Precordial thump for cardiac arrest is effective for asystole but not for ventricular fibrillation
Received 28 April 2009; accepted 20 June 2009. published online 29 June 2009.
Background
Precordial thump for cardiac arrest remains controversial. Although precordial blows can trigger ventricular fibrillation (VF) (i.e., commotio cordis), they paradoxically have been regarded as potential therapy for cardiac arrest. In commotio cordis, impact energy and resultant peak left ventricular (LV) pressure are important variables in VF initiation.
Objective
The purpose of this study was to assess the relationship between LV pressures generated by thumps and their effectiveness in defibrillation of VF or resuscitation of asystole after defibrillation.
Methods
After induction of VF, 10 swine each received 18 chest thumps; two sets of three thumps each with a clenched fist, a 30-mph lacrosse ball, and a 40-mph lacrosse ball. If asystole followed defibrillation, manual thumps were given to induce ventricular depolarizations until resumption of spontaneous rhythm.
Results
During VF, generated LV pressure (mmHg) was 263 ± 52 with manual thumps, 392 ± 179 with 30-mph ball thumps, and 616 ± 182 with 40-mph ball thumps (P <.001). None of the 180 thumps terminated VF. All episodes required electrical defibrillation. During asystole, generated LV pressures were greater for thumps that induced ventricular depolarizations than for those that did not (111 ± 27 mmHg vs 73 ± 23 mmHg, P <.001). A significant association was observed between induction of ventricular depolarizations and thump-generated LV pressures (odds ratio 2.0 per 10 mmHg rise in LV pressure, 95% confidence interval 1.8–2.1).
Conclusion
Despite generating high LV pressures, precordial thumps were not effective in terminating VF. Based on these data, precordial thump for VF in cardiac arrest victims cannot be recommended but for asystolic victims might be beneficial.
⁎Cardiac Arrhythmia Center, Division of Cardiology, Tufts Medical Center, Boston, Massachusetts
†Minneapolis Heart Institute Foundation, Minneapolis, Minnesota
‡Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, Massachusetts
Address reprint requests and correspondence: Dr. Mark S. Link, Cardiac Arrhythmia Center, Division of Cardiology, Tufts Medical Center, 800 Washington Street, Box 197, Boston, Massachusetts 02111
Funding for this study was provided by the Louis J. Acompora Foundation.
ABSTRACT