Time course of fibrillation and defibrillation thresholds after an intravenous bolus of amiodarone--an experimental study

Experimental studies have described an increase in ventricular fibrillation threshold (VFT) by intravenous amiodarone. The aim of this study was to examine the early time course of changes in VFT and defibrillation thresholds (DFT) after an intravenous bolus of amiodarone in an experimental pig model of transient myocardial ischemia. METHODS AND RESULTS: VFT and relative effective ventricular refractory period (ERP) were measured in 15 anaesthetized open-chest pigs after 3 min of regional coronary ischaemia before (time 0) and 2, 15, 30, 60, and 90 min after the intravenous injection of normal saline (group A, n = 5) or amiodarone, 5 mg/kg over 15 s (group B, n = 10). DFT was measured by increasing the strength of DC shocks until defibrillation was accomplished. Amiodarone caused an increase in VFT, starting at 2 min after the infusion (11.4 +/- 8.4 mA versus 9.2 +/- 4.6 mA, P = 0.03), became significant at 15 min (13.7 +/- 6.5 mA, P = 0.009), continued to rise at 30 min (34.2 +/- 28.7 mA, P = 0.03) and reached a plateau at 60 min (50.3 +/- 37.8 mA, P = 0.008). An increase was also observed in the ERP (204 +/- 25 ms at 2 min versus 197 +/- 26 ms at baseline, P = 0.074, 211 +/- 38 ms at 15 min, P = 0.084, 212 +/- 40 ms at 30 min, P = 0.037, 220 +/- 34 ms at 60 min, P = 0.002, and 227 +/- 32 ms at 90 min, P = 0.008). No change was observed in DFT after amiodarone administration. No significant change in VFT, ERP, or DFT occurred in the control group. CONCLUSION: In this porcine model, the intravenous administration of amiodarone increased VFT and ERP over 60 min after the injection, without effect on DFT.     

Myocardial ischaemic preconditioning in the pig has no effect on the ventricular fibrillation and defibrillation thresholds

INTRODUCTION: The effects of myocardial ischaemia preconditioning in pigs on the vulnerability to ventricular fibrillation during subsequent ischaemic events are controversial. This study examined the time course of changes in ventricular fibrillation (VFT) and defibrillation (DFT) thresholds during transient myocardial ischaemia after a 45 min preconditioning period. METHODS AND RESULTS: In five open-chest pigs, VFT was measured after 3 min of regional myocardial ischaemia, at time 0, 2, 15, 30, 60 and 90 min (Control group). In seven other pigs (Test group), VFT was measured before (time 0) and 2, 15, 30, 60 and 90 min after ischaemic preconditioning by three consecutive 5 min periods of regional coronary occlusion, followed by 10 min of reperfusion. DFT was measured by increasing the stored energy systematically until successful defibrillation. Ischaemic preconditioning caused no significant change in the effective refractory period (ERP), VFT or DFT over the 90 min of the experiments. In the Control group, ERP remained stable for 30 min, though was significantly lower at 90 min (178 +/- 28 ms) than at baseline (204 +/- 32 ms, P = 0.007). VFT and DFT remained unchanged throughout the experiments, and no difference was observed in ERP, VFT and DFT between the two groups at any time during the experiment. CONCLUSION: No changes were observed in the refractory duration, ventricular vulnerability or defibrillation energy requirements up to 90 min after ventricular ischaemic preconditioning in the pig.     

Is Ventricular Fibrillation Interval an Indicator of Electrical Defibrillation Threshold?

To clarify whether peak-to-peak interval of the fibrillation wave (VF interval) during VF is an independent indicator of defibrillation efficacy, we measured the transcardiac DFT, VF intervals of the surface and local ECGs (lead II and the right ventricle), and the ERP in 82 open-chest dogs. Both VF intervals showed a negative correlation with heart weight (surface: r = -0.358 [P < 0.005]; local; r = -0.349 [P < 0.005]). DFT was 2.0 +/- 0.7 A and positively correlated with heart weight (r = 0.453 [P < 0.0001]). ERP did not show a significant correlation with heart weight. DFT was negatively correlated with VF interval (vs surface VF interval: r = -0.568 [P < 0.0001]; vs local VF interval: r = -0.504 [P < 0.0001]), but showed only a weak negative correlation with ERP (r = -0.314 [P < 0.005]). Even after allowing for the dependency of DFT and VF intervals on heart weight (normalized to a 100-g heart), the correlation between VF interval and DFT was still significant (vs surface VF interval: r = -0.487 [P < 0.0001]; vs local VF interval: r = -0.414 [P < 0.0002]). These results suggest that VF interval is an indicator of DFT in intact hearts that have not received pharmacological intervention.     

