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PubMed1990

Influence of reflow ventricular fibrillation and electrical defibrillation on infarct size in a canine preparation of myocardial infarction.

STUDY OBJECTIVE - The aim of the study was to investigate the influence of reflow ventricular fibrillation and electrical defibrillation on infarct size in a model of myocardial ischaemia. DESIGN - Myocardial ischaemia was induced in an open chest canine model by occluding the left coronary artery for 2 h. This was followed by 6 h reperfusion. The influence of reflow fibrillation and internal electric defibrillation on infarct size was investigated and compared to dogs which did not develop fibrillation. Infarct size and its major determinants, rate-pressure product (RPP), area at risk (AR), and collateral flow (MBF), were measured and their relationships studied in the two situations, using uni- and multilinear regression analysis. SUBJECTS - 21 adult mongrel dogs of either sex were used in the studies, which were done under pentobarbitone anaesthesia. Two were excluded because they developed ventricular fibrillation soon after coronary occlusion, and one did not survive reflow ventricular fibrillation. Of the remaining 18 dogs, six developed reflow ventricular fibrillation and were compared to the control group of 12 which did not develop fibrillation. MEASUREMENTS and RESULTS - A mean of 70.8(SEM 18.7) joules was required to revive the six dogs with reflow ventricular fibrillation. Difference in mean infarct size in the two groups did not reach significance [49.1(4.4) in fibrillation group v 38(6.2) in the controls]. The multiple linear regression model in the control group accounted for 91% of the variation in infarct size (IS): IS = -3.4 + 0.49 (AR) -21.8 (MBF) + 0.025 (RPP). The equation was not modified by including the reflow fibrillation dogs: IS = -3.1 + 0.52 (AR) - 19 (MBF) + 0.02 (RPP). Ischaemic determinants of infarct size in the reflow fibrillation dogs were computed in the control group equation to compare the infarct size predicted by the model to the measured infarct size in each individual dog in the reflow fibrillation group. There was no significant difference between the means: 12.9(2.9)% (predicted) v 14.9(2.5)% (measured). CONCLUSIONS - In this model of myocardial infarction, reflow ventricular fibrillation and low energy internal electric shocks do not damage the myocardium at risk significantly.

Animals↗

PubMed1985

Amplitude of ventricular fibrillation waveform and outcome after cardiac arrest.

The amplitude of ventricular fibrillation found initially in 394 patients was compared to clinical and logistical findings at the time of cardiac arrest. Peak-to-peak amplitude averaged 0.55 +/- 0.25 mV; a very low amplitude (0.2 mV or less) or "fine" fibrillation was present in 66 patients (17%). The amplitude was not found to be related to clinical histories, but depended on the length of the period from collapse until start of basic life support (p = 0.004) and the delay until assessment by paramedics (p = 0.001). Survival rates were strongly associated with amplitude: only 4 patients (6%) with fine ventricular fibrillation survived, compared to 117 or 328 patients (36%) in whom the initial amplitude was higher (p less than 0.001). Patient outcome related to amplitude even after adjusting for clinical history and logistical delays (p less than 0.005). We conclude that fine ventricular fibrillation is in part the result of delay in initiation of treatment, and that fibrillation amplitude is a powerful indicator of outcome after cardiac arrest.

Aged↗

PubMed1988

Six-year survival of patients with and without painless myocardial ischemia and out-of-hospital ventricular fibrillation.

Out-of-hospital ventricular fibrillation (OHVF) is the most common cause of sudden cardiac death. Of 1,070 patients with OHVF who entered this study, 150 were discharged alive. Of this group, 120 were free of anoxic brain damage. Of these survivors, 67 (57%) had no previously demonstrated anginal symptoms. Treadmill stress testing revealed painless ST depression in 76% of these neurologically intact patients. Exercise ventriculography in a subset of 9 patients without angina before OHVF and in 6 patients with typical anginal symptoms revealed marked left ventricular dysfunction with ST depression in the absence of chest pain in all 15 patients. Sublingual nitroglycerin reversed this evidence of ischemia in the asymptomatic patients. Patients were followed for 6 years after discharge. No statistical difference in mortality could be demonstrated for patients who had previous anginal symptoms vs those who did not, nor was age a predictor of mortality. Women had the same risk of death as men at 2 years after OHVF, but a significantly higher risk by year 6. Myocardial infarction associated with OHVF did not predict lower mortality throughout the study.

