Sinus dysrhythmia

Sympathetic (sympatholytic) Heart Sinus node Atrioventricular (AV node) Slowing Increased refractory period Bradycardia Dysrhythmias, conduction block... 

Cardiac dysrhythmias Exercise caution in patients prone to cardiac dysrhythmias. In a study comparing pergolide and placebo, patients on pergolide had significantly more episodes of atrial premature contractions and sinus tachycardia. 

Serious cardiac dysrhythmias and sudden death have been reported with pulsed methylprednisolone. Oral methyl-prednisolone has been implicated in a case of sinus bradycardia (31). 

The most commonly reported cardiac signs of toxicity are dysrhythmias, such as ventricular ectopic depolarization, second- and third-degree heart block, junctional tachycardia, atrial tachycardia with block, ventricular tachycardia, sinoatrial block, and sinus arrest. 

Two reviews of the cardiac effects of psychotropic drugs briefly mentioned lithium and dysrhythmias, with a focus on sinus node dysfunction (122,123), reports of which, as manifested by bradycardia, sinoatrial block, and sinus arrest, continue to accumulate in association with both toxic (124) and therapeutic (125,126) serum lithium concentrations. The rhythm disturbance normalized in some cases when lithium was stopped (124,126), persisted despite discontinuation... 

In terms of its potential for inducing cardiac dysrhythmias, cannabis is most likely to cause palpitation due to a dose-related sinus tachycardia. Other reported dysrhythmias include sinus bradycardia, second-degree atrioventricular block, and atrial fibrillation. Also reported are ventricular extra beats and other reversible electrocardiographic changes. 

Cardiovascular Cardiac dysrhythmia, congestive heart failure (rare), sinus bradycardia... 

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. 

Ajmaline occasionally causes cardiac dysrh5dhmias (SEDA-17, 219). Of 1995 patients who were given ajmaline 1 mg/kg intravenously during an electrophysiological study, 63 developed a supraventricular tachydysrhythmia (atrial flutter, fibrillation, or tachycardia), and seven an atrioventricular re-entrant tachycardia (2). Those most at risk were older patients, those with underlying cardiac disease, and those with a history of dysrhythmias or sinus node dysfunction. 

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 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. 

Drug Number of subjects Efficacy in converting AF to sinus rhythm (odds ratio versus other drugs ) Efficacy in maintaining sinus rhythm (odds ratio versus other drugs ) Ventricular dysrhythmias (%) Other dysrhythmias %) Dmg withdrawal or dosage reduction (%)... 

Bupivacaine can cause ventricular extra beats (8). Ventricular dysrhythmias and seizures were reported in a patient who received 0.5% bupivacaine 30 ml with adrenaline 5 micrograms/ml for lumbar plexus block, after a negative aspiration test (9). The patient developed ventricular fibrillation and required advanced cardiac life support for 1 hour, including 15 defibrillations, and adrenaline 40 mg before sinus rhythm could be restored. There were no neurological sequelae. 

Digitalis-induced dysrhythmias can be classified according to their sites of origin in the sinus node, the atria and atrioventricular node, and the ventricles. 

It produced a small reduction in hospitalizations due to heart failure (nine per 1000 patients-years) balanced by a significant increase in deaths from presumed dysrhythmias. Digitalis is therefore indicated for a small number of patients who have severe heart failure associated with sinus rhythm after treatment with diuretics, vasodilators, beta-blockers, and spironolactone. It remains the drug of first choice in patients with heart failure accompanied by fast atrial fibrillation, especially if due to myocardial or mitral valve disease. A trial of withdrawal of digitalis therapy can be considered in some cases (as noted in point 3 above). 

Cardiac dysrhythmias in digitalis overdose should be treated only if they are life-threatening. Phenytoin is probably the treatment of choice for ventricular tachydysrhyth-mias, but lidocaine or a beta-adrenoceptor antagonist, such as propranolol, are options. After an overdose of 300 tablets of digoxin (plasma digoxin concentration 50 ng/ml), recurrent ventricular fibrillation was successfully treated with bretylium tosylate (191). Sinus bradycardia may respond to atropine. 

Cibenzoline prolongs the PR interval, the QRS interval, and the QT interval (4—7). It also prolongs the AH and HV intervals (5,8) and shortens the sinus cycle length (5-8). Because of these effects it can cause dysrhythmias (4,6,7,9). 

Dofetihde has been used to convert atrial fibrillation and atrial flutter to sinus rhythm, in maintaining sinus rhythm thereafter, in suppressing paroxysmal supraventricular tachycardia, inducible atrioventricular nodal re-entry tachycardia, and inducible sustained ventricular tachycardia, in suppressing the dysrhythmias of the Wolff-Parkinson-White syndrome, and in facilitating conversion of ventricular fibrillation. 

In a placebo-controlled study in patients with atrial fibrillation or atrial flutter with a median dysrhythmia duration of 62 (range 1-180) days, there was conversion to sinus rhythm in 20 of 66 patients given dofetilide, compared with one of 30 patients given placebo (44). The conversion rate was higher in atrial flutter (seven of 11 patients) than in atrial fibrillation (13 of 55). 

