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Mechanisms and Management of Cardiac Arrhythmias
1st Edition Clifford Garratt Digital Instant Download
Author(s): Clifford Garratt
ISBN(s): 9780727911940, 0727911945
Edition: 1
File Details: PDF, 1.91 MB
Year: 2001
Language: english
Mechanisms and
Management of
Cardiac
Arrhythmias
Clifford Garratt
Professor of Cardiology,
Manchester Heart Centre, Manchester Royal Infirmary,
Manchester M13 9WL, UK
© BMJ Books 2001
BMJ Books is an imprint of the BMJ Publishing Group
All rights reserved. No part of this publication may be reproduced,

stored in a retrieval system, or transmitted, in any form or by any means,
electronic, mechanical, photocopying, recording and/or otherwise,
without the prior written permission of the publishers.
First published in 2001

by BMJ Books, BMA House, Tavistock Square,
London WC1H 9JR
www.bmjbooks.com
British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library
ISBN 0-7279-1194-5
Typeset by Newgen Imaging Systems (P) Ltd., Chennai, India

Printed and Bound by Selwood Printing Ltd, Burgess Hill, West Sussex
To Lucy
This Page Intentionally Left Blank
Contents
Preface vii
PART I CELLULAR AND TISSUE

ELECTROPHYSIOLOGY
1 Ion channels and ion currents 3
2 The cardiac action potential and its relevance to arrhythmias 11
3 Propagation of electrical impulses through cardiac muscle 18
PART II CLINICAL TACHYCARDIAS

4 Classification and nomenclature of clinical tachycardias 29
5 Sinus tachycardia, atrial tachycardia, and atrial flutter 31
6 Atrial fibrillation 43
7 Junctional tachycardias 59
8 Ventricular tachycardia in the setting of a structurally
normal heart 70
9 Ventricular tachycardia and fibrillation in the setting of
ischaemic heart disease 77
10 Ventricular tachycardia and fibrillation in the setting of
dilated or hypertrophic cardiomyopathy 88
11 Ventricular fibrillation in the setting of a structurally
normal heart 93
12 The congenital long QT syndrome 97
13 Arrhythmogenic right ventricular dysplasia/
cardiomyopathy 104
PART III DIAGNOSIS AND MANAGEMENT

14 Clinical management of the patient presenting with
palpitation 115
v
CONTENTS
15 Diagnosis and management of acute episodes of tachycardia 121

16 Antiarrhythmic drug therapy 137
17 Electrophysiologic studies and radiofrequency catheter
ablation techniques 151
18 Implantable cardioverter defibrillators (ICDs) 161
19 Concluding remarks 168
Index 170
vi
Preface
My interest in cardiac arrhythmias stems from my time as a clinical medical

student and house physician at St Bartholomew’s Hospital in London.
A combination of the logical basis to therapy (at least relative to most other
medical disciplines) and the dramatic successes of some forms of treatment
drew me to the subject. I remember being surprised to find that, although
clinical textbooks on arrhythmia management would usually have a section
on “basic electrophysiology” or “the action potential”, there was invariably
no attempt made to explain the clinical arrhythmias in these terms.
Similarly, accounts of the ionic processes underlying activation of cardiac
cells would include a discussion of clinical arrhythmias as an afterthought if
at all. There have been dramatic advances in both fields since that time. My
impression is that this divide remains despite the recent publication of sev-
eral large multiauthored texts which address both areas in a single volume.
The aim of this monograph is to provide medical students, house physicians,
and cardiologists in training with a logical, scientifically based framework
for the management of arrhythmias in which the relevant aspects of basic
electrophysiology are put in the clinical context. The fundamental concepts
introduced in the first three chapters are expanded and illustrated in subse-
quent sections.Thereafter each arrhythmia is discussed in greater detail with
particular emphasis on mechanism, clinical setting, and long term or defin-
itive therapy. Finally the principles of clinical management of arrhythmias
are addressed, with chapters on presentation, acute diagnosis and therapy,
antiarrhythmic drugs, ablation techniques, and implantable cardioverter
defibrillators.
I would like to acknowledge my clinician teachers and colleagues, espe-
cially John Camm, Adam Fitzpatrick, Michael Griffith, Edward Rowland,
and David Ward for their ideas and advice which are contained in this vol-
ume. Finally, I am grateful to Maurits Allessie for an inspiring apprentice-
ship in experimental electrophysiology and to the British Heart Foundation
for allowing me to spend a year in his laboratory in Maastricht.
vii
PART I
CELLULAR AND TISSUE
ELECTROPHYSIOLOGY
1: Ion channels and
ion currents
Each of the cells of the human body is surrounded by a lipid membrane

and, whilst many particles can slowly cross these membranes by diffusion,
most life processes in higher organisms could not occur without more effec-
tive and regulated mechanisms for the transfer of molecules into and out of
cells. Ion channels are integral membrane proteins that are responsible for
rapid transmembrane flow of millions of charged particles per second
thereby generating electrical impulses in the excitable tissues of brain,
nerve, heart, and muscle. The importance of these structures is highlighted
by the fact that some cells use up to 50% of their energy expenditure main-
taining gradients of ions across their membranes. Despite evidence of a
great diversity of different channels within individuals and between species,
the basic structure of these proteins is remarkably well conserved and
voltage-sensitive sodium, calcium, and potassium channels appear to be
members of a closely related gene family (Figure 1.1).
General properties of ion channels

Ion channels show ion selectivity, in that they usually allow only one type
of ion to pass. They can be either open or closed (gating), depending upon
either the electric field across the membrane (voltage-gated), the time
relative to a previous channel event (time-dependent), or the presence
of an appropriate molecule (ligand-gated). The voltage-gated and time-
dependent currents associated with these channels are discussed in more
detail below. Examples of ligand-gated channels are the potassium channels
which open or close in response to acetylcholine and ATP (IK(ACh) and
IK(ATP) respectively). Ion channel gating mechanisms are usually discussed
in relation to a mathematical model of the action potential devised by
Hodgkin and Huxley in 1952–3. In this model, passage of sodium ions is
determined by three “m” gates on the extracellular side of the channel and
one “h” gate on the intracellular side (Figure 1.2). Between each action
potential the m gates are closed and the h gates open (resting state).
Depolarisation (see below) causes the m gates to open and the h gate to
close (voltage dependence) but the closure of the h gate is slightly later than
the m gate opening. Consequently both gates are open for a short period of
time, sodium ions rush into the cell, and the action potential is initiated.
3
MECHANISMS AND MANAGEMENT OF CARDIAC ARRHYTHMIAS
Cyclic CHANNEL EVOLUTION

nucleotide Potassium Calcium Sodium
Present CAMP CGMP
Metazoans
700 million
years ago
Eukaryotes
Monomeric Tetrameric
1400 million
years ago
Primitive (monomeric)
Prokaryotes ancestor
Figure 1.1 Evolution of the family of channel proteins. Near the end of the
Archeozoic period, when eukaryotes evolved from the prokaryotes, a primitive
monomeric channel protein is believed to have given rise to the non-covalently
linked subunits of potassium and cyclic nucleotide-gated channels, and to
tetrameric calcium channels. Later, during the Cambrian period, tetrameric sodium
channels are thought to have evolved from the calcium channels. There appear to
be many more potassium channel subtypes than subtypes of the calcium channel:
evidence that there are even fewer sodium channel subtypes is consistent with their
more recent evolution. (From Katz AM. Ion channels and cardiology: the need for
bridges across a widening boundary. In: Spooner PM, Brown AM, eds. Ion channels
in the cardiovascular system. Aronk, NY: Futura Publishing, 1994.)
Following inactivation, the gates return to their resting state. This model
has been refined in recent years but the basic concepts appear to hold true.
Although the opening of single channels as described above is an “all or
nothing” phenomenon, the total current flowing into the cell is dependent
upon the current through an individual channel, the number of channels in
the cell, and the probability of each channel being open.
Molecular structure of cardiac ion channels

The basic structure of an ion channel is one of a group of protein subunits
embedded within the cell membrane in such a way as to form a central
hydrophilic pore through which ions can pass.
Sodium channels
The sodium channel consists of alpha (central component) and beta (sub-
sidiary) subunits. Each alpha subunit has four homologous domains, linked
by covalent bonds, which wrap around the central pore region, and each
domain can be considered as contributing 25% of the wall of the channel
pore (Figure 1.3A).The domains are made up of six helical protein segments
(S1–S6), all of which traverse the cell membrane (Figure 1.3B). Attempts
have been made to determine the likely function of each segment in terms of
4
ION CHANNELS AND ION CURRENTS
Vm
Im
m m m m
h h
h h
Resting Open Inactivated
Figure 1.2 Proposed role of the m and h gating mechanisms in current flow
through the Na channel. Top and middle: representations of a step change in mem-
brane potential Vm and the resulting current Im. Lower: ion channel movement
through the channel is controlled by activation (m) and inactivation (h) gates (see
text). (From Grant AO. Sodium channel blockade as an antiarrhythmic mechanism.
In: Breithardt G, Borggrefe M, Camm J, Shenasa M, eds. Antiarrhythmic drugs.
Berlin: Springer, 1994.)
the known physiological properties of the sodium channel. The region

