Medmastery_Atrial Fibrillation Management Essentials Handbook

ATRIAL FIBRILLATION
MANAGEMENT ESSENTIALS
HANDBOOK
Franz Wiesbauer
MD MPH
Table of contents
Abbreviation list 3
Atrial fibrillation
Reviewing the basics of atrial fibrillation 5
Diagnosing atrial fibrillation 10
Classifying atrial fibrillation 16
Addressing reversible conditions 20
Anticoagulation
Evaluating stroke risk 24
Deciding when to use anticoagulants 27
Assessing bleeding risk 29
Reviewing anticoagulants 32
Selecting the appropriate anticoagulant 34
Rate and rhythm control

Controlling heart rate in atrial fibrillation 39
Controlling heart rhythm in atrial fibrillation 42
Slowing ventricular rate 45
Restoring sinus rhythm 48
Selecting the appropriate form of cardioversion 51
Maintaining heart rate 54
Maintaining rhythm 57
Choosing between rate and rhythm control 60
Considering ablation 62
Appendix
Reference list 67
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Abbreviation list
AV atrioventricular
ACC American College of Cardiology
ACC / AHA / HRS American College of Cardiology, American Heart
Association, Heart Rhythm Society
ACS acute coronary syndrome
AHA American Heart Association
bpm beats per minute
CHA2DS2-VASc congestive heart failure, hypertension, age (75 or older),
diabetes, history of stroke, vascular disease, age (65–74),
sex category
CYP-3A4 cytochrome P450 3A4
ECG electrocardiogram
HAS-BLED hypertension, abnormal hepatic and / or renal function,
stroke history, bleeding history, labile (or changing) time to
clot, elderly (over 65 years), drug and / or alcohol misuse
HRS Heart Rhythm Society
INR international normalized ratio
IV intravenous
NIP narrow QRS complexes, irregularly spaced QRS complexes,
P waves absent
NOACs novel oral anticoagulants
NSAIDs nonsteroidal anti-inflammatory drugs
SA sinoatrial
TEE transesophageal echocardiography

Chapter 1
ATRIAL FIBRILLATION
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Reviewing the basics of atrial fibrillation
Atrial fibrillation is a type of tachycardia where the heartbeat is fast and
irregular. It is the most common arrhythmia seen clinically. While it is not
immediately life-threatening itself, it can be an indicator of bigger medical
issues and increases the patient’s risk of stroke.
What happens during a normal cardiac cycle?

Each heartbeat, or cardiac cycle, is directed by electrical impulses that move
through the heart, coordinating the contraction and relaxation of the heart’s
chambers. The impulses start at the sinoatrial node, move to the atrioventricular
node, then through the bundle of His, bundle branches, and ventricular muscles.
1. Sinoatrial node
a. A cardiac cycle starts when an action potential is generated at the
sinoatrial node (SA node or sinus node) in the upper right atrium. The SA
node is a natural pacemaker, creating regular impulses between 60–100
beats per minute (bpm).
b. Each impulse spreads from the SA node throughout the right and
left atria.
c. The impulse causes the atria to contract as it travels toward the
atrioventricular (AV) node found at the bottom of the right atrium.
Impulses from the SA node cause atria to contract

2. Atrioventricular node
The AV node acts as a gatekeeper between the atria and the ventricles,
controlling the movement of atria-derived impulses into the ventricles.
3. Bundle of His, bundle branches, and ventricular muscles
Once past the AV node, the impulse travels through the bundle of His, into
the left and right bundle branches, then into the ventricular muscles, causing
them to contract.
Impulses from the AV node cause ventricles to contract
Sinus rhythm
When impulses are generated at a regular interval by the SA node, resulting in a
resting heart rate of 60–100 bpm, this is called sinus rhythm. You can think of it
as a comfortable walking pace for the heart.
What happens during tachycardia?

When the heart feels like it is racing with a resting heart rate faster than 100
bpm, it is in tachycardia.
Sinus tachycardia
The most common form of tachycardia is sinus tachycardia, where the heart
is in normal rhythm, but the heart rate is greater than 100 bpm at rest. On an
electrocardiogram (ECG) the spacing between QRS complexes is even, but the
QRS complexes are closer together than in sinus rhythm.

QRS complexes are closer together
Sinus tachycardia
In sinus tachycardia, the initial impulse is generated at the sinus node, but more
frequently than normal. This is caused by triggers in the body that make the
heartbeat faster, for example, in response to the following:
• Exercise
• Fever
• Pulmonary embolism
Because it takes time for these triggers to travel to the heart, sinus tachycardia
has a gradual onset and a gradual end.
Importantly, heart rate increases when the cause is present and returns to sinus
rhythm when the cause of the episode is gone.
What can cause a sudden arrhythmia?

There are a wide range of pathologies that cause episodes of rapid heart rate
that begin and end suddenly with no obvious explanation. For example, atrial
fibrillation involves episodes that can appear unexpectedly and end randomly, or
not end at all.
The underlying cause of atrial fibrillation is

damage to the atrial tissue, which can result
from any of the following:
• Aging
• Obesity
• Hypertension Atrial fibrillation is caused by
• Various cardiac conditions atrial tissue damage

• Diabetes
• Sleep apnea
• Thyroid disease
• Drug and alcohol use
Electrophysiology of atrial fibrillation

Instead of one impulse being generated at the SA node and moving down the
heart systematically, atrial fibrillation is characterized by multiple impulses
generated outside the SA node, which bounce chaotically within the atria much
like a ball in play on a pinball table.
Most of these impulses do not reach the ventricles thanks to the refractory
period, a brief moment when the AV node is non-conductive. This limits the rate
of ventricular contraction. For this reason, atrial fibrillation is not considered
life-threatening.
Impulses bounce chaotically AV node is non-conductive

within the atria so ventricular contraction is limited
Atrial fibrillation Refractory period
Impulses reach the ventricles at random, creating the characteristic irregular

rhythm of atrial fibrillation, shown below.
Irregular rhythm in atrial fibrillation

Because the atria contract chaotically, they never fully empty. This can lead to
increased risk of clots, atrial tissue damage, and a wide range of symptoms
associated with atrial fibrillation, which we will cover in the next lesson.
Management of atrial fibrillation

There are four therapeutic pillars for the management of atrial fibrillation:
1. Address modifiable risk factors
2. Prevent stroke by reducing the risk of blood clots
3. Control the heart rate
4. Regulate the heart rhythm
We will examine each of these in this course.
Return to table of contents.

Diagnosing atrial fibrillation
New-onset atrial fibrillation is often discovered in clinic during a routine
examination. Sometimes the patient is experiencing symptoms of arrythmia
and will book an appointment for this reason. Other times the patient is not
experiencing symptoms of arrythmia, but an irregular rhythm is found when
evaluating the patient for something else.
What are the symptoms?

