eMedicine Specialties > Emergency Medicine > Cardiovascular
Atrial Flutter: Treatment & Medication
Updated: Jul 2, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Prehospital Care
In general, avoiding class I and III agents (eg, procainamide) in the prehospital setting is safest because of possible induction of 1:1 conduction. Generally, the rate can be slowed safely with calcium channel blockers or beta-adrenergic blockers.
Emergency Department Care
Assess airway, breathing, and circulation. Hemodynamic concerns will dictate initial treatment
Treatment options for atrial flutter include the following:
- Antiarrhythmic drugs/nodal agents
- Direct-current (DC) cardioversion
- Rapid atrial pacing to terminate atrial flutter
- Blood pressure can be supported and rate controlled with medication.
- Look for underlying causes. At times, treatment of the underlying disorder (eg, thyroid disease, valvular heart disease) is necessary to effect conversion to sinus rhythm.
Consultations
- Most cases will require internal medicine or cardiology consultation.
- A cardiologist may become involved, primarily if the patient presents with complicating factors or an obvious ongoing cardiac ischemia (or infarction) not treatable with rate reduction measures and standard chest pain protocols.
Medication
Cardioversion for unstable patients
- If the patient is unstable (eg, hypotension, poor perfusion), synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice.
- Cardioversion may be successful with energies as low as 25 Joules, but since 100 Joules is virtually always successful, this may be a reasonable initial shock strength.
- If the electrical shock results in atrial fibrillation (AF), a second shock at a higher energy level is used to restore normal sinus rhythm (NSR).
Rate control with nodal agents
Rate control is the goal of medication in atrial flutter or atrial fibrillation (see Atrial Fibrillation).
To slow the ventricular response, verapamil or diltiazem may be the appropriate initial treatment. Adenosine produces transient AV block and can be used to reveal flutter waves (see Media file 1). These drugs generally do not convert atrial flutter to normal sinus rhythm.
Type I atrial flutter unmasked by adenosine (Adenocard).
If the flutter cannot be cardioverted, terminated by pacing, or slowed by the drugs mentioned above, digoxin can be administered alone or with either a calcium antagonist or a beta-blocker. Intravenous amiodarone has been shown to slow the ventricular rate and is considered as effective as digoxin.
Digoxin toxicity is very rarely a cause of flutter; however, ascertaining that flutter is not caused by digoxin toxicity is important. Another caveat is to beware of the vagolytic action of quinidine, procainamide, and disopyramide if used to slow the flutter rate. These drugs can effect AV conduction, resulting in a 1:1 ventricular response to the atrial flutter. Before administration of these drugs, be sure to slow the conduction rate with digoxin or calcium channel blockers.
Beta-adrenergic blockers are especially effective in the presence of thyrotoxicosis and increased sympathetic tone.
Other antiarrhythmic drugs that can terminate atrial flutter/fibrillation include procainamide, disopyramide, propafenone, sotalol, flecainide, amiodarone, and ibutilide.
Dronedarone was approved by the US Food and Drug Administration on July 2, 2009. It is a deiodinated derivative of amiodarone that has no organ toxicity. Its use will likely extend to both atrial and ventricular arrhythmias. Dronedarone has multiple actions (all 4 Von Williams class effects). Unlike amiodarone, it does not have the iodine moiety. The lack of iodination may offer a better side-effect profile. Dronedarone has been shown to (1) have antiadrenergic effects, (2) prolong atrial and ventricular refractory periods, and (3) prolong atrioventricular node conduction as well as the paced QRS complex. In animal models, dronedarone has been shown to decrease ischemia-induced ventricular arrhythmias. The clinical effects of dronedarone are currently being examined in patients with atrial fibrillation and in patients with ICDs.
Antiarrhythmic drugs alone control atrial flutter in only 50-60% of patients. Since the early 1990s, radiofrequency catheter ablation has been used to interrupt the re-entrant circuit in the right atrium and prevent recurrences of atrial flutter. Radiofrequency ablation is immediately successful in more than 90% of cases and avoids the long-term toxicity observed with antiarrhythmic drugs.
