Atrial flutter
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Background
- A form of supraventricular tachycardia that is caused by a re-entry circuit, typically within the right atrium
- Second most common arrhythmia, after atrial fibrillation
- Defined by atrial rate of 250-350, classically 300
- Associated with underlying diseases that cause atrial remodeling/dilation, such as hypertension, chronic obstructive pulmonary disease, heart failure, pulmonary hypertension
- Acutely, may be precipitated by antiarrhythmic medications, acute coronary syndrome, or cardiac surgery/procedures
Clinical Features
- Asymptomatic
- Palpitations
- Fatigue
- Dyspnea
- Pre-syncope/syncope
- Hypotension
Differential Diagnosis
Can be difficult to distinguish from atrial fibrillation
Narrow-complex tachycardia
- Regular
- AV Node Independent
- Sinus tachycardia
- Atrial tachycardia (uni-focal or multi-focal)
- Atrial fibrillation
- Atrial flutter
- Idiopathic fascicular left ventricular tachycardia
- AV Node Dependent
- AV Node Independent
- Irregular
- Multifocal atrial tachycardia (MAT)
- Sinus tachycardia with frequent PACs, PJCs, PVCs
- Atrial fibrillation
- Atrial flutter with variable conduction
- Digoxin Toxicity
Wide-complex tachycardia
Assume any wide-complex tachycardia is ventricular tachycardia until proven otherwise (it is safer to incorrectly assume a ventricular dysrhythmia than supraventricular tachycardia with abberancy)
- Regular
- Monomorphic ventricular tachycardia
- PSVT with aberrant conduction:
- PSVT with bundle branch block^
- PSVT with accessory pathway
- Atrial flutter with bundle branch block^
- Sinus tachycardia with bundle branch block^
- Accelerated idioventricular rhythm (consider if less than or ~120 bpm)
- Metabolic
- Irregular
- Atrial fibrillation/atrial flutter with variable AV conduction AND bundle branch block^
- Atrial fibrillation/atrial flutter with variable AV conduction AND accessory pathway (e.g. WPW)
- Atrial fibrillation + hyperkalemia
- Polymorphic ventricular tachycardia
^Fixed or rate-related
Palpitations
- Arrhythmias:
- Non-arrhythmic cardiac causes:
- Psychiatric causes:
- Drugs and Medications:
- Alcohol
- Caffeine
- Drugs of abuse (e.g. cocaine)
- Medications (e.g. digoxin, theophylline)
- Tobacco
- Misc
Evaluation
- ECG
- CBC
- Chem 7
- Magnesium level
- Troponin if patient has chest pain
- Cardiac Echo - if signs of new/worsening heart failure
ECG
- Narrow complex tachycardia
- Usually regular unless variable AV conduction present
- Usually narrow unless aberrancy present
- Typical P waves are absent, but flutter waves (sawtooth pattern) are found in inferior leads
- Hallmark is discordance in flutter wave direction between inferior leads and V1; see below for specific types
- Atrial rate near 300, appearing as flutter waves at 300 bpm
- Ventricular rate = 300 divided by the conduction ratio
- 2:1 block = 150 bpm
- 3:1 block = 100 bpm, and so on
- Conduction ratio depends on sympathetic/parasympathetic balance, AV node refractoriness, AV node disease, AV nodal blockers
- 1:1 conduction can be unstable
- Suggests pre-excitation, sympathetic excess, parasympathetic withdrawal, Class 1C anti-arrhythmic use
- Less common since AV node refractory period prevents 1:1 conduction
- 2:1 conduction is most common
- Suspect atrial flutter whenever ventricular rate is approximately 150
- Note flutter waves may be mistaken for P and T waves
- Conduction >2:1
- More commonly even ratio
- Suggests AV nodal blocking agents or AV node disease
- Variable block
- Difficult to distinguish from atrial fibrillation
- Look for: R-R interval that is multiple of P-P interval and mathematical relationship between R-R intervals (alternating between 2:1, 3:1, 4:1, etc)
- A-fib is completely irregular with no relationship between intervals
- 1:1 conduction can be unstable
- Amal Mattu recommends flipping ECG 180 to easily see inverted P waves or speed machine up to 50 mm/s to stretch out ECG
Types
- Type 1 (Typical Atrial Flutter)
- Re-entry circuit of the cavotricuspid-isthmus (CTI) pathway in the right atrium
- Anticlockwise circuit- 90% of cases
- Inverted flutter waves in inferior leads
- Positive flutter waves in V1
- Clockwise circuit
- Positive flutter waves in inferior leads
- Inverted flutter waves in V1
- Anticlockwise circuit- 90% of cases
- Re-entry circuit of the cavotricuspid-isthmus (CTI) pathway in the right atrium
- Type 2 (Atypical Atrial Flutter)
- Not associated with the CTI pathway, but may be due to arrhythmogenic scars from prior atrial instrumentation
- Does not meet criteria for typical atrial flutter
- Less amenable to treatment
Management
Unstable