between S5 and S6 of each segment is thought to form the pore itself.The S4
segment, unlike the other segments, is positively charged and is considered a
good candidate for the voltage sensor or m gate. The short segment linking
S6 of domain III and S1 of domain IV is identified as a possible candidate for
the h gate that is involved in channel inactivation, possibly by means of a
“hinged lid” mechanism of occluding the pore (see Figure 1.2).The presence
of the beta subunit has a modulating effect on the alpha subunit such that
activation and inactivation of sodium channels are accelerated by its pres-
ence. Abnormalities of the sodium channel underlie some forms of the long
QT syndrome and also the Brugada syndrome (see Chapters 11 and 12).
Potassium channels
Some voltage-gated potassium channels (termed “shaker-related” because of
their abnormal expression in a fruit fly mutant that shakes its legs when
exposed to ether) show striking structural similarity to the sodium channel in
that the pore is formed from an association of four protein structures. These
structures are not covalently bonded, however, but form a non-covalent asso-
ciation: hence they are referred to as alpha subunits rather than domains
(Figure 1.4). These subunits are structurally very similar to the sodium
channel domains, each consisting of six segments: the S4 segment and P
5
(A)
out
β1 α β2
in
Na+
(B)
I II III IV
+ + + +
1 2 34 5 P 6 1 2 3 4 5 P 6 1 2 3 4 5 P 6 1 2 3 4 5 P 6
+ + + +
C
N
Figure 1.3 Structure of the voltage-gated Na channel. (From Jalife J, Delmar M,
Davidenko JM, Anumonwo JMB. Basic cardiac electrophysiology for the clinician.
Armonk, NY: Futura, 1999.)
region (S5–S6) are present and probably play similar roles of voltage sensing
and ion permeation as in the sodium channel. Potassium channels are
thought to undergo inactivation by means of the physical plugging of the
intracellular mouth of the channel with a particle formed by the N-terminal
by what is termed the “ball and chain” mechanism. As well as this N-type
inactivation, some potassium channels show C-type inactivation which
involves the occlusion of the external mouth of the channel pore.The delayed
rectifier currents IKr and IKs occur through shaker-type channels, as does the
transient inward current (ITI). IKr is encoded by the human ether-a-go-go
related gene (HERG) localised on chromosome 7 and the channel protein
underlying IKs is thought to be formed by the coassembly of a shaker-type
channel protein and the minK protein. Mutations in the genes encoding
these proteins are responsible for various forms of the congenital long QT
syndrome (see Chapter 12). Unlike the shaker potassium channels, the
inward rectifier potassium channels (IK1) have only two transmembrane seg-
ments (M1 and M2), similar to the shaker S5 and S6 segments and pore
region: the pore is thought to be formed by a tetrameric assembly.
Calcium channels
The calcium channel consists of multiple subunits: two alpha, one each of
beta, gamma, delta. The alpha subunit forms the pore and the role of the
6
(A)
α out
αα α
β in
K+
(B)
+ + + +
1 2 34 5 6 1 2 3 4 5 6 1 2 3 4 5 6 1 2 34 5 6
+ + + +
N N N N
C C C C
Figure 1.4 Structure of the shaker-related K channel. (From Jalife J, Delmar M,

other subunits remains unclear. Remarkable homology exists between the

alpha 1 subunit of the L-type calcium channel and the pore-forming alpha
subunit of voltage-dependent sodium channels, both having four homologous
domains composed of six transmembrane segments each. The S4 segment
again is likely to be involved in activation gating. The loop between domains
2 and 3 is thought to be important in excitation contraction coupling.
As well as being controlled in the short term by voltage- and time-
dependent mechanisms, ion channel conductance is modulated over longer
time periods by protein phosphorylation and molecular interaction with
guanine nucleotide-binding regulatory proteins (G proteins). These
processes play an essential role in the regulation of cardiac function by hor-
mones and neurotransmitters.
Gap junctional channels

Gap junction channels provide an enclosed conduit for direct exchange of
molecules between cells, with diameters large enough to accommodate
metabolites and signalling molecules with high molecular weights. The
complete structure is made up of two connexons, one from each of the two
7
Gap junction
channel pore Connexin subunit
Plasma one of six
membrane
Cell 1
Plasma
membrane Connexon
Cell 2
Figure 1.5 A gap junctional channel. (From Jongsma HJ, Rook MB. Morphology
and electrophysiology of cardiac gap junction channels. In: Zipes D, Jalife J, eds.
Cardiac electrophysiology from cell to bedside, 2nd edn. Philadelphia: WB Saunders,
1995.)
adjacent cells. Each connexon is composed of six connexin subunits, most

likely arranged so that their third (out of four) transmembrane domains
line the channel lumen (Figure 1.5). Complete gap junction channels are
commonly clustered together and have extremely rapid turnover times,
being exchanged several times a day. At least three types of connexin (C40,
C43, C45) are expressed in the human heart.
Names and symbols for ionic currents

Although all cardiac ion channels share a common basic structure, there is
undoubtedly a great variety of channels and corresponding currents in
human cardiac myocytes. Although the function of all of these currents has
yet to be identified, the majority make some contribution to the generation
of either the resting or action potential (see Chapter 2). These currents can
be influenced to varying degrees by abnormalities of ion channel function
associated with genetic abnormalities, acquired insults such as ischaemia,
and antiarrhythmic drug use.
All ion currents are described by the symbol I, together with a symbol for
the appropriate ion, for example, INa. The direction of the positive charge
defines whether a transmembrane current is described as inward or out-
ward, i.e. an inward current is one in which positively charged ions move
into the cell. This results in the membrane potential becoming more posi-
tive (depolarisation). If positive ions move out of the cell this is referred to
as hyperpolarisation. Current flow across an open ion channel is depend-
ent upon the electromotive force (voltage or potential difference) generated
by the ionic gradient across the membrane. The relationship between cur-
rent flow and voltage may not be linear, in which case the channel is said
to exhibit rectification. Rectification can be inward or outward depending
on whether the conductance is higher in the outward or inward direction.
8
Descriptions of the major ion currents

Sodium current (INa)
This is the major inward current, depolarising cardiac cells in the atria,
ventricles, and Purkinje fibres during phase 0 of the action potential (see
Chapter 2). INa is not thought to be involved in the action potentials of
sinoatrial or atrioventricular nodes. A number of antiarrhythmic agents in
common use have a reduction in INa as their main mode of action (so
called class I action, see Chapter 16).
Calcium currents
Calcium currents are of two types. L-type calcium current (ICa-L) (L for
large and long lasting) is the dominant calcium current in all mature car-
diac cells and (a) provides the sustained inward current that is partially
responsible for the plateau phase (phase 2) of the action potential and (b)
couples the electrical phenomenon of cell depolarisation to cardiac
myocyte contraction. The T-type calcium current (ICa-T) (T for transient) is
usually seen in atrial, Purkinje, and nodal cells whilst in ventricular cells it
is of small amplitude and sometimes cannot be demonstrated, suggesting
it is not vital to excitation contraction coupling. This current is a transient
current elicited by small depolarisations above the resting potential level. It
inactivates rapidly and, unlike ICa-L, is insensitive to dihydropyridines such
as verapamil. The physiological role of ICa-T is most likely to be in pace-
maker impulse generation given its clear demonstration in sinus node and
AV nodal tissue.
Delayed rectifier potassium current (IK )

The delayed rectifier potassium current IK is an outward current important
in the repolarisation of the cardiac action potential. It consists of IKr, a rap-
idly activating current with a sensitivity to the antiarrhythmic agent sotalol,
and IKs, a slowly activating current.
Background potassium current (IK1 )

The background potassium current is a reflection of the much higher con-
centration of K ions within cardiac cells and the relatively high resting per-
meability of cardiac cells to potassium: this outward current is involved in
setting the cell resting membrane potential (see Chapter 2). This current
(also termed inward rectifier) is not usually present in nodal cells, and as a
consequence the resting potentials of these cells are less negative than those
of atrial, ventricular, and Purkinje cells.
Transient outward current (ITO )

ITO is activated by the rapid depolarisation associated with INa and
is responsible for the transient repolarisation in phase 1 of the action
potential.
9
IKur
This current is present in atrial cells only and, together with ITO, is respon-
sible for phase 1 of the action potential of the atria but not the ventricles.
IK(ATP)
IK(ATP) is a current that is sensitive to cytosolic levels of ATP. In the pres-
ence of low ATP levels, such as during ischaemia, the current is activated,
resulting in efflux of potassium and hyperpolarisation.
IK(ACh)
IK(ACh) is a similar current to IK1 and is activated by the acetylcholine
muscarinic receptor on the cell membrane. This receptor is coupled to
the potassium channel via membrane-bound G protein. Activation by
acetylcholine results in potassium efflux and hyperpolarisation of the cell
associated with vagal stimulation.
Hyperpolarisation-activated current or pacemaker current (If )

The hyperpolarisation-activated current or pacemaker current If is one of
the candidates for the generation of pacemaker activity in the sinus node.
F is for “funny” because of the unusual properties of the current: sodium
ions carry the charge through the channel and current activation starts at
approximately 40 mV to 50 mV.
Background pumps
Cardiac cells have ion pumps that are important in the re-establishment of ion
gradients following activity. The sodium potassium pump (3NA : 2K) causes
an outward current because it pumps three sodium ions out for every two
potassium ions in. Activity of this pump is reduced by digoxin, allowing accu-
mulation of intracellular sodium.This then leads to intracellular accumulation
of calcium (via a sodium/calcium exchanger mechanism) that is thought to be
the basis for the positive inotropic and arrhythmogenic effects of this agent.
Non-specific calcium-activated current (ITI or transient inward current)

This is an oscillatory membrane current carried by sodium ions that is trig-
gered by a rise in cytoplasmic calcium concentrations. It is a mechanism of
delayed after-depolarisations and sometimes early after-depolarisations
(see Chapter 2).
Further reading
Catterall WA et al. Molecular bases of ion channel activity. In: Zipes D, Jalife J, eds. Cardiac
electrophysiology from cell to bedside, 2nd edn. Philadelphia: WB Saunders, 1995.
Hodgkin AL, Huxley AF. A quantitative description of membrane current and its application
to conduction and excitation in nerve. J Physiol (Lond) 1952;117:500–44.
Jalife J, Delmar M, Davidenko JM, Anumonwo JMB. Basic cardiac electrophysiology for the
clinician. New York: Futura Publishing, 1999.
Noble D. The initiation of the heart beat. New York: Oxford University Press, 1979.
10
2: The cardiac action
potential and its relevance
to arrhythmias
Whilst it is frequently stated that understanding of the details of the cardiac

action potential is (or will be) important for an understanding of cardiac
arrhythmias in patients, it is not immediately obvious why this should be
true. Most clinical cardiac arrhythmias are caused by abnormalities in
propagation through tissues (see Chapter 3) rather than abnormalities in
physiology of individual cells. Nevertheless, some clinical arrhythmias are
undoubtedly explicable in terms of abnormalities in the action potential
(via abnormalities in ion currents) and these will be discussed following a
description of the normal action potential in cardiac cells.
The resting potential

In the majority of atrial and ventricular myocytes, the voltage across the cell
membrane (resting potential) remains constant between action potentials
at approximately 85 mV, a level which is primarily determined by the fact
that the cell membrane in this state is much more permeable to potassium
than to other ions.The membrane potential is the consequence of a balance
between the chemical or concentration gradient for K ions (high potas-
sium inside, low potassium outside) pushing K ions out of the cell (IK1),
leading to an opposing electrical gradient across the membrane consequent
upon the removal of positive charge from the cell (Figure 2.1).
The action potential

The generation of the sustained depolarisation known as the action poten-
tial is the means whereby electrical impulses are transmitted rapidly
through excitable tissues. The classic description of the cardiac action
potential is based upon that of a Purkinje fibre, in which there are four dis-
tinct phases (Figure 2.2). Phase 0 is the rapid upstroke phase, phase 1 is the
brief initial repolarisation phase, phase 2 is the plateau phase, phase 3 the
rapid repolarisation phase, and phase 4 is the period between the end of
one action potential and the beginning of the next, which in the Purkinje
11
(A) (B) (C)