Death, Sudden↗

PubMed2006

Myocardial ischemia and ventricular fibrillation: pathophysiology and clinical implications.

Ventricular fibrillation (VF) and myocardial ischemia are inseparable. The first clinical manifestation of myocardial ischemia or infarction may be sudden cardiac death in 20-25% of patients. The occurrence of potentially lethal arrhythmia is the end result of a cascade of pathophysiological abnormalities that result from complex interactions between coronary vascular events, myocardial injury, and changes in autonomic tone, metabolic conditions and ionic state of the myocardium. It is also related to the time from the onset of ischemia. Within the first few minutes there is abundant ventricular arrhythmogenesis usually lasting for 30 min. Triggers for ischemic VF occur at the border zone or regionally ischemic heart. The border zone of ischemia is the predominant site of fragmentation. Acute ischemia opens K(ATP) channels and causes acidosis and hypoxia of myocardial cells leading to a large dispersion in repolarization across the border zone. Abnormalities of intracellular Ca2+ handling also occur in the first few minutes of acute myocardial ischemia and may be an important cause of arrhythmias in human coronary artery disease. Substrate on the other hand transforms triggers into VF and serves to maintain it through fragmentation of waves in the ischemic zone. Thrombin levels, stretch, catecholamine, genetic predisposition, etc. are some of these factors. Reentry models described are spiral wave reentry, 3 dimensional rotors, reentry around 'M' cells and figure-of-eight reentry. Continuing efforts to better understand these arrhythmias will help identify patients of myocardial ischemia prone to arrhythmias.

Calcium Channels↗

PubMed1989

Effects of ventricular fibrillation and defibrillation on pacing threshold in the anesthetized dog.

The effects of transthoracic and internal defibrillation on the bipolar ventricular pacing threshold in 20 anesthetized dogs were examined. Ventricular pacing was accomplished with a computer-controlled, constant voltage pacemaker that permitted rapid determination of pacing threshold. Defibrillation at various energy levels was administered during ventricular pacing and after ventricular fibrillation of 5, 15, 30, 45, 60 or 120 s duration in the 20 dogs. Defibrillation during pacing or within 15 s after initiation of ventricular fibrillation did not significantly increase threshold, regardless of defibrillation energy or mode of delivery. Defibrillation after ventricular fibrillation lasting greater than or equal to 30 s increased (p less than 0.05) threshold determined 6 s after defibrillation. The increase in threshold (in volts) determined 6 s after defibrillation was an exponential function of fibrillation duration (30 s = 0.30 +/- 0.09 V; 45 s = 0.53 +/- 0.13 V; 60 s = 2.24 +/- 1.05 V), but was independent of defibrillation energy or mode of delivery. Threshold returned to control values 15 to 30 s after defibrillation. Cardiopulmonary bypass to maintain coronary perfusion prevented the increase in pacing threshold even after ventricular fibrillation of up to 2 min duration. Pacing threshold is not increased by transthoracic or internal defibrillation, but is increased by ventricular fibrillation of sufficient duration to create substantial myocardial hypoxemia.

Anesthesia↗

PubMedDate not supplied

[Ventricular fibrillation after surgical revascularization].

