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PubMed1988

Bidirectional transvenous/subcutaneous defibrillation of ventricular fibrillation in dogs: success rates, energy requirements, currents, voltages and impedance.

Four hundred and thirteen defibrillations of alternating current-induced ventricular fibrillation were performed in 10 halothane-anaesthetized dogs (body weight: 24.5-30.5 kg). Success rates, energy demands, currents, peak voltages and impedance were determined. A transvenous catheter electrode system (Medtronic 6880, right ventricular apex and superior vena cava, distance 100 or 150 mm) and subcutaneous patch electrodes (Intec 67 L, 2nd/3rd and/or 3rd/4th left intercostal space) were used for bidirectional defibrillation. Loading voltages ranged from 600 to 850 V. With an electrode distance of 100 mm and a pulse duration of 2 ms separated by 1 ms, success rates were 100%, 40% and 0% for 850.650 and 600 V, respectively. With a 3-ms pulse duration, the corresponding rates were 100%, 60% and 50%. With a 2-ms pulse duration, successful defibrillation was achieved with energies lower than 15 J in 27%, with energies between 15 and 20 J in 77%, and 100% with energies higher than 20 J. Defibrillation currents were 4.4-9.3 A for pulse 1 (superior vena cava/ventricular apex) and 6.3-13.4 A for pulse 2 (patch/ventricular apex), respectively. Effective peak voltages ranged from 510 to 787 V and from 514 to 777V and averaged 89.6% of the loading voltages. Impedance values (peak voltage/current) were 75.5-117.7 (pulse 1) and 51.7-94.9 Ohms (pulse 2). Fifty consecutive defibrillations in one animal resulted in a decrease of impedance (114.6 to 84.9 Ohms, pulse 1:75.4 to 53.0 Ohms, pulse 2). Defibrillation of ventricular fibrillation can be achieved with acceptably low energies using a bidirectional transvenous/subcutaneous system, avoiding thoracotomy and general anaesthesia for implantation of the defibrillation system.

Animals↗
PubMed2002

Effects of epinephrine and vasopressin in a piglet model of prolonged ventricular fibrillation and cardiopulmonary resuscitation.

OBJECTIVE: We recently demonstrated that vasopressin alone resulted in a poorer outcome in a pediatric porcine model of asphyxial cardiac arrest when compared with epinephrine alone or with epinephrine plus vasopressin in combination. Accordingly, this study was designed to differentiate whether the inferior effects of vasopressin in pediatrics were caused by the type of cardiac arrest. DESIGN: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. SETTING: University hospital laboratory. SUBJECTS: Eighteen piglets weighing 8-11 kg. INTERVENTIONS: After 8 mins of ventricular fibrillation and 8 mins of cardiopulmonary resuscitation, either 0.4 units/kg vasopressin (n = 6), 45 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered. Six minutes after drug administration, a second respective bolus dose of 0.8 units/kg vasopressin, 200 microg/kg epinephrine, or a combination of 200 microg/kg epinephrine with 0.8 units/kg vasopressin was given. Defibrillation was attempted 20 mins after initiating cardiopulmonary resuscitation. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem left ventricular myocardial blood flow 2 mins after each respective drug administration was 65 +/- 4 and 70 +/- 13 mL x min(-1) x 100 g(-1) in the vasopressin group; 83 +/- 42 and 85 +/- 41 mL x min(-1) x 100 g(-1) in the epinephrine group; and 176 +/- 32 and 187 +/- 29 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p <.006 after both doses of epinephrine-vasopressin vs. vasopressin and after the first dose of epinephrine-vasopressin vs. epinephrine, respectively). At the same times, mean +/- sem total cerebral blood flow was 73 +/- 3 and 47 +/- 5 mL x min(-1) x 100 g(-1) after vasopressin; 18 +/- 2 and 12 +/- 2 mL x min(-1) x 100 g(-1) after epinephrine; and 79 +/- 21 and 41 +/- 8 mL x min(-1) x 100 g(-1) after epinephrine-vasopressin (p <.025 after both doses of vasopressin and epinephrine-vasopressin vs. epinephrine). Five of six vasopressin-treated, two of six epinephrine-treated, and six of six epinephrine-vasopressin treated animals had return of spontaneous circulation (nonsignificant). CONCLUSIONS: In this pediatric porcine model of ventricular fibrillation, the combination of epinephrine with vasopressin during cardiopulmonary resuscitation resulted in significantly higher levels of left ventricular myocardial blood flow than either vasopressin alone or epinephrine alone. Both vasopressin alone and the combination of epinephrine with vasopressin, but not epinephrine alone, improved total cerebral blood flow during cardiopulmonary resuscitation. In stark contrast to asphyxial cardiac arrest, vasopressin alone or in combination with epinephrine appears to be of benefit after ventricular fibrillation in the pediatric porcine model.

