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Effects of autonomic manipulation on ventricular fibrillation and internal cardiac defibrillation thresholds in pigs.

Autonomic tone may contribute to cardiac arrhythmogenesis and influence the efficacy of implantable defibrillators. Fifty-two anesthetized pigs were randomized to: (1) methacholine (n = 12); (2) nitroprusside (n = 12); (3) phenylephrine (n = 12); (4) carbachol (n = 8); and (5) saline (n = 8). Ventricular fibrillation threshold (VFT) and triplicate defibrillation thresholds (DFT) were obtained before and during each intervention. Mean (+/- SE) VFT was increased with: methacholine (76 +/- 10.6 V vs 39 +/- 7.1 V, P < 0.001); phenylephrine (68 +/- 10.5 V vs 38 +/- 6.2 V, P < 0.001); and carbachol (106 +/- 11.5 V vs 30 +/- 6.5 V, P < 0.0001). Nitroprusside and saline failed to alter VFT. Mean (+/- SE) DFT was decreased with: methacholine (7.7 +/- 0.8) vs 9.7 +/- 0.8 J, P < 0.001); phenylephrine (9.8 +/- 0.9 J vs 11.3 +/- 1.0 J, P < 0.05); and carbachol (9.2 +/- 0.7 J vs 12.2 +/- 0.8 J, P < 0.0001), remaining unchanged following nitroprusside and saline infusion. Thus, modulation of autonomic tone modified arrhythmia susceptibility and the energy necessary for defibrillation, increased parasympathetic tone, increased VFT, and decreased DFT. Evaluation of autonomic balance, particularly parasympathetic tone, may be useful with the implantation of automatic defibrillators.

Animals↗

On the mechanism of ventricular defibrillation.

The mechanism of ventricular defibrillation can be considered at many different levels. The highest level is considered at strength of the shock given through the defibrillation electrodes. At the next level, the mechanism of defibrillation can be examined in terms of the electrical field that the shock produces throughout the ventricles. Other levels include the effects this electric field has on the activation sequences and on the cellular action potentials that either initiate or inhibit the early sites of activation following the shock. Yet another level considers the mechanism by which the shock field initiates new action potentials or prolongs the action potential by changing the transmembrane potential during the shock. Finally, the subcellular level is considered, which involves the response of the individual ion channels to the shock. This review gives a brief overview of some salient features of defibrillation at each of these mechanistic levels.

Action Potentials↗

An up-down Bayesian, defibrillation efficacy estimator.

In both the clinic and the laboratory, efficacy estimators are used to estimate the shock strength required to achieve a given defibrillation success rate. In the clinic, efficacy estimators are used to estimate highly effective doses (i.e., the shock strength that defibrillates 95% of the time), in order to choose the setting for an ICD. Efficacy estimators are used in the laboratory to compare defibrillation techniques and configurations. Current efficacy estimators are inadequate because they are either difficult to use, can only estimate the shock strength that defibrillates 50% of the time, or do not yield desirable accuracy (low RMS error). This article presents a Bayesian estimation technique that forces the difference between successive test shock strengths (step-size) to be a fixed value after each measurement. Constraining the difference dramatically reduces the computational complexity of the up-down Bayesian method. This new, up-down Bayesian protocol can be used with up to 15 measurements to estimate the shock strength for any given success rate. Simulations show that the added constraint (fixed step-size) only slightly increases the rms error, as compared to the optimum Bayesian protocol. Our simulations also show that protocols can be generated for shock strengths rounded to the nearest 1, 10, or 50 V. without a great increase in RMS error. Experimental results from a subset of all the simulations are reported from six animals, showing a < -2.4% difference between the simulated and measured errors.

Animals↗

Postshock recovery interval of relatively refractory myocardium as a possible explanation for disparate defibrillation efficacy between monophasic and biphasic waveforms.

We investigated the electrophysiological background for the waveform related variability of defibrillation efficacy. In 22 open-chest dogs, a localized potential gradient was created using an 8-V or 16-V field stimulus across a pair of plate electrodes separated by 5 mm. The post shock recovery interval of the nondepolarized myocardium adjacent to the excited area was estimated by the residual refractory period after an appropriately timed field stimulus. The postshock recovery interval and the defibrillation threshold were compared among six different waveforms but with the same total duration of 12 ms (n = 11) or 16 ms (n = 11). Six defibrillation thresholds in individual hearts showed a significant inverse correlation with postshock recovery intervals in most dogs (8/11) tested with a total pulse duration of 12 ms (8 V stimulus: r = -0.80 +/- 0.20 [n = 11]). In contrast, waveforms with a total duration of 16 ms failed to reveal this distinct relationship. We conclude that the waveform related variability of defibrillation efficacy is associated with the refractoriness of relatively refractory myocardium when the total pulse duration is within a certain range. However, the mechanisms responsible for waveform performance may vary as the total pulse duration changes.