Not all patients experience symptoms of atrial fibrillation. Those who do will
present with a rapid heart rate and may also be experiencing the following
symptoms due to the sporadic contractions of the heart:
• Fluttering or pounding sensation in their chest
• Weakness
• Shortness of breath
• Dizziness
However, these symptoms can result from many arrhythmias.
How can you distinguish atrial fibrillation from other

forms of arrhythmia?
An ECG is recommended to establish the diagnosis of atrial fibrillation. For this,
a standard 12-lead ECG is used to detect at least 30 seconds of continuous
atrial fibrillation.
Normal heartbeat ECG

A normal heartbeat (sinus rhythm) will look like the example shown next on an
ECG. P waves indicate atrial contraction, and QRS waves indicate ventricular
contraction. The distance between each P wave and the following QRS complex
is referred to as the PR interval. A normal heartbeat is defined by the following:
• Positive P waves
• P waves appear before the QRS complexes
• PR interval is constant
• Distance between QRS complexes is constant

Positive P waves
P waves appear before QRS complex
PR interval is constant
Distance between QRS complexes is constant

Arrythmias on an ECG
Arrythmias, like atrial fibrillation, can be confirmed using ECG by looking at
these factors:
• Width of the QRS complexes
• Regularity of the QRS complexes
• Presence and position of the P wave
Width of the QRS complex

The width refers to the duration of the QRS complex in seconds (s). When the
duration of the QRS complex is shorter than normal (i.e., 0.12 seconds or less), it
is considered narrow. On the other hand, when it is longer than 0.12 seconds, it is
considered broad.
≤ 0.12 s > 0.12 s
Narrow Broad
Regularity of the QRS complexes

The regularity refers to whether the distance between QRS complexes is constant
(regular) or not (irregular). Below is an example of a regular rhythm.
Consistent distances between QRS complexes

Regular rhythm
The next image is an example of an irregular rhythm, where the distance between
the QRS complexes is random. This is characteristic of atrial fibrillation where
the AV node only lets some impulses through to the ventricles causing them to
contract unpredictably.

Varying distances between QRS complexes
Irregular rhythm
Presence and position of the P wave

Many arrhythmias are regular and narrow, so to help distinguish between them,
look for the P wave. The P wave can be in one of two positions relative to the
isoelectric line:
1. Positive (above)
2. Negative (below)
Positive Negative
Position of P wave relative to isoelectric line
The location of the P wave relative to the QRS complex differs depending on the
type of tachycardia:
• Before
• During (effectively hiding it)
• After
Before QRS During QRS After QRS
Position of P wave relative to the QRS complex

Atrial fibrillation on an ECG
In atrial fibrillation, the QRS complexes should be narrow but irregular and
there are no P waves at all. The rapid, chaotic contractions of the atria are not
strong enough to create them. Let’s make this easier for you to remember. When
diagnosing atrial fibrillation look for NIP:
• Narrow QRS complexes
• Irregularly spaced QRS complexes
• P waves absent
Narrow Irregular P waves absent
Narrow, irregular QRS with P waves absent

Atrial fibrillation
You might also notice that the wave does not return to baseline (the isoelectric
line) between QRS complexes. Instead, it creates a fibrillatory wave that wavers
around the isoelectric line causing a jagged line that looks like the peaks of a
mountain range.
Wave does not return to baseline

Atrial fibrillation
What is the limitation of using an ECG?

Of course, the limitation of using ECG to diagnose atrial fibrillation is that the
patient needs to be experiencing an episode while undergoing the test.

Summary
Okay, let’s quickly review how to distinguish atrial fibrillation from other forms
of tachycardia when looking at an ECG tracing. When presented with a complex
tachycardia:
1. Check if the QRS complexes are narrow
2. Determine if the rhythm is regular or irregular
3. Locate the P wave if you can
Remember to NIP atrial fibrillation in the bud!

Classifying atrial fibrillation
Atrial remodeling refers to the changes in the structure and electrophysiology of
atrial tissue. These changes are central to the development of atrial fibrillation.
How does atrial fibrillation progress?

Scarring or stretching of the atrial tissue can lead to
atrial fibrillation. This damage can be caused by things
such as the following:
• Heart attack
• High blood pressure
• Cardiomyopathy
• Atrial fibrillation itself Atrial tissue damage
Over time, continued tissue damage drives the progression of atrial fibrillation,
causing episodes to occur more frequently and last longer.
How long do episodes last?

While some patients may not notice that they have had an episode of atrial
fibrillation, others may wait months for the fast fluttering heartbeat, chest pain,
dizziness, or fatigue to end, as episodes of atrial fibrillation can last any length of
time before returning to sinus rhythm:
• Minutes
• Hours
• Days
• Weeks
• Months
• Never-ending

Classifying atrial fibrillation
The duration of these episodes is used to classify atrial fibrillation. The 2014
American College of Cardiology (ACC), American Heart Association (AHA), and
Heart Rhythm Society (HRS) guidelines recognize four types of atrial fibrillation:
1. Paroxysmal
2. Persistent
3. Longstanding persistent
4. Permanent
Paroxysmal Persistent Longstanding Permanent

persistent
Four types of atrial fibrillation
Paroxysmal
Paroxysmal atrial fibrillation is defined by the shortest
episodes of irregular tachycardia that start and stop
spontaneously. An episode can last seconds, minutes, or days,
but will resolve within 7 days with or without treatment.
Atrial fibrillation is almost always recurrent with episodes coming and going. As
long as the heart returns to sinus rhythm between episodes and episodes last
fewer than 7 days, it is considered paroxysmal.
Persistent
Persistent atrial fibrillation is defined by
continuous episodes lasting more than 7
days, but less than 12 months. Cases of new-
onset atrial fibrillation can be paroxysmal
or persistent.

Longstanding persistent
Longstanding persistent atrial fibrillation is defined by
continuous episodes lasting more than 12 months.
Permanent
After one or more years of consistent atrial fibrillation, it
can be considered permanent atrial fibrillation. But the
term permanent is not defined by a specific time point or
physiological state. Instead, it is used when the patient and
the clinician accept that the patient’s rapid, irregular heartbeat
is not going away, and they agree to stop trying to restore
sinus rhythm.
As final as it sounds, the permanent classification can be reversed and the

patient may go back to receiving treatments if the symptoms, interventions, or
preferences of the patient and clinician change over time.
How often do episodes occur?

Some people will experience a single episode of atrial fibrillation, and others
will experience recurrent episodes that increase in frequency and duration. The
majority of people with atrial fibrillation will experience recurrent episodes.
Each episode creates cardiovascular stress, causing both structural and

electrophysiological damage in the heart. This damage can accumulate and lead
to progression of atrial fibrillation.
What other terminology is used to classify

atrial fibrillation?
Once we have considered the length of the episodes, we can also classify atrial
fibrillation as either valvular or nonvalvular.

