Amiodarone ventricular

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2). 

The risk of atrial flutter is a 2 1 transmission to the ventricles generating a high ventricular rate. The therapeutic goal is to reduce transmission to 3 1 or 4 1 by administration of either (3-adrenoceptor antagonists, Ca2+ channel blockers or amiodarone. Quinidine must not be used in this arrhythmia, since it accelerates AV-conduction due to its vagolytic effect. 

Ventricular extrasystoles are treated only if they may degenerate into life-threatening arrhythmia. In milder forms the proarrhythmic risk of the diugs overshadows their benefits. In such cases (3-adrenoceptor antagonists may be attempted. For the treatment of ventricular extrasystoles, such as series or runs of extrasystoles, amiodarone or sotalol are used. In the absence of structural heart disease, class I anti-arrhythmic diugs can be considered an alternative. However, they may not be administered during the post-infarction period. 

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. 

Ventricular Rate Control is achieved by inhibiting the proportion of electrical impulses conducted from the atria to the ventricles through the AV node. Therefore, drugs that are effective for ventricular rate control are those that inhibit AV nodal impulse conduction P-blockers, diltiazem, verapamil, and digoxin (Tables 6-5 and 6-6). Amiodarone also inhibits AV nodal conduction, but is not a preferred drug for ventricular rate control in AF due to its unfavorable adverse-effect profile (Table 6-6). 

The Class III effects of amiodarone develop over several weeks. This time-course is similar to that seen in thyroid gland ablation [25]. It is well known that patients with hypothyroidism have long QT intervals which are indicative of prolonged action potentials. Amiodarone has been shown to inhibit the conversion of thyroxine (T4) to triiodothyronine (T3) both in human subjects [26] and in vitro [27]. It has been argued that the Class III effects of amiodarone are due to its effects on thyroid hormones [28]. Others, however, argue that there is no relationship between prolongation of ventricular refractory period by amiodarone and thyroid state [29]. 

Maintenance dose 0.125-0.25 mg PO/IV qd low potassium or magnesium levels potentiate toxicity reduce dose in renal failure toxicity indicated by nausea, headache, visual disturbances (yellow-green halos), ventricular arrhythmias. Quinidine, verapamil, and amiodarone elevate digoxin level. 

Amiodarone is useful in the treatment of supraventricular and ventricular arrhythmias. Amiodarone tends to hove a number of side-effects, such os photosensitivity. Patients ore advised to ovoid exposure to sunlight and apply a sun protection factor on a doily basis. Amiodarone may also cause reversible corneal microdeposits os a result of v/hich patients find night glare irritating and so patients ore advised to ovoid driving at night. 

Amiodarone is an anti-arrhythmic drug indicated in supraventricular and ventricular arrhythmias. One of the main side-effects is photosensitivity and patients are advised to avoid exposure to sunlight and use sun protection factors. 

Amiodarone (16) has been the center of much interest because of its activity as a cardiac depressant useful in treating ventricular arrhythmia and many analogues have been prepared [4. I he originally patented procedure concludes simply by etherification of benzofuran-containing iodonated phenol 15 with 2-halodiethylaminoethane to give amiodarone (16) [5]. The synthesis t)f 15 is not detailed in the reference but the synthesis of benzbromarone contains closely analo-goii.s steps [6]. 

Clinical use of amiodarone is limited because of its high toxicity, which consists of cardiac block, bradycardia, cardiac insufficiency, damaged thyroid gland function, neuropathology, and increased sensitivity to light, all of which significantly limit use of amiodarona, and it is only used in therapy for extremely serious tachyarrhythmias such as reoccurring ventricular fibrillation and hemodynamic unstable ventricular tachycardia, and only under supervision of a physician in a clinical situation. Synonyms of amiodarone are cordarone, rythmarone, and others. 

For the treatment of hemodynamically stable ventricular tachycardia in children, procainamide (loading dose of 15 mg/kg IV infused over 30 to 60 minutes) may be considered as an alternative agent to amiodarone. 

During or after treatment with IV amiodarone, patients may be transferred to oral amiodarone therapy. Use IV amiodarone for acute treatment until the patient s ventricular arrhythmias are stabilized. Most patients require this therapy for 48 to 96 hours, but IV amiodarone may be given safely for longer periods if needed. 

The first 24-hour dose may be individualized for each patient however, in controlled clinical trials, mean daily doses greater than 2100 mg were associated with an increased risk of hypotension. The initial infusion rate should not exceed 30 mg/min. Based on the experience from clinical studies, a maintenance infusion of up to 0.5 mg/min can be cautiously continued for 2 to 3 weeks regardless of the patient s age, renal function, or left ventricular function. There has been limited experience in patients receiving amiodarone IV for more than 3 weeks. 

