Biomedical subjects
Publications and source records attributed to Richard E Kerber.
Primary cardiac lymphomas are extremely rare and can be diagnosed by echocardiography. We present the case of a 79-year-old man with an intracardiac mass, shown to be an aggressive large B-cell lymphoma by mediastinal aspiration, who had rapid regression of the tumor following one cycle of chemotherapy.
BACKGROUND: We have demonstrated previously that triphasic waveform shocks were superior to biphasic waveform shocks for transthoracic defibrillation. Our purpose was to compare the efficacy and safety of quadriphasic versus triphasic shocks for transthoracic defibrillation in a porcine model. METHODS: Sixteen adult swine (19-25 kg, mean: 21.5 kg) were deeply anesthetized and intubated. To simulate impedance of the human chest, fixed electrical resistors (25 or 50 ohms) was placed in series with the defibrillator and the chest of each pig. After 30 s of electrically induced VF, each pig received transthoracic shocks, using either a truncated exponential triphasic waveform (5 ms positive pulse duration, 5 ms negative pulse duration and 5 ms positive pulse duration, total waveform duration 15 ms) or a quadriphasic waveform (5/5/5/5 ms, total waveform duration 20 ms). Each pig received transthoracic triphasic and quadriphasic shocks at three selected energy levels (50, 100 and 150 J) in random sequence. Four shocks were delivered at each energy level to construct an energy versus % success curve. Success was defined as VF termination at 5 s after shock. The total shocks were divided into three groups based on the delivered energy actually delivered to the animal: <40, 40-65 and >65 J. Delivered energy = (animal impedance/total impedance) times selected energy of the shock. RESULTS: For high-impedance animals (86-102 ohms), quadriphasic waveform shocks achieved significantly higher percent shock success than triphasic shocks for the termination of VF at the energy levels of >65 J actually delivered (quadriphasic 72.7+/-12.2%, triphasic 38.9+/-7.7%, p<0.02). No differences in the shock success between quadriphasic and triphasic waveforms were found for other two energy levels. There were no differences in ventricular tachycardia or asystole after shocks between quadriphasic and triphasic waveforms. CONCLUSION: In this porcine model, 20 ms (5/5/5/5) quadriphasic shocks were superior to 15 ms (5/5/5) triphasic shocks for transthoracic defibrillation in animals with impedances that simulated high impedance in humans.
BACKGROUND: We have demonstrated previously that the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine (L-NNA) decreases free radical generation and nitrosative injury via peroxynitrite formation after epicardial dc shocks. OBJECTIVE: Our purpose was to explore the effects of NOS inhibition and NOS donation on cardiopulmonary resuscitation (CPR) success after cardiac arrest of variable duration. We used the non-selective NOS inhibitor L-NNA and the selective neuronal NOS inhibitor ARR-17477, the NOS donor S-nitroso-N-acetylpenicillamine (SNAP) and the vasodilator Enalaprilat, which lowers arterial pressure via a non-NO mechanism. METHODS: Part I: 17 pigs undergoing 4 min supported (i.e. with closed-chest compression and ventilation) ventricular fibrillation (VF) were divided into two groups: a no-L-NNA group (n=8) receiving IV saline and an L-NNA group (n=9) receiving IV L-NNA (5 mg/kg) for 8 min before VF was induced. Part II: 35 pigs undergoing 6-8 min VF were randomized to three groups: a no-L-NNA group (n=13) receiving IV saline, an L-NNA group (n=11) receiving IV L-NNA (5 mg/kg) and an ARR17477 group (n=11) receiving IV ARR17477 (5 mg/kg) before VF. All animals in Part II underwent unsupported VF (no chest compression or ventilation) for 6 min (n=13) or 8 min (n=22); closed-chest compression, ventilation and epinephrine (adrenaline) were employed after defibrillation. Part III: 12 swine were divided into two groups: control (n=6) receiving saline and an LNNA group (n=6) receiving IV LNNA (5 mg/kg). Swine underwent 6 min unsupported VF and 2 min supported VF before defibrillation. Part IV: 25 animals were studied to determine the effect of the NO donor SNAP and the angiotensin-converting enzyme inhibitor Enalaprilat on coronary perfusion pressure (CPP). RESULTS: In Part I, after defibrillation, with continued ventilation, chest compression and