**5. Geometry and lead positioning for cardiac defibrillation**

in the presence of an electric field, discontinuities in tissue conductivity, such as blood vessels, changes in fiber direction, fatty tissue and intercellular clefts, induce a redistribution of intracellular and extracellular currents that can locally hyperpolarize or depolarize the cells. At the depolarization threshold, an excitation wave is emitted.[6,20,21] Conceptually, defib‐ rillation can be considered to be a two-step process. Firstly, the applied shock drives currents that traverse the myocardium and cause complex polarization changes in transmembrane potential distribution. Secondly, post-shock active membrane reactions are invoked that eventually result either in termination of ventricular fibrillation in the case of shock success,

Over a decade ago, bidomain simulations[23] followed by optical mapping studies [24,25] demonstrated that the membrane response in the vicinity of a strong unipolar stimulus involved simultaneous occurrence of positive (depolarizing) and negative (hy‐ perpolarizing) effects in close proximity. This finding of 'virtual electrodes' was in con‐ trast with the established view [26] that tissue responses should only be depolarizing (hyperpolarizing) if the stimulus was cathodal (anodal).[27] Essentially, the virtual elec‐ trode polarization (VEP) theory states that adjacent areas of opposite polarizations exist around the tip of the pacing electrode.[28] Sepulveda et al. [23] showed that the region depolarized (excited) by a strong stimulus has a dog-bone shape, with its long axis per‐ pendicular to the direction of the myocardial fibers. Regions of hyperpolarization (called virtual anodes) exist adjacent to the electrode along the fiber direction. A virtual anode is an example of a virtual electrode. Many researchers have observed these regions of de‐ polarization and hyperpolarization experimentally. [25,29] Depolarization can excite a cell and conversely, hyperpolarization can de-excite a cell. The cellular response to shock-in‐ duced VEP depends on the strength and polarity of the shock, as well as on the electro‐ physiological state of the cell at the time of shock delivery. Positive VEP can result in regenerative depolarization in regions where tissue is at or near diastole; such activation is termed 'make' because it takes place at the onset (make) of the shock. A strong nega‐ tive VEP can completely abolish the action potential (i.e. regenerative repolarization), thus creating post-shock excitable gaps in the virtual anode regions. The close proximity of a de-excited region and a virtual cathode has been shown, in both modelling studies and optical mapping experiments,[25] to result in an excitation at shock end (termed 'break' excitation, i.e. at the break of the shock). The virtual cathode serves as an electri‐ cal stimulus eliciting a regenerative depolarization and a propagating wave in the newly created excitable gap.[27] For a defibrillation shock to succeed, it must extinguish exist‐ ing VF activations throughout the myocardium (or in a critical mass of it), as well as not initiate new fibrillatory wavefronts.[27] A shock succeeds in extinguishing fibrillatory wavefronts and not initiating new re-entry if make/break excitations manage to traverse the shock-induced excitable gaps before the rest of the myocardium recovers from shockinduced depolarization.[27] Defibrillation failure has been explained by one (or both) of the following mechanisms: (I) the shock fails to extinguish all or a sufficient amount of fibrillatory electrical activity and (2) newly created shock-induced wavebreaks by near-

or in reinitiation of fibrillatory activity in the case of shock failure.[22]

32 Cardiac Defibrillation

threshold stimulating fields occurring at existing excitable gaps.[30]

Most models used to describe defibrillation view the myocardial mass as an isotropic conduc‐ tive domain and use the critical mass hypothesis to define successful defibrillation. According to this hypothesis the success of a defibrillation shock depends on rendering a critical mass of the myocardium inexcitable, such that fibrillation wavefronts have no myocardium to depolarize and propagate through.[19] It has been found that raising the extracellular potential gradient above a critical level renders myocardium refractory.[31] Frazier et al.[32] have found the critical level of potential gradient to be close to 5 V/cm, and a commonly accepted value for critical myocardial mass is 95%. [33]

