Amiodarone defibrillator

Ventricular fibrillation should be terminated by electrical defibrillation. Alternatively, lidocaine can be injected intravenously. In cases with lower frequency, ventricular tachyarrhythmia class I diugs such as aj marine, flecainide or propafenone are more effective as a result of the use-dependence of lidocaine. For prophylaxis treatment, amiodarone or sotalol may be helpful or the implantation of a cardioverter-defibrillator system. Acute amiodarone (i.v. in higher doses) can also terminate ventricular tachyarrhythmias. This action, however, seems to be mediated by its INa-blocking side effects and not (or less) by its class III like effects. 

Larsen GC, Manolis AS, Sonnenberg FA, et al. Cost-effectiveness of the implantable cardioverter-defibrillator effect of improved battery life and comparison with amiodarone therapy. J Am Coll Cardiol 1992 19 1323-34. 

The purpose of antiarrhythmic drug therapy after unsuccessful defibrillation and vasopressor administration is to prevent the development or recurrence of VF and PVT by raising the fibrillation threshold. However, the role of antiarrhythmics is limited because clinical evidence demonstrating improved survival to hospital discharge is lacking. Only amiodarone and lidocaine are recommended in the 2005 guidelines for CPR and ECC. 

The Canadian Implantable Defibrillator Study studied ICD therapy versus amiodarone while CASH studied ICD therapy versus a variety of antiarrhythmic medications in patients with resuscitated SCD. Both trials found nonsignificant reductions in mortality with ICD implantation. CIDS showed a relative risk (RR) reduction of 19.7% [p = 0.14] and CASH showed a RR reduction of 23% in mortality [p = 0.08]. 

Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. NEnglJMed. Jan 20 2005 352(3) 225-237. 

Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS) a randomized trial of the implantable cardioverter defibrillator against amiodarone. Circulation. Mar 21 2000 101(11) 1297-1302. 

The cornerstone of therapy for ventricular fibrillation is electrical deflbrillation. In the acute setting, defibrination is first-line therapy. Intravenous bretylium can occasionally contribute to conversion, but this is infrequent. In the management of out-of-hospital cardiac arrest, high-dose epinephrine (5 mg intravenously) improves the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation, when compared with the standard dose of 1 mg. Vasopressin (40 U intravenously) may more effective than 1 mg intravenous epinephrine in out-of-hospital patients with ventricular fibrillation that is resistant to electrical defibrillation. The OPTIC smdy (see Connolly et al., 2006) showed that amiodarone plus jS-blocker is superior than sotalol or jS-blocker alone for reducing ICD shocks in patients with reduced left ventricular function and history of sustained VT, VF, or cardiac arrest. 

Connolly SJ, Dorian P, Roberts RS, Gent M, Bailin S, Fain ES et al. Comparison of beta-blockers, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators the OPTIC Study a randomized trial. JAMA 2006 295 165-71. 

Low doses (100-200 mg/d) of amiodarone are effective in maintaining normal sinus rhythm in patients with atrial fibrillation. The drug is effective in the prevention of recurrent ventricular tachycardia. It is not associated with an increase in mortality in patients with coronary artery disease or heart failure. In many centers, the implanted cardioverter-defibrillator (ICD) has succeeded drug therapy as the primary treatment modality for ventricular tachycardia, but amiodarone may be used for ventricular tachycardia as adjuvant therapy to decrease the frequency of uncomfortable cardioverter-defibrillator discharges. The drug increases the pacing and defibrillation threshold and these devices require retesting after a maintenance dose has been achieved. 

In a 62-year-old man with dilated cardiomyopathy and an implantable cardioverter defibrillator for ventricular tachycardia, microvolt T wave alternans differed when amiodarone was added (55). The onset heart rate with T wave alternans was lower and the alternans voltage higher with amiodarone than without it. 

The effects of amiodarone appeared to be related to exacerbations of ventricular tachycardia and an increased defibrillation threshold. 

HPI CS is a 5 -year-old man admitted for an anterior Ml. Three days after admission, the patient s nurse found him unresponsive. His vital signs included no detectable blood pressure or pulse. ECG showed VT that progressed to ventricular fibrillation (VF). Immediate electrical defibrillation was applied. Other treatments instituted include airway management, chest compression, and establishment of IV access. After three shocks, 1 mg epinephrine was given and patient was shocked again. However, he was still in VF and amiodarone was administered. 

Patients with hemodynamically significant ventricular tachycardia or ventricular fibrillation not associated with an acute Ml who are resuscitated successfully (electrical cardioversion, pressors, amiodarone) are at high risk for death and should receive implantation of an internal cardioverter-defibrillator. 

Strickberger SA, Hummel JD, Bartlett TG, et al. Amiodarone versus implantable cardioverter-defibrillator randomized trial in patients with nonischemic dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia. AMIOVIRT. J Am Coll Cardiol 2003 41 1707-1712. 

The Multicenter Automatic Defibrillator Trial (MADIT) randomized 196 patients with prior MI, class I—III congestive HF, a LVEF <35%, NSVT, and inducible VT on EP study that was not suppressible with procainamide, to an ICD or conventional therapy (16). Most patients in the conventional therapy arm received amiodarone. The trial was stopped early as it demonstrated a statistically significant, and impressive, 54% reduction in total mortality in the ICD arm at 27 months (16% and 39% in the ICD and conventional therapy groups, respectively). MADIT is notable in that it only enrolled a small number of patients and did not have a control group. In addition, more patients in the ICD group received beta-blockers. 

