MD2011

Cardiovascular
Medicine
Dr Lisa Chilton
Lisa.Chilton@jcu.edu.au
Building DB087, Room TV222,
4781 5195

Dysrhythmias

Figures 19-26 (top) & 19-30 (bottom), Copstead and Banasik, 3E

Study Guide 1
1. Explain why dysrhythmias are divided into three classes
2. Explain each of the three common mechanisms of abnormal
sites of impulse initiation (inappropriate automaticity,
triggered activity, and re-entry)
3. Compare and contrast sinus tachycardia, sinus bradycardia,
sinus arrhythmia and sinus arrest
4. Compare and contrast the different types of conduction
blocks
5. Compare and contrast junctional and ventricular escape
rhythms

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 Study Guide 2
6. Explain how abnormal sites of impulse initiation may
produce atrial flutter, atrial fibrillation, ventricular
tachycardia, ventricular fibrillation, and premature
complexes (atrial or ventricular)
7. Define accessory pathways and pre-excitation, using
Wolff-Parkinson-White syndrome as an example
8. Understand how and why the ECG changes in each
dysrhythmia

Dysrhythmias
“Abnormalities of the rhythm of action potential
production and/or the conduction system”
May arise from hypoxia, electrolyte imbalances, trauma,
inflammation, and/or drugs
Significant because they:
May indicate an underlying pathology
Can disrupt normal cardiac function

Three major classes of dysrhythmias:

1. Abnormal rates of sinus rhythm
2. Disturbances in the conduction system
3. Abnormal sites of impulse initiation (ectopic)

Class 1:
Abnormal Rates of Sinus Rhythm

Sinus bradycardia
Sinus tachycardia
Sick sinus syndrome
Sinus arrest

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 Sinus Rhythm
Impulse rate between 60 and 100 impulses/minute
Begins in the sinoatrial node (sinus node)
Follows the normal conduction pathway
PR interval and QRS duration within normal range

Figure 19-17, Copstead and Banasik, 3E

ECG Characteristics of
Normal Sinus Rhythm

Characteristic Findings
Rhythm Regular, PP intervals and RR intervals
may vary as much as 3 mm and still be
considered regular
Rate 60 – 100 bpm
P waves One P wave preceding each QRS
PR Interval 0.12 – 0.20 second, constant
QRS Duration 0.04 – 0.10 second, constant

Source: Table 19-3, Copstead and Banasik, 4E

Abnormal Rates of Sinus Rhythm

Tachycardia: heart rate > 100 bpm
May be perfectly normal (exercise, anxiety, fright)
Commonly associated with increased sympathetic NS activity,
decreased parasympathetic NS activity, fever, pain,
hyperthyroidism, low BP, hypoxia and increased metabolic
rate
If HR is too high to allow the ventricles to fill, CO decreases
and treatment is necessary
Drugs which block sympathetic tone (sympatholytics) and
Ca2+ channel blockers are commonly used

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Abnormal Rates of Sinus Rhythm
Bradycardia: heart rate < 60 bpm
May be normal (athletes)
SA node pacemaker potential depolarisation rate slows due
to parasympathetic activity, sleep, drugs, increased stroke
volume, and acute hypertension
If bradycardia is associated with insufficient CO, then
treatment includes:
Sympathomimetic drugs
Parasympatholytic drugs

Sinus tachycardia

Sinus bradycardia
Figures 19-18 and 19-19, Copstead and Banasik, 3E

Abnormal Rates of Sinus Rhythm

Sinus arrhythmia: variability in sinus rhythm associated with

ventilation and fluctuations in autonomic NS tone
Can be pronounced in children
No treatment is needed
Must be distinguished from sick sinus syndrome, where the
SA node oscillates between periods of tachycardia and
bradycardia (this illness requires an artificial pacemaker)
“Heart Rate Variability” has a diagnostic value in predicting
severity of cardiac disease progression

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 Sinus arrhythmia

Sick Sinus Syndrome

Figure 19-20, Copstead and Banasik, 3E

Abnormal Rates of Sinus Rhythm

Sinus arrest: absence of SA node activity and so of electrical
activity in the heart
Results in no contraction and no CO
Usually, after a period of sinus arrest, slower parts of the
conduction system take over (AV node followed by His bundle
and Purkinje system), restoring excitation at a slower rate

