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

 Class 3:
Abnormal Sites of Impulse Initiation
Premature atrial complexes, premature ventricular
complexes, atrial flutter, atrial fibrillation, ventricular
tachycardia, ventricular fibrillation
Three mechanisms may give rise to ectopic (abnormal) sites
of impulse initiation:
1. Abnormal automaticity
2. Triggered activity
3. Re-entry
Mechanism 1: Inappropriate Automaticity

Atrial or ventricular cells which should lack automaticity

become able to spontaneously depolarise and produce action
potentials
Membrane abnormally leaky to Na+ or Ca2+ ions at rest (in
Phase 4), producing a spontaneous depolarisation
Ischaemia and low ATP levels are associated with an inability
to maintain ion gradients and spontaneous depolarisation
Electrolyte imbalances, especially hypokalaemia, predispose
to spontaneous depolarisation
Ventricular Contractile Myocytes

Normal Phase 4 (RMP):

K1 = dominant K+
current at rest
Small amount of K+,
Na+ & Ca2+ leak
currents
Na+/K+ ATPase &
PMCA + SERCA keep
Figure 14-13, Silverthorn, Human Physiology, 5ed
ion gradients normal
 Mechanism 2: Triggered Activity
Definition: an extra AP that is triggered spontaneously during or
immediately following repolarisation
1. Early afterdepolarisations (EADs) are second action
potentials that are triggered early in the relative refractory
period (Phase 3)
May occur in patients with abnormally long repolarisation times,
as with Long QT Syndrome
Voltage-gated Ca2+ (and Na+) channels recover from inactivation
before membrane potential is below their threshold of
activation, allowing them to open and depolarise the cell
 EADs

Figure 19-14A, Copstead and Banasik, 3E

 Mechanism 2: Triggered Activity

2. Delayed afterdepolarisations (DADs) are depolarisations

that occur after the repolarisation phase is complete
Presents as oscillating depolarisation waves on the ECG
Associated with high intracellular Ca2+ and SR Ca2+ levels,
which trigger Ca2+ release from the SR and evoke an action
potential
Digoxin/digitalis toxicity and excessive catecholamine
stimulation are associated with DADs
 DADs

Figure 19-14B, Copstead and Banasik, 3E

Mechanism 3: Re-entry of Excitation

Mechanism most likely to lead to potentially lethal

ventricular tachycardia (VT) and ventricular fibrillation (VF)
Two types:
1. Functional re-entry occurs when part of the electrical
conduction in the heart is abnormally slowed
2. Anatomical re-entry occurs when part of the electrical
conduction in the heart is through an unusually long
pathway
MI and electrolyte imbalances predispose to re-entry
Mechanisms 3: Re-entry of Excitation
Normally, muscles are absolutely refractory and incapable
of producing an action potential, which prevents re-entry
Reduced absolute refractory period (short AP duration), or
slowed conduction, increase the chance of re-entry
Requirements:
1. A functional or anatomical loop#
2. The absolute refractory period of the re-entered
segment of muscle must be shorter than the conduction
time around the loop #
3. Unidirectional conduction block within the loop*
(# true of re-entry in general; * true of the type described in this lecture)
 Branch in pathway splits wave
of excitation
Wave of excitation then
spreads in both directions in
segment 3
Area behind muscle producing
action potentials refractory
Two waves meeting die out, as
all muscle around are
refractory

Klabunde, Cardiovascular Physiology Concepts

 Segment 2 has a unidirectional
conduction block (action potentials
can propagate in only one direction)
Original wave of excitation is
blocked at segment 2, but
propagated down segment 1
Excitation spreads back to 2 through
segment 3
Unidirectional block allows APs to
pass, exciting segment 1 again if the
muscle is in the relative refractory
period or fully recovered
Cycle repeats
Klabunde, Cardiovascular Physiology Concepts
 Circular path
of APs is
called circus
movement/
excitation

Figure 19-15A, Copstead and Banasik, 3E

www.medicinenet.com
 Abnormal Sites of Impulse Initiation
Atrial Dysrhythmias
1. Premature Atrial Complexes
Atrial depolarisation is initiated by cells within the atria
other than the SA node pacemaker cells
P wave may be abnormal
Timing is faster than sinus rhythm (why?)
Followed by ‘compensatory pause’ where end-diastolic
volume is enhanced and the next beat is stronger
Premature Atrial Complexes (PACs)