1. Valvular
Simply, valvular atrial fibrillation occurs when the patient has moderate to
severe mitral stenosis or a mechanical heart valve.
Mitral stenosis Mechanical heart valve
Valvular atrial fibrillation
2. Nonvalvular
Nonvalvular refers to atrial fibrillation in the absence of those two types of
valvular heart disease. Surprisingly, though, nonvalvular atrial fibrillation
does not exclude other types of valvular heart disease, such as the following:
- aortic stenosis
- mitral regurgitation
- those with valve repair
Aortic stenosis Mitral regurgitation Valve repair
Nonvalvular atrial fibrillation
This terminology can be confusing, and its use is debated for this reason, yet
the importance of this classification will become more obvious when we discuss
medications in a later lesson.

Addressing reversible conditions
Traditionally, there were three pillars in the management of atrial fibrillation:
1. Anticoagulation
2. Rate control
3. Rhythm control
But recent studies show that patients also benefit from a fourth pillar:
4. Address modifiable risk factors
Risk factors can be managed by addressing reversible conditions (e.g., high

blood pressure) and lifestyle choices.
What are the risk factors for atrial fibrillation?

There are many risk factors for the development and progression of atrial
fibrillation, including the following:
• Obesity
• Lack of physical activity
• Obstructive sleep apnea
• Diabetes
• High blood pressure
• Thyroid disease
• Smoking
• Misuse of drugs and / or alcohol
Each of these conditions are considered reversible or modifiable and can be

treated with medication or controlled with lifestyle changes like diet and exercise.
As control over these conditions improves, symptoms of atrial fibrillation are
likely to improve, and episodes will likely occur less often.
How do you modify these risk factors?

Currently, there are no guidelines for risk factor modification, but a
multidisciplinary approach that combines conventional approaches with lifestyle
changes should be considered part of atrial fibrillation management.

Manage atrial fibrillation with a multidisciplinary approach
Obesity
Obesity is a big risk factor for atrial fibrillation. Promoting weight loss through
healthy eating and aerobic exercise will help the patient lose weight gradually.
This will improve their overall health and their atrial fibrillation.
An initial goal of losing 10% of their body weight by doing 20 minutes of

low-intensity exercise 3 times a week is a good place to start patients living
with obesity.
Weight loss through bariatric surgery has proven helpful for atrial
fibrillation management.
Be aware that rapid weight loss through extreme exercise or

the use of weight loss medications can cause symptoms of
atrial fibrillation to get worse.

Sleep apnea
Weight loss and healthy eating will also help to reduce sleep apnea.
Diabetes and high blood pressure

Similarly, lifestyle changes may positively affect conditions like diabetes
and hypertension. As well, controlling blood sugar and blood pressure with
medications can be an effective way to manage atrial fibrillation.
Thyroid disease
Both hyper- and hypothyroidism are also risk factors
for atrial fibrillation. Controlling thyroid hormone levels
with medication (e.g., like methimazole) can help reduce
symptoms and episodes.
Smoking, drugs, and alcohol

Of course, encouraging patients to stop smoking, drinking, or using recreational
drugs, or to seek lifestyle and behavioral counseling, can help patients develop
long-lasting habits to reduce the burden of atrial fibrillation.
So, be sure to add lifestyle interventions and addressing reversible conditions to

your atrial fibrillation management toolbox.

Chapter 2
ANTICOAGULATION
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Evaluating stroke risk
In this chapter, we will discuss the second pillar of atrial fibrillation management—
anticoagulation and stroke prevention.
Why is stroke a risk for patients with atrial fibrillation?

Atrial fibrillation itself is not a life-
threatening medical condition,
but the sporadic contractions
characteristic of atrial fibrillation Thromboembolism
prevent the atria from emptying
Left atrial appendage
fully. As a result, blood collects in
the atria, especially near the left
atrial appendage, with the
potential to form blood clots.
These blood clots, or
thromboembolisms, can travel to Blood left in the atria due to
the brain, block blood flow, and atrial fibrillation can clot
cause a cardioembolic stroke.
The risk of stroke increases with age and a number of chronic conditions often
seen with atrial fibrillation, including the following:
• Congestive heart failure
• Hypertension
• Diabetes
• Vascular disease
This is particularly worrisome as blood clots originating in the heart tend to be

large, with the potential to cause more severe stroke and an increased risk of
major disability or death. For this reason, stroke prevention is a crucial part of
managing atrial fibrillation.

Why do we assess stroke risk?
Since the risk of stroke does not go away in atrial
fibrillation, anticoagulation is generally prescribed
long-term for these patients. Unfortunately, oral
anticoagulants are associated with risks and
side effects that are to be taken seriously. So, it
is important to identify which patients require
anticoagulants to prevent blood clots and which
do not.
How do we assess stroke risk?

Stroke risk is assessed using a points-based scoring system that considers
predictive factors such as age, gender, and comorbidities. This score can be
used when considering anticoagulation as part of atrial fibrillation treatment.
CHA2DS2-VASc system
Both European and American guidelines now recommend the CHA2DS2-VASc
system when evaluating stroke risk in patients with atrial fibrillation. This
updated version of the CHADS2 scoring system better distinguishes low-risk
patients from those with an intermediate or high risk of stroke.
CHA2DS2-VASc stands for:

• Congestive heart failure
• Hypertension
• Aged 75 years or older
• Diabetes
• History of stroke
• Vascular disease
• Age (between 65–74) Sex category
• Sex category (female)
One point is added to the risk score for each of the factors. Note that being
female automatically adds one point to the score.

For example, a 69-year-old female patient living with diabetes would have a
stroke risk score of 3:
Risk score = age 69 years + diabetes + female = 1 + 1 + 1 = 3
There are two factors that add two points to the score:
1. Aged 75 years or older
2. History of stroke
In the next lesson, we will discuss how to use this predictive score when deciding
whether a patient should start anticoagulation to prevent stroke.

Deciding when to use anticoagulants
To start anticoagulation or not to start anticoagulation? That is the question.
What needs to be considered before starting

anticoagulants?
Deciding when to start a patient with atrial fibrillation on an anticoagulant is a
balancing act, having to balance the following:
• Risk of stroke
• Risk of bleeding
• Comorbidities
• Patient preferences
Whether your patient has paroxysmal or permanent atrial fibrillation, your

approach to anticoagulation and stroke prevention should be the same—it is
time to apply the CHA2DS2-VASc score!
The CHA2DS2-VASc score is the primary tool used to decide when to start anti-
coagulation as it includes factors that can predict the risk of stroke and bleeding.
How do you interpret the CHA2DS2-VASc score?

