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Ventricular pacing threshold after transthoracic external defibrillation with two different waveforms: an experimental study

Antonio Carlos Assumpção, Pedro Paulo Martins de Oliveira, Karlos Alexandre de Souza Vilarinho, Pirooz Eghtesady, Lindemberg Mota Silveira Filho, Carlos Fernando Ramos Lavagnoli, Elaine Soraya Barbosa de Oliveira Severino, Orlando Petrucci
DOI: http://dx.doi.org/10.1093/europace/eus288 297-302 First published online: 9 November 2012


Aims Although an increase in the ventricular pacing threshold (VPT) has been observed after administration of transthoracic shock for ventricular defibrillation, few studies have evaluated the phenomenon with respect to the defibrillation waveform energy. Therefore, this study examined the VPT behaviour after transthoracic shock with a monophasic or biphasic energy waveform.

Method and results Domestic Landrace male piglets implanted with a permanent pacemaker stimulation system were divided into three groups: no ventricular fibrillation (VF) induction and transthoracic shock with monophasic or biphasic energy (group I); VF induction, 1 min of observation without intervention, 2 min of external cardiac massage, and transthoracic shock with monophasic or biphasic energy (group II); and VF induction, 2 min of observation without intervention, 4 min of external cardiac massage, and transthoracic shock with monophasic or biphasic energy (group III). After external shock, the VPT was evaluated every minute for 10 min. A total of 143 experiments were performed. At the end of the observation period, groups I and II showed steady VPT values. Group III showed an increase in VPT with monophasic or biphasic external energy, with no difference between the external energy sources. The monophasic but not the biphasic waveform was associated with higher VPT values when the VF was longer.

Conclusion Defibrillation does not have a significant impact on pacing threshold, but a longer VF period is related to a higher VPT after defibrillation with monophasic waveform.

  • Pacing threshold
  • Electric countershock
  • Electric defibrillation
  • Monophasic shock
  • Biphasic shock

What's new?

  • Defibrillation does not appear to have a significant impact on pacing threshold.

  • Longer periods of ventricular fibrillation should receive a biphasic energy source in terms of the postcardioversion ventricular threshold.


More than 200 000 automated external defibrillators (AEDs) are sold yearly in the USA The use of AEDs in communities is associated with higher indices of survival after out-of-hospital cardiac arrest.1 Dysfunction of the sinoatrial node increases with age, with the highest incidence among individuals over 65 years. Because elderly individuals are predicted to account for 30% of the Western population by 2040,2 the number of patients with implanted pacemaker devices and the occurrence of out-of-hospital cardiac arrests are expected to increase in coming years.1

Ventricular capture is mandatory in pacemaker-dependent patients, especially immediately after external countershock within 10min of a cardiac arrest event.3 Several studies have examined pacemaker malfunction and/or ventricular pacing threshold (VPT) increase after transthoracic countershock.46 More recently, studies have evaluated VPT performance after monophasic or biphasic waveform defibrillation from an implanted pacemaker-cardioverter defibrillator.7,8 Nevertheless, the behaviour of the VPT immediately after a counter transthoracic shock remains unclear.

The aims of the present study were to examine changes in the VPT and ventricular electrograph amplitude before, immediately after, and during recovery from an effective transthoracic shock, and to compare biphasic vs. monophasic waveform defibrillation in a relevant animal model of out-of-hospital cardiac arrest.


Animal preparation and pacemaker implant procedure

After approval was obtained from the local ethics committee, experiments were performed with domestic Landrace male piglets weighing 20–30 kg. The animals were anaesthetized with intravenous pentobarbital (20 mg/kg) and intramuscular ketamine (20 mg/kg). Animals were intubated with a cuffed endotracheal tube and maintained on isofluorane inhalant (0.5–2.0%). All experimental protocols were performed in accordance with the standards of the Brazilian Council in Animal Experimentation (COBEA) and the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85-23, revised 1996).

