Atrial fibrillation

Janet Wong, M.D.

1
 Emergent/urgent Cardioversion
€ Poorly tolerated atrial ablation:
• Significant hypotension
• Pulmonary edema
• Significant ischemia
€ DC cardioversion:
• Minimum 200 J. synchronized shock
Atrial fibrillation is the most frequently occurring cardiac arrhythmia,
and it is the main problem that we have to deal with when it comes
to cardiac arrhythmias. There is a 2% risk of atrial fibrillation over
20 years, and the risk increases with age. By the time people reach
75, there is a high prevalence of atrial fibrillation. The risk also
increases with other associated diseases like hypertension, coro-
nary disease, and diabetes.
The main thing we worry about is the risk of stroke in people with
atrial fibrillation. People can be very symptomatic and have func-
tional limitations due to rapid ventricular rate, loss of AV synchrony,
variability of ventricular response, and tachycardia-induced
cardiomyopathy.
Poorly tolerated atrial fibrillation is characterized by significant
hypotension. If their BP is 50, you are going to want to treat it as an
emergency. So you have someone that comes in, their blood
pressure is maintained, but they are developing severe pulmonary
edema or they are complaining of crushing chest pain with ECG
changes, I think you are not wrong in that case to urgently DC
cardiovert those people.
Atrial fibrillation is probably the most difficult arrhythmia to electri-
cally cardiovert. Certainly harder than ventricular tachycardia, often
harder than ventricular fibrillation. It usually takes high energy.
There are two reasons to start with a higher energy. A shock of 50
joules externally stimulates skeletal muscle and that's what makes
it painful. A shock of 200 joules or 300 joules or even 360 joules
hurts just as much. It doesn't hurt any more. So, you are not saving
your patient any discomfort by using a lower energy. When you
shock somebody, you should always recharge the defibrillator
immediately because when you shock somebody there is always
the risk you are going to put them into VF. The risk of causing VF
with the shock is related to the energy. The lower the energy, the
higher the risk of VF because you have incompletely depolarized
the heart.
You can decrease the number of shocks if you use a higher energy
and you can also reduce the risk of causing VF. I routinely start at
200 to 300 joules, and if I have a big barrel-chested person or an
obese person, I just start with 360.
2
 Acute Rate Control
What if the person is stable and you want to just control them
medically when they come in? The rate can be controlled with a
€ IV calcium channel blockers variety of agents. One group of agents is the IV calcium channel
blockers. IV diltiazem is the drug of choice because of the ease of
• Diltiazem 20 - 25 mg bolus, then 10-15 mg/hour infusion
use. After you have loaded the patient with a bolus, which is usually
• Verapamil 2.5 - 5 mg bolus 20 to 25 mg, you can start the patient on an infusion of 10 to 15
mg/hour, and you can titrate the infusion rate to achieve the appro-
€ IV Digoxin
priate heart rate. This strategy is very effective in the short term at
controlling ventricular rate. You want to convert people over that
can take p.o. medications early on if you are going to continue to
need to rate control them.

IV beta blockers work very well. IV Inderal, IV metoprolol; the short-

acting one is esmolol which is difficult to dose. Diltiazem is easier
for that reason.

IV digoxin is not usually recommended for acute rate control be-

cause the onset of action is very long; it can take hours before you
rate control someone. Digoxin is not good at rate control in some-
body with a high catecholamine state. IV digoxin is no longer used
for acute rate control. There is no difference in conversion rate with
IV digoxin.

Rate control that in atrial fibrillation in the setting of the WPW

syndrome. In WPW, there is an accessory pathway connecting the
atrium to the ventricle which bypasses the AV node. The problem
with that is that the AV node limits the number of impulses that can
reach the atrium from the ventricle, maybe in a young healthy
person, to 200 to 220 beats per minute. The accessory pathway
doesn't have that same function and can let 250, even 300, beats
per minute through to the ventricle. The hallmarks of WPW in atrial
fibrillation are a wide QRS complex that is an irregular tachycardia,
and you have changing amounts of preexcitation. So, the QRS is
almost changing beat to beat by the amount of excitation of the
ventricle.

If you give typical AV node blocking drugs in these patients, they

will block the AV node fine, but the ventricle is still going to be
activated rapidly over the accessory pathway. If you give a drug like
verapamil, you may increase conduction over the accessory path-
way. If you give these patients, digoxin, verapamil, or beta blockers,
you can degenerate them to ventricular fibrillation.

