Current emergency cardiovascular care guidelines call for immediate resumption of compressions after defibrillation in out-of-hospital cardiac arrest. These guidelines are based on human and animal data demonstrating the adverse effects of interruptions in chest compression. In studies of animals with prolonged ventricular fibrillation, even if the shock was successful, systolic blood pressure builds gradually, and thus coronary and cerebral blood perfusion is low until well after the initiation of sinus rhythm. In addition, if the shock was not successful, then a period of chest compression before the next defibrillation would increase the likelihood of a successful defibrillation. In human observational data, immediate resumption of chest compressions has been associated with improved survival.

There are, however, animal data showing that chest compressions may cause ventricular activation during asystole or even during sinus rhythm. Chest compression–associated ventricular activation can even cause ventricular fibrillation. This ventricular activation is not unprecedented, as it has been known for decades that chest thumps can cause ventricular activation, and indeed, this method was vital for patients in asystole before the advent of pacing. In addition, chest thumps may terminate ventricular tachycardia, cause ventricular fibrillation if appropriately (or inappropriately, as is really the clinical case) timed during ventricular tachycardia (chest thumping for cardiac arrest) or during sinus rhythm (commotio cordis). The minimal amount of physical energy required to cause ventricular activation is not entirely clear; however, in a commotio cordis model, even baseball impacts of 20 mph (producing a left ventricular pressure increase of as little as 50 mm Hg) cause premature ventricular contractions.

It is thus not surprising that chest compression in humans, especially if vigorous, causes ventricular activation. In the present study, Osorio et al evaluated surface electrocardiographic tracings of automatic external defibrillators and the thoracic impedance data collected by the defibrillators to ascertain ventricular depolarization and chest compression, respectively. Of necessity, ventricular depolarization can be seen only in nonventricular fibrillation situations and thus only in asystole or relatively bradycardic rhythms. Although the tracings demonstrated significant artifacts, there are relatively convincing data that chest compressions caused ventricular depolarization in 7 of 24 patients. However, the association of ventricular fibrillation with chest compression was less convincing. Although ventricular fibrillation was more likely to occur during chest compression than at other time periods, chest compressions should have been performed for most of the time period.

Although concerning, these results are far from conclusive, as Osorio et al themselves admit. Still, because they are biologically plausible, they do raise concern. The 2005 and 2010 emergency cardiovascular care and basic life support guidelines call for more attention to chest compression and do call for immediate resumption of chest compressions without a pulse or rhythm check after defibrillation. These guidelines with an increased focus on chest compressions have been associated with improved survival after out-of-hospital arrest.

What clinical pearls can we take away from this intriguing study? First, the treatment of out-of-hospital arrest should not be altered by this observational study: chest compressions should immediately follow defibrillation. We should be cognizant that ventricular fibrillation may recur, and thus repeat defibrillation may be needed. Second, we need more data to evaluate whether chest compressions may directly trigger ventricular fibrillation and, if so, means to prevent this unwanted arrhythmia. And third, for short time periods of ventricular fibrillation, such as that seen with in-hospital arrests with direct access to defibrillation and thus relatively short ventricular fibrillation times, it is prudent to check the rhythm and pulse before the initiation of chest compressions. Certainly, as has been observed in patients with implantable defibrillators and those patients on cardiac wards, short periods of ventricular fibrillation are generally easily defibrillated with immediate resumption of pulse and blood pressure.