A Model of Ischemically Induced Ventricular Fibrillation for Comparison of Fixed-dose and Escalating-dose Defibrillation Strategies

OBJECTIVES: Fixed- and escalating-dose defibrillation protocols are both in clinical use. Clinical observations suggest that the probability of successful defibrillation is not constant across a population of patients with ventricular fibrillation (VF). Common animal models of electrically induced VF do not represent a clinical VF etiology or reproduce clinical heterogeneity in defibrillation probability. The authors hypothesized that a model of ischemically induced VF would exhibit heterogeneous defibrillation shock strength requirements and that an escalating-dose strategy would more effectively achieve prompt defibrillation. METHODS: Forty-six swine were randomized to fixed, lower-energy (150 J) transthoracic shocks (group 1) or escalating, higher-energy (200 J-300 J-360 J) shocks (group 2). VF was induced by balloon occlusion of a coronary artery. After 1 or 5 minutes of VF, countershocks with a biphasic waveform were administered. The primary endpoint was successful defibrillation (termination of VF for 5 seconds) with < or =3 shocks. RESULTS: VF was induced with occlusion or after reperfusion in 35 animals. Only five of 17 group 1 animals (29%, 95% CI = 10 to 56) could be defibrillated with < or =3 shocks; 15 of 18 group 2 animals (83%, 95% CI = 59 to 96) were defibrillated with < or =3 shocks (p < 0.002 vs. group 1). Nine of the group 1 animals (75%) that could not be defibrillated with 150-J shocks were rescued with < or =3 shocks ranging from 200 to 360 J. CONCLUSIONS: In this ischemic VF animal model, defibrillation shock strength requirements varied among individuals, and when defibrillation was difficult, an escalating-dose strategy was more effective for prompt defibrillation than fixed, lower-energy shocks.     

Myocardial effects of ventricular fibrillation in the isolated rat heart.

OBJECTIVE: Ventricular fibrillation (VF) is known to increase myocardial oxygen requirements and to alter coronary vascular physiology. However, the significance of these effects during cardiac arrest and resuscitation is not well understood. A model was developed in the isolated rat heart to investigate the myocardial effects of VF during a simulated episode of cardiac arrest and resuscitation. We hypothesized that VF would intensify the severity of myocardial ischemia and consequently accentuate postischemic myocardial dysfunction. DESIGN: Prospective and randomized. SETTING: Research laboratory. SUBJECTS: Twenty Sprague-Dawley rats. INTERVENTIONS: Hearts were harvested and perfused at a constant flow rate of 10 mL/min using a modified Krebs-Henseleit solution equilibrated with 95% oxygen and 5% CO2. In five hearts, VF was induced by a 0.05-mA current delivered to the right ventricular endocardium. The perfusate flow was then stopped for a 10-min interval and resumed at 20% of baseline flow for another 10 mins. After 20 mins of VF, the perfusate flow was returned to baseline and a sinus rhythm reestablished by epicardial electrical shocks. The studies were randomized and included three additional groups to control for the effects of ischemia without VF (n = 5), the effects of VF without ischemia (n = 5), and the stability of the preparation (n = 5). MEASUREMENTS AND MAIN RESULTS: Isovolumic indices of left ventricular function were obtained using a latex balloon advanced through the mitral valve and distended to an end-diastolic pressure of 10 mm Hg. The coronary effluent was collected from the right ventricular cavity. VF during myocardial ischemia was associated with a higher coronary effluent PCO2, increased coronary vascular resistance, and development of ischemic contracture as indicated by increases in left ventricular pressure from 9+/-3 to 33+/-6 mm Hg (p < .05). After defibrillation, contractility and relaxation rapidly returned to baseline values, whereas the isovolumic end-diastolic pressure remained elevated for 20 mins. These changes were much less prominent when ischemia was not accompanied by VF. CONCLUSIONS: These findings indicate that VF may adversely affect myocardial ischemia by hastening the development of ischemic contracture, increasing coronary vascular resistance, and favoring the development of diastolic pump failure early after resuscitation from cardiac arrest.     

