Cardiac Dysrhythmias

(Arrhythmias)
Professor Peter Carroll
Sydney Medical School
University of Sydney
Northern Clinical School
Royal North Shore Hospital
COMMONWEALTH OF AUSTRALIA
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 Learning Objectives
• Always remember
- to look after those less
fortunate than you Tent City Homeless Camp, Martin
Place Sydney, SMH August 2017

- that what you walk past is what you accept

- that hubris and greed can be very self
destructive
- that economic rationalism is where
everything is costed but nothing is valued
Reference: Rang and Dale’s Pharmacology, Chapter 21, 8th Edition
 Always have a social
Learning Objectives consciousness

• Understand the conducting system of

the heart and the major components
of the ECG
• Describe the phases of the action
potential of cardiac cells and
understand the ionic movements
which accompany each phase
• Understand how cardiac dysrhythmias
(arrhythmias) may arise
Reference: Rang and Dale’s Pharmacology, Chapter 21, 8th Edition
 Learning Objectives
• Describe the Vaughan Williams classification
of anti-dysrhythmic (anti-arrhythmic ) drugs,
and discuss the properties of a drug from
each class
• List the major side effects of drugs used in
the treatment of cardiac dysrhythmias
(arrhythmias)
• Describe atrial fibrillation, understand why it
may lead to ischaemic stroke, and discuss
how it is treated
Reference: Rang and Dale’s Pharmacology, Chapter 21, 8th Edition
 The Heart
• Automaticity - has the ability to contract on
its own
• Two cell types
- specialised cells which form the conducting
system, and are responsible for initiating and
distributing the electrical stimulus (impulse)
which causes contraction
- contractile cells which allow the heart to contract
• Cardiac muscle contraction follows the
initiation and distribution of the electrical
impulse
Conducting System of the Heart
• Sinoatrial (SA) node
• Atrial internodal pathways
• Atrioventricular (AV) node
• AV bundle (bundle of His)
• Bundle branches
Martini, Anatomy and Physiology, 4th Ed, Prentice Hall

• Purkinje fibres
 Electrocardiogram
• The electrical activity of the heart
is powerful enough to be detected
by electrodes on the skin
• The P wave relates to atrial depolarisation
(the atria contract approximately 100msec
after the start of the P wave)
• The QRS complex relates to ventricular
depolarisation (the ventricles start to contract
shortly after the peak of the R wave)
• The T wave indicates ventricular
repolarisation
 Electrocardiogram
ST Segment Elevation

www.greatwhatsit.com

Martini, Anatomy and Physiology, 4th Ed, Prentice Hall

PR Interval - from the very beginning of the

P wave to the first deflection of the QRS complex
QT Interval - from the beginning of the QRS
complex to the end of the T wave
Action Potential of Cardiac Cell

Rang & Dale’s Pharmacology, 8th Edition, page 248

 Action Potential of Cardiac Cell
• Divided into 5 phases
- Phase 0 (rapid depolarisation) occurs
when the membrane potential reaches
a critical firing threshold (approx -60mV)
with large influx of Na+
- Phase 1 (partial repolarisation) as Na+
influx ceases
- Phase 2 (the plateau) results from an
inward Ca2+ current
- Phase 3 (repolarisation) as inward flow
of Ca2+ ceases and outward flow of K+
commences
- Phase 4 (pacemaker potential) is a
gradual depolarisation during diastole
Rang & Dale’s Pharmacology, 8th Edition, page 247-248
 Action Potential of Cardiac Cell

mV

Martini, Anatomy and Physiology, 4th Ed, Prentice Hall

 Cardiac Rhythm
• The stimulus for cardiac
contraction (heart beat)
normally originates in the
SA node and spreads
across the cardiac muscle
Martini, Anatomy and Physiology, 4th Ed, Prentice Hall

by way of the conducting

system (sinus rhythm)
 Cardiac Rhythm
• Although other cells of
the conducting system
can generate an action
potential (stimulus) and
cause the heart to
contract, the SA node
normally depolarises at a
faster rate and is thus Martini, Anatomy and Physiology, 4th Ed, Prentice Hall

responsible for the heart

beat
 Dysrhythmias (Arrhythmias)
• Cardiac dysrhythmias (arrhythmias,
abnormal rhythms) occur in a number of
ways including
- the stimulus originates from a
site other than the SA node

