Atrial flutter causes

Duration of atrial fibrillation/atrial flutter >48 h or unknown, o Electrical or chemical cardioversion in a patient without adequate anticoagulation may cause embolization of atrial thrombi. 

The predominant mechanism of AF and atrial flutter is reentry, which is usually associated with organic heart disease that causes atrial distention (e.g., ischemia or infarction, hypertensive heart disease, valvular disorders). Additional associated disorders include acute pulmonary embolus and chronic lung disease, resulting in pulmonary hypertension and cor pulmonale and states of high adrenergic tone such as thyrotoxicosis, alcohol withdrawal, sepsis, or excessive physical exertion. 

Supraventricular tachycardia is the major arrhythmia indication for verapamil. Adenosine or verapamil are preferred over older treatments (propranolol, digoxin, edrophonium, vasoconstrictor agents, and cardioversion) for termination. Verapamil can also reduce the ventricular rate in atrial fibrillation and flutter. It only rarely converts atrial flutter and fibrillation to sinus rhythm. Verapamil is occasionally useful in ventricular arrhythmias. However, intravenous verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. 

The authors reviewed the biphasic effect of marijuana on the autonomic nervous system. At low to moderate doses it causes increased sympathetic activity, producing a tachycardia and increase in cardiac output blood pressure therefore increases. At high doses it causes increased parasympathetic activity, leading to bradycardia and hypotension. They thought that this patient most probably had adrenergic atrial flutter. 

It is doubtful whether this differs in its origins or sequelae from atrial fibrillation. The ventricular rate is usually faster (typically, half an atrial rate of 300, where 2 1 block is present), which is too fast to leave without treatment. Since, similarly, the patient is unlikely to have been in this rhythm for a prolonged period, there is less likelihood that atrial thrombus has accumulated. Conversion without prior anticoagulation may occasionally be considered safe but anticoagulation is usually also needed. Patients should not be left in chronic atrial flutter, and DC conversion will usually restore either sinus rhythm or result in atrial fibrillation. The latter is treated as above. Patients who fail to convert, or who revert to atrial flutter should be referred for consideration of radiofrequency ablation that is highly effective and may remove the cause of the atrial flutter > 80% of cases. 

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. 

Amiodarone has been reported to cause atrial flutter in 10 patients who had been given it for paroxysmal atrial fibrillation (56). In nine of those the atrial flutter was successfully treated by catheter ablation. However, during a mean follow-up period of 8 months after ablation, atrial fibrillation occurred in two patients who had continued to take amiodarone this was a lower rate of recurrence than in patients in whom atrial flutter was not associated with amiodarone. The authors therefore suggested that in patients with atrial flutter secondary to amiodarone given for atrial fibrillation, catheter ablation allows continuation of amiodarone therapy. 

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... 

Digitalis can cause supraventricular extra beats or tachycardia. The combination of such dysrhythmias with atrioventricular block is particularly suggestive of digitalis toxicity and carries a high mortality rate (3,36). Rarely atrial fibrillation (37) and atrial flutter (38) may be attributed to digitalis toxicity. The frequency of atrioventricular nodal block is mentioned above. 

In 19 patients with atrial fibrillation and five with atrial flutter, dofetilide 2.5-8.0 micrograms/kg caused conversion to sinus rhythm in 14 (10 with atrial fibrillation and four with atrial flutter) (38). 

In a double-blind, placebo-controlled study in 69 patients with atrial fibriUation or flutter, intravenous dofetihde 2-8 micrograms/kg caused conversion to sinus rhythm in 16 of 51 patients, compared with one of 18 who were given placebo conversion of atrial flutter occurred... 

In a 37-year-old woman with atrial flutter with 1 1 conduction and partial right bundle branch block, intravenous dofetihde 5 micrograms/kg given over 5 minutes not only suppressed the atrioventricular nodal block to 2 1 or 3 1 but also caused complete right bundle branch block and QT interval prolongation (58). 

P-ARK An enzyme that phosphoylates the occupied form of a G-protein coupled receptor, e.g. the 6-adrenoceptor, leading to uncoupling of that receptor and desensitization. ARMI age-related memory impairment, arrhythmia (dysrhythmia) An abnormality of heart rhythm or rate of heartbeat, usually caused by disturbance of the electrical impulses and their conduction within the heart. They include ectopic beats (isolated irregular beats), tachycardias (too fast a heartbeat), bradycardias (too slow a heartbeat) and atrial flutter and ventricular fibrillation. Arthus reaction A severe local inflammatory response, a skin reaction characterized by erythema, oedema, necrosis, local haemorrhage. A type III hypersensitivity reaction. Arunlakshana and Schild plot See Schild plot, ascites fluid The fluid that accumulates in the peritoneal cavity during certain pathological conditions, aspiration The withdrawal of fluid or tissue from the body by suction. 

