MyEClinic
MyEClinic
Health Dictionary Find a Doctor

Atrial flutter

For patient information, click here.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and keywords: A flutter; flutter

Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Roukoz A. Karam, M.D.[3]

Overview

Atrial flutter is an abnormal heart rhythm that occurs in the atria of the heart. When it first occurs, it is usually associated with a fast heart rate or tachycardia, and falls into the category of supra-ventricular tachycardias. While this rhythm occurs most often in individuals with cardiovascular disease (eg: hypertension, coronary artery disease, and cardiomyopathy), it may occur spontaneously in people with otherwise normal hearts. It is typically not a stable rhythm, and frequently degenerates into atrial fibrillation. However, it does rarely persist for months to years.

Classification

There are two types of atrial flutter, the common type I and rarer type II. Most individuals with atrial flutter will manifest only one of these. Rarely someone may manifest both types; however, they can only manifest one type at a time.

Pathophysiology

Atrial flutter is a form of cardiac arrhythmia characterized by an atrial rate ranging from 240 to 400 beats per minute. It is the most common atrial tachycardia after atrial fibrillation, with a uniform and regular continuous wave-form. It is caused by a reentrant rhythm in either the right or left atrium. Some degree of atrio-ventricular block is usually associated with atrial flutter. Similar to atrial fibrillation the rate of ventricular beating depends on the degree of conduction through the atrio-ventricular node. Usual scenario is 2:1 or 4:1 conduction but occasionally there can exist a 1:1 conduction.

Causes

Atrial flutter is caused by a re-entrant rhythm in either the right or left atrium. Causes of atrial flutter can be grouped into two categories, intrinsic diseases and abnormalities of the heart and diseases elsewhere in the body that can affect the heart. Most common causes of atrial flutter are coronary artery disease, hypertensive heart disease and valve abnormalities of the heart.

Differentiating Atrial flutter from other Diseases

Atrial flutter should be differentiated from atrial fibrillation, multifocal atrial tachycardia, SVT and wide complex tachycardia. An electrocardiogram artifact from tremor also can be confused with atrial flutter.

Epidemiology and Demographics

Atrial flutter is more common in elderly males. Men are affected 2.5 times more than women. The incidence of new cases every year in the USA is 200,000.

Risk Factors

Major risk factors for the development of atrial flutter are elderly age, presence of heart disease and high blood pressure.

Diagnosis

History and Symptoms

Common symptoms in patients with atrial flutter are palpitations, fluttery sensation in the chest, breathlessness and lightheadedness.

Physical Examination

The hemodynamic stability of the patient should be first assessed. The patient should also be examined for the presence of reversible causes of atrial flutter.

Electrocardiogram

Characteristic electrocardiographic findings in a patient with atrial flutter include; an atrial rate from 250-350 beats per minute, a “sawtooth” appearance to the tracings due to rapid regular undulations (F waves), and a variable ventricular rate depending on AV conduction.

Echocardiography

Transthoracic echocardiography (TTE) is used in atrial flutter to evaluate the sizes of left and right atria. Transesophageal echocardiography (TEE) is used to evaluate the presence of thrombus and selection of candidates for cardioversion.

Treatment

Medical Therapy

The management of atrial flutter is similar to that of atrial fibrillation with primary goals being control of ventricular rate, restoration of sinus rhythm, and prevention of recurrent episodes and thromboembolic episodes. In the setting of unstable hemodynamics immediate electrical cardioversion is recommended. because of the high success rate and low complication rate radiofrequency ablation is considered superior to medical therapy in atrial flutter.

References

Template:WikiDoc Sources

Historical Perspective

Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

The term flutter first appeared a century ago in 1887, with Mac William who described the visual phenomena resulting from ‘faradic stimulation of the auricles which sets them into a rapid flutter.Its first description a century ago, our understanding of atrial flutter (AFL) has evolved, from a relatively simple and unique electrocardiographic (ECG) pattern corresponding to a right atrial macroreentry, to a variety of atrial tachycardias (ATs) originating from the right atrium as well as the left atrium, and resulting from different mechanisms. The use of multielectrodes catheters and the recent development of sophisticated computerized electroanatomical mapping with virtual anatomical chambers reconstruction and fusion with the actual anatomical radiological image has improved our knowledge of AFL circuits and foci location. These technological improvements have also facilitated curative treatment with radiofrequency (RF) catheter ablation while simultaneously creating some terminological and conceptual confusion about its nature.

