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PubMedDate not supplied

Bretylium tosylate in the management of recurrent ventricular fibrillation complicating acute myocardial infarction.

Eighteen patients with recurrent ventricular fibrillation complicating acute myocardial infarction were treated with bretylium tosylate. All except one patient had been given therapeutic doses of lidocaine and some, in addition, had received other antiarrhythmic agents before bretylium. Bretylium therapy was initiated with intravenous administration of 5 mg/kg body weight and was usually maintained by administering the same dose every 6 to 8 hours by intramuscular route. Ten patients recovered while eight died. Only two of the survivors exhibited heart failure and none of them was in shock, while cardiogenic shock dominated the course of patients with fatal outcome. Postural hypotension invariably occurred but without any clinical deterioration of cardiac function. It is concluded that often bretylium tosylate is an effective therapeutic agent in suppression of recurrent or resistant ventricular fibrillation.

Adult↗

PubMed1999

A randomized controlled clinical trial comparing ventricular fibrillation detection time between two transvenous defibrillator models. The Acute Ventak AV investigator group.

The Ventak AV is an implantable cardioverter defibrillator with dual chamber pacing capability. Features include detection and treatment of ventricular arrhythmias, detection of atrial arrhythmias, as well as dual chamber pacing. The objective of the investigation was to verify the efficacy of the Ventak AV in detecting ventricular fibrillation in the presence of dual chamber pacing. Thirty-three patients, who were to receive an implantable defibrillator were randomized (1:1) in a paired comparison study to the Ventak AV (study device) and the Ventak Mini (control) during defibrillation threshold testing. In order to create a "worst case scenario" for sensing of ventricular fibrillation, pacing was performed at high lower rate limit values (Ventak AV DDD pacing at 150/min, Ventak Mini at VVI 100/min). Ventricularfibrillation was induced and the randomized device was allowed to detect and treat the arrhythmia. This test was repeated for each patient using the alternate device in a randomized order, such that all patients were tested with both devices. The mean ventricular fibrillation detection time for the Ventak AV was 2.0+/-0.11 seconds and for the control device the detection time was 1.8+/-0.11 seconds (P = 0.26). Appropriate tachyarrhythmia therapy decision was documented in all episodes for both devices. The study patient population demonstrated equivalent ventricular fibrillation detection time between the Ventak AV and the Ventak Mini. The Ventak AV demonstrated effectiveness in detecting ventricular fibrillation in the presence of high rate dual chamber pacing.

Adult↗

PubMed2000

Detection of ventricular fibrillation in implantable defibrillators with automatic gain control amplifiers: effects of programming sensitivity.

AIMS: In newer implantable cardioverter-defibrillators with automatic gain control amplifiers the maximum possible sensitivity is programmed with the aim of securing optimal detection of ventricular fibrillation. This study was designed to prove that a reduction in maximum sensitivity is safe with respect to appropriate sensing of ventricular fibrillation, while avoiding sensing of extracardiac signals. METHODS AND RESULTS: Forty-two consecutive patients, undergoing defibrillator implantation/replacement with programmable maximum auto-gain sensing sensitivity (Ventak Mini III, Ventak AV , Guidant, St. Paul, MN, U.S.A.), were prospectively investigated. Thirty-four patients were implanted with a dual-coil lead system, providing integrated bipolar sensing (Endotak, Guidant, St. Paul, MN, U.S.A.), eight patients received a single-coil lead system with true bipolar sensing (Sprint, Medtronic, Minneapolis, MN, U.S.A.). During device implantation and pre-discharge testing, arrhythmia detection times of induced ventricular fibrillation were compared at programmed maximum (0.18 mV) and minimum (0.43 mV) sensitivity in a randomized manner. Seventy-six induced episodes of ventricular fibrillation were analysed. The mean arrhythmia detection times did not differ between the programmed sensing levels (maximum sensitivity: 1612 +/- 307 ms, vs minimal sensitivity: 1,602 +/- 330 ms; P = ns). The results were not affected by the type of implanted lead system (integrated bipolar versus true bipolar sensing). CONCLUSION: In the implantable defibrillator devices, reduction in maximum sensitivity did not impair the detection of induced episodes of ventricular fibrillation.