Let’s discuss how to interpret CHA2DS2-VASc, starting with the lowest score.
• Low-risk score = 0 for male, 1 for female
A score of 0 as a male, or 1 as a female (remember,
women are automatically given 1 point using this
scoring system), indicates a low risk of stroke,
and anticoagulation is not necessary.

• Moderate risk score = 1 for male, 2 for female
A CHA2DS2-VASc score of 1 as a male or 2 as a
female indicates a moderate risk of stroke, and
you may want to consider anticoagulation at this
point. However, for patients with moderate stroke
risk, the benefits of anticoagulation may not
always outweigh the risks. Having a conversation
with your patient to discuss the possibility of
stroke or bleeding, as well as their preferences,
can help decide when to start anticoagulation.
• High-risk score ≥ 2 for male, ≥ 3 for female

Lastly, patients with a CHA2DS2-VASc score of at
least 2 as a male or 3 as a female have a high
stroke risk, and anticoagulation is indicated for
these patients.
Are there any exceptions?

There are two conditions that are associated with stroke that automatically support
the use of anticoagulants regardless of the patient’s CHA2DS2-VASc score:
1. Valvular atrial fibrillation: mitral stenosis or a mechanical heart valve
2. Hypertrophic cardiomyopathy: thickening of the left ventricular walls
If a patient has any of these conditions, anticoagulation is automatically

recommended (so the CHA2DS2-VASc score is not needed).

Assessing bleeding risk
In the previous two lessons, we discussed the CHA2DS2-VASc scoring tool to
determine a patient’s risk of stroke, and whether anticoagulation is right for
the patient. When considering the use of anticoagulants, you may also want to
assess the patient’s risk of bleeding.
Why do you assess bleeding risk?

There is no anticoagulant currently available that reduces the risk of blood clots
without increasing the risk of bleeding. Anticoagulation must balance stroke
prevention and bleeding risk.
When an injury causes bleeding, the body will attempt to limit blood loss by
forming a blood clot to plug the wound.
Without anticoagulants, clots form to heal wounds
Though anticoagulants cannot cause bleeding, they can slow or stop the clotting
needed to resolve small bleeding events. This has the potential to turn a clinically
insignificant bleeding event into a clinically significant one.
Anticoagulant
With anticoagulants, small bleeding events can become severe

How do you assess bleeding risk?
Bleeding risk increases with a number of chronic conditions, including the following:
• Liver disease
• Kidney disease
• Diabetes
• Cancer
The most popular way to assess bleeding risk is to use the HAS-BLED scoring system.
HAS-BLED scoring system

The HAS-BLED scoring system not only identifies risk factors for bleeding but
can direct physicians to correct modifiable risk factors such as blood pressure,
alcohol consumption, and the use of nonsteroidal anti-inflammatory (NSAIDs) or
antiplatelet drugs (e.g., aspirin).
Like CHA2DS2-VASc, when using the HAS-BLED scoring tool, 1 point is given for
each of the predictive factors a patient has:
• Hypertension
• Abnormal hepatic and / or renal function
• Stroke history
• Bleeding history
• Labile (or changing) time to clot
• Elderly (over 65 years)
• Drug and / or alcohol misuse (including aspirin and non-steroidal
anti-inflammatory drugs)

Two of these predictive factors can receive one or two points:
1. Abnormal hepatic and / or renal function
If the patient has either poor liver or renal function you would assign 1 point.
If they have both you would assign 2 points.
2. Drug and / or alcohol misuse

Similarly, if the patient misuses alcohol or drugs you would assign 1 point. If
they misuse both you would assign 2 points.
This means a HAS-BLED score can range from 0–9. The higher the HAS-BLED
score, the higher the risk of bleeding.
• Low bleeding risk < 3
A score below 3 indicates low bleeding risk.
• High bleeding risk ≥ 3

A score of 3 or more suggests a higher risk of bleeding and a more cautious
approach to anticoagulation is needed.
It is recommended that you reassess bleeding risk regularly after starting a

patient on anticoagulation.
Do you need to use both CHA2DS2-VASc and

HAS-BLED?
Because of their similarities, many clinicians
will rely on the CHA2DS2-VASc tool alone to
determine the right time to start anticoagulation,
only using HAS-BLED as a supplement for
specific cases. If you choose to use HAS-BLED,
it should always be used with and secondary to
CHA2DS2-VASc when making this decision.

Reviewing anticoagulants
Once a patient’s risk of stroke and bleeding has been assessed, and
anticoagulation has been found necessary, how do you choose which agent
to use?
Which anticoagulants are recommended?

The 2019 update of the American College of Cardiology, American Heart
Association, and Heart Rhythm Society guidelines recommend five
anticoagulants for the prevention of thromboembolism and stroke in patients
with atrial fibrillation:
• Warfarin
• Four novel oral anticoagulants (NOACs)
These five drugs differ in efficacy, dosing, metabolism, and associated risks.
Warfarin
Warfarin is a vitamin K antagonist. It acts as an anticoagulant by decreasing the
amount of available vitamin K in the blood, which is needed to form clotting
factors. While it helps reduce blood clots, it also increases the length of time
needed for a clot to form, which may put a patient in a life-threatening situation
if a major bleeding event were to occur.
Vitamin K Warfarin
Without anticoagulant Warfarin reduces clotting by

decreasing vitamin K levels
NOACs
The NOACs are a newer class of anticoagulants that prevent clot formation by
directly inhibiting one of two clotting factors, the enzymes thrombin or factor Xa.

Factor Xa Thrombin NOAC
Without anticoagulant NOACs reduce clotting by inhibiting

factor Xa enzyme
Like warfarin, the NOACs increase the time to clot. But compared to warfarin, the
following is true of NOACs:
• Lower risk of intracranial and fatal bleeding
• More predictable pharmacokinetics
• Monitoring not required
• Quicker onset of action
• No food interactions
The four NOACs recommended for use in patients with atrial fibrillation include
dabigatran (a thrombin inhibitor) as well as rivaroxaban, apixaban, and edoxaban
(all factor Xa inhibitors). An easy way to remember the Xa inhibitors is to find an
Xa in the drug name.
NOACs recommended for atrial fibrillation
Now that you are familiar with the available anticoagulants, in the next lesson,
we will discuss how to choose the anticoagulant that is right for your patient.

Selecting the appropriate anticoagulant
When choosing the right drug for your patient, you should consider many factors
including the patient’s history, whether they have valvular or non-valvular atrial
fibrillation, their liver and kidney function, and the potential for drug interactions
if they are taking other medications.
How do you decide which drug to use?

