Sinus bradycardia and

Compare and contrast appropriate nonpharmacologic and pharmacologic treatment options for sinus bradycardia and AV nodal blockade. 

The most common adverse effects are hypotension and bradycardia, which are usually easily managed unless there is preexisting heart disease. Dubovsky et al. (389) reported severe cardiotoxicity when verapamil was combined with lithium in two elderly patients. One had a profound bradycardia with a heart rate of 36 beats/minute another, who had a sinus bradycardia and atrioventricular ectopy, developed an acute myocardial infarction and died. 

Sinus bradycardia and QT interval prolongation occurred in a 25-year-old man taking amisulpride 800 mg/day (16). The dosage of amisulpride was reduced to 600 mg/day and the electrocardiogram normalized within a few days. 

Although betaxolol generally elicits less systemic beta-blockade than do noncardioselective agents, it does cause undesirable systemic effects in some patients. Reported adverse experiences include congestive heart failure, myocardial infarction, respiratory difficulties strongly suggestive of obstructive airway disease, weakness with severe sinus bradycardia, and wheezing with objective reduction in pulmonary function. 

The most common cardiac effects are atrioventricular block, sinus bradycardia, and ventricular extra beats. Occasionally serious dysrhythmias occur (SEDA-17, 219), including ventricular fibrillation (15). ATP can cause transient atrial fibrillation (16). Chest pain occurs in 30-50% of patients and dyspnea and chest discomfort in 35-55%. Chest pain can occur in patients with and without coronary artery disease, and the symptoms are not always tjrpical of cardiac pain. 

Sinus bradycardia and a reversible prolongation of the QT interval have been reported (SEDA-21, 293). 

Clonidine causes sinus bradycardia and atrioventricular block, as illustrated by two cases, one a 10-year-old boy (6) and the other a 71-year-old woman (7), who developed Wenckebach s phenomenon. Clonidine was also studied in seven patients subjected to electrophysiological studies after 5 weeks of therapy (8). It slowed the sinus rate and increased the atrial pacing rate, producing Wenckebach s phenomenon, indicating depressed function of the sinus and AV nodes. 

A 50-year-old man with symptoms of chronic paranoid schizophrenia resistant to typical neuroleptic drugs had a brief syncopal attack with significant electrocardiographic changes (sinus bradycardia and deep anteroseptal inverted T waves and minor ST... 

The combination of disopjramide and practoioi can cause profound sinus bradycardia and asystole (40,41). 

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. 

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. 

Sinus bradycardia and hypotension have been attributed to talipexole (1). 

A 12-year-old girl with terminal renal insnfficiency was given alfacalcidol (0.5 mg/day 0.02 micrograms/ kg) and calcium carbonate (1 g/day) and developed calcification of the papillary muscles, of the ventricular septum, and of the atrioventricnlar valves, with sinus bradycardia and heart block that reqnired a cardiac pacemaker. Her serum calcium was 2.7 mmol/1, phosphate 3.14 mmol/1, and parathyroid hormone 23 pg/ml. Calcidiol and calcinm carbonate... 

Most side effects of the calcium channel blockers are related to their mechanism of action. Verapamil and diltiazem can both cause sinus bradycardia and may worsen CHF. Constipation has been associated with verapamil use. The dihydropyridines often cause symptoms associated with vasodilatation, such as facial flushing, peripheral edema, hypotension, and headache. Because dihydropyridines are potent vasodilators, they can cause reflex tachycardia, which may precipitate palpitations, worsening angina, or Ml. Lastly, all calcium channel blockers can cause Gl complaints and fatigue. 

The toxic effects of propranolol are related to its negative inotropic and chronotropic properties, which can lead to sinus bradycardia and hypotension. These complications should be treated with an acute inotrope such as dopamine or dobutamine. 

AF-DX-116 is an analog of pirenzepinethat differs markedly in its profile of muscarinic activities (102,103). It has greatest affinity for cardiac M2 receptors. Its cardioselectivity is dso observed in humans and may become useful in sinus bradycardia and AV block of vagal origin. 

Sinus bradycardia and atrioventricular rhythms occur frequently during halothane anesthesia but usually are benign and result mainly from a direct depressive effect of halothane on sinoatrial node discharge. Halothane also can sensitize the myocardium to the arrhythmogenic effects of epinephrine. 

Lupanine has been substituted on the 2 (keto)-position, forming benzyl-lupanol and further altered to phenyldehydrosparteine by removal of a molecule of water from the 2 and 3 carbon atoms forming a double bond. With either of these derivatives, a tenfold increase in potency of effects on the isolated frog heart is obtained. Lower concentrations cause ventricular standstill (arrest), sinus bradycardia, and an increase in electrical current (threshold) producing fibrillation (78). 

The adverse effects for fluvoxamine include symptoms of drowsiness, nausea or vomiting, abdominal pain, tremors, sinus bradycardia, and mild anticholinergic symptoms. Toxic doses could produce seizures and severe bradycardia. 

B. Succinylcholine can stimulate vagal nerves, resulting in sinus bradycardia and atrioventricular block. Children are particularly sensitive to vagotonic effects (can prevent with atropine). 

An elderly man with long standing brady-tachycardia was successfully treated for atrial flutter firstly with a temporary pacemaker (later withdrawn) and 600 mg amiodarone daily. Ten days later, and 25 minutes after a permanent pacemaker was inserted under local anaesthesia with 15 mL of 2% lidocaine, severe sinus bradycardia and long sinoatrial arrest developed. He was effectively treated with atropine plus isoprenaline, and cardiac massage. ... 

A man taking digoxin 250 and 375 micrograms on alternate days and reserpine 25 micrograms daily developed sinus bradycardia and carotid sinus supersensitivity. He was hospitalised because of syncope, which resolved when the reserpine was withdrawn. 

Cardiovascular A 57-year-old man with HIV infection taking abacavir, nevirapine, tenofovir, voriconazole, and methadone developed new-onset seizures [69 ]. An electrocardiogram showed sinus bradycardia and a prolonged QT interval of 690 msec. He had several episodes of torsade de pointes and ventricular tachycardia, which resolved spontaneously. They were accompanied by altered cognition and... 

Cardiovascular A case report of a 23-year-old man who presented with sinus bradycardia and second degree Mobiz Type I AV block after ingestion of 42 alprazolam tables, risperidone, acetaminophen and hydrocodone [1 ]. The exact quantity, dose and ingestion times were unknown. The AV block resolved 5 h after his presentation, he refused further follow-up. This case suggests the possibility of potential arrhythmogenicity associated with benzodiazepine exposure. 

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