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PubMed2000

The effects of high-dose epinephrine combined with isoprenaline on isolated rabbit heart and cardiomyocytes after cardioversion of ventricular fibrillation.

The effects of high-dose epinephrine (HDE) combined with isoprenaline (Iso) on myocardial hemodynamics of isolated rabbit heart were studied. The electrophysiology and L-type Ca2+ channel of single ventricular myocyte after cardioversion of ventricular fibrillation were determined. The results suggest that parameters of hemodynamics were significantly enhanced by HDE+Iso than that of HDE (p < 0.01). The OS and Vmax of HDE+Iso increased 83.7 and 10.15% respectively compared to HDE alone. The APF of HDE+Iso is much more rapid than that of HDE (138.38 +/- 9.96 vs. 55.58 +/- 8.63 min(-1), p < 0.001). The APD50 and APD90 of HDE+Iso were significantly decreased; HR was increased (134.16 +/- 1.48 vs 62.20 +/- 6.25 min(-1)); and the amplitude current of through L-type Ca2+ channel was reduced but was significantly higher than the control. We conclude that HDE+Iso can improve the hemodynamics and improve electrophysiology of cardiomyocytes after cardioversion of ventricular fibrillation which is likely interrelated with I(Ca). The combined use of epinephrine and isoprenaline for cardiopulmonary resuscitation of primary ventricular fibrillation may be beneficial when employed in clinical situations.

Action Potentials↗

PubMed1989

The value of the clinical history to assess prognosis of patients with ventricular tachycardia or ventricular fibrillation after myocardial infarction.

Multivariate analysis using 70 variables in 200 patients who suffered from ventricular tachycardia or ventricular fibrillation after myocardial infarction detected eleven variables that were associated with an increased risk of sudden arrhythmic death and cardiac death during a mean follow-up period of 2 years. Four of the 11 variables came from the patient's clinical history: (1) cardiac arrest at the time of the first spontaneous episode of arrhythmia, (2) New York Heart Association functional class for dyspnoea = III, (3) ventricular tachycardia or ventricular fibrillation occurring early (after 3 days and within 2 months) after myocardial infarction, (4) multiple myocardial infarctions before the first episode of ventricular tachyarrhythmia. Total mortality, incidence of sudden arrhythmic death and of non-sudden cardiac death increased with an increasing number (zero, one, two, three, four) of variables seen in individual patients. Patients with zero or one variable had an incidence of sudden death of 2.8% and a 4.2% incidence of non-sudden cardiac death at 26 months, while patients with more than two variables had a 13.5% and a 20.3% incidence respectively of sudden and non-sudden cardiac death. The strongest predictor of sudden death was the occurrence of cardiac arrest during the first spontaneous episode of ventricular arrhythmia. The strongest predictor of non-sudden cardiac death was the New York Heart Association functional class. The use of the four variables to stratify risk revealed seven subgroups of patients with incidences of sudden death ranging from 0 to 28%.(ABSTRACT TRUNCATED AT 250 WORDS)

Death, Sudden↗

PubMed1995

Hospital mortality after out-of-hospital cardiac arrest among patients found in ventricular fibrillation.

The aim of this study was to describe factors associated with in-hospital mortality among patients being hospitalised after out-of-hospital cardiac arrest and who were found in ventricular fibrillation. The study was set in the community of Göteborg, Sweden. The subjects consisted of all patients who were hospitalised alive after out-of-hospital cardiac arrest, being reached by our mobile coronary care unit and who were found in ventricular fibrillation, between 1981 and 1992. In all, 488 patients fulfilled the inclusion criteria of which 262 (54%) died during initial hospitalization. In a multivariate analysis including age, sex, history of cardiovascular disease, chronic medication prior to arrest and circumstances at the time of arrest, the following appeared as independent predictors of hospital mortality: (1) interval between collapse and first defibrillation (P < 0.001); (2) on chronic medication with diuretics (P < 0.01); (3) age (P < 0.01); (4) bystander initiated CPR (P < 0.05); and (5) a history of diabetes (P < 0.05). In a multivariate analysis considering various aspects of status on admission to hospital, the following were independently associated with death: (1) degree of consciousness (P < 0.001) and (2) systolic blood pressure (P < 0.05). In conclusion, among patients with out of hospital cardiac arrest found in ventricular fibrillation and being hospitalised alive, 54% died in hospital. The in-hospital mortality was related to patient characteristics before the cardiac arrest as well as to factors at the resuscitation itself.

Adolescent↗

PubMed2006

Role of the posterior papillary muscle and purkinje potentials in the mechanism of ventricular fibrillation in open chest dogs and Swine: effects of catheter ablation.