When considering drug therapy for atrial flutter/fibrillation, remember the treatment caveat "electrical cardioversion is the preferred modality in the patient whose condition is unstable."
Calcium channel blockers
These agents reduce the rate of AV nodal conduction and control ventricular response. Formulations administered IV are discussed only as they relate to the control of severe symptoms (eg, rapid ventricular rate in emergent situations).
Diltiazem (Cardizem)
DOC during depolarization. Inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium.
Adult
Initial dose: 0.25 mg/kg IV over 2 min as bolus; repeat at 0.35 mg/kg if inadequate rate reduction after 15 min
Maintenance dose: 5-10 mg/h (up to 15 mg/h) IV can be infused for up to 24 h
Pediatric
Not established
May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and decrease in cardiac output; when given with beta-blockers, may increase cardiac depression; cimetidine may increase levels
Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur
Verapamil (Calan, Isoptin, Verelan)
Second DOC. Can diminish PVCs associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia. By interrupting re-entry at AV node, can restore normal sinus rhythm (NSR) in patients with paroxysmal supraventricular tachycardias (PSVT).
During depolarization, inhibits calcium ion from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium.
Adult
2.5-5 mg IV bolus initially reduces ventricular rate within 5 min; can be repeated to total of 15 mg IV, follow by maintenance infusion of 0.05-0.2 mg/min
Pediatric
<1 years: 0.1-0.2 mg/kg IV bolus over at least 2 min under continuous ECG monitoring; usual single-dose range 0.75-2 mg
>1 years: 0.1-0.3 mg/kg IV bolus over at least 2 min; usual single-dose range 2-5 mg; not to exceed 5 mg
May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; coadministration with amiodarone can cause bradycardia and decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase levels
Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hepatocellular injury may occur; transient elevations of transaminase levels with and without concomitant elevations in alkaline phosphatase and bilirubin levels have occurred (elevations have been transient and may disappear with continued verapamil treatment); monitor liver functions periodically
Beta-blockers
These agents slow the sinus rate and decrease AV nodal conduction. Beta-blockers now have more of a secondary role in rate control in atrial flutter/fibrillation. Be sure to monitor blood pressure carefully.
Metoprolol (Lopressor)
Selective beta 1-adrenergic receptor blocker that decreases automaticity of contractions.
Adult
5-15 mg IV over 5-15 min in 5-mg increments
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly decreasing pharmacologic effects; toxicity may increase with coadministration of sparfloxacin, phenothiazines, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, and contraceptives; may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Documented hypersensitivity; uncompensated CHF; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia or hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG
Esmolol (Brevibloc)
Ideal for use in patients at risk of complications from beta-blockade, especially patients with mild-moderate LV dysfunction or peripheral vascular disease. Has short half-life of 8 min; thus, easily titratable to desired effect and may be stopped quickly if necessary.
Adult
Initial: 500 mcg/kg/min (0.5 mg/kg/min) IV infusion over 1 min, followed immediately by maintenance dose of 50 mcg/kg/min (0.05 mg/kg/min) IV over 4 min; if adequate therapeutic effect observed over 5 min of drug administration, maintain maintenance infusion dosage with periodic adjustments prn; if adequate therapeutic effect not observed, repeat same loading dosage over 1 min followed by an increased maintenance infusion rate of 100 mcg/kg/min (0.1 mg/kg/min)
A quick calculation method is to take patient's body weight in kg, divide by 2 (eg, 70 kg/2 = 35 mg); this is loading dose over 1 min; multiply this dose by 0.1 (0.1 X 35 = 3.5 mg) to obtain mg/kg/min drip rate
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly decreasing pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, astemizole (recalled from US market), calcium channel blockers, quinidine, flecainide, or contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, or catecholamine-depleting agents
Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May mask signs and symptoms of acute hypoglycemia or hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm, may worsen when medication withdrawn abruptly; withdraw drug slowly and monitor patient closely
Class I antiarrhythmics
These agents are used for chemical conversion into sinus rhythm. They alter the electrophysiologic mechanisms responsible for arrhythmia.