Electrophysiological Effects of Monophasic and Biphasic Stimuli in Normal and Infarcted Dogs

Though some biphasic waveforms significantly decrease the energy required for defibrillation, little is known about the effect of biphasic stimulation on the determination of other electrophysiological parameters in normal and infarcted hearts. To evaluate this, nine normal dogs and 12 dogs with myocardial infarction had activation threshold (AT), effective refractory period (ERP), strength-interval curves, and ventricular fibrillation threshold (VFT) determined with constant current stimulation to a pair of right ventricular plunge electrodes, and upper limit of vulnerability (ULV) and defibrillation threshold (DFT) determined with truncated exponential shocks delivered to a pair of wire electrodes coiled to contour the right and left ventricular epicardium. Each electrophysiological parameter was determined with a 5.5 msec monophasic and 5.5-msec biphasic (3.5 msec first phase) waveform. Though AT and VFT were not significantly different for the two waveforms, the ERP was significantly longer, the strength-interval curve shifted rightward, and the threshold for repetitive responses higher for biphasic stimuli. Compared to the monophasic waveform, the ULV and DFT were significantly decreased in a parallel fashion for the biphasic waveform. Neither the presence nor size of myocardial infarction significantly affected any of the measured electrophysiological parameters. In six additional dogs, sigmoid defibrillation probability curves were constructed from biphasic shocks of four energies including that of the DFT and ULV. The ULV energy predicted an effective dose that defibrillated 97% of the time (range 90%-100%). In conclusion, the increased defibrillation efficacy of the biphasic waveform is independent of its ability to activate fully repolarized myocardium and cannot be explained by a greater ability of biphasic waveforms to activate partially depolarized tissue. The parallel decrease in the ULV and DFT for biphasic stimulation and the finding that the ULV energy defibrillates with a high probability of success suggest similar underlying mechanisms for the ULV and defibrillation.     

Effect of ventricular fibrillation duration on the defibrillation threshold in humans

Early during ventricular fibrillation, the defibrillation threshold may be low, as ventricular fibrillation most probably arises from a localized area with only a few wavefronts and the effects of global ischemia, ventricular dilatation, and sympathetic discharge have not yet fully developed. The purpose of this study was to explore the effect of the timing of shock delivery in humans. During implantation of an ICD in 26 patients (24 men, 60 +/- 11 years, 19 coronary artery disease, NYHA 2.2 +/- 0.4, left ventricular ejection fraction 0.42 +/- 0.16), the defibrillation threshold was determined after approximately 10 and 2 seconds of ventricular fibrillation. Ventricular fibrillation was induced by T wave shocks. Mean defibrillation threshold was 9.9 +/- 3.6 J after 10.3 +/- 1.0 seconds. Within 2 seconds, 20 of 26 patients could be successfully defibrillated with < or = 8 J. In these patients, the mean defibrillation threshold was 4.0 +/- 2.1 J after 1.4 +/- 0.3 seconds compared to 9.5 +/- 3.1 J after 10.2 +/- 1.1 seconds (P < 0.001). There were no clinical differences between patients who could be successfully defibrillated within 2 seconds and those patients without successful defibrillation within 2 seconds. In the majority of patients, the defibrillation threshold was significantly lower within the first few cycles of ventricular fibrillation than after 10 seconds of ventricular fibrillation. These results should lead to exploration of earlier shock delivery in implantable devices. This could possibly reduce the incidence of syncope in patients with rapid ventricular tachyarrhythmias and ICDs.     

A comparison of electrically induced cardiac arrest with cardiac arrest produced by coronary occlusion

