ARRHYTMIA

Terminology and Basics

Ectopic Beats or Rhythms

• beats or rhythms that originate in places other than the SA
node
• the ectopic focus may cause single beats or take over and
pace the heart, dictating its entire rhythm
• they may or may not be dangerous depending on how they
affect the cardiac output
• Causes of Ectopic Beats or Rhythms
• hypoxic myocardium - chronic pulmonary disease,
pulmonary embolus
• ischemic myocardium - acute MI, expanding MI, angina
• sympathetic stimulation - nervousness, exercise, CHF,
hyperthyroidism
• drugs & electrolyte imbalances - antiarrhythmic drugs,
hypokalemia, imbalances of calcium and magnesium
• bradycardia - a slow HR predisposes one to arrhythmias
• enlargement of the atria or ventricles producing stretch
in pacemaker cells
Terminology and Basics

Arrhythmia or Dysrhythmia?
• dysrhythmia accurate, but arrhythmia most widely

Supraventricular: origin is above the ventricle, i.e.,

SA, atrial muscle, AV or HIS origin
Ventricular: origin is in ventricle
Arrhythmia is generally named for anatomical
site or chamber of origin
 Mechanisms
Automaticity: Spontaneous Phase 4 Depolarization (SA, AV,
Purkinje tissue)
• rate dependent on:
• Threshold potential
• slope of phase 4 depolarization
• resting membrane potential

Mechanisms of Arrhythmias
• Altered automaticity
• Normal, enhanced normal, abnormal
• Triggered activity
• Reentry
1. Altered Automaticity

Change slope,
change rate. 1o
sympathetic
mechanism;

Change threshold, PNS dec phase 4

change rate. slope and
hyperpolarize

Change RMP,
change rate From: Berne and Levy, “Physiology”,
Mosby, 1983.
 From: Berne and Levy, “Physiology”,
Mosby, 1983.

• hypothermia decrease, hyperthermia increase phase 4 slope

• hypoxia & hypercapnia both increase phase 4 slope
• cardiac dilation increases phase 4 slope
• local areas of ischemia or necrosis increases automaticity of neighboring
cells
• hypokalemia increases phase 4 slope, increases ectopics, prolongs
repolarization
• hyperkalemia decreases phase 4 slope; slow conduction, blocks
2. Triggered Activity
• Afterdepolarization reaches threshold
– Early: interrupt repolarization
• Congenital or acquired long QT syndrome: altered K+ and Na+
currents during phase 2 can produce dangerous V-tach
– Delayed: after completion of AP

3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)

• Anatomic: nodal tissue, Purkinje, BB, accessory path
– Example: WPW
• Functional
– Local differences in conduction velocity and membrane characteristics
 3. Reentry (circus movement, reciprocal or echo beat, reciprocating tachycardia)
• Anisotropic:
– circuit determined by difference in conduction velocity through length of fiber
• Reflection
– Parallel pathways with depressed segments
• Requires: available circuit, unidirectional block, and different conduction speed in limbs of circuit
– Conditions that depress conduction velocity or shorten refractory period promote functional block
– Exp: WPW reciprocating tachycardia, AV-nodal reentry, V-tach due to bundle branch reentry, infarcted area.
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Electrical Impulse
Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

Tissues with these type of circuits may exist:

• in microscopic size in the SA node, AV node, or any type of heart tissue
• in a “macroscopic” structure such as an accessory pathway in WPW
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms
Premature Beat Impulse
Cardiac
Repolarizing Tissue Conduction
(long refractory period) Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

1. An arrhythmia is triggered by a premature beat

2. The beat cannot gain entry into the fast conducting
pathway because of its long refractory period and
therefore travels down the slow conducting pathway only
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

3. The wave of excitation from the premature beat

arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast
pathway
The “Re-Entry” Mechanism of Ectopic Beats & Rhythms

Cardiac
Conduction
Tissue
Fast Conduction Path Slow Conduction Path
Slow Recovery Fast Recovery

4. On arriving at the top of the fast pathway it finds the

slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
 Re-entry Circuits as Ectopic Foci and Arrhythmia Generators

Atrio-Ventricular Nodal Re-entry

• supraventricular tachycardia
Atrial Re-entry Ventricular Re-entry
• atrial tachycardia • ventricular tachycardia
• atrial fibrillation
• atrial flutter

Atrio-Ventricular Re-entry
• Wolf Parkinson White
• supraventricular tachycardia
Clinical Manifestations of Arrhythmias
• many go unnoticed and produce no symptoms
• palpitations – ranging from “noticing” or “being aware” of ones heart
beat to a sensation of the heart “beating out of the chest”
• if Q is affected (HR > 300) – lightheadedness and syncope, fainting
• drugs & electrolyte imbalances - antiarrhythmic drugs, hypokalemia,
imbalances of calcium and magnesium
• very rapid arrhythmias u myocardial oxygen demand r ischemia
and angina
• sudden death – especially in the case of an acute MI
• mechanism differentiation from ECG very difficult to impossible
Clinical Application
• No rhythms precisely regular
• Incidence: common (PVC, PAC), increase with age
• ECG differentiation may be impossible
• Monitor leads V1 or MCL1: L&R ventricular ectopy, RBBB &
LBBB, good P-waves
• Where to look for clues
• P-wave morphology
• PR interval
• QRS morphology
• QTc interval
• Matching atrial rate with ventricular
• Look for gaps in the rhythm
Clinical Application
• Eight basic rhythm disturbances
• early beats (extrasystole)
• unexpected pauses (nonconducted atrial extrasystole)
• bradycardia (sinus bradycardia)
• tachycardia (ventricular or atrial)
• bigeminal rhythm (ventricular or supraventricular extrasystolic)
• group beating (2nd degree heart block)
• total irregularity (atrial fibrillation)
• regular non-sinus rhythm at normal rate (accelerated AV rhythm)
 ARRHYTHMIA THERAPIES
1. Pharmacological Treatment
• Accordingly, drugs which may reduce
ventricular rate by reducing AV nodal
conduction include:
–  calcium channel blockers (verapamil
(Isoptin, Calan), diltiazem
(Cardiazem))
–  beta-adrenergic receptor blockers
(propranolol (Inderal)), and
–  digitalis glycosides.
 1. Pharmacological Treatment
• Treatment of atrial fibrillation: Verapamil
(Isoptin, Calan) & Diltiazem (Cardiazem)
– Blocks cardiac calcium channels in slow response
tissues, such as the sinus and AV nodes.
• Useful in treating AV reentrant tachyarrhythmias and in
management of high ventricular rates secondary to atrial flutter
or fibrillation.
– Major adverse effect (i.v. administration) is
hypotension. Heart block or sinus bradycardia can also
occur.
2. Implantable Cardioverter Defibrillators
• implantable cardioverter defibrillators
(ICDs) attempt to terminate
tachyarrhythmias once they have been
initiated by altering the
electrophysiological substrate of the
heart through electrical stimulation
3. Ablation Therapy
4. Gene and Cell Therapy