Procainamide (Pronestyl, Procanbid)
Class IA antiarrhythmic used for PVCs. Increases refractory period of atria and ventricles. Myocardial excitability reduced by an increase in threshold for excitation and inhibition of ectopic pacemaker activity.
Adult
17 mg/kg IV at rate of 20-30 mg/min under continuous cardiac monitoring
Stop infusion if QRS widening or hypotension occurs
Control heart rate (<100 bpm) with IV digoxin or calcium channel blockers first to avoid 1:1 AV conduction
Pediatric
Not established
Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, or quinidine; may increase effects of skeletal muscle relaxants, quinidine, lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity
Documented hypersensitivity; complete heart block or second- or third-degree heart block if pacemaker not in place; torsade de pointes; systemic lupus erythematosus
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for hypotension; plasma concentrations of procainamide and active metabolite, NAPA, may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; caution in complete AV block, digitalis intoxication, organic heart disease, renal disease, or hepatic insufficiency
Quinidine (Cardioquin, Quinora)
Prolongs effective refractory period and increases conduction time. Also has indirect anticholinergic effects, decreases vagal tone, and facilitates conduction in conversion of AF.
Adult
200 mg PO q2-3h for 5-8 doses with subsequent daily increases until sinus rhythm restored or side effects occur; not to exceed 3-4 g/d in any regimen
Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers
Pediatric
30 mg/kg/d PO in 5 divided doses
Phenytoin, rifampin, and phenobarbital may decrease concentrations; toxicity increased when taken with ritonavir, sparfloxacin, beta-blockers, amiodarone, verapamil, cimetidine, alkalinizing agents, or nondepolarizing or depolarizing muscle relaxants; may enhance effect of anticoagulants
Documented hypersensitivity; complete AV block; intraventricular conduction defects; concurrent ritonavir or sparfloxacin
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in G-6-PD deficiency and patients with a tendency to develop granulocytopenia; avoid use in myocardial depression, hepatic or renal insufficiency, and myasthenia gravis
Class III antiarrhythmics
These agents establish a chemical conversion to sinus rhythm.
Amiodarone (Cordarone)
Prolongs action potential and refractory period in myocardium, inhibits adrenergic stimulation, and may inhibit AV conduction and sinus node performance. Blocks sodium channels with high affinity for inactive channels. Blocks potassium channels and weakly blocks calcium channels. In addition, noncompetitively blocks alpha- and beta-adrenergic receptors.
Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers.
Adult
5 mg/kg IV over 30 min followed by 1200 mg/d
Pediatric
6.3 mg/kg (average loading dose) IV
Increases blood levels and effects of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause additive effect and decrease myocardial contractility further; cimetidine may increase levels
Documented hypersensitivity; complete AV block; intraventricular conduction defects; concurrent ritonavir or sparfloxacin
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Adverse effects include pulmonary toxicity and fibrosis, which can be life threatening
Caution in thyroid or liver disease
Dofetilide (Tikosyn)
Prototype of "pure" class III agent. Blocks delayed rectifier current (IKr) and prolongs action potential duration; indeed, even at higher magnitudes, has no effect upon other depolarizing potassium currents (IKs and IKl). Terminates induced re-entrant tachyarrhythmias (atrial fibrillation/flutter and ventricular tachycardia) and prevents their re-induction. At clinically prescribed concentrations, has no effect on sodium channels, which are associated with class I effects. Furthermore, no effect noted on alpha- or beta-adrenergic receptors.
Indicated for maintenance of NSR in patients with atrial fibrillation/atrial flutter lasting >1 wk who have been converted to NSR. Also indicated for conversion of AF and atrial flutter to NSR. Has not been effective for patients with paroxysmal AF. Torsade de pointes is only arrhythmia showing dose-response relationship. Prevalence with supraventricular arrhythmia is 0.8%. Majority of torsade de pointes episodes occur within first 3 d of therapy.
If patients do not convert to NSR within 24 h of initiation of therapy, electrical cardioversion should be considered.
Has no effect on cardiac output, cardiac index, stroke volume index, or systemic vascular resistance. Does not affect blood pressure.
