ECG Apib PDF

Practical Procedures
An analysis tool for 12-lead

ECG interpretation
Joanne Gregory introduces a systematic analysis tool which can be used as an aid to ECG
interpretation. The tool consists of six steps, which are each explored in detail.
T
he NHS Plan: An Action Guide for requires thoroughness and care. Mistakes
Nurses, Midwives and Health Visitors are commonly made through the failure to
(Department of Health (DH), 2001) detect subtle, although sometimes critical
highlights the need to build a highly skilled findings. For example, overlooking a short
nursing workforce within specialist areas. PR interval could result in a missed
For nurses caring for cardiac patients this diagnosis of Wolff-Parkinson-White
involves developing competence in the syndrome, a congenital abnormality which
realm of electrocardiogram (ECG) analysis. is associated with potentially fatal 5 mm 1 mm
Accurate 12-lead ECG interpretation arrhythmias (Keating et al, 2003). In
addition, practitioners will often assume 1 mm
that ST segment and T wave changes are an 40 ms
indication of acute coronary syndromes,
Establish rate but it is important to realize that many
R
and rhythm 5 mm
other conditions, including bundle branch 200 ms
blocks and left ventricular hypertrophy can
also cause alterations to this area of the Figure 2. ECG graph paper
ECG (Pollehn et al, 2002; Wang et al,
Is there evidence 2003). A systematic approach to ECG on the horizontal axis. These parameters are
P
of pre-excitation analysis is therefore essential in obtaining a confirmed by a paper speed of 25 mm/sec-
correct diagnosis. ond (Spiers and Stinchcombe, 2002).
A number of different systematic analy- Although there are many methods for
sis tools have been published (Purcell and working out the QRS rate, probably the
Q
Calculate Haynes, 1984; Rowlands, 1988; Goldberger, simplest is illustrated in Figure 3 . Find the
QRS axis 1999; Garcia, 2001). As a cardiac lecturer tip of one QRS complex, then calculate the
running a 12-lead ECG course, the author number of large boxes between this and the
has been adapting an analysis tool to use as tip of the next QRS complex. If there is
a framework for teaching. This course is only one large box between the two, the
Is there evidence of
aimed at post-registration nurses who are rate is 300 beats per minute (bpm). If there
R right or left bundle
studying to diploma or degree level and are two large boxes, the rate is 150 bpm and
branch block
who work with adults in acute cardiac or so on. In cases where the spacing between
critical care areas. The tool consists of six QRS complexes is irregular, you will need
steps, illustrated in Figure 1, which are each to alter the technique. The ‘six second rule’
explored in the following discussion. For requires the interpreter to count the
Scan chest and limb leads
ease of use, the steps can be committed to
w P waves Joanne Gregory is Senior Lecturer in
S memory using the mnemonic RPQRST.
w QRS dimensions and Cardiac Care, Faculty of Health and
morphology Social Care Sciences, St. George’s
w ST segments and T
Step 1: Establish rate and
rhythm University of London, London SW17
waves ORE
Before considering the rate, it is first neces-
sary to look at the ECG graph paper illus-
Key words
trated in Figure 2. The graph is composed
Translate findings into w 12-lead ECG
T of 1 mm squares which each represent
meaningful conclusions w Pre-excitation
0.04 seconds (40 milliseconds (ms)) in w Bundle branch block
time on the horizontal axis. You will also w Ventricular hypertrophy
notice darker lined boxes, each containing 25 w Acute coronary syndromes
Figure 1. Analysis tool for 12-lead ECG small boxes and measuring 5 mm squared. Accepted for publication 13 February 2006
interpretation using RPQRST Each large box represents 200 milliseconds
216 British Journal of Cardiac Nursing May 2006 Vol 1 No 5
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and Pritchett, 1999). In a normal heart,

300 150 100 75 60 50 impulses from the atria can only enter the
ventricles through the AV node, the func-
tion of which is to delay the signal before it
then enters the ventricles. This delay is
important for two reasons.
Firstly, it allows AV synchrony to occur.
Thus the atria have time to depolarize, con-
tract and empty their contents, before the
impulse is then passed to the ventricles,
causing depolarization, contraction and
subsequent emptying of blood. Maximum
efficiency of the heart as a pumping system
is thus ensured.
Secondly, delay of the impulse protects
the ventricles from developing very fast
rates. An example of this would be atrial
fibrillation. This arrhythmia can cause the
atria to depolarize at a rate of over 300 times
Figure 3. Simple method for QRS rate calculation. The rate is approximately per minute. If all of these impulses were
90 beats per minute. allowed to pass through the AV node, the
identical in morphology and followed by a same rate would be forced on the ventricles
number of QRS complexes between 30 QRS complex. The PR interval should also and cardiac output could not be maintained.
large boxes, which equates to six seconds in be constant. The parameters of normal In a heart with a normal AV node, only
time. The figure obtained is then simply sinus rhythm are depicted in Figure 5 . A around a half to one third of these impulses
multiplied by ten to produce the heart rate description of cardiac arrhythmias is travel into the ventricles (Conover, 2003;
(Garcia and Holtz,, 2001). This method is beyond the remit of this article. However it Huszar, 2002).
illustrated in Figure 4 . is important to confirm the patient is in Patients with Wolff-Parkinson-White
If the rate is very slow, i.e. less than sinus rhythm before continuing with the syndrome have an accessory pathway,
60 bpm, or fast, greater than 100 bpm, you tool as arrhythmia interpretation requires a called the bundle of Kent. This allows
need to ask yourself why this could be the different approach. Sinus rhythm is usually impulses to travel directly from the atria to
case. Tachycardia may be an appropriate confirmed in lead II as this generally pro- the ventricles, without the delay incurred
response in a patient suffering from anxiety vides the most informative view point at the AV node. In reality, both routes are
or pain, or it may be a sign of underlying (Meek and Morris, 2003; Spiers and often used, leading to fusion beats. An
pathophysiology, such as hypovolaemic Stinchcombe, 2002). illustration of this can be seen in Figure 6
shock, heart failure or thyrotoxicosis (Spiers, and the subsequent ECG features are listed
2002). Equally, bradycardia is common in fit Step 2: Is there evidence of in Table 1.
individuals, but could equally be a sign of pre-excitation There are two reasons why it is important
conditions such as myocardial infarction Pre-excitation is the early activation of ven- to identify patients with Wolff-Parkinson-
(Spiers, 2003; Zimetbaum and Josephson, tricular tissue by an atrial impulse. The most White. The condition can lead to danger-
2003). When assessing the significance of a common form of this is Wolff-Parkinson- ous tachyarrhythmias which can be pre-
patient’s heart rate, it is important to con- White syndrome, a congenital abnormality vented with appropriate treatment. In
sider the individual circumstances. caused by defective foetal development of addition, it presents with ECG changes
The next component of this step is to con- the AV ring, a sheet of inert tissue separat- which are common to other abnormalities,
sider the rhythm. Every P wave should be ing the atria from the ventricles (Al-Khalib leading to the possibility of inaccurate
6 seconds = 30 large boxes
Figure 4. The six second rule method of QRS rate calculation. The rate is approximately 80–90 beats per minute
British Journal of Cardiac Nursing May 2006 Vol 1 No 5 217

PR
interval
120-200 ms
T
P
QRS
QRS
duration
100 ms
Figure 5. Parameters for normal sinus

rhythm. Every P wave must be followed by
a QRS complex and T wave
Table 1.
Typical ECG features of Wolff-
Parkinson-White syndrome
w Short PR interval (<0.12 seconds)
w Delta waves (initial slurring to the
QRS complex)
w Widened QRS complexes
w ST-T wave changes
w May be an axis deviation
Figure 6. Cardiac conduction and ECG changes in patients with
Wolff-Parkinson-White syndrome.
interpretation (Al-Khalib and Pritchett,
1999; Keating et al, 2003). For example,
wide QRS complexes may lead the inexpe- L ef
t ax
rienced interpreter to suspect bundle is
x is de
branch block. ST and T wave changes can a vi a
e ti o
masquerade as acute coronary syndromes. n at
n
i
Axis deviations are common to ventricular

m
er
hypertrophy and hemi-blocks as well as

et
In d
Wolff-Parkinson-White syndrome (Garcia Atrioventricular node
and Holtz, 2001). For this reason, if Wolff-

Parkinson-White syndrome is detected,
Left atrium
any further analysis is problematic.
Left bundle branch
Step 3: Calculate QRS axis Sinoatrial node
Anterior fascicle
Frontal plane QRS axis refers to the mean
direction of electrical forces within the Right atrium
Left ventricle
ventricles. In sinus rhythm, the electrical Posterior fascicle

impulse, or wave of depolarization, is gen-
erated at the sinoatrial node in the right
atrium. It travels across the atria and then Right ventricle
through the atrioventricular node and into Right bundle branch

the ventricles. The angled position of the
No
heart in the chest, together with the mus-

n
m r
io
al
at
cular and electrical dominance of the left ax

i
v is
de
ventricle explain why the normal QRS axis xi s
usually lies downwards and to the left.
a
ht
Ri g
Figure 7 illustrates the conduction system
and the normal parameters for axis.
Although there are several methods for Figure 7. The cardiac conduction system and the four quadrants of axis

Table 2. Table 4.
Simple method for QRS axis determination Typical ECG features of left
and right bundle branch block
Normal axis Right axis deviation Left axis deviation
Left bundle branch block
Lead I Positive Negative Positive
w Widened QRS complexes (at least
Lead II Positive Positive or negative Negative
120 milliseconds)
Lead III Positive or negative Positive Negative
w Deep, wide S wave in V1–V3
w May see loss of septal q wave in
V6
Table 3. w ST depression and T wave
Causes of QRS axis deviation inversion
in V4–V6, I and aVL
Causes of left axis deviation Causes of right axis deviation w ST elevation VI–V3
Normal variation in pregnancy, Normal variation in children and thin adults
obesity Right bundle branch block
Ascites, abdominal distention or Chronic lung disease w Widened QRS complexes (at least
tumour 120 milliseconds)
Left anterior hemiblock Left posterior hemiblock w Slurred S wave in V6
Left ventricular hypertrophy Right ventricular hypertrophy w Dominant R in VI (rSR’ or qR
Wolff-Parkinson-White syndrome Wolff-Parkinson-White syndrome complex)
Inferior myocardial infarction Anterolateral myocardial infarction w ST depression and T wave
inversion in VI-V3
axis determination, the simplest relies on Bundle branch block is essentially the non-
inspection of the QRS complexes in leads I, conduction of impulses through one or Parkinson-White syndrome and anterior
II and III (Meek and Morris, 2003). This is other of the bundle branches. These are ST elevation MI (Garcia and Holtz, 2001).
described in Table 2. structures within the conduction system Because left bundle branch block in par-
Frequently students ask the relevance of which straddle the interventricular sep- ticular alters the ECG so profoundly, it is
axis determination. It can in fact be very tum. Damage here can result typically from difficult to make any other assessment here
helpful in the diagnosis of several condi- infarction or ischaemia involving one of and further analysis of the QRS complexes
tions. For example, a finding of left anterior the blood vessels supplying the region. In is challenging.
or left posterior hemi-block relies on evi- addition, high pressures within either of
dence of a left axis or right axis deviation the ventricles, as would occur with hyper- Step 5: Scan chest leads and
respectively. Hemi-blocks imply damage tension on the left side of the heart and limb leads
within one or other of the fascicles in the pulmonary pathologies on the right, can Chest leads
left bundle branch. In acute settings, diag- also result in bundle branch impairment QRS dimensions and morphology
nosis can identify patients at high risk of (Garcia and Holtz, 2001). The R wave should be small in V1, progres-
more serious conduction blocks. Because the bundle branches provide a sively increasing in size through to V6.
Recognition of axis deviation can also help fast route for impulses to be transmitted Conversely, the S wave should be deep in
significantly in establishing evidence for throughout the ventricles, damage within V1 gradually disappearing through the rest
ventricular hypertrophy (Tilley and either one of them will delay depolarization of the chest leads. By V5 or V6, a small q
Petersen, 2003). Causes of axis deviation of the affected chamber, causing a signifi- wave is present (Conover, 2003). The nor-
are listed in Table 3 . cant widening of the QRS complex (Conover, mal progression of the R wave across the
2003). The ECG manifestations of right chest leads is illustrated in Figure 8 . Poor R
Step 4: Is there evidence of and left bundle branch block are listed in wave progression, where the R wave does
right or left bundle branch Table 4 . not develop as expected, can be caused by
block? Right bundle branch block has charac- a number of abnormalities, including ante-
Assuming pre-excitation has not been teristically dominant R waves and ST-T rior MI, left ventricular hypertrophy, left
found and QRS axis has been calculated, wave changes predominantly in V1–V3, bundle branch block and chronic obstruc-
the interpreter can move on to assess for which can mimic posterior myocardial tive airways disease. Conversely, abnor-
evidence of bundle branch block. Again, it infarction (MI) and right ventricular mally dominant R waves in V1 and V2 can
is important to rule this out early in any hypertrophy. In contrast, left bundle branch be a sign of posterior MI, right bundle
assessment because of the variety of condi- block has characteristics in common with branch block and right ventricular hyper-
tions that cause this pattern on the ECG. left ventricular hypertrophy, Wolff- trophy (Jenkins and Gerred, 2005). The

with the baseline, although slight elevation

of less than 2 mm is also considered a nor-
mal variant. ST elevation or depression and
T wave inversion are classic signs of the
acute coronary syndromes. However, it
should be noted that a range of other con-
ditions present with similar findings, for
example, ventricular hypertrophy, bundle
branch block and Wolff-Parkinson-White
syndrome. In addition, conditions such as
left ventricular aneurysm, pericarditis,
ventricular paced rhythm and non cardiac
conditions such as subarachnoid haemor-
rhage will specifically produce ST elevation
(Edhouse et al, 2002; Chan et al, 2005).
Figure 8. Normal R wave progression in the chest leads. When ST and T wave changes are present,
it is important to consider these changes in
the context of the patient’s presentation
Table 5. Table 6. and other findings on the ECG.
Typical features of right Typical features of left
Limb leads
ventricular hypertrophy ventricular hypertrophy QRS dimensions and morphology
w R wave amplitude greater than S w High QRS voltages (Cornell voltage Unlike the chest leads, there can be consid-
wave in VI criteria = S wave in V3 + R wave in erable normal differences in the morphol-
aVL > 28mm in men or 20mm in ogy of the limb leads. AVR should be pre-
w S wave amplitude greater than R
women) dominantly negative and lead II predomi-
wave in V6
nantly positive, whereas leads I, III, aVF
w Right axis deviation w ST-T wave changes in V4-V6, II, III,
and aVL can be variable. The R wave
aVF
w ST–T wave changes in VI, V2, II, III, amplitude should be less than 20 mm in
aVF w Left axis deviation each of the leads and normal q waves may
w Evidence of right atrial enlargement w Evidence of left atrial enlargement be seen in any of the leads I, aVL, II, III and
aVF. These should be narrow and of low
amplitude, i.e. <40 ms wide and no more
ECG features of right ventricular hypertro- obstructive airways disease (Jenkins and than 25% of the associated R wave ampli-
phy are listed in Table 5 . Gerred, 2005). tude (Conover, 2003).
R waves in any of the chest leads should
not normally exceed 27mm in height and ST segments and T waves ST segments and T waves
S waves do not normally exceed 30 mm As a general rule, the T wave should be Normal T waves in the limb leads usually
in depth (Meek and Morris, 2003). In the concordant with the preceding QRS com- have an amplitude of less than 5 mm (Chan
absence of Wolff-Parkinson-White syn- plex. Thus, if the QRS is predominantly et al, 2005) and in contrast to the chest
drome or bundle branch block, high volt- above the baseline, or positive, the T wave leads, there should be less than 1 mm ST
ages in the QRS complexes may denote should also be positive. Conversely, if the elevation (Conover, 2003) ST displacement
left ventricular hypertrophy, although QRS complex is predominantly negative, and T wave abnormalities can again be a
these upper limits can sometimes also be the T wave should also be negative. Although sign of a number of abnormalities includ-
exceeded in individuals who are tall and this applies in most leads, V1–V3 coming myocardial ischaemia or infarction,
thin and in young men (Meek and Morris, monly have discordant T waves i.e. positive bundle branch block, hypertrophy and
2003; Spiers, 2003). Various criteria for T waves associated with predominantly neg- Wolff-Parkinson-White syndrome.
left ventricular hypertrophy have been ative QRS complexes (Conover, 2003). T
proposed (Chan et al, 2005; Magdic and waves should be at least one eighth, but less P waves
Saul, 1997) and the main features are list- than two thrids of the amplitude of the cor- P waves in the limb leads should be upright
ed in Table 6. responding R wave. In healthy individuals, in I, II and aVF, negative in aVR and may be
Abnormally small QRS complexes can the T wave amplitude rarely exceeds 10 mm positive, negative or biphasic in III and aVL
also represent abnormalities. It is generally in the chest leads (Meek and Morris, 2003). (Conover, 2003). Upright P waves in the
accepted that at least one R wave on the The QRS complex terminates at the J limb leads should be less than 120 ms wide
12-lead ECG should be 8 mm or more in point or ST junction and the ST segment and less than 2.5 mm tall (Meek and Morris,
amplitude (Spiers, 2003). Low voltage lies between the J point and the beginning 2003). In cases of left atrial enlargement, the
QRS complexes can be the result of obes- of the T wave (Meek and Morris, 2003). P wave may become broad and notched in
ity, pericardial effusion and chronic Generally, this segment should be level lead II, whereas right atrial enlargement is

often manifested by abnormally tall P waves.

