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PubMed2003

Strategies for reversing shock-resistant ventricular fibrillation.

PURPOSE OF REVIEW: Shock-resistant ventricular fibrillation is defined as ventricular fibrillation persisting after three defibrillation attempts. In approximately 10 to 25% of all cardiac arrests, shock-resistant ventricular fibrillation develops, and 87 to 98% of these patients die. RECENT FINDINGS: In the treatment of shock-resistant ventricular fibrillation, defibrillation using biphasic waveforms is considered as an intervention of choice. Intravenous amiodarone is also acceptable, safe, and useful, based on evidence from two randomized clinical trials. Intravenous vasopressin is acceptable and probably safe and useful, but the evidence supporting this recommendation is coming from a small, randomized clinical trial. Procainamide is acceptable but not recommended. In the presence of acute myocardial infarction and recurrent ventricular fibrillation, if all other therapies fail, beta-blockers can be considered. Magnesium, lidocaine, and bretylium are not recommended in the treatment of shock-resistant ventricular fibrillation. SUMMARY: Biphasic defibrillation and intravenous amiodarone are useful in shock-resistant ventricular fibrillation.

Adrenergic beta-Antagonists↗
PubMed2005

Waveform analysis of ventricular fibrillation to predict defibrillation.

PURPOSE OF REVIEW: Ventricular fibrillation occurs during many cases of cardiac arrest and is treated with rescue shocks. Coarse ventricular fibrillation occurs earlier after the onset of cardiac arrest and is more likely to be converted to an organized rhythm with pulses by rescue shocks. Less organized or fine ventricular fibrillation occurs later, has less power concentrated within narrow frequency bands and lower amplitude, and is less likely to be converted to an organized rhythm by rescue shocks. Quantitative analysis of the ventricular fibrillation waveform may distinguish coarse ventricular fibrillation from fine ventricular fibrillation, allowing more appropriate delivery of rescue shocks. RECENT FINDINGS: A variety of studies in animals and humans indicate that there is underlying structure within the ventricular fibrillation waveform. Highly organized or coarse ventricular fibrillation is characterized by large power contributions from a few component frequencies and higher amplitude. Amplitude, decomposition into power spectra, or probability-based, nonlinear measures all can quantify the organization of human ventricular fibrillation waveforms. Clinical data have accumulated that these quantitative measures, or combinations of these measures, can predict the likelihood of rescue shock success, restoration of circulation, and survival to hospital discharge. SUMMARY: Many quantitative ventricular fibrillation measures could be implemented in current generations of monitors/defibrillators to assist the timing of rescue shocks during clinical care. Emerging data suggest that a period of chest compressions or reperfusion can increase the likelihood of successful defibrillation. Therefore, waveform-based prediction of defibrillation success could reduce the delivery of failed rescue shocks.

Decision Making↗
PubMed1986

Inducible sustained ventricular tachycardia and ventricular fibrillation in conscious dogs with isolated right ventricular infarction: relation to infarct structure.

The susceptibility of infarcted right ventricular myocardium to inducible ventricular tachyarrhythmias was serially evaluated in 18 conscious dogs during the first 2 weeks after permanent right coronary artery occlusion. Properly timed double premature stimuli applied to the right ventricular outflow tract induced sustained (longer than 1 minute) ventricular tachycardia at rates of 190 to 400 beats/min in nine dogs, and ventricular fibrillation in six dogs. No ventricular arrhythmias could be induced in the remaining three dogs. The zone of premature coupling intervals within which ventricular tachyarrhythmias could be induced decreased in each dog as the infarct aged, and by day 12 after occlusion, no ventricular arrhythmias could be induced in any of the dogs studied. Both the size and the degree of patchiness (graded from 0 for no patchiness to +4 for patchiness throughout the infarct) of the infarct appear to be related to the nature of the induced rhythm. Infarcts with greater heterogeneity and those that were larger than 8% of the right ventricular volume were associated with a higher incidence of ventricular fibrillation, and infarcts with a lesser degree of patchiness were more suitable for sustained ventricular tachycardia (3.4 +/- 1.2 versus 1.4 +/- 0.4, p less than 0.05). These findings indicate that the infarcted right ventricular myocardium, independent of left ventricular involvement, can be associated with malignant ventricular tachyarrhythmias, ventricular tachyarrhythmias can be induced only during a well defined postinfarction period; and both the size and geometry of the right ventricular infarct determine the nature of the induced ventricular rhythm.