In a recent study Yang et al. examined the effect of coil position on active-can single-coil ICD defibrillation efficacy by using a finite difference thoracic model which incorporated realistic geometries and conductive inhomogeneities of human thoracic tissues. [34] Four electrode configurations with the coil placed, respectively, in the right ventricular (RV) apex, in the middle of RV cavity, along the free wall in RV, or along the septal wall in RV, were simulated and their defibrillation efficacies were evaluated based on a set of metrics including voltage defibrillation threshold (VDFT) and current defibrillation threshold. It was found that the optimal electrode configuration is to position the coil in the middle of the RV cavity.

The RV cavity-to-can configuration had more endocardium exposed to the more uniform and relatively high voltage gradient fields. Other configurations exposed only endocardic surfaces near the electrodes to high voltage gradient fields and the voltage gradient drops more quickly in myocardial tissue as its resistivity value is one-third larger than blood's.

Aguel et al[35] used a high-resolution finite element model of a human torso that includes the fiber architecture of the ventricular myocardium to find the role of lead positioning in a transvenous lead-to-can defibrillation electrode system. They found that, among single lead systems, posterior positioning of leads in the right ventricle lowers VDFTs. Furthermore, a septal location of leads resulted in lower VDFTs than free-wall positioning. Increasing the number of leads, and thus the effective lead surface area in the right ventricle also resulted in lower VDFTs. However, the lead configuration that resulted in the lowest VDFTs is a combi‐ nation of mid-cavity right ventricle lead and a mid-cavity left ventricle lead.

Since the shape of the myocardial mass–voltage gradient curve is determined entirely by the geometry of the model and the lead design,[35] an improvement in defibrillation efficacy may be achieved by adjustment of the defibrillation lead surface and position, as this allows a more even distribution of the voltage gradient field over a wider surface of the myocardium.[36] Although centering the coils inside the heart chambers is probably not feasible with the current leads, positioning the coil in the middle of the RV cavity functioned equivalently in this sense as it had almost the entire RV endocardial surface exposed to a relatively evenly distributed voltage gradient field considering blood's resistivity is significantly less than the resistivity value of myocardium.

Current density distribution is another important parameter to use in evaluating the efficacy of defibrillation. The cross-sectional current density distribution showed that in the full tissue model skeletal muscle provided an alternative pathway for the current flow. By calculating the current flowing through various regions in the cross-sections it was found that more than 25% of the total current passing through the cross-sections flowed through the skeletal muscle around the outer boundary of the thorax, independent of electrode configuration. On average, 10% of the current was shunted through the relatively high resistivity fat on the outer boun‐ daries of the thorax and another 10% was shunted though the left lung. This suggests that the amount of skeletal muscle, fat and lungs impact the amount of current reaching the heart. This finding is consistent with the results reported by Geddes et al.[37] that indicates body size or shape has a significant influence on the amount of current required for successful defibrillation, though it was based on studies of transthoracic ventricular defibrillation. Examining the current flowing through the heart in the cross-sections on the average, less than 10% of the current flowed through the myocardium, and a major portion of the current flowing through the heart region was shunted through the blood chambers.[34] In a simplified view, the current from the electrode in the RV can propagate up through the blood chambers to the base of the heart, great vessels, and lung to the can, or out through the myocardial wall to the skeletal muscle and up to the can. Both paths are used, but as the ventricles become more enlarged as in patients with advanced heart failure, the low resistivity blood shifts more current up through the base of the heart and away from the skeletal muscle.[34] This would suggest that the large heart chambers of patients in heart failure, or with an enlarged heart, would tend to shunt the current away from the myocardial tissue in the middle regions of the heart, thus resulting in the need for higher defibrillation currents.[34]

**Figure 1.** Single chamber dual coil ICD system with the lead placed in the apex of the right ventricle (arrow). Postero-