Because of the interconnection of all four
cardiac chambers, atrial enlargement often Key Points
accompanies evidence of ventricular w Mistakes in ECG interpretation are commonly made through the failure to recognize
enlargement (Magdic and Saul, 1997). subtle, although critical findings and to consider differential diagnoses.
w A systematic approach is therefore essential if an accurate ECG interpretation is to
Step 6: Translate findings be made.
The assessor is asked to translate the find-
ings into meaningful conclusions. Is there w The author introduces an analysis tool to be used as an aid to 12 lead ECG
evidence for pre-excitation, bundle branch interpretation.
block, hypertrophy, ischaemia or infarc- w The tool has seven steps and requires the interpreter to look systematically for a
tion? Do the conclusions fit with the range of common abnormalities.
patient’s clinical picture? For example, does
the patient with ST elevation have chest
Al-Khalib SM, Pritchett ELC (1999) Clinical features of Brady WJ, Camm J (eds). ABC of Clinical
pain or other symptoms consistent with an Wolff-Parkinson-White syndrome. Am Heart J 138: Electrocardiology. BMJ, London: 1–4
acute coronary syndrome? If there is evi- 403–13 Pollehn T, Brady WJ, Perron AD, Morris F (2002) The
Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P electrocardiographic differential diagnosis of ST
dence of left ventricular hypertrophy, does (2005) ECG in Emergency Medicine and Acute Care. segment depression. Emerg Med J 19: 129–35
the patient have a history of hypertension Mosby, Philadelphia PA Purcell JA, Haynes L (1984) Using the ECG to detect
Conover MB (2003) Understanding Electrocardiography MI. Am J Nurs 84: 627–42
or other associated pathophysiology? The 8th edn. Mosby, St Louis Rowlands D (1988) Understanding the
ECG cannot be viewed in isolation, but Department of Health (2001) The NHS Plan: An Action Electrocardiogram: A New Approach. ICI,
should form part of the data used to for- Guide forNurses, Midwives and Health Visitors. DH, Manchester
London Spiers C (2002) Arrhythmia interpretation in the
mulate a diagnosis. Edhouse J, Brady W, Morris F (2002) ABC of clinical perioperative arena. British Journal of Anaesthetic
electrocardiography-acute myocardial infarction: and Recovery Nursing 3(3): 12–8
Part II. BMJ 324: 963–6 Spiers C, Stinchcombe E (2002) An introduction to
Conclusions Garcia TB, Holtz NE (2001) 12-lead ECG: The Art of cardiac monitoring and rhythm interpretation.
ECG analysis tools help ensure accurate Interpretation. Jones and Bartlett Publishers, London British Journal of Anaesthetic and Recovery Nursing
Goldberger AL (1999) Clinical Electrocardiography: A 3(1): 8–14
interpretation. A systematic approach pre- Simplified Approach 6th edn. Mosby, St Louis Spiers C (2003) The normal 12-lead ECCG. British
vents the assessor from overlooking subtle Huszar RJ (2002) Basic Dysryhthmias: Interpretation Journal of Anaesthetic and Recovery Nursing. (4): 12–
and Management 3rd edn. Mosby, St Louis 5
but important changes and encourages the Jenkins RD, Gerred SJ (2005) ECGs by example. 2nd Tilley P, Petersen D (2003) Pulling axis together.
consideration of a range of abnormalities, edn. Churchill Livingstone, Philadelphia PA Dimens Crit Care Nurs 22: 210–5
some of which have similar findings. An Keating L, Morris FP, Brady WJ (2003) Wang K, Assinger RW, Marriott HJL (2003) ST-
Electrocardiographic features of Wolff-Parkinson- segment elevation in conditions other than acute
analysis tool has been adapted as a frame- White syndrome. Emerg Med J 20: 491–3 myocardial infarction. New Engl J Med 349: 2128–
work for teaching post-registration nurses. Magdic KS, Saul LM (1997) ECG Interpretation of 35
Chamber Enlargement. Crit Care Nurse 17: 13–7 Zimetbaum PJ, Josephson ME (2003) Use of the
This approach can be helpful in promoting Meek S, Morris F (2003) Introduction. 1-Leads, rate, electrocardiogram in acute myocardial infarction. N
best practice and building confidence. rhythm and cardiac axis. In: Morris F, Edhouse J, Engl J Med 348: 933–40

ECG Interpretation Series
Understanding the ECG.

Part 1: Anatomy and physiology
Michael Sampson, BHF Arrhythmia Nurse Specialist, St George’s Hospital and Senior Lecturer, School of Health
and Social Care, London South Bank University, and BHF Alliance member, London;and Anthony McGrath, Head
of Department, Department of Adult Nursing and Midwifery Studies, School of Health and Social Care, London
South Bank University, London. Email: michael.sampson@nhs.net
C
ardiovascular disease is one of the electrical system, the size of the heart standing of the way in which our cells
main causes of death in the UK, and chambers, and the supply of blood to the function. A firm grounding in basic cell
a common cause of hospital heart muscle (Hampton, 2008). ECGs are physiology will help readers to understand
admission (Bhatnagar et al, 2015). It is pivotal in the diagnosis of cardiac ischae- how the heart works, and to appreciate the
important, therefore, that health-care mia and infarction, provide the evidence implications of findings on the ECG. This
practitioners develop their skills and for pacemaker implantation, and detect section will introduce you to a number of
knowledge in relation to this problem if inherited abnormalities such as cardiomy- terms that are important if you wish to
patients are to obtain the best possible care opathy and long-QT syndrome (Jowett and interpret and understand an ECG, such as
in a timely manner. One of the most Thompson, 2007). ECGs are also useful in resting potential, repolarisation, depolari-
important diagnostic tests is the 12-lead detecting non-cardiac pathology, for exam- sation and action potential.
electrocardiogram (ECG) (Society for ple, pulmonary emboli and electrolyte dis- The body is composed of millions of
Cardiological Science & Technology, 2014). orders (Garcia, 2015). individual cells, each enclosed by a fatty
Despite its widespread use, many people From many practitioners’ perspective, cell membrane and surrounded by extra-
struggle to master the basics of ECG ECGs are perceived as complex and diffi- cellular fluid (Alberts et al, 2010). Both the
interpretation and errors in interpretation cult to understand—a ‘black art’ under- cells and the surrounding fluid contain
can lead to misdiagnosis and delays in stood by the few (Wetherell, 2013). multiple substances including water, pro-
appropriate treatment. One of the reasons However, the premise of this series is that teins and electrolytes. It is the concentra-
for this is a limited knowledge of ECG this doesn’t have to be the case. We will put tion of electrolytes, inside and outside the
interpretation resulting from a lack of forward the argument that ECGs can be cell, and their ability to cross the cell mem-
appropriate training (Richley, 2013). understood by anyone with the time and brane, that creates electrical activity in the
This is the first in a series of articles that patience to build the necessary knowledge. cell. In the heart, the most important elec-
will aim to: trolytes are sodium, potassium and calci-
w Explore why ECGs are important tools Electrolytes and electricity um (Klabunde, 2012). Figure 1 shows a
in the diagnosis and management of It is important to develop a good under- typical cardiac cell.
heart disease
w Explore how they can be interpreted
w Provide the reader with an understand-
ing of the anatomy and physiology of the
heart and conducting system.
This first article will explore and discuss
the anatomy and physiology of the heart’s
electrical system. This electrical activity is
fundamental in coordinating the function
of the heart, and it is this activity that ECG
machines record and display.
The ECG
The ECG is an important screening tool
that offers practitioners a wealth of infor-
mation that can be used alongside the his-
tory and clinical findings (Younker, 2011).
An ECG provides a measurement of the
rate and rhythm of the heart. It also pro-
vides information about the health of the Figure 1. The cardiac cell
548 British Journal of Cardiac Nursing November 2015 Vol 10 No 11

There is considerable interchange

between the cells and the extracellular Plateau phase
fluid. Although water and oxygen, for
example, cross the cell membrane freely,
Ca++
Depolarisation Repolarisation
the cell membrane has limited permeabili-
ty to electrolytes (Marieb and Hoehn,
2015). There are two ways that the move- 1 2
ment of electrolytes across the cell mem- 20
brane is increased. Firstly, they are moved
0
into and out of the cell by pumps embed-
ded in the cell membrane. The most impor- 3
Voltage (mv)
-20
tant of these is the sodium-potassium K++
Na+ 0
pump (Levick, 2010). -40
The sodium-potassium pump moves
sodium out of the cell and pumps potassi- -60
um in. Because it pumps continuously,
potassium accumulates inside the cell, -80 4 4
leading to a higher concentration inside
than outside. In the same way, sodium con- -100
centration increases in the extracellular Time
fluid outside the cell. The second way that
electrolytes cross the cell membrane is Figure 2. The action potential
through ion channels. Ion channels are
‘doors’ in the cell membrane that open and Triggering contraction: and calcium enters the cell. This stabilises
close in response to stimuli (Grant, 2009). the action potential the electrical charge across the cell mem-
It is important to note that ion channels The heart is made up of the following three brane and closes the sodium channels.
are specific to one electrolyte; for example, main tissue types (Levick, 2010): Calcium flows slowly into the cell, creating
sodium channels only allow sodium w Fibrous an electrical plateau phase during which
through. When an ion channel or ‘door’ w Electrical the electrical potential does not change
opens, the electrolyte moves into or out of w Contractile. (Fogoros, 2007). Calcium is also released
the cell depending on the concentration Fibrous tissue provides a supporting skele- from intracellular stores at this time. The
gradient. In other words, it moves from the ton to the muscle mass, and forms the increase in calcium concentration inside
area of highest to the area of lowest con- heart valves. Fibrous tissue does not con- the cell triggers mechanical contraction of
centration. When potassium channels tract and, importantly, does not conduct the cell (Aaronson et al, 2013).
open, potassium leaves the cell. In contrast, electricity (Garcia, 2015). In contrast, elec- When contraction is complete, calcium
sodium enters the cell when its ion chan- trical cells are highly conductive, and have channels close and potassium channels
nels open (Pappano and Wier, 2013). pacemaker properties that will be dis- open. Potassium flows briefly from the cell.
The result of these opposing concentra- cussed shortly. Before doing so, let us turn This causes repolarisation; the return of
tions of electrolytes is an electrical charge our attention to the final type of tissue: the resting electrical potential. The whole
across the cell membrane. All electrolytes contractile cells or myocytes. These pro- process of depolarisation and repolarisa-
are electrically charged. Sodium (Na+) and vide the pumping action that moves blood tion is described as an action potential. The
potassium (K+) carry a single positive through the heart, and are the commonest phases of the action potential are usually
charge, while calcium (Ca++) carries two cardiac cell type by far (Tortora and numbered from 0–4, as shown in Figure 2
(Kaplan and Kellum, 2010). At rest, the Nielsen, 2014). (Woods et al, 2010).
inside of the cell membrane has a negative At rest, the inside of the myocyte cell Once one cell depolarises, the action
charge of around -90 mv, compared with membrane is slightly negative. This chang- potential spreads rapidly from cell to cell
the outside (Grant, 2009). es when an electrical impulse arrives at the across the heart muscle. This results in a
This difference in electrical charge is cell membrane. The electrical impulse wave of electrical activity that spreads rap-
called the resting potential (Woods et al, causes sodium channels in the cell mem- idly across the tissue, swiftly followed by
2010). The resting potential changes when brane to open, allowing sodium to enter mechanical contraction. The wave of depo-
ion channels open in the cell membrane, into the cell along its concentration gradi- larisation continues until all cells are depo-
and electrolytes enter or leave the cell along ent. This sudden influx of sodium alters the larised, or it meets non-conducting tissue
their concentration gradient. This change electrical polarity of the cell membrane—it (Christoffels and Moorman, 2009). A good
in electrical potential is used to trigger cel- goes from being negative on the inside to analogy is the throwing of a stone into a
lular activity in many parts of the body being slightly positive (Figure 2). This pond. Once the stone hits the water, the
including the nerves and skeletal muscles. change in electrical potential is called ripples travel in all directions until they
In the heart, however, it triggers mechani- depolarisation (Grant, 2009). Once the cell meet a solid object such as the pond edge
cal contraction (Marieb and Hoehn, 2015). has depolarised, calcium channels open and they then stop. The electrical wave-
British Journal of Cardiac Nursing November 2015 Vol 10 No 11 549

Myocyte Electrical cell

20 20
0 0
Voltage (mv)
Voltage (mv)
-20 -20
-40 -40
-60 -60
-80 -80
-100 -100
Time Time
Figure 3. The action potential in myocytes and electrical cells
front travels through the heart muscle in a blockers are used to treat angina, hyperten- comes to the muscle via the brain and
similar manner. sion and arrhythmias (Sargent, 2006). Two nervous system (Marieb and Hoehn, 2015).
Once a cell has been depolarised, it drugs in this group, diltiazem and vera- The heart is different. In the heart, the
becomes refractory for a brief time (Marieb pamil, slow the heart rate by blocking cal- stimulus comes from its specialised electri-
and Hoehn, 2015). To put it simply, the cell cium channels in the sinus node. Other cal cells. The sole purpose of these cells is
cannot be re-stimulated until its electrical drugs block sodium or potassium chan- to generate and conduct the electrical
activity has returned to near resting state. nels, for example, flecainide (sodium) and impulses that trigger contraction of the
Cardiac cells exhibit two types of refracto- sotalol (potassium) (Opie and Gersch, myocytes (Aaronson et al, 2013). Their
ry period. During the initial absolute 2013). Amiodarone, one of the most com- principal feature is automaticity.
refractory period, the cell is completely monly used anti-arrhythmic drugs, works Automaticity means that the cell is able to
incapable of further depolarisation. by blocking multiple ion channels act as a pacemaker. It does this by sponta-
Following this, a short relative refractory (O’Donovan, 2006). neously depolarising itself. In the myocyte,
period exists before the full resting state is the cell membrane is electrically stable at
restored. During the relative refractory Electrical cells and automaticity rest. There is no electrical change until an
period, the cell may be depolarised again if We have described how an initial electrical impulse arrives from an adjacent cell. In
a large enough stimulus is applied. The stimulus depolarises a myocyte, and is then contrast, there is a constant leakage of ions
refractory period prevents the cell from propagated across the entire muscle mass. across the cell membrane of the electrical
being stimulated again too quickly, as can In a skeletal muscle, the initial impulse cell. This results in a gradual movement
happen in skeletal muscles affected by
© Peter Lamb
tetany (Klabunde, 2012).
It would be fantastic if everybody’s heart
behaved in this textbook fashion.
Unfortunately, patients are subject to dis-
ease processes and health issues that may
interfere with normal electrical function.
Electrolyte imbalance, ion channel abnor- Left atrium
malities and medications can all affect the
normal movement of electrolytes across Sinoatrial node (SA)
the cell membrane (Grant, 2009). A good Bundle of His
example of electrolyte imbalance is hypoka-
laemia (low serum potassium level).
Right atrium
Left bundle branch (LBB)
Hypokalaemia changes the normal potas-
sium concentration gradient, and makes Atrioventricular node (AV) Left ventricle
patients more vulnerable to ventricular
arrhythmias (Resuscitation Council UK,
2010). Ion channel abnormalities are
Right ventricle
genetic mutations that change the normal
function of one or more channels. This Purkinje fibres (PF)
results in conditions such as long-QT and
Brugada syndrome which are associated
with fatal arrhythmias (Martin et al, 2012). Right bundle branch
Finally, ion channel function is affected by
commonly used drugs. Calcium channel Figure 4. The cardiac conduction system