1 2 1 2 1 2
+ – – –
+ + – –
– + – + – +
– +
+ – + –
+ –
+ + +
– – + – +
– –
+ – + + – +
– –
– + + + +
+ + +
+ – – – – –
Chemical gradient Chemical gradient Chemical gradient
Electric gradient Electric gradient
Figure 2.1 Origin of the resting potential. A vessel is divided into two compart-
ments (1 and 2) by a membrane that is permeable to positive ions (potassium) but
impermeable to negative ions. Placing an ionisable solution into compartment 1
creates a chemical concentration gradient for the flow of positive ions toward
compartment 2(A). As positive ions move across the membrane, they leave negative
ions behind, generating an electric gradient of direction opposite to the chemical one
(B). Steady state is achieved when the magnitude of the chemical and electric gradi-
ents are equal (C). (From Jalife J, Delmar M, Davidenko JM, Anumonwo JMB. Basic
cardiac electrophysiology for the clinician. Armonk, NY: Futura Publishing, 1999.)
fibre corresponds to the non-excited or resting potential. The action poten-

tial as described above can be considered an “all-or-nothing” phenomenon,
i.e. once phase 0 has been triggered, the remaining phases automatically
follow (time dependence).
Ionic changes associated with the action potential

The inward sodium current is activated once the membrane potential of
a Purkinje fibre depolarises above a certain threshold value (threshold
potential) (Figure 2.3).The concentration of Na in the extracellular space
is significantly greater than the intracellular space (140 mM v 4 mM) and
once the Na channels open there is a very large, rapid influx of positively
charged Na ions into the cell, resulting in phase 0 depolarisation. After a
few milliseconds the Na channels are inactivated and the depolarisation
stops at approximately 20 mV. In most cardiac cells the phase 1 repolari-
sation is provided by the transient outward current (ITO) of potassium ions
which itself inactivates very rapidly. The dominant currents during
the plateau phase of the action potential are the inward long-lasting
calcium current (ICa-L ) (maintaining depolarisation) and the delayed
12
THE CARDIAC ACTION POTENTIAL AND ITS RELEVANCE TO ARRHYTHMIAS
SA Atrium Purkinje Ventricle

1
2
0 3
4
INa
ICa
ITO
IK1
IK
ICl
If
Figure 2.2 Phases of the action potential in a Purkinje fibre and differences in
action potential morphology in myocytes from different parts of the heart. (From
Hondeghem LM. Use dependence and reverse use dependence of antiarrhythmic
agents: pro and antiarrhythmic actions. In: Breithardt G, Borggrefe M, Camm J,
Shenasa M, eds. Antiarrhythmic drugs. Berlin: Springer, 1994.)
(A) (B)
Vth
(–70 mV)
Vr (–85 mV)
Ith
Figure 2.3 Generation of the action potential requires depolarisation of the

membrane potential (by a current injection) above a certain threshold value (B).
If this threshold is not reached (A) no action potential results. (From Jalife J, Delmar
M, Davidenko JM, Anumonwo JMB. Basic cardiac electrophysiology for the clinician.
New York: Futura, 1999.)
rectifier potassium outward current (IK) (causing repolarisation). Phase 3

occurs when Ca2 channels are inactivated and the outward potassium
currents are unopposed. The delayed rectifier current inactivates as the cell
repolarises, and finally IK1 predominates (phase 4).
13
Action potentials in specialised cardiac cells

The classic action potential as described above shows important variations
depending upon exactly which cardiac cells are involved (see Figure 2.2).
Perhaps the most important variation relates to the action potential of the
sinus node, where normal cardiac electrical activity is initiated. Sinus node
cells, unlike atrial or ventricular myocytes, spontaneously depolarise with-
out any excitatory stimulus being required from another cell. This pace-
maker activity is associated with two major differences in action potential
characteristics from a “generic” myocyte.
● During phase 4 there is a slow spontaneous depolarisation that brings
the membrane potential from its most negative point at the end of repo-
larisation (approximately 60 mV in sinus node cells) to the threshold
potential at the onset of the next action potential (see Figure 2.2).
Despite many years of research, the mechanisms responsible for this
vital “pacemaker current” remain controversial. The most commonly
held view is that it results from a hyperpolarisation-activated sodium
current called If.
● The action potential upstroke of sinus nodal cells is slower than that of
ventricular myocytes and starts at a more negative threshold potential.
These characteristics are the result of the depolarisation being depend-
ent on Ca2 ions through channels similar to those mediating ICa2 in
ventricular cells. The sodium current and inward rectifier potassium
current (IK1) are virtually absent from sinus node cells.
(A) (B) (C)

0
0
50
mV
0
M
Epi
Endo
400 ms 400 ms 2s
Figure 2.4 Quinidine-induced early after-depolarisations and triggered activity in

an M cell. (From Antzelevitch C, Di Diego JM, Sicouri S and Lukas A. Selective
pharmacological modification of repolarising currents: antiarrhythmic and pro-
arrhythmic actions of agents that influence repolarisation in the heart. In:
Breithardt G, Borggrefe M, Camm J, Shenasa M, eds. Antiarrhythmic drugs. Berlin:
Springer, 1994.)
14
Atrioventricular nodal cells in the centre or N region of the AV node show

action potentials similar to sinus node cells and indeed have intrinsic pace-
maker properties, although spontaneous depolarisations are at a slower rate
than those from the sinus node.
M cells are located in the middle myocardium (between the subendocar-
dial and subepicardial regions) and have longer action potential durations
than cells located in the other regions (Figure 2.4A).
Relevance of the action potential to

clinical arrhythmias
Abnormalities of the action potential that have the potential to cause clini-
cal cardiac arrhythmias have historically been classified into three broad
groups.
Normal automaticity of a cardiac cell can cause tachycardias if the rate of
spontaneous phase 4 depolarisation increases but such situations are very
rarely pathological. The most common example is that of exercise-related
sinus tachycardia in which phase 4 depolarisation of the sinus node is
increased by sympathetic activation and vagal inhibition.
Abnormal automaticity has been described in isolated atrial or ventricular
cells in which the resting potential has been made less negative than nor-
mal by some intervention such as ischaemia.This can result in spontaneous
phase 4 depolarisations carried by Ca2 ions (Figure 2.5). It has yet to be
shown convincingly that such preparations have a clinical counterpart but
animal studies have suggested that they may play a role in ventricular
arrhythmias in the early period after myocardial infarction.
Triggered activity refers to depolarisations caused by oscillations in mem-
brane potential that follow an action potential upstroke and are termed
after-depolarisations (Figure 2.6). If such after-depolarisations occur dur-
ing phases 2 or 3 they are referred to as early after-depolarisations (EADs),
and if they are in phase 4, as delayed after-depolarisations (DADs).
Experimentally, there is a wide variety of agents and conditions that can
give rise to EADs but in general they share the common feature of pro-
longing repolarisation. An EAD occurs when, for some reason, the balance
of repolarising currents changes so that there is a net inward movement of
charge.This can occur as a consequence of a decrease in outward potassium
–65
Figure 2.5 Action potentials from isolated Purkinje fibres in the endocardial
border zone of a 24 hr old canine infarct, demonstrating spontaneous phase 4 depo-
larisations (abnormal automaticity). Heart rate is 140 bpm. (From Janse MM.
Mechanisms of arrhythmias. New York: Futura, 1994.)
15
A B C
0
–90
D E
0
–90
1000 msec 750 msec

60/min 80/min
Figure 2.6 The development of triggered activity in association with early and
later after-depolarisations.The solid trace in panel A shows the normal action poten-
tial of a Purkinje fibre. The dashed trace and arrow show the change in membrane
potential during an early after-depolarisation. In panel B the arrow shows a second
upstroke during phase 3 which was triggered by an early after-depolarisation. Panel
C shows the second upstroke and two additional triggered impulses. In panel D a
delayed after-depolarisation is indicated by the arrow. Delayed after-depolarisation
amplitude increases when the stimulus rate is increased, as shown in panel E.
Triggered activity occurs at the arrow when the after-depolarisation reaches thresh-
old potential. (From Wit AL, Rosen MR. Cellular electrophysiology of cardiac
arrhythmias. Modern concepts of cardiovascular disease. 1981:50 7–11.)
current or an increase in the inward sodium or calcium currents. EADs

occur more readily in Purkinje fibres than in ventricular or atrial muscle.
However, the M cell located in the deep subepicardium and midmy-
ocardium is prone to the development of EADs (Figure 2.4). They may
well play a role in in the long QT syndrome (see Chapter 12), in which ven-
tricular arrhythmias are associated with prolongation of the QT interval on
the surface electrocardiogram.
Delayed after-depolarisations (DADs) occur in experimental prepara-
tions of cellular Ca2 overload and are thought to be implicated in arrhyth-
mias associated with digoxin toxicity. Calcium overload, from whatever
cause, results in a transient inward sodium current (ITI) through a calcium-
dependent non-specific ion channel, giving rise to a DAD. Exogenously
administered adenosine has been used as a specific test for the diagnosis
of tachycardias dependent upon DADs. Adenosine reduces Ica indirectly by
inhibiting adenylate cyclase and cAMP. Adenosine terminates and sup-
presses right ventricular outflow tract tachycardia suggesting that the
mechanism of this arrhythmia is cAMP-mediated triggered activity (see
Chapter 8).
16
Further reading
Hoffman BF, Rosen MR. Cellular mechanisms for cardiac arrhythmias. Circ Res 1981;49:1–15.
Lerman BB, Belardinelli L, West GA et al. Adenosine-sensitive ventricular tachycardia:
evidence suggesting cyclic AMP-mediated triggered activity. Circulation 1986;74:270–280.
Noble D. The initiation of the heart beat. New York: Oxford University Press, 1979.
17
3: Propagation of electrical
impulses through cardiac
muscle
Whilst much attention has been directed at the electrical events involved in
excitation of single cardiac cells, in terms of the generation of clinical tachy-
cardias it is likely that the mechanisms of propagation of the cardiac
impulse between cells are just as important (or perhaps more so).
Local current spread (electrotonic propagation)

Injection of current across the membrane of a single myocyte will not only
lead to the depolarisation of the membrane of that particular cell but will
also lead to propagation of excitation across the intercellular gap junctions
to the neighbouring cells. The voltage change that results from such a cur-
rent injection is described by the “cable equations” originally devised to
characterise changes in a transatlantic telegraphic cable. They describe the
changes in voltage along a continuous passive fibre in which resistance is
constant throughout. When a current pulse is introduced into such a fibre
the amplitude of the resulting depolarisation decays exponentially with dis-
tance (Figure 3.1).This form of propagation of cellular excitation occurs in
the absence of generation of action potentials and describes the behaviour
of cell membrane below threshold levels (electrotonic propagation). The
diameter of the fibre has a major influence on the cable type properties,
with intracellular resistances increasing as fibre diameter is reduced. In
other words, the length of the fibre that is influenced locally by a given
current pulse from a point source is greater in a thick than a thin fibre.
There are limitations to the use of cable equations in that propagation
along cardiac tissue is not perfectly uniform and there are microscopic dis-
continuities in the form of gap junctions. Nevertheless, under normal cir-
cumstances the small delays imposed by the gap junctions are of relatively
minor significance.
Propagation of the action potential