Defibrillation and Cardiac Geometry http://dx.doi.org/10.5772/55120 35

It was advised to place the RV coil towards the apex to reduce the DFTs, mainly driven by data obtained before the active can configurations were introduced.[38] Without the hot can pulling current toward the apex, it was important to have the RV coil tip deep in the apex. Otherwise, the current would tend to follow the blood pool back to the SVC coil, shunting the defibrillation energy away from the LV myocardium and raising the VDFT. [38] With a chest electrode ("hot can") in place, the RV apical position is not as critical because current is pulled directed from whatever position in the RV that the coil resides, through the apex to the pectoralis major muscle and to the hot can, thereby including the LV myocardium in the wave front's path.[39] Actually with a hot can, and with no SVC coil, the apical position was shown to be inferior in terms of DFTs.[34] If a hot can and an SVC coil are used the data available seems to suggest a slight advantage for the RV apex position. Clinical studies comparing the DFT for an RV coil tip in the apex versus in the right ventricular outflow tract using biphasic waveforms and a hot can showed that the mean benefit of an apical position was approximately 10% DFT reduction.[38,40,41] This relatively small benefit must be weighed against the increased risk of perforation associated with apical lead positioning.[38,42] Based on the current data the best compromise position of the RV coil tip seems to be along the septum midway (Figure 2)

anterior (PA) and lateral (LAT) radiographic views.

between the apex and RVOT (Figure 3).

#### **5.1. Clinical aspects of right ventricular lead positioning for defibrillation**

Until relatively recently lead placement in the RV apex has been the standard of care for patients requiring pacemaker or defibrillator lead placement (Figure 1).[38]

transvenous lead-to-can defibrillation electrode system. They found that, among single lead systems, posterior positioning of leads in the right ventricle lowers VDFTs. Furthermore, a septal location of leads resulted in lower VDFTs than free-wall positioning. Increasing the number of leads, and thus the effective lead surface area in the right ventricle also resulted in lower VDFTs. However, the lead configuration that resulted in the lowest VDFTs is a combi‐

Since the shape of the myocardial mass–voltage gradient curve is determined entirely by the geometry of the model and the lead design,[35] an improvement in defibrillation efficacy may be achieved by adjustment of the defibrillation lead surface and position, as this allows a more even distribution of the voltage gradient field over a wider surface of the myocardium.[36] Although centering the coils inside the heart chambers is probably not feasible with the current leads, positioning the coil in the middle of the RV cavity functioned equivalently in this sense as it had almost the entire RV endocardial surface exposed to a relatively evenly distributed voltage gradient field considering blood's resistivity is significantly less than the resistivity

Current density distribution is another important parameter to use in evaluating the efficacy of defibrillation. The cross-sectional current density distribution showed that in the full tissue model skeletal muscle provided an alternative pathway for the current flow. By calculating the current flowing through various regions in the cross-sections it was found that more than 25% of the total current passing through the cross-sections flowed through the skeletal muscle around the outer boundary of the thorax, independent of electrode configuration. On average, 10% of the current was shunted through the relatively high resistivity fat on the outer boun‐ daries of the thorax and another 10% was shunted though the left lung. This suggests that the amount of skeletal muscle, fat and lungs impact the amount of current reaching the heart. This finding is consistent with the results reported by Geddes et al.[37] that indicates body size or shape has a significant influence on the amount of current required for successful defibrillation, though it was based on studies of transthoracic ventricular defibrillation. Examining the current flowing through the heart in the cross-sections on the average, less than 10% of the current flowed through the myocardium, and a major portion of the current flowing through the heart region was shunted through the blood chambers.[34] In a simplified view, the current from the electrode in the RV can propagate up through the blood chambers to the base of the heart, great vessels, and lung to the can, or out through the myocardial wall to the skeletal muscle and up to the can. Both paths are used, but as the ventricles become more enlarged as in patients with advanced heart failure, the low resistivity blood shifts more current up through the base of the heart and away from the skeletal muscle.[34] This would suggest that the large heart chambers of patients in heart failure, or with an enlarged heart, would tend to shunt the current away from the myocardial tissue in the middle regions of the heart, thus resulting in

nation of mid-cavity right ventricle lead and a mid-cavity left ventricle lead.

value of myocardium.