There are some guidelines to keep in mind when making this decision. Consider
the following factors to help you decide:
1. Valvular versus non-valvular atrial fibrillation
2. Liver and kidney function
3. History of gastrointestinal bleeding
4. Drug interactions
5. Patient compliance
Valvular or non-valvular atrial fibrillation

The type of atrial fibrillation is very important to consider.
1. Non-valvular atrial fibrillation
NOACs are recommended for patients with non-valvular atrial fibrillation, as
of 2019.
NOACs
2. Valvular atrial fibrillation

NOACs should not be used in patients with valvular atrial fibrillation.
This means that for patients with moderate to severe mitral stenosis or a
mechanical heart valve, the only option is warfarin.

With valvular atrial fibrillation, warfarin is the only option
Liver and kidney function

If you are considering an NOAC for a patient with atrial fibrillation, you should
first evaluate the patient’s liver and kidney function. This should be re-evaluated
at least once a year as long as the patient is on an NOAC. These compounds are
metabolized at the liver and excreted by the kidneys to varying degrees, so it is
important to monitor both liver and kidney health to ensure effectiveness and to
avoid adverse effects.
For patients with severe liver disease,

end-stage kidney disease, or those on dialysis,
we recommend either of the following:
• Warfarin
• Apixaban
History of gastrointestinal bleeding

Even though NOACs have been associated with
lower rates of intracranial and fatal bleeding,
dabigatran and rivaroxaban have been
associated with gastrointestinal bleeding. So,
if your patient has a history of gastrointestinal
bleeding, avoid the following:
• Dabigatran
• Rivaroxaban
Drug interactions
There are many drug interactions to consider when prescribing an anticoagulant.

Warfarin
Drug interactions with warfarin can lead to a longer time to clot, increased risk of
bleeding, and reduced efficacy in preventing clotting. The following drugs can all
affect the performance of warfarin:
• Antimicrobials
• Acetaminophen
• NSAIDs
• Antiplatelet medications
• Antiarrhythmic amiodarone
NOACs
The performance of NOACs can also be affected by the activity of other drugs.
The bioavailability of NOACs involves P-glycoprotein at the intestines, and
metabolism involves cytochrome P450 3A4 (CYP-3A4) at the liver. When drugs
that increase or decrease the activity of these proteins are taken alongside an
NOAC, anticoagulation may not be as effective. Examples of drugs to be wary of
include the following:
• Ritonavir
• Conazoles
• Rifamycins
• Carbamazepine
So, always be sure to check for possible drug interactions before prescribing
anticoagulants to your patient with atrial fibrillation.
Patient compliance
It is important to factor patient compliance and preference into your decision-
making as well.
Dabigatran and apixaban require twice daily dosing. Whereas rivaroxaban and
edoxaban are only taken once daily but can cause symptoms of intolerance like
the following:
• Nausea
• Dizziness
• Headache

How do you monitor bleeding risk?
When starting warfarin for a patient with atrial fibrillation, the patient’s clotting
ability should be tested at least once a week to monitor its effectiveness and
check for bleeding concerns. This is done by testing the amount of time needed
for a clot to form in a blood sample. This is known as the prothrombin time which
is reported as an international normalized ratio (INR).
The effective therapeutic range of warfarin for patients with atrial fibrillation is
an INR of 2.0 to 3.0.
Clotting ability is reported as INR
Once the therapeutic range has been reached, testing can be performed less
frequently, starting at once a month.
Note that as of 2019, the American College of Cardiology,

American Heart Association, and Heart Rhythm Society
guidelines no longer recommend the use of aspirin as an
anticoagulant in patients with atrial fibrillation. Aspirin has
been shown to offer no advantage over a placebo in stroke
prevention and is no longer part of the guidelines for the
management of atrial fibrillation.

Chapter 3
RATE AND RHYTHM

CONTROL
www.medmastery.com
Controlling heart rate in atrial fibrillation
Let’s talk about the third pillar of atrial fibrillation management—rate control. As
the name suggests, rate control is used in patients with atrial fibrillation to slow
and regulate heart rate.
How is heart rate affected by atrial fibrillation?

The term heart rate is used to describe how quickly the ventricles contract. A
normal heart rate ranges from 60 to 100 beats—or ventricular contractions—per
minute. Heart rate is expected to gradually increase with activity and gradually
decrease when the activity has stopped.
In atrial fibrillation, the rate of atrial contraction can reach 400 beats per min
(bpm)! That is really fast.
Most of these impulses do not reach the ventricles thanks to the non-conductive
refractory period of the atrioventricular (AV) node. This allows the atria and
ventricles to have different rates of contraction. Even so, the resting ventricular
rate (or heart rate) in atrial fibrillation is higher than normal, between
100 and 175 bpm.
Resting heart rate in atrial fibrillation
When the ventricles beat too fast there isn’t enough time for the muscle to relax
fully before contracting again. This leads to blood collecting in the ventricles so
less blood is being pumped with each contraction.

What happens to blood pressure during
atrial fibrillation?
The longer a patient’s heart rate remains high, the lower their blood pressure
becomes. If heart rate is not controlled, blood pressure will eventually become
too low to supply enough oxygen to the body, causing the patient to become
hemodynamically unstable. This can cause a range of symptoms:
• Low blood pressure
• Chest pain
• Confusion
• Shortness of breath
• Dizziness
• Cold hands and feet
Prolonged rapid heart rate can also contribute to the damage of the cardiac
muscle, or cardiomyopathy, that is associated with atrial fibrillation.
How can we control heart rate?

We want to reduce the rate of ventricular contraction to alleviate symptoms,
reduce the risk of hemodynamic instability, and prevent damage to the heart.
Because the AV node is typically the only electrical pathway connecting the atria
and ventricles, it is the target of rate control strategies.
Rate control drugs slow the conduction of impulses into the ventricles by
lengthening the refractory period of the AV node. This slows the ventricular rate.
Without rate control drugs

Ventricular rate slowed by rate control drugs

Controlling heart rhythm in atrial fibrillation
Now let’s discuss the fourth and last pillar of atrial fibrillation management—
rhythm control. Like rate control, rhythm control is used to lessen symptoms and
prevent damage to the heart tissue.
The role of the sinoatrial node

Sinus rhythm is the result of impulses generated at the sinoatrial (SA) node, the
pacemaker of the heart. A healthy heart will beat evenly 60–100 times per minute.
Normal resting heart rate
When impulses are no longer generated at the SA node, this creates an irregular
heartbeat as in atrial fibrillation. It can lead to fainting, stroke, and even
cardiac arrest.
Impact of irregular heart rhythm

Atrial fibrillation is characterized by a rapid heart rate as well as an irregular
heart rhythm where ventricular contractions occur unevenly.
Recall from an earlier lesson, the acronym NIP stands for the three key features
on electrocardiogram (ECG) that define atrial fibrillation:
1. Narrow QRS complex
2. Irregular rhythm
3. P waves absent

An irregular rhythm can lead to blood clots and stroke, hemodynamic instability,
cardiac tissue damage, and even death. Any damage within the heart promotes
more frequent and longer episodes of atrial fibrillation, creating a feedback cycle
that furthers the progression.
Irregular rhythm Clots, low blood pressure,

and cardiac damage
Restoring sinus rhythm with rhythm control will help lessen symptoms of
arrhythmia, reduce stroke risk, and protect the heart tissue and function by
breaking the feedback loop.
Irregular rhythm Clots, low blood pressure,

and cardiac damage
Controlling heart rhythm

In most patients with new-onset atrial fibrillation, sinus rhythm will return to
normal spontaneously, without intervention, within the first 48–72 hours. But
for those where this isn’t the case, you should attempt to restore sinus rhythm
before starting long-term rate or rhythm control strategies.