It can be seen from the above that the electrotonic form of propagation
through cardiac muscle is unlikely to be an effective means of rapid spread
18
PROPAGATION OF ELECTRICAL IMPULSES THROUGH CARDIAC MUSCLE
100
80
Vx =Voe –x /
∆V (mV)
60
40 = space constant
20
0 1 2 3
Distance (x )
(mm)
Figure 3.1 The exponential decay of potential difference across the cell mem-
brane with distance. (From Jalife J, Delmar M, Davidenko JM, Anumonwo JMB.
Basic cardiac electrophysiology for the clinician. Armonk, NY: Futura, 1999.)
of electrical activity throughout the heart because of the rapid fall in volt-
age with distance along the muscle fibre. Co-ordinated activation of the
heart is made possible by the generation of action potentials, the all or
nothing nature of which provides a “boost” for the propagating impulse as
each cell is reached, thereby ensuring there is no decay of voltage with dis-
tance. The depolarisation current generated by the first action potential
propagates electrotonically to the next cell which then reaches its threshold
potential and a second action potential occurs with a new influx of inward
current which becomes the source of current for cells further downstream.
In a linear cable composed of electrically interconnected excitable cells,
impulse propagation is determined primarily by the ratio between the cur-
rent available to excite cells (the source) and the current required by cells
downstream to be excited (referred to as the sink), i.e. the likelihood of suc-
cessful propagation (sometimes termed safety factor for conduction) from
proximal to distal cells in such a cable is proportional to the excess of
source current over the requirement of the distal cells that form the sink.
Slow conduction and/or conduction block may result from a progressive
decrease in this ratio or safety factor.
The current generated by the proximal part of the cable (source) is deter-
mined by:
● The maximum rate of rise of the action potential upstroke
● Action potential amplitude
● Action potential duration.
Antiarrhythmic drugs may cause conduction slowing or conduction block
by reducing any of these factors (see Chapter 16).
Passive membrane properties related to cell-to-cell communication may
also modulate the amount of excitatory current delivered by the source.
Perhaps less intuitively obvious is the influence of the sink. If the distal
19
(A) +
+
+
+
+
+ +
+ + + +
Source + + Sink
+ +
(B)
Source Sink
Figure 3.2 If a small group of myocytes acts as a source for current spread to a
significantly greater number of distal cells, the source may be insufficient to depo-
larise the “sink” and the impulse may slow or fail to propagate. If a proximal group
of cells activates distal cells over a broad area (as in the case of a curved wave front)
conduction slowing and failure of propagation is more likely than if the source acts
as a planar wave. (From Jalife J, Delmar M, Davidenko JM, Anumonwo JMB. Basic
cardiac electrophysiology for the clinician. Armonk, NY: Futura, 1999.)
myocytes being activated are in a two-dimensional sheet (or a three-dimen-

sional block) rather than behaving as a single cable, there may come a point
during propagation of an action potential when a single myocyte or a small
group of myocytes must act as the source for current spread to a signifi-
cantly greater number of distal cells (Figure 3.2A). This situation may
occur when a thin unbranched uniform array of cardiac cells exists in the
middle of infarcted ventricular muscle connected to a broad sheet of
healthy ventricular myocytes on the edge of the infarcted area. Under these
circumstances the source may provide insufficient current to depolarise the
broad sheet of distal cells and the impulse may fail to propagate. In other
words, there is a “loading effect” imposed by the cells downstream on a
proximal source. In this way the geometry of cardiac muscle fibres can
greatly influence the likelihood of successful propagation of the cardiac
impulse throughout the heart.
20
Figure 3.3 Structure of cardiac muscle showing a schematic drawing of two

adjacent “unit bundles” of cardiac muscle cells and their interconnections. It can be
seen that the myocardium is better coupled in the direction of the long axis of its cells
and bundles (anisotropy), because of the architecture of the myocytes and position-
ing of the gap junctions. (From Sommer JR and Dolber PC. Cardiac muscle: ultra-
structure of its cells and bundles. In Paes de Carvalho A, Hoffman BF, Lieberman M,
eds. Normal and abnormal conduction in the heart. Mt Kisco, NY: Futura, 1982.)
Anisotropic propagation
One of the fundamental characteristics of electrical propagation through
cardiac tissue is that it is directionally dependent: this is the consequence
of the rod-like shape of adult cardiac myocytes, the heterogeneous distri-
bution of gap junctions and the orientation of cell bundles along the long
axis of the cells (Figure 3.3). As a consequence, speed of propagation is
three to five times greater in the longitudinal direction (parallel to fibre
direction) than the transverse direction. This directional dependence of
propagation is referred to as anisotropy. Although conduction velocity is
greater in the longitudinal direction, the directional dependence of the
safety factor for conduction may be greater in the longitudinal or transverse
direction depending upon, amongst other factors, relative resistivity in
the two directions. Asymmetry in the safety factor for conduction may
result in conduction block occurring in one particular direction (unidirec-
tional block) and this is likely to be important in the generation of cardiac
arrhythmias (see later).
Propagation of curved wave fronts

It follows from the discussion of the influence of a distal sheet of cells on
propagation velocity and safety factor for conduction that the shape of a
propagated wave front is a major determinant of success or failure of prop-
agation. It is clear that the relative area of distal tissue to be excited (the
sink) ahead of a convexly curved wave front (the source) is larger than the
area forming the sink in front of an equivalent plane wave (Figure 3.2B).
The more convexly curved a wave front, the lower its velocity of propaga-
tion and the higher the likelihood of failure of conduction.
21
Relevance of abnormalities in propagation to cardiac

arrhythmias: the generation of re-entry
The great majority of clinical tachycardias have a re-entrant mechanism,
i.e. are caused by abnormalities in propagation of the electrical impulse
through cardiac tissue rather than abnormalities in activation of individual
cells. Re-entry is the circulation of the cardiac impulse around an obstacle
(anatomical or functional) leading to repetitive excitation at a frequency
that depends on the conduction velocity of the impulse and the perimeter
of the obstacle. There are three principal requirements for re-entrant activ-
ity to occur (Figure 3.4).
● The presence of a circuit which can be either anatomically or function-
ally determined. The classic example of an anatomic re-entrant circuit
SA node
(A)
Accessory
AV node pathway
Two anatomic
pathways
SA node
(B)
Atrial
premature beat
Unidirectional
block and
conduction
slowing
(C) SA node
Reentrant
circuit
Figure 3.4 Requirements for re-entrant activity as demonstrated in the anatomic

re-entrant circuit associated with the Wolff–Parkinson–White syndrome.
(A) The existence of two potential routes for electrical wave fronts (in this case the
AV node and accessory pathway). (B) An atrial premature beat finds one route
refractory (the accessory pathway), leading to unidirectional block in the accessory
pathway. The prematurity of the atrial beat also leads to conduction slowing within
the AV nodal tissue. (C) By the time the impulse reaches the ventricular end of the
accessory pathway it is no longer refractory and a stable re-entrant circuit is formed.
22
is that associated with the Wolff–Parkinson–White syndrome (see

Chapter 7), in which a clear and fixed anatomic abnormality exists. The
circuit may be considered functionally determined if there is no well-
defined anatomic circuit but a wave front circulates round a region of
cardiac tissue that is inexcitable (or at least unexcited) in certain cir-
cumstances. The functional group of mechanisms probably underlies
re-entrant activity associated with atrial and ventricular fibrillation.
● The need for unidirectional block for the initiation of circulating
activity. This may occur as a consequence of a disparity in either refrac-
toriness or safety factor for conduction between the two arms of the
re-entrant circuit.
● The presence of slow conduction in some part of the circuit.
Anatomic re-entry
It is clear that for stable re-entrant activity to occur the rotation time
around the circuit should be longer than the time required for recovery
(termed refractory period) of any segment of the circuit. In other words, the
wave length of refractoriness, which is the product of the refractory period
and the conduction velocity, must be shorter than the perimeter of the cir-
cuit. Under these circumstances, an excitable gap will appear between the
head of the circulating impulse and its own refractory tail (Figure 3.5A).
The shorter the wave length (due to either short refractoriness and/or slow
conduction velocities), the larger the excitable gap, and the more stable the
re-entrant tachycardia. Re-entrant activity will be stable in the presence of
a large excitable gap because the re-entrant wave front will find only fully
recovered tissue in its path. Tissue that is partially recovered may be
excitable but may also lead to failure of propagation.
As will be discussed in later chapters, anatomic re-entry is responsible for
many clinical tachycardias, including atrial flutter, AV nodal re-entrant
tachycardia, tachycardias associated with the Wolff–Parkinson–White syn-
drome and several forms of ventricular tachycardia.
Functional re-entry
Functional re-entry occurs in the absence of a predetermined structural
circuit.
The leading circle model of functional re-entry

According to the leading circle concept, a propagated wave turns back on
its own refractory “tail” and re-entrant activity occurs: (1) without an
excitable gap and (2) with a size that is determined by refractoriness of the
cardiac tissue (Figure 3.5B). It is postulated that the central core of tissue
around which the impulse propagates remains inexcitable because it is
continually being depolarised electronically by the circulating wave and
therefore continually refractory.
23
(A) Reentrant circuit defined by anatomy

AV node Accessory
pathway
(B) Reentrant circuit defined by

tissue refractoriness
(C) Reentrant circuit defined by

tissue conduction properties
Refractory tissue
Partially refractory
tissue
Fully excitable
tissue
Figure 3.5 Different forms of re-entry.