Must be initiated with continuous ECG monitoring and monitoring continued for >12 h after conversion. Dose must be individualized according to CrCl and QTc (use QT interval if heart rate <60/min). No information on use of this drug for heart rates <50/min. Patients with AF should receive anticoagulant therapy according to established practice. Anticoagulation should be continued after cardioversion as per usual practice.
Adult
Step 1. Determine QTc using average of 5-10 beats; if QTc >440 ms (500 ms in those with ventricular conduction abnormalities), dofetilide is contraindicated
Step 2. Calculate CrCl prior to administration, using formulas:
CrCl (male) = (140-age) X body weight (kg)/72 X serum creatinine (mg/dL)
CrCl (female) = (140-age) X body weight (kg) X 0.85/72 X serum creatinine (mg/dL)
Step 3. Determine starting dose as follows:
CrCl >60 mL/min: 500 mcg PO bid
CrCl 40-60 mL/min: 250 mcg PO bid
CrCl 20-40 mL/min: 125 mcg PO bid
CrCl <20 mL/min: Contraindicated
Step 4. Administer dofetilide and begin continuous ECG monitoring
Step 5. 2-3 h after administration of first dose, determine QTc; if QTc has increased by >15% compared to baseline or if QTc is >500 ms (550 ms in those with ventricular conduction abnormalities), adjust subsequent doses as follows:
Starting dose 500 mcg bid: 250 mcg bid
Starting dose 250 mcg bid: 125 mcg bid
Starting dose 125 mcg bid: 125 mcg qd
Step 6. Continuously monitor for minimum of 3 d or for a minimum of 12 h after conversion to NSR, whichever is greater
Pediatric
<18 years: Not established
Drugs known to increase plasma levels of dofetilide include verapamil, cimetidine, trimethoprim, and ketoconazole; known inhibitors of renal cation transport include prochlorperazine and megestrol; drugs that prolong QT interval include, but are not limited to, phenothiazines, cisapride, bepridil, tricyclic antidepressants, and certain oral macrolide antibiotics
Class I or class III antiarrhythmic agents should be held for at least 3 half-lives prior to dosing (terminal half-life is 10 h)
Does not affect pharmacokinetics of digoxin, but concomitant use of these 2 drugs has been associated with higher incidence of torsade de pointes; warfarin pharmacodynamics not altered by this medication
Congenital or acquired long QT syndromes; baseline QT interval or QTc >440 ms (500 ms in patients with ventricular conduction abnormalities); severe renal impairment (CrCl <20 mL/min); concomitant use of verapamil, cimetidine, trimethoprim, ketoconazole, or any drug that increases plasma levels of dofetilide, inhibits renal cation transport, or prolongs QT interval
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Use caution in renal impairment (CrCl guides dosing), hepatic impairment (dofetilide has not been studied in patients with severe hepatic impairment), or cardiac conduction problems (drug has no effect on AV node conduction in patients with first-degree heart block, but effects in second- and third-degree block not studied); has been used safely in conjunction with pacemakers
Ibutilide (Corvert)
Newer class III antiarrhythmic agent that may work by increasing action potential duration and thereby changing atrial cycle length variability. Mean time to conversion is 30 min. Two thirds of patients who converted were in sinus rhythm at 24 h. Ventricular arrhythmias occurred in 9.6% of patients and mostly were PVCs. The incidence of torsades de pointes was <2%.
Adult
<60 kg: 0.01 mg/kg IV over 10 min
>60 kg: 1 mg IV over 10 min; a second infusion of equal strength can be given 10 min after first prn
Pediatric
Not established
Ibutilide increases toxicity of quinidine and procainamide; concurrent administration of ibutilide with tricyclic antidepressants and phenothiazines may prolong QT interval (one report noted an 8.3% incidence of torsades de pointes); toxicity of digoxin increases when administered concurrently with ibutilide
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal or hepatic impairment
Antiarrhythmic Agent, Miscellaneous
Dronedarone is an antiarrhythmic agent with properties belonging to all 4 Vaughn-Williams antiarrhythmic classes.
