Minor Variations in Electrode Pad Placement Impact Defibrillation Success.

Defibrillation is essential for resuscitating patients with ventricular fibrillation (VF), but shocks often fail to defibrillate. We hypothesized that small variations in pad placement affect shock success, and that defibrillation waveform and shock dose could compensate for suboptimal pad placement. In 10 swine experiments, electrode pads were attached at 3 adjacent anterolateral positions, less than 3 centimeters apart. At each position, 24 episodes of VF were induced and shocked, 8 episodes for each of 3 defibrillation therapies. This resulted in 9 tested combinations of pad position and defibrillation therapy, with 80 episodes of VF for each combination. An episode consisted of 15 seconds of untreated VF, followed by a first shock and, if necessary, a repeat shock. Episodes were separated by four minutes of recovery. Both electrode pad position and therapy order were randomized by experiment. Primary outcome was defined as successful VF termination after the first shock; secondary outcome was the cumulative success of the first and second shocks. First shock efficacy varied widely across the 9 tested combinations of pad position and defibrillation therapy, ranging from 11.3% to 86.3%. When grouped by therapy, first shock efficacy varied significantly between the 3 pad positions: 38.3%, 48.3%, 36.7% (p = 0.02, ANOVA), and, when grouped by pad position, it varied significantly between therapies: 15.0%, 32.5%, 75.8% (p < 0.001, ANOVA). Cumulative 2-shock success varied significantly with therapy (p < 0.001, ANOVA) but not with pad position (p = 0.30, ANOVA). The lowest first shock success was at one position in 6 of 10 animals, at another position in 4 of 10 animals, and never at the third position. Small variations in pad placement can significantly affect defibrillation shock efficacy. However, anatomical variation between individuals and the challenging conditions of real-world resuscitations make optimal pad placement impractical. Suboptimal pad placement can be overcome with defibrillation waveform and shock dose.

Evaluation of acute cardiac and chest wall damage after shocks with a subcutaneous implantable cardioverter defibrillator in Swine.

BACKGROUND: A subcutaneous implantable cardioverter defibrillator (S-ICD) could ease placement and reduce complications of transvenous ICDs, but requires more energy than transvenous ICDs. Therefore we assessed cardiac and chest wall damage caused by the maximum energy shocks delivered by both types of clinical devices. METHODS: During sinus rhythm, anesthetized pigs (38 ± 6 kg) received an S-ICD (n = 4) and five 80-Joule (J) shocks, or a transvenous ICD (control, n = 4) and five 35-J shocks. An inactive S-ICD electrode was implanted into the same control pigs to study implant trauma. All animals survived 24 hours. Troponin I and creatine kinase muscle isoenzyme (CK-MM) were measured as indicators of myocardial and skeletal muscle injury. Histopathological injury of heart, lungs, and chest wall was assessed using semiquantitative scoring. RESULTS: Troponin I was significantly elevated at 4 hours and 24 hours (22.6 ± 16.3 ng/mL and 3.1 ± 1.3 ng/mL; baseline 0.07 ± 0.09 ng/mL) in control pigs but not in S-ICD pigs (0.12 ± 0.11 ng/mL and 0.13 ± 0.13 ng/mL; baseline 0.06 ± 0.03 ng/mL). CK-MM was significantly elevated in S-ICD pigs after shocks (6,544 ± 1,496 U/L and 9,705 ± 6,240 U/L; baseline 704 ± 398 U/L) but not in controls. Electrocardiogram changes occurred postshock in controls but not in S-ICD pigs. The myocardium and lungs were histologically normal in both groups. Subcutaneous injury was greater in S-ICD compared to controls. CONCLUSION: Although CK-MM suggested more skeletal muscle injury in S-ICD pigs, significant cardiac, lung, and chest wall histopathological changes were not detected in either group. Troponin I data indicate significantly less cardiac injury from 80-J S-ICD shocks than 35-J transvenous shocks.

Alternating fast and slow chest compression rates during CPR improved hemodynamics.

