,35].
Sudden cardiac death generally arises from either ventricular fibrillation or asphyxial hypoxia. In an effort to translate the cardioprotective effects of adenosine and lidocaine (AL) from hemorrhagic shock to cardiopulmonary resuscitation, we examined the effect of AL on hemodynamics and electrocardiogram (ECG) stability in the rat model of asphyxial hypoxia.
Male Sprague-Dawley rats were randomly assigned to 1 of 4 groups (n = 8): saline (SAL), adenosine (ADO), lidocaine (LIDO), and AL. Cardiac arrest (mean arterial pressure < 10 mm Hg) was induced by clamping the ventilator line for 8 minutes. A 0.5-mL intravenous drug bolus was injected followed by chest compressions (300 min^− 1), which were repeated every 5 minutes for 1 hour.
Return of spontaneous circulation was achieved in 5 SAL (62.6%), 4 ADO (50%), 7 LIDO (87.5%), and 8 AL rats (100%) within 5 minutes but could not be sustained. During chest compressions, mean arterial pressure was consistently higher in the AL-treated rats compared with all groups (P < .05; 35-45 and 55 minutes) followed by the LIDO group and was lowest in the ADO and SAL groups (P < .05). Systolic pressure followed a similar pattern. In addition, diastolic pressure in the AL-treated rats was significantly higher from 25 to 60 minutes than LIDO and ADO alone or SAL, and heart rate was 30% to 40% lower. Improved ECG rhythm and R-R variability were apparent in AL-treated rats during early compressions and hands-off intervals.
We conclude that a small bolus of 0.9% NaCl AL improved hemodynamics with possible diastolic rescue and ECG stabilization during chest compressions compared with ADO, LIDO, or SAL controls.
A randomized trial of compression first or analyze first strategies in patients with out-of-hospital cardiac arrest: Results from an Asian community
2012, Resuscitation
Citation Excerpt :
For asystole or pulseless electrical activity (PEA), uninterrupted CPR is the most important treatment.1 For VF or VT, animal studies showed that CPR before shocks could increase the likelihood of defibrillation success and survival.15–18 A three-phase time-sensitive model suggests distinct optimal therapeutic approach of resuscitation.19
It is still under debate whether a period of cardiopulmonary resuscitation should be performed prior to rhythm analysis for defibrillation for out of hospital cardiac arrests (OHCA). This study compared outcomes of OHCA treated by “compression first” (CF) versus “analyze first” (AF) strategies in an Asian community with low rates of shockable rhythms.
This randomized trial was conducted in Taipei City between February 2008 and December 2009. Dispatches of suspected OHCA that activated advanced life support teams were randomized into the CF and AF strategies. Patients assigned to CF strategy received 10 cycles of CPR prior to analysis by automatic external defibrillator. The primary outcome was sustained (>2 h) return of spontaneous circulation (ROSC) and secondary outcome was survival to hospital discharge.
We included 289 cases in the final analysis after exclusion by pre-specified criteria, 141 were allocated to CF strategy and 148 to AF strategy. Baseline characteristics were similar. Thirty-seven (26.2%) of those receiving CF strategy and 49 (33.1%) of the AF strategy achieved sustained ROSC (p = 0.25). In a post-hoc analysis of patients who achieved ROSC, those that received CF strategy were more likely to be discharged alive from the hospital (16/37 = 43.2% vs. 11/49 = 22.4%, p = 0.02).
In this study population of low rates of shockable rhythms, there was no difference in ROSC for CF or AF strategies. Considering the EMS operation situations, a period of paramedic-administered CPR for up to 10 cycles prior to rhythm analysis could be a feasible strategy in this community.
Resuscitation feedback and targeted education improves quality of pre-hospital resuscitation in Scotland
2012, Resuscitation
Citation Excerpt :
Chest compressions aim to provide some perfusion to vital organs, including the brain and heart, during cardiac arrest, prolonging the time before irreversible ischaemic damage occurs.3 Periods during which chest compressions are not performed result in poor blood flow to vital organs, making successful defibrillation less likely.4 Recent studies have demonstrated the adverse physiological consequences of poor resuscitation technique and have shown that quality of CPR is a critical determinant of outcome from OHCA.5,6
Out-of-hospital cardiac arrest (OHCA) is a leading cause of mortality and serious neurological morbidity in Europe. Recent studies have demonstrated the adverse physiological consequences of poor resuscitation technique and have shown that quality of cardiopulmonary resuscitation (CPR) is a critical determinant of outcome from OHCA. Telemetry of the defibrillator transthoracic impedance (TTI) trace can objectively measure quality of pre-hospital resuscitation. This study aims to analyse the impact of targeted resuscitation feedback and training on quality of pre-hospital resuscitation.
Prospective, single centre, cohort study over 13 months (1st December 2009–31st December 2010). Baseline pre-hospital resuscitation data was gathered over a 3-month period. Modems (n = 40) were fitted to defibrillators on ambulance vehicles. Following a resuscitation attempt, the event was sent via telemetry and the TTI trace analysed. Outcome measures were time spent performing chest compressions, compression rate, the interval required to deliver a defibrillator shock and use of automatic or manual cardiac rhythm analysis. Targeted resuscitation classes were introduced and all ambulance crews received feedback following a resuscitation attempt. Pre-hospital resuscitation quality pre and post intervention were compared.
111 resuscitation traces were analysed. Mean hands-on-chest time improved significantly following feedback and targeted resuscitation training (73.0% vs 79.3%, p = 0.007). There was no significant change in compression rate during the study period. There was a significant reduction in median time-to-shock interval from 20.25 s (IQR 15.50–25.50 s) to 13.45 s (IQR 2.25–22.00 s) (p = 0.006). Automatic rhythm recognition fell from 50% to 28.6% (p = 0.03) following intervention.
Telemetry and analysis of the TTI trace following OHCA allows objective evaluation of the quality of pre-hospital resuscitation. Targeted resuscitation training and ambulance feedback improves the quality of pre-hospital resuscitation. Further studies are required to establish possible survival benefit from this technique.
Transthoracic defibrillation potential gradients in a closed chest porcine model of prolonged spontaneous and electrically induced ventricular fibrillation
2010, Resuscitation
Citation Excerpt :
It has been suggested that pre-shock chest compressions may restore depleted high energy phosphate stores, minimize intracellular calcium accumulation or “wash out” toxic metabolites. These theories have recently been questioned.17 Of note, experimental studies supporting the use of chest compressions before defibrillation have all utilized electrically induced VF in canine or porcine cardiac arrest models with an unobstructed coronary vasculature.
The purpose of this study was to measure the local electrical field or potential gradient, measured with a catheter-based system, required to terminate long duration electrically or ischaemically induced ventricular fibrillation (VF). We hypothesized that prolonged ischaemic VF would be more difficult to terminate when compared to electrically induced VF of similar duration.
Thirty anesthetized and instrumented swine were randomized to electrically induced VF or spontaneous, ischaemically induced VF, produced by balloon occlusion of the left anterior descending coronary artery. After 7 min of VF, chest compressions were initiated and rescue shocks were attempted 1 min later. The potential gradient for each shock was measured and the mean values required for defibrillation compared for the VF groups.
The number of shocks and the shock strength required for termination of VF were not significantly different for the groups. The potential gradient of the first successful defibrillating shock was significantly greater in the spontaneous, occlusion-induced VF group (12.80 ± 2.82 V/cm vs 9.60 ± 2.48 V/cm, p = 0.002). The number of refibrillations was greater in the ischaemic group than in the non-ischaemic electrical group (6 ± 4 vs 1 ± 1, p < 0.001). The number of animals requiring a shock at 360 J was 2.5 times greater for the ischaemic group.
Defibrillation of prolonged VF produced by acute myocardial ischaemia requires a significantly greater potential gradient to terminate than prolonged VF induced by electrical stimulation of the right ventricular endocardium. The VF duration used in this study approximates that occurring in victims of out-of-hospital cardiac arrest. Our findings may be of clinical importance in the management of such patients.

