Chapter 12 / External Defibrillation



External Defibrillation
Gregory P. Walcott, MD,
Cheryl R. Killingsworth, DVM, PhD,
and Raymond E. Ideker, MD, PhD

The history of applying electrical shocks to the heart began in the 1700s with direct
current derived from a Leyden jar. In 1775, Abildgard described having shocked a
chicken into lifelessness and on repeating the shock, bringing the bird back to life (1).
Transthoracic defibrillation was first performed clinically in the mid-1950s when Zoll
introduced the alternating current (AC) defibrillator (2). Several years later, Lown
introduced the direct current (DC) defibrillator as an improvement on Zoll’s device in
several important areas, specifically that it caused less damage to the patient and that
it could be made portable (3). Today, internal cardioverter defibrillators are the size of
a small bar of soap and can monitor and correct a patient’s rhythm for several years
between replacements. Likewise, the external defibrillator has been made smaller and
so much simpler to operate that sixth graders can use the device successfully.

The study of external defibrillation can build on much of what has been learned about
internal defibrillation. A large amount of work has been done to understand the mechanisms of defibrillation following short durations of electrically induced ventricular fibrillation (VF) using internal defibrillation electrodes (4–7). VF is maintained by multiple
From: Contemporary Cardiology: Cardiopulmonary Resuscitation
Edited by: J. P. Ornato and M. A. Peberdy © Humana Press Inc., Totowa, NJ


either hyperpolarization or depolarization. the bidomain predicts that hyperpolarization of the transmembrane potential occurs under the extracellular anodal electrode and depolarization of the transmembrane potential occurs under the extracellular cathodal electrode. A shock that is large enough but delivered during the plateau of the action potential will modify an ongoing action potential without . If the shock is delivered just after local activation. The bidomain model extends the one-dimensional cable model into two or three dimensions (11). the bidomain model hypothesizes that there should be changes in the transmembrane potential. a defibrillation shock must stop most or all of the fibrillation wavefronts (10. the extracellular and intracellular spaces are represented as single continuous domains that are separated by the highly resistive cell membrane. Experimental studies have shown that there is a complex pattern of transmembrane potential change during the delivery of a defibrillation shock. the distance from the electrode.20). then it can have one of three effects on the myocardium depending on the local shock strength and its timing with respect to the local action potential. defibrillation is thought to be realized through the electrical pulse causing an alteration in the transmembrane potential of the myocyte. The extension of refractoriness hypothesis is one proposed explanation of how a shock stops fibrillation (19. and the orientation of the myocardial fibers (13). In order to be successful. One-dimensional cable models cannot explain how the transmembrane potential changes at points distant from the shock electrodes. the bidomain formulation begins to give new insights into how shocks change the transmembrane potential. As this represents a large mass of tissue. If a shock only slightly alters the transmembrane potential in a region. relatively unaltered. This change in the transmembrane potential by the shock leads to changes in VF wavefront propagation and initiation of postshock activation fronts that determine whether or not a shock is successful.16–18). Fundamentally. Changes in the transmembrane potential across the heart caused by the shock are predicted by the bidomain model of cardiac tissue. If the shock is large enough and delivered relatively late during the action potential. Defibrillation can be broken down into two parts: halting fibrillation wavefronts and not restarting fibrillation. then activation fronts in the region may continue to propagate. across much of the entire heart (12). after the shock.212 Cardiopulmonary Resuscitation activation fronts that are constantly moving in a pattern of re-entry. According to this model. When realistic tissue resistive anisotropies (changes in conductivity with direction) are included in the model. Similar to the one-dimensional cable model. then it will initiate a new action potential. these alterations must be achieved at a considerable distance from the stimulating electrode. similar to those predicted by the bidomain model (14–16). Additionally. The cable equations predict hyperpolarization of the transmembrane potential adjacent to an extracellular anode and depolarization adjacent to an extracellular cathode with the change in transmembrane potential decreasing exponentially with distance from the electrodes. The change in transmembrane potential elicited by the shock depends on the distribution of intracellular and extracellular current that is affected by the change in the potential gradient with distance. If the shock is large enough. It most likely requires a rapid induction of changes in the transmembrane potential of the myocytes in a critical mass of myocardium (75–90% of the myocardium in dogs [8–10]). then there may be little or no change in the action potential duration. a majority of the heart will see no change in the transmembrane potential as a result of the shock.