The right internal jugular vein was exposed. A bipolar lead (Setrox S 53, Biotronik, Germany) was introduced and advanced to the right ventricular apex under fluoroscopic guidance. The lead was connected to an ICS-3000 pacemaker analyser (Biotronik, Germany) to measure the pacing threshold, R-wave amplitude, and impedance in both the bipolar and unipolar modes. The pacemaker box (Philos SR, Biotronik, Germany) was connected to the lead after the initial measurements. The pacemaker was implanted in a subcutaneous pocket in the right neck of the animal. After the animals recovered from anaesthesia, they were provided with food and water ad libitum for 15 days for postoperative recovery.

Randomization into groups

The groups were computer randomly assigned to one of the following protocols. Group I was exposed to external shock without induction of ventricular fibrillation. Group II was subjected to VF induction for 1min without intervention, 2min of external cardiac massage (CPR), and transthoracic cardiac defibrillation shock. Group III was subjected to VF induction for 2min without intervention, 4min of external cardiac massage, and transthoracic cardiac defibrillation shock.

Induction of VF and cardioversion protocol

At 15 days after pacemaker implant surgery, each animal was anaesthetized with 1.0 mg/kg of propofol. The animals were intubated, and supplemental doses of propofol were administered to keep the animal unconscious and breathing spontaneously. The animals were only actively ventilated during initiation of the external cardiac massage, mimicking the scenario of out-of-hospital cardiac arrest with paramedic assistance initiation after 1 or 2min of cardiac arrest. Pacing threshold, R-wave amplitude, and impedance were recorded with the ICS-3000 pacemaker analyser. Animals were monitored by surface electrocardiography (EP-Tracer, CardioTek, Amerikalaan, Netherlands).

A 22-gauge Quincke needle was inserted through the skin in the subxyphoid position with a cephalic orientation until heart puncture, which was confirmed by the rhythmic movement of the needle. In groups II and III, VF was induced for 3s with a 60 Hz alternating current (9 V) through the Quincke needle. The VF was confirmed by surface electrocardiography, which was maintained throughout the entire experimental protocol. The Quincke needle was removed after VF was established.

Animals were randomly assigned to receive either monophasic or biphasic energy waveform. For transthoracic cardiac defibrillation shock, 360 J were administered by a damped sine monophasic (Codemaster XL +, Hewlett-Packard) or a rectangular biphasic waveform (Cardiomax, Instramed).

At protocol completion, the animals were recovered from anaesthesia and were rested for 2 weeks. After this resting period, the animals were again anaesthetized as described in this subsection, randomized to a different protocol and energy source (monophasic vs. biphasic) employed previously, and submitted to the same experiment design. Before every new experiment, the threshold ventricular capture and lead stability were checked with the specific analyser. Lead placement was checked by radioscopy to ensure that the data were comparable between the groups.

Determination of ventricular pacing threshold

Parameters of the ventricular pacing, such as VPT, R-wave amplitude, and impedance, were measured with a pacemaker analyser before transthoracic shock. The VPT was determined after successful defibrillation and at 1 min intervals for 10min. The VPT was determined by decreasing the pacing output voltage by 0.1 V (starting from 5.0 V, with a fixed pulse width of 0.5 ms) until loss of capture, and then increasing the output voltage until capture recurred. The impedance was measured at 0.5 ms and 5.0 V.

Statistical analysis

The results are reported by comparing the threshold ventricular capture differences between the three groups and the differences between the two types of energy delivery during transthoracic shock (i.e. monophasic vs. biphasic). Continuous variables are reported as means ± SDs. Categorical variables are reported as medians and 95% confidence intervals of the medians. Comparisons were made with two-way analysis of variance for repeated measurements, and the Bonferroni post-hoc test for multiple comparisons was applied as needed. Comparisons for impedance and R-wave amplitude within each group were made with the Student's t-test for paired experiments. Comparisons of the number of necessary shocks in every experiment were made with the Mann–Whitney test. Statistical analyses were performed with the Statistical Package for Social Sciences (SPSS, version 20 for Macintosh). A P value < 0.05 was considered statistically significant.


A total of 143 complete protocols were carried out in 31 animals. Figure 1 shows a flowchart of the experiments. Among the 31 animals included in the study, we observed two lead displacements after external shock and eight defibrillation failures with animal demise (Figure 1). All of the defibrillation failures occurred in group III, including three animals with the biphasic and five animals with the monophasic external energy source. The number of necessary shocks until VF termination or animal demise in every protocol was similar in all groups (Table 1).