- the stimulus spreads across the

heart by way of abnormal
pathways, or is delayed or blocked
• Can occur in different areas of the heart
e.g. atria, AV node or ventricles
 Dysrhythmias (Arrhythmias)
• Supraventricular dysrhythmias
- e.g. atrial ectopic beats (extrasystoles),
paroxysmal atrial tachycardia, atrial
fibrillation
• Ventricular dysrhythmias
•

- e.g. ventricular ectopic beats (extrasystoles),

ventricular tachycardia, ventricular fibrillation
• Heart block
- e.g. stimulus impeded or unable to traverse
the AV node
 Anti-Dysrhythmic (Anti-
Arrhythmic) Drugs
• Medications used in the treatment of
cardiac dysrhythmias (arrhythmias)
basically alter the heart’s electrical
•
properties including
- automaticity
- refractory period
- conduction velocity
• Because of these actions they may at
times actually cause pro-arrhythmic effects
 Anti-Dysrhythmic (Anti-
Arrhythmic) Drugs
• May be classified in a number of ways
• Traditionally classified as possessing one or
more of the four classes of anti-dysrhythmic
(anti-arrhythmic) actions described by
•
Vaughan Williams
- Class IA, IB and IC
- Class II
- Class III
- Class IV Rang & Dale’s Pharmacology, 8th Edition, page 255
 Vaughan Williams
• Class IA - block Na+ channels,
moderate reduction in slope and
peak of phase 0 of action potential,
and increase in duration of action
potential
• Class IB - block Na+ channels,
small reduction in slope and peak of
phase 0 of action potential, and
decrease in duration of action
potential www.cvpharmacology.com

• Class IC - block Na+ channels, large reduction in

slope and peak of phase 0 of action potential, and
no effect on duration of action potential
Rang & Dale’s Pharmacology, 8th Edition, page 255 - 258
 Vaughan Williams
• Class IA - example is
disopyramide
- blocks Na+ channels
- reduces automaticity
- increases refractory period
- slows conduction www.cvpharmacology.com

- may cause QT prolongation and

pro-arrhythmic effects
- exerts anti-cholinergic activity Rang & Dale’s Pharmacology,
8th Edition, page 255 - 258
 Vaughan Williams
• Class IB - example is
lignocaine
- blocks Na+ channels
- reduces automaticity
- decreases refractory period
www.cvpharmacology.com
- may induce pro-arrhythmic effects
- IV treatment of life threatening
ventricular arrhythmias
Rang & Dale’s Pharmacology,
8th Edition, page 255 - 258
 Vaughan Williams
• Class IC - example is
flecainide
- blocks Na+ channels
- reduces automaticity
- no effect on refractory period
www.cvpharmacology.com
- slows conduction
- may prolong the QT interval and
induce pro-arrhythmic effects
Rang & Dale’s Pharmacology,
8th Edition, page 255 - 258
Disopyramide
Lignocaine
Flecainide

Rang and Dale’s Flashcards, 6.04, modified

 Vaughan Williams
• Class II - examples are beta adrenoceptor
blocking agents (beta blockers) e.g.
propranolol
- reduce sympathetic activity on the heart
- reduce phase 4 depolarisation (pacemaker potential)
and slow heart rate (bradycardia)
- prolong the refractory period of the atria
- increase refractory period and increase conduction
time of AV node (slow conduction)
- reduce dysrhythmias (arrhythmias) and mortality
following myocardial infarction
Rang & Dale’s Pharmacology, 8th Edition, page 255 - 258
Propranolol

Rang and Dale’s Flashcards, 6.04, modified

 Vaughan Williams
• Class III - example is amiodarone (acts
primarily on K+ channels)
- decreases automaticity
- prolongs action potential and refractory period
- increases conduction time of AV node
- increases coronary blood flow and decreases
oxygen requirements
- has a long t1/2 (up to 100 days)
- may produce thyroid abnormalities
- QT prolongation and pro-arrhythmic effects
eMIMS September 2016; Rang & Dale’s Pharmacology, 8th Edition, page 255 - 258
 – Amiodarone