Figures 19-24 Copstead and Banasik, 3E

 Abnormal Sites of Impulse Initiation
Atrial Dysrhythmias
2. Atrial Flutter
Atrial depolarisation rate of 240 – 350 bpm
Saw-tooth pattern of P waves
QRS is normal and slower than P rate, as not all atrial
depolarisations are conducted
Re-entry most likely source of abnormality
Acute alcohol toxicity, underlying heart disease, fluid
overload and atrial ischaemia predispose to atrial flutter
 Abnormal Sites of Impulse Initiation
Atrial Dysrhythmias
3. Atrial Fibrillation
Chaotic depolarisation of atria accompanied by a ventricular
depolarisation that is irregular and variable
Multiple and constantly changing re-entry waves underlie the
chaotic electrical activity
All atrial muscle contract and relax randomly, failing to pump blood
from the atria
High probability of clots forming as blood is static (& jiggled)
Treat by cardioversion with electric shock and with anti-arrhythmic
drugs (Ca2+ channel blockers, β-blockers, digitalis, amiodarone)
 Atrial Flutter

Atrial Fibrillation
Figures 19-20 and 19-27, Copstead and Banasik, 3E
 Abnormal Sites of Impulse Initiation
Ventricular Dysrhythmias
1. Premature Ventricular Complexes (PVCs)
A ventricle cell is excited independent of normal activation by
the conduction system
Excitation encompasses the ventricles but not the atria, so sinus
rhythm is unaffected
QRS complex is abnormal and prolonged
T wave is often inverted (repolarisation follows an abnormal
path)
PVC compensatory pause

buried P wave

Figure 19-29, Copstead and Banasik, 3E

 Abnormal Sites of Impulse Initiation
Ventricular Dysrhythmias
1. Premature Ventricular Complexes (PVCs)
Associated with coronary heart disease, drug overdose
and electrolyte imbalances, particularly hypokalemia
and hypomagnesemia (make Phase 4 more depolarised
than normal)
If occur rarely, then no clinical significance
Frequent PVCs may diminish CO and/or progress to VT
and VF
Treat with antiarrhythmic drugs (e.g., amiodarone)
 Abnormal Sites of Impulse Initiation
Ventricular Dysrhythmias
2. Ventricular Tachycardia (VT)
Three or more consecutive QRS complexes at a rate
exceeding 100 bpm
QRS complex normal at slower rates but blend into ST
segments and T waves at higher rates, producing a
characteristic series of large, wide, undulating waves
Sinus rhythm is unaffected and if P waves are seen, the
QRS complex is independent of atrial activity
Ventricular Tachycardia - Monomorphic

Figure 19-30, Copstead and Banasik, 3E

 Abnormal Sites of Impulse Initiation
Ventricular Dysrhythmias
2. Ventricular Tachycardia (VT)
Re-entry is the most common underlying mechanism
associated with MI and ischaemia
High catecholamine levels and electrolyte imbalances
predispose to VT
Serious and potentially fatal dysrhythmia due to
compromised CO
Treat with antiarrhythmic drugs, cardiopulmonary
resuscitation, and electrical cardioversion
 Abnormal Sites of Impulse Initiation
Ventricular Dysrhythmias
2. Ventricular Tachycardia (VT) - polymorphic
Torsade de pointes

drproxy.blogspot.com

Chiang, C.-E. et al. (2000) J Am Coll Cardiol 36:1-12

lifeinthefastlane.com
Abnormal Sites of Impulse Initiation

Ventricular Dysrhythmias
3. Ventricular Fibrillation (VF)
Rapid, choatic rhythm which is completely
uncoordinated
Ventricular muscle quivers rather than contracting in a
coordinated manner
CO is severely compromised
 Abnormal Sites of Impulse Initiation
Ventricular Dysrhythmias
3. Ventricular Fibrillation (VF)
Same conditions which produce VT produce VF (re-entry
associated with MI, ischaemia, high catecholamine
levels and electrolyte imbalance) as VT often progresses
to VF
Treat rapidly with cardiopulmonary resuscitation and
defibrillation
If heart converts, antiarrhythmic drugs are administered
 Summary 1
Abnormal sites of impulse initiation are caused by
premature APs in areas other than the conduction system
Underlying mechanisms: abnormal automaticity,
triggered activity, and re-entry of excitation
Ectopic foci may give rise to premature complexes,
tachycardia, or fibrillation in both the atria and
ventricles
Ventricular fibrillation is the most dangerous
dysrhythmia
 Summary 2
Sinus rhythm may be abnormally fast (tachycardia), slow
(bradycardia), variable (atrial arrhythmias; Sick Sinus
Syndrome) or absent (sinus arrest)
Escape rhythms occur when the SA node fails and the AV
node (junctional escape) or Purkinje fibres (ventricular
escape) take over generating the pacemaker signal
Disruption of electrical conduction profoundly affects heart
rate and cardiac output (AV blocks)
Abnormal conduction pathways may undermine normal
activation of the ventricles (pre-excitation)