PHYSIOLOGY
The electrocardiogram
Emrys Kirkman
A large number of cardiac muscle fibres become activated syn-
chronously and generate sufficient electrical disturbance to be
recorded at the body’s surface: this forms the basis of the ECG.
An examination of the ECG reveals detail of the pathways along
which electrical activity travels in the heart. The ECG does
not represent the electrical activity of any single fibre, but the
­combined activity of all the muscle fibres at any one instant.
Electrical views of the heart
Twelve ECG ‘leads’ are usually recorded. It is important not to
confuse an ECG ‘lead’ with the ‘wires’ connected to the elec-
trodes used to make the recording. In ECG terms, ‘lead’ refers to
an electrical view of the heart.
Standard leads: there are six standard leads (I, II, III, VR, VF,
VL), which view the heart in the vertical plane (e.g. lead II looks
at the left lateral surface of the heart from about the left hip,
while VR looks at the heart from the right shoulder). The detail
of the other views are given in Figure 1. A further six leads
(V1, V2, V3, V4, V5, V6) view the heart in the horizontal plane
(Figure 2). The differential amplifiers used to record the ECG
are configured such that if a wave of depolarization moves along
sequential cardiac muscle fibres towards the view­ing point there
is an upward deflection of the trace away from an isoelectric
starting point. ­ Depolarization moving away from the viewing
point gives a downward ­ deflection below the isoelectric point.
Conversely, repolarization moving towards the viewing point
gives a downward deflection, and repolarization moving away
from the viewing point gives an upward deflection. When there
is no movement of de- or re-polarization from cell to cell with
respect to the viewing point (i.e. all of the cardiac muscle fibres
are either repolarized (phase 4 of the myocardial action poten-
tial) or depolarized (phase 2 of the myocardial action potential))
then the trace returns to the isoelectric point. Consideration of
these rules and the pathway along which the action potential is
normally spread from fibre to fibre through the heart (see page
259) can be used to explain the pattern seen in the ECG.
Emrys Kirkman, PhD, is Team Leader in Surgical Sciences at Dstl,
Porton Down. He has a PhD from Manchester University and has
worked at the MRC Trauma Group, Manchester. He also holds honorary
Senior Lectureships at the University of Durham in the Academic
Division of James Cook University Hospital, Cleveland. His research
interests include trauma-induced changes in cardiovascular control
mechanisms, the underlying central nervous pathways and the
resulting alterations in haemodynamics and oxygen transport.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 7:8
Normal ECG from the standard leads
VR VL
I
II
III
VF
Reproduced with permission from Hampton J R. The ECG made easy. Churchill
Livingstone, 1998.
Figure 1
For a lead II view (Figures 1, 3) there is an initial upward
deflection as action potentials (and hence depolarization) radiate
outwards from the SA node across the atria, predominantly in
the direction of the viewing point on the left hip. The wave is not
very tall; the signal is relatively weak because it involves only
a small amount of tissue (thin atrial walls). This is the P wave
(Figure 3). Once the action potentials invade the AV node they
move almost imperceptibly from fibre to fibre through the AV
node (slow conduction within the AV node), hence the trace
returns to the isoelectric line and is flat for a period. The action
potential then emerges from the AV node and proceeds along
the bundle of His, activating cells in the septum. This causes
activity to spread in the septum from left to right, generally away
from the viewing point. Although action potentials also travel
along the bundle of His towards the apex of the heart, the bundle
itself constitutes only a small amount of tissue. Since the trace is
influenced by the combined activity at any instant, the predomi-
nant direction of activity (taking quantity of tissue into account)
is away from the viewing point, giving the small downward
Q wave. The next major event is the activation of the bulk of the
ventricular ­myocardium, from the endocardial to the epicardial
surface: activity in a large amount of tissue moving from cell
to cell towards the viewing point. This gives the large upward
R wave. Finally, the few muscle fibres at the base of the heart
are depolarized, giving a small downward S wave. At this point,
all the ventricular muscle fibres are depolarized and are on the
shoulder (phase 2) of the cardiac muscle action potential (see
pages 256 and 260). Thus, there is no wave of ­ depolarization
264 © 2006 Published by Elsevier Ltd.
 PHYSIOLOGY

Normal ECG from V1–V6

Left ventricle
2
3
4

V6
V1 V6
V5
V2 V5
V4
V1 V2 V3 V3 V4

Right ventricle

Reproduced with permission from Hampton J R. The ECG made easy. Churchill Livingstone, 1998.

Figure 2

moving with respect to the viewing point, so the trace returns
to the isoelectric line. Finally, after 200–300  ms the myocardial
fibres repolarize (phase 3 of the myocardial action potential).
However, those of the epicardial surface of the heart have a
shorter-duration action potential (nearer 200  ms) than those
Waves of a typical lead II ECG showing mean
(range) for relevant intervals and durations
R
1.0
of the endocardial surface (nearer 300  ms), so that the wave of
repolarization moves away from the viewing point, giving a final
upward wave, the T wave (Figure 3). Atrial repolarization occurs
coincident with ventricular depolarization and, because of the
greater amount of tissue involved in the ventricles, the wave
produced by the atrial repolarization is lost in the QRS ­complex.
The normal durations of the waves and intervals between them
are given in Figure 3. If the viewing point is transferred to the
right shoulder (lead VR), then essentially a mirror image is seen
(Figure 1) with the bulk of the myocardial depolarization ­moving
away from the viewing points and with a predominant large
downward wave in the QRS complex.
In summary, the P wave represents atrial depolarization; the
QRS complex, in its entirety, represents ventricular ­depolarization;
and the T wave represents ventricular repolarization.