OBJECTIVE: The present study was undertaken to compare an animal model of electrically induced VF with ischemically induced VF. In a preponderance of models of cardiac arrest and resuscitation in intact animals, ventricular fibrillation (VF) is induced by an alternating current delivered directly to the epicardium or endocardium. Yet, the applicability of such animal models has been challenged for it is not an electrical current alone but rather a current generated in the ischemic myocardium that triggers VF. Accordingly, a potentially more clinically relevant model was investigated in which spontaneous VF followed acute myocardial ischemia. METHODS: Twenty anesthetized pigs were randomized to either electrical fibrillation or myocardial ischemia following transient occlusion of the left anterior descending (LAD) coronary artery. RESULTS: VF was untreated for 7 min in both models after which mechanical ventilation and precordial compression were begun. Defibrillation was attempted after 5 min of CPR in both groups. VF appeared within 5.7+/-2.0 min of LAD occlusion. CONCLUSIONS: A significant increase in the number of post-resuscitation premature ventricular beats and recurrent VF followed ROSC and a significantly greater number of shocks was required for restoration of spontaneous circulation (ROSC) after LAD occlusion. Nevertheless, early post-resuscitation myocardial dysfunction, neurological recovery and 72 h survival were indistinguishable between the two models.     

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.     

Left Ventricular Function after Monophasic and Biphasic Waveform Defibrillation: The Impact of Cardiopulmonary Resuscitation Time on Contractile Indices

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.     

Potential benefit of transesophageal defibrillation: an experimental evaluation

INTRODUCTION: Because of the proximity of the esophagus to the heart, transesophageal defibrillation might increase defibrillation success. We assessed the defibrillation threshold (DFT) of transesophageal defibrillation compared with standard transthoracic defibrillation. METHODS: Defibrillation success and DFTs were determined in 22 female pigs with high (68+/-4 kg, n=12) or low body weight (39+/-1 kg, n=10). After induction of ventricular fibrillation, biphasic shocks were delivered between two cutaneous patch electrodes (sternal and apical position) or between an esophageal and two cutaneous patch electrodes in a sternal and apical position. The esophageal electrode was integrated into a latex sheath covering a standard transesophageal echocardiography probe. RESULTS: In 5 of 12 pigs with high body weight, external defibrillation failed despite 3 consecutive 200-J shocks, whereas subsequent transesophageal defibrillation was successful with the first shock. In the remaining 7 pigs, a more than 50% reduction in DFT was obtained with transesophageal defibrillation compared with standard biphasic external defibrillation (67+/-27 vs 164+/-23 J, P<.001). Pigs with lower body weight were successfully defibrillated by both transthoracic and transesophageal shocks. The DFT in pigs with low body weight was significantly lower using transesophageal defibrillation compared with transthoracic shocks (65+/-15 vs 99+/-38 J, P<.05). CONCLUSIONS: In this animal model, nonresponders to standard external defibrillation could successfully be defibrillated via an esophageal-cutaneous electrode configuration. Overall, an almost 50% DFT reduction was achieved by transesophageal defibrillation. Transesophageal defibrillation may provide an additional tool for terminating VF, which is refractory to external defibrillation, eg, in patients with very high body weight.     

Effects of rotigaptide, a gap junction modifier, on defibrillation energy and resuscitation from cardiac arrest in rabbits

The gap junction modifier Rotigaptide (ZP123), which promotes cellular coupling, was hypothesized to decrease defibrillation thresholds during prolonged ventricular fibrillation (VF). Thirty-two New Zealand white rabbits were randomized to receive saline (control, n = 16) or Rotigaptide (n = 16). Following 4 min of untreated VF, biphasic defibrillation shocks were applied through chest wall patches, starting either at 300 volts (V) (n = 16) or 500 V (n = 16), with 200 V increasing steps to 900 V in case of shock failure. Rotigaptide significantly decreased defibrillation voltage requirements (average cumulative voltage of all shocks: 1206 +/- 709 V in control group vs. 844 +/- 546 V in treated group, P = .002). Rotigaptide had no effect on heart rate, QRS duration, QT interval, ventricular effective refractory period, monophasic action potential duration or on connexin 43 density using immunofluorescence. Rotigaptide improves the ability to defibrillate after untreated VF.     