Focal activation is also frequently observed following defibrillation shocks. In adjacent regions. the front will be stopped because it cannot propagate into the region of refractory tissue (23).31). showed that as pacing rate increases. do not always lead to fibrillation. Cao et al. Banville et al. it is possible that the activation front arose from the border of a directly excited region that is located intramurally.Chapter 12 / External Defibrillation 213 initiating a new action potential (21. Chattipakorn et al.22). Foci have also been observed with the electrical induction of VF during the vulnerable period (30). If the first activation front that forms after a defibrillation shock encounters tissue with an extended refractory period. Understanding how postshock arrhythmias progress is important to understanding how shocks ultimately succeed or fail. Using video-imaging techniques. One mechanism for the induction of these postshock arrhythmias is described by the critical point hypothesis. examined the induction of fibrillation by rapid pacing in dogs (34). a spatial heterogeneity of conduction velocities occurs. For successful shocks near the defibrillation threshold. Cato et al. By the time the wavefront re-encounters the tissue that was previously refractory. Much of our understanding about the mechanism of postdefibrillation arrhythmia induction comes from studying the simpler process of induction of fibrillation by shocks during paced rhythms. which leads to functional re-entry and VF. Chattipakorn et al. have shown in isolated rabbit hearts that the centers of re-entrant wavefronts induced by shocks delivered in paced rhythms can be moved by changing the shock strength that is delivered and the coupling interval at which it is delivered (27). whether they are focal or re-entrant. The critical point hypothesis postulates that functional reentry is initiated in myocardium in which a dispersion of shock potential gradients intersects a dispersion of refractoriness (26). the first few beats following the shock are not sinus beats (32). direct excitation of recovered tissue and refractory period extension in relatively refractory tissue occur. paced the heart after delivering a shock that was 50 to 100 V greater than the defibrillation threshold and that. At least three rapidly paced cycles after this shock were necessary for induction of VF. in which activation is first observed at one site followed by propagation away from this site in all directions (28). have suggested that whether or not a shock near the defibrillation threshold will defibrillate depends on the number and timing of activations that occur following the shock (33). it has recovered and the wavefront re-enters. The cause of the foci is unknown although it has been observed that foci during defibrillation can occur in myocardial regions exposed to shock fields of 2 to 6 V/cm. This activation front could appear to be focal when it is conducted to the epicardium. Focal origins of activation fronts were first observed with recordings confined to the epicardial surface (28). when given by itself without pacing.25). This idea has been formalized in the upper limit of vulnerability hypothesis for defibrillation that states that failed defibrillation by a shock that is near the defibrillation threshold occurs by the same mechanism as VF induction caused by a premature stimulus of the same strength delivered during the vulnerable period (24. Threedimensional mapping with plunge needles has demonstrated that foci following a shock can arise intramurally at sites in which foci were not present during VF before the shock (29). Ectopic activations following a shock. raising the possibility of early or delayed after depolarizations as the source of the foci (28. . Excitation blocks in the direction of the tissue with refractory period extension and propagates away from and around it. always defibrillated. In these cases.