Historical Perspective

  • The term flutter first appeared a century ago in 1887, with Mac William who described the visual phenomena resulting from faradic stimulation of the auricles which sets them into a rapid flutter.[1][2]
  • It was only 23 years later that Jolly and Ritchie, using the Cambridge model of Einthoven’s string galvanometer recorded the first ECG example of AFL.[3]
  • A single wave circus movement mechanism was initially proposed by Lewis, but the possibility to reproduce the ECG morphology of AFL with high pacing rate or with focal aconitine injection supported a focal mechanism as another possible hypothesis.[4]
  • Both mechanisms are easily observed, the circus movement theory has been finally accepted as being by far the most frequent in man.[5]
  • A macroreentrant mechanism was finally proven by detailed mapping in the operating room, as well as in the electrophysiology laboratory.[6]

References

  1. ↑ McWilliam JA (October 1887). “Fibrillar Contraction of the Heart”. J. Physiol. (Lond.). 8 (5): 296–310. doi:10.1113/jphysiol.1887.sp000261. PMC 1485090. PMID 16991467.
  2. ↑ SCHERF D, TERRANOVA R (October 1949). “Mechanism of auricular flutter and fibrillation”. Am. J. Physiol. 159 (1): 137–42. doi:10.1152/ajplegacy.1949.159.1.137. PMID 15391089.
  3. ↑ Jolly WA, Ritchie WT (January 2003). “Auricular flutter and fibrillation. 1911”. Ann Noninvasive Electrocardiol. 8 (1): 92–6. doi:10.1046/j.1542-474x.2003.08114.x. PMID 12848819.
  4. ↑ Levy, Robert L. (1926). “AURICULAR FIBRILLATION WITH REGULAR VENTRICULAR RHYTHM AND RATE OVER SIXTY”. Archives of Internal Medicine. 38 (1): 116. doi:10.1001/archinte.1926.00120250121008. ISSN 0003-9926.
  5. ↑ “AURICULAR arrhythmias”. S. Afr. Med. J. 27 (42): 925–6. October 1953. PMID 13122200.
  6. ↑ SCHERF D (February 1947). “Studies on auricular tachycardia caused by aconitine administration”. Proc. Soc. Exp. Biol. Med. 64 (2): 233–9. doi:10.3181/00379727-64-15754. PMID 20287386.


Template:WikiDoc Sources CME Category::Cardiology

Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Atrial flutter was previously classified as either type I or type II. That terminology is no longer used. Most individuals with atrial flutter will manifest only one of these. Rarely someone may manifest both types; however, they can only manifest one type at a time. New classification is of two types, typical and atypical atrial flutter.

Old Classification

Atrial flutter was previously classified as either type I or type II. That terminology is no longer used.

  • Type I atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 340 beats/minute. However, this rate may be slowed by antiarrhythmic agents. The re-entrant loop circles the right atrium, passing through the isthmus – a body of fibrous tissue in the lower atrium between the inferior vena cava, and the tricuspid valve. Type I flutter is further divided into two subtypes, known as counterclockwise atrial flutter and clockwise atrial flutter depending on the direction of current passing through the loop. Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen. The flutter waves in this rhythm are inverted in ECG leads II, III, and aVF. The re-entry loop cycles in the opposite direction in clockwise atrial flutter, thus the flutter waves are upright in II, III, and aVF.
  • Type II flutter, also known as atypical flutter, follows a significantly different re-entry pathway to type I flutter, and is typically faster, usually 340–430 beats/minute. This type of atrial flutter is non-isthmus dependent and is believed to be due to an intraatrial reentrant circuit.

