Arrhythmia

Introduction
o Cardiac arrhythmia involves a group of conditions in which the
heartbeat is irregular, too slow, or too fast.
oIrregularity of heartbeat occurs when the electrical impulses in the heart
that coordinate heartbeats don't function properly.
oThe heart has two basic properties, namely,
an electrical property and
a mechanical property.
oArrhythmias Can be broadly grouped into bradyarrhythmia and
tachyarrhythmia. 2
Normal cardiac conduction

3
Cardiac action potential

4
Abnormal conduction
oThe mechanisms of tachyarrhythmias have been classically divided
into two general categories:
those resulting from an abnormality in impulse generation
“automatic” tachycardias and
those resulting from an abnormality in impulse conduction
“reentrant” tachycardias.

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Cont….
oAutomatic tachycardias depend on spontaneous impulse generation in latent
pacemakers and may be a result of several different mechanisms, such as:

Drugs (digoxin or catecholamines), and conditions (hypoxia, hypokalemia,

cardiac dilation).

may lead to an increased slope of phase 4 depolarization in cardiac tissues

other than the SA node.

oIf the rate of spontaneous impulse generation of the abnormally automatic

tissue exceeds that of the SA node, then an automatic tachycardia may result.
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Cont….
oAutomatic tachycardias have the following characteristics:

The onset of the tachycardia is unrelated to an initiating event such as a

premature beat,

The initiating beat is usually identical to subsequent beats of the tachycardia,

The tachycardia cannot be initiated by programmed cardiac stimulation, and

 The onset of the tachycardia is usually preceded by a gradual acceleration in

rate and termination is usually preceded by a gradual deceleration in rate.

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Cont….
o Clinical tachycardias resulting from the classic forms of enhanced automaticity are
not as common as once thought.
 sinus tachycardia and junctional tachycardia are major examples.

o Triggered automaticity is also a possible mechanism for abnormal impulse generation.

o Triggered automaticity refers to transient membrane depolarizations that occur

during repolarization (early afterdepolarizations[EADs]) or
after repolarization (delayed afterdepolarizations [DADs]) but prior to phase 4 of
the action potential.

o Afterdepolarizations may be related to abnormal calcium and sodium influx during or

just after full cellular repolarization.
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Cont….
o Triggered automatic rhythms possess some of the characteristics from both automatic
tachycardias and reentrant tachycardias.

o Reentry is a concept that involves indefinite propagation of the impulse and continued
activation of previously refractory tissue.

o There are three conduction requirements for the formation of a viable reentrant focus:

 two pathways for impulse conduction,

 an area of unidirectional block (prolonged refractoriness) in one of these pathways, and

slow conduction in the other pathway.

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Cont….

first
second

third
fourth

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Cont….
oUsually, a critically timed premature beat initiates reentry.

oThis premature impulse enters both conduction pathways but encounters

refractory tissue in one of the pathways at the area of unidirectional block.

oThe impulse dies out because the tissue is still refractory from the previous
(sinus) impulse.

oAlthough it fails to propagate in one pathway, the impulse may still proceed
in a forward direction (antegrade) through the other pathway because of this
pathway’s relatively shorter refractory period.

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Cont…..
oThe impulse may then proceed through a loop of tissue and “reenter” the
area of unidirectional block in a backward direction (retrograde).

oBecause the antegrade pathway has slow conduction characteristics, the area
of unidirectional block has time to recover its excitability.

oThe impulse can proceed in a retrograde fashion through this previously

refractory tissue and continue around the loop of tissue in a circular fashion.

oThus, the key to the formation of a reentrant focus is crucial conduction

discrepancies in the electrophysiologic characteristics of the two pathways.

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Cont….
oThe reentrant focus may excite surrounding tissue at a rate greater than
that of the SA node, leading to formation of a clinical tachycardia.

oAnother model of reentry, referred to as a functional reentrant loop or

leading circle model, may also occur.

o In a functional reentrant focus, the length of the circuit may vary

depending on the conduction velocity and recovery characteristics of
the impulse.

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Cont….
oThe area in the middle of the loop is continually kept refractory by the
inwardly moving impulse.

oThe length of the circuit is not fixed but is the smallest circle possible,
such that the leading edge of the wave front is continuously exciting tissue
just as it recovers.

oIt differs from the anatomic model in that the leading edge of the
impulse is not preceded by an excitable gap of tissue, and it does not have
an obstacle in the middle.