Sinus rhythm can be restored using electrical or pharmaceutical cardioversion.
Just like the shock you feel when ice cold water is thrown in your face,
cardioversion shocks the heart into an even rhythm of contraction. This shock is
meant to interrupt the sporadic contractions, reminding the heart how to control
its beat at a steady, even rate.

Slowing ventricular rate
Now that you know what rate and rhythm control are, let’s talk about when and
how to use them for the management of atrial fibrillation.
The management of new-onset atrial fibrillation is typically a three-step process:

1. Slow the ventricular rate
2. Restore sinus rhythm
3. Maintain a normal heart rate and regular rhythm
However, when a patient is unstable, as in the case of hemodynamic instability

or signs of heart attack or heart failure, it is more important to restore sinus
rhythm by cardioversion first. This will lessen the risk of a serious cardiac event.
Identifying an appropriate target heart rate

The goal of rate control is to slow and regulate ventricular rate, but what is the
target heart rate for patients with atrial fibrillation?
Well, if your patient has few or no symptoms and good left ventricular function, a
resting heart rate below 110 bpm is okay. This is called lenient rate control. It is
believed lenient control will still help prevent cardiomyopathy.
On the other hand, if your patient is symptomatic and / or has poor left ventricular
function (e.g., heart failure), aim for a resting heart rate below 80 bpm and below
110 bpm with exertion.
Treating patients with rate control drugs

Patient presentation Goal heart rate
Few symptoms and

< 110 bpm at rest
good left ventricular function
Symptomatic and /or < 80 bpm at rest

poor left ventricular function < 110 bpm with exertion
Improved rate control in these patients will lead to better symptom control and
better heart function.

Medical intervention to slow ventricular rate
Atrial fibrillation can often be managed in the outpatient setting. For patients with
no symptoms or only mild symptoms, oral rate control medication can be used.
However, if the patient is symptomatic and uncomfortable because of their

symptoms, intravenous (IV) rate control can help slow the ventricular rate and
relieve symptoms faster. This can still be done in the outpatient setting if an
equipped facility is available.
When treating initial atrial fibrillation in hospital, IV dosing provides a fast-acting

option when slowing the heart rate and is recommended. Once controlled, the
patient can be switched to oral tablets for the long-term maintenance of
rate control.
Does the patient have symptoms?
No symptoms or Symptomatic and

mild symptoms uncomfortable
Oral medication IV medication

as an inpatient or outpatient
Switch to oral medication

once heart rate is controlled
To achieve long-term rate control, the 2014 American College of

Cardiology (ACC) / American Heart Association (AHA) / Heart Rhythm Society
(HRS) guidelines recommend the use of beta-blockers like bisoprolol and
metoprolol, or calcium channel blockers like diltiazem and verapamil, to slow
ventricular rate for all classifications of atrial fibrillation.

How to choose the correct medication for your patient
There are two specific conditions to be careful of when choosing a rate
control medication:
1. Pre-excitation atrial fibrillation
Patients with pre-excitation atrial fibrillation—where impulses move
between the atria and ventricles along abnormal, or accessory, pathways—
should only receive oral beta-blockers for rate control.
2. Heart failure
Patients with heart failure should NOT receive calcium channel blockers.
Other medical options for optimizing rate control

Though not the drug of choice, the antiarrhythmic amiodarone can also be used
for rate control. The IV formulation is useful in critically ill patients without
preexcitation, and the oral dose should be considered when other rate control
options are not working.
Recently, digoxin has become less popular as a rate control medication, except
for specific patient populations including those with heart failure, hemodynamic
instability, or acute coronary syndrome (ACS).
Heart failure Hemodynamic Acute coronary

instability syndrome

Restoring sinus rhythm
Remember that the management of atrial fibrillation is a three-step process:
Let’s discuss the second step—restoring sinus rhythm. That is, when and how do
we stimulate the heart to return to an even, regular rhythm?
When should you intervene to restore sinus rhythm?

In many cases the heart will return to sinus rhythm spontaneously within
72 hours. When it does not, cardioversion is used. Restoring sinus rhythm
improves symptoms and quality of life as well as reduces the risk of serious
cardiac events.
Sometimes resetting the heart’s rhythm is more urgent than slowing the heart
rate. But most of the time cardioversion is elective and used in the non-emergency
setting after ventricular rate has been slowed in stable symptomatic patients.
What is cardioversion?
There are two forms of cardioversion:
1. Electrical
2. Pharmaceutical
Electrical cardioversion
Electrical, or direct current, cardioversion delivers a shock of energy to the heart,
causing all of the cells in the heart to contract at the same time with the aim of
returning the heart to sinus rhythm.
It is performed in hospital when the patient is sedated. The shock is delivered

by two electrodes that are either placed on the chest, or by one on the chest and
one on the back. The latter option is preferred for better current flow. The shock
is generated by a defibrillator in time with the R wave of the QRS cycle.

Electrical cardioversion is different from defibrillation where a higher energy is
used, and the shock is not timed with the cardiac cycle.
Because results can be seen right away, electrical cardioversion is used for
emergency cardioversion in unstable patients and scheduled (or elective)
cardioversion in stable patients. It is more effective than pharmaceutical
cardioversion with few risks and is the preferred method to restore sinus rhythm.
Be sure to check out Medmastery’s Emergency Procedures Part I course to learn

more about how to perform cardioversion.
Pharmaceutical cardioversion
Pharmacological cardioversion uses antiarrhythmic drugs to restore sinus
rhythm. It is most effective in new-onset atrial fibrillation and though it is less
effective than electrical cardioversion, it does not require sedation.