New Classification

Typical atrial flutter

  • The designation of “typical” atrial flutter involves a macroreentrant circuit traversing the cavo-tricuspid isthmus (CTI)[1][2].
  • Isthmus is the region of right atrial tissue between the orifice of the inferior vena cava and the tricuspid valve annulus. If this isthmus is involved, it is called “typical” atrial flutter or CTI-dependent atrial flutter.
  • The circuit is usually a counterclockwise rotation around the tricuspid valve, exhibiting a classic sawtooth appearance in the inferior electrocardiogram (ECG) leads (II, III, aVF).
  • If the circuit is clockwise, it is called “reverse” or “clockwise” typical flutter, exhibiting positive flutter waves in the inferior ECG leads.

Atypical atrial flutter

  • If the CTI is not involved in the underlying mechanism, then it is called “atypical” atrial flutter.[3][4]
  • This type of flutter can involve any region of the right or left atria, around areas of scar tissue due to intrinsic heart disease or surgical/ablated scar tissue. Surgical repair of congenital heart disease may lead to macroreentrant atrial flutter circuits, both typical (cavotricuspid isthmus dependent) and atypical.
  • These circuits are usually right atrial, related to anatomic obstacles and surgical scars (cavotricuspid isthmus, right atriotomy scar, atrial septal defect repair, etc).
  • Incomplete ablation lines created in attempts to cure atrial fibrillation with ablation can promote atypical atrial flutter circuits in the left atrium (mitral isthmus flutter, etc).
  • Focal atrial tachycardias with atrioventricular block may also mimic atypical atrial flutter by ECG appearance, but by electrophysiologic study the focal mechanism can be differentiated from the macroreentry seen in atrial flutter.

References

  1. ↑ Bun SS, Latcu DG, Marchlinski F, Saoudi N (September 2015). “Atrial flutter: more than just one of a kind”. Eur. Heart J. 36 (35): 2356–63. doi:10.1093/eurheartj/ehv118. PMID 25838435.
  2. ↑ Ouali S, Anselme F, Savoure A, Cribier A (June 2003). “An atypical atrial flutter of focal origin: a study using a noncontact mapping system”. Pacing Clin Electrophysiol. 26 (6): 1410–2. doi:10.1046/j.1460-9592.2003.t01-1-00200.x. PMID 12822758.
  3. ↑ Cosío FG (June 2017). “Atrial Flutter, Typical and Atypical: A Review”. Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  4. ↑ Rostock T, Konrad T, Sonnenschein S, Mollnau H, Ocete BQ, Bock K, Spittler R, Huber C, Theis C (September 2015). “[Surface ECG characteristics of right and left atrial flutter]”. Herzschrittmacherther Elektrophysiol (in German). 26 (3): 208–13. doi:10.1007/s00399-015-0386-2. PMID 26260681.

Template:WH Template:WS CME Category::Cardiology

Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Atrial flutter is a form of cardiac arrhythmia characterized by an atrial rate ranging from 240 to 400 beats per minute. It is the most common atrial tachycardia after atrial fibrillation, with a uniform and regular continuous wave-form.[1] It is caused by a reentrant rhythm in either the right or left atrium. Some degree of atrio-ventricular block is usually associated with atrial flutter. Similar to atrial fibrillation the rate of ventricular beating depends on the degree of conduction through the atrioventricular node. The usual scenario is 2:1 or 4:1 conduction but occasionally there can exist a 1:1 conduction.

Pathophysiology

Normal Conduction in the Heart

  • The natural pacemaker of the heart, the sinoatrial (SA) node is located in the right atrium. Impulses originate from this sinus node and travel accross the atrium to reach the AV node.
  • The atrioventricular node is an area of specialized conducting tissue between the atria and the ventricles of the heart, which conducts the normal electrical impulse from the atria to the ventricles.
  • The atrioventricular node delays impulses for ~0.1 second before allowing impulses through to the His-Purkinje conduction system, which spreads impulses to the ventricular walls. The reason it is important to delay the cardiac impulse is to ensure that the atria have ejected their blood into the ventricles before the ventricles contract.[2]

Conduction in Atrial Flutter

Typically initiated by a premature electrical impulse arising in the atria, atrial flutter is propagated due to differences in refractory periods of atrial tissue. This creates a self-perpetuating loop of electrical activity moving around the atrium.