Amplifiers, Electronic↗

PubMed1998

Efficacy of a beta-adrenergic receptor antagonist, propranolol, in preventing ischaemic ventricular fibrillation: dependence on heart rate and ischaemia duration.

OBJECTIVES: To investigate the prevention of ventricular fibrillation with a beta-adrenergic receptor (beta-AR) antagonist in anaesthetized, open-chest pigs in a model of ischaemia, intended to reproduce what happens either in anginal attack or in the first hour of infarction. METHODS: Ventricular fibrillation threshold (VFT) was determined with trains of diastolic stimuli of 100 ms duration delivered by a subepicardial electrode inserted in the area subjected to ischaemia. Ischaemia was obtained by the complete occlusion of the left anterior descending coronary artery, either near its origin during brief but increasing periods (30, 60, 90, 120, 150, 180, 240, 300 s), or half-way from its origin for a much longer time (more than 60 min). RESULTS: During transient proximal occlusion and isoprenaline infusion (0.25 microgram/kg/min), propranolol (50 micrograms/kg plus 2 micrograms/kg/min) attenuated both tachycardia and the fall in VFT to 0 mA. The shortening of MAP duration accompanying depolarization of the fibres was concurrently slowed down, and time to fibrillation prolonged (122 +/- 15 to 262 +/- 14 s, p < 0.001). In the absence of isoprenaline infusion, propranolol exerted similar effects, but to a lesser degree, in proportion to heart rate dependent on sympathetic activity. In contrast, it became unable to raise VFT before and during ischaemia, when heart rate was kept constant by pacing. After persistent midportion occlusion, significant differences in VFT were found only at the 5th min, depending on whether heart rate was accelerated by isoprenaline (0.8 +/- 0.2 mA), left normal (1.8 +/- 0.3 mA) or slowed down by propranolol (1.6 +/- 0.3 mA). Later on, especially after 15 and 25 min of ischaemia, VFT, which was below 1.0 mA, did not appear to be influenced by the activation or blockade of beta-ARs: spontaneous fibrillations were observed in the same number in this period with or without the administration of propranolol. Beyond 30 min after occlusion, the rise in VFT, subsequent to the first irreversible cell damage, also occurred in the same way. CONCLUSIONS: The prevention of ischaemic ventricular fibrillation by a beta-AR antagonist, judged from VFT, is easily checked experimentally when ischaemia is only transitory, especially if sympathetic activity is high. The maintenance of VFT at a relatively high level is essentially related to the depressant effect on the sinus rate. The same animal model does not give support to an effective protection in the first hour of infarction. However, the control of heart rate may also be beneficial in these circumstances by attenuating systemic haemodynamic disorders.

Adrenergic beta-Agonists↗

PubMed2002

Prognosis of patients with ventricular fibrillation in out-of-hospital cardiac arrest in Hong Kong: prospective study.

OBJECTIVE: To determine the prognosis of patients with ventricular fibrillation in out-of-hospital cardiac arrest in Hong Kong and examine its relationship with the other links in the chain of survival. DESIGN: Prospective descriptive study. SETTING: Three accident and emergency departments, Hong Kong. PARTICIPANTS: Patients older than 18 years with non-traumatic out-of-hospital cardiac arrest who were transported to the hospitals by ambulance between 15 March 1999 and 15 October 1999. MAIN OUTCOME MEASURES: Demographic data, characteristics of the cardiac arrest and the response times of the emergency medical service according to the Utstein style, and survival to hospital discharge rate. RESULTS: Three hundred and twenty patients were included. The incidence of ventricular fibrillation in this group of patients was 14.1%. The chance of survival to hospital discharge was significantly higher for patients with ventricular fibrillation than those with other rhythms of cardiac arrest (4.4% versus 0.7%). Approximately 40.0% of all cardiac arrests were witnessed. The bystander cardiopulmonary resuscitation rate was low at 15.6%. The median intervals for recognition to activation of the emergency medical service, time to cardiopulmonary resuscitation, time to defibrillation, and time to advanced life support were 1, 8, 9, and 27 minutes, respectively. CONCLUSION: Patients with ventricular fibrillation in out-of-hospital cardiac arrest have a better chance of survival than those with other cardiac rhythms. Further improvement requires simultaneous strengthening of all four links in the chain of survival.