Animals↗

Effect of the superior vena cava electrode surface area on defibrillation threshold in different lead systems.

Little data is available comparing the efficacy of the Transvene, Endotak C 70 series, and the active CAN configuration on defibrillation success. In addition, the impact of the superior vena cava (SVC) electrode surface area and length on the active CAN system is unknown. Therefore, we compared the defibrillation efficacy of the Transvene and Endotak C 70 series lead systems with and without the active CAN in dogs. Defibrillation threshold (DFT) testing was randomly performed in 20 dogs. In protocol I (10 dogs), DFT energy was compared in three RV/SVC lead systems with an SVC electrode defibrillating surface area of 90 mm2 (Transvene-90), 160 mm2 (Transvene-160), 617 mm2 (Endotak), and an RV/CAN configuration. In protocol II (10 dogs), DFT comparison was performed in the Transvene-90/CAN, Transvene-160/CAN, Endotak/CAN, and RV/CAN configurations. In protocol I, increasing the SVC surface area from 90 to 160 mm2 and from 160 to 617 mm2 significantly lowered DFT energy. The Endotak and the RV/CAN systems provided the lowest DFT energy requirements. In protocol II, the Endotak/CAN system significantly lowered DFT energy compared to the other three lead configurations. In both protocols, the impedance decreased as the SVC surface area increased from 90 to 160 mm2. However, no significant reduction in DFT impedance occurred as the SVC surface area increased from the Transvene-160 to the Endotak lead. Increasing the SVC surface area from 90 to 617 mm2 in a two coil lead system lowered DFT energy to similar levels provided by the RV/CAN configuration. The addition of an SVC electrode with a surface area of 90 or 160 mm2 did not reduce DFT energy compared to the RV/CAN configuration. The Endotak/CAN system, however, provided the lowest DFT requirements.

Animals↗

Effect of a class III antiarrhythmic drug on the configuration of dose response curve for defibrillation.

Antiarrhythmic agents with a Class III action are known to increase defibrillation efficacy. We investigated whether a Class III drug simply shifts the dose-response curve for defibrillation or more extensively alters the curve. Forty-five dogs were divided into four groups according to the shock waveform and the presence or absence of treatment with a novel Class III drug, MS-551 (2 mg/kg bolus + 0.02 mg/kg per min). In addition to the conventional transcardiac DFT, dose-response curves were obtained by fitting the results of 40 fibrillation-defibrillation sequences at five shock strengths to a logistic model. MS-551 significantly decreased DFT regardless of the shock waveform (control vs MS-551 = 306 +/- 79 V vs 229 +/- 72 V [monophasic shock, P < 0.05], or 227 +/- 42 V vs 176 +/- 26 V [biphasic shock, P < 0.005]). The dose-response curves in dogs treated with MS-551 had a gentler slope than those without treatment, and the ratio of the voltages corresponding to 50% and 90% defibrillation success (V90/V50) was significantly greater in the MS-551 group (monophasic: 1.21 +/- 0.06 vs. 1.62 +/- 0.42 [P < 0.005], biphasic: 1.20 +/- 0.05 vs 1.37 +/- 0.18 [P < 0.01]). The V90/DFT ratio was also significantly larger in the MS-551 group (monophasic: 1.22 +/- 0.12 vs 1.66 +/- 0.37 [P < 0.001]; biphasic: 1.19 +/- 0.11 vs 1.44 +/- 0.79 [P < 0.005]). Thus, this Class III drug decreased the shock strength corresponding to relatively higher success rate (approximately 90%) less markedly than that for moderate success rate (approximately 50%). These results suggest that a Class III drug does not simply shift the dose response curve in proportion to the change in DFT, but more extensively alters its configuration.

Action Potentials↗

Surgical open-chest ventricular defibrillation: triphasic waveforms are superior to biphasic waveforms.

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.