epinephrine, 8/9 L-NNA pigs achieved ROSC versus 4/8 control pigs (p=0.11). After 60 s of CPR, 7/9 pigs in the L-NNA group achieved ROSC versus 2/8 pigs in the no-L-NNA group (p<0.05). Only 2/9 pigs receiving L-NNA required epinephrine (1 mg) after defibrillation, compared to 6/8 pigs requiring at least one dose of epinephrine in the no-L-NNA group (p<0.05). In Part II, there was no significant difference between L-NNA, ARR17477 and control pigs in ROSC. However, control pigs required 6.8+/-1.4S.E. mg epinephrine; L-NNA pigs and ARR17477 pigs required less epinephrine (3.7+/-0.7 and 3.0+/-0.3 mg, both p=0.01). Shorter chest compression was required in the L-NNA group (252+/-38 s, p<0.05) and in ARR17477 group (222+/-15 s, p<0.05) compared to the control group (405+/-77 s). In Part III, L-NNA infusion caused a significant increase in mean blood pressure at baseline, but did not change CPP throughout the experiment. In Part IV, there were no significant differences in the changes of mean blood pressure and CPP between SNAP and Enalaprilat group in all animals throughout the experiment. CONCLUSION: NOS inhibition pre-arrest did not improve survival, but did reduce requirements for epinephrine and closed-chest compression in a swine resuscitation model.
Lay rescuer automated external defibrillator (AED) programs may increase the number of people experiencing sudden cardiac arrest who receive bystander cardiopulmonary resuscitation (CPR), can reduce time to defibrillation, and may improve survival from sudden cardiac arrest. These programs require an organized and practiced response, with rescuers trained and equipped to recognize emergencies, activate the emergency medical services system, provide CPR, and provide defibrillation. To determine the effect of public access defibrillation (PAD) programs on survival and other outcomes after SCA, the National Heart, Lung, and Blood Institute, the American Heart Association (AHA), and others funded a large prospective randomized trial. The results of this study were recently published in The New England Journal of Medicine and support current AHA recommendations for lay rescuer AED programs and emphasis on planning, training, and practice of CPR and use of AEDs. The purpose of this statement is to highlight important findings of the Public Access Defibrillation Trial and summarize implications of these findings for healthcare providers, healthcare policy advocates, and the AHA training network.
BACKGROUND: Induced hypothermia is recommended to improve neurological outcomes in unconscious survivors of out-of-hospital ventricular fibrillation (VF) cardiac arrest. Patients resuscitated from a VF arrest are at risk of refibrillation, but there are few data on the effects of already existing hypothermia on defibrillation and resuscitation. METHODS AND RESULTS: Thirty-two swine (mean+/-SE weight, 23.0+/-0.6 kg) were divided into 4 groups: normothermia (n=8), mild hypothermia (35 degrees C) (n=8), moderate hypothermia (33 degrees C) (n=8), and severe hypothermia (30 degrees C) (n=8). Hypothermia was induced by surrounding the animal with ice, and VF was electrically induced. After 8 minutes of unsupported VF (no CPR), the swine were defibrillated (biphasic waveform) with successive shocks as needed and underwent CPR until resumption of spontaneous circulation or no response (> or =10 minutes). First-shock defibrillation success was higher in the moderate hypothermia group (6 of 8 hypothermia versus 1 of 8 normothermia; P=0.04). The number of shocks needed for late defibrillation (> or =1 minute after initial shock) was less in all 3 hypothermia groups compared with normothermia (all P<0.05). None of the 8 animals in the normothermia group achieved resumption of spontaneous circulation compared with 3 of 8 mild hypothermia (P=NS), 7 of 8 moderate hypothermia (P=0.001), and 5 of 8 severe hypothermia (P=0.03) animals. Coronary perfusion pressure during CPR was not different between the groups. CONCLUSIONS: When VF was induced in the setting of moderate or severe hypothermia, resuscitative measures were facilitated with significantly improved defibrillation success and resuscitation outcome. The beneficial effect of hypothermia was not due to alteration of coronary perfusion pressure, which suggests that changes in the mechanical, metabolic, or electrophysiological properties of the myocardium may be responsible.