In Type 1 atrial flutter most commonly the conduction is in counterclockwise direction around the tricuspid valve causing a caudocranial activation of the atrial septum. Clockwise activation around the tricuspid annulus is less common compared to the counterclockwise direction and is called isthmus dependent flutter or reverse typical atrial flutter. The slowly conducting reentrant circuit is believed to be located in the low right atrial isthmus.

Type 2 atrial flutter also known as atypical flutter usually results from an intra-atrial reentrant circuit that is short. It is believed to be originating from abnormal anatomy in the right atrium or the left atrium (surgical scars, irregular pulmonary veins, disturbed mitral annulus).

The impact and symptoms of atrial flutter depend on the heart rate of the patient. Heart rate is a measure of the ventricular rather than atrial activity. Impulses from the atria are conducted to the ventricles through the atrio-ventricular node. Due primarily to its longer refractory period, the AV node exerts a protective effect on heart rate by blocking atrial impulses in excess of about 180 beats/minute (This block is dependent on the age of the patient, and can be calculated roughly by subtracting patient age from 220). If the flutter rate is 300/minute only half of these impulses will be conducted, giving a ventricular rate of 150/minute, i.e., 2:1 block. The addition of rate-controlling drugs or conduction system disease can increase this block substantially (see image below).

References

  1. ↑ Dhar S, Lidhoo P, Koul D, Dhar S, Bakhshi M, Deger FT (2009). “Current concepts and management strategies in atrial flutter”. South. Med. J. 102 (9): 917–22. doi:10.1097/SMJ.0b013e3181b0f4b8. PMID 19668035. Unknown parameter |month= ignored (help)
  2. ↑ Campbell, N., & Reece, J. (2002). Biology. 6th ed. San Francisco: Benjamin Cummings.

Template:WH Template:WS CME Category::Cardiology

Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vendhan Ramanujam M.B.B.S [2]

Overview

Atrial flutter is caused by a re-entrant rhythm in either the right or left atrium. Causes of atrial flutter can be grouped into two categories which are intrinsic diseases of the heart and extrinsic diseases that can affect the heart. The most common causes of atrial flutter are coronary artery disease, hypertensive heart disease and valve abnormalities of the heart.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular Aortic regurgitation, aortic stenosis, atrial myxoma, cardiomyopathy, congenital heart disease, congestive heart failure, coronary artery disease, dilated cardiomyopathy, holiday heart syndrome, hypertensive heart disease, hypertrophic cardiomyopathy, ischemic heart disease, Lown-Ganong-Levine syndrome, mitral regurgitation, mitral valve prolapse, mitral valve stenosis, myocardial infarction, myocardial ischemia, neonatal coxsackie myocarditis, pericarditis, rheumatic fever, rheumatic heart disease, sick sinus syndrome, Wolff-Parkinson-White syndrome
Chemical / poisoning Carbon monoxide poisoning
Dermatologic No underlying causes
Drug Side Effect Amphetamines, cyclophosphamide, disopyramide, febuxostat, flecainide, Ixabepilone, lacosamide, lithium, orlistat, procainamide, propafenone, quinidine, type Ia antiarrhythmic agents, type Ic antiarrhythmic agents, type III antiarrhythmic agents
Ear Nose Throat No underlying causes
Endocrine Hyperthyroidism, pheochromocytoma, thyrotoxicosis
Environmental No underlying causes
Gastroenterologic Crohn’s disease, ulcerative colitis
Genetic Myotonic dystrophy
Hematologic Nonimmune hydrops fetalis
Iatrogenic Cardiac surgery, cardiac transplantation, heart bypass surgery, incomplete ablation procedures, open heart surgery, temporary cardiac pacing
Infectious Disease Amoebiasis, neonatal coxsackie myocarditis, rheumatic fever
Musculoskeletal / Ortho Myotonic dystrophy
Neurologic Subarachnoid hemorrhage
Nutritional / Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Atrial myxoma, lung cancer
Opthalmologic No underlying causes
Overdose / Toxicity Alcohol, caffeine, cocaine, digitalis toxicity
Psychiatric Anxiety
Pulmonary Chronic obstructive pulmonary disease, emphysema, hypoxia, lung cancer, obstructive sleep apnea, pneumonia, pulmonary embolism
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Ankylosing spondylitis, juvenile idiopathic arthritis, psoriatic arthritis, reactive arthritis, sarcoidosis, spondyloarthritis
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Stress