The common supraventricular tachycardias that often require drug treatment are (1) atrial fibrillation or atrial flutter, (2) paroxysmal supraventricular tachycardia, and (3) automatic atrial tachycardias. Other common supraventricular arrhythmias that usually do not require drug therapy include premature atrial complexes (PACs), wandering atrial pacemaker, sinus arrhythmia, and sinus tachycardia. As an example, PACs rarely cause symptoms and never cause hemodynamic compromise, and therefore, drug therapy usually is not... 

These rhythms are usually not directly life-threatening, nor do they generally cause hemodynamic collapse or syncope, but 1 1 atrial flutter (ventricular response 300 beats per minute) is an exception. Also, patients with underlying forms of heart disease that are heavily reliant on atrial contraction to maintain adequate cardiac output (e.g., mitral stenosis and obstructive cardiomyopathy) will display more severe symptoms of atrial fibrillation/flutter. 

AV conduction = ventricular rate of 150 beats per minute 3 1 AV conduction = ventricular rate of 100 beats per minute). Atrial flutter may occur in two distinct forms (type I and type II). Type I flutter is the more common classic form with atrial rates of approximately 300 beats per minute and the typical sawtooth pattern of atrial activation, as shown by the surface ECG. Type II flutter tends to be faster, being somewhat of a hybrid between classic atrial flutter and atrial fibrillation. Although the ventricular response usually has a regular pattern, atrial flutter with varying degrees of AV block or that occurs with episodes of atrial fibrillation ( fib-flutter ) can cause an irregular ventricular rate and pulse. 

It is generally accepted that the predominant mechanism of atrial fibrillation and atrial flutter is reentry. Atrial fibrillation appears to result from multiple atrial reentrant loops (or wavelets), and atrial flutter is due to a single, dominant reentrant substrate (counterclockwise circus movement around the tricuspid annulus). Atrial fibrillation or flutter usually occurs in association with forms of organic heart disease that causes atrial distension. Forms of heart disease that commonly lead to atrial stretch and precipitate atrial fibrillation or flutter include... 

In addition, through an effect in the central nervous system cardiac glycosides cause an increase in parasympathetic activity and therefore slow conduction through the AV node, hence their usefulness in atrial flutter and atrial fibrillation. 

Dofetilide is an antiarrhythmic agent that causes blockade of the cardiac ion channel carrying the rapid component of the delayed rectifier potassium currents. Dofetilide is indicated in maintenance of normal sinus rhythm (delay in time to recurrence of atrial fibrillation/atrial flutter [AF/AFl]) in patients with AF/AFl of more than 1 week duration who have been converted to normal sinus rhythm and in conversion of AF/AFl to normal sinus rhythm. 

Adverse Effects Flecainide usually produces few subjective complaints dose-related blurred vision is the most common noncardiac adverse effect. It can exacerbate CHF in patients with depressed left ventricular performance. The most serious adverse effects are provocation or exacerbation of potentially lethal arrhythmias. These include acceleration of ventricular rate in patients with atrial flutter, increased frequency of episodes of reentrant ventricular tachycardia, and increased mortality in patients convalescing from myocardial infarction. These effects likely result from Na+ channel block. Flecainide also can cause heart block in patients with conduction system disease. 

Class IV anti-arrhythmic drugs usually interfere with calcium conductance such as verapamil hydrochloride. Verapamil inhibits the aetion potential of the upper and middle nodal regions of the heart where the slow inward ealeium-ion-mediated current contributes to depolarisation. This is responsible for the bloekade of slow-ehannel eonduetion in the atrioventricular node. It has been found to inhibit one limb of the re-entry circuit which is assumed to underlie most paroxysmal supraventricular tachycardias, thereby causing the reduction of ventricular rate in atrial flutter and fibrillation. 

Dofetilide is a Type III antiarrhythmic agent used in the treatment of chronic atrial fibrillation or atrial flutter. Physicians and hospital staff need to complete a dofetilide education program before the drug can be received by the hospital and prescribed. Dofetilide can cause fife-threatening ventricular arrhythmias and should therefore be used in select patients. 

The increase in QTc interval after intravenous ibutilide 2 mg was less in patients treated with propafenone (5 patients) or flecainide (1 patient) than in 85 other patients who had taken ibutilide alone (34 versus 65 milliseconds). The effect appeared to be dose-related, with higher propafenone doses causing the largest attenuation in the ibutilide-induced QT prolongation. The efficacy of ibutilide was unaltered. In a further study, 71 patients with atrial fibrillation or atrial flutter receiving either propafenone 300 to 900 mg daily or flecainide 100 to 300 mg daily underwent cardioversion with a single intravenous dose of ibutilide 1 mg over 10 minutes, followed if necessary by a further dose after an interval of 10 minutes. Torsade de pointes occurred in one patient with profound sinus node suppression after cardioversion, but the mean ibutilide-induced QTc interval was attenuated (20 + 54 milliseconds compared to reported range of 47 to 90 milliseconds) without a decrease in efficacy. However, the authors note that the risk of sustained torsade de pointes in this study appears to be similar to that seen in other studies of ibutilide. ... 

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