Download Atrial Flutter

Atrial Flutter
Chris Caulfield
AM Report
2/19/10
Definition
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Atrial Flutter is rapid, regular atrial
depolarizations at a characteristic rate of
approximately 300 beats/min.
Prolonged atrial flutter can ultimately
impair cardiac output, increase myocardial
oxygen demand, and cause atrial
thrombus formation.
Epidemiology
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In one study, estimated that the incidence of in
the United States is about 200,000 new cases per
year, and occurs more common in men and in
older adults.
Risk of developing atrial flutter increased 3.5
times in patients with heart failure and 1.9 times
in those with chronic obstructive lung disease
Unusual to occur in a normal heart, and is
especially uncommon in children and young
adults
Classification of Type
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Type I is considered typical and has an
atrial rate 240 to 340 beats/min
Type II is considered atypical and has an
atrial rate of 340 to 440 beats/min
Type I Atrial Flutter
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Typical atrial flutter, or "isthmus-dependent"
flutter, is a macroreentrant arrhythmia that
involves a long slow path with an excitable gap,
forming a circuit within the right atrium.
Slowly conducting reentrant circuit is located in
the low right atrial isthmus.
The isthmus of tissue is between the inferior
vena cava and tricuspid annulus.
Type I
Type I
Type II Atrial Flutter
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Atypical atrial flutter lacks an excitable gap and
is not isthmus-dependent.
Usually this rhythm results from an intra-atrial
reentrant circuit that is very short.
May be due abnormal anatomy within the right
or left atrium (i.e. surgical scars, irregular
pulmonary veins, disturbed mitral annulus)
Symptoms
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Palpitations
Fatigue
Lightheadedness
Shortness of breath
Less common symptoms include angina,
hypotension, or syncope
Diagnosis: EKG
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EKG will typically show 2:1 conduction across
the AV node (even ratios of conduction are more
common than odd ratios)
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1:1 conductive response suggests catecholamine
excess, parasympathetic withdrawal, or the existence
of an accessory bypass tract in pre-excitation
May need to administer adenosine to slow conduction
through AV node
Diagnosis: EKG
Diagnosis: EKG
Diagnosis: Underlying Causes
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Rheumatic heart
disease (if MV
involved)
LV dysfunction/heart
failure
Sick sinus syndrome
Pericarditis
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Uncommon complication of acute MI and digitalis toxicity
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Pulmonary embolism
Chronic obstructive
pulmonary disease
Mitral valve prolapse
Hyperthyroidism
Status post CABG
Further Diagnosis
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Serum electrolytes, pulmonary and thyroid function tests
should be ordered if appropriate.
Transthoracic echocardiography should be performed to
evaluate for structural and valvular abnormalities along
with LV systolic function.
Holter monitoring or event recorders could be provided in
an ambulatory setting if symptoms are non-specific and
an arrhythmia is considered but has not been detected.
Electrophysiological studies may be required at a later
point for further diagnosis and therapy.
Treatment
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Control of ventricular rate
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Reversion to NSR
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Maintenance of NSR
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Prevention of systemic embolization
Control of ventricular rate
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Intravenous calcium channel blockers (Diltiazem
or Verapamil) or beta blockers (Esmolol) may be
used to control rapid ventricular rate.
Digoxin is not typically used except occasionally
in patients with heart failure.
Amiodarone can also be used for control of rapid
ventricular response, but could promote
conversion to sinus rhythm, increasing risk of
embolization if not anticoagulated.
Reversion to NSR
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The optimal outcome of atrial flutter is reversion to and maintenance
of normal sinus rhythm, not ventricular rate control.
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Cardioversion can be performed by electrical or chemical means.
DC cardioversion is the choice for reversion to sinus rhythm if the
patient is hemodynamically unstable and is uninstrumented. (starting
at 50 to 100 J with biphasic defibrillators)
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Stable patients may convert after watchful waiting.
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Factors that predict spontaneous reversion to sinus rhythm or a
successful cardioversion include:
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Left atrial size less than 4.5 to 5 cm
Atrial flutter of recent onset with little or no heart failure
No underlying reversible cause (i.e. hyperthyroidism)
Chemical Cardioversion
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Anti-arrhythmic agents that can be used for cardioversion include
flecainide, dofetilide, propafenone, ibutilide, and amiodarone.
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Flecainide is contraindicated in CAD, structural heart disease, and
LVH (as per CAST)
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LV hypertrophy without ischemia or conduction delay, class III agents,
specifically amiodarone, can be used.
Ischemic heart disease, sotalol or amiodarone can be used. (Avoid class
IC agents)
Significant systolic dysfunction, amiodarone and dofetilide can be used.
(Avoid class IC agents)
Slowing of the atrial flutter rate with anti-arrhythmics alone can lead
to 1:1 conduction.
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Class IA and IC drugs should be administered in conjunction with an AV
nodal blocking agent (beta blocker or calcium channel blocker)
Anticoagulation
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It is unusual to have thrombus form in the left atrial appendage
because of the regularity of atrial contractions in atrial flutter.
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However, atrial fibrillation can be a rhythm underlying atrial flutter.
As in Afib, if atrial flutter persists for more than 48 hours, 4 weeks
of adequate anticoagulation or TEE is needed before attempting
cardioversion to sinus rhythm.
If TEE does not visualize the presence of left atrial thrombus,
cardioversion can be performed with continuation of warfarin for
four weeks after cardioversion. However, the safety of this approach
has not been formally studied in atrial flutter.
Among patients with atrial fibrillation and flutter, the choice between
warfarin and aspirin is based upon the estimated stroke risk using
the CHADS2 score.
Ablation
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Radiofrequency ablation interrupts the reentrant circuit in order to
prevent the recurrence of atrial flutter.
With recurrent symptomatic Type I atrial flutter, there is a success
rate of higher than 95% with ablation.
 Ablation is commonly performed at the 6:00 position on the
tricuspid valve isthmus.
Type II atrial flutter is also amenable to ablation and success rate is
close to 95%, but recurrence is more common than Type I.
In patients with atrial flutter treated with ablation who subsequently
develop a fib (56% in one study), ablation of the AV junction may
need to be performed with placement of pacemaker.
Take Home Points
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Typical atrial flutter (Type I) is an “isthmusdependent” flutter involving a macroreentrant
arrhythmia down a long slow path, due to an
isthmus of tissue between the IVC and tricuspid
annulus.
Atypical atrial flutter (Type II) is not isthmusdependent and involves an intra-atrial reentrant
circuit that is very short and related to abnormal
anatomy within the right or left atrium.
Take Home Points
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IV calcium channel blockers (Diltiazem or Verapamil) or beta
blockers (Esmolol) may be used to control rapid ventricular rate.
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The optimal outcome of atrial flutter is reversion to and
maintenance of normal sinus rhythm, not ventricular rate control.
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Cardioversion can be performed by electrical or chemical means.
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If TEE does not visualize the presence of left atrial thrombus,
cardioversion can be performed with continuation of warfarin for
four weeks after cardioversion.
Radiofrequency ablation should be considered prior to starting an
antiarrhythmic agent.