Atrioventricular block treatment

Verapamil s cardiotoxic effects are dose-related and usually avoidable. A common error has been to administer intravenous verapamil to a patient with ventricular tachycardia misdiagnosed as supraventricular tachycardia. In this setting, hypotension and ventricular fibrillation can occur. Verapamil s negative inotropic effects may limit its clinical usefulness in diseased hearts (see Chapter 12 Vasodilators the Treatment of Angina Pectoris). Verapamil can lead to atrioventricular block when used in large doses or in patients with atrio-ventricular nodal disease. This block can be treated with atropine and -receptor stimulants. In patients with sinus node disease, verapamil can precipitate sinus arrest. 

The causes of syncope in patients with Alzheimer s disease treated with donepezil have been reported in 16 consecutive patients (12 women, 4 men) with Alzheimer s disease, mean age 80 years, who underwent staged evaluation, ranging from physical examination to electrophy-siological testing (54). The mean dose of donepezil was 7.8 mg/day and the mean duration of donepezil treatment at the time of syncope was 12 months. Among the causes of syncope, carotid sinus syndrome (n = 3), complete atrioventricular block (n = 2), sinus node dysfunction (n = 2), and paroxysmal atrial fibrillation (n = 1) were diagnosed. No cause of syncope was found in six patients. Non-invasive evaluation is recommended before withdrawing cholinesterase inhibitors in patients with Alzheimer s disease and unexplained syncope. 

The incidence of atrioventricular block has been reported in 600 consecutive patients who underwent stress myocardial perfusion imaging with adenosine (140 micrograms/kg/minute for 6 minutes), and of whom 43 had first-degree heart block before adenosine and 557 had a baseline PR interval less than 200 ms (Table 1) (31). The heart block in all cases was of short duration, was not associated with any specific symptoms, and in no case required specific treatment. The risk of atrioventricular block during adenosine infusion was not increased by the presence of other drugs that might have caused atrioventricular block (digitalis, beta-blockers, diltiazem, verapamil). 

Amiodarone and carvedilol have been used in combination in 109 patients with severe heart failure and left ventricular ejection fractions of 0.25 (16). They were given amiodarone 1000 mg/week plus carvedilol titrated to a target dose of 50 mg/day. A dual-chamber pacemaker was inserted and programmed in back-up mode at a basal rate of 40. Significantly more patients were in sinus rhythm after 1 year, and in 47 patients who were studied for at least 1 year the resting heart rate fell from 90 to 59. Ventricular extra beats were suppressed from 1 to 0.1/day and the number of bouts of tachycardia over 167 per minute was reduced from 1.2 to 0.3 episodes per patient per 3 months. The left ventricular ejection fraction increased from 0.26 to 0.39 and New York Heart Association Classification improved from 3.2 to 1.8. The probability of sudden death was significantly reduced by amiodarone plus carvedilol compared with 154 patients treated with amiodarone alone and even more so compared with 283 patients who received no treatment at all. However, the study was not randomized, and this vitiates the results. The main adverse effect was s)mptomatic bradycardia, which occurred in seven patients two of those developed atrioventricular block and four had sinoatrial block and/or sinus bradycardia one patient developed slow atrial fibrillation. 

Atrioventricular block is very rare after arsenic trioxide treatment for refractory acute promyelocjdic leukemia (16). 

Huang CH, Chen WJ, Wu CC, Chen YC, Lee YT. Complete atrioventricular block after arsenic trioxide treatment in an acute promyelocytic leukemic patient. Pacing Clin Electrophysiol 1999 22(6 Pt l) 965-7. 

Five patients with acute accidental poisoning with V. album rapidly developed nausea, vomiting, abdominal pain, hypotension, and bradycardia (26). In four cases the electrocardiogram showed sinus bradycardia and in one there was complete atrioventricular block with an ectopic atrial bradycardia and an intermittent idioventricular rhythm. Symptomatic treatment and/or atropine led to recovery within a few hours. 

Variceal bleeding is a frequent and serious event in cirrhosis, and carries an increased risk of death (SEDA-22, 218). Therapy to prevent bleeding is therefore essential in these patients. Propranolol alone has been compared with propranolol plus isosorbide-5-mononitrate in a randomized, double-blind study in 95 patients (21). The combined treatment reduced the incidence of variceal bleeding compared with propranolol alone, but without any improvement in survival Isosorbide-5-mononitrate added to propranolol appeared to be less well tolerated than propranolol alone, since seven patients had to be withdrawn from treatment because of adverse effects (four with feehngs of faintness, two with headache, one with angina-like chest pain), compared with one with atrioventricular block taking propranolol alone. 

The safety of oral propafenone in the treatment of dysrhythmias has been studied retrospectively in infants and children (40). There were significant electrophysiolo-gical adverse effects and prodysrhythmia in 15 of 772 patients (1.9%). These included sinus node dysfunction in four, complete atrioventricular block in two, aggravation of supraventricular tachycardia in two, acceleration of ventricular rate during atrial flutter in one, ventricular prodysrhythmia in five, and unexplained sjmcope in one. Cardiac arrest or sudden death occurred in five patients (0.6%) two had a supraventricular tachycardia due to Wolff-Parkinson-White syndrome the other three had structural heart disease. Adverse cardiac events were more common in the presence of structural heart disease and there was no difference between patients with supraventricular and ventricular dysrhythmias. 