towards depolarisation. Once a threshold is ten times slower than through the sur- nervous system in order to depolarise. This
reached, calcium channels open and calci- rounding muscle (Klabunde, 2012). This means that the heart will continue to beat
um floods into the cell, completing depo- slowing of conduction allows the atria to even when removed from the body, pro-
larisation. The action potential created finish contracting before the impulse pass- vided it is supplied with oxygen and nutri-
spreads through both the electrical system es into the ventricles. Slow conduction ents (Marieb and Hoehn, 2015). This fea-
and the surrounding myocytes (Fogoros, through the AV node also limits how many ture has recently been exploited to keep
2007). Figure 3 compares the electrical beats per minute the node can conduct. donated hearts alive prior to transplant,
activity in the myocyte and the electrical This is an important mechanism that pro- using a machine called an Organ Care
cell. Note that the baseline is constantly tects the ventricles from high atrial rates System (Transmedics Inc, 2015). Despite
moving upward in the electrical cell, unlike during atrial arrhythmias such as atrial this self-reliance, the heart is heavily inner-
the flat baseline of the myocyte. Also, the fibrillation (Lafuente-Lafeunte et al, 2009). vated by the autonomic nervous system.
electrical cell has no plateau phase because From the AV node, the electrical impulse Nerves from both sympathetic and para-
it does not contract. enters the bundle of His. The bundle of His sympathetic branches of this system run
penetrates the atrial wall and enters the from the brain to the heart (Levick, 2010).
The heart’s conduction system interventricular septum. It also crosses the These nerves help to regulate the rate at
This is a key section to understand as it fibrous layer that separates the atria and which the heart beats, as well as the speed
provides insight into the waves recorded ventricles. Because fibrous tissue does not of electrical conduction and the force of
on the ECG and what they mean. The conduct electricity, the AV node and bun- contraction. This allows the brain to match
heart’s electrical cells are arranged in a con- dle of His is the only route of electrical cardiac output to circulatory demand.
duction system that carries the electrical conduction from atria to ventricles in the Sympathetic nerves act as the heart’s
impulse to every part of the organ normal heart. ‘accelerator’, increasing heart rate, speed of
(Figure 4). This ensures that the atria con- The bundle of His divides within the conduction, and contractility. Sympathetic
tract before the ventricles, and that ven- septum to produce the left- and right- activity increases during exercise and
tricular contraction is coordinated and bundle branches. These carry the electrical stress. Its opposite, the parasympathetic
efficient (Hampton, 2008). The Conduction impulse into the left and right ventricles. system, acts as the ‘brakes’ and slows the
system comprises of the sinoatrial node The bundle branches terminate in a branch- heart at rest. The parasympathetic nerve
(SA or sinus node), atrioventricular node ing network of Purkinje fibres that carry running to the heart is the Vagus nerve
(AV node), bundle of His, left and right the electrical impulse to every part of the (Tortora and Nielsen, 2014).
bundle branches, and Purkinje fibres ventricle almost simultaneously, ensuring At rest, the heart is said to exhibit vagal
(Garcia, 2015). rapid and effective contraction of the tone, meaning that parasympathetic tone
Normally, the electrical impulse that ini- chamber (Pappano and Wier, 2013). predominates. As the demand for cardiac
tiates the heart beat originates in the sinus Conduction through the His-Purkinje sys- output rises, for example, during exertion,
node. This small patch of electrical cells is tem is extremely rapid, much faster than parasympathetic tone diminishes and sym-
located in the right atrium, near its junc- through the muscle cells of the ventricles. pathetic tone increases (Klabunde, 2012).
tion with the superior vena cava If the system is damaged, for example, by A ‘vasovagal reaction’ occurs when a phys-
(Christoffels and Moorman, 2009). The ischaemic heart disease, conduction to the ical or emotional stimulus causes a sudden
sinus node acts as the primary pacemaker ventricles may be delayed or fail complete- increase in parasympathetic outflow to the
because it has the fastest rate of depolarisa- ly (Jowett and Thompson, 2007). These heart. The sudden drop in heart rate and
tion. If it slows down, or fails, the next fast- problems can be seen on the ECG and are contractility lowers blood pressure, and
est pacemaker takes over. The normal rate referred to as heart blocks (Bennett, 2013). causing dizziness or loss of consciousness
of depolarisation of the different parts of Complete heart block occurs when no elec- (Blanc et al, 2015).
the conduction system is shown in Table 1. trical impulses are able to travel from the The other important extra-cardiac influ-
This is an important fail-safe feature of the atria to the ventricles. This often results in ence on the heart is the endocrine system.
system, and ensures that the heart contin- severe bradycardia and is a life-threatening Many hormones influence cardiac electri-
ues to beat even if the sinus node is dis- condition (Swift, 2013). cal activity including thyroid and growth
eased or damaged. Sinus node disease is hormones (Levick, 2010). Clinically, the
common in older individuals and is caused Extra-cardiac influences most important group of hormones affect-
by fibrosis of the conduction tissue. The Because of automaticity, electrical cells in ing the heart are the catecholamines, epine-
node may also be damaged by myocardial the heart do not need stimulation from the phrine and norepinephrine. These bind to
infarction, surgery or diseases of the heart
muscle such as cardiomyopathy (Houghton Table 1. Rates of depolarisation
and Gray, 2014). Area of the conduction system Depolarisation rate
From the sinus node, the electrical
impulse spreads across both atria, causing SA node 60–100 beats per minute
the atrial myocytes to depolarise. The
AV node 40–60 beats per minute
impulse also arrives at the AV node, locat-
ed in the inferoseptal right atrium (Garcia, His-Pukinje system 20–40 beats per minute
2015). Conduction through the AV node is

Figure 6. ECG waveforms
duction to the waves recorded on the ECG

such as the, P-, QRS- and T-wave, which in
Figure 5. The 12-lead ECG turn will provide a firm understanding of
the ECG as this series progresses.
receptor sites on the heart, increasing heart heart (Khan, 2006). Beta-blockers slow the By placing electrodes on the skin, we can
rate, conduction speed and contractility. heart rate during sinus rhythm, and are record the electrical activity of the heart
Synthetic forms of epinephrine and nore- used to slow AV node conduction during and the resulting waveforms. Depending
pinephrine are used to maintain cardiac atrial arrhythmias such as atrial fibrillation on the type of machine used, and the
output and blood pressure in critically ill (Camm et al, 2010). number of electrodes that are placed, mul-
people (Parry, 2012). Other drugs have the tiple views of the heart’s electrical activity
opposite effect. The ECG can be recorded. Most health-care practi-
Beta-blockers, for example, prevent cate- The ECG is simply a recording of the tioners will be familiar with the use of
cholamines from binding to their receptor heart’s electrical activity (Hampton, 2008). 12-lead ECG machines. A 12-lead ECG
sites and therefore reduce their effect on the This section will provide you with an intro- measures and records 12 different electri-
cal views of the heart (Figure 5). In other
words, it records the electrical activity as
Key Points seen from 12 different points around the
heart. Lead II, for example, records the
Contraction of the heart relies on electrical stimulation. Electrical activity is
w electrical activity as seen from the inferior
generated by the movement of electrolytes through ion channels in the cell (diaphragmatic) surface of the heart. This
membrane lead is often used for rhythm monitoring
(Bennett, 2013). Other types of ECG
Depolarisation is the reversal of the electrical charge across the cell membrane,
w machine include bedside monitors and
and triggers contraction of the muscle cells. Repolarisation is the return to resting ambulatory ECG recorders such as Holter
electrical state. Between these two extremes is a refractory period when it is monitors. Electrical activity can also be
impossible, or difficult, to depolarise the cell again recorded from electrodes inside the body;
Specialised electrical cells have automaticity and act as the heart’s pacemaker.
w for example, through pacemaker leads or
The sinus node is the normal pacemaker, but all parts of the electrical system are implantable loop recorders (Diemberger et
capable of this function al, 2015).
Three principal waveforms are recorded
After spreading through the atria, the electrical impulse is delayed in the AV node.
w by the ECG (Figure 6):
This allows the atria to finish emptying, and protects the ventricles from high atrial w The P-wave
rates during atrial arrhythmias w QRS complex
The electrical impulse passes from the AV node into the His-Purkinje system. This is
w w T-wave.
the only electrical connection between the atria and ventricles in the normal heart, The P-wave is created by depolarisation of
and its failure causes heart blocks the atria, the QRS by depolarisation of the
ventricles, and the T-wave by repolarisa-
Although the electrical system is self-contained, input from the nervous and
w
tion of the ventricles (Hampton, 2008). In
endocrine system help to regulate cardiac activity in response to the body’s needs
most people, these waveforms occur in a
Cardiac electrical activity can be recorded using skin electrodes, and displayed or
w repeating rhythm called sinus rhythm, so
printed using a variety of ECG machines. Typical waveforms are recorded;the called because it originates in the sinus
P-wave, QRS complex and T-wave. Occasionally, U-waves are seen, although their node. In some people, a fourth waveform
significance remains controversial called a U-wave can be seen. This is usually
seen at slower heart rates. The significance

of the U-wave remains uncertain. Some

authors think that it represents the late
stages of ventricular repolarisation, while
BHF Resources
others describe it as a post-repolarisation The British Heart Foundation (BHF) is committed to sharing our knowledge to
phenomenon (Rautaharju et al, 2009). prevent heart disease devastating people’s lives. We’ve created a range of
U-wave abnormalities have been described resources that can be used by health professionals to support people with a
in various disease states including ischae- heart or circulatory condition. Resources relevant to this article are listed below:
mic heart disease (Kukla et al, 2014).
The basis of ECG interpretation is w A wealth of online information on a variety of heart conditions, tests and
formed upon the recognition of abnor- treatments—Find out more at bhf.org.uk/tests
malities in the size, shape, pattern and tim-
ing of these waveforms (Gregory, 2006). w Tests—A booklet for adults describing the tests that are commonly used to
Next month, we will delve into ECG wave- help diagnose heart diseases or assess the current condition of people with a
forms in more depth, examine the timing heart condition
of events, and describe sinus rhythm and w Electrocardiogram—Your quick guide. A short illustrated leaflet that helps
its variations. We will also consider a sys- adults understand what to expect if they’re having an ECG. It explains the
tem for rhythm interpretation, and discuss different types of ECG, including Holter monitoring and exercise stress tests
issues of accuracy. w Your guide to heart tests and treatments—A series of films following 18 real
To conclude, it is important that anyone people’s journeys through a variety of cardiac tests and treatments. By seeing
wishing to interpret ECGs has a firm phys- the actual procedures, patients know what to expect and how to prepare.
iological foundation to help them under- Available online at bhf.org.uk or on DVD, there are three films covering ECG:
stand why ECGs record what they do, as Your guide to ECG; Your guide to 24 hour blood pressure and Holter monitoring
well as enabling them to explore the com- tests;and Your guide to exercise ECG (stress test). The DVD version includes
plexities of ECGs further. By providing subtitles in English, Bengali, Hindi, Gujarati, Punjabi and Urdu, and optional
readers with some insight into how electro- in-vision BSL interpretation
lytes work, how contraction occurs, and View, download and order these items free at bhf.org.uk/publications
the resulting waveforms, it is hoped that
The BHF Alliance is a free membership scheme that supports professionals
they will be in a better position to begin
working with people affected by, or at risk of developing, cardiovascular disease.
reading and interpreting ECGs with more
confidence. BJCN
Join today at bhf.org.uk/alliance
References
Aaronson PI, Ward JPT, Connolly MJ (2013) The
cardiovascular system at a glance. 4th edn. (2015) Holter ECG for pacemaker/defibrillator Concepts. 2nd edn. Lippincott Williams &
Wiley-Blackwell, Chichester carriers: what is its role in the era of remote Wilkins, Baltimore
Alberts B, Bray D, Hopkin K, Johnson A, Lewis J, monitoring? Heart 101(16): 1272–8. doi: Kukla P, Baranchuk A, Jastrzębski M, Bryniarski L
Raff M, Roberts K, Walter P (2010) Essential 10.1136/heartjnl-2015-307614 (2014) U wave variability in the surface ECG.
Cell Biology. 3rd edn. Garland Science, Fogoros RN (2007) Antiarrhythmic drugs, a Ann Noninvasive Electrocardiol 19(6): 601–3.
Abingdon practical guide. 2nd edn. Blackwell Publishing, doi: 10.1111/anec.12160
Bennett DH (2013) Bennett’s Cardiac Oxford Lafuente-Lafuente C, Mahé I, Extramiana F
Arrhythmias: Practical notes on interpretation Garcia TB (2015) 12-lead ECG: The Art of (2009) Management of atrial fibrillation. BMJ
and treatment. 8th edn. Hodder Arnold, Interpretation. 2nd edn. Jones and Bartlett, 339: b5216. doi: 10.1136/bmj.b5216
London Burlington Levick JR (2010) An Introduction to
Bhatnagar P, Wickramasinghe K, Williams J, Grant AO (2009) Cardiac ion channels. Circ Cardiovascular Physiology. 5th edn. Hodder
Rayner M, Townsend N (2015) The Arrhythm Electrophysiol 2(2): 185–94. doi: Arnold, London
epidemiology of cardiovascular disease in the 10.1161/CIRCEP.108.789081 Marieb EB, Hoehn KN (2015) Human Anatomy &
UK 2014. Heart 101(15): 1182–9. doi: 10.1136/ Gregory J (2006) An analysis tool for 12-lead Physiology. 10th edn. Pearson, Cambridge
heartjnl-2015-307516 ECG interpretation. British Journal of Cardiac Martin CA, Matthews GD, Huang CL (2012)
Blanc JJ, Alboni P, Benditt DG (2015) Vasovagal Nursing 1(5): 216–21. doi: 10.12968/ Sudden cardiac death and inherited
syncope in humans and protective reactions in bjca.2006.1.5.21118 channelopathy: the basic electrophysiology of
animals. Europace 17(3): 345–9. doi: 10.1093/ Hampton JR (2008) The ECG made easy. 7th edn. the myocyte and myocardium in ion channel
europace/euu367 Churchill Livingstone, London disease. Heart 98(7): 536–43. doi: 10.1136/
Camm AJ, Kirchhof P, Lip GY et al (2010) Houghton AR, Gray D (2014) Making Sense of the heartjnl-2011-300953
Guidelines for the management of atrial ECG: A hands-on guide. 4th edn. CRC Press, O’Donovan K (2006) Amiodarone as a class III
fibrillation: the Task Force for the Management Boca Raton antiarrhythmic drug. British Journal of Cardiac
of Atrial Fibrillation of the European Society of Jowett NI, Thompson DR (2007) Comprehensive Nursing 1(11): 530–9. doi: 10.12968/
Cardiology (ESC). Eur Heart J 31(19): 2369– Coronary Care. 4th edn. Bailliere Tindall, bjca.2006.1.11.530
429. doi: 10.1093/eurheartj/ehq278 London Opie L, Gersch B (2013) Drugs for the Heart. 8th
Christoffels VM, Moorman AF (2009) Kaplan LJ, Kellum JA (2010) Fluids, pH, ions and edn. W.B.Saunders, Philadelphia
Development of the cardiac conduction system: electrolytes. Curr Opin Crit Care 16(4): 323–31. Pappano AJ, Wier WJ (2013) Cardiovascular
why are some regions of the heart more doi: 10.1097/MCC.0b013e32833c0957 Physiology. 10th edn. Elsevier/Mosby,
arrhythmogenic than others? Circ Arrhythm Khan E (2006) Beta blockers: Types and clinical Philadelphia
Electrophysiol 2(2): 195–207. doi: 10.1161/ implications. British Journal of Cardiac Nursing Parry A (2012) Inotropic drugs and their uses in
CIRCEP.108.829341 1(3): 132–8. doi: 10.12968/bjca.2006.1.3.20743 critical care. Nurs Crit Care 17(1): 19–27. doi:
Diemberger I, Gardini B, Martignani C et al Klabunde RE (2012) Cardiovascular Physiology 10.1111/j.1478-5153.2011.00476.x. Epub 2011

Rautaharju PM, Surawicz B, Gettes LS et al (2009) com/252rlm (accessed 9 October 2015) Stand 27(22): 48–56
AHA/ACCF/HRS recommendations for the Richley D (2013) New training and qualifications Tortora GJ, Nielsen MT (2014) Principles of
standardization and interpretation of the in electrocardiography. British Journal of Human Anatomy. 13th edn. Wiley, Hoboken
electrocardiogram: part IV: the ST segment, T Cardiac Nursing 8(1): 38–42. doi: 10.12968/ TransMedics Inc (2015) Organ Care System.
and U waves, and the QT interval: a scientific bjca.2013.8.1.38 http://tinyurl.com/q2grojn (accessed 9 October
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Association Electrocardiography and blockers in hypertension, angina and Wetherell H (2013) ECGs for the faint hearted. Br
Arrhythmias Committee, Council on Clinical supraventricular tachycardia. British Journal of J Cardiol 20(2): 52
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Cardiology Foundation; and the Heart Rhythm bjca.2006.1.5.21124 Motzer S, Bridges EJ (2010) Cardiac Nursing.
Society: endorsed by the International Society Society for Cardiological Science & Technology 6th edn. Lippincott Williams & Wilkins,
for Computerized Electrocardiology. (2014) Recording a standard 12-lead Philadelphia
Circulation 119(10): e241–50. doi: 10.1161/ electrocardiogram. http://tinyurl.com/p7kpbhx Younker J (2011) Assessment of the
CIRCULATIONAHA.108.191096 (accessed 9 October 2015) cardiovascular system. In: Humphreys M, ed.
Resuscitation Council UK (2010) The Swift J (2013) Assessment and treatment of Nursing the Cardiac Patient. Wiley-Blackwell,
Resuscitation Guidelines. http://tinyurl. patients with acute unstable bradycardia. Nurs Chichester: 19–35
H N
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F R S
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Understanding the ECG