The treatment of choice for atrial fibrillation in the setting of WPW

is electrical cardioversion if the patient is unstable. Procainamide is
the drug of choice given intravenously because it may convert the
atrial fibrillation, and it suppresses conduction over the accessory
pathway, and it will limit the number of impulses getting to the
ventricle. A potentially life-threatening complication may occur with
the usual rate control medications.

3
 Elective Cardioversion
Patients who have been in atrial fibrillation for less than 48 hours
can be safely cardioverted without anticoagulation. Elective cardio-
€ > 24 - 48 hours version can be accomplished pharmacologically with either intrave-
nous procainamide or ibutilide. Or you can use oral loading of
€ Pharmacologic
quinidine or disopyramide (Norpace). External electrical cardiover-
• Intravenous: procainamide/ibutilide sion can be used. Internal cardioversions may also be effective in
the patients who are resistant to external DC cardioversions.
• Oral loading
€ Electrical In atrial fibrillation that has been present for more than 48 hours,
after you cardiovert them, you need to maintain anticoagulation due
• External
to the high risk of embolic events during that period. Patients that
• Internal have been in chronic atrial fibrillation, the atria are stunned and
they don't contract very well. Patients are at continued risk for
stroke even though they are in sinus rhythm for a period of three
Anticoagulation for three months after cardioversion is recom- months after conversion from atrial fibrillation.
mended because of high-risk of embolic events during this
The standard approach is you put them on Coumadin and wait four
period. to six weeks and then bring them in for an elective cardioversion.
The down side is there is a delay in cardioversion. You also end up
having more prolonged anticoagulation with the risks attendant with
warfarin and you delay the recovery of atrial function. The longer
you leave somebody in atrial fibrillation, the longer it takes the
atrium to recover. The quicker you get somebody out of atrial
fibrillation, the longer they will stay out of fibrillation.

Transesophageal echo should be used to select candidates for

early cardioversion. Heparin therapy should be instituted and the
rate should be controlled, and you do a TEE and you look for
thrombus. In patients who do not have a thrombus, you can go
ahead and cardiovert. So, you have an overall shorter duration of
warfarin therapy--four to six weeks less–and a more rapid return of
atrial function, and fewer incidents of thromboembolism. In patients
in whom left atrial thrombi was excluded, you can safely cardiovert
these people.

If you decide to cardiovert somebody you don't always have to

shock them right off. What we do in our hospital is often bring them
in for elective cardioversion, we will give them a load of intravenous
procainamide, and if they don't convert then we go ahead and do
the DC cardioversion. The standard dose of procainamide, 15
mg/kg over 20 to 30 minutes. It is probably more effective at this
faster rate because you get a higher peak plasma level of the
procainamide, and that is probably what accounts for the acute
conversions. The patient should be monitored for hypotension,
QRS widening and QT prolongation.

A new class III antiarrhythmic drug called ibutilide (Corvert) works

by prolonging the action potential duration. It works well for up to
50%. With atrial fibrillation, with a 30% conversion rate. There is a
significant risk of torsades de pointes with ibutilide. It is much
easier to give than procainamide - you can give it quicker. Patients
develop polymorphic VTs, sustained in almost 2%, 2.5% non-
sustained. Some people even developed monomorphic VT. You
can see a 9% incidence of ventricular proarrhythmia in these pa-
tients. It is okay to use it; you just have to be aware of this and use
it in the proper setting. So, if you give this in the ER, patients have
to be monitored closely for 4 hours after you use it. If you use it in
the hospital, they have to be in a telemetry setting where you are
comfortable with the people on your telemetry floors that they can
recognize this and treat it very rapidly.