Animals↗
PubMed1988

Long-term arrhythmic outcome in survivors of ventricular fibrillation with absence of inducible ventricular tachycardia.

While programmed electrical stimulation of the heart is useful in directing therapy in cardiac arrest survivors who exhibit inducible ventricular tachycardia (VT), controversy exists as to the risk of recurrent ventricular fibrillation (VF) and need for antiarrhythmic therapy in patients without inducible VT during drug-free control programmed stimulation studies. In this study, the clinical features and arrhythmic outcome of 43 survivors of VF without inducible VT at control programmed stimulation were examined. In 38 patients, factors that may have played a potentiating role in the genesis of VF included ischemia in 15, proarrhythmia in 18, rapid rate response to atrial fibrillation in 3 and acute alcoholism in 2. Three patients required antiarrhythmic drugs for supraventricular tachyarrhythmia and 40 patients were discharged without antiarrhythmic therapy. At 32 +/- 21 months (range 1 to 82), 37 (92%) have remained free of arrhythmic recurrence while 3 have had sustained subsequent major arrhythmic events (syncope 1 patient, VF 1, sudden cardiac death 1). Thus, survivors of VF without inducible VT at drug-free control programmed stimulation are characterized by (1) potentiating factors--often identifiable and correctable--that may be important to the genesis of VF; (2) generally low risk of arrhythmic recurrence; and (3) effective long-term management often achieved without the use of additional antiarrhythmic drugs or antitachycardia/defibrillation devices.

Adult↗
PubMed1990

Determinants of prognosis in symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction. The Dutch Ventricular Tachycardia Study Group of the Interuniversity Cardiology Institute of The Netherlands.

In a multicenter study, 390 patients with sustained symptomatic ventricular tachycardia or ventricular fibrillation late after acute myocardial infarction were prospectively followed up to assess determinants of mortality and recurrence of arrhythmic events. Patients were given standard antiarrhythmic treatment, which consisted primarily of drug therapy. During a mean follow-up period of 1.9 years, 133 patients (34%) died; arrhythmic events and heart failure were the most common cause of death (41 patients [11%] died suddenly, 31 [8%] died because of recurrent ventricular tachycardia or ventricular fibrillation and 23 [6%] died of heart failure). One hundred ninety-two patients (49%) had at least one recurrent arrhythmic event; 85% of first recurrent arrhythmic events were nonfatal. Multivariate analysis of data from patients who developed the arrhythmia less than 6 weeks after infarction identified five variables as independent determinants of total mortality: 1) age greater than 70 years (risk ratio 4.5); 2) Killip class III or IV in the subacute phase of infarction (risk ratio 3.5); 3) cardiac arrest during the index arrhythmia (risk ratio 1.7); 4) anterior infarction (risk ratio 2.2); and 5) multiple previous infarctions (risk ratio 1.6). Multivariate analysis of data from patients developing the arrhythmia greater than 6 weeks after infarction identified four variables as independently predictive of total mortality: 1) Q wave infarction (risk ratio 2.1); 2) cardiac arrest during the index arrhythmia (risk ratio 1.7); 3) Killip class III or IV in the subacute phase of infarction (risk ratio 1.7); and 4) multiple previous infarctions (risk ratio 1.4). The results of the two multivariate analyses were used in a model for prediction of mortality at 1 year. The average predicted mortality rate varied considerably according to the model: for 243 patients (62%) with the lowest risk, it was 13%, corresponding to an observed mortality rate of 12%; for 92 patients (24%) with intermediate risk, it was 27%, corresponding to an observed rate of 28%; for 55 patients (14%) with the highest risk, it was 64%, corresponding to an observed rate of 54%. This study shows that patients with symptomatic ventricular tachycardia or ventricular fibrillation late after myocardial infarction who are given standard antiarrhythmic treatment have a high mortality rate. The predictive model presented identifies patients at low, intermediate and high risk of death and can be of help in designing the appropriate diagnostic and therapeutic strategy for the individual patient.

Aged↗
PubMed1998

Low prevalence of coronary artery spasm in patients with normal coronary angiograms and unexplained ventricular fibrillation.

