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CVM Lecture Week4 Lecture Notes
CVM Lecture Week4 Lecture Notes
Cardiovascular
Medicine
Dr Lisa Chilton
Lisa.Chilton@jcu.edu.au
Building DB087, Room TV222,
4781 5195
Dysrhythmias
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
1
Mechanism 1: Inappropriate Automaticity
2
EADs
DADs
3
Mechanism 3: Re-entry of Excitation
4
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
www.medicinenet.com
5
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
6
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
7
PVC compensatory pause
buried P wave
8
Ventricular Tachycardia - Monomorphic
drproxy.blogspot.com
9
lifeinthefastlane.com
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
10
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)
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