How do you convert somebody electrically? When external cardio-

version fails, internal cardioversion with a catheter may be success-

4
 Treatment of Atrial Fibrillation
€ Treat underlying cause if present
€ Rate control
€ Anticoagulating
€ Maintenance of sinus rhythm in selected patients
ful. The catheter has a platinum electrode on it is floated into the
right atrium, and then you shock between the tip of the catheter and
the back patch. So, you are actually shocking from inside the heart.
The results have been really encouraging. Significantly more people
were cardioverted with internal cardioversion than with external.
The long-term outcomes were no different. It is useful in the pa-
tients who will benefit from sinus rhythm, but you can't get into
sinus rhythm with external shocks.
Treatment of atrial fibrillation includes treatment of underlying
causes. The most common disorders are thyrotoxicosis and
pericarditis.
5
 Anticoagulation Recommendations
€ Strong contraindication to warfarin: Aspirin 325 mg per day
€ Lone atrial fibrillation, less than 65: No treatment or aspirin
€ Low-risk: Aspirin
€ One or more risk factors: Warfarin (INR 2.0-3.0)
€ $70, low-risk: Warfarin (INR 2.0) or aspirin
People who have atrial fibrillation have a 6-fold increased risk of
stroke. The very high risk patients tend to be the older patients with
diabetes, hypertension, previous strokes and TIAs, CHF, coronary
disease, and mitral valve disease. High risk patients greater than
65, with one of these risk factors have a 5% per year risk. The low
risk patients are the patients less than 60 with normal hearts, with
normal blood pressures and glucoses, and the risk is probably even
less than 1% per year.
With Coumadin there is an overall 65% reduction in stroke presen-
tations with atrial fibrillation. Anticoagulation is important in atrial
fibrillation.
There is a significant reduction in the risk of stroke with Coumadin
over platelet inhibitors. So, in the general population, including the
high-risk patients, Coumadin is clearly better than aspirin alone. In
patients that are low-risk, who have essentially structural normal
hearts, that have no hypertension, no LV dysfunction, no prior
embolic events, even if they are older, aspirin is probably better
than warfarin in those patients. High risk patients should be on
Coumadin.
With strong contraindications to warfarin, you need to put them on
aspirin. In patients with lone atrial fibrillation that are relatively
young, either nothing or aspirin is recommended. If it is a male
patient that is 55 years old, having him take an aspirin a day may
have some added benefit in coronary disease, so I like to tell them
to take an aspirin anyway.
Low-risk patients can be treated with aspirin alone. If they have one
or more risk factors, warfarin is recommended with an INR between
2 and 3, usually shooting between 2 to 2.5. Greater than 70 puts
them in high-risk; however, those are the people that have a higher
incidence of bleeding. What I tend to do in people that have rela-
tively normal hearts even if they are older than 70, I will often use
aspirin alone, or if I do use Coumadin I will tend to shoot on the
lower side of the INR. You have to individualize it for each patient.
6
 Treatment Goals
Treatment goals in treating atrial fibrillation include alleviation of
symptoms, prevention of ischemia with high heart rates. Some
€ Alleviate symptoms patients with atrial fibrillation due to the loss of AV synchrony and
the irregularness of their rate have more CHF and keeping them in
€ Prevent ischemia
sinus will improve hemodynamics. You would like to prolong life
€ Improve hemodynamics and prevent sequelae.
€ Prolonge life in prevent sequelae
There is no data at present that supports reduction in stroke or
Maintenance of sinus rhythm with an antiarrhythmic has not prolongation of life with antiarrhythmic maintenance of sinus
rhythm.
been proven to reduce risk of stroke or prolong life
Antiarrhythmics in patients that had no history of CHF did not
cause a significant increase in mortality. Patients with a history of
CHF and no antiarrhythmics, clearly they did less well than those
patients that had no history of CHF, but the surprising finding was
that if you looked at the survival curve for the patients that both had
a history of CHF and were receiving antiarrhythmics to maintain
sinus rhythm, their survival is much worse than the other groups.

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 Rate Control
Rate control in chronic atrial fibrillation. There are pharmacologic
agents, digitalis, beta blockers, calcium channel blockers and even
€ Pharmacological amiodarone for rate control and there are some non-pharmacologic
approaches such as AV node modification or ablation of the AV
• Calcium blockers
node and physiologic pacing.
• Beta-blockers
• Digitalis
• Amiodarone
€ Non-pharmacological
• AV node modification
• AV node ablation plus physiologic pacing

