History
Symptoms in patients with atrial flutter typically reflect decreased cardiac output as a result of the rapid ventricular rate. Typical symptoms include the following:
-
Palpitations
-
Fatigue or poor exercise tolerance
-
Mild dyspnea
-
Presyncope
Less common symptoms include angina, profound dyspnea, or syncope resulting from compromised left ventricular function. Thromboembolic events are possible with this arrhythmia. In addition, patients may have symptoms of the conditions that are causing the atrial flutter. These may be noncardiac (eg, hyperthyroidism or pulmonary disease) or cardiac.
The clinician should attempt to elicit information about factors that may have precipitated the episode of atrial flutter, including alcohol, as well as medical conditions (eg, pneumonia or acute myocardial infarction) and surgical procedures. An effort should also be made to elicit any history of using stimulant drugs (eg, ginseng, cocaine, ephedra, or methamphetamine).
Determining when the onset of symptoms occurred is critical, in that the duration of the episode affects management. For atrial flutter lasting longer than 48 hours, anticoagulation with warfarin or transesophageal echocardiography is required to rule out thrombus in the left atrium before cardioversion to sinus rhythm. In patients with a history of atrial flutter, the history should include precipitating causes and modes of termination of the arrhythmia.
Atrial flutter rhythm itself is unstable and usually reverts either to atrial fibrillation or to sinus rhythm. It would be unusual but certainly not impossible for a patient to remain in stable chronic atrial flutter. A history of preexcitation syndrome (Wolff-Parkinson-White) indicates a need for caution; these patients are at risk for 1:1 conduction of the flutter waves, which can cause ventricular fibrillation.
Patients with concurrently diagnosed new rapid atrial fibrillation or atrial flutter and new reduced left ventricular ejection fraction typically have heavy alcohol intake and a high rate prevalence of left atrial appendage thrombi. [10]
Physical Examination
The patient’s general appearance and vital signs are important for determining the urgency of restoring sinus rhythm. Thus, the initial cardiopulmonary evaluation and monitoring for signs of cardiac or pulmonary failure help guide initial management.
Pay careful attention to the heart rate, blood pressure, and oxygen saturation. Tachycardia may or may not be present, depending on the degree of atrioventricular (AV) block associated with the atrial flutter activity.
The heart rate is often approximately 150 beats/min because of a 2:1 AV block. (This depends on the atrial firing rate, which may be influenced by medications as well as by intrinsic cardiac factors.) The venous pulsations may be more rapid at the rate of the flutter. Because the AV block may be variable, the pulse may be regular or slightly irregular. Hypotension is possible, but normal blood pressure is more commonly observed.
Other elements of the physical examination are as follows:
-
Palpate the neck and thyroid gland for goiter
-
Evaluate the neck for jugular venous distention
-
Auscultate the lungs for rales or crackles
-
Auscultate the heart for extra heart sounds and murmurs
-
Palpate the point of maximum impulse on the chest wall
-
Assess the lower extremities for edema or impaired perfusion
If embolization has occurred from intermittent atrial flutter, findings are related to brain or peripheral vascular involvement. In addition to neurologic insult, other complications of atrial flutter may include the following:
-
Embolization (arterial)
-
Congestive heart failure
-
Severe bradycardia
-
Myocardial rate–related ischemia
-
Anatomy of classic counterclockwise atrial flutter. This image demonstrates an oblique view of the right atrium and shows some crucial structures. The isthmus of tissue responsible for atrial flutter is seen anterior to the coronary sinus (CS) orifice. The eustachian ridge is part of the crista terminalis that separates the roughened part of the right atrium from the smooth septal part of the right atrium. IVC = inferior vena cava; SVC = superior vena cava.
-
Typical counterclockwise atrial flutter. This 3-dimensional electroanatomic map of a tricuspid valve and right atrium shows the activation pattern displayed in color format. Red is early and blue is late, relative to a fixed point in time. Activation travels in counterclockwise direction.
-
A 12-Lead electrocardiogram of typical atrial flutter. Note the negative sawtooth pattern of the flutter waves in leads II, III, and aVF.
-
Electrocardiogram of atypical left atrial flutter.
-
3-Dimensional electroanatomic map of typical atrial flutter. Colors progress from blue to red to white and represent the relative conduction time in the right atrium (early to late). An ablation line (red dots) has been created on the tricuspid ridge extending to the inferior vena cava. This ablation line interrupts the flutter circuit. CSO = coronary sinus os; IVC = inferior vena cava; RAA = right atrial appendage; TV = tricuspid valve annulus.
-
Rhythm strips demonstrating typical atrial flutter unmasked by adenosine (Adenocard).
Tables
Type of Tachycardia |
Treatment (Grade) |
Not Mentioned in 2019 Guidelines |
Narrow QRS tachycardias |
Verapamil and diltiazem; beta-blockers (now all are grade IIa) |
Amiodarone, digoxin |
Wide QRS tachycardias |
Procainamide, adenosine (both grade IIa); amiodarone (IIb) |
Sotalol, lidocaine |
Inappropriate sinus tachycardia |
Beta-blockers (IIa) |
Verapamil/diltiazem, catheter ablation |
Postural orthostatic tachycardia syndrome |
Salt and fluid intake (IIb) |
Head-up tilt sleep, compression stockings, selective beta-blockers, fludrocortisone, clonidine, methylphenidate, fluoxetine, erythropoietin, ergotaminel octreotide, phenobarbitone |
Focal atrial tachycardia |
Acute: beta-blockers (IIa); flecainide/propafenone, amiodarone (IIb) |
Acute: procainamide, sotalol, digoxin |
Chronic: beta-blockers; verapamil and diltiazem (all IIa) |
Chronic: amiodarone, sotalol, disopyramide |
|
Atrial flutter |
Acute: ibutilide (I); verapamil and diltiazem, beta-blockers (all IIa); atrial or transesophageal pacing (IIb); flecainide/propafenone (III) |
Acute: digitalis |
Chronic: — |
Chronic: dofetilide, sotalol, flecainide, propafenone, procainamide, quinidine, disopyramide |
|
Atrioventricular nodal re-entrant tachycardia (AVNRT) |
Acute: — |
Acute: amiodarone, sotalol, flecainide, propafenone |
Chronic: verapamil and diltiazem; beta-blockers (all IIa) |
Chronic: amiodarone, sotalol, flecainide, propafenone, “pill-in-the-pocket” approach |
|
Atrioventricular re-entrant tachycardia (AVRT) |
Beta-blockers (IIa); flecainide/propafenone (IIb) |
Amiodarone, sotalol, “pill-in-the-pocket” approach |
SVT in pregnancy |
Verapamil (IIa); catheter ablation (IIa when fluoroless ablation is available) |
Sotalol, propafenone, quinidine, procainamide |
Adapted from Brugada J, Katritsis DG, Arbelo E, et al, for the ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2019 Aug 31;ehz467. https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz467/5556821 |
||