INTRODUCTION: Mechanical chest compression devices allow for variation in chest compression (CCs) characteristics from moment to moment, enabling therapy that is not feasible for manual CCs. Effects of varying compressions over time have not been studied. In a randomized trial in an experimental model of prolonged cardiac arrest, we compared time-varying CPR (TVCPR), alternating between 100 and 200 compressions per minute (cpm) every 6 s, to guidelines CPR (Control). METHODS: Ventricular fibrillation (VF) was electrically induced in 20 anesthetized pigs (28.4-45.8 kg). Following 10 min of untreated VF, cardiopulmonary resuscitation (CPR) began, randomized to TVCPR or Control. Rate of return of spontaneous circulation (ROSC), 4-h survival, and hemodynamics during the first 5 min of CPR were compared between groups. Moment-to-moment hemodynamic effects of changing the CC rate were analyzed. RESULTS: TVCPR improved the proportion of ROSC over time compared to Control (p < 0.05) but ROSC (9/10 vs. 5/10) and 4-h survival (8/10 vs 5/10) did not differ significantly between groups. During CPR, coronary and cerebral perfusion pressures and femoral artery pressure did not differ between groups; however, end-tidal CO2 and mixed venous O2 saturation were higher, and pulmonary artery pressure was lower (p < 0.05) for TVCPR than Control. During TVCPR, switching to 100 cpm increased coronary perfusion pressure (p < 0.05), and switching to 200 cpm increased cerebral perfusion pressure (p < 0.05). CONCLUSIONS: Time-varying CPR significantly improved indicators of net forward blood flow and proportion of ROSC over time without negatively impacting perfusion pressures. Alternating CC rate alternates between perfusion pressures favoring the brain and those favoring the heart. Time-varying CPR represents a new avenue of research for optimizing CPR. INSTITUTIONAL PROTOCOL NUMBER: University of Alabama at Birmingham Institutional Animal Care and Use Committee (IACUC) Protocol Number 140406860.

Comparison of low-energy versus high-energy biphasic defibrillation shocks following prolonged ventricular fibrillation.

INTRODUCTION: Since the initial development of the defibrillator, there has been concern that, while delivery of a large electric shock would stop fibrillation, it would also cause damage to the heart. This concern has been raised again with the development of the biphasic defibrillator. OBJECTIVE: To compare defibrillation efficacy, postshock cardiac function, and troponin I levels following 150-J and 360-J shocks. METHODS: Nineteen swine were anesthetized with isoflurane and instrumented with pressure catheters in the left ventricle, aorta, and right atrium. The animals were fibrillated for 6 minutes, followed by defibrillation with either low-energy (n = 8) or high-energy (n = 11) shocks. After defibrillation, chest compressions were initiated and continued until return of spontaneous circulation (ROSC). Epinephrine, 0.01 mg/kg every 3 minutes, was given for arterial blood pressure < 50 mmHg. Hemodynamic parameters were recorded for four hours. Transthoracic echocardiography was performed and troponin I levels were measured at baseline and four hours following ventricular fibrillation (VF). RESULTS: Survival rates at four hours were not different between the two groups (low-energy, 5 of 8; high-energy, 7 of 11). Results for arterial blood pressure, positive dP/dt (first derivative of pressure measured over time, a measure of left ventricular contractility), and negative dP/dt at the time of lowest arterial blood pressure (ABP) following ROSC were not different between the two groups (p = not significant [NS]), but were lower than at baseline. All hemodynamic measures returned to baseline by four hours. Ejection fractions, stroke volumes, and cardiac outputs were not different between the two groups at four hours. Troponin I levels at four hours were not different between the two groups (12 +/- 11 ng/mL versus 21 +/- 26 ng/mL, p = NS) but were higher at four hours than at baseline (19 +/- 19 ng/mL versus 0.8 +/- 0.5 ng/mL, p < 0.05, groups combined). CONCLUSION: Biphasic 360-J shocks do not cause more cardiac damage than biphasic 150-J shocks in this animal model of prolonged VF and resuscitation.

Effect of timing and duration of a single chest compression pause on short-term survival following prolonged ventricular fibrillation.

BACKGROUND: Pauses during chest compressions are thought to have a detrimental effect on resuscitation outcome. The Guidelines 2005 have recently eliminated the post-defibrillation pause. Previous animal studies have shown that multiple pauses of increasing duration decrease resuscitation success. We investigated the effect of varying the characteristics of a single pause near defibrillation on resuscitation outcome. METHODS: Part A: 48 swine were anesthetized, fibrillated for 7min and randomized. Chest compressions were initiated for 90s followed by defibrillation and then resumption of chest compressions. Four groups were studied-G2000: 40s pause beginning 20s before, and ending 20s after defibrillation, A1: a 20s pause just before defibrillation, A2: a 20s pause ending 30s prior to defibrillation, and group A3: a 10s pause ending 30s prior to defibrillation. Part B: 12 swine (Group B) were studied with a protocol identical to Part A but with no pause in chest compressions. Primary endpoint was survival to 4h. RESULTS: The survival rate was significantly higher for groups A1, A2, A3, and B (5/12, 7/12, 5/12, and 5/12 survived) than for the G2000 group (0/12, p<0.05). Survival did not differ significantly among groups A1, A2, A3, and B. CONCLUSIONS: These results suggest that the Guidelines 2005 recommendation to omit the post-shock pulse check and immediately resume chest compressions may be an important resuscitation protocol change. However, these results also suggest that clinical maneuvers further altering a single pre-shock chest compression pause provide no additional benefit.

