CommentaryWhy do chest compressions aid delayed defibrillation?☆
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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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.