Not all biphasic waveforms are superior to monophasic waveforms. More recently. the polarity of the shock does not change at each electrode throughout the entire duration of the shock. For example.40). Within each type.41. (B) Truncated exponential biphasic waveform. The electric shock that is delivered is called the waveform. In biphasic waveforms. waveforms can be described as truncated exponential or damped sinusoidal shapes. Because of the inductor necessary to shape the damped sinusoidal waveform. (A) Truncated exponential monophasic waveform. (D) Quasi-sinusoidal biphasic waveform. In monophasic waveforms.214 Cardiopulmonary Resuscitation Fig. most external defibrillators until recently have used damped sinusoidal waveforms. and (b) a mechanism to actually deliver that shock. In contrast. if the second phase of the biphasic waveform becomes much longer than the first phase. The optimum durations of the two . then the energy required for defibrillation increases and can eventually rise to a level above the energy required to defibrillate with a monophasic waveform equal in duration to the first phase of the biphasic waveform (38. Many studies. have shown that biphasic waveforms can defibrillate with less current and energy than monophasic waveforms (35–38). these defibrillators tend to be large and heavy.42). (C) Damped sinusoidal monophasic waveform. both animal and human. Most implantable cardioverter defibrillators use truncated exponential biphasic waveforms. Quasi-sinusoidal biphasic waveforms are used in external defibrillators in Russia and similar to truncated exponential biphasic waveforms. the polarity of the shock reverses at each electrode part way through the shock. 1. lighter external defibrillators have been developed that use truncated exponential biphasic waveforms. The two most common waveform shapes used clinically are monophasic and biphasic waveforms (Fig. DEFIBRILLATION METHODOLOGY Defibrillators consist of two parts: (a) a mechanism for determining whether or not it is necessary to deliver a shock to the patient. have been shown to have an improved efficacy over monophasic waveforms (39. 1). similar those used in internal defibrillators.

First. For truncated exponential waveforms. showed that the transmembrane potential changed with a time constant varying from 1. because current or energy delivered after that point is wasted. if the waveform is long enough.6 to 14. although choosing a single time constant may be too simplistic.50. defibrillation efficacy follows a strength-duration relationship similar to cardiac stimulation (47. The voltage across the network is then calculated for each time point during the defibrillation pulse. There is some evidence that this RC network is a reasonable if simplified model of the heart during defibrillation. the higher the voltage. On the basis of this observation. waveforms that rise gradually should have an improved efficacy over waveforms that reach their maximum value immediately. . as the waveform gets longer. This minimum does not extend indefinitely.6 to 6 ms depending on shock size and polarity (Fig. for square waveforms of the same current. several groups have suggested that cardiac defibrillation can be mathematically modeled using a parallel resistor-capacitor (RC) network (Fig. however. Zhou et al. Schuder and colleagues showed that if the duration of the waveform gets too long. at very long waveform durations.52]). Ascending ramps defibrillate with a greater efficacy than do descending ramps (56.58). Therefore. approaching a minimum called the rheobase (49). Likewise.57). In one version of the model. then it is no longer capable of defibrillating (55). its polarity and the time during the action potential that it is delivered. Second. showed that the time constant for the transmembrane response varied from 1. However.48). Zhou et al. the lower the defibrillation threshold. 3). Both of these studies show that the cells of the heart respond to a shock with a time constant on the order of a few milliseconds. the model voltage rises. the average current necessary to successfully defibrillate 50% of the time becomes progressively less. it has been determined that the time constant for the parallel RC network is in the range of 2.2 ms depending on the size of the shock. Mowrey et al. Unlike stimulation. Several observations can be made from this model. measured the transmembrane potential response to shocks in an isolated rabbit heart model using optical techniques (53). recorded the transmembrane potential of cells in a rabbit papillary muscle during delivery of a defibrillation sizes shock using a double-barrel micro-electrode technique (52). the voltage across the network gets progressively higher and approaches an asymptote or rheobase. Several groups have shown that for square waveforms of duration less than 20 to 30 ms. as the waveform duration gets longer. This prediction has been shown to hold true for both internal and external defibrillation (56.5 to 5 ms (44–46).46. In supporting this prediction. begins to decrease. The relative defibrillation efficacy of different waveform shapes and durations can be compared by holding the peak current of the waveform constant and comparing the maximum voltage values achieved by each waveform. Empirically.Chapter 12 / External Defibrillation 215 phases of the biphasic waveform depend on electrode impedance and defibrillator capacitance (43–46). this condition only occurs for waveforms more than 30 seconds in duration. strength-duration relationships for waveform leading edge voltage at the defibrillation threshold for truncated exponential waveforms in both animals (46) and humans (54) do not approach an asymptote but rather reach a minimum and remain constant over a range of waveform durations. 2 [44. the model predicts that monophasic exponential waveforms should be truncated at a time when the peak voltage across the RC network is reached. reaches a peak and then. Mowrey et al. the model predicts that the heart acts as a low-pass filter (51). Therefore. the average current necessary to defibrillate rises. a current waveform is applied to the RC network (46).