Amiodarone (Cordarone, Pacerone) [Ventricular Antiarrhythmic/Adrenergic Blocker] Uses RecumMit VF or hemo-dynamically unstable VT, supraventricular arrhythmias, AF Action Class III antiarrhythmic (Table VI-7) Dose Adul. Ventricular arrhythmias IV 15 mg/min... 

On the basis of two large randomized trials aimed at suppressing premature ventricular complexes after MI, so-called warning arrhythmias, it was discovered that many common antiarrhythmic medications actually increase the risk of mortality [20, 21]. Amiodarone also has been shown to have no definitive effect on mortality in patients after an MI, including in the recent SCD-HeFT trial [22-24]. In fact, of all antiarrhythmic medications, only beta blockers have been clearly shown to prevent SCD after MI [25], particularly among those with depressed LV function [11]. 

Cairns JA, Connolly SJ, Roberts R, et al. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations CAMIAT. Canadian Amiodarone myocardial infarction arrhythmia trial investigators. Lancet. Mar 8 1997 349(9053) 675-682. 

Class Ill-agents, used clinically, are rare, with amiodarone as the best-known example. Several experimental preparations are the subject of clinical investigation. Amiodarone has shown to be effective in the treatment of various ventricular tachyarrhythmias and one of its major advantages is... 

Class II Ventricular tachycardia WPW syndrome Postoperative atrial fibrillation (i.v. amiodarone)... 

Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with Udo-caine for shosk-resistant ventricular fibrillation. NEJM 2002 346(12) 884-90. 

ICD implantation is recommended for prevention of sudden cardiac death in patients with ARVC with documented sustained VT or ventricular fibrillation. Drug therapy with amiodarone or stalol can be effective in selected patients with ARVC. 

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. 

III Amiodarone Bretylium Sotalol Prolong ventricular action potential, prolong refractoriness, inhibit potassium repolarization currents. Prolong QTc interval. Potential for proarrhythmia (torsades de pointes tachyarrhythmia). 

Amiodarone Hemodynamically unstable ventricular tachycardia Ventricular fibrillation... 

The dominant effect on ventricular myocardium that has been chronically exposed to either amiodarone or desethylamiodarone is a prolongation in the action potential with an associated increase in the refractory period and a modest decrease in Vmax as a function of stimulus frequency. Amiodarone inhibits the delayed outward potassium current, a finding consistent with the observation of a prolonged action potential. Both amiodarone and its metabolite significantly decrease the ac-... 

Amiodarone relaxes vascular smooth muscle one of its most prominent effects is on the coronary circulation, reducing coronary vascular resistance and improving regional myocardial blood flow. In addition, its effects on the peripheral vascular bed lead to a decrease in left ventricular stroke work and myocardial oxygen consumption. Therefore, amiodarone improves the relationship between myocardial oxygen demand and oxygen supply. IV administration may be associated with profound hypotension requiring volume expansion therapy. 

Amiodarone is available as an IV formulation as well as an oral preparation. IV amiodarone is indicated for initiating treatment and for prophylaxis of frequently recurring ventricular fibrillation and hemody-... 

Amiodarone may elicit life-threatening side effects in addition to presenting substantial management difh-culties associated with its use. The oral formulation of amiodarone is indicated only for the treatment of life-threatening recurrent ventricular arrhythmias (e.g., recurrent ventricular hbrillation and/or recurrent hemo-dynamicaUy unstable ventricular tachycardia) that have not responded to other potentially effective antiarrhythmic drugs or when alternative interventions could not be tolerated. Despite its efficacy as an antiarrhythmic agent, there is no evidence from clinical trials that the use of amiodarone favorably affects survival. 

Ventricular tachycardia, atrial fibrillation, and flutter (can convert recent-onset fibrillation or flutter to sinus rhythm). Amiodarone is used in the management of patients with supraventricular and ventricular arrhythmias, and arrhythmias associated with the WPW syndrome... 

Procainamide is effective against most atrial and ventricular arrhythmias. However, many clinicians attempt to avoid long-term therapy because of the requirement for frequent dosing and the common occurrence of lupus-related effects. Procainamide is the drug of second or third choice (after lidocaine or amiodarone) in most coronary care units for the treatment of sustained ventricular arrhythmias associated with acute myocardial infarction. 

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