Dronedarone (Multaq)
Blocks sodium channels, blocks beta1-adrenergic site, and alters adenyl cyclase generation (ie, negative inotropic effects); blocks potassium channels (eg, hERG) and therefore prolongs cardiac repolarization.
In a multinational clinical trial (n >4600), dronedarone reduced cardiovascular hospitalization or death from any cause by 24% compared with placebo.
Indicated to reduce risk for cardiovascular hospitalization in patients with paroxysmal or persistent atrial fibrillation (AF) or atrial flutter (AFL), with a recent episode of AF/AFL and associated cardiovascular risk factors (ie, age >70 y, hypertension, diabetes, history of CVA, LAD >50 mm or LVEF <40%) who are in sinus rhythm or who will be cardioverted.
Adult
400 mg PO bid with meals
Pediatric
Not established
CYP3A4 substrate, moderate CYP3A4 and CYP2D6 inhibitor; P-gP inhibitor
Avoid coadministration with CYP3A4 inhibitors (eg, itraconazole, azithromycin, erythromycin, grapefruit juice) that may decrease clearance and thereby increase dronedarone plasma levels (see Contraindications); avoid use with CYP3A4 inducers (eg, rifampin, carbamazepine) because of increased clearance and consequent reduction in dronedarone serum levels; use with other drugs that prolong QT interval (eg, phenothiazine, TCAs, macrolide antibiotics, class I and III antiarrhythmic agents) may cause life-threatening arrhythmias (see Contraindications)
When coadministered with P-gP substrates (eg, digoxin), P-gP substrate bioavailability may increase (consider discontinuing P-gp substrate or decrease P-gP substrate dose by 50%)
Coadministration increases serum levels of HMG-CoA reductase inhibitors (eg, atorvastatin), thereby increasing risk for adverse effects (eg, myopathy); monitor serum levels of CYP3A substrates with narrow therapeutic indexes (eg, sirolimus, tacrolimus) if coadministered
Coadministration with beta-blockers or calcium channel blockers requires lowered dose of these agents and dose should only be increased after ECG verification of tolerability
Documented hypersensitivity; severe heart failure (ie, NYHA class IV) or NYHA class II-III with recent decompensation requiring hospitalization or referral to heart failure program; second- or third-degree heart block or sick sinus syndrome (unless functioning pacemaker in place); bradycardia <50 bpm; QTc interval >500 milliseconds (coadministration with other drugs that prolong QT interval may cause torsade de pointes[en dash]type ventricular tachycardia); severe hepatic impairment; strong CYP3A4 inhibitors
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Boxed warning: May cause critical adverse reactions, including death, in patients with recent severe heart failure
Common adverse reactions include diarrhea, nausea, vomiting, fatigue, and asthenia; discontinue if new or worsening heart failure develops; monitor QT interval; hypomagnesemia and hypokalemia may increase risk for serious arrhythmic event
Cardiac glycosides
Cardiac glycosides decrease AV nodal conduction primarily by increasing vagal tone. They are used mainly in the context of atrial fibrillation (AF) and atrial flutter with congestive heart failure (CHF).
Digitalis, Digoxin (Lanoxin)
Has direct inotropic effects in addition to indirect effects on cardiovascular system. Effects on myocardium involve both direct action on cardiac muscle that increases myocardial systolic contractions and indirect actions that result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.
Adult
In previously undigitalized patients: 400-600 mcg (0.4-0.6 mg) IV initial single dose usually produces detectable effect in 5-30 min, which becomes maximal in 1-4 h
Pediatric
<2 years: Not established
2-5 years: 25-35 mcg/kg IV
5-10 years: 15-20 mcg/kg IV
>10 years: 8-12 mcg/kg IV
Medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid
Documented hypersensitivity; beriberi heart disease; idiopathic hypertrophic subaortic stenosis; constrictive pericarditis; carotid sinus syndrome
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hypokalemia may reduce positive inotropic effect; IV calcium may produce arrhythmias in digitalized patients; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis
More on Atrial Flutter |
| Overview: Atrial Flutter |
| Differential Diagnoses & Workup: Atrial Flutter |
 Treatment & Medication: Atrial Flutter |
| Follow-up: Atrial Flutter |
| Multimedia: Atrial Flutter |
| References |
| Further Reading |
| « Previous Page | Next Page » |
References
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Sassone B, Leone O, Martinelli GN, Di Pasquale G. Acute myocardial infarction after radiofrequency catheter ablation of typical atrial flutter: histopathological findings and etiopathogenetic hypothesis. Ital Heart J. May 2004;5(5):403-7. [Medline].