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 Pharmacologic Rate Control
€ Digitalis is indicated if history of CHF
• Poor choice in active patients
• Excessive slowing during sinus rate or at rest
€ Beta-blockers
• Excellent in active patients
• Using combination with and antiarrhythmics
• First choice in thyrotoxicosis
• First choice in ischemic patients
• May not be tolerated in patients with CHF or lung dis-
ease
• ISA in patients with tachy-bradycardia syndrome
€ Calcium channel blockers
• Good in active patients
• First choice in patients with lung disease
• Acceptable in patients with ischemia
• May not be tolerated in patients with CHF
€ Amiodarone
• May work when nothing else does
• Good in patients with enhanced AV conviction
• May be beneficial in patients with LV dysfunction
and/or Nonsustained ventricular tachycardia
If you are going to go ahead with pharmacologic rate control it is
important to confirm that the patient is rate controlled. A significant
number of patients who their physicians thought were adequately
rate-controlled were in atrial fibrillation with rates of 140 to 150 at
rest. Before people leave the hospital, I will get them up and put
them on the stairs while they are still on telemetry and see what
their heart rate does. After I send them out, I will either get a tread-
mill test, or it is even better to send them home with a Holter moni-
tor and tell them, "I want you to go do all of the things that you are
normally going to do." You really want to do surveillance Holters
when they are back doing the things that they do because when
these people get active, their heart rates often shoot up much
higher than you thought.
Beta blockers are an excellent choice for active patients. Use in
combination with antiarrhythmics is well tolerated. It is the first
choice in patients with thyrotoxicosis. It is the first choice in patients
with ischemia. It may not be tolerated in patients with moderate
CHF or lung disease, although patients with mild CHF should be
put on beta blockers. A beta blocker like Pindolol, with intrinsic
sympathomimetic activity, may be advantageous in patients with
tachy-bradycardia syndrome, where you could avoid a pacemaker.
But I am not sure how good that is.
Calcium channel blockers, I think, are very good agents for rate
control. They are good in the active patients. They are the first
choice of patients with lung disease who can't use beta blockers. I
think they are the first choice of patients with atrial fibrillation and
LVH because of the beneficial effects of calcium channel blockers
in these patients and the regression of LVH. It may not be tolerated
in patients with CHF. Negative inotropic effects.
Digitalis is only recommended in patients with a history of CHF
because you have the added benefit in those patients. It is very
poor in active patients. The problem with digoxin is that you have
excessive slowing of the sinus rate at rest but not good control
during exertion. So, you push the dig to a point where someone has
a heart rate of 60 at rest and then they get up and start doing things
like climbing stairs and stuff and their heart rate goes up to 170 or
140. Digoxin, especially in the active patient, is not recomended.
Amiodarone may work when nothing else can control the heart rate.
It is good in patients that have enhanced AV nodal conduction is a
very rare entity where people go into atrial fibrillation and go very
rapidly up to 250 or 350 beats per minute. It may be beneficial in
patients with LV dysfunction and/or nonsustained VT where you get
the added benefit of reducing the risk of sudden death.
AV junctional ablation for rate control of atrial fibrillation. The
response of patients is really dramatic, and people do really well
with this procedure. Indications include failure of the multiple AV
nodal blocking drugs. So, patients that you just can't rate control no
matter what you use. Patients in whom even though their rate is
controlled the irregularity of the atrial fibrillation still bothers them.
Drug intolerance. Patients that when they take the drugs that rate
control, they get admitted five times a year with CHF and their heart
rate is 150 because they never take their medications. Also, patient
preference.
What do we do with patients with atrial fibrillation and heart failure?
Twenty five percent of patients with heart failure may also have
atrial fibrillation. These are the patients that are at highest risk of
proarrhythmia from antiarrhythmic drugs. Congestive heart failure
9
 Chemical Cardioversion can lead to atrial fibrillation, and atrial fibrillation can lead to and
worsen congestive heart failure. Chronic tachycardia is associated
with the development of a cardiomyopathy and it appears to be
reversible.
€ Procainamide
Ablation and pacing results in an improvement in EF from 25% to
• 15 mg/kg IV over 20-30 minutes (750-1500 mg) 52%. Dramatic increases in injection fraction. With severe LV
• Watch for hypotension, QRS widening, QT prolonga- dysfunction, after you ablate their AV node and put in a pacemaker;
it is almost back to normal. I think that is a really important point
tion. that people don't fully understand yet. Patients with mean heart
rates of 60 to 100 beats per minute on a Holter that had depressed
LV function underwent AV junctional ablation and showed a signifi-
cant improvement in function after this.

Regularization of ventricular response. Even if you have somebody

rate controlled, the ventricle is being activated very irregularly.
Regularization of rhythm provides significant hemodynamic bene-
fits. In patients with AF, an increase in pulmonary capillary wedge
pressure were seen with irregular rhythm as opposed to regular
rhythm; therefore, both rapid rate and irregularity leads to de-
creased LV function.

If you have patients that are difficult to manage and are having
repeated visits to the hospital with CHF and have chronic atrial
fibrillation, AV junctional ablation with pacing is something to
consider. It may help you manage their CHF.