INTRODUCTION: Ventricular fibrillation (VF) presents a complete disintegrated myocardial activity associated with hemodynamic collapse and loss of consciousness requiring urgent reanimation. VF mostly occurs following myocardial infarction and endstage of ischemic heart disease in patients with ejection fraction less than 30%. MATERIAL AND METHODS: This paper analyzes occurrence of VF following coronary artery revascularization in patients undergoing surgery at the Institute of Cardiovascular Diseases in Sremska Kamenica. During the period 1994-1998, 3.186 patients underwent coronary artery revascularization procedure, whereas following it VF occurred in 20 patients (0.63%). RESULTS AND DISCUSSION: In all patients VF presented in the first postoperative week, while in 16 patients it occurred in the first 3 days following surgery. Nine patients with VF underwent left coronary artery revascularization with endarterectomy, 9 patients underwent right coronary artery revascularization with endarterectomy. One patient had a left-ventricular aneurysmectomy and 80% of patients had low ejection fraction rate--20-35%. After VF in 75% of patients urgent reoperation was performed, and only one suffered from thrombotic occlusion, that is perioerative infarction. After defibrillation patients were treated with xylocaine, amiodarone and beta-blockers. During the 30-day period following surgery, there were no lethal outcomes, whereas in the 24-month period after surgery 3 patients died. Cardiac-related death occurred in one patient, while two died due to cerebral insult. CONCLUSION: VF was not a frequent complication in our patients. Effective antiarrhythmic drugs prevent repeated VF. Beta-blockers, xy-locaine and amiodarone are drugs of choice for the treatment of malignant cardiac rhythm disturbances.

Coronary Artery Bypass↗

PubMed1977

The significance of intraoperative ventricular fibrillation during aortic valve replacement.

The effect of the spontaneous occurrence of ventricular fibrillation during aortic valve replacement and coronary arterial perfusion was studied in a consecutive series of 361 such operations. All operations were performed in a standard manner before 1972. One fourth of the patients experienced ventricular fibrillation,and the early mortality rate of this group was significantly (p less than 0.005) higher 7.3 per cent) than in the nonfibrillating group (1.5 per cent). The total mortality rate was 3 per cent. However, late results among survivors of the operations showed no effect of fibrillation. These findings indicate that ventricular fibrillation should be avoided in these patients. Whether or not countershock is advisable if and when fibrillation occurs remains an unanswered question.

Adult↗

PubMed1984

Comparison of programmed electrical stimulation and ambulatory electrocardiographic (Holter) monitoring in the management of ventricular tachycardia and ventricular fibrillation.

Forty-four patients with primary ventricular fibrillation or recurrent ventricular tachycardia were stabilized on an antiarrhythmic drug regimen before electrophysiologic study and 24 to 72 hours of ambulatory electrocardiographic monitoring were performed. The long-term predictive value of these two tests was then compared retrospectively for a 12 to 32 month (mean 18) follow-up period, during which all patients continued receiving the same antiarrhythmic drug regimen. Electrophysiologic testing induced ventricular tachycardia (greater than or equal to 3 beats) in 26 patients; 23 had a poor clinical outcome (positive predictive value 88%), defined as sudden death or sustained ventricular tachycardia. In 18 patients with a negative electrophysiologic test, only 1 had a poor clinical outcome (negative predictive value 94%). Ambulatory electrocardiographic monitoring accurately predicted outcome in 7 of 10 patients with a positive recording (positive predictive value 70%), defined as three or more consecutive ventricular extrasystoles, and in 17 of 34 patients with negative ambulatory monitor recordings (negative predictive value 50%). The long-term predictive accuracy of the electrophysiologic study was significantly higher than that of the ambulatory electrocardiographic monitor (p less than 0.001). Electrophysiologic studies offer advantages over ambulatory electrocardiographic monitoring in this high risk patient group, providing a high degree of accuracy in predicting the long-term clinical response to antiarrhythmic drugs for at least 18 months.

Adult↗

PubMed1976

Toward preventing coronary death from ventricular fibrillation.

Sudden coronary death from ventricular fibrillation is the biggest and possibly the most remediable of the major public health problems at the moment. Most of those liable to sudden death can be identified and it is possible that by the use of beta-adrenergic blocking or other antiarrhythmic drugs, by reducing the consumption of cigarettes and perhaps, by different therapies for hypertension, a substantial proportion of coronary deaths might be prevented or, at least, postponed.

Adult↗

PubMed2002

Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation.