Braunwald E. Heart disease: A Textbook of Cardiovascular Medicine. 5th ed. Philadelphia, Pa: WB Saunders Co; 1997:1997:641-656.
Galve E, Rius T, Ballester R, et al. Intravenous amiodarone in treatment of recent-onset atrial fibrillation: results of a randomized, controlled study. J Am Coll Cardiol. Apr 1996;27(5):1079-82. [Medline].
Goodacre S, Irons R. ABC of clinical electrocardiography: Atrial arrhythmias. BMJ. Mar 9 2002;324(7337):594-7. [Medline].
Gronefeld GC, Wegener F, Israel CW, Teupe C, Hohnloser SH. Thromboembolic risk of patients referred for radiofrequency catheter ablation of typical atrial flutter without prior appropriate anticoagulation therapy. Pacing Clin Electrophysiol. Jan 2003;26(1 Pt 2):323-7. [Medline].
Niebauer MJ, Chung MK. Management of atrial flutter. Cardiol Rev. Sep-Oct 2001;9(5):253-8. [Medline].
Perry JC, Fenrich AL, Hulse JE, Triedman JK, Friedman RA, Lamberti JJ. Pediatric use of intravenous amiodarone: efficacy and safety in critically ill patients from a multicenter protocol. J Am Coll Cardiol. Apr 1996;27(5):1246-50. [Medline].
Pritchett EL. Management of atrial fibrillation. N Engl J Med. May 7 1992;326(19):1264-71. [Medline].
Prystowsky EN, Benson DW Jr, Fuster V, et al. Management of patients with atrial fibrillation. A Statement for Healthcare Professionals. From the Subcommittee on Electrocardiography and Electrophysiology, American Heart Association. Circulation. Mar 15 1996;93(6):1262-77. [Medline].
Sawhney NS, Feld GK. Diagnosis and management of typical atrial flutter. Med Clin North Am. Jan 2008;92(1):65-85, x. [Medline].
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Vidaillet H, Granada JF, Chyou PH, et al. A population-based study of mortality among patients with atrial fibrillation or flutter. Am J Med. Oct 1 2002;113(5):365-70. [Medline].
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Further Reading
Clinical guidelines
ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). European Heart Rhythm Association, Heart Rhythm Society, Zipes DP, Camm AJ, Borggrefe M, et al, American College of Cardiology, American Heart Association Task Force, European Society of Cardiology Committee for Practice Guidelines. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society [trunc]. J Am Coll Cardiol 2006 Sep5;48(5):e247-346. [1085 references] PubMed
Antithrombotic therapy in atrial fibrillation. American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Singer DE, Albers GW, Dalen JE, Fang MC, Go AS, Halperin JL, Lip GY, Manning WJ. Antithrombotic therapy in atrial fibrillation: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008 Jun;133(6 Suppl):546S-92S. [281 references] PubMed
Keywords
atrial flutter, heart flutter, auricular flutter, catheter ablation, atrial flutter treatment, atrial flutter causes, atrial flutter symptoms, atrial fibrillation, bradyarrhythmia, tachyarrhythmia, arrhythmia, heart disease, acute myocardial infarction, AMI, congestive heart disease, CHD, coronary artery disease, CAD, cardiovascular disease, heart attack, rhythm disturbance, palpitations, fatigue, poor exercise tolerance, dyspnea, angina, syncope, rhythm disturbance of the atria, congestive heart failure, CHF, peripheral embolization, left ventricle dysfunction, long-standing hypertension, valvular heart disease, rheumatic heart disease, left ventricular hypertrophy, diabetes, depressed left ventricular function, myotonic dystrophy, postoperative revascularization, digitalis toxicity, pulmonary embolism