Causes in Alphabetical Order

References

  1. ↑ Gutierrez SD, Earing MG, Singh AK, Tweddell JS, Bartz PJ (2012). “Atrial Tachyarrhythmias and the Cox-maze Procedure in Congenital Heart Disease”. Congenit Heart Dis. doi:10.1111/chd.12031. PMID 23280242. Unknown parameter |month= ignored (help)
  2. ↑ Granada, J.; Uribe, W.; Chyou, PH.; Maassen, K.; Vierkant, R.; Smith, PN.; Hayes, J.; Eaker, E.; Vidaillet, H. (2000). “Incidence and predictors of atrial flutter in the general population”. J Am Coll Cardiol. 36 (7): 2242–6. PMID 11127467. Unknown parameter |month= ignored (help)
  3. ↑ Murali, A.; Balu, K.; Paari, V.; Rajendiran, G. (2011). “Atrial flutter and pericarditis–a rare complication of right lobe amoebic liver abscess”. Med J Malaysia. 66 (5): 499–500. PMID 22390111. Unknown parameter |month= ignored (help)
  4. ↑ Fukamizu S, Sakurada H, Hayashi T; et al. (2012). “Macroreentrant Atrial Tachycardia in Patients without Previous Atrial Surgery or Catheter Ablation: Clinical and Electrophysiological Characteristics of Scar-Related Left Atrial Anterior Wall Reentry”. J. Cardiovasc. Electrophysiol. doi:10.1111/jce.12059. PMID 23279349. Unknown parameter |month= ignored (help)
  5. ↑ Nevzorov, R.; Ben-Gal, T.; Strasberg, B.; Haim, M. (2012). “Atrial flutter in a post-transplant recipient”. Isr Med Assoc J. 14 (7): 448–9. PMID 22953623. Unknown parameter |month= ignored (help)
  6. ↑ FRIEDBERG, CK.; DONOSO, E. (1960). “Arrhythmias and conduction disturbances due to digitalis”. Prog Cardiovasc Dis. 2: 408–31. PMID 13825021. Unknown parameter |month= ignored (help)
  7. ↑ JULIAN DG, VALENTINE PA, MILLER GG (1964). “DISTURBANCES OF RATE, RHYTHM AND CONDUCTION IN ACUTE MYOCARDIAL INFARCTION: A PROSPECTIVE STUDY OF 100 CONSECUTIVE UNSELECTED PATIENTS WITH THE AID OF ELECTROCARDIOGRAPHIC MONITORING”. Am J Med. 37: 915–27. PMID 14246092.
  8. ↑ Namboodiri N, Stiles MK, Young GD, Sanders P (2012). “Electrophysiological features of atrial flutter in cardiac sarcoidosis: a report of two cases”. Indian Pacing Electrophysiol J. 12 (6): 284–9. PMC 3513242. PMID 23233762. Unknown parameter |month= ignored (help)
  9. ↑ Varma, N.; Helms, R.; Benson, DW.; Sanagala, T. (2011). “Congenital sick sinus syndrome with atrial inexcitability and coronary sinus flutter”. Circ Arrhythm Electrophysiol. 4 (5): e52–8. doi:10.1161/CIRCEP.111.964213. PMID 22010118. Unknown parameter |month= ignored (help)
  10. ↑ Tolat, A.; Krishnan, S.; Lippman, N.; Dell’Orfano, J.; Berns, E. (2010). “Advanced heart block and atrial flutter in a patient with HLA B27 spondyloarthropathy”. Europace. 12 (6): 903–4. doi:10.1093/europace/euq008. PMID 20118489. Unknown parameter |month= ignored (help)

Template:WH Template:WS CME Category::Cardiology

Differentiating Atrial flutter from other Diseases

Differentiating Atrial flutter from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Syed Hassan A. Kazmi BSc, MD [3]

Overview

Atrial flutter should be differentiated from atrial fibrillation, multifocal atrial tachycardia, SVT and wide complex tachycardia. An electrocardiogram artifact from tremor also can be confused with atrial flutter.