An investigation of inter-shock timing and electrode placement for double-sequential defibrillation.

BACKGROUND: Double-Sequential Defibrillation (DSD) is the near-simultaneous use of two defibrillators to treat refractory VF. We hypothesized that (1) risk of DSD-associated defibrillator damage depends on shock vector and (2) the efficacy of DSD depends on inter-shock time. METHODS: Part 1: risk of defibrillator damage was assessed in three anaesthetized pigs by applying two sets of defibrillation electrodes in six different configurations (near-orthogonal or near-parallel vectors). Ten 360J shocks were delivered from one set of pads and peak voltage was measured across the second set. Part 2: the dependence of DSD efficacy on inter-shock time was assessed in ten anaesthetized pigs. Electrodes were applied in lateral-lateral (LL) and anterior-posterior positions. Control (LL Stacked Shocks; one vector, two shocks ∼10 s apart) and DSD therapies (Overlapping, 10 ms, 50 ms, 100 ms, 200 ms, 500 ms, 1000 ms apart) were tested in a block randomized design treating electrically-induced VF (n = ∼89 VF episodes/therapy). Shock energies were selected to achieve 25% shock success for a single LL shock. RESULTS: Part 1: peak voltage delivered was 1833 ± 48 V (mean ± 95%CI). Peak voltage exposure was, on average, 10-fold higher for parallel than orthogonal vectors (p < 0.0001). Part 2: DSD efficacy compared to Stacked LL shocks was higher for Overlapping, 10 ms, and 100 ms (p < 0.05); lower at 50 ms (p < 0.05); and not different at 200 ms or longer inter-shock times. CONCLUSION: Risk of DSD-associated defibrillator damage can be mitigated by using near-orthogonal shock vectors. DSD efficacy is highly dependent on the inter-shock time and can be better, worse, or no different than stacked shocks from a single vector. INSTITUTIONAL PROTOCOL NUMBER: University of Alabama at Birmingham Institutional Animal Care and Use Committee (IACUC) Protocol Number 06860.

Porcine defibrillation thresholds with chopped biphasic truncated exponential waveforms.

PURPOSE: Conventional biphasic truncated exponential (BTE) waveforms have been studied extensively but less is known about "chopping modulated" BTE shocks. Previous studies comparing chopped and unchopped waveforms have found conflicting results. This study compared the defibrillation thresholds (DFTs) of a variety of chopped and unchopped BTE waveforms. METHODS: Six anesthetized pigs were defibrillated after 15s of electrically induced ventricular fibrillation (VF). Three waveform types were studied: unchopped BTE, "short" duration chopped, and "long" duration chopped waveforms. Each type included waveforms generated with 50, 100, and 200 microF capacitances, giving 9 total waveforms. Shocks were delivered in a standard up-down protocol and the order of the waveforms was randomized. Defibrillation thresholds were calculated using a Bayesian logistic regression model. RESULTS: DFTs of the 50, 100, and 200 microF unchopped waveforms were 122+/-22, 124+/-22, and 126+/-22 J. Short chopped DFTs were at least 75+/-23 J higher than unchopped DFTs. Long chopped DFTs averaged 66+/-20 J more than short chopped DFTs. There is a 99.5% probability that the best of the chopped waveforms has a higher DFT than the worst of the unchopped waveforms, and a 95% probability that the difference is at least 37 J. DFT differences between capacitor values were less than 7 J for all waveform types. CONCLUSIONS: When treating swine with short-duration VF, chopped waveforms require more energy to defibrillate than unchopped waveforms. More study is required to assess the performance of chopped waveforms when treating cardiac arrest patients.

Sustained reentry in the left ventricle of fibrillating pig hearts.