Part 2: ECG basics
Michael Sampson, BHF Arrhythmia Nurse Specialist, St George’s Hospital, Senior Lecturer, School of Health and
Social Care, London South Bank University, and BHF Alliance member, London; and Anthony McGrath, Head of
Department, Department of Adult Nursing and Midwifery Studies, School of Health and Social Care, London
South Bank University, London. Email: michael.sampson@nhs.net
T
he 12-lead electrocardiogram (ECG) In this second article, we take a more particular perspective (Garcia, 2015).
is one of the most commonly detailed look at the 12-lead ECG. Our aim Therefore, when we carry out a 12-lead
performed cardiac investigations, and is to familiarise you with the layout of the ECG, we are recording cardiac electrical
provides a wealth of clinical data (Whitbread, 12-lead ECG, and to help you to under- activity from 12 different perspectives
2006). Correct interpretation of this data, stand the relationship between ECG leads (Hampton, 2013). Imagine you are visiting
however, requires that practitioners have a and the different areas of the heart. We a historic building and taking photographs
good understanding of how it is presented, also consider common factors that affect of it. If you take 12 photographs from
and approach the data in a methodical and the accuracy of recording, and offer the around the building, each one will show a
thorough fashion (Gregory, 2006). Equally reader a method of interpretation that we different aspect; for example, the front, the
important is a recognition of the factors that believe facilitates systematic analysis of sides and the back of the building. Together,
can influence recording accuracy, and a the ECG. Finally, we describe the first step they build up a three-dimensional record
knowledge of how each aspect of the in this system of interpretation: the assess- of the building’s shape and appearance. A
recording relates to the structure and ment of heart rate, rhythm and intervals. 12-lead ECG builds up a three-dimension-
function of the heart (Crawford and al picture of the heart’s electrical activity in
Doherty, 2008). Normal and abnormal Leads a similar way.
values must be understood, and applied to I remember once being approached by a Let’s look at an ECG more closely and
the clinical context (Garcia, 2015). junior member of staff in the Emergency hopefully you’ll see what we mean. Figure 1
The first article in this series explored and Department who informed me that the shows a normal 12-lead ECG. The first
discussed the anatomy and physiology that ECG machine was broken. ‘There are only thing to note is that there are two groups of
underpins the ECG (Sampson and McGrath, 10 leads,’ she told me, ‘instead of the 12 that six leads: one group to the left and one to
2015). We discussed the way in which car- there should be’. After a simple explanation the right. Below them is a longer printout
diac electrical activity arises from the move- of what lead means in ECG terms, she real- of lead II, which is called a rhythm strip.
ment of electrolytes, and outlined the main ised that she had a fully functioning piece Most ECGs are laid out in this fashion,
features of the cardiac conduction system. of equipment. although some may print a different lead
We then introduced the principal wave- To put it simply, an ECG lead is not an for the rhythm strip, typically V1, and oth-
forms and considered different types of electrical cable but a recording of the ers may not print a rhythm strip at all
ECG recording. heart’s electrical activity, seen from one (Eldridge and Richley, 2014). You’ll see
from Figure 1 that the leads to the left are
marked with either a roman numeral or
three letters starting with ‘a’. These six leads
are derived from the four electrodes placed
on the arms and legs. For this reason, they
are called the ‘limb leads’. These can be
further divided into the basic limb leads (I,
II, III) and the augmented limb leads (aVR,
aVL, aVF) (Houghton and Gray, 2014).
Moving to the right-hand side of the
ECG, we can see that the six leads on that
side all start with the letter V followed by a
number: V1 through to V6. These leads are
© 2015 MA Healthcare Ltd
called the chest or precordial leads. Each

one corresponds with a single electrode
placed on the chest wall. On some
machines, these leads are labelled as C1 to
Figure 1. Layout of the 12-lead ECG C6 (Garcia, 2015).
588 British Journal of Cardiac Nursing December 2015 Vol 10 No 12

The final lead on the ECG is our rhythm towards the back. This anatomical
© Peter Lamb
strip. As mentioned, this is a longer print- arrangement of the chambers is not obvi-
out of one of the 12 leads, usually lead II. A ous when the heart is depicted from the
aVR aVL
rhythm strip is useful in evaluating heart front, as it is in most textbooks. From this
rate and rhythm, because it gives you a perspective, we can see that V1 and V2 are
longer recording through which to evalu- looking in at part of the right ventricle;
ate the pattern of ECG waveforms however, their main view is of the septum I
(Bennett, 2013). between the two ventricles. We can there-
fore refer to these leads as the septal leads.
The 12 views Leads V3 and V4 are further around
The next step in getting to know the towards the left side of the body, and see
12-lead ECG is to think about which parts the anterior or front surface of the LV.
III II
of the heart the 12 leads are ‘seeing’ elec- These leads can therefore be referred to as
aVF
trically. The heart is a complex structure the anterior leads. More commonly, leads
and if we required a truly three-dimen- V1 to V4 are grouped together as the anter- Figure 2. The limb leads
sional picture, we would need a lot more oseptal leads (Jowett and Thompson,
© Peter Lamb
than 12 leads. Imagine trying to interpret 2007). Finally, leads V5 and V6 look in
a 48- or 60-lead ECG—this would be from the left side of the chest and see the
impractical. Therefore, the 12 leads are lateral wall of the LV. The area they see is
predominantly grouped around the left similar to leads I and aVL (Hampton,
ventricle (LV), as this is the most impor- 2013). It is important that cardiac nurses V2
V1
tant chamber in terms of maintaining develop a full understanding of what each V3
V4 V5 V6
cardiac output (Aaronson et al, 2013). The group of leads sees in order to be able to
two sets of leads view the heart in two dif- assess the ECG for signs of structural
ferent planes (Kligfield et al, 2007): heart disease, such as hypertrophy or
w The limb leads in a frontal plane ischaemia (Jabbour and Touquet, 2014).
w The chest leads in a transverse plane. Our aim is to provide a more detailed Posterior
Figure 2 shows how the limb leads view overview of these areas in a future article.
the heart. You can see that all six leads LV Left
ECG paper RV V6 lateral

look in from the sides of the body. Leads I
V5
and aVL look in from near the left arm We are fortunate that the graph paper on V4
and see the lateral (side) wall of the LV. which the ECG is recorded can provide us V1 V2
V3
Anterior
Leads II, III and aVF look in from below, with a great deal of information. The way
as if you were looking up the legs. These in which the paper is laid out allows the Figure 3. The chest leads
three leads see the inferior surface of the interpreter to measure the timing of
LV, the part that rests on the diaphragm. events, as well as the size of the various
Finally, lead aVR looks in from the area of waveforms. It is important to note that
the right arm, seeing predominantly the accurate interpretation of both timing and
right atrium (Garcia, 2015). As you can see, size relies on the machine being properly
the limb leads do not see the front surface set up, and the electrodes being placed
of the heart, which is why the chest leads correctly. Let us now consider these points
are necessary (Houghton and Gray, 2014). in turn.
The chest leads look in through the When you look at ECG paper, you note
front of the chest wall. As the electrodes that it is divided into small and large
are now closer to the heart, the waveforms squares (Figure 4). Each small square is Figure 4. ECG paper
are generally larger. However, this is not 1 mm x 1 mm, and each large square
always the case. Conditions such as obes- 5 mm x 5 mm. Time is measured along waveforms on the ECG will be wider and
ity and lung disease may increase the dis- the horizontal (X) axis. Each small square further apart, which will confuse your
tance between the heart and the recording represents 0.04 seconds (40 milliseconds) analysis. When you are interpreting an
electrodes, which in turn reduces the size and each large square, 0.2 seconds ECG, it is important that you check the
of the waveforms (Low et al, 2012). (200 milliseconds) (Garcia, 2015). speed. This is printed out in the bottom
Figure 3 shows the relationship between Therefore, if events on the ECG are five left corner of the paper (Figure 4).
the chest leads and the heart. In this large squares apart, then one second sepa- The vertical, or Y axis, of the ECG
image, we are looking down on the heart rates them in time. These timings assume measures the amplitude of the waveforms
from above, with the sternum at the front that the paper speed of the ECG machine in millivolts. The amplitude, or size, of the
and the spine at the back. You can see that is set up normally. Standard paper speed waveforms reflects the size of the cham-
the right ventricle is towards the front of is 25 mm/second (Eldridge and Richley, bers that are depolarising. The QRS com-
the body, and the left ventricle, more 2014). If the paper speed is increased, plex is much taller than the P-wave
British Journal of Cardiac Nursing December 2015 Vol 10 No 12 589

many more cells than a normal heart a suitable written guide. Crawford and
Rate, rhythm and intervals? (Gosse et al, 2012). The standard calibra- Doherty (2008), for example, provide an
R tion for amplitude is 10 mm per millivolt. in-depth, step-by-step guide to correct
In other words, one millivolt of electricity lead placement.
will move the stylus up or down by 10 mm
P Pre-excitation?
on the paper (Kligfield et al, 2007). As Systematic ECG interpretation
with paper speed, amplitude settings can The strength of the 12-lead ECG is the
be altered on the ECG machine. Increasing amount of detail that it contains; however,
Q QRS axis the setting to 20 mm/mv will double the this also poses its greatest challenge. A
size of the waveforms on the ECG. The structured approach to interpretation is
amplitude calibration is printed in the recommended, and reduces the chance
R Right or left bundle bottom left corner of the ECG, next to the that you will miss important information
branch block? paper speed. This should also be checked (Whitbread, 2006).
Scan each lead: when you are interpreting the ECG. Research suggests the use of interpreta-
S • P-waves A second factor to consider when tion tools improves accuracy in both expe-
• QRS dimensions and morphology assessing the accuracy of waveform ampli- rienced and novices (Sibbald et al, 2013).
• ST segments and T waves
tude is electrode placement. Electrodes While we acknowledge that there are a
T that are placed in the wrong position can number of systems of interpretation avail-
Translate findings result in increased or decreased amplitude able, we propose to use a modified version
of the ECG waveforms. In a study of of the RPQRST system. This system was
Figure 5. System of interpretation adapted
120 health-care practitioners, devised by Gregory (2006) and has the
from Gregory (2006), with kind permission
Rajaganeshan et al (2008) found that advantage of being simple and memorable
because the ventricles are much larger, errors in chest electrode placement were (Figure 5). We believe using a tool ensures
and thicker-walled, than the atria especially common, with V1/V2 and V5/ you work through each aspect in turn
(Klabunde, 2012). Clinically, this can be V6 often placed too high on the chest. before making a diagnosis. This ensures a
useful when assessing the ECG for Limb electrodes may also be incorrectly thorough and systematic evaluation of the
enlargement of the heart. The ECG of a placed. Eldridge and Richley (2014) point information contained on the ECG, which
patient whose heart has enlarged, because out that these electrodes should be placed in turn reduces the risk of jumping to con-
of long-standing hypertension, for exam- on the wrists and ankles, not on the upper clusions or reaching an incorrect diagno-
ple, may show QRS complexes that are limbs or torso. Practitioners who are sis. Let us now consider the first step in the
taller than normal. This is because the unsure of correct lead placement should RPQRST system; the evaluation of heart
thickened walls of the ventricles contain consult a more experienced colleague, or rate, rhythm and intervals.
Large Heart rate

squares (beats/min)
1 300
2 150
3 100
4 75
5 60
6 50
Figure 6. The R-R method of estimating heart rate
Six QRS complexes: the heart rate is around 60 beats per minute
Figure 7. The 30-square method of estimating heart rate

Evaluating heart rate infallible and may miscalculate the heart

The heart rate is an important piece of rate (Southern and Arnsten, 2009). It is
information, not only from a diagnostic important therefore that practitioners
point of view, but also in terms of patient should be able to calculate rate manually
safety. Extremely low or high heart rates to check the machine’s findings. Second,
suggest serious rhythm abnormalities, practitioners may need to calculate heart
and the possibility of patient decompen- rate from a rhythm strip that has no rate
sation or cardiac arrest (Pitcher and printed on it. There are a number of ways
Nolan, 2015). Heart rate is therefore an of calculating heart rate from the ECG,
important factor in overall patient assess- some of which require a calculator.
ment, as well as one aspect to be consid- However, we would like to propose
ered when assessing the ECG (Jevon, two simple methods that require no Figure 8. Time intervals of the ECG
2010). The first step in evaluating heart
rate is to understand the normal range Box 1. Rhythm evaluation questions
of values. 1. Is the rhythm regular?
During sinus rhythm, the heart rate is 2. Is the heart rate between 60 and 100 beats per minute?
set by how quickly the sinus node depo-
3. Are there upright P-waves, and are they all the same shape?
larises (Levick, 2010). We discussed vari-
ous factors that influence sinus rate last 4. Is there one P-wave in front of each QRS complex?
month, including the autonomic nervous 5. Is the PR interval normal (3 to 5 small squares?)
system, hormones and medications 6. Is the QRS complex narrow (less than 3 small squares wide?)
(Sampson and McGrath, 2015). At rest,
normal sinus rate is usually defined as
60–100 beats per minute (Bennett, 2013;
Hampton, 2013; Houghton and Gray,
2014; Garcia, 2015). Rates below 60 are
described as bradycardia, although there
is evidence that rates as low as 50 are both
normal and common, especially in physi-
cally fit individuals. Spodick et al (1992)
measured the resting heart rate of
500 healthy, unmedicated individuals and
found a range of 46–93 beats per minute
in men, and 51–95 beats per minute in
women. Sinus bradycardia is also com-
mon during sleep, when the heart slows as
a result of decreased demand for cardiac
output (Marieb and Hoehn, 2015). Rates Figure 9. Calculating QTc using Bazett’s formula
above 100 are described as tachycardia
(Garcia, 2015). Sinus tachycardia is nor-
mal during exercise, and increases cardiac
output to meet the demand of working
muscles (Kenney et al, 2015). Other caus-
es of sinus tachycardia include pain, anxi-
ety, fever and blood loss. Sinus tachycar-
dia should always be investigated to deter-
mine and treat the underlying cause, for
example, giving analgesia for pain (Bench Normal QT: The QTc is 394 ms
and Brown, 2011).
Once we understand the normal values
for heart rate, we are ready to evaluate
them on the ECG. At first glance, it would
appear that the easiest way to determine
the heart rate is to use the figure calculat-

ed by the machine. While this is accepta-
ble in most circumstances, there are QT prolongation: The QTc is 532 ms
several potential pitfalls that must be con-
sidered. First, ECG machines are not Figure 10. Comparison of normal and prolonged QT intervals

equipment. The first is the ‘R-R method’, Because each P-wave comes from the variation of sinus rhythm is present, such
the second, the ‘30 large square’ method. same place in the heart, each one should as sinus tachycardia. Recognising abnor-
be the same size and shape (Bennett, mal rhythms will be the focus of the next
R-R method 2013). P-waves should also be upright article in this series.
The R-R method gives a quick estimate of (positive) in all leads except aVR, which is
heart rate based on the number of large usually negative, and leads III and V1, Intervals
squares between each QRS complex which may have positive or negative The final element in this first stage of ECG
(Figure 6). The number of large squares is P-waves (Garcia, 2015). interpretation is to evaluate the time
divided into 300 to give the approximate This can be explained by the way in intervals on the ECG. We have already
heart rate. The more squares between the which ECG machines record electrical considered the PR interval and the QRS
QRS complexes, the lower the heart rate activity. An electrical impulse moving duration in our discussion of rhythm. The
(Hampton, 2013). In Figure 6, we can see towards an ECG lead creates an upright other important time measurement is the
that there are four large squares between waveform, while an impulse moving away QT interval (Houghton and Gray, 2014).
QRS complexes: 300 divided by four gives results in a negative one. The sinus node is The QT interval is the time from the
us a heart rate of 75 beats per minute. Some at the top of the heart, while most of the beginning of the QRS complex to the end
people prefer to memorise the heart rate recording leads are lower down. The of the T-wave, and represents the entire
for a given number of large squares, as impulse from the sinus node is therefore process of ventricular depolarisation and
shown in Figure 6. travelling towards most of the leads, and repolarisation (Figure 8). Prolongation of
The advantage of the R-R method is that causes a positive P-wave (Hampton, 2013). the QT interval increases the risk of ven-
it gives a very quick and easy estimate of The QRS is also upright in most leads, tricular arrhythmias, particularly a type of
heart rate. The disadvantages are that the although various abnormalities in cardiac ventricular tachycardia called Torsades de
rate is only a very rough estimate, and that structure or electrical function can alter Pointes (Attin and Davidson, 2011). A
the system cannot be used when the this, as we shall see as we progress through prolonged QT interval may occur because
rhythm is irregular. This is because in this series of articles. From a rhythm per- of a genetic abnormality in ion channel
irregular rhythms, the interval between spective, a more important consideration function, creating a condition known as
QRS complexes is not the same for each when assessing the QRS is its width or long-QT syndrome (Martin et al, 2012).
beat (Garcia, 2015). duration. We know that the electrical The QT interval may also be increased by
impulse spreads through the ventricles cardiac drugs such as amiodarone, flecain-
30 large square method very rapidly because of the extensive His- ide and sotalol, as well as by many non-
For a more accurate estimate of heart rate, Purkinje system (Tortora and Nielsen, cardiac drugs including erythromycin and
or when the rhythm is irregular, the 30 2014). The QRS is therefore narrow in haloperidol (Fogoros, 2007; Nachimuthu et
large square method is better (Hampton, normal health, and occurs in less than al, 2012).
2013). To use this method, mark a point 0.12 seconds (less than 3 small squares of Measurement of the QT interval is more
on the rhythm strip and count off 30 large ECG paper) (Hampton, 2013). A wide complex than assessment of the PR inter-
squares before making another mark. QRS suggests one of two possibilities. val or QRS duration for several reasons.
Now count the number of QRS complexes Either the electrical impulse has not trav- First, the QT interval appears longer in
between the marks. Multiply this number elled normally through the conduction some ECG leads than others. The
by ten to give the heart rate. In the example system (for example, because of heart American Heart Association recommends
in Figure 7, there are six QRS complexes block) or, more alarmingly, the rhythm simultaneous analysis of all 12 leads to
between the marks. Six multiplied by ten itself has originated in the ventricles. determine the earliest QRS complex and
gives us a heart rate of 60 beats per minute. Because broad complex arrhythmias can the latest T-wave, thereby measuring the
cause cardiac arrest, any ECG with a wide longest possible QT interval (Rautaharju
Evaluating rhythm QRS complex must be carefully evaluated et al, 2009). Yaldren and Richley (2014)
Once we know the heart rate, the next (Tough, 2008). point out that this is not feasible in every-
step is to evaluate the rhythm. The normal The final major consideration from a day practice, and suggest that the most
rhythm of the heart is sinus rhythm. We rhythm point of view is the time taken for important aspect of accurate QT measure-
can understand the ECG appearance of the electrical impulse to pass through the ment is selecting a lead in which the end of
sinus rhythm by reflecting on our knowl- conduction system. This is measured from the T-wave is clearly visible. They suggest
edge of the cardiac conduction system. the start of the P-wave to the start of the using lead II if the T-wave is clearly defined,
The sinus node depolarises at regular QRS complex, and is called the PR inter- otherwise leads I, III or V5.
intervals. Sinus rhythm therefore has a val. The normal PR interval is between The second complication with QT
regular pattern. The electrical signal 0.12 and 0.2 seconds (3–5 small squares) measurement is variability with heart rate.
spreads through the atria, creating the (Klabunde, 2012). As heart rate increases, the QT interval
P-wave on the ECG, and then spreads Checking if all these normal features are shortens. This makes comparison with
through the ventricles to create the QRS present will tell you whether the rhythm is normal values difficult. QT interval is
complex. The P-wave therefore comes in sinus or not. Box 1 lists the key questions therefore corrected for heart rate to give
front of the QRS complex, and there that you need to ask. If any answer is QTc. QTc represents the QT interval as it
should only be one P-wave to every QRS. no, either the rhythm is not sinus or a would be at 60 beats per minute (Hampton,