5. 4. 3. 4. The model response does not change polarity until phase-2 duration is longer than 2 ms. Phase 2 was truncated after 1. 6. Waveforms were truncated at 1. 2. Leading edge current of the input waveforms was 10A.216 Cardiopulmonary Resuscitation Fig. 7. 2. and 10 ms. The model response approaches a maximum assymptotically. (A) A schematic of the parallel RC circuit. The input is a square wave. 6. Model responses to a monophasic and biphasic truncated exponential waveform with a time constant of 7 ms. 2. and 8 ms. (B) The model response to a monophasic waveform. The model response reaches a peak at 4 ms and then begins to decrease despite continued current delivery. 5. 8. (C) The model response to a biphasic waveform. 3. . Phase 1 was truncated at 6 ms.

Several groups have suggested that the optimal first phase of a biphasic waveform is the optimal monophasic waveform (43. whereas opposite polarity caused hyperpolarization (dotted lines). One shock polarity caused depolarization (solid lines). Shock strength was 11 V/cm. . and interval between arrows 2 and 3 represents duration of second phase of a biphasic shock.46).Chapter 12 / External Defibrillation 217 Fig. Each tracing includes recordings of 9th S1-induced action potential and 10th S1-induced action potential during which a 10-ms monophasic (top) or 10/10-ms (middle) or 5/5 ms (bottom) biphasic shock was applied. Kerber et al. Studies in both animals and humans support this prediction. If this is true. Voltage and time scales are given at bottom right. it appears that the role of the second phase is to return the model voltage response to 0 as quickly as possible to maximize the increased efficacy of the biphasic waveform over that of the monophasic waveform with the same duration as phase one of the biphasic waveform. Measurements of shock-induced transmembrane potential change (b Vm). Third. Each action potential tracing is accompanied with an extracellular recording during which no shock artifact was recorded when both double-barrel microelectrode tips were outside the cell membrane. efficacy is lost. Tracings for the same shock waveform but opposite polarity are superimposed. Swerdlow and colleagues have shown in humans that the “best” second phase of a biphasic waveform is one that returns the model response close to 0 (46). showed in 347 patients who received 1009 shocks using a damped sinusoidal monophasic waveform that there was a clear relationship between peak current and shock success (59). Arrows indicate timing of a shock: interval between arrows 1 and 2 represents duration of a monophasic shock or first phase of a biphasic shock. the model predicts that the most appropriate measure of a defibrillation waveform is current rather than energy. If the network voltage does not reach 0 or if it greatly overshoots 0. 3. then what does the model predict as the “best” second phase of a biphasic waveform? Empirically. Horizontal dark bars in 9th action potential indicate time interval during which shocks were actually given in 10th S1-induced action potential.

