Amiodarone, dysrhythmias

Should be administered only by clinicians experienced in treatment of life-threatening dysrhythmias who are thoroughly familiar with the risks and benefits of amiodarone therapy... 

Procainamide (Pronestyl, Pronestyl SR, Procanbid) [Antiarrhythmic] WARNING Only use in life-treating arrhythmias hematologic tox can be severe Uses Supraventricular/ventricular arrhythmias Action Class 1A antiarrhythmic (Table VI-7) Dose Adults. Recurrent VF/pulseless VT 20 mg/min slow IV inf to a max of 17 mg/kg or until QRS T by 50% or dysrhythmia resolves Maint inf 4 mg/min (mix 1 gm in 250 mL NS to make 4 mg/mL use 60 gtt set—60 gtt/min = 4 mg) Peds. Loading dose 15-50 mg/kg IV/IO Caution [C, +] Contra Complete heart block, 2nd- or 3rd-degree heart block w/o pacemaker, torsades de pointes, SLE Disp Tabs caps 250, 500 mg SR tabs 500, 750, 1000 mg inj 100, 500 mg/mL SE 1 BP, lupus-like synd, GI upset, taste perversion, arrhythmias, tach, heart block, angioneurotic edema, blood dyscrasias Interactions T Effects W/ acetazolamide, amiodarone, cimetidine, ranitidine, trimethoprim T effects OF anticholinergics, antihypertensives i effects W/ procaine, EtOH EMS Monitor BP and ECG use caution to prevent rapid... 

Apart from its effects on thyroid function tests, amiodarone is also associated with both functional hyperthyroidism and hypothyroidism, in up to 6% of patients. The frequency of thyroid disease in patients taking amiodarone has been retrospectively studied in 90 patients taking amiodarone 200 mg/day for a mean duration of 33 months (35). Hypothyroidism occurred in five patients and hyperthyroidism in 11. Hyperthyroidism became more frequent with time and was associated with recurrent supraventricular dysrhythmias in four of the 11 patients. 

Two patients with cardiomyopathy and resistant dysrhythmias developed thyrotoxicosis while taking amiodarone (71). Despite medical therapy, they failed to improve. Both underwent total thyroidectomy without difficulty or complications. Most reported cases of amiodarone-induced thyrotoxicosis that have been treated surgically have been of type II, i.e. with no underlying thyroid disease. 

Amiodarone is highly effective in treating both ventricular and supraventricular dysrhythmias (1). Its pharmacology, therapeutic uses, and adverse effects and interactions have been extensively reviewed (2-14). 

In a comparison of amiodarone (n = 23) with sotalol (n = 22) in patients with spontaneous sustained ventricular tachydysrhythmias secondary to myocardial infarction, sotalol was much more effective, 75% of those taking it remaining free of dysrhythmias compared with 38% of those taking amiodarone (34). Adverse effects requiring withdrawal occurred in 17% of those taking amiodarone at a median time of 3.5 months. The adverse effects included malaise, rash, headaches, flushing, and dyspnea due to pulmonary fibrosis. 

The incidence of cardiac dysrhythmias with amiodarone is under 3% (42), lower than with many other antidysrhythmic drugs, and several randomized controlled trials have failed to show any prodysrhythmic effect (43). 

Ventricular dysrhjdhmias due to drugs can be either mono-morphic or poljmorphic. The class la drugs are particularly likely to cause poljmorphic dysrhjdhmias, as is amiodarone (although to a lesser extent). In contrast, the class Ic drugs are more likely to cause monomorphic dysrhythmias (46). 

It is not clear that the dysrhythmias in these cases were due to amiodarone, particularly since the doses had been very low and the serum concentrations no higher than the usual target range QT intervals were not reported. 

Amiodarone can sometimes cause atrial flutter, even though it is also used to treat it (SEDA-25, 180). There has been a report of seven cases (six men and one woman, aged 34-75 years) of 1 1 atrial flutter with oral amiodarone (57). Four of them had underlying cardiac disease none had hjrperthyroidism. The initial dysrhythmia was 2 1 atrial flutter (n = 4), 1 1 atrial flutter n = 2), or atrial fibrillation (n — 1). Qne patient was taking amiodarone 200 mg/day and one was taking 400 mg/day plus... 

Qf 2559 patients admitted to an intensive cardiac care unit over 3 years, 64 with major cardiac iatrogenic problems were reviewed (59). Qf those, 58 had dysrhythmias, mainly bradydysrhythmias, secondary to amiodarone, beta-blockers, calcium channel blockers, electrolyte imbalance, or a combination of those. Amiodarone was implicated in 19 cases, compared with 44 cases attributed to beta-blockers and 28 to calcium channel blockers. Qf the 56 patients with sinus bradycardia, 10 were taking a combination of amiodarone and a beta-blocker, six were taking amiodarone alone, and three were taking amiodarone plus a calcium channel blocker. 