Several publications involving 962 patients treated with an intravenous infusion of racemic sotalol have been reviewed, with the aim of describing the risk of torsade de pointes (5). Torsade de pointes occurred in only one case (0.1% 95% Cl = 0.003, 0.6), which is less often than with oral sotalol (2-4%). This difference can be explained by the shorter duration of treatment. The other reported complications were hypotension (0.3%), severe bradycardia (0.2%), and atrioventricular block necessitating drug withdrawal (0.03%). 

A 79-year-old white woman developed extreme fatigue and dizziness (34). Her heart rate was 40/minute and her blood pressure 80/40 mmHg. An electrocardiogram showed complete atrioventricular block, an escape rhythm at 50/minute, and QT interval prolongation to 583 milliseconds. This event was attributed to concomitant treatment with verapamil 480 mg/day and erythromycin 2000 mg/day, which had been prescribed 1 week before admission. 

The calcium channel blockers generally are considered seconder third-line options for preventive treatment when other drugs with established clinical benefit are ineffective or contraindicated. Verapamil is the most widely used calcium chaimel blocker for preventive treatment, but it provided only modest benefit in decreasing the frequency of attacks in two placebo-controlled studies." The therapeutic effect of verapamil may not be noted for up to 8 weeks after initiation of therapy. Side effects of verapamil may include constipation, hypotension, bradycardia, atrioventricular block, and exacerbation of congestive heart failure. Evaluations of nifedipine, nimodipine, diltiazem, and nicardipine have yielded equivocal results. ... 

The main effect of atropine on the heart is the alteration of the rate. At low doses, the rate is slowed (bradycardia) without a change in blood pressure or cardiac output. Higher doses cause an increase in pulse rate (tachycardia). Atropine may be used in the initial treatment of a myocardial infarction or high-grade atrioventricular block. 

A patient with bitemporal epilepsy took lacosamide 12 g, gabapentin 56 g, topira-mate 2 g, and zonisamide 2.8 g [104 ]. He became comatose and had repeated generalized tonic-clonic seizures, aspiration, and subsequent pneumonia, hypotension, and first-degree atrioventricular block. He recovered completely after several days of supportive treatment. 

Complete atrioventricular block developed 60 hours after the start of an octreotide infusion 50 micrograms/hour for the treatment of vari-ceal bleeding in a patient with hepatic cirrhosis and resolved 6 days after withdrawal of octreotide. The presence or absence of other drugs was not reported. Atropine and saline increased heart rate without a change in rhythm. 

Deaner A, Fluck D, Timmis AD. Exertional atrioventricular block presenting with recurrent syncope successful treatment by coronary angioplasty. Heart 1996 75 640-641. 

The authors of a review of the cardiac toxicity associated with paclitaxel treatment concluded that the overall incidence of serious cardiac events is low (0.1%). The causal relation of paclitaxel to atrial and ventricular dysrhythmias and cardiac ischemia is not entirely clear [32 ]. Reported events include ventricular tachycardia, Mobitz I (Wenckebach syndrome), Mobitz U atrioventricular block, complete atrioventricular block (requiring pacemaker insertion), acute myocardial infarction, supraventricular tachycardia, and atrial fibrillation. 

Case series In a retrospective series of 19 patients poisoned by mad honey , all had rmusea, vomiting, sweating, dizziness, and weakness several hours after ingestion [103"]. There was hypotension in 15, sinus bradycardia in 15, and complete atrioventricular block in four. The hypotension and conduction disorders resolved with atropine treatment, resulting in complete recovery within 24 hours. 

Drugs that block beta-1 receptors on the myocardium are one of the mainstays in arrhythmia treatment. Beta blockers are effective because they decrease the excitatory effects of the sympathetic nervous system and related catecholamines (norepinephrine and epinephrine) on the heart.5,28 This effect typically decreases cardiac automaticity and prolongs the effective refractory period, thus slowing heart rate.5 Beta blockers also slow down conduction through the myocardium, and are especially useful in controlling function of the atrioventricular node.21 Hence, these drugs are most effective in treating atrial tachycardias such as atrial fibrillation.23 Some ventricular arrhythmias may also respond to treatment with beta blockers. 

Atropine is an antimuscarinic agent that blocks the depressant effect of acetylcholine on both the sinus and atrioventricular nodes, thus decreasing parasympathetic tone. During asystole, parasympathetic tone may increase because of the vagal stimulation that occurs secondary to intubation, the effects of hypoxia and acidosis, or alterations in the balance of parasympathetic and sympathetic control. Unfortunately, there are no large randomized trials showing benefit from atropine for the treatment of asystole. Evidence is limited to small case series or retrospective reviews. " ... 

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