It has been proposed that ventricular fibrillation (VF) is driven by sustained reentry. However, mapping studies have not detected such "mother rotors" in large mammalian hearts. We mapped VF from three 21x12 unipolar electrode arrays in 6 pigs. Two of the arrays were adjacent to each other on the left-ventricular epicardium. Electrode spacing was 2 mm. The third array consisted of 21 needles (0.5-mm diameter, 12 electrodes, 1-mm spacing) inserted in a row (2-mm spacing) between the epicardial arrays. A total of 88 5-second VF epochs were analyzed with automatic reentry detection algorithms. Although intramural reentry was sporadically present (29 total occurrences), it was always short-lived with a mean life span of 127+/-57 ms. However, in 3 of the 6 animals, sustained epicardial reentry (ie, reentry persisting for more than a few cycles) was consistently present, often lasting for several seconds. For each epoch, we computed indices characterizing (1) the relative duration of reentry on the two epicardial arrays (R), (2) the flow of wavefronts between epicardial arrays (W), and (3) the relative activation rates of the two epicardial arrays (F). R did not correlate with either W or F indicating that rotor-containing regions did not produce a net outflow of wavefronts and were not faster than neighboring regions. Thus, sustained epicardial, but not intramural, rotors were consistently present in some large animal hearts during VF. However, we found no evidence that these rotors were responsible for sustaining VF through the mechanisms outlined in the mother rotor hypothesis.

Quantification of activation patterns during ventricular fibrillation in open-chest porcine left ventricle and septum.

BACKGROUND: A single stationary mother rotor has been hypothesized to be responsible for maintenance of ventricular fibrillation (VF) in the guinea pig. Previous studies have pointed to the ventricular septum as a possible location for a mother rotor in the pig heart. OBJECTIVES: The purpose of this study was to test the hypothesis that a mother rotor is located in the septum. METHODS: In seven open-chest pigs, we mapped the first 20 seconds of electrically induced VF simultaneously from the posterior left ventricle (LV) and right side of the septum with two electrical arrays. Each array contained 504 electrodes (21 x 24) spaced 2 mm apart in the LV and 1.5 mm apart in the septum. RESULTS: The percentage of VF wavefronts that formed reentrant circuits was significantly lower in the septum (1% +/- 1% [mean +/- SD]) than in the LV (2% +/- 1%). The peak frequency during VF also was significantly smaller in the septum (8.6 Hz +/- 3.0 Hz) than in the LV (10.4 Hz +/- 3.4 Hz). The mean direction of spread of activation of VF wavefronts was away from the region where the posterior LV free wall intersects the posterior septum in both the LV and septum. CONCLUSIONS: The lower incidence of reentry and lower peak frequency in the mapped region of the septum than in the LV indicate that a mother rotor is not present in swine on the RV side of the septum. The mean directions of the VF activation sequences in the LV and septum suggest that if a mother rotor is present during the first 20 seconds of VF, it exists where the posterior LV free wall joins the septum, the region where the posterior papillary muscle inserts.

Comparison of six clinically used external defibrillators in swine.

BACKGROUND: External defibrillation has long been practiced with two types of monophasic waveforms, and now four biphasic waveforms are also widely available. Although waveforms and clinical dosing protocols differ among defibrillators, no studies have adequately compared performance of the monophasic or the biphasic waveforms. This is the first study to compare defibrillation efficacy among biphasic external defibrillators, and does so as part of a study comparing all commonly available waveforms using their respective manufacturer-provided and clinically used doses. METHODS AND RESULTS: Efficacy of six waveforms was tested in 852 short-duration ventricular fibrillation episodes in 14 swine. Protocol 1: 200-J monophasic damped sine (MDS) and monophasic truncated exponential (MTE) shocks were compared to 150-J biphasic shocks in six swine at the low-impedance of these animals. Protocol 2: Four commercially available biphasic defibrillators were compared using their respective manufacturer-recommended dose protocols in eight swine at low and simulated high-impedance. At low-impedance, all biphasic shocks achieved near-perfect success, while efficacy was significantly lower for MDS (67%) and MTE (30%) shocks. In protocol 2, first-shock success rates of the four biphasic defibrillators were uniformly high (97, 100, 100, and 94%) for low-impedance shocks, and decreased for high-impedance shocks (62, 92, 82, and 64%). There were statistically significant differences in efficacy among devices. CONCLUSIONS: Commonly used MDS and MTE waveforms provide markedly dissimilar efficacies. Despite impedance-compensation schemes in biphasic defibrillators, impedance has an impact on their efficacy. At high-impedance, modest efficacy differences exist among clinically available biphasic defibrillators, reflecting differences in both waveforms and manufacturer-provided doses.