BACKGROUND: Papillary muscle (PM) ablation may terminate ventricular fibrillation (VF) in rabbit hearts. Whether or not PM ablation prevents ventricular fibrillation (VF) induction in large animals is unknown. METHODS: We performed noncontact endocardial mapping and/or high-density epicardial mapping during VF in 12 dogs and 16 swine and tested the effects of posterior PM (PPM) ablation on VF inducibility. RESULTS: During VF in progressive global ischemia (3 swine and 2 dogs), the highest dominant frequency (DF) was near PPM. The majority of the reentrant wavefronts during a propranolol infusion (swine) were anchored to the PPM. Purkinje potentials onset were recorded on the PPM both during sinus rhythm and during VF. Radiofrequency (RF) ablation of the endocardium on the PPM with a linear extension of the ablation line from the PPM to the mitral valve annulus and then the left ventricular apex in 7 dogs reduced the VF inducibility from 100% at baseline to 22% after ablation (P < 0.0001). RF applications to the anterolateral wall of dogs (n = 3) did not prevent VF induction. The application of RF energy near the PPM frequently initiated VF in swine (n = 7), preventing subsequent testing of VF inducibility. CONCLUSION: In dogs and swine, the highest DF and majority of reentrant wavefronts during VF with acute global ischemia or during a propranolol infusion were located on the PPM. RF ablation targeted at the PPM reduced the inducibility of VF in normal dogs. However, the same ablation provoked incessant VF in swine, preventing subsequent testing of VF inducibility.

Animals↗

PubMed1999

Induction of ventricular fibrillation by T wave shocks: observations from monophasic action potential recordings.

INTRODUCTION: Shocks given during the vulnerable period of cardiac repolarization may induce ventricular fibrillation (VF). However, the relationship of the vulnerable period and the monophasic action potential (MAP) has not yet been reported in humans. The purpose of this study was, therefore, to determine how the monophasic action potential recorded from the right ventricle correlates with inducibility of VF using T wave shocks during ventricular pacing. METHODS: Eleven patients undergoing implantable cardioverter defibrillator (ICD) implantation had a MAP catheter positioned in the right ventricle (RV). The local monophasic action potential duration at 90% repolarization (MAP90) duration was measured during pacing at 400 ms. VF induction was attempted by pacing at 400 ms for 10 cycles and then giving a 1.0 joule monophasic T wave shock at varying coupling intervals (CI) to the last paced stimulus. The maximum and minimum CI that induced VF were determined and mapped in relation to the MAP90 recording. RESULTS: The average paced MAP duration was 275 +/- 20 ms. The minimum and maximum CI to induce VF were 255 +/- 24 ms and 325 +/- 36 ms respectively. This ranged from 93% to 118% of the MAP90 duration but because of delay in conduction time to the MAP catheter, shocks that induced ventricular fibrillation occurred between 74% and 99% of local repolarization time. CONCLUSION: VF is inducible with low energy T wave shocks falling during the last 25% of the right ventricular MAP90 recording. This corresponds with VF initiation during phase III repolarization.

Action Potentials↗

PubMed1996

Comparison of patients with acute myocardial infarction with and without ventricular fibrillation.

Among 1,590 patients with acute myocardial infarction from 1990 to 1994, the rate of primary ventricular fibrillation was 3.6%. The prevalence of smoking, complete left bundle branch block, hypokalemia, and decreased left ventricular function was higher in patients with ventricular fibrillation while those on thrombolytic therapy and those with non-Q-wave myocardial infarction were significantly lower.

Case-Control Studies↗

PubMed2002

The effects of acute and chronic amiodarone on activation patterns and defibrillation threshold during ventricular fibrillation in dogs.