Differentiating Atrial flutter from other Diseases


Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)[1][2]
  • Irregularly irregular
  • Absent
  • Fibrillatory waves
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter[3][4]
  • Regular or Irregular
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Sawtooth pattern of P waves at 250 to 350 bpm
  • Biphasic deflection in V1
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)[5][6][7][8]
  • Regular
  • 140-280 bpm
  • Slow-Fast AVNRT:
    • Pseudo-S wave in leads II, III, and AVF
    • Pseudo-R’ in lead V1.
  • Fast-Slow AVNRT
  • Slow-Slow AVNRT
  • Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)
  • Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • QRS alternans may be present
Multifocal Atrial Tachycardia[9][10]
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Varying morphology from at least three different foci
  • Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)[11][12]
  • Regular except when disturbed by premature beat(s)
  • 80-120 bpm
  • Upright
  • > 0.12 second
  • May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node
  • Ashman’s Phenomenon:
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome[13][14]
  • Regular
  • Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm
  • Less than 0.12 seconds
  • A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway
  • A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.
Ventricular Fibrillation (VF)[15][16][17]
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia[18][19]
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent
  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

References

  1. ↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). “The ECG as a tool to determine atrial fibrillation complexity”. Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
  2. ↑ Harris K, Edwards D, Mant J (2012). “How can we best detect atrial fibrillation?”. J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
  3. ↑ Cosío FG (June 2017). “Atrial Flutter, Typical and Atypical: A Review”. Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
  4. ↑ Boyer, Melissa; Koplan, Bruce A. (2005). “Atrial Flutter”. Circulation. 112 (22). doi:10.1161/CIRCULATIONAHA.105.540476. ISSN 0009-7322.
  5. ↑ Katritsis DG, Josephson ME (August 2016). “Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia”. Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
  6. ↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). “Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway”. Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
  7. ↑ “Atrioventricular Nodal Reentry Tachycardia (AVNRT) – StatPearls – NCBI Bookshelf”.
  8. ↑ Schernthaner C, Danmayr F, Strohmer B (2014). “Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias”. Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
  9. ↑ Scher DL, Arsura EL (September 1989). “Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment”. Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
  10. ↑ Goodacre S, Irons R (March 2002). “ABC of clinical electrocardiography: Atrial arrhythmias”. BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
  11. ↑ Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). “Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome”. J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
  12. ↑ Strasburger JF, Cheulkar B, Wichman HJ (December 2007). “Perinatal arrhythmias: diagnosis and management”. Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
  13. ↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). “Evaluation and management of wolff-Parkinson-white in athletes”. Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
  14. ↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). “Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues”. Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
  15. ↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). “Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction”. J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
  16. ↑ Samie FH, Jalife J (May 2001). “Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart”. Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
  17. ↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). “Sudden cardiac death: epidemiology and risk factors”. Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
  18. ↑ Koplan BA, Stevenson WG (March 2009). “Ventricular tachycardia and sudden cardiac death”. Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
  19. ↑ Levis JT (2011). “ECG Diagnosis: Monomorphic Ventricular Tachycardia”. Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

Template:WH Template:WS CME Category::Cardiology

Risk Factors

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Farima Kahe M.D. [2]

Overview

Common risk factors in the development of atrial flutter include thyrotoxicosis, obesity,pericarditis, pulmonary embolism and diabetes. Less common risk factors include acute myocardial infarction, cardiac surgery, digitalis toxicity, electrolyte imbalance and antiarrhythmic drugs.

Risk Factors

Common risk factors in the development of atrial flutter include thyrotoxicosis, obesity, pericarditis, pulmonary embolism and diabetes.

