Cardiac & Resuscitation

A Double Sequential External Defibrillation Review and Discussion

Issue 12 and Volume 41.

One Tuesday morning, a Bernalillo County Fire Department (BCFD) engine and paramedic rescue unit are dispatched to a 58-year-old male who’s suffering a witnessed cardiac arrest at his home in a very rural service area. They arrive on scene simultaneously with Albuquerque Ambulance, the ALS transport service, nine minutes after the 9-1-1 call.

Family members are providing dispatcher-assisted bystander CPR. The crews jump into action and began resuscitation according to local protocols, which includes manual pit crew CPR for a non-hypoxic adult cardiac arrest (specifically, six minutes of continuous chest compressions and passive/apneic oxygenation via non-rebreather [NRB] with brief interruptions every two minutes to analyze and treat the cardiac rhythm). The Physio-Control LIFEPAK 15 is attached to the patient and, after the first round of EMS provider CPR, the patient’s initial rhythm is coarse v fib.

The crew delivers the first biphasic defibrillation at the maximum energy setting of 360 J using the LIFEPAK. Additionally, the crew places two nasopharyngeal airways, an EtCO2 sampling cannula, and an NRB at 10 Lpm. The initial EtCO2 reading is 27 mmHg, and the patient has spontaneous respirations at 17 breaths per minute throughout the resuscitation. After six minutes of pit crew CPR, the patient remains in v fib and the crew places a laryngeal mask airway supraglottic device (LMA Supreme) and begins positive pressure ventilations. Over the next 25 minutes, the patient is given six doses of 1:10,000 epinephrine, 3 mg/kg of lidocaine, 2 grams of magnesium sulfate, and is defibrillated 11 times using the LIFEPAK at 360 J with anterior-apex pad placement.

The patient remains in refractory v fib despite these interventions, and the crew contacts the on-call EMS physician for further advice. They receive an order for 1 mEq/kg of sodium bicarbonate, and are advised to set up for double sequential external defibrillation (DSED). A second set of pads is placed in the anterior-posterior orientation and attached to a ZOLL E Series monitor, which is the only other manual defibrillator monitor on scene. Neither the crew nor the physician know if the two devices are compatible, but they’re ready try it to help the patient.

The LIFEPAK is charged to its maximum of 360 J, and the ZOLL E series is charged to its maximum of 200 J, and both shock buttons are depressed in rapid sequence. Chest compressions are immediately resumed, and a rapid and sustained increase in EtCO2 to 57 mmHg is observed, which is very promising.

After two minutes of chest compressions with asynchronous ventilations, the rhythm check reveals a narrow complex sinus tachycardia with corresponding palpable carotid and femoral pulses. The patient is started on vasopressor support and maintains return of spontaneous circulation (ROSC) throughout his transport.

Refractory V Fib

V fib has the highest survival rates of any cause of sudden cardiac death.1 It’s a disorganized chaotic electrical activity in the heart causing the muscle to quiver and become unable to contract uniformly or pump blood, resulting in tissue ischemia. Without cardiac output, unconsciousness occurs in seconds and irreversible central nervous system damage begins in just a few minutes, eventually followed by death if not corrected.

V fib almost never spontaneously reverses and defibrillation is the definitive therapy for the lethal cardiac rhythm.

The exact mechanism of v fib isn’t completely understood but often occurs in the setting of acute cardiac ischemia or myocardial infarction. It’s important to mention that v tach often precedes v fib and may be seen if the patient arrests in the presence of EMS or if response times are very short.

Risk factors for v fib may be divided into structural heart disease, nonstructural heart disease and non-cardiac disease. Examples of structural heart disease include: coronary artery disease, cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and valvular heart disease.

Examples of nonstructural heart disease include ion channel abnormalities such as long/short QT syndrome and Brugada syndrome, heart blocks, and idiopathic v fib.

Finally, causes of non-cardiac v fib include drug-induced QT prolongation, aortic dissection, pulmonary embolism, electrolyte or metabolic disturbances, and hypoxia.