2013). A number of formulae are available

to calculate QTc, of which Bazett’s is the
most widely used (Yaldren and Richley,
Key Points
The 12 leads of the ECG build a three-dimensional picture of the heart’s electrical
w
2014). Bazett’s formula states that the QTc activity, and are divided into the six limb leads and six chest leads
is equal to the QT interval (in millisec-
onds) divided by the square root of the ECG leads can also be grouped according to the area of the left ventricle that is
w
R-R interval (in seconds). An example of seen (i.e. inferior, lateral or anteroseptal). This becomes important when assessing
a QTc calculation using Bazett’s formula is for structural heart disease and ischaemia
shown in Figure 9. Suggested maximum The ECG is printed on graph paper with small and large squares. Time is shown
w
values for QTc are 450 milliseconds for along the horizontal axis, and amplitude on the vertical axis
men, and 460 milliseconds for women
(Rautaharju et al, 2009; National Institute Paper speed and amplitude must be correctly set on the machine for accurate
w
for Health and Care Excellence (NICE), interpretation. Incorrect electrode placement will also affect accuracy
2010). Measuring QTc manually is quite The use of a system of interpretation ensures that the 12-lead ECG is evaluated
w
time-consuming, so many practitioners thoroughly, and that important details are not overlooked. We propose the use of
rely on the ECG machine’s calculation. the RPQRST system
While this is usually highly accurate, a
quick visual check is essential in case of The first stage in this system is to evaluate heart rate, rhythm and
w
machine error. Garcia (2015) points out conduction intervals
that the normal QT is less than half of the The normal heart rate is 60–100 beats per minute, with slower rates described as
w
R-R distance and suggests this method as bradycardia and faster rates as tachycardia
a quick visual check. Figure 10 compares
Normal sinus rhythm has a number of key features including: regularity, P-waves that
w
ECGs with normal and prolonged
are consistent and upright in most leads, one P-wave in front of every QRS, and a
QT intervals.
normal PR interval. The QRS is usually narrow
Conclusion In addition to evaluating QRS width and PR interval, the QT interval should also be
w
The 12-lead ECG provides detailed infor- measured. QTc is used owing to variability of the interval at different heart rates
mation about the heart’s electrical activity.
The use of a structured interpretation tool
is recommended to ensure that this infor-
mation is handled in a systematic and
BHF Resources
thorough fashion. In this article, we have The British Heart Foundation (BHF) is committed to sharing our knowledge to
provided you with one system of analysis, prevent heart disease devastating people’s lives. We have created a range of
as well as the essential building blocks for resources that can be used by health professionals to support people with a
a deeper understanding of the ECG and heart or circulatory condition. Resources relevant to this article are listed below:
how it is recorded. We have also endeav- A wealth of online information on a variety of heart conditions, tests and
oured to provide you with a better under- treatments—Find out more at bhf.org.uk/tests
standing of the layout of the ECG, and the w Tests—A booklet for adults describing the tests that are commonly used to
orientation of the various leads.We believe help diagnose heart diseases or assess the current condition of people with a
that this is an essential first step in devel- heart condition
oping your 12-lead interpretation skills.
w Electrocardiogram—Your quick guide. A short illustrated leaflet that helps
Next month, we aim to consolidate
adults understand what to expect if they’re having an ECG. It explains the
and develop your knowledge further
different types of ECG, including Holter monitoring and exercise stress tests
by examining in detail the common
rhythm abnormalities. BJCN
w Your guide to heart tests and treatments—A series of films following 18 real
people’s journeys through a variety of cardiac tests and treatments. By seeing
References the actual procedures, patients know what to expect and how to prepare.
Aaronson PI, Ward JPT, Connolly MJ (2013) The Available online at bhf.org.uk or on DVD, there are three films covering ECG:
Cardiovascular System At A Glance. 4th edn. Your guide to ECG; Your guide to 24 hour blood pressure and Holter monitoring
Wiley-Blackwell, Chichester
tests; and Your guide to exercise ECG (stress test). The DVD version includes
Attin M, Davidson JE (2011) Using QRS morphology
and QTc interval to prevent complications and subtitles in English, Bengali, Hindi, Gujarati, Punjabi and Urdu, and optional
cardiac death. Crit Care Nurs Q 34(3): 246–53. doi: in-vision BSL interpretation
10.1097/CNQ.0b013e318221477c
View, download and order these items free at bhf.org.uk/publications
Bench S, Brown KM (2011) Critical Care Nursing:

Learning From Practice. Wiley-Blackwell, West The BHF Alliance is a free membership scheme that supports professionals
Sussex
Bennett DH (2013) Bennett’s Cardiac Arrhythmias: working with people affected by, or at risk of developing, cardiovascular disease.
Practical Notes on Interpretation and Treatment. Join today at bhf.org.uk/alliance
8th edn. Hodder Arnold, London
Crawford J, Doherty L (2008) Recording a standard

in over 16s. [CG109]. www.nice.org.uk/guidance/

BHF Doctor’s comment cg109 (accessed 18 November 2015)
Pitcher D, Nolan J (2015) Peri-arrest Arrhythmias.
Achieving optimal clinical outcomes provides a clear understanding of the Resuscitation Council UK, London. http://tinyurl.
requires accurate diagnosis, and this in principles and practice needed to record com/ogeh2jt (accessed 18 November 2015)
Rajaganeshan R, Ludlam CL, Francis DP, Parasramka
turn is dependent on accurate and interpret the ECG. SV, Sutton R (2008) Accuracy in ECG lead
interpretation of tests, as well as precision placement among technicians, nurses, general
in undertaking the test in the first place. Dr Mike Knapton physicians and cardiologists. Int J Clin Pract 62(1):
This review, the second in the series, BHF Medical Director 65–70. Epub 2007
Rautaharju PM, Surawicz B, Gettes LS et al (2009)
AHA/ACCF/HRS recommendations for the
standardization and interpretation of the
12-lead ECG: filling in gaps in knowledge. Kenney WL, Wilmore J, Costill D (2015) Physiology
electrocardiogram: part IV: the ST segment, T and
BJCardN 3(12): 572–7. doi: 10.12968/ of Sport and Exercise. 6th edn. Human Kinetics,
Champaign U waves, and the QT interval: a scientific
bjca.2008.3.12.31804
Eldridge J, Richley D (2014) Clinical Guidelines by Klabunde RE (2012) Cardiovascular Physiology statement from the American Heart Association
consensus. Recording a standard 12-lead Concepts. 2nd edn. Lippincott Williams & Wilkins, Electrocardiography and Arrhythmias Committee,
electrocardiogram: An approved methodology by Baltimore Council on Clinical Cardiology; the American
the Society for Cardiological Science & Technology Kligfield P, Gettes LS, Bailey JJ et al (2007) College of Cardiology Foundation; and the Heart
(SCST). http://tinyurl.com/p7kpbhx (accessed 17 Recommendations for the standardization and Rhythm Society: endorsed by the International
November 2015) interpretation of the electrocardiogram: part I: the Society for Computerized Electrocardiology.
Fogoros RN (2007) Antiarrhythmic Drugs: A Practical electrocardiogram and its technology a scientific Circulation 119(10): e241–50. doi: 10.1161/
Guide. 2nd edn. Blackwell Publishing, Oxford statement from the American Heart Association CIRCULATIONAHA.108.191096
Garcia TB (2015) 12-lead ECG: The Art of Electrocardiography and Arrhythmias Committee, Sampson M, McGrath A (2015) Understanding the
Interpretation. 2nd edn. Jones and Bartlett, Council on Clinical Cardiology; the American ECG. Part 1: Anatomy and physiology. BJCardN
Burlington College of Cardiology Foundation; and the Heart 10(11): 548–54. doi: 10.12968/bjca.2015.10.11.548
Gosse P, Jan E, Coulon P et al (2012) ECG detection Rhythm Society endorsed by the International Sibbald M, de Bruin AB, van Merrienboer JJ (2013)
of left ventricular hypertrophy: the simpler, the Society for Computerized Electrocardiology. J Am Checklists improve experts’ diagnostic decisions.
better? J Hypertens 30(5): 990–6. doi: 10.1097/ Coll Cardiol 49(10): 1109–27 Med Educ 47(3): 301–8. doi: 10.1111/medu.12080
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Gregory J (2006) An analysis tool for 12-lead ECG small QRS voltages. Singapore Med J 53(5): 299– erroneous computer interpretation of ECGs on
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Understanding the ECG

Part 4: Conduction blocks
and Social Care, London South Bank University, and BHF Alliance member, London.
Email: michael.sampson@nhs.net
In this fourth article of the British Journal

© Peter Lamb
of Cardiac Nursing’s ECG Interpretation

Series, we examine the conduction blocks
commonly encountered in clinical prac-
tice, and discuss how they can be recog-
nised on the electrocardiogram (ECG). As
with the previous article in this series
Left atrium
(Sampson, 2016), we also place each block
in context by briefly considering why it
Sinoatrial node (SA) occurs, its clinical significance, and any
Bundle of His treatment that might be necessary.
Right atrium
Left bundle branch (LBB) Rhythm evaluation
We have discussed systematic rhythm eval-
Atrioventricular node (AV) Left ventricle uation in a previous article (Sampson and
McGrath, 2015). Readers may wish to
refresh their memories of this information
Right ventricle before reading further. For convenience,
the key steps are reproduced in Box 1.
Purkinje fibres (PF)
Sinoatrial block
The sinus node is a relatively large struc-
Right bundle branch
ture, divided into functionally different
Figure 1. The cardiac conduction system: sites of conduction block include the sinoatrial areas. The electrical impulse arises in one
(SA) node, atrioventricular (AV) node, and the left and right bundle branches part of the node, and is conducted through
the surrounding nodal tissue before reach-
I
n the normal heart, the electrical their journey through the conduction sys- ing the atrial myocardium. Conduction
impulse arising from the sinus node is tem, or fail to arrive in the ventricles at all. block occurring in this surrounding tissue
conducted to the ventricles via the Conduction may be normal through one will prevent the impulse from exiting the
atrioventricular (AV) node, bundle of His, bundle branch, but be blocked in the other sinus node (Monfredi et al, 2010). This
and bundle branches (Klabunde, 2012) (Garcia, 2015). All of these conduction phenomenon is referred to as sinoatrial
(Figure 1). The normal operation of this problems are referred to as ‘blocks’, block, or sinus exit block. Because the
specialised system ensures that every although their effect on heart rate, rhythm, non-conducted beats do not reach the
impulse from the sinus node is conducted and patient wellbeing vary considerably. main body of the atria, no P-wave is gener-
to both ventricles in a rapid and efficient
manner (Marieb and Hoehne, 2015). Box 1. Key steps in systematic rhythm evaluation
Unfortunately, this process of impulse Rhythm evaluation questions
conduction is not normal in every indi-
1. Is the rhythm regular?
vidual. The cardiac conduction system is
subject to the same disease processes that 2. Is the heart rate between 60 and 100 beats per minute?
impair the function of other parts of the 3. Are there upright P-waves, and are they all the same shape?
heart, and the result is a range of conduc- 4. Is there one P-wave in front of each QRS complex?
tion disturbances (Chow et al, 2012).
5. Is the PR interval normal (3 to 5 small squares?)
Impulses from the sinus node may fail to
conduct through the atria, be delayed in 6. Is the QRS complex narrow (less than 3 small squares wide?)
British Journal of Cardiac Nursing February 2016 Vol 11 No 2 71

2013). Figure 4 shows a junctional escape

beat that occurs following a sinus pause.
Because the escape beat arises in the
AV junction, the electrical wavefront trav-
els upward through the atria instead of
downward. This results in an inverted
Figure 2. Sinoatrial block. The pause is exactly 2 cycle lengths P-wave that may occur before or after the
QRS, depending on conduction times and
the location of the subsidiary pacemaker.
In many cases, as in Figure 4, the P-wave
occurs at the same time as the QRS, and is
therefore hidden by it. The QRS is narrow
because conduction to the ventricles is
Figure 3. Sinus arrest. The pause is around 3.5 cycle lengths
normal (Aehlert, 2011).
Escape beats are a normal back-up fea-
ture of the heart, and ensure that prolonged
asystole does not occur (Klabunde, 2012).
If the sinus node fails entirely, an escape
rhythm from the AV junction will usually
Figure 4. Sinus pause followed by a junctional escape beat take over. This is referred to as junctional
rhythm, and appears as a series of junc-
tional escape beats (Figure 5). The rate is
usually slow, as pacemakers in the AV junc-
tion fire more slowly than those in the
sinus node (Jowett and Thompson, 2007).
Figure 5. Junctional rhythm. In this example, there is an inverted P-wave before the QRS The ECG features of junctional rhythm are
as follows:
w A regular rhythm, often between 40 and
60 beats per minute
w P-waves are either inverted, or hidden by
the QRS
w The QRS is narrow.
If a complete block in conduction occurs
Figure 6. First-degree AV block. The PR interval is 340 milliseconds lower in the conduction system, for exam-
ple in the AV node, a subsidiary pacemaker
ated. The electrical impulse does not arrive sinus bradycardia, chronotropic incompe- below the level of the block usually ensures
at the AV node, and is not conducted to tence, and paroxysmal atrial fibrillation or that the ventricles continue to depolarise.
the ventricles, so there is no QRS complex flutter. Collectively, these problems are If the subsidiary pacemaker is within the
or T-wave either (Aehlert, 2011). On the referred to as sick sinus syndrome (Ewy, bundle of His, the resulting escape rhythm
ECG, this results in a single missed beat in 2014). The most common cause of sick will have a narrow QRS. If it is in the bun-
an otherwise regular rhythm (Figure 2). sinus syndrome is age-related degenera- dle branches or Purkinje fibres, the QRS
Because the sinus node is still firing regu- tion of the sinus node, resulting in fibrosis will be broad. Subsidiary pacemakers in
larly, the pause is a multiple of the usual or ion-channel dysfunction, although it the lower parts of the conduction system
cycle length. For example, if the sinus may also be a result of coronary heart are much slower than those in the AV junc-
node is firing once every second, the pause disease (Monfredi et al, 2010). Its symp- tion, and are more unreliable. If they fail,
will be 2 seconds if a single impulse is toms include: dizziness; loss of conscious- asystole occurs (Bennett, 2013).
blocked (Houghton and Gray, 2014). ness; palpitations; breathlessness; and
A similar pause occurs if the sinus node exercise intolerance (Jensen et al, 2014). Atrioventricular blocks
fails to fire at all. This is referred to as sinus Permanent pacemaker implantation is AV blocks occur when conduction between
arrest (Figure 3). The pause produced by necessary in symptomatic individuals, the atria and ventricles is delayed, intermit-
sinus arrest is variable in length, and does especially if there is a history of syncope tently blocked, or fails completely. Unlike
not correspond with cycle length as it does (Bennett, 2013). sinoatrial block, the electrical impulse exits
in sinoatrial block (Hampton, 2013). the sinus node normally and is conducted
Otherwise, the two problems are very Escape beats and rhythms through the atria, creating a P-wave on the
similar in ECG appearance. If sinoatrial block or sinus arrest result in a ECG (Vogler et al, 2012). Conduction fail-
Sinoatrial block and sinus arrest occur long enough pause, a subsidiary pacemak- ure occurs further down the system, in the
most commonly in older people, often in er in the AV junction may fire. This is AV node, bundle of His or bundle branch-
association with related disorders such as referred to as an escape beat (Bennett, es. On the ECG, effects of AV block can be
72 British Journal of Cardiac Nursing February 2016 Vol 11 No 2