OBJECTIVES: The goal of this study was to evaluate the effects of acute and chronic amiodarone on activation patterns during ventricular fibrillation (VF), ventricular effective refractory period (VERP) and defibrillation threshold (DFT). BACKGROUND: Acute and chronic amiodarone may act through different mechanisms. METHODS: The VERP, VF activation patterns and DFT were determined in 24 dogs. Twelve dogs received acute intravenous amiodarone (10 mg/kg, n = 6) or saline (n = 6), and 12 dogs received chronic oral amiodarone (20 mg/kg/day, n = 6) or placebo (n = 6). Epicardial VF activation patterns were recorded with 504 electrodes. Quantitative descriptors of VF were calculated. RESULTS: The DFT was unchanged by acute or chronic amiodarone. Although chronic amiodarone significantly extended the VERP, acute amiodarone did not. In the mapped region, acute and chronic amiodarone decreased the number of VF wavefronts by 42% and 60%. Acute amiodarone decreased conduction block by 22%, while chronic amiodarone increased block by 41% but decreased wave fractionation by 50%. Both chronic and acute amiodarone increased the size of the core of re-entrant circuits and decreased the incidence of re-entry by 44% and 57%; however, chronic amiodarone increased wavelength, while acute amiodarone did not. CONCLUSIONS: Neither acute nor chronic amiodarone change the DFT. While both acute and chronic amiodarone decrease the number of wavefronts, decrease the incidence of re-entry and increase the size of re-entrant cores in the mapped region during VF, they achieve these antiarrhythmic effects through different electrophysiologic mechanisms. Chronic amiodarone prolonged the VF cycle length and slowed conduction velocity, indicating it increased the wavelength and/or the excitable gap.

Amiodarone↗

PubMed2005

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.

Animals↗

PubMedDate not supplied

Changes in ventricular fibrillation threshold induced by contrast agents during acute coronary artery occlusion.

In the first few hours after acute coronary thrombosis, clinical coronary angiography is associated with enhanced risk of ventricular fibrillation. In these experiments, the ventricular fibrillation threshold (VFT) was measured in anesthetized dogs before and during acute occlusion of the left circumflex coronary artery. Ischemia alone reduced the fibrillation threshold. Angiography with 1- or 2-ml does of Renografin 76 lowered VFT significantly more than did equal doses of iohexol or iopamidol. It is concluded that nonionic agents may be safer for coronary angiography in the presence of acute coronary insufficiency.

Angiography↗

PubMed2005

New model of ventricular fibrillation.

The purpose of this study was to develop a more efficient and stable model of ventricular fibrillation (VF) in the isolated rabbit heart, because there is not a satisfactory model with this animal. We also observed the effects of increasing extracellular calcium in the stability and reversibility of the arrhythmia. After suspending the hearts in a classical Langendorff preparation, VF was induced by burst stimulation (current = 2.0 mA, pulse duration = 3 milliseconds, frequency = 50 Hz, voltage = 10 V, duration of stimulation = 5 minutes). The hearts were then divided into 2 groups, A and B. The hearts in group B were perfused with a modified Krebs-Henseleit solution, which contained twice as much calcium as the solution used in the other group. The rate of success with this model was 100% for both groups. The hearts fibrillated up to 30 minutes in group A and more than 40 minutes in group B, longer then all studies ever published in rabbit hearts. Ventricular fibrillation reverted to sinus rhythm in 100% of the hearts of group A when treated with an antifibrillatory drug, whereas no reversion at all was observed in the hearts of group B. We conclude that high extracellular calcium makes the reversion to sinus rhythm more difficult in this model. Our high rate of success and the exceptionally stable and long-lasting VF turn our model very effective for the study of antiarrhythmic interventions in the isolated rabbit heart.

Animals↗

PubMed1996

Ventricular fibrillation in the patient with blunt trauma: not always exsanguination.

Three cases of successful prehospital resuscitation of blunt trauma patients sustaining cardiac arrest resulting from ventricular fibrillation are reported. Although probably uncommon, ventricular fibrillation not caused by severe hypovolemia, exsanguination, or severe hypoxia in the setting of blunt trauma might be a treatable cause of cardiac arrest. Early electrocardiographic monitoring of patients with blunt trauma, including those with cardiac arrest, can detect this small, yet easily salvageable group of patients.

Adolescent↗

PubMed1987

Role of QT prolongation secondary to a postextrasystolic pause as a possible mechanism for the induction of ventricular fibrillation. Report of two cases.

Two patients developed ventricular fibrillation (VF) while undergoing continuous electrocardiographic monitoring. Analysis showed that VF appeared only when a particular combination of circumstances occurred: a postextrasystolic pause, QT prolongation of the subsequent beat and a premature ventricular beat that did not have a short coupling interval. The relevance of this sequence as a trigger mechanism of VF is discussed.

Aged↗

PubMed2004

Ventricular fibrillation frequency characteristics and time evolution in piglets: a developmental study.