The 2014 ACC / AHA / HRS guidelines recommends using one of two types of
medication for pharmaceutical cardioversion:
• Class I sodium-channel blocker like flecainide or propafenone
• Class III potassium-channel blocker like dofetilide or intravenous ibutilide
Because the restoration of sinus rhythm is delayed compared to electrical

cardioversion, pharmacological cardioversion is only used for non-emergencies.
During pharmacological cardioversion, antiarrhythmic medications are delivered

intravenously or orally in hospital or clinic. Generally, sinus rhythm is restored
within 15 minutes using intravenous delivery, and 30–60 minutes with
oral delivery.
There is a pill-in-the-pocket approach that can be used at the start of an episode

by select outpatients with new onset paroxysmal atrial fibrillation. For this, either
oral flecainide or propafenone can be used.
Finally, if pharmacological cardioversion fails to restore sinus rhythm, the patient

is typically scheduled for electrical cardioversion.

Selecting the appropriate form
of cardioversion
Now that you know about the differences between electrical and pharmacological
cardioversion, how do you choose which one is appropriate for your patient?
When choosing between pharmacological and electrical cardioversion,

you should consider the risks and benefits of each. For example, electrical
cardioversion requires sedation but results are immediate, whereas
pharmacological cardioversion does not require sedation but there is a risk of
side effects and drug interactions.
Use of anticoagulants with cardioversion

Regardless of the method used, patients undergoing cardioversion should be on
an anticoagulant to lessen the risk of displacing any existing blood clots in the
heart and causing stroke.
Within the first 48 hours of an atrial fibrillation episode, patients with low stroke
risk can start anticoagulation the same day they undergo cardioversion because
the risk of clots is low for such a short duration of arrythmia.
With short duration arrythmia and low stroke risk, use

cardioversion and anticoagulation

In two subsets of patients, cardioversion should be delayed until they have been
on an anticoagulant for at least three weeks:
• Patients that have been experiencing atrial fibrillation for more than 48 hours
or for an unknown duration
• Patients with a high risk of stroke
If cardioversion is considered urgent and there is no time for anticoagulation, as

in the case of a hemodynamically unstable patient, transesophageal
echocardiography (TEE) can be used to confirm that there are no blood clots in
the left atrium prior to cardioversion. Anticoagulation should be started as soon
as possible.
In urgent situations, use TEE to rule out clots

before cardioversion
In all cases, anticoagulation should be continued for at least four weeks

after cardioversion.
Frequency of cardioversion treatment

Generally, people with recent-onset atrial fibrillation will only require one shock to
cardiovert. If cardioversion does not work the first time, it can be repeated. There
is no limit to how many times a patient can undergo cardioversion, but if after
many attempts the rhythm is still irregular, it is unlikely additional cardioversion
will be effective.
Similarly, for individuals with persistent atrial fibrillation where episodes last
weeks or months, cardioversion can be repeated as long as they are able to
maintain sinus rhythm for a reasonable amount of time between treatments.

Cardioversion is not for everyone
Cardioversion may not always be the best choice. For example, you should not
attempt cardioversion for a patient who cannot receive anticoagulants or who
has a blood clot in the left atrium. Also, you should consider a different strategy
for asymptomatic patients or those who have failed cardioversion in the past.

Maintaining heart rate
Once again, you may recall that the management of atrial fibrillation is a
three-step process:
Let’s discuss the third step in managing atrial fibrillation—maintenance.
Once ventricular rate has been slowed and sinus rhythm restored, you should
consider long-term treatment to prevent future episodes of atrial fibrillation. To
do this you will need to choose either a rate control or a rhythm control
therapeutic strategy. Both are used long-term with the aim of reducing
symptoms, frequency and duration of episodes of atrial fibrillation, as well as
preventing cardiomyopathy.
Rate control
There are three reasons that a rate control strategy is usually the first choice to
prevent future episodes of atrial fibrillation:
1. It can address symptoms.
2. It can slow the progression of atrial fibrillation.
3. It is considered less risky than rhythm control which can worsen instead of
prevent arrhythmia in a phenomenon known as proarrhythmic effects.

Which medications can be used in a rate control
therapeutic strategy?
The approach is similar to slowing ventricular rate in the acute setting. Long-
term maintenance of heart rate for all types of atrial fibrillation can be achieved
with beta-blockers like bisoprolol or metoprolol, or calcium channel blockers like
diltiazem or verapamil.
Oral amiodarone can also be used, but only when other rate control efforts have
been unsuccessful or are contraindicated.
Medications for long-term heart rate control
What is the target heart rate for maintenance therapies?

For the long-term management of atrial fibrillation, a target heart rate of less
than 80 bpm is recommended.
When selecting a long-term rate control medication, it is recommended that you

assess how effective it is with exertion to see if any pharmacological changes
need to be made. For this, a 6-minute moderate exercise walk-test or an exercise
ECG test can be used.

Assess medication effectiveness with a moderate walk test or exercise ECG
All rate control drugs are effective when the patient is at rest, but beta-blockers
are the most effective for active patients.
Beta-blockers are most effective for active patients

Maintaining rhythm
Since you can use rate control or rhythm control strategies to prevent future
atrial fibrillation, let’s talk about rhythm control strategies now.
Rhythm control
Maintenance rhythm control uses the same antiarrhythmic drugs used for
pharmacological cardioversion, but in oral formulation and taken long-term with
the aim of maintaining sinus rhythm.
Antiarrhythmic drugs to maintain sinus rhythm
There are three common reasons to consider rhythm control:

1. Persistent symptoms (even when the heart rate is controlled).
2. Heart rate is not controlled.
3. Rate control is not an option (e.g., if the patient cannot tolerate rate
control drugs).
Which medications can be used in a rate control

therapeutic strategy?
Drugs used for rhythm control slow the generation of electrical impulses within
the atria, slowing the heart rate and restoring a regular heart rhythm.

According to the 2014 ACC / AHA / HRS guidelines the following medications are
recommended for patients with atrial fibrillation:
• Potassium channel blockers
- amiodarone
- dofetilide
- dronedarone
- sotalol
• Sodium channel blockers
- flecainide
- propafenone
When selecting an antiarrhythmic drug for long-term use, you will need to
consider a number of factors:
• Heart disease or coronary artery disease
• Classification of atrial fibrillation (paroxysmal or permanent)
• Patient’s other medications
This will help you ensure the drug is effective, while avoiding drug interactions,
intolerance, and adverse events. For example, sodium channel blockers should
be avoided in patients with heart failure, coronary artery disease, or atrial flutter.
When atrial fibrillation becomes permanent, antiarrhythmic drugs should be

stopped, and if clinically possible, patients should be shifted to a rate control
strategy for the management of symptoms. This is based on evidence that
suggests antiarrhythmic drugs can increase serious cardiac events in patients
with permanent atrial fibrillation.
Stop antiarrhythmic drugs with permanent atrial fibrillation

Finally, amiodarone, which can be used for both rate and rhythm control, has
been shown to be very effective, but it can be quite toxic and should only be used
when other agents are contraindicated or have failed.