AIMS: The aetiology of ventricular fibrillation in patients without identifiable structural heart disease is unknown. Recently, high prevalence of silent ischaemia due to coronary artery spasm has been reported in such patients. However, in at least one report, all patients had non-critical coronary artery lesions. Identification of coronary artery spasm as the underlying aetiology of ventricular fibrillation has important therapeutic implications. METHODS AND RESULTS: We performed ergonovine provocation tests in 18 patients (14 males, and four females; mean age, 36 years) with documented ventricular fibrillation in the absence of identifiable structural heart disease who had undergone aborted sudden death. In group I (n = 7) ergonovine provocation tests were performed at a mean interval of 31 months (range 21-42 months) after the index episode. These patients had already received an implantable cardioverter defibrillator, after failed electrophysiologically guided antiarrhythmic therapy. In group II (n = 11) the ergonovine provocation test was performed prospectively as part of the diagnostic evaluation. All patients were off antiarrhythmic drugs, calcium entry or beta-adrenoceptor blockers at the time of the ergonovine provocation test. Ergonovine was administered intravenously as a bolus injection, beginning with 0.05 mg followed every 3 min by incremental doses up to a cumulative maximum dose of 0.45 mg. Predefined end-points were (1) recording of ischaemic ST segment shifts of > or = 1 mm in at least two corresponding leads of the 12-lead electrocardiogram; (2) induction of ventricular tachycardia or ventricular fibrillation; and (3) administration of a cumulative dose of 0.45 mg. A positive response to ergonovine was seen in only one patient (5%) in group I in whom there developed ST segment elevation without angina and a short burst of rapid ventricular tachycardia. CONCLUSIONS: This study found a low prevalence of coronary artery spasm in patients with aborted sudden death resulting from documented ventricular fibrillation and non-apparent underlying heart disease. All patients had normal coronary angiograms and a negative history for spontaneous episodes of chest pain. The mechanism of arrhythmogenesis in such patients remains largely unknown.

Adult↗
PubMed1976

[Ventricular fibrillation and asystole precursors in myocardial infarct].

Ventricular fibrillation and asystole are a frequent cause of death in myocardial infarction. The data of continuous monitoring the heart in 134 patients with acute myocardial infarction and ventricular fibrillation and asystole. The immediate precursors of ventricular fibrillation were predominantly ventricular extrasystoles. A frequent precursor of ventricular fibrillation consists in paroxysmal ventricular tachycardia. In some patients the ventricular fibrillation was preceded by the block of the bundle of His, non-paroxysmal ventricular tathycardia, escaping contractions and some other arrhythmias. A factor providing for the development of ventricular fibrillation consists in the Q-T interval lengthening on ECG. Ventricular asystole is usually preceeded by atrioventricular block, Stage II-III, and the block of the bundle of His, as well as by ventricular tachycardia and extrasystole, in some cases--by sinus bradycardia and sinoauricular block (weakness of the sinus node). The examination of the rhythm and conductivity disorders preceeding the ventricular fibrillation is of great importance in view of the possibilities of prevention of "arrhythmic death".

Acute Disease↗
PubMed1986

Survival to leave hospital from ventricular fibrillation.

In 125 consecutive patients with 173 arrests due to ventricular fibrillation, 53 survived to leave hospital. At the initial arrest and using univariate analysis, those who had primary ventricular fibrillation, had ventricular fibrillation less than 24 hours from the onset of symptoms, received the first DC shock less than 1 minute after the onset of ventricular fibrillation, who required less than 4 shocks to terminate the ventricular fibrillation, whose first established rhythm within the first minute of correction of ventricular fibrillation was atrial fibrillation, sinus rhythm or paced rhythm, or who were not receiving prior antiarrhythmic agents had a significantly improved survival to leave hospital (p less than 0.05). To predict survival to leave hospital using discriminant function analysis, the most significant factors ranking in order of importance at the time of the initial arrest were: less than or equal to 5 shocks to correct ventricular fibrillation, no prior antiarrhythmic therapy, primary ventricular fibrillation, and time from onset of ventricular fibrillation to first shock less than 1 minute. For the last arrest, the most significant factors were: no prior cardiac arrest, less than or equal to 5 shocks to correct ventricular fibrillation, no prior antiarrhythmic therapy, and primary ventricular fibrillation. The most significant factors measured at the time of the last arrest provided a better prediction of survival to leave hospital (sensitivity 77%, specificity 75%) than did similarly defined factors for the initial arrest (sensitivity 59%, specificity 89%).

Adolescent↗
PubMed1991

Emergency intracardiac defibrillation for refractory ventricular fibrillation during routine electrophysiologic study.