Animals↗

Ventricular fibrillation resulting from synchronized internal atrial defibrillation in a patient with ventricular preexcitation.

This case describes ventricular proarrhythmia as a result of a synchronized internal atrial defibrillation shock in a 29-year-old man with Ebstein's anomaly referred for radiofrequency ablation of a right posterior accessory pathway. During the electrophysiologic study, atrial fibrillation was induced and 3/3 msec shocks of various strengths were delivered between two decapolar defibrillation catheters in the coronary sinus and right atrial appendage. A 2.0-J biphasic shock synchronized to an R wave after a short-long-short ventricular cycle length pattern with a preshock coupling interval of 245 msec induced ventricular fibrillation, which was externally defibrillated with 200 J. This observation has implications for the development of implantable atrial defibrillators.

Adult↗

The effects of ventricular fibrillation duration and a preceding unsuccessful shock on the probability of defibrillation success using biphasic waveforms in pigs.

INTRODUCTION: While the defibrillation threshold has been reported to increase with ventricular fibrillation (VF) duration for monophasic waveforms, the effect of VF duration for biphasic waveforms is unknown. METHODS AND RESULTS: The ED 50 requirements (the 50% probability of defibrillation success) for an endocardial lead system, which included a subcutaneous array, were determined by logistic regression using a recursive up-down algorithm for a biphasic waveform (6/6 msec). The study was performed in two parts, each with eight pigs. In part 1, ED 50 was compared for shocks delivered after 10 seconds of VF and for shocks delivered after 20 seconds of VF following a failed first shock at 10 seconds. Energy at ED 50 decreased from 6.5 +/- 0.9 J for shocks delivered after 10 seconds of VF to 4.9 +/- 0.8 J (P < 0.01) for shocks delivered after 20 seconds. To determine if improved second shock efficacy was a result of preconditioning by the failed first shock or a function of VF duration, part 2 of the study compared defibrillation efficacy between shocks delivered after 10 seconds of VF with shocks delivered after 20 seconds of VF with and without a failed first shock at 10 seconds. Mean energy at ED 50 decreased from 10.1 +/- 2.4 J for shocks delivered after 10 seconds of VF to 7.9 +/- 2.4 J (P < 0.01) and 7.5 +/- 3.2 J (P < 0.01) for shocks delivered after 20 seconds of VF with and without a failed first shock, respectively. The mean energy at ED 50 for shocks delivered after 20 seconds of VF with and without a failed first shock was not significantly different (P = 0.53). A strong linear correlation for energy at ED 50 was found between shocks delivered after 10 seconds of VF and shocks delivered after 20 seconds of VF following a failed first shock (r = 0.95, P < 0.01). CONCLUSION: (1) As opposed to monophasic shocks, ED 50 is significantly lower for biphasic shocks delivered after 20 seconds of VF compared with shocks delivered after 10 seconds of VF in pigs. (2) An unsuccessful biphasic shock in pigs does not affect the defibrillation efficacy for a subsequent shock. (3) ED 50 for a biphasic shock delivered after 20 seconds of VF is linearly related to ED 50 for a shock delivered after 10 seconds of VF.

Animals↗

Success and failure of the defibrillation shock: insights from a simulation study.

INTRODUCTION: This simulation study presents a further inquiry into the mechanisms by which a strong electric shock fails to halt life-threatening cardiac arrhythmias. METHODS AND RESULTS: The research uses a model of the defibrillation process that represents a sheet of myocardium as a bidomain. The tissue consists of nonuniformly curved fibers in which spiral wave reentry is initiated. Monophasic defibrillation shocks are delivered via two line electrodes that occupy opposite tissue boundaries. In some simulation experiments, the polarity of the shock is reversed. Electrical activity in the sheet is compared for failed and successful shocks under controlled conditions. The maps of transmembrane potential and activation times calculated during and after the shock demonstrate that weak shocks fail to terminate the reentrant activity via two major mechanisms. As compared with strong shocks, weak shocks result in (1) smaller extension of refractoriness in the areas depolarized by the shock, and (2) slower or incomplete activation of the excitable gap created by deexcitation of the negatively polarized areas. In its turn, mechanism 2 is associated with one or more of the following events: (a) lack of some break excitations, (b) latency in the occurrence of the break excitations, and (c) slower propagation through deexcited areas. Reversal of shock polarity results in a change of the extent of the regions of deexcitation, and thus, in a change in defibrillation threshold. CONCLUSION: The results of this study indicate the paramount importance of shock-induced deexcitation in both defibrillation and postshock arrhythmogenesis.