BACKGROUND: Derived variables of ventricular fibrillation, such as the frequency distribution by fast Fourier transformation and its evolution over time, have been used to determine the optimum timing for defibrillation. We hypothesized that these frequency variables would differ among neonatal, young child and older child populations due to cardiac developmental and size differences. Such differences may have important implications for developing defibrillation algorithms for pediatric patients and for extrapolating adult defibrillation algorithms to children in VF. METHODS: Ventricular fibrillation was induced and recorded for 6 min in 4 kg (n = 11), 14 kg (n = 10), and 24 kg (n = 16) piglets, corresponding to neonatal, young child and older children. Mean, median, and dominant frequencies were computed in 30 s intervals and compared among weight classes. RESULTS: All frequency variables in all weight groups showed first a decline at 1.25-1.75 min, followed by a gradual rise and plateau. There were significant differences for mean, median and dominant frequencies among weight classes. Specifically, 14 kg piglets showed higher frequency variables overall with a time evolution that was different from that of 4 and 24 kg piglets. Mean frequency showed the most stable time evolution with the least moment-to-moment variability. CONCLUSION: The frequency waveform characteristics and time course are somewhat different in 14 kg piglets compared with 4 and 24 kg piglets. If similar differences are demonstrable among children of different weights and ages, AEDs designed to determine optimal timing of defibrillation shocks in adults by frequency waveform characteristics may require modification for use in children with VF.

Animals↗

PubMed2000

[Recurrent ventricular fibrillation after defibrillation in a patient with pacemaker].

HISTORY: A 62-year-old patient was admitted for an operation of a hernia of the right groin in the surgical department. He had a dual chamber pacemaker because of a binodal disease. Pre-operatively the patient was reanimated because of ventricular fibrillation in dilated cardiomyopathy and was defibrillated 12 times, unexpectedly often. DIAGNOSIS: The reason of the repeated ventricular fibrillation was a spike-on-T-phenomenon due to loss of the sensing function of the pacemaker (entrance bloc). TREATMENT: Therefore, the pacemaker was explanted, and the ventricular fibrillation came to an end. The patient recovered. CONCLUSIONS: The repeated defibrillations with the electrodes over the basis and the apex of the heart damaged the pacemaker. The following fibrillation episodes were founded on a spike-on-T-phenomenon. In order to prevent such damage of pacemakers, pacemaker patients should be defibrillated and cardioverted in anterior-posterior position of the electrodes.

Cardiomyopathy, Dilated↗

PubMed1987

Demonstration of exercise-induced painless myocardial ischemia in survivors of out-of-hospital ventricular fibrillation.

To ascertain if myocardial ischemia is the mechanism of out-of-hospital ventricular fibrillation (VF), left ventricular (LV) function was assessed at rest and during submaximal exercise in 15 patients who survived out-of-hospital VF. They were separated into asymptomatic (9 patients, group A) and symptomatic (6 patients, group S) groups for a history of angina or myocardial infarction. Both groups had significant (at least 70% diameter stenosis) coronary artery disease. At catheterization no patient had angina during exercise, but 12 of 15 had ST depression or increased ST depression (group A, 1.9 +/- 1.4 mm; group S, 1.1 +/- 1.2 mm) and 11 had abnormal wall motion. From rest to exercise, patients in group S had increased LV end-diastolic pressure (from 21 +/- 9 to 37 +/- 11 mm Hg, p = 0.009) and volume (from 100 +/- 25 to 107 +/- 26 ml/m2, p = 0.006), with no significant change in LV ejection fraction (from 40 +/- 13 to 42 +/- 12%). In group A LV end-diastolic pressure increased from 19 +/- 4 to 31 +/- 8 mm Hg (p = 0.001), but neither end-diastolic volume nor ejection fraction changed significantly (from 83 +/- 13 to 92 +/- 23 ml/m2 and from 55 +/- 13% to 46 +/- 13%, respectively). Thus, patients with coronary artery disease who survive out-of-hospital VF may have evidence of myocardial ischemia during exercise without pain. Painless ischemia may have a role in out-of-hospital VF.

Adult↗

PubMed1993

Plasma potassium, serum magnesium and ventricular fibrillation: a prospective study.

Low plasma potassium and magnesium concentrations have been advanced as risk factors for ventricular fibrillation (VF). For potassium, this assertion is based almost exclusively on retrospective data; for magnesium the evidence shows an association with ventricular arrhythmias but no direct association with VF. We studied the relationship between these electrolytes and VF prospectively. Plasma potassium and serum magnesium concentrations were measured on admission to our coronary care unit. Drug therapy, time from onset of symptoms, ECG, enzyme changes and clinical status were all recorded. VF was confirmed by analysis of 24 h monitoring tapes. Mean plasma potassium in the 21 patients with VF who had measurements prior to their arrhythmia was 3.49 +/- 0.54 mmol/l, lower than that of the 1165 patients without VF (mean K 3.88 +/- 0.57 mmol/l, p < 0.05). Plasma potassium concentrations in the 17 patients with myocardial infarction and VF were lower (mean 3.58 +/- 0.41 mmol/l) than in those without VF (n = 417, mean 3.89 +/- 0.61 mmol/l) (p < 0.05). Mean serum magnesium in the 12 patients with VF, measured prior to their arrhythmia (all with myocardial infarction) was 0.80 +/- 0.07 mmol/l, which was not different from the mean for patients without VF (n = 781, 0.82 +/- 0.09 mmol/l) or from the mean of 0.81 +/- 0.08 mmol/l for those with infarction but not VF (n = 331). Low plasma potassium concentrations are associated with increased risk of ventricular fibrillation, but low serum magnesium concentrations are not.