Ventricular fibrillation refractory to cardiopulmonary resuscitation including multiple transthoracic defibrillations occurred in four patients during 1,215 consecutive ventricular tachycardia induction studies. A technique of emergency intracardiac defibrillation for management of refractory ventricular fibrillation is described. In four patients, stable monomorphic ventricular tachycardia (320 to 570 ms cycle length) was induced during the study and overdrive ventricular pacing resulted in ventricular fibrillation. These patients did not respond to prompt transthoracic defibrillations (5 to 15 attempts/patient) and cardiopulmonary resuscitation, including antiarrhythmic therapy. As a last resort, intracardiac defibrillation was performed with use of a previously inserted standard right ventricular quadripolar catheter as cathode and a posterior skin patch as anode. High energy intracardiac defibrillation pulses (100 to 500 J) delivered from a standard defibrillator successfully terminated each arrhythmia. Intracardiac defibrillation is technically simple and appears effective in terminating refractory ventricular fibrillation in the electrophysiology laboratory. However, further research is necessary to determine the safety and efficacy of this technique, as well as potential applications in other emergency settings.

Aged↗
PubMed2001

Diagnosis and long-term follow-up of the Brugada syndrome in patients with idiopathic ventricular fibrillation.

AIMS: Some patients with idiopathic ventricular fibrillation may suffer from the Brugada syndrome. The diagnostic criteria for the Brugada syndrome are uncertain and arbitrarily set. Therefore, we studied the prevalence of the Brugada syndrome using various diagnostic criteria and long-term follow-up in 37 idiopathic ventricular fibrillation patients. METHODS AND RESULTS: Idiopathic ventricular fibrillation was diagnosed after thorough clinical evaluation in 37 survivors of an out-of-hospital cardiac arrest referred to our institute (UMC Utrecht). Retrospectively, nine patients (24%, group I) were classified as potentially having the Brugada syndrome based on the presence of (in)complete right bundle branch block and ST-segment elevation in leads V(1)-V(3)of > or =1 mm. Only three patients (8%, group II) showed (in)complete right bundle branch block and > or =2 mm ST-segment elevation. With the intermittent presence of these ECG features and/or their (re)appearance with class I antiarrhythmic drugs included as criteria, the percentage of the Brugada syndrome was attenuated in group I (2/37; 5%) and group II (1/37; 3%). Sixteen (43%) of all idiopathic ventricular fibrillation patients (mean follow-up 77+/-41 months) had a recurrent episode of syncope, ventricular tachyarrhythmias or sudden death. Recurrence rate was 3/9 (33%) in Brugada patients group I, 2/3 (66%) in group II and 13/28 (46%) in patients without the Brugada syndrome (P=ns). CONCLUSIONS: Depending on the diagnostic criteria used, the Brugada syndrome was observed in 3% to 24% of patients with idiopathic ventricular fibrillation, underlining the importance of defining the precise diagnostic criteria in these patients. For all idiopathic ventricular fibrillation patients, the ventricular tachyarrhythmia recurrence rate was substantial during an average follow-up of more than 6 years.

Adolescent↗
PubMed1990

Correlation between the ventricular electrogram amplitude in sinus rhythm and in ventricular fibrillation.

During testing of implantable defibrillators, ability to sense ventricular fibrillation is assessed by observing electrograms and the emitted ECG interpretation channel during induced ventricular fibrillation. We hypothesized that ventricular electrogram amplitude in sinus rhythm could be used to predict the ventricular electrogram amplitude in ventricular fibrillation and serve as a first approximation of the "safety margin" for sensing ventricular fibrillation. We compared the peak-to-peak epicardial ventricular electrogram during sinus rhythm and ventricular fibrillation in 12 patients undergoing defibrillator implantation. The ventricular electrogram was recorded with an integrated bipolar lead and filtered at 10-50 Hz. Ventricular fibrillation was induced by alternating current and the ventricular electrogram measured from cessation of alternating current to the first countershock. The mean ventricular electrogram amplitude in sinus rhythm was 15.3 +/- 5.4 mV (range 7.1-25.5) and in 37 episodes of ventricular fibrillation was 8.3 +/- 3.6 mV (range 2.1-16.3). There was a significant relationship between the mean ventricular electrogram amplitude in sinus rhythm and in ventricular fibrillation (R = 0.7, P less than 0.001). There was wide variation among individuals in the decrease in the mean ventricular electrogram amplitude during ventricular fibrillation, with the ratio of mean ventricular electrogram in sinus rhythm to mean ventricular electrogram in ventricular fibrillation ranging from 0.29 to 1.05 (mean 0.55 +/- 0.20). This suggests that up to a fourfold decrease may be expected in the mean ventricular electrogram amplitude during ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗
PubMed2000

Laplacian electrograms and the interpretation of complex ventricular activation patterns during ventricular fibrillation.

