Do or die?

Double defibrillation, harnessing two defibrillators to administer simultaneous or double sequential shocks (sometimes called the “one-two punch”), has seen increased use among various EMS agencies.

Though well-intentioned and considered by some as an innovative approach to treating shock-resistant ventricular fibrillation (v fib), biphasic double defibrillation is also controversial, off-label and poorly studied.

What Do We Actually Know?

Double defibrillation is based on the belief that a very high energy shock (achieved by coupling two defibrillators) is needed when v fib is unresponsive to a series of standard shocks at maximum output. How often is this necessary?

Studies have shown that while many patients with out-of-hospital cardiac arrest require multiple shocks during the course of care, the vast majority of v fib cardiac arrests ultimately prove to be shock-terminated, making shock-refractory v fib a relatively rare event for the added equipment and training double defibrillation requires.1,2

Nonetheless, just the possibility of shock failure seemingly begs the need for alternative approaches to such patients, whether that be higher energy “double” shocks or something else. This said, a potential problem with a high-energy, double shock approach to v fib is that electricity, like drug therapies, also has dose-dependent toxicity.

In the case of drugs, this is exemplified by the ill-effects from high doses of antiarrhythmic drugs3 or epinephrine,4 and (in the case of electricity) by the injuries sustained from things like accidental electrocution.

Similarly, clinical and experimental studies have shown that higher peak currents resulting from high energy defibrillation can be pro-arrhythmic. These excessively high currents reduce rather than enhance defibrillation success and may actually promote v fib/v tach,5-8 a concern that could also apply when lower biphasic shock energies are substantially increased by double defibrillation. This approach also raises additional questions and challenges.

How Often Is Post-Shock V Fib Truly Shock-Resistant?

More often than not, so-called shock-resistant v fib is a victim of mistaken identity. In most patients with cardiac arrest, the v fib seen after one or more shocks is the result of its recurrence, not shock-resistance.

By definition, v fib that can’t be terminated by shock is shock-resistant; whereas v fib that returns sometime after being successfully terminated, is considered recurrent.

Distinguishing between these two presentations of post-shock v fib can be clinically challenging since, under current American Heart Association Guidelines, CPR is typically resumed immediately after shock delivery. During this time, the ECG is usually distorted by chest compression artifact and not easily interpretable until the next pause in CPR about two minutes later.

In studies where rhythms during these two minute periods of post-shock CPR were formally analyzed by experts using techniques that minimized chest compression artifact, v fib was most often found to have been successfully terminated by the shock; but its effects were short-lived because v fib subsequently recurred.1,9

Such recurrent v fib is usually caused by ongoing myocardial ischemia or other characteristics of the heart fostering electrical instability, not shock failure, and is best treated with rhythm-stabilizing drugs or other medical measures along with standard shocks. Deploying dual shocks in such circumstances isn’t only unnecessary, but hazardous.

In addition to risking greater electrical injury to the heart, dual shocks can expose the circuitry of one defibrillator to a large shock from the other, potentially damaging one or both devices and rendering them useless.10 Accordingly, this practice is discouraged by all defibrillator manufacturers.

Why Do Shocks Sometimes Fail?

The answer here requires a brief lesson in electricity. Defibrillator settings are displayed as joules, but “joules” don’t actually defibrillate the heart; it’s current (amps) applied over time that accomplishes this task.6 Here’s how it happens. The defibrillator shock creates a voltage gradient through the tissues between the patient’s two electrode pads (i.e., high voltage on one end, and low voltage on the other). Sustaining this voltage gradient for a sufficient time interval is what ultimately “pushes” enough current across the heart, resulting in defibrillation.

The magnitude of the current, in turn, depends on the resistance between the two pads. This resistance is related to electrode size and skin contact, along with the resistance of the organs lying between the electrodes.

Anything that increases resistance along the path of this voltage gradient results in a smaller current. For example, if the interface between the patches and skin creates an unusually high resistance, much of the energy from the defibrillator will be dissipated in the patches or at the skin level, with little current making its way to the heart.

This often occurs because of poor electrical contact between the pads and skin. Resistance-not energy-is often the major roadblock to effective defibrillation. Although applying higher energy can partly compensate for the problem, if resistance itself isn’t addressed, the effort will usually be self-defeating.