Genesis of Sigmoidal Dose-Response Curve During Defibrillation by Random Shock: A Theoretical Model Based on Experimental Evidence for a Vulnerable Window During Ventricular Fibrillation

The sigmoidal dose-response curve (percent success vs shock energy) suggests a probabilistic nature of defibrillation. The mechanism is still largely unknown, however, random variation in the excitable state during ventricular fibrillation (VF) is suspected. A canine defibrillation study was designed to determine whether random variation in absolute VF voltage (AVFV) (a crude marker of number of excitable cells) was related to success of defibrillation, using a DC shock successful at the 50% level. The results were: (a) transmyocardial resistance (73.4 +/- 1.4 vs 73.6 +/- 1.5 ohms) and delivered energy (6.1 +/- 1.2 vs 6.2 +/- 1.2 joules) were similar; however, (b) AVFV 2 msec prior to DC shock was greater for successful as compared to unsuccessful attempts (0.5 +/- 0.1 vs 0.3 +/- 0.0 mV, P less than 0.01). A mathematical model was subsequently developed based on fluctuation in the number of excitable cells. Variation in the state of excitability resulted in a cyclic window potentially vulnerable to defibrillation. The vulnerable window occurred at a point when the number of excitable cells was low, i.e., a higher state of total depolarization, which was in agreement with the experimental finding. For a given VF pattern, duration of the vulnerable window was regulated by the shock energy. A larger shock energy generated a wider vulnerable window and, in turn, a higher success rate. Finally, the sigmoidal dose-response curve of defibrillation was theoretically constructed by calculating the variable chances of a random DC shock occurring either in a vulnerable window or elsewhere during VF. It is concluded that a vulnerable window susceptible to defibrillation can be demonstrated in the early stages (10 sec) of VF. The mathematical model provides a theoretical basis for the vulnerable window and helps elucidate the probabilistic nature of defibrillation.     

A comparison of cardiopulmonary resuscitation with cardiopulmonary bypass after prolonged cardiac arrest in dogs. Reperfusion pressures and neurologic recovery.

Resuscitability and outcome after prolonged cardiac arrest were compared in dogs with standard external cardiopulmonary resuscitation (CPR) vs. closed-chest emergency cardiopulmonary bypass (CPB). Ventricular fibrillation (VF) was with no blood flow from VF 0 min to VF 10 min. Subsequent CPR basic life support (BLS) was from 10 min to VF 15 min. Then, group I (n = 13) received CPR advanced life support (ALS) from VF 15 min until restoration of spontaneous circulation to occur not later than VF 40 min. Group II (n = 14) received CPR-ALS from VF 15 min to VF 20 min without defibrillation, and then total CPB to defibrillation attempts started at VF 20 min, followed by assisted CPB to 2 h. Total ischemia time (no-flow time plus CPR time of MAP less than 50 mmHg) was unexpectedly shorter in group I (14.3 +/- 2.5 min) than in group II (18.6 +/- 2.3 min) (P less than 0.01). During CPR-BLS, coronary perfusion pressures were 25 +/- 9 mmHg in group I and 18 +/- 8 mmHg in group II (NS). Epinephrine during CPR-ALS, before countershock, raised coronary perfusion pressure to 40 +/- 10 mmHg in group I and 27 +/- 10 mmHg in group II (NS). In group II, coronary perfusion pressure increased during total CPB to 58 +/- 16 mmHg (P less than 0.01 vs. group I). Spontaneous normotension was restored in 11/13 dogs of group I and all 14 dogs of group II (NS). Ten dogs in each group followed protocol and survived to 96 h. Five of ten in group I and six of ten in group II were neurologically normal (NS). We conclude that: (1) Reperfusion with CPB yields higher coronary perfusion pressures than reperfusion with CPR-ALS; and (2) even after no blood flow for 10 min, optimized CPR can result in cardiovascular resuscitability and neurologic recovery, similar to those achieved by CPB.     

Myocardial protection during ventricular fibrillation by reduction of proton-driven sarcolemmal sodium influx

Although the inhibition of proton-driven sarcolemmal sodium influx ameliorates ischemic injury in the quiescent myocardium, the effects when ventricular fibrillation is present are largely unknown. We used an isolated rat heart model to investigate whether inhibition of the sodium-hydrogen exchanger isoform-1 (with the benzoylguanidine derivatives HOE-694 and cariporide) with or without concomitant inhibition of the sodium-bicarbonate co-transporter (with perfusate buffered with N-2-hydroxyethylpiperazine-N-2-ethanesulfonic acid [HEPES]) during ischemia and ventricular fibrillation could ameliorate functional myocardial abnormalities presumed to limit cardiac resuscitability. Ischemic contracture, which typically develops during ventricular fibrillation, was ameliorated by HOE-694 when either a bicarbonate-buffered (20 +/- 7 mm Hg vs 15 +/- 5 mm Hg, P <.05) or a HEPES-buffered (14 +/- 5 mm Hg vs 10 +/- 3 mm Hg, P <.04) perfusate was used. Maximal amelioration occurred when cariporide and HEPES-buffered perfusate were used simultaneously (25 +/- 14 mm Hg vs 11 +/- 3 mm Hg, P <.01), and this was accompanied by lesser leftward shifts of the end-diastolic pressure-volume curves after defibrillation. Intramyocardial sodium increases of 76% during ischemia and ventricular fibrillation (P <.05) were ameliorated by the sodium-influx-limiting interventions. Thus interventions limiting sarcolemmal sodium influx during ischemia and ventricular fibrillation may facilitate successful resuscitation from ventricular fibrillation.     