Female↗

PubMed1994

[Correlation between reperfusion ventricular fibrillation and postoperative enzyme release in coronary artery bypass grafting].

Twenty patients who had undergone elective coronary artery bypass grafting were divided into two groups according to the cardiac rhythms after aortic declamping. Eight patients had ventricular fibrillation (Vf group) and 12 patients had spontaneous resumption of heart beating in regular sinus rhythm (SPB group). In Vf group, percent CK-MB and absolute value of CK-MB on the first postoperative day showed significant increase compared with those of the SPB group (p < 0.01). Furthermore, duration of ventricular fibrillation after aortic declamping tended to be positively correlated (r = 0.7018) with absolute value of CK-MB on the first postoperative day, although this did not reach statistic significance (p = 0.0523). To the contrary, between the two groups no significant difference was found in percent LDH1, absolute value of LDH1, and ratio of LDH1 to LDH2 on the first and third postoperative day. It is suggested that ventricular fibrillation after aortic declamping plays a crucial role in increasing postoperative CK-MB level, and its duration is presumably correlated with the absolute value of CK-MB on the first postoperative day.

Adult↗

PubMed1994

Active compression-decompression CPR improves vital organ perfusion in a dog model of ventricular fibrillation.

OBJECTIVES: This study was designed to assess whether a new method of cardiopulmonary resuscitation (CPR), termed active compression-decompression CPR, or ACD-CPR, improves organ perfusion when compared with standard (S) CPR in a dog model of ventricular fibrillation. BACKGROUND: ACD-CPR has recently been shown to improve hemodynamic and respiratory parameters during cardiac arrest when compared with standard CPR. However, to our knowledge, the effects of ACD-CPR on tissue perfusion have not been investigated. METHODS: Ventricular fibrillation was induced in eight anesthetized, intubated animals. ACD-CPR and standard CPR were each performed twice in alternating order. All interventions were preceded by 1 min of ventricular fibrillation, in which no CPR was performed, and consisted of 6 min of CPR with either technique during which tissue perfusion was measured. Compressions were performed at 80/min with a 50 percent duty cycle and 175 to 200 N downward force applied to the chest wall for both techniques. Epinephrine was administered at the beginning of each 6-min CPR interval. Hemodynamic monitoring of aortic and right atrial pressure was performed continuously and myocardial, cerebral, and renal blood flows were measured using the radiolabeled microsphere technique at baseline and during all interventions. RESULTS: Baseline organ perfusion and hemodynamics were similar for all dogs. Baseline left ventricular, brain, and renal blood flows were 62.0 +/- 5.5, 14.1 +/- 2.1, and 476.3 +/- 55.5 ml/min/100 g, respectively (mean +/- SEM). Compared with standard CPR, ACD-CPR resulted in higher global left ventricular (22.5 +/- 6.2 vs 14.1 +/- 4.0 ml/min/100 g, p < 0.01), cerebral (12.0 +/- 2.4 vs 8.5 +/- 2.3 ml/min/100 g, p < 0.01), and renal cortical (27.8 +/- 5.0 vs 17.5 +/- 5.0 ml/min/100 g, p < 0.05) blood flows. Regional flows to the epicardium, endocardium, and midmyocardium as well as to the frontal, parietal, and occipital lobes of the brain were all significantly improved by ACD-CPR. Aortic systolic (61.7 +/- 4.1 vs 49.5 +/- 3.1 mm Hg, p < 0.01), aortic mean (31.6 +/- 2.8 vs 27.2 +/- 2.2 mm Hg, p = 0.001), and myocardial perfusion pressure (12.9 +/- 3.4 vs 10.4 +/- 3.4 mm Hg, ACD-CPR vs standard CPR, p < 0.01) were all higher during ACD-CPR than during standard CPR. CONCLUSIONS: We conclude that ACD-CPR improves tissue perfusion and systemic hemodynamics compared with standard CPR.

Animals↗