Suboptimal defibrillator pad location is yet another correctable obstacle to successful defibrillation.11 Defibrillator pads that fail to encompass the heart completely (by being located too high, too low, or too medially in relation to the heart) may misdirect needed current to surrounding organs instead of to the heart itself, resulting in a failed shock regardless of its strength.

If placed too close together, the current will take the path of least resistance and be shunted between the patch electrodes themselves, bypassing the heart completely.

The direction of current flow across the heart can also be a factor in defibrillation success. Biphasic defibrillation takes advantage of this by changing the direction of the shock in midstream, resulting in a current that heads in one direction, followed by taking the opposite direction.

Similarly, changing pad location (e.g., from anterolateral to anterior-posterior) creates a differently-oriented shock. Because this shock traverses the heart from an alternate direction, it might more effectively reach different regions of fibrillating myocardium.

Indeed, the success frequently attributed to dual defibrillator shocks may be due to differences in pad location and the altered direction of the second shock compared to the first, rather than to the effects from the dual shock itself.

Finally, defibrillation also has an element of chance. During v fib, cells in the heart are in varying states of depolarization, repolarization or resting. Each state responds differently to shock, such that the effect of a shock can vary from one moment to the next depending on the phase of those cells at that instant.12

This explains why, all other things being equal, an identical energy shock may defibrillate on one occasion but not on another. In fact, the occasional apparent efficacy of a double shock doesn’t necessarily mean that another standard shock wouldn’t have worked as well!

If Used, How Quickly Should Dual Defibrillator Shocks Be Given?

Timing is critical when successive shocks are administered from two separate defibrillators, and is perhaps the least appreciated pitfall of dual defibrillation. Human reaction time is about 200 milliseconds (0.2 seconds).

Thus, even one person pushing two separate buttons on two separate defibrillators, whether simultaneously or sequentially, doesn’t guarantee that the resulting shocks will be administered with the desired timing; these can be off-target by 200 milliseconds in any direction. By comparison, the therapeutic window for double shocks is much shorter and its margin of safety extremely narrow.

To illustrate, experimental work has shown that the interval between the delivery of dual biphasic shocks must either be < 10 milliseconds (0.01 seconds) or 75-125 milliseconds (0.075-0.125 seconds) apart to improve defibrillation efficacy; whereas if the second shock follows the first by longer periods, its effects are more likely to be one-in-the-same as two separately administered single shocks.

More ominous, if the delay between the each of the dual shocks is 10-75 milliseconds (0.01-0.075 seconds), v fib becomes more difficult to defibrillate or can even result in the re-induction of v fib by the second shock that had already been terminated by the first one.13

In sum, the degree of precision in button-pushing required to safely and effectively administer dual biphasic shocks isn’t only daunting, but in light of reaction time probably not even close to achievable by human hands.

Are Dual Shocks Still Biphasic?

The simple answer to this question is yes and no. Unlike monophasic shock, the biphasic waveform consists of two phases: an initially “positive” wave (creating a current going in one direction) followed almost immediately by a “negative” wave (or current going in the opposite direction).

The “two-waves-in-one” make the biphasic waveform more effective than monophasic shock, but also more complicated and less suitable for dual defibrillation. This is because double defibrillator shocks result in the superimposition or cancellation of one or the other (or both) of these biphasic shock waves, depending on shock timing and pad location. For example, if the timing of shock delivery is such that the two positive waves from a double shock happen to be partly or completely superimposed upon one another, the resulting higher voltage gradient will result in some regions of the heart receiving a greater or even excessive amount of current.

Alternatively, if the timing and direction of a double shock is such that the positive wave from one shock is partially or wholly cancelled by the negative wave of another, the resulting lower voltage gradient means other fibrillating regions of the heart may receive little or no current at all.

Double defibrillation can thus create a myriad of augmented and cancelled shock waves whose net effect on
v fib becomes an uncertain and potentially risky gamble. Some might even dare say, a “crapshoot.”

Are There Better Alternatives?

To date, evidence supporting a benefit from dual defibrillator biphasic shocks rests entirely on isolated case reports or small case series with mixed outcomes. Understandably, resorting to dual defibrillator shock stems from an imperative to “do something!” when other resuscitation interventions and therapies appear to be failing. The question, however, is whether there are other, better alternatives for treating such patients? Consider these:

1. Is the v fib/v tach truly shock-refractory, or just recurrent? If recurrent, a change in shock energy is unlikely to be helpful. Such patients are better benefitted by other rhythm-stabilizing medical interventions.