(A) Re-entrant circuit defined by anatomy: in this example orthodromic tachycar-
dia associated with an accessory pathway. In this situation the size of the re-entrant
circuit is defined by anatomic boundaries. At any particular moment a length of the
electrical tissue within the circuit is completely refractory (the wavelength of refrac-
toriness, defined as refractory period conduction velocity). A further length will
be partially refractory and the remaining length remains available for excitation
(excitable gap). The larger the excitable gap the less likely that the advancing wave
front will encounter refractory tissue and the more stable the re-entrant circuit.
(B) Re-entrant circuit defined by tissue refractoriness. In the leading circle model
of functional re-entry an advancing wave front rotates back upon itself, the diame-
ter of the rotating circuit being limited only by the wavelength of refractoriness (see
above). In this model there is no excitable gap and the core of the wavelet is ren-
dered continuously refractory by continuous re-excitation from the surrounding
circulating electrical activity.
(C) Re-entrant circuit defined by tissue conduction properties. In this form of func-
tional re-entry (spiral wave hypothesis) the size of the re-entrant circuit is deter-
mined by the ability of the wave front to curve back upon itself. In contrast to the
leading circle model of functional re-entry, in this scheme an excitable gap may exist
and the core remains available for excitation.
24
Figure 3.6 Wavefront curvature is highest at the centre of a spiral wave and as a
consequence conduction is slowest at this point. (From Jalife J, Delmar M,
Spiral waves
Some authors have suggested that the properties of functional re-entrant
waves are governed mainly by the properties of curved wave fronts rather
than the leading circle explanation discussed above. It is suggested that the
formation of rotating spiral waves is a common feature of excitable tissues
throughout biology and that their formation is related to the effect of
curvature on propagating wave fronts. It can be seen that, during spiral
wave activity, curvature of the wave front is extremely high at the centre of
the spiral and it is proposed that (due to source/sink mismatch) it is suffi-
ciently high to result in failure of propagation (Figure 3.6): thus the dynam-
ics of propagation of curved wave fronts may explain the origin of this core.
A consequence of the above hypothesis is that, as opposed to the leading
circle mechanism, an excitable gap may well be present during these rotat-
ing waves (Figure 3.5C), and indeed this can be demonstrated directly by
the fact that externally induced propagating waves with lower curvature
(and therefore higher speed) are able to invade the core region during
spiral wave activity. Because the core remains excitable during spiral wave
activity, it is not surprising that small changes in the condition of the spiral
wave tip (such as small changes in the excitability of the tissue) may lead
to shifts in the trajectory of the spiral wave, leading to “drifting spirals”.
This is currently a popular hypothesis for the mechanism of atrial and
ventricular fibrillation.
Anisotropic re-entry
Anisotropic re-entry may be considered as a form of functionally deter-
mined re-entry in which initiation and maintenance of the re-entrant
25
activity is based on the directional properties of the tissue. As has been dis-
cussed previously, propagation velocity in cardiac muscle is three to five
times faster in the longitudinal axis of the cells than along the transverse
axis. Similarly, there is asymmetry in the safety factor for propagation as
well as conduction velocity. Thus, anisotropy may set the stage for hetero-
geneity of functional properties and unidirectional block and lead to the
initiation and maintenance of re-entry. Clear clinical examples of such
forms of re-entry are difficult to come across, however. It has been sug-
gested, based on a dog model of ventricular tachycardia following myocar-
dial infarction, that anisotropic propagation may play a major role in the
initiation and maintenance of re-entry in ventricular tissue surviving a
myocardial infarction.
Further reading
Danse PW, Garratt CJ, Allessie MA. Preferential depression of conduction around a pivot
point in rabbit ventricular myocardium by potassium and flecainide. J Cardiovasc
Electrophysiol 2000;11:262–273.
El-Sherif N. Re-entrant mechanisms in ventricular arrhythmias. In: Zipes D and Jalife J eds.
Cardiac electrophysiology from cell to bedside, 2nd edn. Philadelphia: WB Saunders, 1995.
Fast VG, Kleber AG. Role of wavefront curvature in propagation of the cardiac impulse.
Cardiovasc Res 1997;33:258–271.
26
PART II
CLINICAL TACHYCARDIAS
4: Classification and
nomenclature of
clinical tachycardias
Tachycardias are usually classified according to their presumed site of

origin. It is obvious that, as knowledge about the site of origin of tachycardias
has increased, so the terms used to describe arrhythmias have become more
specific. It is usual to classify arrhythmias into three broad groups based on
whether they originate in the atrium, the atrioventricular junction, or the ven-
tricle. The following description is not an exhaustive list, but includes all the
common tachycardias and all those discussed in this book.This classification
acts as a framework for the subsequent chapters and includes some terms
that will be fully defined and described in the relevant section.
(A)
Atrium “fast”AV
“slow”
nodal
AV nodal
pathway
pathway
Ventricle
(B)
Atrium
Accessory
AV node
pathway
Right bundle
branch
Left bundle
branch
Ventricle
Figure 4.1 Anatomic basis for the two common forms of junctional tachycardia:
atrioventricular nodal re-entrant tachycardia (A) and atrioventricular re-entrant
tachycardia utilising an accessory pathway (B).
29
Tachycardias originating in the atrium

● Sinus tachycardia
● Atrial tachycardia
● Atrial flutter
● Atrial fibrillation.
Tachycardias originating in the atrioventricular junction (Figure 4.1)

● Atrioventricular nodal re-entrant tachycardia (AVNRT)
● Accessory pathway mediated re-entrant tachycardia (sometimes referred
to as atrioventricular re-entrant tachycardia or AVRT)

Prior to the full description of the source of these tachycardias they were
often referred to as PAT (paroxysmal atrial tachycardia) or PSVT (parox-
ysmal supraventricular tachycardia). When the precise diagnosis is unclear
but thought to be either AVNRT or AVRT, then the phrase paroxysmal
junctional tachycardia is appropriate.
Tachycardias originating in the ventricle

Subclassification of ventricular arrhythmias is based primarily on their elec-
trocardiographic morphology (Figure 4.2):
● Monomorphic ventricular tachycardia (including right ventricular out-
flow tract tachycardia, left ventricular fascicular tachycardia)
● Polymorphic ventricular tachycardia (sometimes referred to as torsade
de pointes, when there is a typical “twisting of the points” appearance or
(more loosely) if polymorphic ventricular tachycardia occurs in the set-
ting of a long QT interval
● Ventricular fibrillation (polymorphic ventricular tachycardia that is asso-
ciated with cessation of cardiac output and does not self-terminate)
● Ventricular flutter – very rapid monomorphic ventricular tachycardia
(usually 300 beats/min or more) that is associated with cessation of
cardiac output.
(A)
(B)
(C)
(D)
Figure 4.2 Monomorphic ventricular tachycardia (A), polymorphic ventricular

tachycardia (B), ventricular fibrillation (C), and ventricular flutter (D).
30
5: Sinus tachycardia,
atrial tachycardia, and
atrial flutter
Sinus tachycardia
Sinus tachycardia is the normal physiological response to a number of
stimuli, including exercise, anxiety, fever, pain, hypotension, pulmonary
embolism, and other acute medical conditions. The key electrocardio-
graphic feature of sinus tachycardia is the presence of P waves of normal
morphology during tachycardia (Figure 5.1). Under these circumstances it
is not appropriate to attempt to slow the heart rate, as the tachycardia may
be the only thing maintaining an adequate circulation. The cause of the
tachycardia should be sought and treatment directed appropriately.
There are two conditions in which sinus tachycardia is not a normal
physiological or compensatory response. Sinus node re-entrant tachycardia
(SNRT), as the name implies, is a re-entrant tachycardia in which the cir-
cuit involves the sinus node or perinodal tissue, and may represent a spe-
cific form of focal atrial tachycardia (see below). It differs from other forms
of sinus tachycardia in that it has a sudden (within one beat) onset and off-
set. P wave morphology is, by definition, normal. Patients rarely present
with this tachycardia and much more frequently it is a coincidental finding
at electrophysiology study. Treatment is rarely necessary but beta blockade
or verapamil are usually effective.
Inappropriate sinus tachycardia usually occurs in young people, predomi-
nantly women, and may be an expression of what is known as the hyper-
adrenergic syndrome. In this syndrome the presentation is with troublesome
palpitation that may be present throughout most of the day. Attempts to
record cardiac rhythm coincident with symptoms reveals sinus tachycardia
only, usually in the 110–140 beats per minute range. This syndrome over-
laps with orthostatic intolerance syndrome, which is characterised by
symptoms of lightheadedness and fatigue in addition to palpitations and is
associated with a marked rise in heart rate on standing. This syndrome in
turn overlaps with the chronic fatigue syndrome. It has been suggested that
the hyperadrenergic syndromes are an expression of oversensitivity of the
heart to circulating catecholamines, and certainly these patients have a par-
ticularly high heart rate in response to intravenous catecholamine infusion.
31
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure 5.1 12-lead ECG of sinus tachycardia. Normal P waves can clearly be seen preceding the QRS complexes.
SINUS TACHYCARDIA, ATRIAL TACHYCARDIA, AND ATRIAL FLUTTER
Beta blockade should be attempted in the first instance, but these patients
are usually poorly tolerant of this and other medication. As a result, these
patients commonly progress from one medication to another (and often
one doctor to another) with little improvement.
Attempts to modify the sinus node in cases of inappropriate sinus tachy-
cardia have shown that extensive radiofrequency applications must be per-
formed in order to accomplish a moderate sinus rate reduction. There is a
high recurrence rate and such a procedure is certainly one of last resort.
Patients must understand that only those symptoms clearly associated with
a rapid heart rate can improve with sinus node ablation.
Atrial tachycardias
Atrial tachycardias are defined as supraventricular arrhythmias that require
atrial tissue only (i.e. not AV junctional or ventricular tissue) for initiation
and maintenance. A variety of features have been used to classify these
arrhythmias, such as the putative cellular mechanism, features of the surface
electrocardiogram, response to drugs and the presence or absence of prior
cardiac surgery. For instance, atrial tachycardias that can be terminated by
intravenous adenosine are thought to have an automatic mechanism,
whereas those that can reproducibly be initiated or terminated by atrial
premature beats are thought to have a re-entrant mechanism. Increasingly,
however, they are classified with catheter ablation techniques in mind and
can be subdivided as follows.
Tachycardias that arise from a focal area of

atrial tissue
These tachycardias can be cured by delivery of radiofrequency application
at a specific site. The most common atrial sites which can give rise to such
arrhythmias are the terminal crest (crista terminalis) in the right atrium, the
junction of the left atrium with the pulmonary veins, and the junction of
the superior caval vein with the right atrium (Figure 5.2). It is unclear why
such sites are particularly important in the generation of atrial tachycardia,
but it may be that local discontinuities of atrial structure are important in
the generation of micro re-entry. Alternatively such sites may be more sus-
ceptible to stretch-induced abnormal automaticity.
Although a likely cellular mechanism (re-entry, automaticity, or triggered
activity) may be delineated in some cases, successful application of radiofre-
quency energy (and cure) is independent of the suggested cellular mechanism.
Clinical and electrocardiographic presentation