Another cause of v fib is a condition called “electrical storm,” in which the myocardium is made hyper-excitable from an uncontrolled surge in adrenaline. In this situation, additional administration of epinephrine can worsen the irritable foci and make the rhythm more refractory. Therefore, an alternate or additional treatment for refractory v fib frequently includes an IV push of beta-blockers or antiarrhythmic at some point in the algorithmic approach to help facilitate conversion.2,3

DSED for refractory v fib or pulseless v tach is a recent hot topic in the national and international EMS arena. The number of interventions needed prior to officially diagnosing refractory v fib varies, but is commonly considered after at least 3–4 standard defibrillation attempts with any device (including public access or provider AEDs or ALS-operated manual devices) and possibly after a full dose of antiarrhythmic medication.

It’s extremely important to note that refractory v fib or v tach is different than recurrent v fib, which is defined as v fib that converts to a different rhythm at some point during the resuscitation and then reverts back to v fib.

It’s also now common practice in EMS systems across the U.S. to begin standard defibrillation at the maximum joule setting for any given defibrillator without progressing through the escalating power settings. This is because the number of shocks needed to terminate v fib or v tach is an independent predictor of survival to hospital discharge.4 DSED has been used successfully both in the hospital and prehospital arenas in adult patients for more than 10 years, and is an excellent treatment option when faced with a truly refractory v fib patient who isn’t responding to standard therapy.5

We don’t know for sure how DSED works, but there are a few theories, including: optimization of the electrical vector direction, increased myocardial surface area affected, and increased power delivered. Standard defibrillation vector change is the most common advised first step.

A vector refers to an electrical force traveling in a certain direction across the myocardium. Because a standard defibrillation travels from one defibrillation pad to the other and back again (biphasic wave), it’s possible we may miss some of the myocardial cells that aren’t aligned with the pads. This could allow “unshocked” cells to remain excitable and available to re-propagate the disorganized rhythm to the rest of the myocardium that was successfully treated. By changing or adding a different vector with DSED, we can affect a larger myocardial surface area, and hopefully reset all the excitable cells at once.

One study proved that defibrillation energy level significantly impacted the success of electrical termination of v fib, and that increased energy levels could be used to overcome suboptimal pad placement.6 Certain patients may benefit from the increased energy level that DSED provides. Each patient has different anatomy and a different transthoracic impedance level that the defibrillator must overcome to deliver an effective shock. Each person has a slightly different size and shape of the heart, different location of the heart in the thoracic cavity, and different positioning of the heart related to body position (e.g., supine or standing). Body habitus also plays a role when delivering shocks; adipose tissue conducts electricity very well, whereas air (e.g., a barrel-chested chronic obstructive pulmonary disease patient) doesn’t conduct electricity as easily.

The ideal combination of pad placement and energy level is being investigated, but it’s also likely different for every patient. The recommended DSED pad placement varies between EMS systems, but often includes some combination of anterior-apex and anterior-posterior positions. Pad placement also varies based on operational practicality, such as avoiding the central chest footprint of a mechanical compression device. (See Figure 1.)

Figure 1: Placement of AED pads during double sequential external defibrillation
Double Sequential External Defibrillation

Dual Shocks

The goal of performing DSED is to perform sequential—not simultaneous—shocks. We don’t yet know what the ideal coordination and timing of the biphasic waves is, but there are some theoretical concerns to getting this right. According to Physio-Control, each biphasic defibrillation takes approximately 0.015 seconds (150 milliseconds) to deliver. If two shocks are delivered in an overlapping fashion within those 150 milliseconds, the positive and negative waves could actually cancel each other out, significantly decreasing the effective current across the heart. Additionally, during those 150 milliseconds, the monitor’s circuit is “closed” and the circuit board is vulnerable to a second device’s shock. One or both devices could possibly be damaged if the shocks are overlapping during those 150 vulnerable milliseconds. At all other times when the monitor is working (i.e., powered on and attached to the patient, but not actively delivering a shock), this circuit is “open” and the machine is shockproof.