Myocardial performance index following electrically induced or ischemically induced cardiac arrest

OBJECTIVES: We sought to investigate the echocardiographic myocardial performance index (MPI) to assess post-resuscitation myocardial function following electrically and ischemically induced ventricular fibrillation (VF). MATERIALS AND METHODS: VF was induced in fourteen anesthetized pigs weighing 38+/-4 kg. VF was induced electrically in seven animals and ischemically, following transient occlusion of the left anterior descending coronary artery (LAD), in the remaining seven animals. VF was untreated for 7 min after which CPR, including precordial compression and mechanical ventilation was begun. Defibrillation was attempted after 5 min of CPR. MPI, ejection fraction (EF) and fractional area change (FAC) were measured hourly during the following 4 h interval post-resuscitation. RESULTS: Five of seven animals were resuscitated in the electrically induced VF group, and four of seven animals in the ischemically induced VF group. No difference in EF and FAC were observed between the two groups. The MPI, however, was significantly greater at 60 min and 120 min post-resuscitation in animals after ischemically induced VF (p<0.05). CONCLUSION: In this model, left ventricular (LV) MPI was a more sensitive and useful quantitative parameter to assess the LV function than the EF and FAC measurements used routinely. MPI measurements indicated that post-resuscitation myocardial dysfunction may be more severe after ischemically induced VF compared to the electrically induced VF.     

Adjustable atrial and ventricular temporary electrode for low-energy termination of tachyarrhythmias early after cardiac surgery

Supraventricular and ventricular tachycardias are common and serious postoperative complications early after cardiac surgery. We introduce a completely removable temporary adjustable defibrillation electrode (TADE) for low energy cardioversion/defibrillation of postoperative atrial and ventricular tachyarrhythmias. The electrode consists of three loops of steel wires connected to one steel wire, which are movable within an isolation sheet for adjusting the active surface to the individual size of the heart chambers. Evaluation of the electrode was performed in 10 open-chest beagles with a mean weight of 25.5 kg. The electrodes were first positioned on the left and right atrium. Atrial fibrillation (AF) was induced via a bipolar temporary heart wire. Atrial defibrillation thresholds (DFTs) were measured according to a step-down shock protocol (5-0.4 J). Thereafter, the electrodes were adjusted and positioned on the right and left ventricle. Ventricular fibrillation (VF) was induced and DFTs were recorded the same way. Aortic flow and pressure and left ventricular pressure were continuously monitored throughout the experiment. For termination of AF, mean DFTs were 0.4 +/- 0 J (lowest possible shock level) with a mean shock impedance of 70 +/- 7.6 ohms. VF was terminated with a mean DFT of 3 +/- 1.1 J with a mean impedance 56.1 +/- 7.9 ohms. Complete transcutaneous removal of the electrodes was possible in all animals without any complications. In conclusion, successful low energy termination of AF and VF is possible with the tested temporary adjustable electrode. A clinical study is planned for further evaluation.     

Myocardial cytokine IL-8 and nitric oxide synthase activity during and after resuscitation: preliminary observations in regards to post-resuscitation myocardial dysfunction