The clinical settings in which this type of atrial tachycardia occur are very
much those of atrial flutter and atrial fibrillation (see Chapter 6). Clinical
presentation is usually with palpitations but may be with symptoms associ-
ated with a tachycardia-induced cardiomyopathy. P wave morphology is
abnormal (unlike sinus tachycardia) and gives a good indication of the site
33
SA
RA LA
SVC
IVC
AV
Figure 5.2 Schematic representation of usual sites of focal atrial tachycardias: the
terminal crest in the right atrium and at the junction with the pulmonary veins in
the left atrium.
of origin of the tachycardia (Figure 15.2). Positive P waves in the inferior

leads indicate a superior (rather than inferior) origin and a positive P wave
in V1 indicates a left atrial origin. Rarely, P wave morphology may be vari-
able (“multifocal” atrial tachycardia), particularly if it is occurring in the
setting of illnesses associated with elevated right-sided intracardiac pres-
sures such as acute exacerbations of pulmonary disease.
Therapy
Pharmacological treatment of patients with focal atrial tachycardias has
been somewhat disappointing, and there are no controlled trials of medical
therapy for these arrhythmias. Digoxin is frequently used in order to control
the ventricular rate but does not affect the atrial tachycardia itself. Drugs
such as flecainide and propafenone have been found to have efficacy rates of
approximately 50% and amiodarone has also been shown to be moderately
effective in terms of terminating and suppressing these arrhythmias. As with
many other arrhythmias, recent attention has shifted to the role of radiofre-
quency catheter ablation as a curative treatment. Identification of the pre-
cise site of tachycardia origin (and therefore appropriate site for ablation
lesions) at electrophysiology study is in general more difficult than for junc-
tional tachycardias as sites are not limited to one anatomic structure, such
as the AV junction. Reported success rates are in the order of 80–100% but
recurrence may occur if there is widespread underlying atrial disease.
Tachycardias that involve re-entry with macroscopic

anatomic and/or surgical barriers
In this category the critical re-entrant circuit involves (and is dependent
upon) a region of atrial tissue (isthmus) that is delineated by anatomic
34
SINUS TACHYCARDIA, ATRIAL TACHYCARDIA, AND ATRIAL FLUTTER
SVC Anterior
scar
Posterior
scar IVC
Figure 5.3 Representation of the re-entrant circuit in a patient with atriotomy-

related atrial tachycardia, in this instance following repair of atrial septal defect.The
presence of slowly conducting tissue between “islands” of non-conducting scar
tissue predisposes to re-entrant arrhythmias. (Modified from Nakagawa et al.
Characterisation of re-entrant circuit in macro re-entrant right atrial tachycardia
after surgical repair of congenital heart disease. Circulation 2001; 103:699–709.)
boundaries such as surgical atriotomy scars (Figure 5.3). Such “incisional”

re-entrant atrial tachycardias involve a combination of natural and surgi-
cally created (incisions, patches, conduit material) barriers in patients
following reparative surgery for congenital heart disease. In this situation
a line (series of individual lesions) of radiofrequency lesions across the
conducting isthmus is required to abolish the arrhythmia.
Clinical and electrocardiographic presentation

These arrhythmias can complicate repair of atrial septal defect, transposition
of the great arteries (Mustard, Senning and Rastelli procedures) and Fontan
procedures for tricuspid atresia, double inlet single ventricle, or other more
complex anomalies. Incisional atrial tachycardias are usually sustained and
may present several years after surgery. Usually the arrhythmias are of sud-
den onset and offset, and the electrocardiogram reveals a constant atrial cycle
length of more than 0.2 seconds with an abnormal P wave morphology.
Therapy
The successful management of arrhythmias in these patients can be very
challenging. As with the “focal” forms of atrial tachycardia, antiarrhythmic
drugs are frequently ineffective. In addition, antiarrhythmic agents have the
potential to adversely affect myocardial function and exacerbate coexisting
sinus node dysfunction in such patients. Radiofrequency catheter ablation
(as discussed above) is potentially curative in many such arrhythmias but
requires a very high level of expertise in terms of mapping of the tachycardia
35
circuit, identification of a critical isthmus and delivery of an uninterrupted

line of lesions across this isthmus. Clinical reports in the literature indicate
an acute success rate of 75–100% in terms of termination of these arrhyth-
mias during ablation procedures, but there is a relatively high recurrence
rate and overall success is probably not as high as that for junctional tachy-
cardias (see Chapter 7). In severely symptomatic patients with
tachycardia-induced cardiomyopathy (or the potential for this condition
as indicated by an incessant arrhythmia with a rapid ventricular rate),
radiofrequency ablation of the AV junction and pacemaker implantation
may be considered. This may be a considerable challenge itself, depending
upon the complexity of the underlying anatomy.
Atrial flutter
Atrial flutter was first described in 1911 and is a common arrhythmia that
occurs in settings (and has the same causes) similar to atrial fibrillation (see
following chapter). The two arrhythmias often coexist in the same patients.
Clinical presentation
Atrial flutter, like atrial fibrillation, can present in a paroxysmal or chronic
form. Its most common presentation is a fast regular tachycardia with a
ventricular rate of 150 beats per minute, representing an atrial rate of
300 beats/min conducted with 2:1 AV block (Figure 5.4). In situations in
which AV nodal conduction is enhanced (for instance by high cate-
cholamine drive or vagal withdrawal) or the flutter rate is slowed (usually
by antiarrhythmic drugs), AV conduction may become 1:1 with associated
marked haemodynamic deterioration (Figure 5.5). In addition to
palpitations, patients may present with left ventricular dysfunction second-
ary to prolonged periods (weeks and months) of rapid ventricular rates,
i.e. tachycardia-related cardiomyopathy.
Mechanism
“Typical” atrial flutter results from a large anatomic re-entrant circuit
within the right atrium with the impulse travelling in a caudo-cranial direc-
tion up the interatrial septum and a cranio-caudal direction down the right
free wall adjacent to the tricuspid annulus (referred to as a counterclock-
wise atrial flutter) (Figure 5.6). The tricuspid valve ring forms the anterior
anatomic barrier of the circuit and a combination of the terminal crest and
the eustachian ridge (between the inferior vena cava and the coronary
sinus os) form the posterior anatomical barrier. More rarely, electrical
activity travels in the reverse direction (counterclockwise) (Figure 5.7). An
area of slow conduction is present in the muscular “isthmus” between the
tricuspid valve ring and the inferior vena cava: this undoubtedly contributes
to the stability of the anatomic re-entrant circuit (see Chapter 3) but is
unlikely to be the primary abnormality as the electrophysiological charac-
teristics of this area are similar in people without atrial flutter. It is more
36
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GETTING RICH.
When the Society purchased the property in St James Street they
were very poor and had to take a bond on the property, and when, a
year or two later, the adjacent property in Park Street was purchased,
the amount of the bond was increased, the total being £830. Now, in
1878, the committee found themselves in a position to pay out the
bondholders, and accordingly this was done. The views of the
committee on the subject of “bonds,” as reported in the minutes, are
interesting and worthy of quotation. They state:
“The uplifting of the bonds has entailed a considerable expense to this
Society. The amount was advanced by four separate parties, who had each to
be secured by a separate bond. We should draw a lesson from this which
might be beneficial to us in the future, to make us beware that this or any of
our respective local societies never have a ‘bond’ on any property where it is
possible to get co-operative money.”
At this point it may be interesting to note the apparent effect which
the withdrawal of the trade of Barrhead Society had on the Bakery.
For the ninth year the average turnover of the Society was 223 sacks
per week, while in the tenth year this fell to an average of 188. The
position is more fully illustrated by taking the totals for the two
years; that for the ninth year being 11,588 sacks, while that for the
tenth year had fallen to 9,774 sacks. About this time the members
were beginning to be uneasy about the Oakmill Society, in which they
had invested £200, and at one quarterly meeting a delegate wished
to know whether the committee considered the shares of this society
a safe investment. The meeting was assured by Messrs Barclay and
M‘Nair, who were both members of the Oakmill Society, that they
considered the investment quite a safe one. At the quarterly meeting
in March 1879 question was again raised, when Mr Alexander, the
treasurer of the Baking Society, gave it as his opinion that “the loan
capital in Oakmill Society was as safe as ever it was.”
FURTHER EXTENSIONS PROPOSED.
Meantime negotiations had been going on as the result of which
the tenants in the bolt and rivet shop agreed to remove, and their
boiler, engine, and shafting were purchased by the Society for use in
driving the machinery which was being installed in the bakery. A new
roof was also being put on the bakery, and the question of erecting
two new ovens in the premises vacated by their tenant was being
considered, when the news came that Johnstone Society had decided
to start baking on their own account. This put an end for the time
being to any thought of erecting new ovens, as the withdrawal of this
society would again reduce the trade to below the capacity of the
ovens already erected, but, notwithstanding that fact, it was decided
that the whole question should be submitted to the quarterly meeting
for its decision. The 40th quarterly meeting was held on 1st March
1879. The society had now been in existence for ten years, and
although the outlook at the moment was not very bright, yet worse
times had already been met and overcome. Doubtless, the members
of committee were looking forward to the time when other societies
at a distance from the centre would begin baking on their own
account, but they knew also that the membership of the societies in
the immediate vicinity of the Bakery was increasing, and hoped to
recoup themselves in this way. At the quarterly meeting a general
discussion on the question of building new ovens, in view of the fact
that Johnstone Society was withdrawing, took place, but no decision
was come to.
THE RESULTS OF TEN YEARS’ WORK.
In considering the trade for the ten years during which the Society
had been established, it is to be noted that that for the ninth year was
the greatest, 11,588 sacks having been turned into bread and biscuits
in that year. The tenth year was the first in which there was a fall in
the turnover, each of the first nine years showing a steady increase
over that immediately preceding, and the reason for the drop in the
tenth year was so obvious and so insurmountable that no uneasiness
arose in consequence. From the second quarter in the seventh year
the dividend each quarter was almost uniformly a shilling or over,
and by the end of the tenth year no less than £8,051 had been
allocated in dividend, as well as £75 as dividend to non-members;
while £1,548 had been paid as interest on share and loan capital.
Thus in the first ten years, those associated with the Bakery had
received nearly £10,000, which they certainly would not have
received had the Baking Federation not been started. In addition,
they had a valuable property represented by shares and loans
amounting to £5,706, while private loan-holders had also £544
invested. At the same time, in addition to the employees being paid
wages equal to those paid elsewhere in the trade, £766 had been
divided amongst them in the form of bonus. The directors were also
extremely liberal in their depreciations, for during the ten years
£4,270 had been written off property, stocks, machinery, fittings,
and live stock. This made for the stability of the Society. In view of
the fact that the capital was small and the capital outlay
comparatively large, the financial policy adopted of devoting large
sums to depreciation instead of paying them away in dividends was a
sound one, and enabled the committee to undertake with a light
heart extensions which would otherwise have caused them
considerable anxiety. They had established on a sound financial basis
a structure which was to prove of lasting benefit to the co-operative
movement, and which was to bear no uncertain testimony in future
years to the ability of the builders and to the soundness of the
principles on which they were carrying on their business.
CHAPTER VII.
ST JAMES STREET: CONGESTION.
A FALL IN MEMBERSHIP—RELATIONS WITH EMPLOYEES—