Electric Countershock↗

Effects of sildenafil citrate on defibrillation efficacy.

INTRODUCTION: Although fatal arrhythmia and sudden death have been reported in patients taking sildenafil citrate, its effect on defibrillation efficacy has not been investigated. The aim of this study was to test the hypothesis that sildenafil citrate increases the shock strength required to successfully defibrillate during ventricular fibrillation (VF). METHODS AND RESULTS: A total of 26 pigs (20-25 kg) were randomly assigned into three groups. In each group, the defibrillation threshold (DFT) was determined at the beginning of the study using a three-reversal up/down protocol. Each shock (RV-SVC, biphasic) was delivered after 10 seconds of VF. Group 1 (n = 10) received 50 mg and group 2 (n = 10) received 100 mg of sildenafil citrate intravenously at a rate of 2 mL/minute for 50 minutes. Group 3 (n = 6) received 100 mL of saline intravenously at the same rate as in group 1. The DFT was determined again after the drug (drug-DFT) and saline (saline-DFT) administration. For 100-mg sildenafil citrate infusion, the DFT (483 +/- 39 V, 18 +/- 3 J) was significantly (P < 0.003 and P < 0.01, respectively) higher than the control-DFT (407 +/- 123 V, 13 +/- 7 J). This sildenafil citrate infusion increased the DFT approximately 19% by voltage, and approximately 38% by total energy. After 50-mg sildenafil citrate infusion, the DFT (454 +/- 28 V, 15 +/- 2 J) was not different than the control DFT (449 +/- 28 V, 15 +/- 2 J). Saline infusion (391 +/- 18 V, 12 +/- 1 J) did not alter the control DFT (399 +/- 22 V, 12 +/- 1 J). CONCLUSION: The 100-mg sildenafil citrate infusion, representing a supra-therapeutic plasma level, significantly increased the DFT. This finding indicates that VF occurring during supra-therapeutic sildenafil citrate treatment would require a stronger shock to successfully defibrillate.

Animals↗

Left ventricular function after monophasic and biphasic waveform defibrillation: the impact of cardiopulmonary resuscitation time on contractile indices.

UNLABELLED: Previous work has suggested that low-energy biphasic waveform defibrillation (BWD) is followed by less post-resuscitation left ventricular (LV) dysfunction when compared with higher-energy monophasic waveform defibrillation (MWD). To the best of the authors' knowledge, the effect of cardiopulmonary resuscitation (CPR) duration and total ischemia time on LV function after countershock, controlling for waveform type, has not been evaluated. OBJECTIVE: To determine the effect of CPR duration on LV function after MWD and BWD. METHODS: VF was electrically induced in anesthetized and instrumented swine. After 5 minutes of VF, the animals were randomized to MWD (n = 22) or one of two BWDs (n = 46). If countershock terminated VF but was followed by a nonperfusing rhythm, conventional manual CPR without drug therapy was performed until restoration of spontaneous circulation (ROSC), defined as a systolic arterial pressure >60 mm Hg for 10 minutes without vasopressor support. Systolic LV pressure (LVP), LV dP/dt (first derivative of pressure measured over time), and cardiac output (CO) were measured at intervals for 60 minutes postresuscitation. CPR times (times to ROSC) and hemodynamic variables for the three groups were compared. Multivariable linear regression was performed to assess the contribution of defibrillation waveform, total joules, and CPR time on LVP, LV dP/dt, and CO at 15, 30, and 60 minutes postresuscitation. RESULTS: When analyzed as groups, significant differences in median number of shocks to terminate VF, total joules, or CPR time were not observed between waveform groups. Regression analysis demonstrated that increasing CPR time was associated with a significant effect on indices of LV function at 15 and 30 minutes postresuscitation. Global LV function was not influenced by waveform type or total joules. CONCLUSIONS: Adjustment for CPR time, a determinant of total myocardial ischemia time, is necessary when defibrillation waveforms are compared for their effect on postresuscitation cardiac function and short-term outcome.

Animals↗

Defibrillators in general practice.