BACKGROUND: Patent foramen ovale (PFO) is commonly demonstrated by transesophageal echocardiography (TEE) in patients with a recent transient ischemic attack or stroke. Our purpose was to determine how the TEE visualization of a PFO alters anticoagulation therapy. METHODS: We retrospectively identified 100 patients with transient ischemic attack or stroke referred for TEE; 50 had a PFO and 50 did not (control patients). RESULTS: Both groups were similar in regard to age, sex, the occurrence of transient ischemic attack versus stroke, and history of stroke. The PFO group had a higher incidence of a mobile interatrial septum, interatrial septal aneurysm, or both ( P < .001 by Fisher exact test). Both groups had similar pre-TEE aspirin, other antiplatelet, and warfarin use. After TEE, warfarin was instituted in 8 of 50 patients with PFO versus 2 of 50 in the control group ( P = .05) and aspirin use was discontinued in 9 of 50 patients with PFO versus 3 of 50 in the control group ( P = .12). CONCLUSION: The main effect of demonstrating a PFO by TEE after an ischemic cerebral event was the institution of warfarin; there was a trend toward discontinuing aspirin.
A probe assembly for simultaneous transesophageal echocardiography and transesophageal cardioversion has been developed. This probe allows cardioversion with the delivery of much lower energy than the standard external approach. Details of the probe construction and its use are described, as is the prospect for future practice. The use of a combined probe may be the technique of choice for patients who require both cardioversion and transesophageal echocardiography.
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BACKGROUND: Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented. METHODS: In 39 swine (21.4+/-1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30 degrees C) (n=10), (2) severe H followed by N (n=10), (3) N followed by moderate H (33 degrees C) (n=10) and (4) moderate H followed by N (n=9). After 30s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20J, 30J, 50J and 100J in random order in both N and H conditions. RESULTS: For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58; p<0.0001), despite the fact that impedance rose from 39+/-3Omega (N) to 42+/-3Omega (H) (p<0.001) and current fell from 22+/-8 (N) to 21+/-7A (H) (p<0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (p=0.0002). CONCLUSION: Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.
We studied the feasibility and efficacy of transesophageal echocardiography (TEE) combined with transesophageal cardioversion (TEC). Secondary aims were to study left atrial flow velocities before and 1 and 5 minutes after TEC, biochemical markers of myocardial damage, and patient tolerability. TEC after a short period of anticoagulation and exclusion of a clot with TEE was safe. TEC was well tolerated and efficacious. The use of a combined probe for TEE and TEC therefore can save time and be more effective. A custom-made probe for combined TEE plus TEC was used. TEC was performed with a step-up protocol (20 J to between 30 and 50 J) and with biphasic shocks. Presence of spontaneous echo contrast was scored. Cumulative energy needed to achieve sinus rhythm was calculated. Discomfort was scored on a scale of 0 to 10. Twenty-six patients underwent combined TEE/TEC. Sinus rhythm was achieved in 24 of 26 patients (92%) with a mean cumulative energy of 42.3 J. Sixteen of 26 patients were cardioverted with a 20-J shock, and 6 of these patients had early recurrence of atrial fibrillation. All biochemical markers were unaffected, and TEE/TEC was well tolerated. Left atrial appendage velocity decreased significantly after TEC. Thus, the use of a TEE/TEC probe offers effective cardioversion with low energy levels, is well tolerated, and hemodynamics during and immediately after cardioversion can be monitored. Early cardioversion after exclusion of a clot with this combined probe is time saving and cost effective.
OBJECTIVES: to demonstrate that nitric oxide (NO) contributes to free radical generation after epicardial shocks and to determinethe effect of a nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NNA), on free radical generation. BACKGROUND: Free radicals are generated by direct current shocks for defibrillation. NO reacts with the superoxide (O2*-) radical to for peroxynitrite (O = NOO-), which is toxic and initiates additional free radical generation. The contribution of NO to free radical generation after defibrillation is not fully defined. METHODS AND RESULTS: Fourteen open chest dogs were studied. In the initial eight dogs, 40 J damped sinusoidal monophasic epicardial shocks was administered. Using electron paramagnetic resonance, we monitored the coronary sinus concentration of ascorbate free radical (Asc*-), a measure of free radical generation (total oxidative flux). Epicardial shocks were repeated after L-NNA, 5 mg/kg IV. In six additional dogs, immunohistochemical staining was done to identify nitrotyrosine, a marker of reactive nitrogen species-mediated injury, in post-shock myocardial tissue. Three of these dogs received L-NNA pre-shock. After the initial 40 J shock, Asc*- rose 39 +/- 2.5% from baseline. After L-NNA infusion, a similar 40 J shock caused Asc*- to increase only 2 +/- 3% form baseline (P < 0.05, post-L-NNA shock versus initial shock). Nitrotyrosine staining was more prominent in control animals than dogs receiving L-NNA, suggesting prevention of O = NOO- formation. CONCLUSION: NO contributes to free radical generation and nitrosative injury after epicardial shocks; NOS inhibitors decrease radical generation by inhibiting the production of O = NOO-.