CANVASSING FOR TRADE—GOOD BREAD—GROUND
ANNUAL PURCHASED—DIFFERENTIAL TREATMENT—
PRESIDENT AND TREASURER RETIRE—KEEPING DOWN
PRICES—OAKMILL FAILURE—A PECULIAR COMPLAINT
FROM KINNING PARK—FURTHER EXTENSIONS—COSTLY
LITIGATION—TRANSFERABLE CAPITAL—STILL FURTHER
EXTENSIONS.
In the preceding chapter the decline in the turnover of the

Federation, and the circumstances to which that decline was due,
have been detailed. During the latter half of the tenth year three
societies had withdrawn or been paid out, and the membership of the
Federation, which had consisted of twenty-six societies at the
beginning of the year, consisted of only twenty-three at the end. For
three years no new societies had joined, and the increase which had
taken place in the trade was due entirely to increased membership of
the societies which were members of the Federation, and to a
growing demand on the part of the members for co-operatively
produced bread. Two of the societies whose names had been struck
off the roll had been little more than nominal members for years, and
their loss scarcely affected the trade at all, while, by the beginning of
the eleventh year, the substantial decrease which had resulted from
the withdrawal of Barrhead Society showed signs of being completely
overcome. The turnover, which had averaged 185 sacks per week in
the last two quarters of 1878, as compared with 226 in the third
quarter of 1877, rose in the first quarter of 1879 to 207 sacks, and by
the end of that year was up to 216¾ sacks. The prospects for the
immediate future were not too bright, however, as Johnstone
Society, in reply to a letter which had been sent by the Bakery board,
stated that they had definitely decided to begin baking for
themselves. On 21st February 1880 the committee had before them
the formal notice from the society of their withdrawal from the
Federation, which was accepted. At the same meeting Mr Green, who
had been the representative of Johnstone Society on the committee
for eight years, was thanked by the committee for the great interest
he had taken in, and the valuable services he had rendered to, the
Baking Society. Mr Small, Johnstone, who had been one of the
auditors since the beginning of 1876, had resigned six months
earlier, in view of the fact that his society proposed withdrawing
from the Federation.
Notwithstanding the fact that the withdrawal of Johnstone Society
was imminent, and that the quarterly meeting of delegates had given
no decision on the subject when it was before them at the fortieth
quarterly meeting, the committee, by a majority of 9 votes to 2,
decided at their next meeting to proceed with the erection of two
ovens additional in the premises just vacated by their tenants. At the
same time the work of installing machinery was proceeding, and by
the middle of the summer the work was completed, as was also that
of reslating the bakery roof. The whole of this work was earned out at
a cost of almost a thousand pounds, and placed the Federation in a
position to handle a considerably larger trade than they were doing
at the moment.
RELATIONS WITH EMPLOYEES.
At the same time they were considering the wages of their bakers
and vanmen. These workers had always been paid the wages current
in the trade, and now it was reported to the committee that the wages
of bakers in the city had been reduced by 2/ per week. The subject
was discussed on several occasions, being postponed month after
month for lack of precise information, and perhaps, also because
they were loth to take the step of reducing wages. Finally, a decision
was arrived at. The information was to the effect that nineteen
bakers, eight vanmen and stable hands, and four employees in the
breadroom and office were receiving a total of £46, 16s. per week.
The details of the bakery wages showed that the ordinary bakers
were being paid 29/ per week; the ovensmen, 32/; the stockkeeper,
33/; the biscuit baker, 35/; and the under foreman, £2, 2s.; and it
was agreed that the wages all round be reduced by 2/ per week. The
vanmen who had charge of two-horse vans had their wages reduced
from 27/ to 25/; one man who had 24/ had his wage reduced to 23/;
and those who were being paid 21/ had no reduction made.
Naturally, this reduction did not meet with the approval of the
employees, but for three months they do not seem to have taken any
action. At the end of that period, however, the committee were
memorialised by both bakers and vanmen, and the request made
that their wages should be brought up to the former figures. In reply
to the vanmen’s request, the committee said that after careful
consideration they could see no good reason why they should alter
their former decision. The reply to the bakers was couched in
somewhat different terms, but it was to the same effect. It was stated
that the reduction was entirely due to the state of the labour market
in the country. From the reports which had appeared in the public
press, it seemed that similar reductions had been made in other
baking establishments, and, as the Federation had advanced wages
when advances were given elsewhere, when reductions were made
they were only following the usual course which regulated wages in
the trade. The minute continues: “But to show that we have no wish
to take any undue advantage of their position, if they can establish to
the satisfaction of this committee that the United Baking Society are
paying less than the standard wage current in Glasgow, we as a
committee would have much pleasure in reconsidering the whole
question at next meeting. Until that is done we adhere to our former
agreement.”
CANVASSING FOR TRADE.
Meantime, the committee had not been idle. They visited a
number of societies which were taking bread from them, but not all
that they required, with the view of getting them to place the whole
of their orders with the Society. They also visited several societies
which were within a comparatively short distance of Glasgow, and
one of these—Renfrew Equitable—was so pleased with the quality of
the bread supplied that after a comparatively short trial they agreed
to take the whole of their supplies from the Federation. This was
cheering news, and offset some of the other worries which were
cropping up occasionally. Flour at this time was rising very rapidly in
price. During the quarter it had risen by 10/6 per sack, the last rise
being 4/6, and the bread had, in consequence, to be advanced in
price—the common bread to 7d. per 4–lb. loaf and the “fine” to 8d.
Some trouble was also being experienced with the engine which they
had put in. New rings had been put on the piston rod, and the
engineer informed them that this would require to be done about
once in every six months. At first the committee were sceptical, but
inquiries elsewhere confirmed the engineer’s opinion. The trade at
this time was fairly prosperous, for the profit realised was averaging
about £30 per week. They were very particular also to see that their
financial position was kept on safe lines, and spent a good part of one
night discussing the allocation of the cost of the additions to the
property to the various accounts. The result was that they agreed to
add the cost of the new machinery to fixed stock account, the cost of
the new ovens and division wall to property account, to be
depreciated according to rule, while the cost of reroofing the bakery
and refitting the breadroom they decided to pay out of revenue. The
latter decision was challenged at next quarterly meeting, but on a
division the delegates by a large majority upheld the decision of the
committee. Towards the end of 1879 they made another comparison
of their bread with that of their competitors, and came to the
conclusion that, as the minute puts it, “the Society’s bread was
superior both in shape and colour, while the members had great
reason to be satisfied with the great improvement which had been
made in the french and pan bread. A unanimous expression of
opinion was given that it had been the best comparison they could
remember where the Bakery bread stood in such a pre-eminently
favourable position.” After making due allowance for the partiality of
the committee for bread of their own manufacture, it would, appear
that the expectations of good to be derived from the installation of
machinery were being realised. The committee also this year issued
calendars to the societies. This had been done on at least one
previous occasion.
THE GROUND ANNUAL.
At one of the last meetings held in 1879 Mr Slater drew attention
to the fact that the payment of the ground annual for the land on
which the bakery was built was costing the Society £68 a year. He
suggested that this should be bought out, giving the probable cost as
about £1,400, and also that the necessary money might be raised by
means of loans from societies and individuals connected with the
movement, pointing out that it would be a good investment for the
Society and a safe one for those who lent the money. The suggestion
was very favourably received by the members of the committee, and
was brought to the notice of the delegates at the first general meeting
of the Society. There the committee were instructed to put it on the
programme of business for the annual meeting of the Society. At that
meeting, however, the question was shelved for the time being, a
motion being agreed to “that they delay at present taking any active
steps to purchase the ground annual, and that the matter be left in
the hands of the committee to bring it up again when they consider
that the Society is in a position to do it with advantage.” It was not
until a meeting of committee held on 18th November 1882 that the
subject was raised again, and again this was done by the secretary in
the form of a definite motion “that steps be taken to purchase the
ground annual.” He pointed out that they were paying £68 per
annum to persons outside who had no other interest in the
movement, and that this sum would be retained for the benefit of the
Federation, while the purchase would also assist to a certain extent
in the solution of the problem of what to do with their surplus
capital. The other members of the committee agreed, and it was
decided to call a special meeting at the end of the 56th quarterly
meeting to consider the question. At this meeting the committee
were empowered to make the purchase at once, and entered into
negotiations with the proprietors, with the result that after a
considerable amount of negotiation and delay the Society became the
owner of the ground annual at a cost of £1,652, 2s. 6d., being twenty-
three and a half years’ purchase of the sum paid annually. The
Society was now so wealthy that the directors were able to pay this
sum from the bank balance without interfering with their deposits in
the Wholesale Society.
DIFFERENTIAL TREATMENT.
For some reason which is not very easy to understand after the
lapse of time the committee did not treat alike all the societies which
withdrew from the Federation. For instance, Barrhead Society had
no deduction made from its capital on withdrawing, while Johnstone
Society, two years later, was asked to pay 7½ per cent. toward the
reserve and depreciation funds. As the circumstances which led to
the withdrawal of the two societies were practically similar, and as
the financial position of the Federation had changed, if at all, for the
better in the interval, to find a reason for the differentiation is a little
difficult. Parkhead Society, which withdrew shortly after Johnstone,
were charged 10 per cent., but in this case the society had not been
regular or consistent customers of the Federation, and at the meeting
at which intimation of their withdrawal was given very serious
complaints of their unco-operative methods were made by the sub-
committee.
PRESIDENT AND TREASURER RETIRE.
The year 1880 was notable for the retiral of two officials of the
Society who had given long and faithful service. Mr Alexander, who
had been treasurer almost from the beginning, was defeated at the
annual meeting held in March, Mr James M‘Murran, Glasgow
Eastern, receiving the greater number of votes. At the same meeting
Mr Andrew Brown, who had been president of the Federation from
1872, intimated that it was not his intention to seek re-election, his
reason for this course being that his society, Paisley Provident, had
decided to open a bakery of their own. At the following quarterly
meeting the delegates decided to present Mr Brown with £30 as a
token of esteem for the manner in which he had conducted the
business of the Society during the years in which he had been
president. This decision called forth a protest from Paisley Equitable
Society—in the first place from the committee of the society, and
later by the authority of a quarterly meeting—but the committee of
the Baking Federation held that as the decision had been that of the
delegates the matter was one in which they could not interfere, and
in due course the presentation to Mr Brown took place. Mr
Alexander Fraser, Busby, was elected president in succession to Mr
Brown, and during his term of office the Society entered on a period
of prosperity much greater than any which had been experienced
hitherto.
By the withdrawal of Johnstone and Parkhead societies the
membership of the Federation now numbered only twenty-one
societies, and for four quarters there was no addition. But although
societies did not join up with the Federation very rapidly customers
on a non-member basis were coming in. First there was a request
from Allander Society for supplies, coupled with the promise that in
a very short time an application for membership would follow, and
the committee agreed to supply them provided that the accounts
were settled fortnightly. In September the Society was admitted to
membership. Owing to the coming withdrawal of Paisley Provident
Society the committee took energetic steps to make good the deficit
in the output which would occur when this took place. They selected
Greenock district as a likely field to tap, with such good results that
Greenock East-End Society soon became purchasers and were
admitted to membership early in the following year. Port-Glasgow
Society followed, and after a little Ann Street Society, Greenock,
became a customer, to be followed shortly afterwards by Dalmuir,
Clydebank, and Cowlairs societies. Then came Clippens Society and
Greenock Industrial. To get in all these societies, however, had taken
nearly two years, and there had been decided fluctuations in the
output during the period. With the withdrawal of Paisley Provident
Society, notwithstanding the increased trade which came from
Greenock, the number of sacks baked had dropped from 235 in the
48th quarter to 186 in the 51st; then there began a gradual rise until
the 63rd quarter showed an average output of 267 sacks per week.
The withdrawal of Paisley Provident Society had meant a loss to the
Baking Society of trade amounting to about £2,000 a quarter.
KEEPING DOWN PRICES.
There is nothing new under the sun. During the war period it has
been common knowledge that the U.C.B.S. was responsible for
keeping down the price of bread when the other master bakers
desired to raise it. This was not an entirely new role for the Society to
play, however. In 1880 it was successful in forcing the bakers of
Glasgow to reduce the price of bread within a fortnight after having
raised it, because of the Society’s refusal to raise the price also.
THE OAKMILL INVESTMENT.
The members of the committee had been somewhat chary about
investing any money in the Oakmill Society, although it was finally
decreed by the quarterly general meeting of the Society that this
should be done. For some time there had been reports that all was
not well with this society, and more than once questions had been
asked in the Baking Society’s general meetings on the subject. At
length matters were coming to a crisis, however, and a circular was
issued to the societies by the S.C.W.S. in which that society wished to
be informed how much they were prepared to give to Oakmill Society
on loan. The Baking Society’s committee replied that they could do
nothing until they had consulted the general meeting of members.
The circular had been issued in June, and in August the committee
decided to withdraw the amount of interest on their loan to Oakmill
Society which had been allowed to accumulate, and now amounted
to £47. At this meeting it was also decided that the question of a
further loan be not brought before the quarterly meeting. Shortly
afterwards the society went into liquidation, and when the final
settlement was made the Baking Society found that they had lost
£122, 11s. 8d. This sum was liquidated by being paid from the reserve
fund.
In 1882 a disaster befell Barrhead Society, their bakery being
burned down, and during the time it was being rebuilt they got their
bread from the U.C.B.S. This meant an immediate increase of twenty
sacks per week in the turnover, which was of importance at the time;
but what was of still more importance, it served to lessen the breach
which had opened between the Federation and the society and paved
the way for the return of the society to the fold at a later date.
During the earlier years of the Society’s history the mention of
letters in “red ink,” sent as reminders to societies that their
indebtedness to the Federation was exceeding reasonable limits, was
frequent in the minutes, but in these later years such “red ink”
circulars do not seem to have been sent. At anyrate, mention of them
no longer appears. This did not mean, unfortunately, that all the
societies were now sufficiently alive to the need of paying their debts
promptly and that they had the cash at hand wherewith to pay them.
The position of some of the societies was still a matter of grave
concern to the Baking Society’s committee, and in one or two cases
societies went into liquidation. One such society was Allander, which
had only joined the Federation in 1881, and which went into
liquidation towards the end of 1883. From this society they got one
shilling in the pound. Another case was that of Petershill Society,
which went into liquidation early in the same year and which had
paid its debt to the Baking Society in full.
At one time there was trouble with Kinning Park Society of a
peculiar kind. The committee of that society sent a letter to the
Baking Society’s committee, in which it was stated that the
impression in that society was “That if a situation is wanted in the
Bakery, the most effective way to secure it is to denounce Co-
operation, and the Kinning Park Society in particular.” The board, in
discussing this letter, expressed the opinion that it was a matter with
which they had nothing to do. It was no business of theirs where
their employees did or did not purchase their goods. This sound
business rule is one which is still in operation in all well-regulated
societies. At the same time, it must be admitted that when a man is
working for a principle as well as for a livelihood, his work is likely to
be better done. There are still workers in the movement, however,
who, while professing to work for it, treat it worse than they would be
allowed to treat a private employer, by denying it the efficient, loyal,
and painstaking service which they would be compelled to render for
wages alone. No more was heard of Kinning Park complaint. The
terms of the letter were probably an exaggeration of whatever
grievance there was.
FURTHER EXTENSIONS.
For some years the fluctuations in the trade of the Society had
been such that further extensions had been unnecessary, but, by the
end of 1882, the congestion had become so great that it was
necessary that further baking accommodation should be procured at
an early date. This raised a debate as to the respective merits of
increasing the oven accommodation at St James Street or putting
down a branch bakery at Greenock to supply the societies in that
area. The societies in the Greenock and Port-Glasgow area were all
members of the Federation, but there were both difficulty and
expense entailed in sending the bread from Glasgow, and, especially
in winter, when there was fog on the river, there was occasionally
irritating delay. The result of the debate was that a committee was
appointed to consider the different schemes and report.
When the special committee reported on the various points which
had been remitted to them to discuss there was considerable
difference of opinion amongst the members of the Bakery board as to
which was the best plan to adopt. Finally, on a vote being taken, it
was agreed, by a majority, to recommend to the general meeting the
erection of a branch bakery in Greenock. When the question came
before the delegates at the quarterly meeting, however, the scheme
for a branch in Greenock was not adopted, and it was decided to
proceed with the erection of two additional ovens at St James Street.
In 1884, however, the trade was again outgrowing the
accommodation, and in November of that year the committee
decided to rent a bakehouse in Scotland Street in order to relieve the
congestion. The membership of the Federation was again up to 26
societies, and the output at the end of 1884 was 281 sacks per week.
For a considerable part of this period the Federation were buying
much of the flour they used elsewhere than from the Wholesale
Society, and discussions on the subject took place from time to time.
The contention of the Bakery board was that they were being asked
by the Wholesale Society to pay considerably more for flour than
they could buy the same quality for elsewhere, and from the minute
of an interview which took place between representatives of the two
boards, it appears that the Wholesale representatives agreed that this
was the case at the time. The Wholesale board could not see their
way to make any alteration at the time on their method of charging,
however. Nevertheless, it is gratifying to know that in a short time
the Wholesale Society was in a position to meet competitors on level
terms, and towards the end of 1884 a large proportion of the flour
used was purchased from the Federation.
COSTLY LITIGATION.
Early in 1884, the Society became involved in a lawsuit. An
accident took place through which a horse belonging to the Glasgow
Tramway and Omnibus Company was killed, and as it was found
impossible to come to any arrangement which would be satisfactory
to both parties, the Sheriff-Substitute for Renfrewshire was called
upon to decide. The committee were agreeable to take responsibility
for the accident, which had been caused by one of their horses
running away while being unyoked. The Tramway Company valued
the animal killed at £35, while the veterinary surgeon employed by
the Society to value it immediately after the accident placed its value
at £16, but the Tramway Company manager refused to make any
concession. After the dispute had dragged on for a month, during
which the case was taken into Court and the Society lodged £20 in
full of all claims, the Tramway Company’s agent offered to try and
induce his clients to accept £30 in full of all claims, each party to pay
their own expenses. This offer the Society refused to accept, but
when the case came before the Sheriff-Substitute he decreed for £35;
at the same time passing severe strictures on the method in vogue at
the bakery when horses were being yoked and unyoked. An appeal to
the Sheriff-Principal was lodged, but he also decided against the
Society, with the result that, instead of settling for £35, they had also
a heavy bill to pay for expenses.
At the quarterly meeting held in June 1884, some reorganisation
of the work of the office took place. As a preliminary step, the office
of treasurer to the Society was abolished. With the exception of a
short period at the beginning, this office had been held by two men—
Mr Alexander of Paisley and Mr M‘Murran of Glasgow Eastern
Society. At the meeting at which the office of treasurer was
abolished, an attempt was made to make all the capital of the Society
transferable, but this proposal was defeated by a narrow majority;
fifty-eight delegates voting for the proposal and thirty-two against it.
As a two-thirds majority was necessary, the vote in favour was six
short of the necessary number.