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Possible mechanism of proarrhythmia in the anatomic model
of reentry

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Mechanism of reentry and proarrhythmia

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Cont……
o Reentrant tachycardias have the following characteristics:

the onset of the tachycardia is usually related to an initiating event (ie, premature beat),

the initiating beat is usually different in morphology from subsequent beats of the
tachycardia,

the initiation of the tachycardia can usually be incited with programmed cardiac
stimulation, and

the initiation and termination of the tachycardia is usually abrupt without an

acceleration or deceleration phase.

o Examples of reentrant tachycardias include AF, atrial flutter (AFl), AV nodal reentrant
tachycardia (AVNRT), AV reentrant tachycardia (AVRT), and recurrent VT.
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Anti-arrhythmic drugs (AADs)
oDrugs have antiarrhythmic activity by directly altering conduction in several
ways.

1. A drug may depress the automatic properties of abnormal pacemaker cells.

2. Drugs may alter the conduction characteristics of the pathways of a

reentrant loop.
A drug may facilitate conduction (shorten refractoriness), or
a drug may further depress conduction (prolong refractoriness).

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Classifications of AADs

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Types of arrhythmias
BRADYARRHYTHMIAS (<60bpm)
oSinus bradycardia
oSinoatrial (SA) block
oSinus pause
oSinus arrest (slow junctional rhythm)
TACHYARRYTHMIAS (>100bpm)
o Supraventricular Arrhythmias
Sinus tachycardia
Atrial fibrillation or Atrial flutter
 Automatic (ectopic) atrial tachycardia
 Multifocal atrial tachycardia
Atrioventricular nodal reentrant
tachycardias
o Ventricular Arrhythmias
Premature ventricular beats
Ventricular tachycardia
Ventricular fibrillation 20
Atrial fibrillation/ flutter
oAF continues to be the most common sustained arrhythmia encountered in
clinical practice, affecting between 2.7 and 6.1 million Americans.
oThe overall prevalence of AF is 0.4% to 1%, and this increases with age.
o The prevalence of AF also appears to increase as patients develop more
severe HF.
oThe general lifetime risk for AF in men and women at least 40 years of age is
estimated to be 1 in 4.

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Cont…..
oAF and AFl may present as a chronic, established tachycardia, an acute
tachycardia, or a self-terminating, paroxysmal form.
acute AF - onset within 48 hours,
paroxysmal AF - terminates spontaneously in less than 7 days,
recurrent AF - two or more episodes,
persistent AF - duration longer than 7 days and does not terminate spontaneously,
long-standing persistent AF - duration longer than 12 months, and
permanent AF - patient and provider jointly decide to stop attempts to restore or
maintain SR.

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Cont…..
oAF is characterized by extremely rapid (atrial rate of 400 to 600 beats/min) and
disorganized atrial activation.

oSupraventricular impulses penetrate AV conduction system to variable degrees,

resulting in irregular ventricular activation and irregularly irregular pulse
(120–180 beats/min).

oAtrial flutter has rapid (270–330 atrial beats/min) but regular atrial activation.

oVentricular response usually has a regular pattern and a pulse of 300 beats/min.

oThis arrhythmia occurs less frequently than AF but has similar precipitating
factors, consequences, and drug therapy.
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Cont….
oThe predominant mechanism of AF and atrial flutter is reentry,
which is usually associated with organic heart disease that causes atrial
distention (e.g., ischemia or infarction, hypertensive heart disease, and
valvular disorders).

oAdditional associated disorders include

 acute pulmonary embolus and chronic lung disease, resulting in
pulmonary hypertension and cor pulmonale, and
states of high adrenergic tone

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Clinical presentation
oClinical manifestations may ranging from no symptoms to minor
palpitations or irregular pulse to severe and even life-threatening symptoms.

oPatients with AF or AFl may experience the entire range of symptoms

associated with other supraventricular tachycardias,
although syncope as a presenting symptom is uncommon.

oMost often, patients complain of rapid heart rate/palpitations, chest pain,

dyspnea, dizziness, and fatigue.

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Diagnosis
oAF is an irregularly irregular supraventricular rhythm with no discernible,
consistent atrial activity (P waves).

oVentricular rate is usually 90 to 170 beats/min and the pulse is irregular.

oAFl is (usually) a regular supraventricular rhythm with characteristic

flutter waves reflecting more organized atrial activity.

oCommonly, the ventricular rate is in factors of 300 beats/min.

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Treatment
oThe goals of treating AF or atrial flutter are
restoring sinus rhythm,
preventing thromboembolic complications, and
preventing further recurrences

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Cont….
oTreatment of AF involves several sequential goals.

First, evaluate need for acute treatment (usually with drugs that slow
ventricular rate).

Next, consider methods to restore sinus rhythm, considering risks

involved (eg, thromboembolism).