Triphasic shocks have been evaluated for endocardial defibrillation but not for open-chest epicardial defibrillation. The purpose of this study was to compare the efficacy and safety of biphasic versus triphasic shocks for epicardial defibrillation in a porcine model. Twenty-two adult swine (18-28 kg) were deeply anesthetized and intubated. After 30 seconds electrically induced VF, each pig received truncated exponential biphasic (7.2-ms positive pulse duration and 7.2-ms negative pulse duration, total waveform duration 14.4 ms) and triphasic (4.8/4.8/4.8 ms, total waveform duration 14.4 ms) epicardial shocks. Pigs in group 1 (n = 11) received epicardial biphasic and triphasic shocks from large hand held paddle electrodes (44.2 cm2); pigs in group 2 (n = 11) received shocks from small paddle electrodes (15.9 cm2). Shocks were given at five selected energy levels (3-30 J) in random sequence. Four shocks were delivered at each energy level to construct an energy versus percentage of success curve. In group 1 (large paddle electrodes), percentage of shock success was significantly higher for triphasic shocks at the energy levels of 3, 5, 10, and 20 J compared to biphasic shocks. In group 2 (small paddle electrodes), triphasic shocks yielded a significantly higher percentage of shock success than biphasic shocks at the energy levels of 5, 10, and 20 J). Shock induced ventricular tachycardia was similar for both waveforms; asystole was rare. For open-chest defibrillation, triphasic waveform shocks were superior to biphasic waveform shocks for VF termination at energy levels of 3-20 J and were as safe as biphasic shocks.
OBJECTIVES: Our objective was to evaluate the efficacy of triphasic waveforms for transthoracic defibrillation in a swine model. BACKGROUND: Triphasic shocks have been found to cause less post-shock dysfunction than biphasic shocks in chick embryo studies. METHODS: After 30 s of electrically induced ventricular fibrillation (VF), each pig in part I (n = 32) received truncated exponential biphasic (7.2/7.2 ms) and triphasic (4.8/4.8/4.8 ms) transthoracic shocks. Each pig in part II (n = 14) received biphasic (5/5 ms) and triphasic shocks (5/5/5 ms). Three selected energy levels (50, 100, and 150 J) were tested for parts I and II. Pigs in part III (n = 13) received biphasic (5/5 ms) and triphasic (5/5/5 ms) shocks at a higher energy (200 and 300 J). Although the individual pulse durations of these shocks were equal, the energy of each pulse varied. Nine pigs in part I also received shocks where each individual pulse contained equal energy but was of a different duration (biphasic 3.3/11.1 ms; triphasic 2.0/3.2/9.2 ms). RESULTS: Triphasic shocks of equal duration pulses achieved higher success than biphasic shocks at delivered low energies: <40 J: 38 +/- 5% triphasic vs. 19 +/- 4% biphasic (p < 0.01); 40 to <50 J: 66 +/- 7% vs. 42 +/- 7% (p < 0.01); and 50 to <65 J: 78 +/- 4% vs. 54 +/- 5% (p < 0.05). Shocks of equal energy but different duration pulses achieved relatively poor success for both triphasic and biphasic waveforms. Shock-induced ventricular tachycardia (VT) and asystole occurred less often after triphasic shocks. CONCLUSIONS: Triphasic transthoracic shocks composed of equal duration pulses were superior to biphasic shocks for VF termination at low energies and caused less VT and asystole.