Defibrillation threshold and cardiac responses using an external biphasic defibrillator with pediatric and adult adhesive patches in pediatric-sized piglets.

Before recommendations for using an automatic external defibrillator on pediatric patients can be made, a protocol for the energy of a biphasic waveform energy dosing needs to be determined that will allow ventricular defibrillation of 8 year olds while causing only a minimal amount of cardiac damage to infants. Pediatric- and adult-sized electrode patches were alternately applied to 10 isoflurane-anesthetized piglets weighing 3.8-20.1 kg to approximate the body weights of newborns to children < 8 years old. The defibrillation threshold (DFT) was determined for biphasic truncated exponential waveform shocks. Additional shocks, varying from the DFT to 360 Joules (J), were delivered during sinus rhythm or following 30 s of ventricular fibrillation (VF). The DFT was 2.4+/-0.81 and 2.1+/-0.65 J/kg for pediatric and adult patches, respectively (P = N.S.). The change in left ventricular (LV) dP/dt from baseline as a function of shock strength was significantly different at 1 and 10 s after shocks of increasing energy that were delivered in sinus rhythm, and 1, 10, 20, and 30 s after defibrillation shocks. There was no significant difference in LV dP/dt with increasing shock energy at 60 s with either patch size. The time to return of sinus rhythm, ST-segment deviation, and cardiac output were also not significantly different from baseline 60 s following shocks of up to 360 J delivered during sinus rhythm or VF with either patch. The same amount of energy delivered with a biphasic external defibrillator successfully defibrillated VF whether adult or pediatric patches were used. Cardiac rhythm and hemodynamic variables were unaltered at 60 s after shocks delivered at energies of up to 360 J. These data suggest that there is a substantial safety margin above a DFT strength shock for this biphasic waveform in piglets.

Fiberglass needle electrodes for transmural cardiac mapping.

We developed a new method for fabricating plunge needle electrodes for use in cardiac mapping. The needles have 12 electrodes with 1-mm spacing, are 0.5 mm in diameter, and are fabricated from fiberglass reinforced epoxy. They are stiff enough to be easily inserted into beating hearts and durable enough to be reused many times. We found that these new needles elicit smaller, more quickly resolving injury potentials, and when inserted in a row with 2-mm spacing, disrupt ventricular fibrillation activation patterns less than traditional steel needles.

Transmural recording of shock potential gradient fields, early postshock activations, and refibrillation episodes associated with external defibrillation of long-duration ventricular fibrillation in swine.

BACKGROUND: Knowledge of the shock potential gradient (nablaV) and postshock activation is limited to internal defibrillation of short-duration ventricular fibrillation (SDVF). OBJECTIVE: The purpose of this study was to determine these variables after external defibrillation of long-duration VF (LDVF). METHODS: In six pigs, 115-20 plunge needles with three to six electrodes each were inserted to record throughout both ventricles. After the chest was closed, the biphasic defibrillation threshold (DFT) was determined after 20 seconds of SDVF with external defibrillation pads. After 7 minutes of LDVF, defibrillation shocks that were less than or equal to the SDVF DFT strength were given. RESULTS: For DFT shocks (1632 +/- 429 V), the maximum minus minimum ventricular voltage (160 +/- 100 V) was 9.8% of the shock voltage. Maximum cardiac nablaV (28.7 +/- 17 V/cm) was 4.7 +/- 2.0 times the minimum nablaV (6.2 +/- 3.5 V/cm). Although LDVF did not increase the DFT in five of the six pigs, it significantly lengthened the time to earliest postshock activation following defibrillation (1.6 +/- 2.2 seconds for SDVF and 4.9 +/- 4.3 seconds for LDVF). After LDVF, 1.3 +/- 0.8 episodes of spontaneous refibrillation occurred per animal, but there was no refibrillation after SDVF. CONCLUSION: Compared with previous studies of internal defibrillation, during external defibrillation much less of the shock voltage appears across the heart and the shock field is much more even; however, the minimum nablaV is similar. Compared with external defibrillation of SDVF, the biphasic external DFT for LDVF is not increased; however, time to earliest postshock activation triples. Refibrillation is common after LDVF but not after SDVF in these normal hearts, indicating that LDVF by itself can cause refibrillation without requiring preexisting heart disease.

Panoramic optical mapping reveals continuous epicardial reentry during ventricular fibrillation in the isolated swine heart.

