Ventricular fibrillation case studies

The incidence of major adverse reactions to dipyridamole was determined in a multicenter retrospective study, involving 73 806 patients who underwent intravenous dipjridamole stress imaging in 59 hospitals and 19 countries (4). The main conclusion was that the risk of serious dipjridamole-induced adverse effects is very low, a conclusion that is in line with other reports (5), and comparable to that reported for exercise testing in a similar patient population. Combined major adverse events among the entire patient population included 7 cardiac deaths (0.95 per 10000), 13 non-fatal myocardial infarctions (1.76 per 10000), 6 non-fatal sustained ventricular dysrhythmias (0.81 per 10000) (ventricular tachycardia in 2 and ventricular fibrillation in 4), 9 transient cerebral ischemic attacks (1.22 per 10000), 1 stroke, and 9 severe cases of bronch-ospasm (1.22 per 10000). Minor non-cardiac adverse effects were less frequent among the elderly and more frequent in women and patients taking maintenance aspirin. 

Truppmann and Ellenby routinely used cardiac monitoring when doing phenol peels, and detected many arrhythmias. In 1979, they published the results of a study on 48 patients treated with phenol peels. Saponified and non-saponified Baker or Litton formulas were studied. They report that 23% of patients treated with phenol showed arrhythmia, on average 17.5 minutes after the phenol was first applied. These arrhythmias were often premature ventricular (Figure 28.3) or supraventricular contractions, bigeminy, or supraventricular (Figure 28.2) or ventricular tachycardias (Figure 28.7). Tachycardia, which in extreme cases can sometimes reach 220—230 beats per minute, can turn into ventricular fibrillation and lead to cardiac arrest. 

Dekker LR, Bezzina CR, Henriques JP, et al. Familial sudden death is an important risk factor for primary ventricular fibrillation a case-control study in acute myocardial infarction patients. Circulation 2006 114(11) 1140—5. 

Underdetection Ventricular tachycardia will not be detected in some cases, even in the presence of adequate sensing. One troublesome cause of underdetection is slow ventricular tachycardia with rates that are lower than the programmed tachycardia detection rate. Patients who receive concomitant antiarrhythmic drugs may be predisposed to this problem owing to slowing of ventricular tachycardia. In one study, 8% of patients who received ICDs developed ventricular tachycardia with rates that had significant overlap with spontaneous sinus rates (89). Similarly, irregularity of the tachycardia, which causes sensed rates to straddle two zones (between sinus rhythm and ventricular tachycardia or between ventricular tachycardia and ventricular fibrillation). 

The adverse effects of propafenone in placebo-con-trolled trials in patients with atrial tachydysrhythmias have been reviewed (16). The following effects were reported after single intravenous oral doses to produce conversion of atrial fibrillation to sinus rhythm. Non-cardiac adverse effects included mild dizziness. Mild hypotension was also noted, but only required withdrawal of propafenone in one of 29 patients in one study. There have been prodysrhythmic effects in several studies, including atrial flutter with a broad QRS complex, which can occur in up to 5% of cases in some cases atrial flutter can have a rapid ventricular response due to 1 1 atrioventricular conduction, which has been attributed to slowing of atrial conduction and reduced refractoriness of the atrioventricular node. Other prodysrhythmic effects in a few patients included sinus bradycardia with sinus pauses and effects on atrioventricular conduction. 

The use of propafenone in atrial fibrillation (SEDA-23, 202) has been studied in a randomized, double-bhnd, placebo-controUed trial in 55 patients (17). The dose of propafenone was chosen according to body weight 450, 600, and 750 mg for those weighing 50-64, 65-80, and over 80 kg respectively. Propafenone converted atrial fibrillation to sinus rhythm significantly more quickly than placebo, and most patients given propafenone had converted by 6 hours. However, by 24 hours there was no significant difference between the two groups. Four patients had hypotension after propafenone, in three cases transiently. The patient with sustained hypotension had poor left ventricular systolic function, but it responded promptly to the administration of fluids and electrical cardioversion. In one patient with transient hypotension there was a brief episode of sinus bradycardia and in another an isolated sinus pause. 

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