BACKGROUND: Lidocaine has been the initial antiarrhythmic drug treatment recommended for patients with ventricular fibrillation that is resistant to conversion by defibrillator shocks. We performed a randomized trial comparing intravenous lidocaine with intravenous amiodarone as an adjunct to defibrillation in victims of out-of-hospital cardiac arrest. METHODS: Patients were enrolled if they had out-of-hospital ventricular fibrillation resistant to three shocks, intravenous epinephrine, and a further shock; or if they had recurrent ventricular fibrillation after initially successful defibrillation. They were randomly assigned in a double-blind manner to receive intravenous amiodarone plus lidocaine placebo or intravenous lidocaine plus amiodarone placebo. The primary end point was the proportion of patients who survived to be admitted to the hospital. RESULTS: In total, 347 patients (mean [+/-SD] age, 67+/-14 years) were enrolled. The mean interval between the time at which paramedics were dispatched to the scene of the cardiac arrest and the time of their arrival was 7+/-3 minutes, and the mean interval from dispatch to drug administration was 25+/-8 minutes. After treatment with amiodarone, 22.8 percent of 180 patients survived to hospital admission, as compared with 12.0 percent of 167 patients treated with lidocaine (P=0.009; odds ratio, 2.17; 95 percent confidence interval, 1.21 to 3.83). Among patients for whom the time from dispatch to the administration of the drug was equal to or less than the median time (24 minutes), 27.7 percent of those given amiodarone and 15.3 percent of those given lidocaine survived to hospital admission (P=0.05). CONCLUSIONS: As compared with lidocaine, amiodarone leads to substantially higher rates of survival to hospital admission in patients with shock-resistant out-of-hospital ventricular fibrillation.

Aged↗

PubMed1995

Out-of-hospital ventricular fibrillation in children and adolescents: causes and outcomes.

STUDY OBJECTIVE: To compare causes and outcomes of patients younger than 20 years with an initial rhythm of ventricular fibrillation versus asystole and pulseless electrical activity. DESIGN: Retrospective cohort study. SETTING: Urban/suburban prehospital system. PARTICIPANTS: Pulseless, nonbreathing patients less than 20 years who underwent out-of-hospital resuscitation. Patients with lividity or rigor mortis or who were less than 6 months old and died of sudden infant death syndrome were excluded. RESULTS: Ventricular fibrillation was the initial rhythm in 19% (29 of 157) of the cardiac arrests. Rhythm assessment was performed by the first responder in only 44% (69 of 157) of patients. All three rhythm groups were similar in age distribution, frequency of intubation (96%), and vascular access (92%); 93% of ventricular fibrillation patients were defibrillated. The causes of ventricular fibrillation were distributed evenly among medical illnesses, overdoses, drownings, and trauma, only two patients had congenital heart defects. Seventeen percent were discharged with no or mild disability, compared with 2% of asystole/pulseless electrical activity patients (P = .003). CONCLUSION: Ventricular fibrillation is not rare in child and adolescent prehospital cardiac arrest, and these patients have a better outcome than those with asystole or pulseless electrical activity. Earlier recognition and treatment of ventricular fibrillation might improve pediatric cardiac arrest survival rates.

Adolescent↗

PubMed1992

Developmental changes of ventricular fibrillation threshold and spontaneous defibrillation in young dogs.

This study was conducted to systematically investigate whether induction and maintenance of ventricular fibrillation in the canine heart, change with age during the early postnatal development. Forty-eight mongrel puppies from seven litters, were randomly selected for size and studied at weekly intervals from 1-6 weeks for determination of ventricular fibrillation threshold and incidence of spontaneous defibrillation. Another fourteen mongrel puppies 8-11 weeks old and 10 adult dogs were similarly studied. Ventricular fibrillation threshold increased progressively with age up to the eighth week (VFTmA = 8.38 + 2.67 wk-0.134.wk2, r = 0.995) and thereafter reached a plateau, which was not significantly different from the ventricular fibrillation threshold of adult dogs (26.5 +/- 2.2 mA). In contrast, the high incidence of spontaneous defibrillation at early age decreased rapidly between second and fourth week and became rare thereafter, (%SDF = 281.e-0.60wk, r = 0.94. This rapid drop could not be explained by the increase in mean body weight, which did not change significantly during this early period (BWkg = 0.59.e0.23wk, r = 0.97). Our findings suggest first, that the vulnerability of the neonatal dog heart to electrical induction of ventricular fibrillation decreases progressively during early age. Second, that spontaneous defibrillation decreases precipitously between the second and fourth week of age, a change not sufficiently explained by the modest body weight gain during that time. Thus, it appears that about the third week of age ventricular vulnerability to fibrillation and ability to defibrillation reach a critical point, where lethal arrhythmias may become both inducible and sustainable, to result in death.