2. Are defibrillator pads optimally positioned?

3. Can resistance be minimized? Applying manual pressure to pads can help lower resistance at the electrode pad-skin interface. Using gloved hands, press a thick, folded dry towel(s) on one or both pads during shock delivery. This can substantially reduce pad resistance, resulting in higher defibrillation success.14

4. Should defibrillator pads be relocated? Administering shocks in a different direction (e.g., anterior-posterior vs. anterolateral) might afford greater success.

5. Is this a circumstance where rapid transport to a cardiac catheterization laboratory is the ultimate solution? Shock-refractory v fib and recurrent polymorphic ventricular tachycardia are common signs of acute myocardial ischemia and infarction, which may only be correctable by emergent revascularization.

Summary

Apart from anecdotal reports, there’s little clinical evidence to support a benefit from double defibrillator biphasic shock. Conversely, there are substantial reasons to question its safety, efficacy and necessity. More research is needed before dual defibrillation is deployed clinically. In the interim, given the other available approaches to treat refractory v fib, it’s best to consider the sage advice from Hippocrates himself: Primum non nocere, or, first, do no harm.

References

1. Kudenchuk PJ, Cobb LA, Copass MK, et al. Transthoracic incremental monophasic versus biphasic defibrillation by emergency responders (TIMBER): A randomized comparison of monophasic with biphasic waveform ascending energy defibrillation for the resuscitation of out-of-hospital cardiac arrest due to ventricular fibrillation. Circulation. 2006;114(19):2010-2018.

2. Holmen J, Hollenberg J, Claesson A, et al. Survival in ventricular fibrillation with emphasis on the number of defibrillations in relation to other factors at resuscitation. Resuscitation. 2017;113:33-38.

3. Brown DL, Skiendzielewski JJ. Lidocaine toxicity. Ann Emerg Med. 1980;9(12):627-629.

4. Stiell IG, Hebert PC, Weitzman BN, et al. High-dose epinephrine in adult cardiac arrest. N Engl J Med. 1992;327(15):1045-1050.

5. Jones JL, Jones R. Postshock arrhythmias-A possible cause of unsuccessful defibrillation. Crit Care Med. 1980;8(3):167-171.

6. Kerber RE, Martins JB, Kienzle MG, et al. Energy, current and success in defibrillation and cardioversion. Circulation. 1988;77(5):1038-1046.

7. Tung L, Tovar O, Neunlist M, et al. Effects of strong electrical shock on cardiac muscle tissue. Ann N Y Acad Sci. 1994;720(1):160-175.

8. Buensch DP, Hu J, Fischer K, et al. T1 and T2 mapping detect myocardial edema after repeated 200J electrical cardioversion. J Cardiovasc Mag Reson. 2014;16(Suppl 1):P157.

9. van Alem AP, Chapman FW, Lankj P, et al. A prospective, randomized and blinded comparison of first shock success of monophasic and biphasic waveforms in out-of-hospital cardiac arrest. Resuscitation. 2003;58(1):17-24.

10. Gerstein NS, McLean AR, Stecker EC, et al. External defibrillator damage associated with attempted synchronized dual-dose cardioversion. Ann Emerg Med. May 27, 2017. [Epub before print.]

11. Esibov A, Chapman FW, Melnick SB, et al. Minor variations in electrode pad placement impact defibrillation success. Prehosp Emerg Care. 2016;20(2):292-298.

12. Dosdall DJ, Fast VG, Ideker RE. Mechanisms of defibrillation. Annu Rev Biomed Eng. 2010;12:233-258.

13. Johnson EE, Alfernes CA, Wolf PD, et al. Effect of pulse separation between two sequential biphasic shocks given over different lead configurations on ventricular defibrillation efficacy. Circulation. 1992;85(6):2267-2274.

14. Persse DE, Dzwonczyk PE, Brown CG. Effect of application of force to self-adhesive defibrillator pads on transthoracic electrical impedance and countershock success. Ann Emerg Med. 1999;34(2):129-133.