A 77-year-old man without a history of lung disease was given amiodarone 7 days after bypass surgery because of supraventricular dysrhythmias and non-sustained ventricular tachycardia (74). He had taken 1600 mg/ day for a week followed by a maintenance dosage of 400 mg/day, and 15 days later became pale, sweaty, febrile, and tachypneic. His blood pressure was 100/60 and his heart rate 100/minute. There were reduced breath sounds and crackles throughout the lung fields. 

The safety and efficacy of amiodarone for supraventricular tachycardia have been studied in 50 infants (mean age 1.0 month, 35 boys) (222). They had congenital heart disease (24%), congestive heart failure (36%), or ventricular dysfunction (44%). Six, who were critically ill, received a loading dose of intravenous amiodarone 5 mg/kg over 1 hour, and all took 20 mg/kg/day orally for 7-10 days, followed by 100 mg/day if this failed to control the dysrhythmia, oral propranolol (2 mg/kg/day) was added. Follow-up was for an average of 16 months. Rhythm control was achieved in aU patients. Growth and... 

A few studies have also reported the effects and adverse effects of intravenous amiodarone in patients with atrial fibrillation. Of 67 patients with atrial fibrillation, of whom 33 received amiodarone and 34 received placebo, conversion to sinus rhythm occurred in 16 of the patients who received amiodarone and in none of those who received placebo (242). In five patients the systolic blood pressure fell significantly during the first trial of intravenous drug administration. There were no cardiac dysrhythmias. Thrombophlebitis occurred in 12 patients who received amiodarone. 

Antidysrhythmic dmgs can themselves cause cardiac dysrhythmias, their major adverse effect. The risk of antidysrhythmic-induced cardiac dysrhythmias (prodys-rhythmic effects) has been estimated at about 11-13% in non-invasive studies (18,19) and at up to 20% in invasive electrophysiological studies. However, the risk varies from dmg to drug and is particularly low with class III drugs. In one study the quoted risks of dysrhythmias were flecainide 30%, quinidine 18%, propafenone 7%, sotalol 6%, and amiodar-one 0% (20). However, amiodarone does cause dysrhythmias, especially when the QT interval is over 600 ms. 

In patients with heart failure, amiodarone is often required for the treatment of serious ventricular dysrhythmias. The beneficial effects of carvedilol on left ventricular remodeling, systolic function, and symptomatic status were not altered by amiodarone in 80 patients with heart failure. Adverse effects that necessitated withdrawal of carvedilol were no more frequent in patients taking amiodarone than in those taking carvedilol alone (26 versus 25%) (4). 

The combination of flecainide with amiodarone can result in reduced conduction, predisposing to bundle branch block and dysrhythmias (69,70). 

Current concepts of resuscitation after local anesthetic cardiotoxicity have been reviewed (17). Vasopressin may be a logical vasopressor in the setting of hypotension, rather than adrenaline, in view of the dysrhythmogenic potential of the latter. Amiodarone is probably of use in the treatment of dysrhythmias. Calcium channel blockers, phenytoin, and bretyllium should be avoided. In terms of new modes of therapy targeted at the specific action of local anesthetics, lipid infusions, propofol, and insulin/ glucose/potassium infusions may all have a role, but further research is necessary. 

Serious ingestions require cardiac monitoring in an intensive-care setting. Hypotension may be resistant to dopamine and dobutamine. Norepinephrine can also be used. Bradycardia can be treated with atropine and a temporary pacemaker as needed. Digoxin-specific FAB antibody fragments have been used with some success for cardiac conduction abnormalities after a yew exposure. If no contraindication, lido-caine, amiodarone, or procainamide may be used for ventricular dysrhythmias. 

Prolong repolarization ventricular dysrhythmias shortness of breath,/dyspnea) Amiodarone HC1... 

Amiodarone is administered in life-threatening ventricular dysrhythmias, not asystole. 

Cardiovascular Amiodarone-induced torsade de pointes has been reported in a patient with Wolff-Parkinson-White syndrome who had been given intravenous amiodarone for a wide-complex tachycardia [24 ]. Aas sinus rhythm was restored, QT interval prolongation and T wave alter-nans occurred, followed by symptomatic torsade de pointes. The dysrhythmia spontaneously terminated after discontinuation of intravenous amiodarone. 

Presentation Atrial fibrillation can be induced by amiodarone-induced thyrotoxicosis even some time after drug withdrawal, as has been described in a patient who had taken oral amiodarone for 2.5 years for ventricular dysrhythmias, in whom it had been withdrawn 6 months before [37 ]. 

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