OBJECTIVE: To determine if cardiac injury following DC shocks includes impairment of coronary vascular reactivity. METHODS: 36 dogs (18-32 kg) were anesthetized and a thoracotomy was performed. Either antioxidant enzymes, superoxide dismutase (SOD, 15,000 U/kg) plus catalase (55,000 U/kg) or the NO synthase inhibitor N(G)-nitro-L-arginine (L-NNA, 5 mg/kg) was administered IV prior to sham (no shocks) or DC shock treatment, and the results were compared to dogs which did not receive SOD/catalase or L-NNA. In sham dogs, electrodes cradled the heart, but no shocks were delivered. In shock dogs, three 20 Joule DC shocks were delivered to the epicardium using hand-held paddles. Other dogs were allowed a 3-hour recovery period after the shocks. Epicardial microvessels and conduit rings were studied in vitro. Antagonists were not added to the bath of the study vessel. Internal diameter was measured in microvessels after constriction with endothelin. Tension of conduit arteries was measured after constriction with PGF(2alpha). Responses to acetylcholine (Ach, 10(-10)-10(-4) M), bradykinin (10(-14)-10(-6) M), the calcium ionophore A23187 (A23187, 10(-12)-10(-4) M) or nitroprusside (SNP, 10(-10)-10(-4) M) were measured. RESULTS: Bradykinin, A23187 and SNP dependent dilation was not different between vessels from sham and shocked animals. Dilation to Ach was attenuated in vessels from shocked dogs. Superoxide production probably contributed to the impaired dilation to Ach since treatment with SOD/catalase improved dilation. Treatment with L-NNA also improved vascular function after DC shock. CONCLUSION: DC shocks cause endothelial dysfunction, as demonstrated by impaired dilation to acetylcholine, in both canine coronary microvascular and conduit arteries. Since pretreatment with either SOD/catalase or L-NNA protects against this damage, a free radical mechanism, possibly involving eNOS, may contribute to endothelial dysfunction.DC shocks for cardioversion and defibrillation cause myocardial injury that may be free radical mediated.
OBJECTIVE: Our objective was to determine if magnesium reduces free radicals generated by direct current countershock and preserves left ventricular contractile function. BACKGROUND: We have previously shown that magnesium reduces free radicals in a coronary occlusion-reperfusion model, and therefore also might reduce free radical generation by direct current shocks. METHODS: In eight swine weighing 18-27 kg (mean: 22 kg), using electron paramagnetic resonance, we monitored continuously the coronary sinus concentration of ascorbate free radical, a measure of free radical generation (total oxidative flux). Epicardial shocks (30 J) using a truncated exponential biphasic waveform (5/5 ms) were administered. Each animal received two shocks, one without and one with magnesium, 80 mg/min IV, beginning 10 min before the shock and continuing to 15 min after the shock. Percent fractional area shortening of the left ventricular cavity was determined by 2-dimensional echocardiography. RESULTS: Magnesium shocks resulted in a significantly lower increase in the ascorbate free radical concentration (0.6+/-4.6%) than no-magnesium shocks (16+/-3.3%, P<0.05) at 12 min after the shock. Total radical flux was reduced 72% (P<0.05), and left ventricular fractional area shortening was preserved: baseline: 69+/-2.6%, no-magnesium shocks: 41+/-2.8% (P<0.05, versus baseline) and magnesium shocks 61+/-3.7%. CONCLUSIONS: Magnesium pre-treatment reduced oxygen free radicals generated by direct current shocks; post-shock left ventricular contractile function was not impaired. Magnesium may be cardioprotective during epicardial ('surgical') defibrillation.