Aged↗

PubMed1976

Electrical induction of ventricular fibrillation in the human heart. A study of excitability levels with alternating current of different frequencies.

An experimental study was made on induction thresholds for ventricular fibrillation with alternating currents at frequencies ranging between 6 and 1 600 c/s. The tests were performed on experimental dogs and on patients in association with open-heart surgery. The most vulnerable range was found to be between 12 and 60 c/s. A close similarity was demonstrated between canine and human hearts. The induction of ventricular fibrillation during open-heart surgery is discussed. Ventricular fibrillation, caused by electricity, is either accidental or deliberately induced for medical purposes. The myocardial threshold of excitability towards alternating currents is dependent on two parameters, current and frequency. The vulnerability of the heart towards current has been thoroughly investigated by several authors (Walter, 1969; Dalziel & Lee, 1969; Nickel & Spang, 1965; Kugelberg, 1975). A frequency of 50-60 c/s was utilized in all these determinations, as this is the one of choice in networks for distribution of electric power all over the world. Thus, accidental ventricular fibrillation is most likely to occur with currents of this frequency, and inductions for medical purposes, i.e. during open-heart operations, are achieved in the easiest way with simple transformers delivering the same frequency.

Accidents↗

PubMed1982

Cholinergic modulation of enhanced vulnerability to ventricular fibrillation evoked by adrenergic stimulation in the isolated rat heart.

We investigated whether acetylcholine could antagonize the enhanced vulnerability to ventricular fibrillation evoked by adrenergic stimulation. Epinephrine, 5 X 10(-7)M, caused an 80% reduction in the ventricular fibrillation threshold and a 130% increase in the tissue level of cAMP. Acetylcholine 1 X 10(-7)M, 5 X 10(-7)M, and 1 X 10(-6)M, reduced the epinephrine-induced fall in the ventricular fibrillation threshold by 42%, 100%, and 94%, respectively. This antifibrillatory effect of acetylcholine could not be related to tissue levels of cGMP but rather was associated with reduced tissue levels of cAMP. These results demonstrate cholinergic modulation of the epinephrine-enhanced vulnerability to ventricular fibrillation and suggest that reduced accumulation of cAMP may underlie this effect.

Acetylcholine↗

PubMed1992

[Early and late ventricular fibrillation in myocardial infarction. Prognostic value of clinical and echocardiographic indicators].

Our studies were aimed at evaluating the prognostic value of certain clinical and echocardiographic parameters as well as cardiac arrhythmias in patients with acute myocardial infarction complicated by ventricular fibrillation. The studies comprised 66 patients with previous ventricular fibrillation selected out of 637 patients undergoing treatment after recent myocardial infarction at the Clinic of Cardiology, Institute of Cardiology, Medical Academy, Poznań. The group included 51 males and 15 females aged 30-83, mean age 68. Anterior and/or lateral infarction were diagnosed in 44 patients (67%) whereas inferior and/or posterior infarction in 22 patients (33%). Fifty-eight patients (88%) had transmural infarction. The 2D and M-mode echocardiographic examinations and 24-hour Holter monitoring were performed in all patients. The group of patients resuscitated successfully was compared to the group of deceased patients. The observation period ranged from 1 to 7 years, mean 4 years. The analysis indicated that high mortality of patients with late ventricular fibrillation results from an extensive myocardial infarction and severe ventricular contractility disorders. In patients with late ventricular fibrillation, the main prognostic factor proves to be congestive heart failure and intraventricular conduction disorders with the fascicular and/or bundle-branch block types.

Adult↗

PubMed1987

Electrophysiological mechanisms for the initiation and maintenance of ventricular fibrillation in nonischemic rabbit hearts.