Common Risk Factors

Less Common Risk Factors

References

  1. ↑ Rahman F, Wang N, Yin X, Ellinor PT, Lubitz SA, LeLorier PA, McManus DD, Sullivan LM, Seshadri S, Vasan RS, Benjamin EJ, Magnani JW (January 2016). “Atrial flutter: Clinical risk factors and adverse outcomes in the Framingham Heart Study”. Heart Rhythm. 13 (1): 233–40. doi:10.1016/j.hrthm.2015.07.031. PMC 4698205. PMID 26226213.
  2. ↑ FRIEDBERG CK, DONOSO E (March 1960). “Arrhythmias and conduction disturbances due to digitalis”. Prog Cardiovasc Dis. 2: 408–31. doi:10.1016/s0033-0620(60)80002-3. PMID 13825021.
  3. ↑ Suda K, Matsumura M, Hayashi Y (February 2004). “Myotonic dystrophy presenting as atrial flutter in childhood”. Cardiol Young. 14 (1): 89–92. doi:10.1017/s1047951104001179. PMID 15237679.

Template:WH Template:WS CME Category::Cardiology

Screening

Screening

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Roukoz A. Karam, M.D.[2]

Overview

There is insufficient evidence to recommend routine screening for atrial flutter.

Screening

There is insufficient evidence to recommend routine screening for atrial flutter.

References


Template:WikiDoc Sources CME Category::Cardiology

Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Atrial flutter by nature occurs and then subsides. There are several complications that can occur, including hypotension, heart failure, angina, stroke, ventricular fibrillation, and sudden cardiac death. Prognosis varies from person to person and depends on the underlying cause and the presence of other risk factors.

Natural History, Complications, and Prognosis

Natural History

Atrial flutter is by nature unstable. It usually reverts back to either sinus rhythm or atrial fibrillation. Chronic atrial flutter state is very rare.[1][2]

Complications


Prognosis

The prognosis of the patient depends on the underlying cause of flutter. After treating the acute episode of atrial flutter, sinus rhythm is usually restored and chronic therapy is not usually required. It is more difficult to control the heart rate in flutter compared to that in atrial fibrillation. It is very difficult to control the rate in a chronic flutter, as it is not responsive to antiarrhythmic agents. The risk for thromboembolism in atrial flutter is nearly similar to that of atrial fibrillation. The recurrence rate of flutter is very low in patients undergoing catheter ablation for type 1 flutter indicating a good prognosis.

References

  1. ↑ Halligan SC, Gersh BJ, Brown RD, Rosales AG, Munger TM, Shen WK; et al. (2004). “The natural history of lone atrial flutter”. Ann Intern Med. 140 (4): 265–8. doi:10.7326/0003-4819-140-4-200402170-00008. PMID 14970149.
  2. ↑ Halligan SC, Gersh BJ, Brown RD, Rosales AG, Munger TM, Shen WK; et al. (2004). “The natural history of lone atrial flutter”. Ann Intern Med. 140 (4): 265–8. doi:10.7326/0003-4819-140-4-200402170-00008. PMID 14970149.
  3. ↑ C. J. Lanzarotti & B. Olshansky (1997). “Thromboembolism in chronic atrial flutter: is the risk underestimated?”. Journal of the American College of Cardiology. 30 (6): 1506–1511. doi:10.1016/s0735-1097(97)00326-4. PMID 9362409. Unknown parameter |month= ignored (help)

Template:WH Template:WS CME Category::Cardiology

Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | EKG Examples | Chest X Ray | Echocardiography | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical Therapy | Surgery | Primary Prevention | Secondary Prevention | Cost-Effectiveness of Therapy | Future or Investigational Therapies

Case Studies

Case Studies

Case #1

Related Chapters


Template:WikiDoc Sources CME Category::Cardiology

Looking for the patient version?

Back to the patient-friendly article

Imprint

Privacy Policy

Terms and Conditions

© 2026 MyEClinic – IFTM Institut für Telematik in der Medizin GmbH