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^☆: A Spanish translated version of the summary of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2007.11.010.

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CommentaryWhy do chest compressions aid delayed defibrillation?☆

Summary

Introduction

Section snippets

The new wisdom

Limitations of the metabolic hypothesis

The complex haemodynamics of cardiac arrest

An alternative view

Implications for resuscitation

Relevance to the ERC guidelines

Conflict of interest

Acknowledgements

Disparate effects of three types of extracellular acidosis on left ventricular function

Am J Physiol Heart Circ Physiol

Cellular mechanisms of ischemia-reperfusion injury

Ann Thorac Surg

No-reflow after cardiac arrest

Intensive Care Med

Resuscitation after cardiac arrest: a 3-phase time-sensitive model

JAMA

Ischemic contracture of the heart: stone heart

Am J Cardiol

Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation.

JAMA

Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial

JAMA

American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 5: Electrical therapies

Circulation

European Resuscitation Council Guidelines for Resuscitation 2005. Section 3. Electrical therapies: automated external defibrillators, defibrillation, cardioversion and pacing

Resuscitation

Myocardial oxygen delivery/consumption during cardiopulmonary resuscitation: a comparison of epinenephrine and phenylephrine

Ann Emerg Med

Treatment of prolonged ventricular fibrillation Immediate countershock versus high-dose epinephrine and CPR preceding countershock

Circulation

Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation

JAMA

Adverse effects of interrupting precordial compression during cardiopulmonary resuscitation

Crit Care Med

Predicting outcome of defibrillation by spectral characterization and nonparametric classification of ventricular fibrillation in patients with out-of-hospital cardiac arrest

Circulation

Effects of interrupting precordial compressions on the calculated probability of defibrillation success during out-of-hospital cardiac arrest

Circulation

Commentary
Why do chest compressions aid delayed defibrillation?☆