FIGURE 1.6 Kaplan-Meier estimates of death from any cause in patients with both ischemic and nonischemic cardiomyopathy randomized to amiodarone, placebo, or implantable cardioverter-defibrillator therapy in SCD-HeFT. (From Ref. 29, with permission.)... 

Singh SN, Poole J, Anderson J, et al. Role of amiodarone or implantable cardioverter/defibrillator in patients with atrial fibrillation and heart failure. Am Heart J 2006 152(5) 974. e7-ll. 

A 64-year-old woman was treated for hypertrophic cardiomyopathy with amiodarone 1.2 g daily and atenolol 50 mg daily. Five days later the atenolol was replaced by metoprolol 100 mg daily. Within 3 hours she complained of dizziness, weakness and blurred vision. On examination she was found to be pale and sweating with a pulse rate of 20 bpm. Her systolic blood pressure was 60 mmHg. Atropine 2 mg did not produce chronotropic or haemodynamic improvement. She responded to isoprena-line (isoproterenol). Severe hypotension has been reported in another patient taking sotalol when intravenous amiodarone (total dose 250 mg) was given. Another report describes cardiac arrest in one patient on amiodarone, and severe bradycardia and ventricular fibrillation (requiring defibrillation) in another, within 1.5 and 2 hours of starting to take propranolol. ... 

In one study, 10 elderly patients (9 with symptomatic atrial fibrillation and one with an implanted defibrillator and frequent ventricular tachycardia) taking metoprolol (mean daily dose 119 mg) were also given amiodarone 1.2 g daily for 6 days. The metoprolol AUC and plasma levels were increased by about 80% and 75%, respectively, by the amiodarone, the extent varying by CYP2D6 genotype. None of the patients included in the study were poor metabolisers. 

A woman with congenital heart disease and atrial and ventricular arrhythmias managed by an implanted cardioverter defibrillator, epicardial pacing and amiodarone 400 mg daily, experienced deterioration in the control of her condition. She developed palpitations and experienced a shock from the defibrillator. Her amiodarone serum levels were 40% lower than 2 months previously, and her A-desethylamiodarone levels were undetectable. It was noted that 5 weeks earlier rifampicin 600 mg daily had been started to treat an infection of the pacing system. The amiodarone dose was doubled, but the palpitations continued. Amiodarone and A-desethy-lamiodarone levels increased after rifampicin was discontinued. Rifampicin is a potent enzyme inducer and it may have increased the metabolism and clearance of amiodarone. This case suggests that combined use of amiodarone and rifampicin should be well monitored. 

Cardiovascular Torsade de pontes has been attributed to cisapride 10 mg tds in a 36-year-old woman, in association with low serum potassium and magnesium concentrations [S ]. She had recurrent episodes, which required 50-70 defibrillation shocks per day, while several antidysrhyth-mic agents, including bretylium, phenytoin, isoprenaline, amiodarone, lidocaine, and magnesium sulfate, were ineffective. When cisapride was withdrawn the episodes of torsade de pointes resolved within a day. 

Bardy GH, Lee KL, Mark DB, Poole JE, Packer DL, Boineau R, Domanski M, Troutman C, Anderson J, Johnson G, McNulty SE, Clapp-Channing N, Davidson-Ray LD, Fraulo ES, Fishbein DP, Luceri RM, Ip JH. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med 2005 352 225-37. 

Huang J, Skinner JL, Rogers JM, Smith WM, Hohnan WL, Ideker RE. The effects of acute and chronic amiodarone on activation patterns and defibrillation threshold during ventricnlar fibrillation in dogs. J Am Coll Cardiol 2002 40 375-83. 

The original intent of the ICD was to prevent recurrent cardiac arrest due to ventricular tachycardia and fibrillation. Secondary prevention of recurrent cardiac arrest was initially the prime reason for ICD implant. Five multicenter prospective randomized secondary prevention trials have been completed AVID (Antiatrhythmics Versus Implantable Defibrillator), CASH (Cardiac Arrest Study Hamburg), CIDS (Canadian Implantable Defibrillator Study), DEBUT (Defibrillator versus beta-Blockers for Unexplained death in Thailand), and MAVERIC (The Midlands Trial of Empirical Amiodarone versus Electrophysiology-guided Interventions and Implantable (Tardioverter-defibrillators) (Table 14.3) (77,118,121,149,170). 

AVID (antiarrhythmics versus implantable defibrillator, 1997) ICD vs. amiodarone/sota-lol for VTA F CAD (81%), prior MI (67%) l,016pts Cardiac arrest sustained VT with syncope or snstained VT with EF < 40% and symptomatic because of hemodynamic compromise from the arrhythmia... 

CIDS (Canadian Implantable Defibrillator Study, 1998) ICD vs. amiodarone for VTA F Most CAD, prior MI (74%) VT with syncope VT > ISObpm with EF < 35%, or inducible VT with syncope, VF... 

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