without compromise of defibrillation efficacy (67). showed that for both monophasic and biphasic shocks. Electroporation can cause massive ion exchange across the cell membrane. . the cell is paralyzed electrically being both unresponsive and unable to conduct an action potential. 200 to 360 J of energy is necessary for successful defibrillation when the defibrillation electrodes are located on the body surface. showed that transthoracic defibrillation with biphasic shocks resulted in less postshock electrocardiogram evidence of myocardial dysfunction than standard monophasic damped sinusoidal waveforms. However. Less energy is required for a truncated exponential biphasic waveform. The transmembrane potential changes temporarily to a value almost equal to that of the plateau of a normal action potential. Thus. The shape of the waveform alters the strength of the shock at which these detrimental effects occur.218 Cardiopulmonary Resuscitation The location of the defibrillation electrodes affects the magnitude of the shock necessary to defibrillate the heart. the probability of defibrillation success begins to drop (62). During this period. The probability of 200 to 360 J monophasic shocks converting atrial fibrillation to sinus rhythm is higher if the electrodes are on the anterior and posterior chest walls than if they are on the anterior and lateral chest walls (61). as occurs in transthoracic defibrillation with a damped sinusoidal monophasic waveform. a potential gradient in the myocardium of 71 ± 6 V/cm was required for conduction block when a 5-ms/5-ms truncated exponential biphasic shock was used. Use of a 10-ms truncated exponential monophasic waveform for VF in dogs resulted in temporary conduction block in regions in which the potential gradient was greater than 64 ± 4 V/cm (65). increasing shock strength does not always improve the probability of successful defibrillation and may in fact increase the incidence of postshock arrhythmias (64). only 4 to 20% of the current that is delivered to transthoracic defibrillation electrodes ever reaches the heart. Most of the current is shunted around the heart through the muscles of the chest wall (60). Reddy et al. The very high voltage can result in disruption of the phospholipid membrane bilayer and the formation of pores that permit the free influx and efflux of ions and macromolecules. biphasic waveforms are less apt to cause electro-physiologic damage or dysfunction in high potential gradient regions than monophasic waveforms. EFFECT OF HIGH-SHOCK FIELDS ON THE MYOCARDIUM What happens if a defibrillation shock gets very large? At high-shock strengths. Moving the location of electrodes on the chest wall can also affect defibrillation efficacy. One mechanism that has been implicated for the mechanism of shocks causing damage to the myocardium is electroporation. It is thought that at large strengths. Addition of a second phase to a monophasic waveform—making it a biphasic waveform—reduced the damage sustained by cultured chick myocytes compared to that induced by the monophasic waveform alone (66). Electroporation may occur in regions in which the shock potential gradient is high (>50–70 V/cm) and had been hypothesized to occur in regions in which the potential gradient is much less than 50 V/cm (68). Cates et al. defibrillation shocks can have detrimental effects on the heart. results in arrhythmic beating and at very high potential gradients necrosis may occur (69). probably greater than 150 V/cm. the formation of holes or pores in the cell membrane. Typically. Exposure of the myocardium to yet higher potential gradients. In contrast. Shocks that created even higher potential gradients in the myocardium prolonged the duration of this conduction block. Increasing the shock strength to very high levels (>1000 V with transvenous electrodes) can result in activation fronts arising from regions of high potential gradient that re-induce VF (63).