Lastly, consider ways to prevent long-term complications, such as

recurrent arrhythmia and thromboembolism

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Cont….
o In patients with new-onset AF or atrial flutter with signs and/or symptoms of
hemodynamic instability,
direct-current cardioversion (DCC) is indicated to restore sinus rhythm
immediately.

o If patients are hemodynamically stable, the focus should be directed toward

controlling ventricular rate.

o Use drugs that slow conduction and increase refractoriness in the AV node as
initial therapy.

o In patients with normal LV function, IV β-blockers (propranolol, metoprolol, and

esmolol), diltiazem, or verapamil are recommended as first-line therapy.
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Cont…..
oIn patients with LVEF less than or equal to 40%, avoid IV diltiazem and
verapamil, and use IV β-blockers with caution.

oIn patients having an exacerbation of HF symptoms, use IV digoxin or

amiodarone as first-line therapy for ventricular rate control.

oIV amiodarone can also be used in

 patients who are refractory or
have contraindications to β-blockers, non dihydropyridine calcium
channel blockers, and digoxin.

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Cont….
oAfter treatment with AV nodal blocking agents and a subsequent decrease in
ventricular response,
assess the patient for the possibility of restoring sinus rhythm if AF
persists.

oIf sinus rhythm is to be restored, initiate anticoagulation prior to

cardioversion because return of atrial contraction increases risk of
thromboembolism.

o Patients become at increased risk of thrombus formation and a subsequent

embolic event if the duration of AF exceeds 48 hours.

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Cont….
• Patients with AF for longer than 48 hours or an unknown duration should
receive
warfarin, a low-molecular weight heparin or dabigatran for at least 3
weeks prior to cardioversion.

• Patients with AF less than 48 hours in duration do not require

anticoagulation prior to cardioversion,
 but they should receive either IV unfractionated heparin or a low-
molecular-weight heparin at presentation prior to and proceeding to
cardioversion.

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Cont…..
oIf cardioversion is successful, continue anticoagulation with either warfarin or
dabigatran for at least 4 weeks.

oFor patients at high or intermediate risk for stroke,

oral anticoagulation is preferred over aspirin or aspirin plus clopidogrel;
dabigatran should be used rather than warfarin.

oFor patients at low risk for stroke, either no antithrombotic therapy or aspirin
is recommended;
however, no therapy is preferred.

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Cont….
oAmiodarone is the most effective and most frequently used class III
agent for preventing AF recurrences despite its potential for significant
organ toxicity.

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Evaluation
oThere are some therapeutic outcomes that are unique to certain
arrhythmias.

oFor instance, patients with AF or AFl need to be monitored for

thromboembolism and for complications of antithrombotic therapy
(bleeding, drug interactions).

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Cont….
oThe most important monitoring parameters for most patients fall into
the following categories:

mortality (total and sudden cardiac death);

arrhythmia recurrence (duration, frequency, symptoms);

hemodynamic consequences (heart rate, blood pressure, symptoms);

and

treatment complications (side effects or need for alternative or

additional drugs, devices, surgery).

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Case study
J.K., a 66-year-old man, presents with complaints of mild shortness of
breath (SOB) and palpitations for the last 2 weeks. He experienced
palpitations of shorter duration three times in the last year, but these
were not associated with SOB. His medical history includes type II
diabetes mellitus for the past 5 years, hypertension, and gout. There is
no history of rheumatic heart disease, MI, HF, pulmonary embolism, or
thyroid disease. Medications include glyburide 5 mg twice a day (BID),
hydrochlorothiazide 25 mg/day, and allopurinol 300 mg/day. J.K. does
not smoke or drink alcohol.
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Cont….
Physical examination reveals a blood pressure (BP) of 136/84 mmHg, pulse of
154 beats/minute with an irregularly irregular pattern, respiratory rate (RR) of 16
breaths/minute, and temperature of 98.2◦F. He has bilateral rales on chest
auscultation.

Cardiac examination reveals an irregularly irregular rhythm without murmurs,

gallops, or rubs. His jugular vein is distended 4 cm. His extremities have 1+
pitting edema. The ECG shows AF and the chest radiograph is compatible with
mild HF. A cardiac echocardiogram reveals the atrial size to be <5 cm (normal)
and a previously unknown ejection fraction (EF) of 35% (low). In view of his
history and previous episodes, J.K. is diagnosed with PAF. 38
Cont…..
1. Which of J.K.’s other medical problems may predispose him to AF development?
What other conditions commonly are associated with AF?

2. What clinical findings demonstrated by J.K. are typically associated with AF?

3. J.K. is given a 1-mg loading dose of digoxin, followed by a 0.25-mg every day
(QD) maintenance dose. What is the purpose of administering digoxin? What are
the relative advantages and disadvantages of digoxin compared with other agents
to control ventricular rate?

4. What other drugs can be used for ventricular rate control, and what are their
relative advantages and disadvantages compared with digoxin?

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