Animals↗
PubMed2001

Successful treatment with an implantable cardioverter defibrillator for spontaneous ventricular fibrillation in dilated cardiomyopathy with very high defibrillation thresholds.

A 72-year-old male patient with idiopathic dilated cardiomyopathy who had shown recurrent episodes of drug refractory ventricular fibrillation underwent implantation of a transvenous implantable cardioverter defibrillator (ICD). Ventricular fibrillation (VF) was induced by a T wave shock at the implantation. However, the ICD device with a maximum energy of 30 J failed to terminate the VF. Reversing defibrillation polarity and/or adding a defibrillation electrode lead at the site of a high superior vena cava were also ineffective. The ICD was programmed to a maximum energy of 30 J when the device sensed spontaneous VF. During the follow-up period of 5 months, two episodes of spontaneous VF were recorded from ICD telemetry, and the ICD device terminated VF successfully with the first therapy shock in both episodes. No previous reports have shown failure to terminate induced VF at implantation of the ICD with successful termination of spontaneous VF during follow-up. Careful follow-up is needed in ICD patients, especially those with very high defibrillation thresholds.

Aged↗
PubMed1980

Myocardial metabolic changes related to ventricular fibrillation.

The cause of death in patients who die suddenly or after an acute myocardial infarction is, in most cases, ventricular fibrillation. Most of these patients suffer from ischemic heart disease and atherosclerotic narrowing of the coronary arteries. Ischemic changes include hypoxia, accumulation of metabolites, depletion of energy-yielding substrates, ionic shifts and structural changes. There is an increased sympathetic activity and often a higher vagal tone. Recent observations support the idea that there is an elevated regional adrenergic activity in the ischemic area with increased tissue levels of cyclic AMP. This seems to be one of several important factors contributing to the occurrence of ventricular fibrillation. Increased sympathetic activity might mediate reentry mechanisms as well as enhanced automaticity.

Arrhythmias, Cardiac↗
PubMed1983

The repetitive extrasystole as an index of vulnerability to ventricular fibrillation during myocardial ischemia in the canine heart.

The repetitive extrasystole threshold (RET) is a reliable measure of vulnerability to ventricular fibrillation (VF) during diverse interventions in the normal heart. Whether this relationship also holds during varying degrees of myocardial ischemia has not been adequately explored. In 15 chloralose-anesthetized dogs, circumflex coronary blood flow (CBF) was decreased progressively with the use of an externally applied balloon occluder. There was a statistically significant correlation between the RET and ventricular fibrillation threshold (VFT) until left circumflex coronary artery flow was reduced by 90% of control values (r = 0.92). During reductions of CBF of 90% or greater, the VFT fell more than the RET and the RET/VFT ratio was disrupted. Total coronary occlusion, whether performed abruptly or gradually (5 minutes), likewise resulted in a disproportionate decline in VFT. During sustained total coronary occlusion, the VFT recovered to control values within 15 minutes, and the relationship between the RE and VF thresholds was restored. We conclude that the vulnerable period threshold for provoking repetitive extrasystole is a reliable index of vulnerability to VF during myocardial ischemia and remains so until nearly total occlusion of a major coronary vessel.

Animals↗
PubMed1994

[Acute ischemia, autonomic reflexes, and ventricular fibrillation].