34 Cardiac Defibrillation

the need for higher defibrillation currents.[34]

**5.1. Clinical aspects of right ventricular lead positioning for defibrillation**

patients requiring pacemaker or defibrillator lead placement (Figure 1).[38]

Until relatively recently lead placement in the RV apex has been the standard of care for

**Figure 1.** Single chamber dual coil ICD system with the lead placed in the apex of the right ventricle (arrow). Posteroanterior (PA) and lateral (LAT) radiographic views.

It was advised to place the RV coil towards the apex to reduce the DFTs, mainly driven by data obtained before the active can configurations were introduced.[38] Without the hot can pulling current toward the apex, it was important to have the RV coil tip deep in the apex. Otherwise, the current would tend to follow the blood pool back to the SVC coil, shunting the defibrillation energy away from the LV myocardium and raising the VDFT. [38] With a chest electrode ("hot can") in place, the RV apical position is not as critical because current is pulled directed from whatever position in the RV that the coil resides, through the apex to the pectoralis major muscle and to the hot can, thereby including the LV myocardium in the wave front's path.[39] Actually with a hot can, and with no SVC coil, the apical position was shown to be inferior in terms of DFTs.[34] If a hot can and an SVC coil are used the data available seems to suggest a slight advantage for the RV apex position. Clinical studies comparing the DFT for an RV coil tip in the apex versus in the right ventricular outflow tract using biphasic waveforms and a hot can showed that the mean benefit of an apical position was approximately 10% DFT reduction.[38,40,41] This relatively small benefit must be weighed against the increased risk of perforation associated with apical lead positioning.[38,42] Based on the current data the best compromise position of the RV coil tip seems to be along the septum midway (Figure 2) between the apex and RVOT (Figure 3).

If the SVC coil is used, (given the lower DFTs for the mid-septal/RVOT position) an apical or apical-septal position may be considered (Figure 1). If the SVC coil is not used, the mid-septal location (Figure 2) appears to give lower DFTs than the apical tip location according to a

Defibrillation and Cardiac Geometry http://dx.doi.org/10.5772/55120 37

The effect of waveform polarity has been studied using both monophasic and biphasic wave‐ forms, and the available data shows 15-20% DFT mean reduction when an anodal RV coil con‐ figuration is being used. [38,43] These results are predicted by the virtual electrode hypothesis of defibrillation[44] that predicts that post-shock virtual electrodes launch new wavefronts to‐ ward the anode.[38] A right ventricular cathode produces expanding, pro-arrhythmic wave‐ fronts, whereas a right ventricular anode produces collapsing, self-extinguishing wavefronts. [38] An additional beneficial effect of anodal RV shocks may be to increase the homogeneity of

Another element of lead technology that can affect the efficiency of a defibrillation system is the SVC coil. Studies on patients with active-can lead configurations suggest that the addition of the SVC coil decreases the DFT and reduces impedance. With an apically placed RV coil and a prepectoral hot can, major current flow is to the pectoralis major and to the ICD can. Minimal current flows to the posterior base. The addition of an SVC coil directs some current

There are several detrimental effects from the use of the SVC coil, especially for a coil placed in the right atrium. The low SVC coil diverts current from the apex and LV free wall because the RV and atrial blood pool provide a lower resistance path. In addition, a low cathodal SVC coil could launch wavefronts into basal RV. And, additionally, the extraction of a dual-coil lead is much more challenging because the adherences that can form between the SVC coil and