OBJECTIVES: To demonstrate that nitric oxide (NO) contributes to free radical generation after epicardial shocks and to determine the effect of a nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NNA), on free radical generation. BACKGROUND: Free radicals are generated by direct current shocks for defibrillation. NO reacts with the superoxide (O(2).(-)) radical to form peroxynitrite (O=NOO(-)), which is toxic and initiates additional free radical generation. The contribution of NO to free radical generation after defibrillation is not fully defined. METHODS AND RESULTS: Fourteen open chest dogs were studied. In the initial eight dogs, 40 J damped sinusoidal monophasic epicardial shocks was administered. Using electron paramagnetic resonance, we monitored the coronary sinus concentration of ascorbate free radical (Ascz.(-)), a measure of free radical generation (total oxidative flux). Epicardial shocks were repeated after L-NNA, 5 mg/kg IV. In six additional dogs, immunohistochemical staining was done to identify nitrotyrosine, a marker of reactive nitrogen species-mediated injury, in post-shock myocardial tissue. Three of these dogs received L-NNA pre-shock. After the initial 40 J shock, Ascz.(-) rose 39+/-2.5% from baseline. After L-NNA infusion, a similar 40 J shock caused Ascz.(-) to increase only 2+/-3% from baseline (P<0.05, post-L-NNA shock versus initial shock). Nitrotyrosine staining was more prominent in control animals than dogs receiving L-NNA, suggesting prevention of O=NOO(-) formation. CONCLUSIONS: NO contributes to free radical generation and nitrosative injury after epicardial shocks; NOS inhibitors decrease radical generation by inhibiting the production of O=NOO(-).
BACKGROUND: During reperfusion of ischemic myocardium nitric oxide (NO) reacts with superoxide radicals to form cardiotoxic peroxynitrite, which causes lipid peroxidation. Our hypothesis was that infusion of a NO donor S-nitroso-N-acetylpenicillamine (SNAP) during ischemia-reperfusion would exacerbate the oxidative damage to the myocardium by increased formation of nitrogen radicals. METHODS AND RESULTS: In 19 open-chest dogs, left anterior descending (LAD) coronary occlusion (15 min)-reperfusion (15 min) sequences were created. Using electron paramagnetic resonance (EPR), we monitored the coronary sinus concentration of ascorbate free radical (Ascz*-), a measure of free radical generation (total oxidative flux). Seven control dogs (Group 1) received intravenous saline infusion during occlusion-reperfusion, while 12 dogs received SNAP infusion (Group 2: 2.5 microg/min per kg SNAP, and Group 3: 5 microg/min per kg SNAP). Left ventricular fractional area shortening was determined by echocardiography. Dogs in Group 3 receiving a high dose of SNAP (5 microg/min per kg) demonstrated a higher Ascz*- concentration increase than the control group. Percent fractional area shortening in Group 1 declined from 77+/-4.0 (baseline) to 54+/-9.0% during ischemia (P<0.05), and then fully recovered to 74+/-3.7% with reperfusion. In the SNAP-treated dogs, the percent fractional area shortening during reperfusion was significantly lower than baseline in Group 2 (55+/-3.9 vs. baseline 74+/-4.4%, P<0.05) and in Group 3 (49+/-5.0 vs. baseline 71+/-4.5%, P<0.01). In five additional dogs, nitrotyrosine immunohistochemistry showed heavy staining of the ischemic-reperfused myocardium. CONCLUSIONS: The NO donor SNAP increased free radical concentration and exacerbated myocardial oxidative damage after ischemia-reperfusion.
The aim of the study was to compare biphasic versus monophasic shocks for open-chest epicardial defibrillation. Transthoracic biphasic waveform shocks require less energy to terminate ventricular fibrillation compared to monophasic waveform shocks. However, if biphasic shocks are effective for open-chest epicardial ("surgical") defibrillation has not been established. Twenty-eight anesthetized adult swine (15-25 kg) underwent a midline sternotomy. Ventricular fibrillation was electrically induced. After 15 seconds of ventricular fibrillation, each pig in group 1 (n = 16) randomly received damped sinusoidal monophasic epicardial shocks and truncated exponential biphasic epicardial shocks from large (44.2 cm2) paddle electrodes at eight energy levels (2-50 J). Pigs in group 2 (n = 12) received monophasic and truncated exponential biphasic shocks from small (15.9 cm2) paddle electrodes. In group 1 (large paddle electrodes), the overall percent shock success rose from 15 +/- 9% at 2 J to 97 +/- 3% at 50 J. In this group there was no significant difference in percent of shock success between damped sinusoidal monophasic and biphasic waveform shocks. In group 2 (small paddle electrodes), biphasic shocks yielded a significantly higher percent of shock success than monophasic shocks at mid-energy levels from 7 to 20 J (all P < 0.01). With small surgical paddle electrodes, biphasic waveform shocks demonstrated a significantly higher percent of shock success rate compared to monophasic waveform shocks. With large paddle electrodes, the two waveforms were equally effective.