Two series of experiments were carried out using isolated, perfused rabbit hearts to elucidate the mechanisms of initiation and maintenance of ventricular fibrillation in the absence of ischemia. In the first series, either single premature or rapid electrical stimulation induced ventricular fibrillation, during which the spread of excitation was studied by recording electrograms from the endocardial and epicardial surfaces of both ventricles. Left ventricular endocardial stimulation appeared to induce fibrillation most easily. Initiation of ventricular fibrillation was preceded by the spread of areas showing a conduction delay. In certain instances, excitation of the endocardial and subendocardial tissue was necessary for the maintenance of repetitive responses. Injury to the endocardial and subendocardial layers of a ventricle (or both ventricles) by formaldehyde perfusion made the initiation of fibrillation more difficult, although complete prevention of fibrillation required extensive injury with a significant reduction in the excitable myocardial mass. In the second series of experiments, sustained ventricular fibrillation was produced by rapid electrical stimulation and the effects of several antiarrhythmic agents or electrolytes were studied by recording transmembrane action potentials of subepicardial ventricular muscle fibers with microelectrodes. Quinidine, lidocaine, and high K+ concentration significantly decreased the frequency of cellular depolarization and terminated fibrillation in all the 14 hearts studied. These agents suppressed local responses and small action potentials, and made the action potentials more uniform. In 5 of the 14 hearts in these three groups, termination of fibrillation was followed by either transient or prolonged periods of regular ventricular tachycardia. High Mg2+ concentration and bretylium tosylate tended to hyperpolarize the cell membrane, but less markedly decreased the frequency of cellular discharge. Defibrillation was achieved in only two of the ten hearts in which these two interventions were tested. Lanatoside C shortened the action potential duration, sometimes increased the frequency of cellular depolarization, and tended to sustain fibrillatory movements. These observations suggest the role of numerous microreentry movements in both the initiation and maintenance of ventricular fibrillation, although unifocal, ectopic impulse formation may not be definitely ruled out as an initiating mechanism. The possible defibrillating effect of certain antiarrhythmic agents is suggested.

Animals↗

PubMed1987

Calcium antagonists and acute myocardial ischemia: comparative effects of gallopamil and nifedipine on ischemia-induced and reperfusion-induced ventricular arrhythmias, epicardial conduction times, and ventricular fibrillation thresholds.

The comparative effects of the calcium-antagonists gallopamil and nifedipine on ischemia-induced and reperfusion-induced ventricular arrhythmias, particularly ventricular fibrillation (VF), were assessed in a total of 40 mongrel dogs in two experimental preparations. In part I of the study, changes in the time course of spontaneous ventricular arrhythmias and VF parallel to changes in epicardial conduction following acute coronary artery occlusion lasting 20 minutes and followed by subsequent reperfusion were determined. In part II, repeated coronary artery occlusions (20 min) followed by reperfusion (60 min) were performed, and changes in ventricular fibrillation threshold (VFT) were assessed. Gallopamil proved to be highly effective in preventing ventricular arrhythmias and VF following coronary delay was reduced. The ischemia-induced fall in conduction delay was reduced. The ischemia-induced fall in VFT occurring during the first few minutes after occlusion (phase Ia) was significantly reduced. In contrast, nifedipine failed to influence the incidence of ventricular arrhythmias and VF. Following reperfusion, neither drug reduced the incidence of VF nor the associated fall in VFT at the onset of reperfusion. The time course of recovery of epicardial conduction was not affected by either drug. However, the increase in the VFT during the early postreperfusion period was significantly enhanced by both agents. The effects of gallopamil were more pronounced than those of nifedipine. Delayed reperfusion ventricular arrhythmias arising 5 to 10 minutes after release of coronary artery obstruction were significantly reduced by gallopamil whereas nifedipine proved ineffective. The results show that calcium antagonists display direct antiarrhythmic and cardioprotective actions in acute transient myocardial ischemia. The different effectiveness of gallopamil compared to nifedipine can be explained by differences in electrophysiological properties of the drugs. Enhanced ventricular vulnerability following acute transient coronary artery occlusion and subsequent release of coronary artery obstruction, first described by Tennant and Wiggers, has been extensively investigated over the past decade in a variety of experimental and clinical settings. However, the basic mechanisms underlying ischemia- and reperfusion-induced ventricular arrhythmias and ventricular fibrillation (VF) have not yet been fully elucidated. Furthermore, the results of pharmacological approaches to prevent ventricular arrhythmic activity are conflicting. The present study aimed to evaluate the antiarrhythmic efficacy of calcium antagonists in acute myocardial ischemia and reperfusion. We have examined the effects of gallopamil and nifedipine on the time course of ventricular arrhythmias during the first 20 minutes after acute coronary artery occlusion and subsequent reperfusion. We have studied the underlying mechanisms by mapping epicardial conduction and by assessing the electrically induced ventricular fibrillation threshold (VFT) both within and outside ischemic areas.