Aging↗

PubMed1979

The effects of coronary artery disease on the ventricular fibrillation threshold in man.

The ventricular fibrillation threshold (VFT) was measured in 28 patients at the time of cardiac surgery. The VFT was measured with a 100 Hz train of 24 rectangular pulses positioned across the ST segment and T wave. Current was applied to the epicardial surface of either ventricle with a bipolar electrode probe. In six patients, the normal right VFT was 24.3 +/- 5.2 mA, and in 10 patients the normal left VFT was 33.6 +/- mA (p less than 0.05). In 12 patients with greater than or equal to 75% obstruction of the left anterior descending coronary artery, the left VFT was 18.6 +/- 6.9 mA. This value was significantly less than the left VFT in patients without coronary artery disease (p less than 0.001). This study shows that the VFT can be measured in man and that coronary artery disease reduces this parameter.

Adult↗

PubMed1981

Studies on the preventive method of lowered ventricular fibrillation threshold during experimental acute myocardial infarctions. A comparison between disopyramide phosphate and lidocaine.

This study was performed to investigate the prophylactic effect of disopyramide phosphate on ventricular fibrillation in acute myocardial infarction. Lidocaine and disopyramide phosphate were compared in terms of their effects on the lowered ventricular fibrillation threshold in experimental myocardial infarction produced by coronary ligation in dogs. The following results were obtained: 1) The effect of lidocaine i.v. + infusion appeared promptly and the ventricular fibrillation threshold exceeded control levels from 45 min onwards (p less than 0.01). 2) The i.m. injection of lidocaine was effective in a dose of 10 mg/Kg. The minimally effective blood level was 1.7 mcg/ml. 3) Disopyramide phosphate 5 mg/Kg i.v. produced a tendency towards recovery from 15 min onwards. After 30 min, the ventricular fibrillation threshold was significantly higher than control (p less than 0.01). 4) Disopyramide phosphate 5 mg/Kg i.m. was initially effective after 45 min. The effect was significant from 1 hour and 30 min onwards, compared with control (p less than 0.01). The minimally effective blood level was 2.4 mcg/ml. 5) Disopyramide phosphate 2 mg/Kg i.m. produced a tendency towards recovery but the difference from the control was not significant. 6) In equivalent i.m. doses, disopyramide phosphate tended to be more potent than lidocaine in increasing the ventricular fibrillation threshold. 7) In the aforementioned doses, disopyramide phosphate did not cause any marked changes in PQ interval or QT time in ECG. These results suggest that the intramuscular injection of disopyramide phosphate is a hopeful clinical treatment to prevent ventricular fibrillation in the very early stages of acute myocardial infarction.

Animals↗

PubMed2005

Successful management of air embolism-induced ventricular fibrillation in orthotopic liver transplantation.

Ventricular fibrillation (VF) although less common during noncardiac surgery often brings about severe complication as an aftermath. We report a case of VF which was highly suspected to be induced by air embolism at the moment when the surgeon was dissecting the collateral vessels of portal vein in liver transplantation surgery. The outcome of this patient was excellent due to aggressive resuscitative measures including open-chest cardiac massage. Transesophageal echocardiogram (TEE) was not applied in this patient in fear of increased risk of esophageal varicose bleeding in a liver cirrhotic patient. However, some reports described the use of TEE in cirrhotic patients without obvious complications. In this case, venous air embolism (VAE) happened during the dissection of collateral vessels of the portal vein, which to our knowledge was ever been reported in liver transplantation surgery. The related literature has been reviewed and the success of the resuscitation is also herein discussed.

Echocardiography, Transesophageal↗

PubMed1998

Regional expansion during myocardial ischemia predicts ventricular fibrillation and coronary reocclusion.