ECG appearance: Mobitz type-I or

Wenckebach, and Mobitz type-II. There are
prognostic differences between these types
of second-degree block (Aehlert 2011).
Mobitz type-I (Wenckebach)

Figure 7. Mobitz type I. The PR interval lengthens progressively until a beat is dropped In Mobitz type-I, conduction from the
sinus node to the ventricles becomes pro-
gressively slower with each beat, until an
impulse fails to conduct at all. On the ECG,
this results in progressive lengthening of
the PR interval until a P-wave is not fol-
lowed by a QRS complex (Figure 7). After
the dropped beat, the PR interval returns
to its shortest length before starting to
Figure 8. Mobitz type II. The PR interval is constant. Note the frequent dropped beats,
lengthen again. The dropped beats make
and broad QRS complex
the rhythm regularly irregular (Houghton
and Gray, 2014). The ECG findings in
Mobitz type-I are therefore:
w There are more P-waves than QRS com-
plexes
w The PR interval gets longer with each beat,
until a P-wave is not followed by a QRS
Figure 9. Second-degree AV block with 2:1 conduction. The QRS complex is narrow w After a dropped beat, the PR interval
‘resets’ and the cycle starts again
seen in changes in the PR interval, P-waves First-degree AV block does not affect the w The rhythm is regularly irregular (areas
that are not followed by QRS complexes, or heart rate or rhythm, and does not generally of regular rhythm are separated by
in complete electrical dissociation of the cause symptoms. It is often considered dropped beats)
atria and ventricles (Hampton, 2013). benign, and is a normal finding in young w The QRS complex is narrow, unless there
Based on the degree of conduction block, people and athletes, in whom it is usually is concurrent bundle branch block.
AV blocks are classified as first-, second- or owing to high vagal tone (Bennett, 2013). Like first-degree AV block, Mobitz type-I
third-degree in nature (Chow et al, 2012). Early research into first-degree AV block may be caused by slow conduction within
supports this benign view, demonstrating a the AV node. In young, healthy people, this
First-degree AV block low rate of progression to higher degrees of is a normal finding at night, and is caused
In first-degree AV block, the electrical block, and no increase in mortality (Packard by high vagal tone. In older people, and
impulse is delayed on its journey from the et al, 1954; Mymin et al, 1986). However, during the day, Mobitz type-I is less likely
sinus node to the ventricles. It is not, there- these findings were recently challenged by to be harmless, and more likely to be
fore, a block at all but rather a form of Cheng et al (2009) who point out that the caused by damage to the distal conduction
conduction delay (Aehlert, 2011). Most early studies were based on healthy young system. In this case, it carries a similar
commonly, the delay occurs within the men, and are not generalisable to a wider prognosis to Mobitz type-II (Bennett, 2013).
AV node; however, slow conduction population. Their study, which followed
through the atria or His-Purkinje system 7575 people over five decades, found that Mobitz type-II
may also be responsible (Vogler et al, individuals with first-degree AV block at Mobitz type-II is also a form of intermit-
2012). On the ECG, first-degree AV block baseline were twice as likely to develop tent heart block. Unlike type-I, however,
is characterised by prolongation of the atrial fibrillation, and three times as likely to there is no progressive slowing of conduc-
PR interval (Figure 6). In every other need permanent pacing. Mortality rates also tion prior to a dropped beat (Figure 8). In
respect, the rhythm is normal, and can eas- increased moderately (Cheng et al, 2009). conducted beats, the PR interval remains
ily be mistaken for normal sinus rhythm constant (Hampton, 2013). On the ECG,
(Houghton and Gray, 2014). The key ECG Second-degree AV block its key features are:
findings are therefore: In second-degree AV block, there is inter- w There are more P-waves than QRS com-
w A regular rhythm with a normal P-wave mittent conduction between the atria and plexes
in front of every QRS ventricles. In other words, some impulses w The PR interval does not change from
w A long PR interval (>200 milliseconds or are conducted through the electrical system beat to beat
5 small squares) successfully, while others fail to conduct. w Some P-waves are not followed by
w The PR interval is the same for every beat On the ECG, this results in some P-waves QRS complexes
w The QRS is narrow unless ventricular that are not followed by QRS complexes. w The rhythm is regularly irregular
conduction block is present (e.g. bundle Second-degree AV block is further subdi- w The QRS may be narrow, but is
branch block). vided into two distinct types according to often broad.

Complete heart block is the most alarm-

QRS QRS QRS QRS
ing of the AV blocks, and warrants imme-
diate assessment and treatment because of
the risk of haemodynamic compromise
and cardiac arrest (Pitcher and Nolan,
P P P P P P P
2015).
Causes and treatment

Figure 10. Third-degree AV block. Note the regular P-waves and QRS complexes. There As discussed, high vagal tone may account
is no association between them. The QRS is wide, and the rate slow. There is a P-wave for first-degree or Mobitz type-I AV blocks
buried in the third T-wave in younger, healthy people, in which case no
Mobitz type-II is usually a result of con- have no relationship with the QRS. In treatment is required. In older people, these
duction failure within the bundle branches, effect, there are two rhythms superim- lower level AV bocks may be owing to age-
and is a more sinister finding than Mobitz posed on each other; one from the sinus related degeneration of the conduction tis-
type-I. There is a significant risk that it will node, and one from the ventricles sues, or structural heart disease. Nonetheless,
progress to third-degree heart block (Hampton, 2013). P-waves may distort treatment is not generally necessary unless
(Vogler et al, 2012). T-waves or QRS complexes, or may be hid- significant bradycardia is documented, and
den by them. Mapping out the P-wave the patient is symptomatic (Bennett, 2013).
Second-degree 2:1 conduction rhythm with a piece of paper can be useful In the acute setting, first-degree heart block
Second-degree AV block may occur in a in predicting where P-waves should be. and Mobitz type-I can occur during myo-
pattern where every other beat is blocked, The key ECG features of complete heart cardial infarction (MI), in which case there
resulting in 2:1 conduction to the ventricles block are: is a risk of progression to higher degrees of
(Figure 9). So is this Mobitz type-I or Mobitz w P-waves are regular, but may be superim- block. These patients should be closely
type-II? It is impossible to say. The key fea- posed on the T-waves or QRS complexes monitored (Aehlert, 2011).
ture that separates the two types of second- w QRS complexes are also regular, and Mobitz type-II and complete heart block
degree AV block is the progressive length- occur at a slower rate than the P-waves are never benign findings. Both can cause
ening of the PR interval in type-I. In w There is no relationship between the significant bradycardia or result in sudden
2:1 block, we have only one PR interval to P-waves and the QRS complexes cardiac death as a result of asystole. As with
examine before conduction fails. Thus, we w The QRS may be narrow if the block is sick sinus syndrome, idiopathic degenera-
cannot say whether the PR interval is get- within the AV junction, but broad if it is tion of the conduction system is a common
ting longer (Aehlert, 2011). This leaves us lower down. cause, accounting for around 50% of cases
with a certain amount of prognostic uncer-
tainty. Bennett (2013) suggests that 2:1 block
with a broad QRS is likely to be type-II, and
should be treated as such. Further testing
(e.g. Holter monitoring) may be useful in
determining which type of block is present
(Vogler et al, 2012).
Third-degree (complete) AV block

Third-degree AV block is also referred to as
complete heart block. It occurs when there
is no conduction between the atria and
ventricles. Impulses arise in the sinus node
as normal, and are conducted through the
atria, creating regular P-waves on the ECG.
Every impulse is blocked in the conduction
system, however, and none arrive in the
ventricles. In most cases, a subsidiary pace-
maker below the block starts to fire, result-
ing in a slower ventricular escape rhythm.
The QRS complexes may be broad or nar-
row, depending on the level of the block,
and, therefore, the site of the subsidiary

pacemaker (Garcia, 2015).
On the ECG, third-degree heart block
appears as a regular rhythm (Figure 10).
There are regular P-waves; however, these Figure 11. Normal R-wave progression

Predominant direction of depolarisation

Box 2. Comparison of left- and right-bundle branch block
Right-bundle branch block Left-bundle branch block
QRS width >120 milliseconds >120 milliseconds
Right Left
V6
V1/V2 RSR pattern Deep S-waves
T-waves often inverted
V5 V6 Wide S-wave Tall, monophasic R-wave
V4 T-waves often inverted
V1 V2 V3
Transition complex
will return with recovery. Otherwise, a eral important concepts. Firstly, an electri-
pacemaker should be implanted without cal wavefront moving towards a lead cre-
delay, given the risk of collapse or sudden ates a positive ECG deflection, while one
death (Bennett, 2013). moving away creates a negative one.
Figure 12. R-wave progression in context Secondly, although the depolarisation wave
Bundle branch blocks travels through the heart in many direc-
(Vogler et al, 2012). Rarely, AV blocks A bundle branch block occurs when con- tions, the largest wavefront will dominate
occur as an isolated congenital abnormali- duction through either the left- or right- the ECG, and dictate the orientation of the
ty, but more often, are found in association bundle branch fails entirely. Because con- ECG complexes. The left ventricle has
with congenital heart disease or acquired duction continues normally in the other much thicker walls than the right, and
disorders such as coronary heart disease, branch, every impulse from the atria is con- therefore generates more electricity. The
endocarditis and cardiac surgery (Tunaoglu ducted to the ventricles. Thus, unlike the predominant direction of the depolarisa-
et al, 2010). Drugs that alter cardiac con- AV blocks, bundle branch blocks do not tion wave is therefore towards the left,
duction (e.g. beta-blockers) may also pre- cause a change in heart rhythm (Houghton away from V1 and towards V6, as shown in
cipitate heart blocks, as may electrolyte and Gray, 2014). To understand how they Figure 12 (Hampton, 2013).
disturbances and hypoxia (Fogoros, 2007). affect the appearance of the 12-lead ECG,
AV blocks are also a common complication we need to think about conduction through Abnormal ventricular
of MI (Hreybe and Saba, 2009). the ventricles, and how this creates the nor- depolarisation
In the acute setting, any patient with mal pattern of QRS complexes in the pre- In bundle branch blocks, only one ventricle
second- or third-degree AV block should cordial leads. is depolarised normally. The other ventri-
be assessed using an A-to-E approach and cle has to wait for the electrical impulse to
placed under regular observation with R-wave progression spread across from the other side of the
continuous ECG monitoring. A 12-lead In the normal conduction system, the elec- heart, through the muscle cells. This is
ECG should be recorded (Swift, 2013). trical impulse is rapidly conducted to every much slower than depolarisation via a nor-
Severe bradycardia is possible, which can part of both ventricles by the bundle mal conduction system, and hence the
cause significant haemodynamic compro- branches and extensive network of Purkinje QRS complex widens. This abnormal depo-
mise. Initial treatment in this case is atro- fibres. This results in efficient distribution larisation also changes the normal pattern
pine, given intravenously in 500 micro- of the electrical impulse, and a narrow QRS of QRS complexes on the ECG, most obvi-
gram doses, and repeated every 3–5 min- complex (Klabunde, 2012). It also creates a ously in the precordial leads (Bennett,
utes to a maximum of 3 grams (Pitcher and particular pattern of QRS complexes that 2013).
Nolan, 2015). If atropine fails to increase we associate with a normal 12-lead ECG. Figure 13 shows a typical example of
the heart rate, temporary pacing should be Let’s look at this normal pattern in the pre- right-bundle branch block (RBBB). The
initiated. Transcutaneous pacing may be cordial leads. first thing to note is the width of the
tried initially, although it is not always suc- Figure 11 shows leads V1 to V6 from a QRS complex. This is around 140 millisec-
cessful and is painful for the patient (Swift, normal 12-lead ECG. You can see that V1 onds, or three and a half small squares.
2013). A temporary transvenous pacing has a small initial upward deflection (an In QRS width, small differences are impor-
wire, placed via the femoral, brachial or R-wave) followed by a deep downward tant so this is abnormally wide. If we look
jugular vein, is a more reliable alternative, deflection (an S-wave). As we move across at the precordial leads, we can see that the
but insertion requires advanced skills that the precordium towards V6, the R-wave R-wave progression is also abnormal, with
are not available in every practice setting gradually grows in size, usually reaching its a very tall R-wave in V1 and V2. The QRS
(Sharma et al, 2012; McNaughton, 2013). greatest height by V5. In contrast, the complex in these leads has an RSR pattern,
Transfer to a more specialised setting may S-wave gradually diminishes in size. This which is sometimes described as M-shaped,
be necessary. normal pattern is referred to as ‘R-wave or like rabbit ears (Aehlert, 2011). The QRS
In the longer term, patients who remain progression’. The ‘transition’ point at which goes upward (R-wave), then drops back
in Mobitz type-II or third-degree AV block the R-wave exceeds the S-wave is usually (S-wave) before climbing again (another
will need permanent pacing. This may be between V3 and V4 (Garcia, 2015). R-wave). If we look across at the left-sided
delayed in acute conditions, such as MI, if To understand why the QRS complexes precordial leads, and particularly at V6, we
there is a chance that normal conduction change this way, we need to consider sev- see a wide S-wave following the R-wave.

Figure 13. Right-bundle branch block. Note the RSR in V1/V2, and wide S-wave in V6. The QRS is broad
Figure 14. Left-bundle branch block. Note the deep S-waves in V1–V3, and notched, monophasic R-wave in V6. The QRS is broad
Both the RSR in V1 and/or V2, and the transition to a positive QRS in the left-sided Marrow, with its two Rs in the middle, is
wide S-wave in V6, are characteristic fea- precordial leads. The upright QRS complexes RBBB. The M is the RSR in V1, and the W
tures of RBBB (Surawicz et al, 2009). The in V5 and V6 are short, stumpy, and notched. at the end is the wide S-wave in V6
final thing to note is the T-wave inversion These are typical findings in LBBB (Kumar et (Houghton and Gray, 2014).
in the right precordials (V1 to V3). T-wave al, 2013). If you look at the QRS in V6, you
inversion, and ST-segment abnormalities, can see that the QRS is also monophasic—it Causes and treatment
are also common features of bundle branch is all R-wave, with no preceding Q-wave. The The left-bundle branch is a much more
blocks (Garcia, 2015). upright QRS complexes in the left precordials extensive structure than the right, and
Figure 14 shows left-bundle branch block also have inverted T-waves. These are also receives a blood supply from both the left
(LBBB). The QRS is again wide, and in this common findings (Garcia, 2015). Box 2 com- and right coronary arteries (Josephson
example is over 170 milliseconds (more than pares the principal features of left- and right- 2010). Although LBBB may be caused by
four small squares). Superficially, the R-wave bundle branch block. age-related degeneration of the conduction
progression appears more normal than in Some people find the mnemonic system, more often, it results from disease
RBBB. We start out with a small R-wave and ‘William Marrow’ helpful in remembering processes affecting the left ventricle. These
deep S-wave in V1 as you would expect; how- bundle branch blocks. William has two Ls include hypertension, valvular heart dis-
ever, there is no growth of the R-wave as we in the middle, and represents LBBB. The W ease, cardiomyopathy, myocarditis and
move through V2 and V3, and the S-waves is the wide, deep S-wave in V1, and the M coronary heart disease (Kumar et al 2012).
remain deep and wide. There is a sudden is the stumpy and notched R-wave in V6. Any patient presenting with previously