Isoelectric line V1–V6: these leads view the heart in the horizontal plane
(­Figure 2). V1 and V2 view the heart from the right and V5 and
0.5
PR segment ST segment V6 from the left, with V3 and V4 in between. Because the ­septal
T depolarization arises before ventricular depolarization, and occurs
mV P from left to right, initial parts of the ventricular depolarization
U
0 are shown by an upward deflection in V1 and V2 but downward
deflections in V5 and V6 (Figure 2). Thereafter, the main mass
Q of ventricular tissue is depolarized. However, since there is a
PR interval
much greater mass in the left ventricle, during ­ventricular depo-
0.18 ms 0.18 ms
(1.2–2.0)
larization the predominant movement is away from V1 and V2,
S (to 0.10)
–0.5
QRS duration 0.40 ms giving a downward deflection, and towards V5 and V6, ­giving an
QT interval (to 0.43) upward deflection in these views (Figure 2).
0 0.2 0.4 0.6
Convention for naming waves: the waves of the ECG are labelled
Time (s)
P, Q, R, S and T (with an additional U wave sometimes visible).
Reproduced with permission from Ganong W F. Review of Medical Physiology.
McGraw-Hill, 2001.
If the first deflection after a P wave (if it exists) is downward it
is called a Q wave. An upward deflection is called an R wave,
Figure 3 whether or not it is preceded by a downward wave. A deflection

ANAESTHESIA AND INTENSIVE CARE MEDICINE 7:8 265 © 2006 Published by Elsevier Ltd.
 PHYSIOLOGY
below the isoelectric line after an R wave is called an S wave,
whether or not a Q wave has been seen.
Ectopic foci and conduction problems
It is beyond the scope of this article to discuss any ECG abnor-
malities in detail, but a few examples are given. It should be
stressed that a single abnormality in a few leads can be the result
of a range of problems, and that the entire picture from all leads
and other clinical signs must be integrated.
Ectopic foci can develop in the atria or ventricles. They lead
to an abnormal sequence of spread of the action potentials from
fibre to fibre through the heart, and hence abnormalities of
the ECG. Atrial ectopic foci can give rise to abnormally shaped
P waves (e.g. inverted P waves in lead II). Furthermore, since the
focus may be much closer to the AV node, the P–R interval may
be abnormally short. However, the spread of the action potentials
should be essentially normal from the AV node onwards, and
the QRS complex should be normal. Conversely, a ventricular
ectopic focus gives rise to an abnormally shaped QRS complex,
which is not preceded by a P wave. The shape of the abnormal-
ity occurs because of the altered sequence of fibres along which
the myocardial action potential travels within the ventricles. The
QRS complex is much wider (occurs over a greater period of
time) because the spread of the action potentials does not make
proper use of the fast conduction system.
In some circumstances, the myocardial action potential is pro-
longed, which in turn prolongs the QT interval. Long QT syn-
drome is a recognized condition associated with sudden death
and often associated with ventricular arrhythmias and fibrillation.
The problem is that during the repolarization of the ventricles the
heart is in a critical state, termed the vulnerable period. At this
time (which corresponds to the rising phase of the T wave of the
ECG) some of the ventricular myocytes have repolarized while
others have incompletely repolarized or are still ­ depolarized.
ANAESTHESIA AND INTENSIVE CARE MEDICINE 7:8
Under these circumstances an ectopic beat can establish a re-
entry (see page 261) and a circus of action potentials leading to
fibrillation.
Conduction problems in the AV node can be indicated by a
prolonged P–R interval. If all of the P waves result in a QRS
complex this is referred to as a first-degree heart block. In other
instances some, but not all, P waves result in a QRS complex:
this is second-degree heart block. In more extreme circumstances
there is complete block at the AV node and no P wave results in
a QRS complex. This is third-degree heart block and in this case
ventricular beating is driven by an alternative ventricular pace-
maker. In this latter circumstance there may be regular P waves
and regular QRS complexes, but they occur at different rates.
Sinus arrhythmia
Examination of the ECG in the normal individual reveals that the
heart rate is often not steady at rest: the R–R interval becomes
progressively increased during expiration and shortened during
inspiration. This rhythmical fluctuation in heart rate in phase
with respiration is called sinus arrhythmia. It reflects resting
vagal tone to the heart: during inspiration the vagus nerve is
inhibited as a consequence of activity in medullary inspiratory
neurons and because of inhibition from an afferent pathway ori­
ginating in pulmonary stretch receptors. On expiration the inhibi-
tion is lost and vagal activity increases, leading to a bradycardia.
The degree of sinus arrhythmia in part depends on the level of
resting vagal tone. If this is high, there is considerable scope
for inhibition during inspiration, while if resting vagal activity
is low, there is little scope for inhibition during inspiration and
sinus arrhythmia is weak or absent. Sinus arrhythmia can there-
fore be used as a test of vagal activity. It is reduced by anxiety, a
decline in cardiovascular fitness and pathological states affecting
the vagus nerve, therefore care must be taken when interpreting
the results. ◆
266 © 2006 Published by Elsevier Ltd.