After a successful pilot scheme introduced in 1975, when six portable defibrillators were provided for health centres, an additional 50 defibrillators were provided in February 1982 for general practitioners to use. Between December 1975 and February 1984 defibrillation was attempted in 54 patients who collapsed with clinical cardiac arrest in the presence of general practitioners or less than five minutes before their arrival. A cardiac output was achieved in 32 patients, 28 survived to reach hospital via a mobile coronary care unit, and 22 were discharged alive. Of the 28 admitted to hospital, 24 were found to have myocardial infarction. If all general practitioners carried defibrillators they might make an important dent in the early mortality from myocardial infarction in addition to that achieved by a mobile coronary care unit.

Adult↗

Use of automated external defibrillator by first responders in out of hospital cardiac arrest: prospective controlled trial.

OBJECTIVE: To test the hypothesis that the use of an automated external defibrillator by police and fire fighters results in higher discharge rates for out of hospital cardiac arrest. DESIGN: Controlled clinical trial with initial random allocation of automated external defibrillators to first responders in four of the eight participating regions; each region switched from control to experimental, and vice versa, every four months. SETTING: Amsterdam and surroundings, the Netherlands. PARTICIPANTS: Patients with witnessed out of hospital cardiac arrests, identified by the emergency medical system between January 2000 and January 2002. MAIN OUTCOMES MEASURES: Survival to hospital discharge; return of spontaneous circulation; admission to hospital. RESULTS: 243 patients (65% in ventricular fibrillation) were included in the experimental area and 226 patients (67% in ventricular fibrillation) in the control area. The median time interval between collapse and first shock was 668 seconds in the experimental area and 769 seconds in the control area (P < 0.001). 44 (18%) patients in the experimental area versus 33 (15%) patients in the control area were discharged (odds ratio 1.3 (95% confidence interval 0.8 to 2.2), P = 0.33), 139 (57%) experimental versus 108 (48%) control patients had return of spontaneous circulation (1.5 (1.0 to 2.2), P = 0.05), and 103 (42%) experimental versus 74 (33%) control patients were admitted (1.5 (1.1 to 1.6), P = 0.02). The median delay from receipt of call to dispatch of the ambulance was 120 seconds, and the delay to dispatch of the first responder was 180 seconds. CONCLUSIONS: Use of automated external defibrillators by first responders did not significantly increase survival to discharge from hospital, although it did improve return of spontaneous circulation and admission to hospital. Improved dispatch procedures should increase the success of programmes of first responders using external defibrillators.

Adult↗

Cost effectiveness and cost utility model of public place defibrillators in improving survival after prehospital cardiopulmonary arrest.

OBJECTIVE: To determine the cost effectiveness and cost utility of locating defibrillators in all major airports, railway stations, and bus stations throughout Scotland. DESIGN: Economic modelling exercise with data from Heartstart (Scotland). Parameters used in economic model included direct costs derived for increased accident and emergency attendances, increased hospital bed days, purchase and maintenance of defibrillators, and training in their use; life years gained calculated from increased discharges from hospital and mean survival after discharge; utility (quality of life) obtained from published data. Sensitivity analyses tested the robustness of model. Future gains discounted at 1.5% a year and future costs at 6%. SETTING: Whole of Scotland. SUBJECTS: Records of all prehospital cardiac arrests due to presumed heart disease that occurred in a major airport, railway, or bus station between May 1991 and March 1998 and were not witnessed by ambulance or medical staff. MAIN OUTCOME MEASURES: Observed survival to hospital admission and observed survival to discharge. Predicted survival calculated by applying observed survival in patients attended by ambulance staff within three minutes to those who waited longer. RESULTS: The total discounted direct costs were 18 325 pounds sterling a year. The cost per life year gained was 29 625 pounds sterling (49 625 dollars, 43 151 Euros) and the cost per quality adjusted life year (QALY) gained was pound 41 146 (68 924 dollars, 59 932 Euros). More widespread provision of public place defibrillators would increase these figures. CONCLUSIONS: The cost per QALY calculated for public place defibrillators represents poorer value for money than some alternative strategies for improving survival after prehospital cardiopulmonary arrest, such as the use of other trained first responders. The figure exceeds the commonly discussed cut off levels for funding in the United Kingdom and United States of pound 30 000 and 50 000 dollars per QALY, respectively.

Cost-Benefit Analysis↗

Determinants of successful transthoracic defibrillation and outcome in ventricular fibrillation.