The effects of the autonomic nervous system on malignant arrhythmias, particularly in the setting of ischemic heart disease, have been widely investigated and described. Specifically, while sympathetic hyperactivity is arrhythmogenic, an increased vagal activity often exerts a beneficial effect. New insights on the relationship between autonomic activity and sudden cardiac death have been obtained in conscious dogs in which a healed myocardial infarction, acute myocardial ischemia and exercise are combined. In this chronic animal model myocardial infarction reduces baroreflex sensitivity and heart rate variability (markers of vagal reflex and tonic activity to the heart) and a depressed baroreflex sensitivity or a reduced heart rate variability after myocardial infarction indicates an increased risk for ventricular fibrillation. The clinical relevance of these experimental observations was confirmed in studies in patients with myocardial infarction. Exercise training increases vagal control of heart rate and concomitantly prevents recurrence of ventricular fibrillation during acute ischemia in dogs susceptible to sudden death. The protective effect of vagal activity is further confirmed by the experimental evidence that electrical stimulation of the vagus is able to prevent ventricular fibrillation during acute myocardial ischemia. The possibility of modulating the autonomic control of cardiac activity by means of pharmacologic and non pharmacologic interventions able to increase cardiac vagal activity represents a rational and promising approach to reduce risk for lethal events after myocardial infarction.

Acute Disease↗
PubMed1992

Diltiazem improves resuscitation from experimental ventricular fibrillation in dogs.

OBJECTIVE: To determine the effect of diltiazem on survival immediately after cardiac arrest and cardiopulmonary resuscitation (CPR) in dogs. DESIGN: Prospective, double-blind, randomized trial. SETTING: Laboratory at a large, university-affiliated medical center. SUBJECTS: Twenty-eight mongrel dogs, weighing 12 to 16 kg. INTERVENTIONS: After the administration of anesthesia, catheters were placed in the pulmonary artery, aortic arch, left ventricle, right ventricle, and great cardiac vein (12 dogs) for sample collection, pressure determinations, and induction of ventricular fibrillation. Dogs were randomized to receive either diltiazem, calcium chloride, or placebo (saline) either before or early during CPR. Dogs underwent 3 mins of unassisted fibrillatory arrest followed by 10 mins of standard CPR using a pneumatic device. After 13 mins of ventricular fibrillation, defibrillation was attempted repeatedly for less than or equal to 10 mins. Successful resuscitation was defined as an organized rhythm with an unassisted systolic BP of greater than 60 mm Hg for greater than or equal to 2 mins. MEASUREMENTS AND MAIN RESULTS: The resuscitation rate was significantly greater in diltiazem-treated animals (100%) than in those dogs receiving calcium (57%) or placebo (29%). Diltiazem-treated animals were resuscitated faster and required fewer defibrillation attempts than did dogs in the other groups. During CPR, coronary artery perfusion pressure and blood gases (arterial, venous, and myocardial) were similar among treatment groups. CONCLUSIONS: Diltiazem improves the resuscitation from experimentally induced ventricular fibrillation when administered before or early during CPR. This response may have important clinical implications in the treatment of patients undergoing cardiac arrest and CPR.

Analysis of Variance↗
PubMed1975

Coronary revascularization in patients surviving unexpected ventricular fibrillation.

Coronary angiography and hemodynamic studies were performed in a group of 13 patients who had been successfully resuscitated from unexpected ventricular fibrillation, had had angina pectoris prior to the cardiac arrest, and who had not had an acute myocardial infarction in the periarrest period. Eleven of the 13 had one or more coronary artery lesions which were amenable to surgical intervention, and eight of the 11 accepted surgery. Left ventricular end-diastolic pressure was elevated in most patients, while cardiac index and ejection fraction were depressed. Bypassable lesions were found in the main left coronary artery in one patient, and the proximal left anterior descending artery in two. Both of these patients had disease elsewhere. The remaining five patients had diffuse three-vessel disease. The eight patients have survived for periods ranging from 8 to 32 months (average = 24 months). This contrasts to an overall 1-year mortality of approximately 30% in survivors of hospitalization after unexpected ventricular fibrillation.

Cardiac Catheterization↗
PubMed1992

Cryoblockade in limbic brain (amygdala) prevents or delays ventricular fibrillation after coronary artery occlusion in psychologically stressed pigs.