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Mechanisms and Management of Cardiac

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First published in 2001

British Library Cataloguing in Publication Data

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PART I CELLULAR AND TISSUE

PART II CLINICAL TACHYCARDIAS

PART III DIAGNOSIS AND MANAGEMENT

15 Diagnosis and management of acute episodes of tachycardia 121

My interest in cardiac arrhythmias stems from my time as a clinical medical

Each of the cells of the human body is surrounded by a lipid membrane

General properties of ion channels

Cyclic CHANNEL EVOLUTION

Molecular structure of cardiac ion channels

the known physiological properties of the sodium channel. The region

Figure 1.4 Structure of the shaker-related K channel. (From Jalife J, Delmar M,

other subunits remains unclear. Remarkable homology exists between the

Gap junctional channels

adjacent cells. Each connexon is composed of six connexin subunits, most

Names and symbols for ionic currents

Descriptions of the major ion currents

Delayed rectifier potassium current (IK )

Background potassium current (IK1 )

Transient outward current (ITO )

Hyperpolarisation-activated current or pacemaker current (If )

Non-specific calcium-activated current (ITI or transient inward current)

Whilst it is frequently stated that understanding of the details of the cardiac

The resting potential

The action potential

(A) (B) (C)

Electric gradient Electric gradient

fibre corresponds to the non-excited or resting potential. The action poten-

Ionic changes associated with the action potential

SA Atrium Purkinje Ventricle

Figure 2.3 Generation of the action potential requires depolarisation of the

rectifier potassium outward current (IK) (causing repolarisation). Phase 3

Action potentials in specialised cardiac cells

(A) (B) (C)

Figure 2.4 Quinidine-induced early after-depolarisations and triggered activity in

Atrioventricular nodal cells in the centre or N region of the AV node show

Relevance of the action potential to

1000 msec 750 msec

current or an increase in the inward sodium or calcium currents. EADs

Local current spread (electrotonic propagation)

Propagation of the action potential

myocytes being activated are in a two-dimensional sheet (or a three-dimen-

Figure 3.3 Structure of cardiac muscle showing a schematic drawing of two

Propagation of curved wave fronts