Animals↗

PubMed1999

Flow requirements in ventricular fibrillation: An in vivo nuclear magnetic resonance analysis of the left ventricular high-energy phosphate pool.

STUDY OBJECTIVE: We sought to determine whether flow rates of approximately 60% of normal values are sufficient to preserve the left ventricular myocardial high-energy phosphate pool during ventricular fibrillation (VF). METHODS: Mixed-breed swine (weight 22. 4+/-2.5 kg) were anesthetized with alpha-chloralose, placed in a state of VF, and perfused with extracorporeal circulation at a target flow of 50 mL.kg(-1).min(-1). In vivo whole-wall (average of left ventricular wall) and spatially localized phosphorous-31 nuclear magnetic resonance (NMR) spectra were acquired at baseline and during VF. RESULTS: Mean flow during VF was 58+/-20 mL.kg(-1). min(-1) (+/-SD; 95% confidence interval, 44 to 71) or about 60% of baseline cardiac output (n=13). Whole-wall adenosine triphosphate (ATP) decreased during perfused VF (P <.05), whereas creatine phosphate (CP) remained unchanged from baseline. With spatially localized NMR, the ratios of CP/ATP were similar at baseline in all layers (endocardium --> epicardium) of the left ventricular wall. However, during perfused VF, subepicardial CP/ATP ratios increased by 14% to 40% compared with baseline values, whereas subendocardial CP/ATP ratios remained unchanged (1% to 3% increase). An additional 4 animals perfused at 72+/-10 mL.kg(-1).min(-1) (+/-SD; 95% confidence interval, 56 to 92) during VF had preservation of CP and ATP levels. CONCLUSION: Flow levels equivalent to 60% of baseline cardiac output were insufficient to maintain normal high-energy phosphate levels in the in vivo fibrillating myocardium. At this level of flow, myocardial high-energy phosphate loss is nonhomogeneous within the left ventricular wall.

Adenosine Triphosphate↗

PubMed1992

Ventricular fibrillation produced by stimulation of external transthoracic electrodes--an experimental study.

The threshold for ventricular fibrillation was determined in 12 pentobarbital anesthetized dogs using transthoracic electrodes located at the optimal axillary electroventilation sites. Electroventilation is the name used to designate inspiration produced by stimuli applied to body surface electrodes. The optimal stimulation site for electroventilation was first determined using hand-held electrodes. Then electrodes, 4.1 cm in diameter, were sutured bilaterally to the optimal anterior axillary stimulation site. The threshold current for producing ventricular fibrillation was determined using single pulses ranging from 0.1-10 msec in duration delivered during the vulnerable period of the cardiac cycle. Fibrillation was produced in all dogs with the 10- and 5-msec pulse durations, in 11 dogs with 0.3-msec, in 6 dogs with 0.2-msec, and in 1 dog with 0.1-msec pulse duration. In all dogs, the current required to produce ventricular fibrillation increased greatly as the pulse duration was decreased. The current required for fibrillation was much in excess of that required to produce one tidal volume. With the longer duration pulses, the ratio was about 80. With the 8 microseconds duration pulses used for electroventilation the estimated ratio is about 800.