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 Maintenance of Sinus to Rhythm
Maintenance of sinus rhythm. There is a subset of patients in whom
we are going to want to try and maintain sinus rhythm. There are
€ Pharmacologic pharmacologic approaches, preventative pacing, implantable
defibrillators and ablative therapy.
€ Preventive pacing
€ Implantable defibrillator
€ Ablative therapy
• Surgical
• Catheter

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 Pharmacologic Maintenance of Sinus
to Rhythm
€ Class IA
• Quinidine: diarrhea
• Procainamide: arthritis/rash/lupus
• Disopyramide: urinary retention
€ Class IC
• Flecainide: avoided in ischemia/poor LV function
• Propafenone: avoided in ischemia/poor LV function
€ Class III
• Sotalol: CHF, asthma, bradycardia
€ Amiodarone: end organ toxicity
Pharmacologic agents. The class-I agents are sodium channel
blockers. There is quinidine, procainamide, disopyramide.
Quinidine is a drug that has been used for years and years, but 40
to 50% of patients can't take it because of the diarrhea.
Procainamide maintenance is not recommended because of arthri-
tis, rash, and lupus-like syndromes. Disopyramide (Norpace) is not
good in older men because of urinary retention, but it is very well-
tolerated in younger patients, and in patients with vagally mediated
atrial fibrillation.
The class 1C agents. Flecainide got a very bad name because of
the excess mortality in patients post MI. But I think in patients with
structurally normal hearts, it is probably one of the most effective
agents that we have for controlling atrial fibrillation. It should be
avoided it in patients with ischemia or poor LV function. The same
thing with propafenone (Rythmol). A newer agent, Sotalol can be
very effective because it offers both rate control and an
antiarrhythmic properties, but the beta blocking properties can
cause problems in patients with CHF, asthma, and it can cause
bradycardia.
Amiodarone is a very good drug for controlling atrial fibrillation, but
the end organ toxicities are something to be concerned about. Over
one year's time on quinidine, about 50% are maintained in sinus
rhythm. Propafenone and Sotalol, 50%. With the exception of
amiodarone, the antiarrhythmic drugs are all about 50% effective at
one year. Amiodarone appears to be the most effective
antiarrhythmic at maintaining sinus rhythm. It is 78% effective at
maintaining sinus rhythm in people who had failed a type-I
antiarrhythmic. Amiodarone versus quinidine, again right around
50% versus 79%. Same thing for amiodarone versus Norpace.
Amiodarone is the best drug available for maintaining sinus rhythm.
We have had a lot of good success with using amiodarone, and we
use it in a lot of patients. Toxicity tends to be dose related. So, in
the doses we use in ventricular tachycardia, 400 to 600 mg/day,
there is a significant incidence of pulmonary fibrosis and other end
organ toxicities. At the dose we use for atrial fibrillation, it is 200
mg/day, which is one pill, or even 200 mg every other day, the
incidence of these side effects are very low. The side effects are
reversible. In patients that have failed other drugs and patients that
have LV dysfunction, amiodarone is the drug of choice.
Amiodarone is a very unique drug. The half-life is one month to five
months. It is a very lipophilic drug so when you give it to people it
immediately gets sucked up into their fat stores. Start with a much
higher dose and then we cut the dose back. Start them on 800
mg/day for about two weeks, then I will put them on 400 mg/day for
about a month, then cut them back down to 200 mg/day. Results
have been very good. Patients have tolerated it well and it clearly
works much better than other agents. Anybody over 70 who pres-
ents with atrial fibrillation or who has any LV dysfunction, should be
started on amiodarone as a first line agent.
12
 No Structural Heart Disease
If you have a patient that has no structural heart disease with lone
AF, they are very symptomatic, you don't want to leave these
€ First-line agents people in AF all the time and make them take aspirin and have
them in atrial fibrillation. You can give them drugs to try to maintain
• Class IC (flecainide, propafenone)
sinus rhythm. We have had a lot of success with flecainide in this
• Disopyramide (especially if vagally mediated) population. Norpace is very good especially in vagally mediated AF.
There is a group of patients who get atrial fibrillation after they eat
€ Second-line
big meals or they wake up in the middle of the night. Vagal surges
• Sotalol change the electrophysiologic properties of the atrium and make it
more susceptible to atrial fibrillation. Norpace has some vagolytic
€ Third line
effects and may be effective in those patients. Second line, Sotalol
• Amiodarone is often good in these patients, and you can use amiodarone.