During ventricular fibrillation (VF), activation waves are fragmented and the heart cannot contract synchronously. It has been proposed that VF waves emanate from stable sources ("mother rotors"). Previously, we used new optical mapping technology to image VF wavefronts from nearly the entire epicardial surface of six isolated swine hearts. We found that VF was not driven by epicardial rotors, but could not exclude the presence of stable rotors hidden within the ventricular walls. Here, we use graph theoretic analysis to show that, in all 17 VF episodes we analyzed, it was always possible to trace sequences of wavefronts through series of fragmentation and collision events from the beginning to the end of the episode. The set of wavefronts that were so related (the dominant component) consisted of 92%+/-1% of epicardial wavefronts. Because each such wavefront sequence constitutes a continuous activation front, this finding shows that complete reentrant pathways were always present on the epicardial surface and therefore, that wavefront infusion from nonepicardial sources was not strictly necessary for VF maintenance. These data suggest that VF in this model is not driven by localized sources; thus, new anti-VF treatments designed to target such sources may be less effective than global interventions.

Lifetimes of epicardial rotors in panoramic optical maps of fibrillating swine ventricles.

During ventricular fibrillation (VF), electrical activation waves are fragmented, and the heart cannot contract in synchrony. It has been proposed that VF waves emanate from stable periodic sources (often called "mother rotors"). The objective of the present study was to determine if stable rotors are consistently present on the epicardial surface of hearts comparable in size to human hearts. Using new optical mapping technology, we imaged VF from nearly the entire ventricular surface of six isolated swine hearts. Using newly developed pattern analysis algorithms, we identified and tracked VF wave fronts and phase singularities (PS; the pivot point of a reentrant wave front). We introduce the notion of a compound rotor in which the rotor's central PS can change and describe an algorithm for automatically identifying such patterns. This prevents rotor lifetimes from being inappropriately abbreviated by wave front fragmentation and collision events near the PS. We found that stable epicardial rotors were not consistently present during VF: only 1 of 17 VF episodes contained a compound rotor that lasted for the entire mapped interval of 4 s. However, shorter-lived rotors were common; 12.2 (SD 3.3) compound rotors with lifetime >200 ms were visible on the epicardium at any given instant. We conclude that epicardial mother rotors do not drive VF in this experimental model; if mother rotors do exist, they are intramural or septal. This paucity of persistent rotors suggests that individual rotors will eventually terminate by themselves and therefore that the continual formation of new rotors is critical for VF maintenance.

Effects of burst stimulation during ventricular fibrillation on cardiac function after defibrillation.

The purpose of defibrillation is to rapidly restore blood flow and tissue perfusion following ventricular fibrillation (VF) and shock delivery. We tested the hypotheses that 1) a series of 1-ms pulses of various amplitudes delivered before the defibrillation shock can improve hemodynamics following the shock, and 2) this hemodynamic improvement is due to stimulation of cardiac or thoracic sympathetic nerves. Ten anesthetized pigs received a burst of either 15 or 30 1-ms pulses (0.1-10 A in strength) during VF, after which defibrillation was performed. ECG, arterial blood pressure, and left ventricular (LV) pressure were recorded. Defibrillation shocks and burst pulses were delivered from a right ventricular coil electrode to superior vena cava coil and left chest wall electrodes. Sympathetic blockade was induced with 1 mg/kg timolol and trials were repeated. The first half of this protocol was repeated in two animals that were pretreated with reserpine. Heart rate (HR) after 1-, 2-, 5-, and 10-A pulses was significantly higher than after control shocks without preceding pulse therapy. Mean and peak LV pressure measurements increased 38 and 72%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. Mean and peak arterial pressures increased 36 and 43%, respectively, following shocks preceded by 5- and 10-A pulses compared with shocks preceded by no burst pulses. After beta-blockade, HR, mean and peak arterial pressures, and mean LV pressure were not significantly different after pulses of any strength compared with control shocks. LV peak pressure following the 10-A pulses was significantly higher than with no burst pulses but was significantly lower than the response to the 10-A pulses delivered without beta-blockade. HR, mean and peak arterial pressures, and mean and peak LV pressure responses after 15 or 30 5- or 10-A pulses were similar to the responses to the same pulses after beta-blockade. We conclude that a burst of 15-30 1-ms pulses delivered during VF can increase HR, arterial pressure, and LV pressure following defibrillation. beta-Blockade or reserpine pretreatment prevents most of this postshock increase in HR, arterial pressure, and LV pressure.