As mentioned above, too short of a delay could be ineffective or damage the machine, and there are animal studies that suggest that too long of a delay between double defibrillations would actually be less successful than a single shock alone. This means that if the delay is too long between shocks, the benefit of double sequential shocks is lost, and either the energy threshold needed for successful conversion is increased from the “standard” amount, or the second shock actually re-induces ventricular fibrillation after the first shock converted the rhythm.7,8

Device Compatibility

The official policy from three of the major companies that manufacture defibrillation devices (Physio-Control, ZOLL and Phillips) is that DSED is an off-label use of their device and isn’t recommended. That being said, many of the companies recognize the success of DSED both in hospital and out of hospital for refractory v fib and v tach. There are several unknown details about this procedure (e.g., ideal timing, ideal pad placement, ideal phase of v fib wave) that make it difficult for the manufacturers to give recommendations or to develop a device that performs DSED automatically. Additionally, any change in the current devices’ defibrillation programming would require a lengthy FDA approval process that would include human testing for these extremely rare and hard-to-predict refractory cases. All manufactures suggest maintenance self-checks and possibly sending the device back to the manufacturer to ensure it’s working properly after performing a DSED and before using the device again for another defibrillation. The manufactures are also vague about what performing off-label DSED would mean in regard to device warranty.

We were able to answer one question about device compatibility through our patient. We used two different manufacturer devices: Physio-Control, which delivers a biphasic shock of 360 J, and ZOLL, which delivers a biphasic shock of 200 J. They were compatible and worked effectively together to terminate v fib in our case. Current DSED case studies don’t discuss device compatibility. There are small differences in each device’s type of biphasic waveform (e.g., biphasic truncated exponential, rectilinear biphasic or pulsed biphasic), which explains the different maximum current settings for each one. Despite these differences, based on our experience in this case, it’s reasonable to assume that any biphasic device is compatible with any other biphasic device. Further evidence of device compatibility has been shown by EMS systems that use AEDs combined with manual monitors to deliver the DSED shocks. The only downside to using an AED is that it would have to take time to analyze the rhythm and allow you to charge it before you could deliver the shocks, which would lengthen your pre-shock pauses.

Monophasic monitors are no longer in popular use, so compatibility between monophasic and biphasic devices isn’t known.

Defining Success

DSED success can be considered both in the electrical sense, meaning conversion into a rhythm other than v fib or v tach, or return of spontaneous circulation (ROSC) and neurologically intact outcome. Anecdotally, the survival to hospital discharge for refractory v fib after only standard defibrillations has been very low.

Several case studies are showing electrical success with DSED, but there’s conflicting data regarding the neurologic outcomes of the DSED patients vs. standard defibrillation.1, 9–11

Poor survival reported after DSED may be partially due to delayed use. Many protocols and systems wait until the fifth failed standard defibrillation attempt before using DSED, and the majority of patients require two DSED attempts to terminate v fib.11

Many more studies are needed, but true refractory v fib is a relatively rare event (only 0.1% of all v fib arrests5), making large randomized studies nearly impossible to perform. Consequently, we’re left with only a handful of case series from around the country, which means we should use caution when interpreting these studies and applying them to the general public. One could argue that we should first target electrical success, since it’s easy to measure, and it’s impossible to have any good neurological outcome if the patient never converts out of v fib or v tach.