Rang and Dale’s Flashcards, 6.04, modified

 Vaughan Williams
• Class IV - examples are non-
dihydropyridine calcium channel blocking
agents e.g. verapamil

- block L type voltage gated Ca2+ channels

- slow heart rate

- prolong refractory period of AV node

- increase conduction time of AV node

Rang & Dale’s Pharmacology, 8th Edition, page 255 - 258
 Verapamil
–

Rang and Dale’s Flashcards, 6.04, modified

 Atrial Fibrillation (AF)
• Most common sustained cardiac dysrhythmia
• Very fast, disorganised electrical activity in
the atria
• Atria quiver/squirm faster than 300 times per
minute, and there is no effective atrial
contraction
• Ventricular rate is around 150-160 beats per
minute and irregular (AV node conduction
time and AV refractory period limit ventricular
rate)
https://www.google.com.au/search?q=atrial+fibrillation+and+stroke&biw=1366&bih=622&source=lnms&tbm=isc
h&sa=X&sqi=2&ved=0CAcQ_AUoAmoVChMIi__Z3vPoxwIVR1umCh1ToAX9#imgrc=-qj53THRS2F4xM%3A
 Atrial Fibrillation (AF)
• Atrial fibrillation may be asymptomatic
• If symptoms are present they may
include
- tiredness
- breathlessness
- dizziness
- thumping heart beat
McNamara K and Gellatly R (2015) Australian Pharmacist January, 34-39
 Atrial Fibrillation (AF)
• A thrombus is a clot which forms
at a specific site within the
cardiovascular system and
remains there
• An embolus is a clot which forms
in one location and travels to
another location within the
cardiovascular system
 Atrial Fibrillation (AF)
• Atria quiver/squirm faster than 300 times
per minute, and there is no effective atrial
contraction
• Thrombi (clots) may form in the atria
(particularly in the left atrial appendage)
• If these thrombi (clots) are pumped out of
the heart (emboli) they may cause an
ischaemic stroke or TIA
• Atrial fibrillation is responsible for up to 20%
of all strokes Samardhi H et al, Current Management of Atrial Fibrillation, Australian
Prescriber 2011, 34, 100–4)
www.bostonscientific.com
www.nhlbi.nih.gov/health/dci/Diseases/af/af_all.html
 Atrial Fibrillation (AF)
Treatment options include
• Rhythm control - reversion to, and maintenance of,
sinus rhythm with cardioversion, antiarrhythmic
therapy e.g. amiodarone
• Rate control - control of ventricular rate by slowing
conduction rate and increasing refractory period of
AV node e.g. beta blocker, verapamil, digoxin
eTG Complete, Atrial Fibrillation, July 2015

Refractory Period of AV Node Increased (Rate Control)

 Atrial Fibrillation (AF)
Treatment options include
• Anticoagulants to reduce the risk of
thrombi (clots) and ischaemic stroke

www.nhlbi.nih.gov/health/dci/Diseases/af/af_all.html
CHADS2 Score

NPS Medicinewise, Good Anticoagulant Practice, February 2013

Atrial Fibrillation and the Risk of Stroke

Aspirin is not recommended for people with a CHADS2

score ≥ 1 unless anticoagulation is contraindicated
NPS Medicinewise, Good Anticoagulant Practice, February 2013; NPS Medicinewise, Achieving Good Anticoagulant Practice,
Samardhi H et al, Current Management of Atrial Fibrillation, Australian Prescriber 2011, 34, 100–4)
www.nps.org.au/medicines/heart-blood-and-blood-vessels/anti-clotting-medicines/for-individuals/anticoagulant-medicines/for-
health-professionals/evidence-summary/atrial-fibrillation. Accessed 18/11/14
CHADS2 and CHA2DS2–VASc Scores

NPS Medicinewise, Good Anticoagulant Practice, February 2013