Animals↗

PubMed1984

Bretylium in hypothermia-induced ventricular fibrillation in dogs.

We undertook a study to determine the ability of intravenous bretylium to cause "chemical defibrillation" or facilitate electrical defibrillation of hypothermia-induced ventricular fibrillation in the dog. Two groups of ten dogs were cooled to 22 C and placed into ventricular fibrillation. Following initiation of cardiopulmonary resuscitation, bretylium 15 mg/kg or normal saline was administered and the dogs were defibrillated according to a standard protocol. Both groups were equivalent in mean arterial pressure and arterial blood gases throughout the investigation. Seven dogs in each group were converted from ventricular fibrillation to an organized cardiac rhythm (P greater than .05). Despite the possible value of prophylactic bretylium in the setting of hypothermia, its use as active treatment for hypothermia-induced ventricular fibrillation in dogs does not seem to be beneficial.

Animals↗

PubMed1981

Intracellular recording of in situ ventricular cells during ventricular fibrillation.

Transmembrane action potentials (AP) from ventricular cells during ventricular fibrillation (VF) have not been systematically studied. We have recently developed a motion-compensated micropipette holder that holds a micropipette and moves in synchrony with heart motion. AP of subepicardial ventricular cells were recorded in 14 open-chest anesthetized dogs prior to occlusion (control) of left anterior descending artery (LAD) and during first 10 min of reperfusion-induced VF. During control, characteristics (means +/- SE) of AP are: excitation rate (R), 112 +/- 4 beats/min; resting potential (Vr), -79.3 +/- 1.0 mV; overshoot potential (Vov), 17.9 +/- 1.8 mV; 90% AP duration (APD), 251 +/- 8 ms. During VF, AP from the reperfused areas are: R, 173 +/- 27 beats/min; Vr, -60.6 +/- 2.2 mV; Vov, 3.4 +/- 2.9 mV; APD, 134 +/- 9 ms (significantly different from control at P less than 0.001, except R). During VF, cells from the reperfused areas are made inexcitable with verapamil, but not by tetrodotoxin. In conclusion, during VF accurate AP recording is possible from in situ heart, and subepicardial cells in reperfused areas seem to have AP of slow-channel type.

Action Potentials↗

PubMed1999

The effect of amiodarone on the ventricular fibrillation threshold.

We evaluated the antifibrillatory effect of two different doses of amiodarone after cardiac arrest with a cardiopulmonary resuscitation (CPR) model in 19 pigs. Ventricular fibrillation was induced by pacing the right ventricle using a primary drive train at a cycle length of 270 msec for 8 beats. The minimum current strength necessary to induce sustained ventricular fibrillation was defined as the ventricular fibrillation threshold (VFT) measured in mA. Three VFT determinations were made at baseline, followed by 9 minutes of continuous CPR with two determinations of VFT, and three after stabilization. The pigs were placed into one of three groups: amiodarone 2 or 5 mg/kg, or placebo. The average poststabilization VFT in each group was compared with the average baseline VFT. Pigs receiving amiodarone 2 mg/kg had significantly higher VFT after stabilization than at baseline (22.88+/-12.76 to 27.10+/-10.18 mA, p=0.048), as did those receiving 5 mg/kg (17.03+/-7.01 to 28.08+/-11.58 mA, p=0.002). The deltaVFT was significantly greater with amiodarone 5 mg/kg than with vehicle (placebo), but not with 2 mg/kg. There were no changes in VFT in any group during CPR versus baseline. When active treatments were combined, the trend was toward better survival in the amiodarone groups (13/13) compared with the placebo group (4/6, p=0.076).

Amiodarone↗

PubMed2000

Ventricular fibrillation: mechanisms of initiation and maintenance.