In a randomized, placebo-controlled, crossover study in 15 men, mean age 34 (range 18-63) years, with Wolff-Parkinson-White syndrome and atrial fibrillation or atrioventricular re-entrant tachycardia induced electro-physiologically, six of ten patients who were given dofetilide converted to sinus rhythm, compared with one of five who were given placebo (47). There were no dysrhythmias. 

In 33 patients with sjmptomatic and inducible supraventricular tachycardias single doses of placebo, flecainide 3 mg/kg, or dUtiazem 120 mg plus propranolol 80 mg were used to terminate the dysrhythmia (5). Conversion to sinus rhythm was achieved within 2 hours in 17 patients with placebo, in 20 with flecainide, and in 31 with diltiazem plus propranolol. Time to conversion was shorter with diltiazem plus propranolol (32 minutes) than with flecainide (74 minutes) or placebo (77 minutes). Of those who were given flecainide, two had hypotension and one had sinus bradycardia. 

In a review of 60 original articles detailing 1835 courses of intravenous and/or oral flecainide in both placebo-controlled and comparative studies as well as a large number of uncontrolled studies, unwanted cardiac events occurred in 8% of patients (7). The cardiac events were hypotension (1.3%), heart failure (0.4%), sinus node dysfunction (1.6%), bundle branch block (1.0%), atrial dysrhythmias (1.6%), and ventricular dysrhythmias (1.3%). However, in 8505 patients, 5507 of whom were administered flecainide for more than 4 weeks and most of whom took dosages of 100-300 mg/day, cardiac adverse effects occurred in only about 2% and non-cardiac effects in... 

In a double-blind, randomized, controlled study of 77 children undergoing halothane anesthesia for adenoidect-omy, the effects of atropine 0.02 mg/kg, glycopyrrolate 0.04 mg/kg, and physiological saline were compared (9). There was no difference in the incidence of ventricular dysrhythmias. Atropine prevented bradycardia but was associated with sinus tachycardia in most patients. The bradycardias that occurred in the groups that received glycopyrrolate or placebo were short-lived and resolved spontaneously. 

Hypotension or hypertension, benign sinus or supraventricular tachycardia, and rarely distal cyanosis, have been reported within the first days of treatment in 5-15% of patients receiving high-dose interferon alfa (20). These adverse effects are usually benign, except in high-risk patients with a previous history of dysrhythmias, coronary disease, or cardiac dysfunction. 

Lidocaine can cause dysrhythmias and hypotension. The dysrhythmias that have been reported include sinus bradycardia, supraventricular tachycardia (11), and rarely torsade de pointes (12). There have also been rare reports of cardiac arrest (2) and worsening heart failure (13). Lidocaine can also cause an increased risk of asystole after repeated attempts at defibrillation (14). Lidocaine may increase mortality after acute myocardial infarction, and it should be used only in patients with specific so-called warning dysrhythmias (that is frequent or multifocal ventricular extra beats, or salvos) (15). 

Sinus bradycardia was seen in 18% of patients taking mefloquine (SEDA-12, 693) (14), occurring some 4-7 days after administration the bradycardia was asymptomatic and lasted about 3-4 days. Transient sinus arrhythmia was also reported, without a need for treatment (SEDA-12, 808). Asymptomatic dysrhythmias were also recorded in a dosage comparison trial (SEDA-16, 308). 

The authors of a review of the cardiac toxicity associated with paclitaxel in a number of studies concluded that the overall incidence of serious cardiac events is low (0.1%) (20). Heart block and conduction abnormalities occurred infrequently and were often asymptomatic. Sinus bradycardia was the most frequent, occurring in 30% of patients. The causal relation of paclitaxel to atrial and ventricular dysrhythmias and cardiac ischemia was not entirely clear. There did not appear to be any evidence of cumulative toxicity or augmentation of acute cardiac effects of the anthracydines. 

A comparison between procainamide and propafenone in 62 patients, who had undergone coronary artery bypass grafting or valvular surgery within 3 weeks and developed sustained atrial fibrillation, showed that both drugs converted the dysrhythmia to sinus rhythm in up to 76% of cases, but that propafenone did it more quickly (3). Symptomatic arterial hypotension occurred more frequently with procainamide (nine of 33 patients) than with propafenone (two of 29 patients). Other adverse effects of procainamide were nausea (n = 2) and junctional escape rhythm (n = 2). 

Procainamide prolongs the QT interval (7) and can cause dysrhythmias. It can also impair cardiac conduction and can cause bradycardia and heart block (1). In the sick sinus syndrome it can alter sinus node recovery time (8), although the clinical significance of this is not clear. 

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. 

An unusual dysrhythmia has been attributed to propranolol alternating sinus rhythm with intermittent sinoatrial block. The authors suggested that this was... 

Quinidine has also been incriminated in cases of sinoatrial block and sinus arrest, but it was not clearly established that quinidine was responsible (9,10). The anticholinergic effects of quinidine can increase the risk of dysrhythmias (11). 

A 75-year-old woman received ropivacaine 160 mg intravenously through an epidural catheter (10). After completion of the injection, she suddenly became unresponsive and had a generalized tonic-clonic convulsion accompanied by a sinus tachycardia of 120/minute but no other cardiac dysrhythmias. 

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