View this table:
Table 1

Number of shocks in every protocol

GroupExternal energyNumber of shocks Median (95% CI)Highest/lowest frequency of shocksP
IMonophasic1 (1 to 1)9/10.98
Biphasic1 (1 to 1)4/1
IIMonophasic1 (1 to 1.43)8/10.53
Biphasic1 (1 to 2.65)13/1
IIIMonophasic1 (1 to 1)2/10.59
Biphasic1 (1 to 1)8/1
  • Highest and lowest frequency of shocks for VF termination or animal demise in every protocol.

  • P value with Mann–Whitney test. 95% CI: 95% confidence interval for the median.

Figure 1

Flowchart of the 143 completed experiments. A total of 35 implanted pacemakers were studied, with four animals being excluded from the study.

Ventricular capture threshold

Group I (external shock without VF induction) showed very steady ventricular capture threshold values during the entire observation period (P = 0.71), with no differences between the monophasic and biphasic external energy sources (Figure 2A). Similar behaviour was seen in group II (VF induction, 1 min of observation, 2 min of CPR, and external shock), with steady ventricular capture threshold values for both monophasic and biphasic energy sources (Figure 2B). In group III (VF induction, 2 min of observation, 4 min of CPR, and external shock), the ventricular capture threshold values increased in both groups during the observation period (P < 0.001), but no differences were observed between the external energy sources (P = 0.79, Figure 2C).

Figure 2

Ventricular capture threshold in group I (A), group II (B), and group III (C). Data are expressed as means ± standard errors of the mean (SEM).

Biphasic vs. monophasic external energy source

Additional analyses were made considering a single external shock source and comparing two distinct protocols of ventricular induction or simple external transthoracic shock without VF.

Animals that received monophasic external shock showed increased ventricular capture threshold values when they underwent VF for 2min and external cardiac massage for 4min (group III) compared to the two other protocols (i.e. 1 min of VF + 2 min of external cardiac massage, or external shock without VF induction; P = 0.02). These differences were observed from 4min after external shock delivery until the end of the observation period (Figure 3A). Animals that underwent biphasic external shock displayed increased ventricular capture threshold overall (P = 0.016), with no differences among the three groups (P = 0.313, Figure 3B). The R-wave amplitude and lead impedance before and after an external shock showed no differences among the groups (Table 2).

View this table:
Table 2

Impedance and R–wave amplitude

GroupExternal energyImpedancePR waveP
IMonophasic458.74 ± 131.87432.14 ± 95.530.0511.07 ± 4.8611.55 ± 4.660.29
Biphasic450.70 ± 161.49453.39 ± 146.230.9310.24 ± 4.8311.31 ± 5.410.12
IIMonophasic418.84 ± 107.87401.62 ± 64.030.1910.45 ± 4.6111.34 ± 4.980.14
Biphasic411.22 ± 94.13400.73 ± 65.670.3710.09 ± 4.8210.95 ± 4.660.14
IIIMonophasic447.54 ± 102.48433.33 ± 78.550.3611.94 ± 5.5413.09 ± 5.000.08
Biphasic432.56 ± 97.04442.03 ± 111.420.6211.04 ± 4.2911.30 ± 4.480.48
  • P value before and after shock by Student's t-test for paired experiments.

  • a10 min after transthoracic external energy delivery.

Figure 3

Ventricular capture threshold with monophasic (A) or biphasic external shock (B). *P < 0.05 and **P < 0.001 by Bonferroni post-hoc test for multiple comparisons. Data are expressed as means ± standard errors of the mean (SEM).


This study investigated the safety, effectiveness, and behaviour of ventricular lead, ventricular electrograph amplitude, and ventricular threshold capture after defibrillation with two different external energy sources in a single contemporary device. We observed a stable lead impedance and ventricular electrograph amplitude after transthoracic external defibrillation shock with both biphasic and monophasic energy sources, which demonstrated the safe use of either energy source for the implanted stimulation system in terms of its integrity. Nevertheless, animals with a longer cardiopulmonary arrest displayed a higher ventricular threshold when the monophasic energy source was used compared to animals with no cardiopulmonary arrest in a clinically relevant model of out-of-hospital cardiac arrest. Unexpectedly, the use of a biphasic energy source of defibrillation was similar in all three protocols, in terms of the ventricular threshold values for stimulation.