Weaver et al. Both the mechanical trauma and the hypoperfusion associated with CPR are possible explanations for the correlation between enzyme release and total defibrillation energy. all subsequent shocks were 320 J. there was no difference in survival in patients receiving monophasic or biphasic shocks. In 115 patients with prehospital sudden arrest secondary to VF. both return of spontaneous circulation and survival were inversely related to the total number of shocks delivered but neither of these outcomes was related to the level of energy used for the initial two defibrillation shocks. compared the effect of a protocol using a constant 150 J shock strength vs a protocol using an escalating 200 to 360 J shock strength (71). Grubb et al. A total of 249 patients were randomized to receive either one or two (as necessary) monophasic damped sinusoidal shocks of 175 J or 320 J (2. The total amount of delivered defibrillation energy was also positively correlated with the duration of CPR. A rise in CK-MB and cardiac troponin T occurred in almost all cases. it is desirable that the heart not be damaged by a defibrillation shock. An increased proportion of patients did have return of spontaneous circulation in the 150 J group compared to the 200 to 360 J group but this difference can be explained by the increased defibrillation efficacy of the biphasic waveform compared to the monophasic waveforms. Schneider et al. but were not significantly associated either with the number of defibrillation shocks delivered (mean = 3. measured cardiac enzymes in patients resuscitated from out-of-hospital cardiac arrest (CA) including patients who received no shocks (72). examined the influence of chest compressions and external defibrillation on the release of cardiac enzymes in patients resuscitated from out-of-hospital CA (73). The higher energy shocks were more likely to leave the patient in atrioventricular block following multiple shocks. The 150 J shock was always biphasic. In a three-way analysis of variance. but this difference did not influence survival. A comparison of low and high energy biphasic shocks has yet to be performed in the prehospital setting but is crucial for determining whether a constant low-strength or an escalating shock strength protocol is preferred with biphasic waveforms. A similar study performed by Müllner et al. Both the Weaver study and the Schneider study suggest that there is neither increased survival nor decreased survival with the larger monophasic shocks. Using a multivariate stepwise linear regression model. 80% were monophasic truncated exponential shocks and 20% were monophasic damped sinusoidal shocks. Beyond survival. 41 of 54 patients (75%) had return of spontaneous circulation in the 150 J group compared to 33 of 49 patients (67%) in the 200 to 360 J group (p = NS). Of the escalating 200 to 360 J shocks. compared the effect of two shock strengths on survival (70). range = 1–6) or with the amount of epinephrine administered. If the comparison is limited to patients who were successfully defibrillated. Likewise. There was a modest correlation between enzyme release for both troponin T and CK-MB and the total defibrillation energy delivered among patients without electrocardiographic evidence of acute myocardial infarction (AMI). a similar model was constructed for troponin T concentrations 12 hours after resuscitation and again. and the presence of cardiogenic shock in the postresuscitation period.5 or 4. the duration of CPR. If three or more shocks were required. These studies suggest that damage caused by defibrillation during CPR is either small or nonexistent compared with the damage and dysfunction caused by the underlying pathology and period of no-flow ischemia. the number of defibrillation shocks administered was not significant in the model. .6 J/kg for a 70 kg individual). they showed that CK-MB concentrations 12 hours after CPR were positively associated with the presence of AMI. Patients received from 0 to no less than 2000 J of total defibrillation energy.Chapter 12 / External Defibrillation 219 Two clinical trials have been performed comparing the effect of shock energies on survival after prehospital sudden CA.

Results showed that biphasic waveforms had significantly lower voltage and energy thresholds at all fibrillation durations and that their relative efficacy improved with increasing fibrillation duration. Jones et al. 4). B/M was 0. The ratio between the biphasic waveform threshold and the monophasic waveform threshold (B/M) decreased to 0. whereas defibrillation threshold for monophasic waveform was significantly different after 5 minutes of fibrillation vs after 15 seconds of fibrillation.62 at 15 seconds.67 that for the monophasic waveform after 5 seconds of fibrillation. defibrillation threshold for biphasic waveform was significantly different from that of monophasic waveform.05 compared to the defibrillation threshold at 15 seconds). . The biphasic waveform energy threshold was 0. Defibrillation threshold for biphasic waveform did not change significantly with duration of fibrillation. 4. Defibrillation thresholds in terms of energy for quasi-sinusoidal biphasic waveform and critically damped sinusoidal monophasic waveform after 15 seconds and after 5 minutes of fibrillation. Walcott et al.220 Cardiopulmonary Resuscitation Fig. In both cases. usually 15 to 45 seconds in duration. In contrast. compared the efficacy of a monophasic waveform (5 ms rectangular) and an asymmetrical biphasic waveform (5 ms each pulse. EFFECT OF THE DURATION OF VF ON DEFIBRILLATION EFFICACY Most defibrillation studies have been performed on healthy hearts after short periods of electrically induced VF. 15.52. compared the relative efficacy of a damped sinusoidal monophasic and damped sinusoidal biphasic waveform after 15 seconds and 5 minutes of VF (3 minutes of unsupported VF followed by 2 minutes of femoral–femoral venous–arterial circulation at 1 L per minute) in a canine model (40). V2 = 50% V1) at 5. Yet most patients who suffer sudden CA are away from immediate medical care and fibrillate for 5 to 7 minutes before defibrillation. At 30 seconds. The defibrillation threshold increased by 40% for the damped sinusoidal monophasic waveform (p < 0. the defibrillation threshold increased by 10% for a damped sinusoidal biphasic waveform ( p = NS defibrillation threshold at 5 minutes compared to the threshold at 15 seconds) (Fig. and 30 seconds using a working rabbit heart model of defibrillation (74).