- Synchronized cardioversion
- Atrial flutter - start at 50 J
- Atrial fibrillation - start at 200 J
- Indications: ischemic chest pain, SBP < 90, acute pulmonary edema, altered mental status
- If shock does not work:
- Verify not preexcitation
- Increase diastolic BP to perfuse the heart
- Push-dose phenylephrine
- Will maintain BP when give rate-control medications
- 50-200mcg q2-5min with goal DBP >60
- Push-dose phenylephrine
- Amiodarone 150mg over 10min (preferably through central venous access) OR diltiazem 2.5mg/min until HR<100 or max 50mg
Stable and Asymptomatic
- If mild or no symptoms and pulse only mildly elevated (<110bpm) ok to manage with PO meds
- Less reactive to PO medication than atrial fibrillation
- Cardioversion is preferred and treats 96-97% of atrial flutter[1]
Stable and Symptomatic
- Goal <110bpm
- Make sure you are not slowing down a normal physiologic response (e.g. fever, hypoxia, etc)
- RACE-II trial demonstrated that lenient control (goal HR < 110bpm) was noninferior to strict control (HR < 80 bpm) in preventing the primary outcome[2]
Cardioversion
- Consider for:[3]
- Symptoms <48hr
- New diagnosis
- No history of similar episodes
- No LV dysfunction
- No mitral valve disease
- No prior thromboembolic event
- Already Anticoagulated
- If cardioversion is considered, pretreatment with rate or rhythm control medications can reduce effectiveness[4]
- 90% effective, 60% effective with pretreatment
Anticoagulation Prior to Cardioversion
- Anticoagulation with Heparin or LMWH should be considered before cardioversion if time permits, otherwise immediately after cardioversion. (unless you are sure it has been <48 hours since onset of afib) [5][6] [7]
- Generally cardioversion while anti-coagulated is believed to be safe with a 1.3% risk of thromboembolism if on aspirin or other anticoagulant[8] However the risk may be as great as 2% risk after 48 hours and preference should be given to anticoagulation prior to cardioversion in longer cases[9]
Evidence of preexcitation
- Avoid AV nodal agents
- Unstable:
- Unsynchronized cardioversion (200J)
- Procainamide (if cardioversion unsuccessful)
- 20-50mg/min until arrhythmia is controlled, hypotension occurs, QRS complex widens by 50% of original width, or total of 17mg/kg is given; followed by continuous infusion of 1-4mg/min
- Stable:
- Try to avoid cardioversion without adequate anticoagulation
Disposition
Admission
- Ongoing symptoms/complications (respiratory distress, chest pain, pulmonary edema, myocardial ischemia)
- Infusion needed for rate control
Discharge
- Consider consult with cardiology prior
- Patients with good rate/rhythm control and anticoagulation can usually be discharged after an appropriate work-up
- Ensure follow-up is arranged
See Also
External Links
- IBCC - Atrial Fibrillation and Flutter complicating critical illness
- emDOCS - Atrial Flutter
- Merck Manual - Atrial Flutter
References
- ↑ Gallagher MM, Guo XH, Poloniecki JD, et al. Initial energy setting, outcome and efficiency in direct current cardioversion of atrial fibrillation and flutter. J Am Coll Cardiol 2001; 38:1498.
- ↑ Van Gelder IC et al. Lenient versus strict rate control in patients with atrial fibrillation. N Engl J Med. 2010 Apr 15;362(15):1363-73. full text
- ↑ Ottowa Aggressive Protocol
- ↑ Blecher GE, et al. Use of rate control medication before cardioversion of recent-onset atrial fibrillation or flutter in the emergency department is associated with reduced success rates. CJEM. 2012;14(3):169-177.
- ↑ You JJ, Singer DE, Howard PA, Lane DA, Eckman MH, Fang MC, Hylek EM, Schulman S, Go AS, Hughes M, Spencer FA, Manning WJ, Halperin JL, Lip GY. Antithrombotic therapy for atrial fibrillation: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012 Feb;141(2 Suppl):e531S-75S
- ↑ FusterV et al;American Collegeof Cardiology/ American Heart Association Task Force on Practice Guidelines; European Society of Cardiology Committee for Practice Guidelines; European Heart Rhythm Association; Heart Rhythm Society. 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): developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Circulation. 2006;114(7):e257-e354.
- ↑ Camm AJ, Kirchhof P, Lip GY, et al; European Heart Rhythm Association; European Association for Cardio-Thoracic Surgery. Guidelines for the management of atrial fibrillation: the task force for the management of atrial fibrillation of the European Society of Cardiology (ESC). Eur Heart J. 2010;31(19):2369-2429.
- ↑ 48hr Cardioversion for A.fib.
- ↑ Nuotio I. et al. Time to cardioversion for acute atrial fibrillation and thromboembolic complications. JAMA. 2014 Aug 13;312(6):647-9