A recent study analyzed comparatively the DFTs for active and inactive SVC coils.[46] The results depended on the single coil impedance. If the single coil impedance was >58Ω, then an active SVC coil almost always lowered the DFT. If the single coil impedance was already in the normal range (<58 Ω), then the effect of the SVC coil was split.[38] Half of patients had a lower DFT and half had a higher DFT. Interestingly, if the SVC coil was active, its position was important: an SVC coil in the SVC/right atrial junction increased the DFT, and an SVC coil

Total subcutaneous implantable subcutaneous defibrillators (S-ICDs) have been developed as alternative ICD strategies allowing more widespread application of ICD therapy for the pri‐ mary prevention of sudden death. The optimal device and electrode configurations for S-ICDs are not well known. Image-based defibrillation finite element models have been used to predict the myocardial electric field generated during defibrillation shocks in a variety of subcutaneous electrode positions, in order to determine factors affecting optimal lead positions for subcutane‐

ous ICDs (S-ICD), and ultimately to improve the efficacy of these defibrillation systems.

membrane time constants in comparison with cathodal shocks.[38,45]

placed in the SVC/ innominate junction decreased the DFT.[46]

**6. Electrode configurations for subcutaneous ICDs**

modeling study.[34,38]

vertically and toward the posterior.

the venous wall.[38]

**Figure 2.** Single-chamber single-coil ICD system with the lead placed in a mid-septal location (arrow). Postero-anterior (PA) and lateral (LAT) radiographic views.

**Figure 3.** Single-chamber dual-coil ICD system with the lead placed at the base of the right ventricular outflow tract (arrow). Postero-anterior (PA) and lateral (LAT) radiographic views.

If the SVC coil is used, (given the lower DFTs for the mid-septal/RVOT position) an apical or apical-septal position may be considered (Figure 1). If the SVC coil is not used, the mid-septal location (Figure 2) appears to give lower DFTs than the apical tip location according to a modeling study.[34,38]

The effect of waveform polarity has been studied using both monophasic and biphasic wave‐ forms, and the available data shows 15-20% DFT mean reduction when an anodal RV coil con‐ figuration is being used. [38,43] These results are predicted by the virtual electrode hypothesis of defibrillation[44] that predicts that post-shock virtual electrodes launch new wavefronts to‐ ward the anode.[38] A right ventricular cathode produces expanding, pro-arrhythmic wave‐ fronts, whereas a right ventricular anode produces collapsing, self-extinguishing wavefronts. [38] An additional beneficial effect of anodal RV shocks may be to increase the homogeneity of membrane time constants in comparison with cathodal shocks.[38,45]

Another element of lead technology that can affect the efficiency of a defibrillation system is the SVC coil. Studies on patients with active-can lead configurations suggest that the addition of the SVC coil decreases the DFT and reduces impedance. With an apically placed RV coil and a prepectoral hot can, major current flow is to the pectoralis major and to the ICD can. Minimal current flows to the posterior base. The addition of an SVC coil directs some current vertically and toward the posterior.

There are several detrimental effects from the use of the SVC coil, especially for a coil placed in the right atrium. The low SVC coil diverts current from the apex and LV free wall because the RV and atrial blood pool provide a lower resistance path. In addition, a low cathodal SVC coil could launch wavefronts into basal RV. And, additionally, the extraction of a dual-coil lead is much more challenging because the adherences that can form between the SVC coil and the venous wall.[38]

A recent study analyzed comparatively the DFTs for active and inactive SVC coils.[46] The results depended on the single coil impedance. If the single coil impedance was >58Ω, then an active SVC coil almost always lowered the DFT. If the single coil impedance was already in the normal range (<58 Ω), then the effect of the SVC coil was split.[38] Half of patients had a lower DFT and half had a higher DFT. Interestingly, if the SVC coil was active, its position was important: an SVC coil in the SVC/right atrial junction increased the DFT, and an SVC coil placed in the SVC/ innominate junction decreased the DFT.[46]