VF lasted for 9. Ouyang et al. there appeared to be two populations of spontaneous arrhythmias. Other reports either did not find increases in defibrillation thresholds after coronary artery occlusion (79. Thus. 5). Weaver et al. defibrillation efficacy does not appear to decrease with VF duration for biphasic waveforms. Occlusion or embolization of a coronary artery has been reported to increase defibrillation current and energy thresholds during the 30 to 60 minutes following the onset of myocardial ischemia in dogs (77. The lowest energy threshold for defibrillation was determined in 10 open chest dogs with reversible 10-minute coronary occlusions at various sites for each of 44 VF events.2 ± 2. measured the defibrillation threshold for a biphasic waveform with both electrically induced VF and spontaneous VF secondary to acute ischemia (83). Bardy et al. one that was defibrillated with relatively low strength shocks and a second that was defibrillated with much higher shock strengths or not at all (Fig. Despite similar masses of ischemia. determined the defibrillation threshold for spontaneous arrhythmias induced by acute ischemia using a monophasic waveform and electrodes directly on the heart (82). showed that 86% of patients were defibrillated with the first shock using a 130 J biphasic truncated exponential waveform following a failed internal defibrillation shock (76). defibrillation success was not improved when the shock strength was increased to 320 J. One possible explanation for why the defibrillation threshold is higher for spontaneous VF secondary to acute ischemia is that the shock actually does defibrillate but that the heart refibrillates before the electrocardiogram amplifiers have recovered from the shock. Similar results were seen in swine. They showed that the defibrillation threshold for electrically induced VF was 65 ± 28 J but was 228 ± 97 J for spontaneous VF secondary to acute ischemia in a dog model. Walcott et al. The same comparison can be made for biphasic waveforms. Higgins et al. VF lasted for about 15 seconds before shock delivery.9 minutes. EFFECT OF ISCHEMIA ON DEFIBRILLATION EFFICACY Whether or not acute regional ischemia affects defibrillation efficacy of electrically induced VF is controversial. two times as much energy was required for defibrillation of spontaneous VF (whether after occlusion or reperfusion) as for electrically induced VF. showed that 96% of patients were defibrillated with a 200 J damped sinusoidal monophasic waveform in patients in the electrophysiology laboratory following a failed internal defibrillation test shock (75). Of note. showed that 96% of patients were defibrillated with the first shock using the same biphasic truncated exponential waveform except for shock strength. mirroring the animal data presented above. More important than the effect of ischemia on defibrillation is whether the arrhythmia starts spontaneously during acute ischemia or is induced electrically. These studies suggest that there is a decrease in defibrillation efficacy with VF duration for the monophasic damped sinusoidal waveform in humans. measured the defibrillation threshold for electrically induced VF in 15 . More recently. Schneider et al. showed that 61% of patients were defibrillated with a 175 J damped sinusoidal monophasic waveform in patients suffering (70) VF outside the hospital. Furthermore. which was 150 J (71).78).Chapter 12 / External Defibrillation 221 It is not possible to perform a paired comparison of defibrillation shock efficacy in humans but we can compare the results from different studies to estimate how shock efficacy changes with VF duration. Qin et al.80) or found a lower threshold (81).

5. fibrillation was induced electrically. Human studies stratifying patient characteristics as a function of defibrillation threshold have shown that heart dimensions and body dimensions but not underlying heart disease are correlated with the defibrillation threshold of electrically induced VF for internal elec- . one that is defibrillated at a relatively low energy level and one that is defibrillated at a much higher energy level. pigs before ischemia and then the efficacy of a shock 1.222 Cardiopulmonary Resuscitation Fig.6 ± 5. The incidence of delayed recurrence (at least one organized electrical beat before VF recurrence) after electrically induced nonischemic (3%) or ischemic (20%) VF was significantly lower than after spontaneous VF (75%). Open bar = reperfusion. ND = the VF could not be defibrillated and the animal died. Mean VF recurrence time after spontaneous VF was 4.3 seconds. If VF was not induced during 20 minutes of ischemia. These data suggest that shocks often stop spontaneous fibrillation but that fibrillation quickly recurs and that if the first two to three shocks fail then drug therapy might be more appropriate than continued shock delivery EFFECT OF INFARCTION ON DEFIBRILLATION EFFICACY It does not appear that previous MI has an effect on defibrillation efficacy. It appears that there are two populations of arrhythmias. Histogram of the number of arrhythmic episodes that were successfully defibrillated as a function of energy level. Defibrillation efficacy at 1.5 times the measured threshold during acute regional ischemia although recording a fast recovering electrogram and blood pressure trace (84).5 times the electrically induced VF defibrillation threshold was significantly higher for electrically induced ischemic VF (76%) than for spontaneous VF (31%). solid bar = occlusion.