Neomammalian and paleomammalian (limbic) brain structures control different behaviors and the autonomic support specific to each. Both neural systems are involved in cardiovascular disorders. Our previous studies showed that bilateral cryoblockade of a neomammalian structure (the frontal lobes) reduces blood pressure elevations in experimental hypertension and prevents lethal arrhythmogenesis in experimental myocardial infarction. Other studies showed that bilateral lesions in a paleomammalian structure (amygdala) also reduce the blood pressure elevations. Thus, we hypothesized that cryoblockade of the amygdala would prevent lethal arrhythmogenesis. We found that cooling of cryoprobes implanted bilaterally in the amygdala prevented ventricular fibrillation in five of eight pigs during a 20-minute period of reversible myocardial ischemia, whereas cryoblockade in structures surrounding the amygdala (five pigs), unilateral cryoblockade in the amygdala (two pigs), or sham operations (three pigs) did not prevent ventricular fibrillation (p less than 0.003). In two of the five pigs with amygdaloid blockade, the cooling was reversed at 20 minutes while the coronary occlusion continued (24 hours), and still ventricular fibrillation did not occur. In all other cases, ischemia was reversed at 20 minutes so that the heart could recover; this enabled histochemical documentation that the heart was normal at the time(s) ischemia was induced, and it allowed within-subject control experiments. Amygdaloid cryoblockade produced a small but significant increase in heart rate (10 beats per minute) without a change in blood pressure. We conclude that the paleomammalian brain, like its neomammalian counterpart, mediates brain effects on fatal arrhythmogenesis.

Amygdala↗
PubMed1991

Effect of palmitic acid and fatty acid binding protein on ventricular fibrillation threshold in the perfused rat heart.

The effects of increased free fatty acid (FFA) levels on ventricular arrhythmias remain controversial. Using ventricular fibrillation threshold (VFT), we examined the relationship between FFA levels and ventricular arrhythmias. Isolated rat hearts were perfused with palmitate bound to either albumin or fatty acid binding protein (FABP) by Langendorf's method. The VFT was determined by electrical stimulation. Perfusion with 0.12 mM albumin alone, 0.12 mM palmitate bound to 0.12 mM albumin, and 0.36 mM palmitate bound to 0.12 mM albumin did not lower the VFT significantly. However, 0.60 mM palmitate bound to 0.12 mM albumin lowered VFT from 2.19 +/- 0.20 mA to 1.56 +/- 0.13 mA. The perfusion of 0.36 mM palmitate bound to 0.12 mM FABP lowered the VFT from 2.05 +/- to 0.19 mA to 1.47 +/- 0.23 mA, but 0.12 mM FABP alone did not affect the VFT. Perfusion with 0.36 mM palmitate bound to 0.12 mM FABP caused the VFT to fall more than perfusion with 0.36 mM palmitate bound to 0.12 mM albumin. Then the effects of verapamil perfusion or a low concentration of perfusate Ca2+ on VFT were examined. VFT was determined by electrical stimulation. Palmitate (0.6 mM) bound to 0.12 mM albumin lowered VFT. Verapamil 10(-7) M perfusion and a low concentration of Ca2+ (Ca2+ 1.67 mM) suppressed the FFA-induced fall of VFT. These results suggested that the arrhythmogenic action of FFA was related to Ca2+ overload in myocardial cells.

Albumins↗
PubMed1995

How can we facilitate spontaneous termination of ventricular fibrillation and prevent sudden cardiac death? A working hypothesis.

Ventricular fibrillation (VF) is one of the most life-threatening arrhythmias encountered in daily clinical practice. Its occurrence cannot be completely prevented by currently used antiarrhythmic drugs, and, in most instances, VF is sustained and leads to the patient's death unless a successful DC defibrillation is applied. However, spontaneous reversion of VF to sinus rhythm has been observed in various animals and occasionally even in man. Hence, facilitation of self-ventricular defibrillation must be explored as an alternative therapeutic approach. In experimental studies using several mammalian species, we have found that self ventricular defibrillation requires a good intercellular coupling and well synchronized electrical activity in the ventricles, which, in untreated animals, depend on their myocardial catecholamine content. It can then be hypothesized that any agent that elevates the catecholamine level during VF would facilitate spontaneous ventricular defibrillation, and drugs inhibiting extraneuronal catecholamine reuptake have indeed been shown to possess this ability. It is suggested that their effects are mediated by an increase in the intracellular cAMP level, and any compounds sharing this property could well prove efficacious in making VF transient and in reducing sudden cardiac death.