OBJECTIVE: To examine factors determining defibrillation success and outcome in patients with ventricular fibrillation. DESIGN: Observational prospective study of age, sex, transthoracic impedance, site of cardiac arrest, ventricular fibrillation duration and amplitude, primary or secondary ventricular fibrillation, aetiology, number of shocks to correct ventricular fibrillation, and drug treatment. SETTING: A teaching hospital and a mobile coronary care unit with a physician. PATIENTS: 70 consecutive patients (50 male, 20 female) mean age 66.5 years. INTERVENTIONS: Before the first countershock was administered transthoracic impedance using a 30 kHz low amplitude AC current passed through 8 cm/12 cm self-adhesive defibrillator electrode pads applied in the anteroapical position was measured. The first two shocks were 200 J delivered energy (low energy) and further shocks of 360 J (high energy) were given if required. MAIN OUTCOME MEASURES: Countershock success and outcome from ventricular fibrillation. RESULTS AND CONCLUSIONS: First shock success was significantly greater in inhospital arrests (37/53) than in out-of-hospital arrests (5/17) and in those receiving antiarrhythmic treatment (13/15, 86.7%) v (27/51, 52.9%). Transthoracic impedance was similar in those who were successfully defibrillated with one or two 200 J shocks (98.7 (26) omega) and those who required one or more 360 J shocks (91.4 (23) omega). Success rates with two 200 J shocks were similar in those patients with "high" transthoracic impedance (that is, greater than 115 omega) and those with transthoracic impedance (less than or equal to 115 omega) (8/12 (67%) v 44/58 (76%]. Fine ventricular fibrillation was significantly more common in the patients with a transthoracic impedance of greater than 95 omega (41% (13/32] than in those with a transthoracic impedance less than or equal to 95 omega (13% (5/38]. Death during arrest was significantly more common in patients who needed high energy shocks (14/18 (78%] than in those who needed low energy shocks (16/52 (31%]. Multiple regression analysis identified ventricular fibrillation with an amplitude of greater than or equal to 0.5 mV, age less than or equal to 70 years, and arrests that needed less than or equal to two shocks for defibrillation, in rank order as independent predictors of survival to discharge.

Aged↗

Left ventricular geometry immediately following defibrillation: shock-induced relaxation.

A previous two-dimensional (2D) ultrasound study suggested that there is relaxation of the myocardium after defibrillation. The 2D study could not measure activity occurring within the first 33 ms after the shock, a period that may be critical for discriminating between shock- and excitation-induced relaxation. The objective of our study was to determine the left ventricular (LV) geometry during the first 33 ms after defibrillation. Biphasic defibrillation shocks were delivered 5-50 s after the induction of ventricular fibrillation in each of the seven dogs. One-dimensional, short-axis ultrasound images of the LV cavity were acquired at a rate of 250 samples/s. The LV cavity diameter was computed from 32 ms before to 32 ms after the shock. Preshock and postshock percent changes in LV diameter were analyzed as a function of time with the use of regression analysis. The normalized mean pre- and postshock slopes (0.2 +/- 2.2 and 3.3 +/- 7.9% per 10 ms) were significantly different (P < 0.01). The postshock slope was positive (P < 0.005). Our results confirm that the bulk of the myocardium is relaxing immediately after defibrillation.

Animals↗

Effect of body hypothermia on transventricular simple-capacitor-discharge defibrillation thresholds.

In 260 successful transventricular simple capacitor-discharge defibrillations performed on 20 mongrel dogs under conditions of body hypothermia, an overall average peak current threshold of 69.5 mA/g of heart (SD 30.4) was found. This value, when compared by means of the unpaired t test with previous data obtained under conditions of relative normothermia (89.5 mA/g of heart, SD 32.8, 346 defibrillations, 20 dogs) yielded a highly significant difference (P less than 0.1%). When comparing the deviation of the regression equation (current vs. temperature) from the horizontal line, the Snedecor F test gave also a high level of significance (P less than 1%). These results led to the conclusion that body hypothermia significantly reduces transventricular defibrillation thresholds. After normalizing the regression equations, this reduction was found to be on the average equal to 4.1%/degrees C (SD 1.4) for current and to 5.9%/degrees C (SD 1.4) for energy over the 20 dogs. In all animals, the coefficient of variation was greater for energy than for current (about twice as much), suggesting that current is a better descriptor of what is needed for electrical defibrillation. The transventricular impedance was rather constant, yielding an overall average of 28.5 omega (SD 6.0).

Animals↗