These findings suggest the safety of external shocks in two different clinical situations considering post-shock ventricular threshold capture: external cardioversion for atrial fibrillation (group I) and external defibrillation in patients with out-of-hospital cardiac arrest (groups II and III). Because use of the monophasic waveform in group III was associated with an increased ventricular threshold, use of a biphasic energy source seems to be safer in the out-of-hospital cardiac arrest scenario in patients with implanted pacemaker devices. Moreover, by utilizing a contemporary cardiac stimulation system, our results provide concrete information regarding the safety of external transthoracic shocks for defibrillation in victims of out-of-hospital cardiac arrest with implanted pacemakers.

Although several reports have shown an increase of ventricular threshold capture in patients with pacemakers,912 few studies have reported the consequences of using external defibrillation in these patients.13 In a prospective randomized trial, Manegold et al.14 evaluated the safety and efficacy of monophasic vs. biphasic external cardioversion of atrial fibrillation in 44 patients with five different brands of implanted rhythm devices. They observed no lead or device dysfunction after external shock delivery. However, they used a different protocol for energy delivery than the present paper, applying a maximum of four shocks at escalating doses (biphasic shocks: 10, 150, 2 × 200 J, monophasic shocks: 200, 300, 2 × 360 J). In contrast, we applied 360 J at every shock until VF was terminated or until the animal died.

In group III, we observed an increase in the pacing threshold after external cardiac massage for 4min and defibrillation with monophasic energy, simulating a clinical scenario of an out-of-hospital cardiac arrest. Similar behaviour was not observed when biphasic energy was administered.

The anaesthetic drug utilized during the VF induction (propofol) has negative effects on heart chronotropism and inotropism, but these effects have been reported to be clinically and experimentally safe.1517 All animals received the same anaesthetic protocol. Therefore, we believe that the observed differences were due to the external energy source or VF duration.

Although the mechanism by which the pacing threshold increases after a defibrillation shock is not clear, potentially responsible elements may include pacing electrode polarization, displacement of the pacing lead by the electrical shock, or myocardial hypoxia due to VF.8 In an experimental setting with dogs on bypass, Reiter et al.18 observed an increase in the threshold ventricular capture with longer periods of preceding ventricular defibrillation. Although they did not observe any relationship between defibrillation energy and the subsequent pacing threshold, they only evaluated internal vs. external defibrillation with a monophasic energy defibrillator. Their findings support ours in terms of the increased capture threshold in group III when a monophasic energy source was used.

In this same paper, Reiter et al. evaluated the ventricular threshold at different levels of partial pressure of oxygen (PO2) during the cardiopulmonary bypass and observed higher pacing thresholds with lower PO2 levels. They concluded that the pacing threshold is increased by sufficient duration of VF to create substantial myocardial hypoxemia. We believe that the observed increase of the pacing threshold in group III with monophasic energy is supported by the findings of Reiter et al., and that perhaps the myocardial ischaemia played an important role. However, we cannot confirm this hypothesis because such information is beyond the protocol design of the present study.

Study limitations

In our study, the pacing threshold was determined with decrementing stimuli during constant rate pacing. This technique was utilized to minimize the effect of post-cardioversion bradycardia,19 but should not affect the validity of our observations. It is difficult to determine whether changes in pacing threshold after a defibrillation shock are due to metabolic deterioration of the myocardium during VF. However, in the present model, we observed differences between the two energy sources in the same scenario in group III. We cannot infer that these differences are clinically relevant. The model used here is not associated with a structural heart disease (e.g. myocardium infarction or coronary artery disease) such as occurs in patients with ventricular fibrillation. However, similar models as those used in the present paper have been reported in the literature.2023


Defibrillation does not appear to have a significant impact on pacing threshold. However, the duration of the preceding VF is related to the change in pacing threshold shortly after defibrillation. Our data indicate that longer periods of VF should receive a biphasic energy source in terms of the post-cardioversion ventricular threshold.

Conflict of interest: none declared.


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