Animals↗
PubMed1999

[Recurrent ventricular fibrillation in a patient with Prinzmetal angina pectoris--case report].

The description of the case of 35 years old patient with paroxysmal ventricular fibrillation in a course of Prinzmetal angina pectoris treated unsuccessfully with antiarrhythmic drugs who required implantation of cardioverter/defibrillator. The via-venous cardioverter/defibrillator was implanted (ICD). During 6 months observation ventricular tachycardia and ventricular fibrillation occurred four times and was effectively interrupted by the cardioverter/defibrillator.

Adult↗
PubMed1988

Differences between patients with ventricular tachycardia and ventricular fibrillation as assessed by signal-averaged electrocardiogram, radionuclide ventriculography and cardiac mapping.

This study examined 65 patients with ventricular tachycardia or fibrillation late after myocardial infarction to determine whether they differed with respect to duration of ventricular activation in sinus rhythm and left ventricular ejection fraction. Patients with spontaneous ventricular tachycardia had a longer ventricular activation time in sinus rhythm than did patients with spontaneous ventricular fibrillation. This difference was detected with the signal-averaged electrocardiogram (ECG) (tachycardia 181 +/- 33 ms, fibrillation 152 +/- 23 ms, p less than 0.001) and at epicardial mapping (tachycardia 210 +/- 17 ms, fibrillation 192 +/- 17 ms, p less than 0.02). Left ventricular ejection fraction was lower in patients with spontaneous ventricular tachycardia (0.22 +/- 0.09) than in patients with spontaneous ventricular fibrillation (0.27 +/- 0.09) (p less than 0.05). The patients with both spontaneous and inducible ventricular fibrillation had a shorter ventricular activation time on the signal-averaged ECG (129 +/- 17 ms) and a higher ejection fraction (0.36 +/- 0.05) than did either patients with spontaneous ventricular fibrillation and inducible ventricular tachycardia (158 +/- 21 ms and 0.25 +/- 0.08, respectively, each p less than 0.01) or patients with both spontaneous and inducible ventricular tachycardia (181 +/- 33 ms and 0.22 +/- 0.09, respectively, each p less than 0.001). Of the patients with inducible ventricular tachycardia, presentation with tachycardia rather than fibrillation was associated with a longer ventricular activation time on the signal-averaged ECG (181 +/- 33 versus 158 +/- 21 ms, p less than 0.02) and a longer cycle length of inducible ventricular tachycardia (290 +/- 61 versus 259 +/- 44 ms, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Effect of sustained stretch on dispersion of ventricular fibrillation intervals in normal rabbit hearts.

OBJECTIVE: To determine the effect of acute left ventricular dilatation on refractoriness in normal hearts. METHODS: During sustained ventricular fibrillation (VF) in isolated perfused hearts, recording of local activation time yields VF intervals which provide an index of local refractoriness. Simultaneous measurement from multiple sites enables study of spatial aspects of changes in refractoriness. We studied the effects of stretch on the magnitude and dispersion of changes in VF interval in 10 isolated, Langendorff-perfused rabbit hearts using a flexible epicardial array containing 240 unipolar electrodes. The left ventricular pressure was increased from 0 to 40 mmHg by inflation of an intraventricular balloon during sustained VF. RESULTS: The current threshold for VF induction fell from 64 +/- 11 mA to 43 +/- 11 mA (mean +/- SE, P < 0.01) following ventricular dilatation. Mean VF interval at 0 mmHg was 79.8 +/- 1.3 ms and fell to 70.2 +/- 1.7 ms (P < 0.01) at 40 mmHg. There was a corresponding increase in dispersion of VF interval (coefficient of variation) from 8.13 +/- 0.8 to 13.3 +/- 0.8 (P < 0.01). There was regional heterogeneity in the areas of greatest reduction in VF interval, which varied between hearts. Following balloon inflation there was an increase in the number of activation waves. CONCLUSIONS: Acute ventricular dilatation produces spatially heterogeneous changes in refractoriness which would predispose to the maintenance of reentrant arrhythmias.

Animals↗
PubMed1983

Ventricular fibrillation in a conscious canine model--its prevention by UM-272.

