Pharmacological Agents Post-DSD
None of the patients in the study by Hoch et al5 received any pharmacological agents between initial unsuccessful attempts at defibrillation and the final application of DSD. As previously noted, all three of the patients in our cases had the full support of ED personnel, as well as the administration of appropriate pharmacological agents.
A randomized controlled trial published in 2006 by Hohnloser et al9 reported clinically significant results in studying the effects of antiarrhythmic agents, particularly amiodarone and sotalol, on defibrillation thresholds. They found that amiodarone increased the defibrillation threshold by 1.29 J, while sotalol decreased the defibrillation threshold by 0.89 J. However, despite their findings, Hohnloser et al9 believed that such differences were highly unlikely to influence patient outcomes.
Post-DSD Effects
The short- and long-term effects of DSD on the human body are unknown. Since the mechanism responsible for the efficacy of DSD is still unclear, many professionals and researchers are concerned that doubling the energy could cause myocardial damage. Although successful return of spontaneous circulation is an important first step in a successful resuscitation, the ultimate goal is to have a patient who is neurologically intact at the time of discharge home, with the capability of maintaining a favorable quality of life.
In 2016, Ross et al10 conducted a larger study comparing CPC scores of 279 patients in refractory V-fib, who received single shock (229 patients) vs DSD (50 patients). They found no statistically significant differences in neurologically intact survival rates between the two groups. This is an important finding that should be the goal for any future studies regarding DSD.10
Limitations to Future Research
For researchers to provide DSD results considered clinically significant, more cross-sectional, randomized-controlled studies need to be performed. Such studies will require a tremendous amount of time, effort, data collection, and a substantial sample size to prove that positive DSD results are not due to chance. As previously noted, the relatively rare incidence of true refractory V-fib makes it difficult for researchers to obtain large enough sample sizes to demonstrate clinically significant study results. Additionally, since medical institutions tend to adhere to different guidelines when running a code for cardiac arrest it would involve extraordinary measures to create and impose a single, standardized procedure/protocol for research purposes that each hospital would have to unanimously agree on.
Another limitation to producing large-scale, clinically significant research is that there is no universally accepted definition of refractory V-fib/pulseless V-tach. In all three of our cases, we defined it as V-fib/pulseless V-tach does not convert after three or more standard shocks, and at least one dose of either IV epinephrine and/or amiodarone. However, other clinicians and institutions define refractory V-fib as patients remaining in cardiac arrest for which the initial rhythm was either V-fib or V-tach, despite at least three defibrillation attempts, 3 mg of epinephrine, and 300 mg of amiodarone.11,12Importantly, DSD currently is neither endorsed as a standard of care nor recommended as part of the ACLS/American Heart Association/American College of Cardiology guidelines.
Conclusion
For every minute a patient remains in V-fib, the chance of survival decreases. Although the application of DSD has not been standardized at this time, we feel that it is a reasonable treatment option for patients in V-fib and pulseless V-tach, after all conventional interventions have failed. Though studies on DSD to date, as well as the three cases presented here, all involved relatively small sample sizes and isolated case reports, the results seem to suggest that DSD does improve chance of ROSC. We believe that DSD deserves further study and may be considered in cases of refractory V-fib and pulseless V-tach.