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 Ischemic Heart Disease
In patients with ischemic heart disease, the class 1C drugs should
be avoided. Sotalol may be a good drug. The beta blocking proper-
€ First-line: ties are good for the ischemic patient, and amiodarone is a good
agent in those patients.
• Sotalol
€ Second-line:
• Amiodarone
€ Avoid class IC

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 CHF/LV Dysfunction
In the patients with CHF and LV dysfunction, you have to avoid
those drugs that are proarrhythmic. Amiodarone may be the best
€ First-line: drug in these patients because you get the added protection from
sudden death. You should also consider the non-pharmacologic
• Amiodarone
approach in these patients because you may see an increase in LV
€ Consider non-pharmacologic approach function after you control their rate with ablation and regularize their
ventricular response with pacing.
€ Avoid class IC

15
 LVH/HCM
In patients that have left ventricular hypertrophy or hypertrophic
cardiomyopathy, class 1C agents are also good. Disopyramide is
€ First-line specifically good in patients with hypertrophic cardiomyopathy
because of the negative inotropic effects. It may decrease the
• Class 1C (flecainide, propafenone)
gradient. Sotalol also is very good in these patients, and
€ Second-line: amiodarone is good. In patients with hypertrophic cardiomyopathy,
you should consider non-pharmacologic management, such as
• Sotalol
ablation, because dual-chamber pacing will decrease the pressure
• Amiodarone gradient so you get the added benefit of those two things.
€ Consider nonpharmacologic management (HCM)

16
Outpatient loading of antiarrhythmic medications utilizing a monitoring device is probably safe and cost-effective. Patients get their
first dose of the drug in the hospital, and then were sent out with a loop recorder for 10 days. Every day they transmit a tracing of
their heart rate and their QT interval and they also transmit any palpitations or any adverse effects that they had.

Prophylactic pacing for atrial fibrillation. It is thought that atrial fibrillation is due to multiple re-entrant wave fronts throughout the
atria. Excitation and therefore prolongation of the refractoriness of the tissue in the critical regions of the atrium may prevent the
initiation or maintenance of atrial fibrillation. If you stimulate the heart in more than one place, you may be able to prevent these re-
entrant wave fronts and prevent atrial fibrillation. There are trials that have looked at patients with sick sinus syndrome that got either
dual chamber pacers or ventricular pacers alone. The studies showed that in patients that had atrial pacing, it was a significantly
much lower incidence of atrial fibrillation that had active atrial pacing suggesting that somehow pacing the atrium will decrease the
incidence of atrial fibrillation.

Implantable ventricular defibrillators. This is a device that goes in the pectoral region, has two leads in the right atrium. One in the
right atrium, one in the coronary sinus and one for R-wave synchronization in the RV apex. It is used to cardiovert people out of atrial
fibrillation. It can be done when you have two leads inside the heart like this and you are not shocking externally and you are not
stimulating skeletal muscle. The amount of energy required is only in some patients 0.5 Joule or 1 or 2 Joule. So, although in some
patients that causes a fair amount of discomfort, in some patients it doesn't and the idea of atrial defibrillators are being tested right
now. The big questions are safety. The first patient that has an atrial defibrillator that gets shocked or it fails and they get put into VF
and then dies, that will be the end of the whole idea.

Surgical treatment of atrial fibrillation. The Maze procedure consists of multiple atriotomies which interrupt all the potential re-entrant
circuits. This will restore control of the heartbeat to the atrial pacemaker, which is the sinus node, and it allows activation of the entire
atrial myocardium. The long term results are unclear.

Atrial flutter. Typical atrial flutter is characterized by the typical saw-tooth flutter wave in the inferior leads beneath the positive flutter
wave in lead V1. It is a macroreentrant electrical rhythm confined to the right atrium. So, the electrical wave front goes around the
right atrium, up the septum, down the lateral wall and through this isthmus of tissue between the opening of the IVC and the tricuspid
annulus and the coronary sinus. If we can create a line of conduction block, the patient should not have atrial flutter anymore.

We are now able to terminate atrial flutter and cure people that have typical atrial flutter in about 95% of cases. Antiarrhythmic drugs
are not very effective for atrial flutter, and rate control is much more difficult in atrial flutter than atrial fibrillation because it is hard to
get a reasonable rate control. When somebody presents with atrial flutter for the first time, cardioversion is recommended, and then
the patients are discharged and observed to determine what the natural history is going to be. If they are not going to have atrial
flutter for the next five years, no treatment is necessary. The first time they return with atrial flutter, if it is early on, the first line of
therapy now is ablative therapy and our success rate is very good and the risk is low.

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