complicated by LBBB, often derive symp-

Key Points tomatic benefit from cardiac resynchroni-
sation therapy. In this treatment, a biven-
w Conduction blocks can occur in all parts of the conduction system, causing a
variety of ECG changes. They may be congenital, acquired, idiopathic or
tricular pacemaker is implanted so that
physiological. Age-related degeneration of the conduction system, and coronary
both ventricles can be paced simultane-
heart disease, are common causes
ously (National Institute for Health and
Care Excellence (NICE), 2014).
w Sinoatrial block occurs when the electrical impulse is unable to leave the sinus The right-bundle branch is a long, slen-
node. It results in a pause on the ECG, and is often found in conjunction with der structure, with a blood supply from
other features of sick sinus syndrome. A permanent pacemaker is required in the left coronary artery only. It is more
symptomatic patients prone to damage than the left-bundle
w Atrioventricular (AV) blocks occur when the impulse is delayed or blocked in the branch, and thus, RBBB is a more com-
AV node, bundle of His or bundle branches. It may be first-, second- or third- mon finding on the ECG (Josephson,
degree in nature, depending on whether the electrical impulse is delayed, 2010). Pathological causes of RBBB
intermittently blocked, or always blocked include coronary heart disease, congenital
heart disease (especially Ebstein’s anoma-
w First-degree, and Mobitz type-I AV blocks may be benign, especially in younger ly and atrial septal defect), and pulmo-
people and at night. In older people, they are more often pathological and, in nary embolus (Houghton and Gray, 2014).
the acutely unwell person, can rapidly progress to higher degrees of block Unlike LBBB, RBBB is also found in oth-
w Mobitz type-II and third-degree AV block are associated with bradycardia and erwise normal hearts, in which case it is
asystole, and may cause haemodynamic compromise or cardiac arrest. often considered a benign finding
Systematic patient assessment is essential, followed by emergency treatment if (Bennett, 2013).
necessary. This may include atropine and/or temporary pacing. In the longer A recent study has suggested that this is
term, permanent pacing is often required not always the case. Bussink et al (2013)
demonstrated a 30% increase in mortality
w Bundle branch blocks do not affect heart rate or rhythm, but are often markers in people with RBBB but no known heart
of underlying heart disease, especially in left bundle branch block (LBBB). LBBB disease at initial evaluation. The increase
may also indicate acute myocardial infarction, requiring primary percutaneous in mortality was attributed to the later
coronary intervention. In heart failure, LBBB may cause mechanical development of cardiovascular disease,
dyssynchrony, which can be treated with resynchronisation therapy suggesting that RBBB may be an early
marker of disease in some individuals.
unknown LBBB should therefore be evalu- the most widely evaluated (Sgarbossa et al, Incomplete bundle branch block
ated for an underlying cause. Unlike 1996). Unfortunately, although this criteria In incomplete bundle branch block, con-
AV blocks, bundle branch blocks do not has a high specificity, its sensitivity is low, duction down one bundle branch is delayed
cause bradycardia or asystole, so do not meaning that patients who are in fact hav- but not completely blocked (Houghton and
generally require emergency treatment. ing an infarct may be missed (Tabas et al, Gray, 2014). This results in the characteris-
There are, however, a number of clinical 2008). As a result, current guidelines do tic features of RBBB or LBBB, but the QRS
scenarios in which LBBB influences treat- not suggest its use, and instead recom- complex remains relatively narrow at
ment. The first of these is suspected MI. mend prompt percutaneous coronary between 100 and 120 milliseconds
The ECG is an important tool in the intervention (PCI) in any patient who (Surawicz et al, 2009). Houghton and Gray
assessment of patients presenting with a presents with new LBBB and a history con- (2014) suggest that the causes of incom-
history of chest pain. Abnormalities in the sistent with acute MI (Steg et al, 2012). plete bundle branch block are the same as
T-waves and ST segments are suggestive of The second situation in which LBBB has those of complete bundle branch block.
ischaemia, and are diagnostic in ST eleva- particular clinical relevance is heart fail- Bussink et al (2013), however, suggest that
tion MI (Steg et al, 2012). These changes ure. Delayed depolarisation of the left incomplete right-bundle branch block is
may be masked by the ST and T-wave ventricle results in mechanical dyssyn- usually benign. It was not associated with
abnormalities that normally occur in LBBB chrony. In other words, the right ventricle increased mortality in their study.
(Bennett, 2013). In a patient with chest contracts before the left. This reduces the
pain and LBBB, it is often unclear whether efficiency of the heart, and lowers cardiac Conclusion
ECG changes are a result of ischaemia, or output (Kumar et al, 2013). In people with Both congenital and acquired disease can
simply the result of conduction block, and well-preserved ventricular function, this cause abnormalities in cardiac conduction,
in clinical practice, less than half of these has limited significance. In patients with leading to conduction blocks. In some
patients are found to have an occluded heart failure and poor ejection fraction, it cases, they also occur in the absence of
coronary artery (Jain et al, 2011; Kontos et can cause a critical decline in pump func- identifiable disease. Block may occur in the
al, 2011). Various criteria to differentiate tion, and increased symptoms sinus node, AV junction or bundle branch-
normal LBBB from ischaemic LBBB have (O’Donovan, 2009). People with heart es, resulting in a range of ECG abnormali-
been suggested, of which the Sgarbossa is failure and reduced ejection fraction, ties. Careful evaluation of both heart

rhythm, and QRS morphology across the

precordium, is necessary for their identifi- BHF Resources
cation. Some blocks, such as first-degree
AV block, are relatively benign, while oth- The British Heart Foundation (BHF) is committed to sharing our knowledge to
ers have the potential to cause severe prevent heart disease devastating people’s lives. Visit bhf.org.uk where you’ll
haemodynamic compromise or cardiac find a wide range of resources that you can use to support people with a heart
arrest. Systematic clinical assessment, and or circulatory conditions, including:
appropriate monitoring, are therefore just w A wealth of online information about cardiac arrhythmias, including AV heart
as important as skills in ECG interpreta- blocks
tion. Nurses must also have a working w Short animations explaining some common abnormal heart rhythms such as:
knowledge of the emergency treatment of w Atrial fibrillation
bradycardia to care for these patients safely. w Atrial flutter
For practitioners working in autonomous w Second-degree AV heart block (Mobitz II)
roles, recognising the relationship between w Complete heart block
conduction blocks and heart disease is also
w Information booklets for patients and their families including our Heart
important from a screening standpoint.
rhythms booklet, and videos explaining common cardiac tests and treatments.
This article concludes our review of the
first step in ECG interpretation; the evalu-
ation of rate, rhythm and intervals. We will The BHF Alliance is a free membership scheme that supports professionals
be returning to bundle branch blocks in working with people affected by, or at risk of developing, cardiovascular disease.
2 months’ time, when we discuss the car- Join today at bhf.org.uk/alliance
diac axis and hemiblocks. Next month, we
turn our attention to the next step in our
system of interpretation; evaluating the
ECG for signs of pre-excitation. BJCN BHF Doctor’s comment
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Part 6: QRS axis
and Social Care, London South Bank University, and BHF Alliance member, London
E
lectrical activity in the heart is the 12-lead ECG; however, the most impor- toy gun. The force propelling the dart can
created by the depolarisation of tant is the QRS axis, representing the net be described as a vector—it has direction
individual myocytes (Klabunde, direction of depolarisation within the ven- and magnitude. Now imagine firing a real
2012). The electrical impulse created moves tricles (Hampton, 2013). gun in the same direction. Again, there is a
through the atria before passing into the The QRS axis provides important diag- vector but, in this case, the magnitude is
specialised conduction system and entering nostic information about the flow of elec- much greater. These two vectors could be
the ventricles, where it is distributed to tricity through the ventricles, and is useful represented by two arrows, one short and
both chambers rapidly and efficiently in diagnosing abnormalities in both the one long, as shown in Figure 1.
(Pappano and Wier, 2013). We tend to structure and electrical function of the In many situations, the forces acting on
think of this process as being linear, and heart (Garcia, 2015). Despite its usefulness, objects move in different directions
two-dimensional, because this is how it is it is often considered a difficult subject in (Shankar, 2014). If you’ve ever watched a
depicted in textbooks. In reality, the heart ECG interpretation, and one that students tug-of-war, you will have seen two oppos-
is a three-dimensional structure, and waves struggle to grasp (Davies, 2007; Houghton ing vectors. The two teams are pulling in
of depolarisation are moving in many and Gray, 2014). This difficulty may be opposite directions, and whichever is
directions simultaneously as electrical compounded by a plethora of methods strongest defines the direction that the
activity spreads through the walls of the suggested for axis evaluation, and by a lack rope travels in (Figure 2). If the two teams
heart (Garcia, 2015). of conformity in the literature about where (vectors) are of equal strength (magni-
An electrical axis is the net direction in the normal axis lies, and what causes it to tude), they cancel each other out, and the
which depolarising waves are moving; in be abnormal. rope remains static. The same principles
other words, the predominant direction In this sixth article of the British Journal apply to waves of depolarisation in the
when all the waveforms are added together of Cardiac Nursing ECG Interpretation heart, which can also be described in terms
(Davies, 2007). Electrical axis can be calcu- series, we hope to shed some light on these of vectors (Garcia, 2015). During ventricu-
lated for all the waveforms and intervals on issues, and to describe the QRS axis in lar depolarisation, these vectors are mov-
terms that readers can understand. We will ing in many directions; for example,
present the currently accepted definitions through the anterior and posterior walls of
of both normal and abnormal axis, as both the right and left ventricles. If we add
defined by internationally agreed practice all of these vectors together, the net direc-
guidelines. We will also explain how to tion is the QRS axis (Kuhn and Rose,
evaluate axis on the 12-lead ECG, using 2008). In adults, this travels downward and
simple methods that are appropriate to the toward the left as shown in Figure 3 . This is
Figure 1. The arrow representing the bullet clinical setting. Finally, we will examine the because the vectors produced by the thick-
is longer because the force driving it has most common cause of axis deviation, the er-walled left ventricle outweigh those pro-
much greater magnitude than the plastic fascicular blocks. duced by the right (Aehlert, 2011).
dart
Vectors Defining normal QRS axis
To understand electrical axis, it’s useful to QRS axis refers to ventricular depolarisa-
start with the concept of vectors. A vector tion as seen in a frontal plane; in other
is a mathematical concept used to describe words, from the perspective of the limb
a force that has both direction and magni- leads (Houghton and Gray, 2014). It is
tude (Garcia, 2015). Vectors are usually therefore these leads that are used to evalu-
Figure 2. Both teams are pulling hard, but represented by arrows—with the length of ate it. Some authors describe QRS axis as
the team pulling to the left (vector 1) is the arrow representing magnitude, and the the ‘mean frontal QRS axis’, which makes
stronger (has greater magnitude). When direction demonstrating the direction in this more explicit (Davies, 2007).
the two vectors are added, the result is a which the force is moving (Aehlert, 2011). To evaluate QRS axis, the limb leads are
small vector moving to the left Imagine firing a plastic dart from a child’s placed in the hexaxial reference system
180 British Journal of Cardiac Nursing April 2016 Vol 11 No 4

©Peter Lamb
(Burns, 2014) (Figure 4 ). This system plac-
es the limb leads in a circle surrounding
the heart, according to their electrical
viewpoint. The position of each lead is
measured in degrees, relative to lead I,
which is at 0˚ (Hampton, 2013). Leads in
the lower half of the circle are calculated in
positive degrees moving clockwise from
lead I, while leads in the upper half of the
circle are measured in negative degrees,
moving anticlockwise from the same start-
ing position (Garcia, 2015).
In adults, a variety of ranges for normal
QRS axis have been proposed; however, the
current standard is -30 to +90˚ (Surawicz et
al, 2009). An axis that falls outside of this
range is referred to as axis deviation
(Davies, 2007). Left-axis deviation (LAD)
is from -30 to -90˚, while right-axis devia-
tion (RAD) is from +90 to 180˚ (Surawicz
et al, 2009). Extreme axis deviation, from
-90 to 180˚, is also referred to as ‘no-man’s
land’ or a ‘northwest axis’ (Davies, 2007;
Burns, 2014). Rarely, it is not possible to
determine the QRS axis, in which case it is
described as ‘indeterminate’ (Kilicaslan et
al, 2007).
Axis deviation
The QRS axis is dependent on a number of Figure 3. The normal QRS axis in adults is downward and towards the left
factors including age and body shape, the
size of the ventricles, the route taken by the
electrical impulse, and the placement of −90o
the limb leads (Davies, 2007). This results
in considerable variation in what is consid-
ered normal, as well as the potential for a
range of abnormal findings (Burns, 2014). −150o −30o
In children, the QRS axis is further to the Extreme axis Left axis
right, and moves leftward during growth to aVR deviation deviation aVL
adulthood (Surawicz et al, 2009). A more
rightward axis is also common in tall, thin
individuals in whom the heart is orientated
more vertically in the chest (Davies, 2007). 180o I 0o
RAD may be a normal variant in people with
this body shape. In contrast, when the body
is shorter and wider, the heart may be tilted Right axis Normal
to a more horizontal position, resulting in a deviation axis
more leftward axis (Kuhn and Rose, 2008).
Conditions that increase the size of the abdo-
men, such as ascites or pregnancy, may push
the heart into a more horizontal position, III II
resulting in LAD (Adamson and Nelson- aVF
Piercy, 2007; Goloba et al, 2010).
+120o +60o
Alteration in the relative size of the ventri-
cles also has the potential to alter QRS axis +90o
(Hampton, 2013). In left-ventricular (LV)
hypertrophy, thickening of the LV wall Figure 4. The hexaxial reference system. Note that the position of each limb lead is calcu-
increases the magnitude of depolarising vec- lated according to its position relative to lead I, which is at zero degrees
British Journal of Cardiac Nursing April 2016 Vol 11 No 4 181

This is not seen in limb lead misplacement,

Table 1. Possible causes of axis deviation in adults
which can be confirmed simply by repeat-
Left-axis deviation Right-axis deviation ing the ECG and ensuring the leads are
Left-anterior fascicular block Left-posterior fascicular block placed on the correct limbs (Eldridge and
Inferior myocardial infarction Anterolateral myocardial infarction Richley, 2014).
Left-ventricular hypertrophy Right-ventricular hypertrophy Table 1 lists the more commonly cited
causes of right- and left-axis deviation
Left-bundle branch block Right-bundle branch block
(Davies, 2007; Kuhn and Rose, 2008;
Ventricular pacing Pulmonary embolism Aehlert, 2011; Burns, 2014; Houghton and
Pre-excitation Pre-excitation Gray, 2014 ; Garcia 2015).
Ventricular arrhythmias Ventricular arrhythmias
Pregnancy, ascites or abdominal tumour Dextrocardia Evaluating QRS axis
Before we discuss evaluation of the QRS
Short, squat body shape Tall, thin body shape
axis, we need to reiterate an important
Hyperkalaemia Normal in children and adolescents principle in ECG interpretation concerning
the orientation of waveforms. This principle
tors moving towards the left (Hancock et al, Electrical activation of the ventricles has states that a wave of depolarisation moving
2009). This moves the mean QRS axis to the perhaps the greatest effect on QRS axis towards an ECG lead creates a positive
left, and can result in LAD. The same phe- (Bennett, 2013). We know from our discus- (upward) deflection, while one moving
nomenon is possible in the case of right- sions of bundle branch blocks and pre- away creates a negative (downward) one
ventricular enlargement, in which case the excitation that abnormalities in conduction (Garcia, 2015). We can add to this principle
axis shifts to the right (Josephson, 2010). can alter the pattern of depolarisation in the as follows:
Loss of functioning muscle, for example as a ventricles (Sampson, 2016a; 2016b). These w Many QRS complexes have both positive
result of myocardial infarction, can have the abnormalities can also alter the QRS axis, and negative components. This indicates
opposite effect, shifting the axis away from although Garcia (2015) suggests that this that the depolarising wave is moving at
the damaged area of the heart (Kuhn and rarely occurs, owing to bundle branch an angle to the lead, rather than directly
Rose, 2008). block. In addition, there are two electrical towards or away from it (Davies, 2007)
abnormalities that result in marked axis w When the positive part is larger than the
deviation. The first is a block in one fascicle negative part, the depolarising wave is
of the left bundle branch (Burns, 2014). moving more towards the lead than away
Fascicular blocks are a common and clini- from it. The QRS is described as positive
cally important cause of axis deviation, and (Hampton, 2013)
are discussed further in this article. The w The opposite applies if the negative part is
second is abnormal activation of the ventri- larger (Hampton, 2013)
cles during ventricular arrhythmias (Garcia, w If a QRS complex has positive and nega-
2015). Ventricular tachycardia (VT) can tive parts that are equal, the depolarising
Figure 5. Positive, negative, and isoelectric cause extreme-axis deviation, which is oth- wave is moving at 90˚ to the lead. The
QRS complexes erwise rarely seen (Davies, 2007). QRS complex is described as isoelectric,
Evaluation of QRS axis can therefore be or equiphasic (Garcia, 2015).
useful in distinguishing between VT and
supraventricular tachycardia with aberrant
conduction (Bennett, 2013).
Finally, misplacement of the limb leads
can radically alter the axis, and has the
potential to cause misdiagnosis (Crawford
Top Top
and Doherty, 2008). Most commonly, the left right
arm electrodes are transposed, resulting in
an ECG that suggests right or extreme-axis I
deviation (Harrigan et al, 2012). Careful Bottom Bottom
evaluation of the ECG, however, will dem- left right
onstrate other abnormal features such as
Figure 6. The top left corner of a typical inverted P-waves in lead I, and an upright
12-lead ECG. The machine’s calculations QRS in aVR. It should be noted that similar
can be seen at the top right, and include changes are seen on the ECGs of people
ventricular rate, PR interval and so on. At with dextrocardia (Uchenna et al, 2012). In aVF
the bottom of the list are P-R-T axes. R is this condition, however, the location of the
the QRS axis, which in this case is 48 heart in the right side of the chest also Figure 7. Leads I and aVF can be used to
degrees, and therefore normal results in abnormal R-wave progression. divide the hexaxial system into quadrants

−90o −90o
−150o −150o
−30o −30o I I
aVF aVF
180o I 0o 180o 0o I
I I
aVF aVF
+120o +60o +120o +60o