The v fib amplitude (or “coarseness”) is directly related to the chance of successful defibrillation. The higher the amplitude of the v fib or v tach, the more recent the cardiac arrest (or excellent CPR), and the higher the chance of terminating the arrhythmia with electricity.4 Also, good contact between the skin and the pads is essential for shock success. The surface area of the pads was specifically designed to deliver the optimal shock, so it must have even adhesion to the skin to work properly. Chest hair should be shaved, clothing should be removed, wet skin should be dried, and pads shouldn’t be touching each other. There are studies that suggest there’s minimal risk (but not zero risk) to a provider touching the patient during defibrillation with the newer devices.12,13

It’s possible that in the future we’ll discover a certain phase in the v fib/v tach wave form, or points in the compression-decompression cycle of chest compressions that correlate to higher shock success rates. And, some EMS systems are transporting out-of-hospital cardiac arrest patients in refractory v fib straight to the cath lab with CPR in progress or initiating ECMO (extracorporeal membrane oxygenation) on them while CPR continues.


We still clearly have a lot to learn about optimal cardiac arrest care, CPR and defibrillation, which we used to consider such a basic skill. But it’s clear that DSED makes an excellent tool in the toolbox when confronted with that difficult refractory v fib or unstable v tach patient, and “shockingly,” any two biphasic defibrillators available should do the trick.


1. Daya MR, Schmicker RH, Zive DM, et al. Out-of-hospital cardiac arrest survival improving over time: Results from the Resuscitation Outcomes Consortium (ROC). Resuscitation. 2015;91:108–115.

2. Nademanee K, Taylor R, Bailey WE, et al. Treating electrical storm: sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation. 2000;102(7):742–747.

3. McGovern T, McNamee J. (Nov. 18, 2015.) Emergency interventions for treating cardiac electrical storms. ACEP Now. Retrieved Oct. 24, 2016, from

4. Dalzell GWN, Adgey AAJ. Determinants of successful transthoracic defibrillation and outcome in ventricular fibrillation. British Heart Journal. 1991;65(6):311–316.

5. Hoch DH, Batsford WP, Greenberg SM, et al. Double sequential external shocks for refractory ventricular fibrillation. J Am Coll Cardiol. 1994;23(5):1141–1145.

6. Esibov A, Chapman FW, Melnick SB, et al. Minor variations in electrode pad placement impact defibrillation success. Prehosp Emerg Care. 2015;20(2):292–298.

7. McDaniel WC, Schuder JC, Sweeney RJ, et al. Double pulse transthoracic defibrillation in the calf using percent fibrillation cycle length as spacing determinate. Pacing Clin Electrophysiol. 1999;22(10):1440–1447.

8. Johnson EE, Alferness 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.

9. Cabanas JG, Myers JB, Williams JG, et al. Double sequential external defibrillation in out-of-hospital refractory ventricular fibrillation: A report of ten cases. Prehosp Emerg Care. 2015;19(1):126–130.

10. Lybeck AM, Moy HP, Tan DK. Double sequential defibrillation for refractory ventricular fibrillation: A case report. Prehosp Emerg Care. 2015;19(4):554–557.

11. Merlin MA, Tagore A, Bauter R, et al. A case series of double sequential defibrillation. Prehosp Emerg Care. 2016;20(4):550–553.

12. Lloyd MS, Heeke B, Walter PF, et al. Hands-on defibrillation: An analysis of electrical current flow through rescuers in direct contact with patients during biphasic external defibrillation. Circulation. 2008;117(19): 2510–2514.

13. Perkins GD, Lockey AS. Defibrillation-safety versus efficacy. Resuscitation. 2008;79(1):1–3.


• Fredman CS, Biermann KM, Barold SS, et al. Treatment of refractory ventricular fibrillation by combined internal (epicardial) and eternal (transthoracic) defibrillation. Pacing Clin Electrophysiol. 1996;19(6):1003–1005.

• Kerber RE, Bourland JD, Kallok MJ, et al. Transthoracic defibrillation using sequential and simultaneous dual shock pathways: Experimental studies. Pacing Clin Electrophysiol. 1990;13(2):207–217.

• Jones DL, Klein GJ, Rattes MF, ,et al. Internal cardiac defibrillation: Single and sequential pulses and a variety of lead orientations. Pacing Clin Electrophysiol. 1988;11(5):583–591.

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• 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. (n.d.) American Heart Association. Retrieved Feb. 25, 2016, from