Ventricular fibrillation (VF) is the major immediate cause of sudden cardiac death. Traditionally, VF has been defined as turbulent cardiac electrical activity, which implies a large amount of irregularity in the electrical waves that underlie ventricular excitation. During VF, the heart rate is too high (> 550 excitations/minute) to allow adequate pumping of blood. In the electrocardiogram (ECG), ventricular complexes that are ever-changing in frequency, contour, and amplitude characterize VF. This article reviews prevailing theories for the initiation and maintenance of VF, as well as its spatio-temporal organization. Particular attention is given to recent experiments and computer simulations suggesting that VF may be explained in terms of highly periodic three-dimensional rotors that activate the ventricles at exceedingly high frequency. Such rotors may show at least two different behaviors: (a) At one extreme, they may drift throughout the heart at high speeds producing beat-to-beat changes in the activation sequence. (b) At the other extreme, rotors may be relatively stationary, activating the ventricles at such high frequencies that the wave fronts emanating from them breakup at varying distances, resulting in complex spatio-temporal patterns of fibrillatory conduction. In either case, the recorded ECG patterns are indistinguishable from VF. The data discussed have paved the way for a better understanding of the mechanisms of VF in the normal, as well as the diseased, human heart.

Animals↗

PubMed1992

Ventricular fibrillation detection using the evoked electrogram from the braided endocardial defibrillation lead.

Life-threatening consequences can be the result of inappropriate classification of ventricular fibrillation for patients with implantable cardioverter defibrillators. The objective of this study was to determine if analysis of the asynchronously paced evoked electrogram using the braided endocardial defibrillation lead could improve the detection of ventricular fibrillation. The depolarization portion of the evoked electrogram was integrated to obtain the paced depolarization integral. The results demonstrated that the mean of the paced depolarization integral, its SD, and the mean +/- SD were significantly different between sinus rhythm and ventricular fibrillation (p < 0.005, p < 0.05, p < 0.01, respectively). These results suggest that the paced depolarization integral obtained with the braided endocardial defibrillation lead could improve the specificity and sensitivity of ventricular fibrillation detection.

Animals↗

PubMed2006

The natural biochemical changes during ventricular fibrillation with cardiopulmonary resuscitation and the onset of postdefibrillation pulseless electrical activity.

OBJECTIVE: The objective of this study was to document the biochemical changes during ventricular fibrillation (VF) with cardiopulmonary resuscitation (CPR), and to identify factors associated with postdefibrillation pulseless electrical activity (PD-PEA). BACKGROUND: It has been reliably estimated that as much as 60% of out-of-hospital sudden cardiac death can be attributed to the onset of PD-PEA (Niemann JT, Cruz B, Garner D et al. Immediate countershock versus CPR before countershock in a 5-minute swine model of ventricular fibrillation arrest. Ann Emerg Med 2000;36:543-6). Previous attempts to treat reversible causes of pulseless electrical activity have not been successful clinically (Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Outcome of out-of-hospital postcountershock asystole and pulseless electrical activity versus primary asystole and pulseless electrical activity. Crit Care Med 2001;29:2366-70). METHODS: This investigation used 22 studies on 14 anesthetized pigs breathing 100% oxygen. Ventricular fibrillation was induced with a right ventricular catheter electrode, and the chest was compressed with a pneumatically driven Chest Thumper (Michigan Instruments) (80-100 lb at 60/min). The electrocardiogram and aortic pressure were recorded continuously. Arterial pH, P(O2), P(CO2), Na+, K+, Ca2+, Cl-, SaO2, glucose, hematocrit, and hemoglobin level were measured at selected times. Ventricular defibrillation was achieved with transchest electrodes. RESULTS: Typically, during VF with CPR, mean aortic pressure was 20 to 25 mm Hg. In all cases aortic P(O2) decreased to about 20% of the initial value in 10 minutes, and aortic blood K+ increased by 50% in 6 minutes. By 5 to 8 minutes, the incidence of PD-PEA was 50%. CONCLUSION: Ventricular fibrillation duration, arterial K+, and arterial P(CO2) were statistically correlated with the onset of PD-PEA in this study. In addition, trends suggest an association of mean arterial blood pressure and arterial P(O2) with the onset of PD-PEA.

Animals↗