The antifibrillatory properties of UM-272 (dimethylpropranolol; Pranolium) were evaluated in a conscious canine model of sudden coronary death. The initial preparation of the animal model was carried out under surgical anesthesia and involved the intraluminal implantation of a Teflon-coated silver wire into the circumflex coronary artery so that 3 mm of the bared electrode was in contact with the endothelial surface. The left anterior descending coronary artery then was occluded for a period of 90 min and reperfused in the presence of a critical stenosis. Three days after myocardial infarction, they were randomized into two groups. One group (n = 10) served as controls and received saline. The second group (n = 10) received UM-272 in a dose of 5 mg/kg every 6 h. On day 4, a 150 microA current was applied to the intimal surface of the left circumflex coronary artery, resulting in transient or permanent alterations in circumflex coronary blood flow accompanied by electrocardiographic evidence of regional myocardial ischemia. The time to onset of ST-segment changes in the saline control group was 99 +/- 34 min and was followed by the appearance of premature ventricular complexes (111 +/- 34 min) and subsequent ventricular tachycardia (131 +/- 37 min) which terminated in ventricular fibrillation in each of the 10 dogs. Animals treated with UM-272 likewise developed ST-segment changes (156 +/- 28 min) and premature ventricular complexes (168 +/- 29 min), but 4 of 10 animals failed to develop ventricular fibrillation (P less than 0.05 vs. saline). These results demonstrate that UM-272, the dimethyl quaternary analog of propranolol, is effective in reducing the incidence of ventricular fibrillation in a conscious canine model in which the superimposition of a transient ischemic event upon an already jeopardized heart leads to the development of sudden death.

Animals↗
PubMed2005

Reliability of old and new ventricular fibrillation detection algorithms for automated external defibrillators.

BACKGROUND: A pivotal component in automated external defibrillators (AEDs) is the detection of ventricular fibrillation by means of appropriate detection algorithms. In scientific literature there exists a wide variety of methods and ideas for handling this task. These algorithms should have a high detection quality, be easily implementable, and work in real time in an AED. Testing of these algorithms should be done by using a large amount of annotated data under equal conditions. METHODS: For our investigation we simulated a continuous analysis by selecting the data in steps of one second without any preselection. We used the complete BIH-MIT arrhythmia database, the CU database, and the files 7001-8210 of the AHA database. All algorithms were tested under equal conditions. RESULTS: For 5 well-known standard and 5 new ventricular fibrillation detection algorithms we calculated the sensitivity, specificity, and the area under their receiver operating characteristic. In addition, two QRS detection algorithms were included. These results are based on approximately 330,000 decisions (per algorithm). CONCLUSION: Our values for sensitivity and specificity differ from earlier investigations since we used no preselection. The best algorithm is a new one, presented here for the first time.

Algorithms↗
PubMed1993

Efficient electrode spacing for examining spatial organization during ventricular fibrillation.

Spatial organization has been observed during episodes of ventricular fibrillation (VF) by recording epicardial unipolar electrograms on a grid of electrodes. In such studies, the choice of spacing between electrodes is an important decision, affecting the resolution and the size of the domain to be studied. A basic tenet of sampling theory, the Nyquist criterion, states that an electrode spacing smaller than half the smallest significant wavelength is required to capture the important details of a spatially sampled process. In this paper, we suggest a method to choose a practical interelectrode spacing by examining wavenumber power spectra of high-resolution VF data recorded from a square 11 x 11 array of electrodes spaced 0.28 mm apart. The plaque was sutured on the epicardium near the left ventricular apex in seven anesthetized pigs. VF was induced with ac simulation. Unipolar extracellular electrograms were simultaneously recorded from each channel for 2 s after the induction of VF. Each signal was sampled in time at 1000 Hz. Wavenumber power spectra were calculated for 100 ms segments using the zero-delay wavenumber spectrum method, for a total of 140 power spectra. All spectra had dominant peaks at the origin and fell off rapidly with increasing wavenumber (decreasing wavelength). In all the spectra, every wavelength shorter than 1.4 mm contributed insignificant power. Furthermore, in 134 of 140 spectra (96%), insignificant power levels were associated with every wavelength shorter than 2.8 mm. These results suggest that, for unipolar extracellular electrodes, an intersensor spacing on the order of 1 mm is appropriate to study organization during early VF.

Animals↗