Primary ventricular fibrillation (VF) complicating acute myocardial infarction is associated with occluded infarction-related arteries. The relationship between VF during ischemia and spontaneous coronary reocclusion was analyzed in 48 anesthetized pigs submitted to 48 min of coronary ligation and 6 h of reflow. Reocclusion was associated with ischemic VF (6 of 11 animals with VF but only 6 of 37 without it had reocclusion) but not with reperfusion arrhythmias, the size of the ischemic area, the magnitude of electrocardiogram changes or contractile dysfunction during ischemia, or the severity of intimal injury at the occlusion site. The increase in end-diastolic length in the ischemic region during coronary occlusion was associated with ischemic VF (15 min after occlusion, end-diastolic length was 116 +/- 2 and 111 +/- 1% of baseline in animals with or without presenting subsequent VF, respectively) and was retained by multiple logistic regression analysis as the only independent predictor of ischemic VF and reocclusion. Thus ischemic VF is strongly associated with an increased rate of spontaneous coronary reocclusion during subsequent reperfusion. Acute expansion of ischemic myocardium appears as a prominent determinant of both ischemic VF and reocclusion.

Animals↗

PubMed1997

Association between hemodynamic parameters and the degeneration of sustained ventricular tachycardias into ventricular fibrillation in rats.

UNLABELLED: Sustained ventricular tachycardias (VT) often degenerate into ventricular fibrillation (VF). In the present study, the impact of VT on mean arterial blood pressure (MAP), myocardial blood flow (MBF), and myocardial oxygen consumption (MVCO2) was assessed. In addition, the degeneration of sustained VT into VF was analysed with respect to MAP. MBF was measured in 48 anesthetized rats with colored microspheres; arterial catecholamine levels were measured by HPLC in 16 additional rats during control conditions and VT. MBF (4. 66+/-1.29 ml/g/min; mean+/-s.d.) did not change with the onset of VT (5.37+/-1.92 ml/g/min, n.s.). Epinephrine (0.22+/-0.13 ng/ml) and norepinephrine (0.37+/-0.12 ng/ml) increased during VT (3.55+/-2.68 ng/ml, P<0.01; 0.88+/-0.44 ng/ml, P<0.05), respectively. VF was more frequent when MAP remained normal (MAP>80 mmHg: 26%) than with hypotension (MAP<80 mmHg: 2%, P<0.05). Mechanical failure was observed in 10% of rats with severe hypotension (MAP<60 mmHg), and 2% with moderate hypotension (MAP 60-80 mmHg). The endo-epicardial MBF ratio in the VF group was significantly lower than that in the non-VF group (0.94+/-0.17 v 1.11+/-0.24, P<0.05). CONCLUSIONS: severe hypotension predisposes to the occurrence of acute mechanical failure during VT; moderate hypotension during VT, however, serves as a protective mechanism against VF in structurally normal hearts. Subendocardial hypoperfusion in the presence of an increased energy demand during VT is suggested to be responsible for the initiation of VF.

Animals↗

PubMed1988

Initiation of ventricular fibrillation by supraventricular beats in patients with acute myocardial infarction.

The role of supraventricular extrasystoles in the initiation of ventricular arrhythmia was studied in 72 consecutive patients who developed primary ventricular fibrillation during the acute phase of myocardial infarction. In six patients (8%), a total of 12 episodes of ventricular fibrillation and 16 episodes of ventricular tachycardia were initiated by supraventricular extrasystoles. Ventricular fibrillation and tachycardia were initiated by single supraventricular extrasystoles in 16 and by salvos greater than or equal to two beats in 12 episodes. The RR coupling interval of the supraventricular impulse immediately preceding ventricular tachycardia ranged from 240 to 420 ms (mean 356 (62)) and was characteristic of R-on-T (prematurity index less than 1) in 63% of episodes. Average peak serum creatine kinase activity in the six patients in whom ventricular tachycardia was initiated by a supraventricular extrasystole was 1275 units compared with 720 units in the remaining 66 patients. Five of these six patients later showed evidence of pump failure. Lignocaine or procainamide or both suppressed the ventricular arrhythmia in five of the six patients. The initiation of ventricular fibrillation or tachycardia by supraventricular extrasystoles in acute myocardial infarction is not uncommon and may reflect the increased vulnerability of the heart after a large infarct. These arrhythmias may respond to drugs that suppress ventricular irritability.

Cardiac Complexes, Premature↗