INTRODUCTION: During ventricular fibrillation (VF), interpretation of a local electrogram and determination of the local activation moment are hampered by remote activity or intervening repolarization waves. Successful defibrillation depends on critical timing of the shock relative to local activation. We tested the applicability of Laplacian electrograms for detection of the moment of local activation during VF. METHODS AND RESULTS: From isolated perfused porcine intact hearts, 247 local unipolar electrograms were recorded simultaneously (13 x 19 matrix, interelectrode distance 0.3 mm) from the left ventricular wall during sinus rhythm, following pacing or during VF. Activation maps were constructed based on local unipolar electrograms, and Laplacian electrograms were calculated from local electrograms and its eight neighbors. The Laplacian electrogram displayed a sharp R/S complex with local activation indicated by the moment of zero crossing without interference from remote activity or repolarization waves. Its amplitude increased with decreasing interelectrode distance. Following epicardial stimulation, Laplacian amplitude was significantly larger than during a breakthrough pattern. During VF, identical unipolar electrograms corresponded to Laplacian complexes with different morphology. Collision of wavefronts was associated with entirely positive Laplacian waveforms; "focal" appearance of activity was associated with an entirely negative waveform. Activation block in the activation maps was correlated with the appearance of sustained episodes of negativity or positivity in the Laplacian electrogram (depending on the location of the recording site relative to the line of block). CONCLUSION: Laplacian electrograms allow detection of the moment of local activation without interference from remote activity or repolarization, especially during complex arrhythmias. The technique applied to automatic sensing devices, such as the internal defibrillator, may optimize defibrillation success.

Action Potentials↗
PubMed2006

Impact of sympathetic innervation on recurrent life-threatening arrhythmias in the follow-up of patients with idiopathic ventricular fibrillation.

PURPOSE: Idiopathic ventricular fibrillation (IVF) is defined as VF in the absence of any identifiable structural or functional cardiac disease. The underlying pathophysiological mechanisms are unknown. This study was performed to investigate the potential impact of sympathetic dysfunction, assessed by (123)I-meta-iodo-benzylguanidine scintigraphy ((123)I-MIBG SPECT), on the long-term prognosis of patients with IVF. METHODS: (123)I-MIBG SPECT was performed in 20 patients (mean age 37+/-13 years) with IVF. Mean follow-up of patients after study entry was 7.2+/-1.5 years (range 4.9-10.5 years). Ten patients (five men, five women; mean age 43+/-12 years; p=NS versus study group) with medullary carcinoma of the thyroid gland served as an age-matched control group. RESULTS: Abnormal (123)I-MIBG uptake was observed in 13 patients (65%). During follow-up, 18 episodes of VF/fast polymorphic ventricular tachycardias occurred in four IVF patients with abnormal (123)I-MIBG uptake whereas only two episodes of monomorphic ventricular tachycardia (and no VF) occurred in a single IVF patient with normal (123)I-MIBG uptake. CONCLUSION: Impairment of sympathetic innervation may indicate a higher risk of future recurrent episodes of life-threatening ventricular tachyarrhythmias in patients with IVF. Studies in larger cohorts are required to validate the significance of (123)I-MIBG SPECT during the long-term follow-up of these patients.

3-Iodobenzylguanidine↗
PubMed1994

Systolic arterial pressure recovery after ventricular fibrillation in pigs.