AIM: Increases in serum cytokines have been reported after successful resuscitation from prolonged ventricular fibrillation (VF). Pro-inflammatory cytokines can stimulate inducible nitric oxide synthase (iNOS) to produce excessive levels of nitric oxide (NO). High levels of both myocardial inflammatory cytokines and nitric oxide levels can depress myocardial contractile function. We hypothesized that myocardial pro-inflammatory cytokines and iNOS activity would increase following successful resuscitation from prolonged ventricular fibrillation cardiac arrest, and that such increases would parallel the development of post-resuscitation myocardial dysfunction. METHODS: Ventricular fibrillation cardiac arrest was induced in seven domestic swine (25+/-5kg). After 10min of untreated VF, the animals were defibrillated and resuscitated. Left ventricular (LV) systolic and diastolic function measurements, serum samples (arterial and coronary sinus) for IL-8 cytokine quantification, and LV myocardial biopsies were collected before, during, and after resuscitation. Quantification of myocardial endothelial (eNOS) and inducible (iNOS) nitric oxide synthase protein levels were determined using immunoblot analyses and protein localization was examined using immunohistochemistry. RESULTS: Post-resuscitation LV systolic and diastolic functions were depressed while increases in both coronary sinus IL-8 levels and myocardial iNOS activity were found. Compared to pre-arrest baseline, levels of iNOS protein increased during VF (p相似文献   

Transvenous Single Lead Atrial Defibrillation: Efficacy and Risk of Ventricular Fibrillation in an Ischemic Canine Model

Transvenous atrial defibrillation with multiple atrial lead systems has been shown to be effective in models without the potential for ventricular arrhythmias. The specific aim of this study was to evaluate the efficacy and safety of transvenous single lead atrial defibrillation in a canine model of ischemia cardiomyopathy. Ten dogs had ischemia cardiomyopathy induced by repeated intracoronary micmsphere injections. The mean LV ejection fraction decreased from 71%± 9% to 38%± 14% (P = 0.003). Spontaneous atrial fibrillation (AF) developed in four dogs, and in six AF was induced electrically. Atrial defibrillation thresholds (ADFTs) were determined with synchronous low energy shocks using a transvenous tripolar lead with two defibrillation coils (right ventricle, superior vena cava) and an integrated sensing lead (RV coil vs electrode tip). The ADFTs derived by logistic regression were compared at 50% and 90% probability of success (ED₅₀, ED₉₀): ED₅₀ was 2.4 ±1.7 J and 2.9 ±2.1 J, respectively, for 5- and 10-ms monophasic shocks, and 1.8 ± 0.9 J and 2.1 ± 1.3 J, respectively, for 5- and 10-ms biphasic shocks. Immediately after 3 of 2,179 (0.1%) synchronized shocks, ventricular fibrillation (VF) developed. VF was induced in 3 of 1,062 (0.3%) shocks with integrated sensing (RV coil vs electrode tip) compared to 0 of 1,117 shocks when a separate bipolar RV sensing electrode was used for synchronization. In our canine model of ischemic cardiomyopathy, low energy atrial defibrillation via a transvenous single lead system was highly effective. However, there was a small but definite risk of VF induction, which seemed to be greater when an integrated as opposed to a true bipolar RV sensing was used.     

Effect of epinephrine on defibrillation in ischemic ventricular fibrillation

Epinephrine is thought to improve the success of defibrillation with countershock therapy. However, a recent study failed to show any effect of epinephrine in dogs with normal coronary arteries undergoing electrically-induced ventricular fibrillation (VF). In the current study, the effects of epinephrine were examined in dogs with coronary occlusion undergoing both spontaneous and electrically-induced fibrillation. Forty pentobarbital-anesthetized dogs were prepared by placing snares around the circumflex and left anterior descending coronary arteries. Fibrillation and subsequent resuscitation were carried out with one coronary artery occluded. Dogs were randomly allocated so that half of the animals underwent spontaneous fibrillation and half were electrically fibrillated. In addition, half received epinephrine (1 mg) during resuscitation and half received normal saline solution (1 ml). After 3 minutes of cardiac arrest, cardiopulmonary resuscitation (CPR) was begun, and 30 seconds later epinephrine or saline were injected. One minute later defibrillation was attempted using successive stored energy doses of 1, 2, 4, 8, 16, and 32 J/kg. Delivered energy and transthoracic impedance were measured for each countershock. Successful defibrillation was defined as conversion to any rhythm other than VF or ventricular tachycardia that degenerated in VF within 10 seconds. No other drugs were given during resuscitation. Neither the type of fibrillation (electrically-induced versus spontaneous) or drug therapy (epinephrine versus placebo) had a significant effect on the incidence of defibrillation or the energy necessary for successful defibrillation. Epinephrine did significantly increase the incidence of resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)