Figure 19-21, Copstead and Banasik, 3E

Class 2: Disturbances of the

Conduction System

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Conduction Pathway Disturbances
causes:
Sinus arrest (producing escape rhythms)
Enhanced excitability, triggered activity, re-entry (producing
premature depolarisations which override the SA node), AV
node damage or malformation, presence of an accessory
pathway
Excitation of the atria may occur due to backward AP
spread from the AV node, or may not occur at all
P wave may be inverted and may occur at any time (or
not at all)
PR interval is abnormal

Conduction Pathway Disturbances

Escape rhythms
1. Junctional escape rhythms
Arise from the AV node (40 – 60 APs/min)
Normal QRS complex

Figure 19-22, Copstead and Banasik, 3E

Conduction Pathway Disturbances

Escape rhythms
2. Ventricular escape rhythms
Arise from the Bundle of His, Bundle Branches, or the
Purkinje fibres (15 – 40 APs/min)
Abnormally wide QRS complex

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Conduction Pathway Disturbances
Escape rhythms
2. Ventricular escape rhythms

Figure 19-23, Copstead and Banasik, 3E

Conduction Pathway Disturbances

Deranged Atrioventricular Conduction
Atrioventricular (AV) Block
Disturbance of conduction of the sinus impulse from
the right atrium to the ventricles
Conduction may be slowed or lost altogether
Functional or pathological defect in the AV node,
Bundle of His or bundle branches
May be first-degree, second-degree Type I or Type II,
or third-degree

Conduction Pathway Disturbances

Abnormal Atrioventricular Conduction
1. First-degree AV Block
PR Interval is prolonged (> 0.20 second)
Rhythm is normal and each QRS complex is
associated with a P wave
Common; occurs without evidence of heart disease
Drugs, MI, and congenital heart defects may
produce first-degree AV block
Manage underlying cause if known

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 Figure 19-17, Copstead and Banasik, 3E

P T

QRS
Normal Lead II

P T

QRS Figure 19-32, Copstead and Banasik, 3E

First-degree AV block

Conduction Pathway Disturbances

Abnormal Atrioventricular Conduction
2. Second-degree AV Block
Not all P waves are conducted to the ventricles (not all P
waves are associated with QRS complexes)
The pattern of blocked P waves determines the type of
second-degree AV block
A. Type I (Mobitz Type I or Wenckebach): the PR Interval
progressively increases until a P wave is not conducted
(dropped beat)
The pattern then repeats

Second-degree AV block, Type I

R R R R R
P P P P P P

Figure 19-33, Copstead and Banasik, 3E

QRS complexes appear clustered

PP intervals are constant within a cluster, but the RR Intervals
vary
Usually caused by reversible ischaemia of the AV node,
associated with acute MI
Treatment only required if progresses to Type II block

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Conduction Pathway Disturbances
Abnormal Atrioventricular Conduction
B. Second-degree AV Block, Type II
Aka Mobitz Type II
Blocked P waves occur with a consistent PR
Interval (no PR prolongation, as seen in Type I)
Associated with damage to the bundle of His, the
right bundle branch, or both
If due to bundle branch failure, the QRS complex
will abnormally wide

Second-degree AV block, Type II

R R R
P P P P P P P P P

Figure 19-34, Copstead and Banasik, 3E

More serious than Second-degree AV block, Type I

Associated with anterior septal MI or fibrosis of the
conduction system
Bradycardia yields low CO
May progress to third-degree AV block
Treatment: implant an artificial pacemaker

Conduction Pathway Disturbances

Abnormal Atrioventricular Conduction
3. Third-degree AV Block
Complete block (no P waves are conducted)
Ventricular escape controls the rhythm of the QRS
complexes (Purkinje fibres take over)
Damage to the AV node, bundle of His, and/or bundle
branches (width of QRS complex reveals site)
Bradycardia may compromise CO
Treatment: implant an artificial pacemaker

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 Third-degree AV block

P P P P P P P P

Figure 19-35, Copstead and Banasik, 3E

Conduction Pathway Disturbances

Abnormal Conduction Pathways
Accessory conduction pathways allow atrial excitation to
spread to the ventricles abnormally quickly
“Pre-excitation syndromes”

Wolff-Parkinson-White Syndrome
Accessory pathways pass from atria to ventricles without
passing through AV node
Short PR Interval, δ waves (abnormal start of QRS
complex) and wide QRS complex

Wolff-Parkinson-White Syndrome

Figure 19-36, Copstead and Banasik, 3E

Accessory pathways may allow re-entry, VT and VF

Treatment includes antiarrhythmia drugs, surgical ablation of
the accessory pathway, and disruption of the conduction
pathway

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