Ventricular fibrillation (VF) is induced during implantable cardioverter defibrillator insertion and can result in cardiovascular collapse. The relation between repeated VF trials of varying duration and systolic blood pressure (SBP) recovery rate was studied in 6 pigs. Two implantable cardioverter defibrillator patches were placed on the heart, and VF was varied in a cyclic pattern until cardiovascular collapse occurred. A negative logarithmic relation between SBP recovery rate and duration of VF was found in 4 of the pigs with correlation coefficients of 0.62 to 0.97 (p < 0.05). The overall correlation coefficient was 0.51 for all 116 data points (p < 0.001). Although there was a significant (p < 0.05) decrease in average (+/- standard error of the mean) baseline SBP in the second half of each experiment (83 +/- 5 mm Hg versus 77 +/- 6 mm Hg), no significant difference in SBP was observed during VF (17 +/- 1 mm Hg versus 16 +/- 1 mm Hg) or after 15 seconds of SBP recovery (51 +/- 4 mm Hg versus 46 +/- 3 mm Hg) between the two halves of the experiments. Cardiovascular collapse occurred without warning; epinephrine was effective in reversing it. In conclusion, SBP recovery rate and duration of VF have a negative logarithmic relation consistent with a negative effect on left ventricular contractility with prolongation of VF. The onset of cardiovascular collapse during implantable cardioverter defibrillator testing cannot be predicted on the basis of monitored blood pressure alone.

Animals↗
PubMed2000

Scaling structure of electrocardiographic waveform during prolonged ventricular fibrillation in swine.

Ventricular fibrillation (VF) is the most common arrhythmia causing sudden cardiac death. However, the likelihood of successful defibrillation declines with increasing duration of VF. Because the morphology of the electrocardiogram (ECG) waveform during VF also changes with time, this study examined a new measure that describes the VF waveform and distinguishes between early and late VF. Surface ECG recordings were digitized at 200 samples/s from nine swine with induced VF. A new measure called the scaling exponent was calculated by examining the power-law relationship between the summation of amplitudes of a 1,024-point (5.12 second) waveform segment and the time scale of measurement. The scaling exponent is a local estimate of the fractal dimension of the ECG waveform. A consistent power-law relationship was observed for measurement time scales of 0.005-0.040 seconds. Calculation of the scaling exponent produced similar results between subjects, and distinguished early VF (< 4-minute duration) from late VF (> or = 4-minute duration). The scaling exponent was dependent on the order of the data, supporting the hypothesis that the surface ECG during VF is a deterministic rather than a random signal. The waveform of VF results from the interaction of multiple fronts of depolarization within the heart, and may be described using the tools of nonlinear dynamics. As a quantitative descriptor of waveform structure, the scaling exponent characterizes the time dependent organization of VF.

Animals↗
PubMed2004

Estimated global transmural distribution of activation rate and conduction block during porcine and canine ventricular fibrillation.

We quantified ventricular fibrillation (VF) activation rate, conduction block, and organization transmurally in pigs and dogs, whose transmural Purkinje distribution differ. In six pigs and five dogs, 75 to 100 plunge needles, containing four electrodes for the right ventricle (RV) and six electrodes for the left ventricle (LV) and septum, were inserted in vivo. Six VF episodes were electrically initiated and allowed to last for 47 to 180 seconds. From the FFT power spectra, dominant frequency (DF), an estimate of activation rate, and incidence of double peaks (DPI), an estimate of conduction block, were calculated every 8 ms at each electrode. DF was highest at the epicardium and lowest at the endocardium, whereas DPI was highest at the endocardium and lowest at the epicardium for the entire LV and the RV base in both pigs and dogs for the first 70 seconds of VF. This distribution changed little throughout the first 3 minutes of VF in pigs but reversed in dogs by 2 minutes of VF. In conclusion, estimated activation rates and conduction block incidence during VF are not uniformly distributed transmurally. During the first minute of VF, the faster activating LV base epicardium exhibits less estimated block than the slower endocardium, raising the possibility that faster activating epicardium generates wavefronts that drive the endocardium early during VF. Constancy of this pattern in pigs but its reversal by 2 minutes in dogs is consistent with the hypothesis that activation during later VF is driven by Purkinje fibers.

Animals↗
PubMed1985

Fatal ventricular fibrillation following verapamil in Wolff-Parkinson-White syndrome with atrial fibrillation.

A 29-year-old man with Wolff-Parkinson-White syndrome and atrial fibrillation developed fatal ventricular fibrillation shortly after receiving intravenous verapamil. The patient presented with an irregular pulse of 190. A total of 23 mg of verapamil was administered in small intravenous doses over 35 minutes. The ventricular rate accelerated as verapamil was administered, and fatal ventricular fibrillation followed. Three theoretical mechanisms by which verapamil may enhance conduction of atrial fibrillation in Wolff-Parkinson-White syndrome, predisposing to ventricular fibrillation, are mentioned.

Adult↗