and in the same perfusion bed as the infarct (88). If automatic external defibrillators are to be used on pediatric patients. Survival in pediatric CA patients in more likely. or cardiac output in piglets weighing between 3. Killingsworth et al. PEDIATRIC DEFIBRILLATION VF is a less common reason for VA in pediatric patients than in adult patients.1 kg and receiving individual external biphasic shocks of up to 90 J/kg (92). Therefore there is growing interest in defibrillation for pediatric patients. Zhang et al. Tacker et al. More recently. both when the acute ischemia is in a different perfusion bed from the infarct. Gutgesell et al.8 and 20. however both creatine kinase and troponin I were within normal limits and echocardiography showed no left ventricular (LV) dysfunction (94). showed a reverse correlation between body weight and the percentage of patients successfully defibrillated by a given shock strength (90). the defibrillation threshold was not different for patients with previous MI when compared to patients with structurally normal hearts (85).Chapter 12 / External Defibrillation 223 trodes in the electrophysiology laboratory (54). Eight-year-old patients weigh 25 kg on average. with a possibility of even higher escalating energy shocks. . a recent panel of experts concluded that a first shock of 150 to 200 J. then shock strengths must be sufficient to defibrillate the larger pediatric patients although not damaging the hearts of the smallest patients. Several investigators have shown that defibrillation shock success is directly related to body weight. in a retrospective human clinical study. exceeds the recommended dose of 2 to 4 J/kg for defibrillation of VF/pulseless ventricular tachycardia (VT) and is inappropriate for children less than 8 years old with a median weight less than 25 kg. Increasing myocardial damage with increasing external monophasic shock strength has been reported at doses greater than 150 J/kg in pigs (96) and 30 J/kg in dogs (98). ST segment deviation. A shock of 50 to 100 J is equivalent to 12 to 25 J/kg for newborn children. reviewed 71 transthoracic monophasic defibrillations in 27 children (93) and showed that the appropriate defibrillation dose for a monophasic waveform is 2–4 J/kg. Previous MI does increase the probability of a sudden CA. Nonetheless. A recent study indicated that there was no indication of persistent myocardial injury based on the time to return of sinus rhythm. A pediatric case report describes a 150 J (9 J/kg) shock that resulted in transient ST segment changes. although. Manufacturers of automatic external defibrillators (AEDs) are currently addressing the need for early defibrillation of pediatric patients with different biphasic waveforms as well as impedance compensating. if VF is present at the time of resuscitation. Animal studies have not shown any change in defibrillation threshold when comparing animals with previous MIs to those animals with normal hearts (78.8 to 20 kg (92). showed that the energy and current necessary to defibrillate using a damped sinusoidal monophasic waveform is related to body weight across different animal species (89). showed that the energy dose at the defibrillation threshold is proportional to the weight of the animal across a group of young swine ranging from 3. Animal studies have shown that a previous myocardial infarction makes it much more likely that an episode of acute ischemia will cause a tachyarrhythmia.87). Animal data with monophasic waveforms suggest a wide margin of safety before myocardial injury is induced (95–97). a dose of 50 to 100 J should be adequate to treat pediatric patients. In a study of 26 patients. have shown that the percent success for 70 J and 100 J biphasic defibrillation shocks is inversely correlated with animal size (91). nonescalating external shocks (99). LV dP/dt. Therefore. Geddes et al.86.

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