Choosing between rate and rhythm control
We used to think that rhythm control medications and strategies had a greater
effect on symptoms and better prevented stroke and hemodynamic instability.
However, we now know that rate and rhythm control strategies are equally
effective, with no difference in rates of stroke or death.
Should you use rate control or rhythm control

strategies to treat your patient?
Because they are equally effective, the decision of which strategy to use will
be individualized for the patient, factoring in comorbidities, medications,
intolerances, and preferences.
Rate and rhythm control strategies do not cure atrial fibrillation. The patient’s
atrial fibrillation will progress, and symptoms, interventions, or preferences
are likely to change, but you can switch the treatment approach as needed.
For example, a patient may need urgent cardioversion, but rate control is the
appropriate choice for their long-term maintenance. Or if rate control just isn’t
working and the patient is still experiencing symptoms, you might want to
consider a rhythm control strategy instead.
How to monitor treatment effectiveness

Once you prescribe a medication,
you will need to track how well it is
working. For outpatients, you can
do this by checking their heart rate
in your office a couple of times in
the first week. Alternatively, you can
use a cardiac monitoring device like
a Holter monitor, which can be used
to determine the efficacy of a new
medication as the patient goes about
their daily activities and can guide
Monitor treatment effectiveness by using
any dosing adjustments.
a Holter monitor during daily activities

If you are interested in learning more about Holter monitoring, you should check
out Medmastery’s Holter Monitoring Essentials course.
Together, the four pillars we have discussed—managing risk factors,

anticoagulation, rate control and rhythm control—support the management of
atrial fibrillation. If these approaches to both rate and rhythm control are not
working, you can then start to think about ablation.

Considering ablation
We have discussed how to manage symptoms and episodes of arrythmia in
patients with atrial fibrillation using strategies that control heart rate and rhythm.
But what do you do when these strategies do not work well enough?
Catheter ablation
Catheter ablation is an effective way to relieve symptoms. It is a rhythm control
procedure designed to interrupt the electrical impulses that cause atrial
fibrillation and to restore sinus rhythm.
This is done by using either heat or cold to cauterize the atrial tissue that
is triggering the abnormal, or ectopic, impulses. By damaging this tissue,
ablation isolates the tissue from the rest of the atria and stops the conduction
of the impulses.
How is catheter ablation performed?

One or more flexible catheters are inserted
into the heart through the jugular vein in the
neck, the subclavian vein at the shoulder,
or the femoral vein near the groin. These
catheters are used to deliver the cauterizing
energy to create small non-conductive scars
in the atrial tissue.

Where is the cauterizing energy targeted?
Ectopic impulses are often associated with the tissue surrounding the four
pulmonary veins where they enter the heart. This tissue is called the myocardial
sleeve and is the most common target of catheter ablation.
Are there risks associated with catheter ablation?

You will want to discuss the risks of the procedure with your patient. Catheter
ablation is an effective way to relieve symptoms, but there are many risks:
• Bleeding and infection
• Blood clots
• Worsening of the arrhythmia
• Damage to the vessels, electrical system, tissues, and valves of the heart
More serious risks are rare but possible:

• Buildup of fluid around the heart
• Narrowing of the pulmonary veins (stenosis)
• Stroke
• Creation of an abnormal pathway, or fistula, connecting the esophagus and
the heart
What does post-procedure monitoring look like for

these patients?
Following catheter ablation, some patients can go home the same day as the
procedure. Others will need to stay in hospital for one or more nights.

Atrioventricular node ablation
AV node ablation is another procedure available for patients with atrial fibrillation.
Where catheter ablation is used to control heart rhythm, AV node ablation can be
used to control heart rate.
How is AV node ablation performed?

Like catheter ablation, AV node ablation uses a catheter inserted into the heart
to apply heat energy to damage the tissue, this time around the AV node to block
impulses from reaching the ventricles.
Because AV node ablation destroys the AV node and its ability to conduct
impulses, the placement of a pacemaker is needed following this procedure to
ensure ventricular contraction.
Pacemaker required after AV node ablation

What are the risks associated with AV node ablation?
AV node ablation itself has fewer risks compared to catheter ablation, but there
are risks associated with the placement of a pacemaker:
• Infection
• Blood clots
• Damage in the area around the pacemaker
What types of patients should get AV node ablation?

Candidates for AV node ablation are highly symptomatic, hemodynamically
unstable, or have cardiomyopathy as a result of atrial fibrillation.
Because of the serious nature of these procedures, both catheter and AV node
ablation should only be considered after all pharmaceutical options for rhythm
and rate have been explored. But they generally have a high success rate.
Post-procedure care
Following either type of ablation, the patient will need to continue anti-
coagulation for at least two months to prevent blood clots and stroke. The
choice of rate or rhythm control medications following ablation will depend on
the patient’s symptoms.

APPENDIX
www.medmastery.com
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ATRIAL FIBRILLATION

Rate and rhythm control

Become an expert at www.medmastery.com. 2

Become an expert at www.medmastery.com. 3

What happens during a normal cardiac cycle?

Impulses from the SA node cause atria to contract

Become an expert at www.medmastery.com. 5

Impulses from the AV node cause ventricles to contract

What happens during tachycardia?

Become an expert at www.medmastery.com. 6

What can cause a sudden arrhythmia?

The underlying cause of atrial fibrillation is

Become an expert at www.medmastery.com. 7

Electrophysiology of atrial fibrillation

Impulses bounce chaotically AV node is non-conductive

Impulses reach the ventricles at random, creating the characteristic irregular

Irregular rhythm in atrial fibrillation

Become an expert at www.medmastery.com. 8

Management of atrial fibrillation

We will examine each of these in this course.

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What are the symptoms?

However, these symptoms can result from many arrhythmias.

How can you distinguish atrial fibrillation from other

Normal heartbeat ECG

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P waves appear before QRS complex

Distance between QRS complexes is constant

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Width of the QRS complex

≤ 0.12 s > 0.12 s

Regularity of the QRS complexes

Consistent distances between QRS complexes

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Presence and position of the P wave

Position of P wave relative to isoelectric line

Before QRS During QRS After QRS

Position of P wave relative to the QRS complex

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Narrow, irregular QRS with P waves absent

Wave does not return to baseline

What is the limitation of using an ECG?

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Remember to NIP atrial fibrillation in the bud!

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How does atrial fibrillation progress?

How long do episodes last?

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Paroxysmal Persistent Longstanding Permanent

Four types of atrial fibrillation

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As final as it sounds, the permanent classification can be reversed and the

How often do episodes occur?

Each episode creates cardiovascular stress, causing both structural and

What other terminology is used to classify

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Mitral stenosis Mechanical heart valve