+90o aVF
+90o aVF
Figure 8. Red arrows indicate an axis moving towards the lead, grey arrows an axis Figure 9. Using leads I and aVF, we can
moving away. When lead I is positive, the axis falls within the right half of the hexaxial place the axis in one quadrant of the hex-
system. When it is negative, the axis is in the left half. Lead aVF divides the system into axial system. This is enough to identify
upper and lower halves in the same way right and extreme axis deviation
These different ECG appearances are illus- This can be done using a quadrant-based tive QRS places it in the left half (Garcia,
trated in Figure 5 . system, or by evaluating the most isoelec- 2015) (Figure 8 ).
So how does this help us with QRS axis? tric limb lead (Garcia, 2015). Next, let’s think about lead aVF. If
Axis cannot be measured directly so it must lead aVF is positive, the axis must be trav-
be inferred from the polarity of the QRS Quadrant approach elling towards +90˚, or within 90˚ either
complexes in the limb leads (Davies, 2007). If we look at the hexaxial system, we can side (Houghton and Gray, 2014) (Figure 8 ).
In other words, by comparing which leads see that lead I sits at the horizontal axis of This locates the axis in the bottom half of
are positive and which negative, we can use the system, and lead aVF at the vertical our hexaxial system (Garcia, 2015). If aVF
logic to work out where the axis lies. Most (Hampton, 2013). If we draw a line across is negative, the axis must be in the top half.
ECG machines perform this calculation, from each of these leads, it divides the sys- As you can see, examination of these two
and display the QRS axis at the top of the tem into four quadrants (Figure 7 ). By leads effectively places the axis within one
print out (Figure 6). In the vast majority of examining the QRS complex in leads I and quadrant of the hexaxial system (Figure 9 ).
cases, this is the most accurate way of deter- aVF, and deciding if it is positive or nega- This is sufficient to determine both right-
mining the axis (Spodick et al, 2008). ECG tive, we can place the QRS axis in one of axis deviation (QRS is positive in aVF but
machines are not infallible, however, and these quadrants. This is the first step in the negative in lead I) and extreme-axis devia-
some machines may not calculate the axis quadrant approach (Garcia, 2015). tion (both lead I and aVF are negative)
(Kuhn and Rose, 2008). Practitioners must So, how does this work? Let’s think about (Davies, 2007). So how about a normal axis
therefore be able to calculate axis manually. lead I, and go back to our first principles. versus left-axis deviation?
Use Figure 4 to remind yourself about lead The difficulty here is that the normal axis
−90o positions as we go along. A wave of depo- occupies more than one quadrant (Garcia,
larisation moving towards 0˚ will create an 2015). If you look at Figure 4 , you can see
entirely upright QRS in lead I (Davies, that the normal axis is between -30 and
−150o
−30o 2007). Either side of zero, the QRS will still +90˚ (Surawicz et al, 2009). There is there-
be more positive than negative (or isoelec- fore a thin wedge of normal axis, between
tric) if the axis is as far left as -90˚, or as far 0 and -30˚, that lies in the upper right
180o 0o right as +90˚ (Garcia, 2015). So, a positive quadrant. If both lead I and aVF are posi-
QRS in lead I locates the axis in the right tive, we know that the axis lies in the bot-
half of our hexaxial system, while a nega- tom right quadrant, and the axis is normal
+120o Table 2. Polarity of leads in each type of axis

II
+90o +60o
(+ = positive, - = negative)
Lead I Lead aVF Lead II
Figure 10. Lead II divides the hexaxial sys- Normal axis + + or − +
tem along a line running from -30 to +150 Left-axis deviation + − −
degrees. If the QRS is positive in lead II,
Right-axis deviation − + + or −
the axis must fall in the bottom half. If lead
I is also positive, the axis is normal Extreme-axis deviation − − −

Now, you might be thinking that this

seems deceptively simple, in which case
you would be right. In many cases, there is
no isoelectric limb lead (Burns, 2014). If
this is the case, we have to make a small
adjustment to our method. Firstly, we
select the limb lead that is closest to isoe-
lectric, or if none are biphasic, the one with
the smallest amplitude (the least tall)
(Garcia, 2015). Let’s look at another exam-
ple in Figure 13 .
Let’s start with quadrants again. Lead I is
positive and aVF is negative. This puts the
axis in the top right quadrant (Burns,
2014). Lead II is negative, so the axis is
between -30 and -90˚, meaning there is
LAD (Surawicz et al, 2009). Can we locate
the axis more exactly using an isoelectric
lead? There are no biphasic leads, they are
all completely positive, or completely nega-
tive. Therefore, we choose the smallest
amplitude, which is lead II. Lead II sits at
+60˚, so the axis must near to -30˚ or +150˚.
Figure 11. Using the isoelectric lead to locate the axis Clearly it is -30˚, because we have placed
the axis in the upper right quadrant. Is the
(Davies, 2007). But what about when lead I of the most isoelectric limb lead. Using this axis at -30˚ exactly? No, because lead II is
is positive, and aVF is negative? This places system, the QRS axis can be located to negative, not isoelectric. Garcia (2015)
the axis in the top right quadrant, and the within 10˚ (Garcia, 2015). suggests that when the smallest, or most
axis could either be normal (i.e. between 0 If you think back to the principles that biphasic lead, is not isoelectric, the axis lies
and -30˚), or there could be left-axis devia- we established earlier on, you might either just beyond, or just before 90˚. By
tion (Burns, 2014). To determine which remember that when a wave of depolarisa- adding or subtracting 10 or 20˚, depending
possibility is correct, we need to examine tion is travelling at 90˚ to an ECG lead, that on how far the lead is from isoelectric, we
lead II. lead will be isoelectric (Garcia, 2015). This can place the axis to within 10˚, as shown
Lead II sits at +60˚, and therefore divides principle can be applied to the cardiac axis. in Table 3 .
the hexaxial system along a line running If we locate an isoelectric limb lead, the In the case of Figure 13 , the QRS in
from -30 to +150˚ (Houghton and Gray, axis will be at 90˚ to that lead. This gives us lead II is entirely negative, suggesting that
2014) (Figure 10 ). In a normal axis, lead II two possible answers, in other words, 90˚ to the axis is between 100 and 110˚ from the
must therefore be positive. We can state the left, or 90˚ to the right (Burns, 2014). If
that when both leads I and II are positive, we already know which quadrant the axis
the axis is normal (Rose and Kuhn, 2009). lies in, we know which of the two possible −150o
When lead I is positive, but lead II is nega- answers is correct (Davies, 2007). This will
Top Top
tive, there is LAD (Burns, 2014). be clearer with an example, so let’s look at left right
Hopefully this makes sense—but if you the ECG in Figure 11. For clarity, we have
are struggling to understand the logic of cut away everything except the limb leads.
axis determination, don’t despair. Simply First, let’s locate the axis using the quad-
learning which leads are positive or nega- rant system. Both I and aVF are positive, so
Bottom
tive in each type of axis will get you by in the axis lies in the bottom right quadrant left
clinical practice. These are summarised in (Garcia, 2015). This is a normal axis, but
Table 2. You may well find that with prac- where is it exactly? By examining each limb Bottom
tice, your understanding improves, and lead, we can see that lead III is isoelectric right
III
you are able to work out the axis from first —its QRS has equally positive and negative +30o
principles. parts. The axis must therefore lie at 90˚ to +120o
that lead. Lead III sits at +120˚, so 90˚ to
Isoelectric lead approach that lead is either +30˚ or -150˚ (Figure 12). Figure 12. If lead III is isoelectric, the axis
This approach can be used to determine It can’t be -150˚ because we know that the must lie at 90 degrees to it. This is either
the axis more accurately, and builds on the axis is in the bottom right quadrant, so the +30 or -150 degrees. Using the quadrant
logic of the quadrant approach (Davies, axis is +30˚. The ECG machine calculated approach tells us which one it is, in this
2007). Its key component is identification this axis as +37˚, so we are within 10˚. case +30 degrees

lead. This places the axis between -40 and

-50˚, well within LAD territory. In fact, the
ECG machine calculated this axis as -41˚.
So why does this patient have LAD? If we
look carefully, we can see that there is a
short PR interval, a broad QRS, and a delta
wave. The patient has pre-excitation owing
to an accessory pathway (Mark et al, 2009).
Clinical relevance of QRS axis

The final topic that we need to consider is
the use of QRS axis in clinical practice.
Table 1 lists some of the more common
causes of axis deviation, but leaves unan-
swered the question of how we distinguish
between them. In some instances, such as
our patient with pre-excitation, systematic
evaluation of the ECG alone can provide a
diagnosis (Houghton and Gray, 2014).
More commonly, however, ECG findings
must be correlated with patient history,
physical examination, and other diagnostic
tests (McGee, 2009). It is often these other
tests, rather than the ECG, that confirm the
cause of axis deviation. A good example of
this is the use of echocardiography to con-
firm left-ventricular hypertrophy
(Oxborough, 2008). Figure 13. When there is no isoelectric lead, select the smallest lead.
This lack of direct relationship between
the QRS axis and a diagnosis is often a interconnected pathways that supply the more robust, and is supplied with blood
cause of concern for students. If the QRS various aspects of the LV and septum from two coronary arteries (Rose and
axis doesn’t tell us what’s wrong with the (Houghton and Gray, 2014). For functional Kuhn, 2009). It travels inferiorly down the
patient, they ask, what is the point of learn- purposes, these pathways are considered back of the LV, carrying depolarisation into
ing (sometimes painfully) how to work it two distinct sub-branches, or fascicles; the the posterior and inferior walls. There are
out? The answer is that QRS axis provides left anterior fascicle, and left posterior fas- multiple anastomoses between the two
important supporting evidence for many cicle (Kumar et al, 2013). fascicles, which means that they are con-
conditions, and may be the first clue that The anterior fascicle is a relatively thin nected electrically into one larger system
suggests a diagnosis (Kuhn and Rose, structure that runs down the front of the (Kumar et al, 2013).
2008). Perhaps more importantly, if all heart, activating the anterolateral walls of Fascicular block, also known as hemiblock,
other causes of axis deviation have been the LV (Josephson, 2010). Its blood supply occurs when one fascicle is diseased, and fails
excluded, a diagnosis of fascicular block comes from a single coronary artery. In to conduct the electrical impulse (Houghton
may be made (Bennett, 2013). These blocks contrast, the posterior fascicle is broader, and Gray, 2014). Depolarisation occurs nor-
have important diagnostic, and prognostic
value, that makes their identification alone Table 3. Locating the axis using the most isoelectric, or small-
a reason to understand the QRS axis. est, limb lead
QRS morphology in smallest/most Approximate location of axis
Fascicular blocks biphasic lead
In this series of articles, we have, until now,
described the left-bundle branch as a single Positive part at least twice the size of 70˚ to the lead
entity. This is a common simplification, negative part
and we now need to move beyond it. Many Positive part larger, but less than twice 80˚ to the lead
people may be familiar with the idea that the size of negative part
the His bundle divides within the interven- Isoelectric (equally positive and negative) 90˚ to the lead
tricular septum to form the left and right
Negative part larger, but less than twice 100˚ to the lead
bundle branches (Sampson and McGrath,
the size of positive part
2015). It is less widely appreciated that the
left bundle branch subdivides soon after it Negative part at least twice the size of 110˚ to the lead
leaves the His bundle, forming a number of positive part

quent study of a large, primary care popula-

Table 4. ECG features of fascicular blocks
tion failed to find any relationship between
Left-anterior fascicular block Left-posterior fascicular block LAFB and CVD (Nielsen et al, 2014).
QRS axis between -45 and -90˚ QRS axis between +90 and 180˚ The second important aspect is that fas-
cicular blocks may be discovered in asso-
qR pattern in lead aVL rS pattern in leads I and aVL
ciation with disease in other parts of the
R-peak time in lead aVL of 45 ms or more qR pattern in leads III and aVF distal conduction system. This indicates
not only a greater degree of damaged con-
QSR duration less than 120 ms QRS duration less than 120 ms
duction tissue, but also a higher risk of
Source: Surawicz et al, 2009 progression to complete heart block
(Houghton and Gray, 2014). If, for exam-
mally in the other fascicle, and spreads across (Vogler et al, 2012). While this may be ple, fascicular block is found in association
to the affected side of the heart via the anas- caused by age-related degeneration of the with right-bundle branch block, the impli-
tomoses between the fascicles. This alters the conduction tissues, it may also result from cation is that two out of three conduction
net direction of depolarisation, and therefore structural heart diseases such as coronary pathways to the ventricles are blocked.
the QRS axis (Rose and Kuhn, 2009). In left- heart disease (Chow et al, 2012). It seems This is commonly referred to as a ‘bifas-
anterior fascicular block (LAFB), left axis logical that people newly diagnosed with cicular block’ (Swift, 2013).
deviation is seen. In contrast, left-posterior fascicular block should undergo screening Even more alarming is a finding of right
fascicular block (LPFB) causes right-axis for underlying cardiovascular disease bundle branch block, fascicular block, and
deviation (Hampton, 2013). Various other (CVD). This is certainly so in the case of first-degree atrioventricular (AV) block.
ECG features are associated with fascicular LPFB, which is rare, and suggests a greater This implies that there is disease, and
blocks, and these are listed in Table 4 . degree of myocardial damage given the impaired conduction, in the one function-
Several points are worth noting. Firstly, robust nature of the posterior fascicle, and ing fascicle, and is commonly, if inaccu-
although fascicular blocks delay ventricu- its dual blood supply (Bennett, 2013). rately, referred to as ‘trifascicular block’(Rose
lar depolarisation slightly, the QRS does The need for screening in the case of and Kuhn, 2009). If this remaining fascicle
not exceed 120 ms (Burns, 2014). Secondly, LAFB is less well established, with a tradi- fails, complete heart block will ensue (Vogler
the current American Heart Association tional view that it carries a relatively benign et al, 2012). Patients with trifascicular block
(AHA) definition suggests that LAD is at prognosis, and might even be considered a require careful follow-up, and ongoing eval-
least -45˚ when it is caused by LAFB consequence of ageing (Josephson, 2010). uation for higher degrees of AV block in the
(Surawicz et al, 2009). This view was recently challenged by functioning fascicle (Brignole et al, 2013). If
In terms of clinical practice, there are Mandyam et al (2013) who demonstrated more significant AV block is detected, a
two aspects of fascicular blocks that are an association between LAFB and atrial permanent pacemaker must be implanted
important. The first is that they indicate fibrillation, chronic heart failure and death. because of the high risk of complete heart
damage to the distal conduction system This study was small, however, and a subse- block (Bennett, 2013).
Figure 14. Right-bundle branch block, left-anterior fascicular block, and 2:1 AV block. The patient received a permanent pacemaker

Because the terms ‘bifascicular’ and ‘tri-

fascicular’ block are inaccurate, the AHA BHF Resources
recommends that they are avoided, and
suggests describing these complex blocks The British Heart Foundation (BHF) is committed to sharing our knowledge to
according to their constituent features prevent heart disease devastating people’s lives. Visit bhf.org.uk where you’ll find
(Surawicz et al, 2009). Accordingly, the a wide range of resources that you can use to support people with a heart or
ECG in Figure 14 shows right-bundle circulatory condition. These resources include:
branch block, left-anterior fascicular block, w A wealth of online information on a variety of heart conditions, tests and
and 2:1 AV block. The patient presented to treatments including cardiac arrhythmias, ECG tests and pacemaker
her GP with dizziness and collapse, and implantation
was transferred to the emergency depart- w Short animations explaining some common abnormal heart rhythms such as
ment by ambulance. She was admitted to a AV heart blocks and complete heart block
monitored bed on the coronary care unit,
w Information booklets for patients and their friends and family including our
and underwent pacemaker implantation
Heart rhythms booklet.
the same night.
Conclusion The BHF Alliance is a free membership scheme that supports professionals
The QRS axis is an important measure- working with people affected by, or at risk of developing, cardiovascular disease.
ment on the 12-lead ECG, albeit one whose
measurement is subject to various pitfalls Join today at bhf.org.uk/alliance
and inaccuracies. These include a wide
natural variation in normal values, changes
that occur in response to ageing and body
shape, and susceptibility to wild inaccuracy BHF Doctor’s comment
if limb leads are transposed. QRS axis is
T
also much misunderstood, and seen as dif- his article, the sixth in strate, it can also be used to useful to the practitioner,
ficult to master. the series, gives a diagnose other non-cardi- who is working to make an
Despite these challenges, accurate assess- clear and practical ac conditions. Critically, accurate diagnosis.
ment of the QRS axis is a vital part of sys- explanation of how to the series also makes clear The outcomes for
tematic 12-lead ECG interpretation. interpret the QRS complex. the pitfalls of being ‘reas- patients depend on accu-
Although axis deviation may be a benign Importantly, the pitfalls sured’ by a normal ECG. rate diagnosis, which in
and normal finding, in many cases it reflects and reasons for The whole series of arti- turn relies on accurate
changes in the structure or electrical activa- misinterpreting the QRS cles on EGC measurement interpretation of diagnos-
tion of the ventricles. This has important axis are also explained. and interpretation repre- tic tests such as the ECG.
ramifications in terms of diagnosis, progno- Working though the sents an invaluable Educational resources
sis, and further evaluation of the patient. simple steps set out here resource for all non-spe- such as this give the practi-
This is especially so in the case of fascicular will ensure accurate cialist practitioners using tioner the confidence to
block in association with right-bundle interpretation of the QRS the ECG as a diagnostic know when they can inter-
branch block, in which case the develop- complex and the clinical tool. The ECG is increas- pret the ECG, and when to
ment of AV block in the remaining fascicle relevance of any ingly available and used in appropriately refer for
can herald the need for permanent pacing. abnormalities. non-specialist settings. specialist advice.
In this review, we have evaluated the The ECG is an indispen- This is both convenient for
importance of QRS axis, and described how sable tool in the diagnosis the patient, saving the
and when it can be useful in clinical practice. of cardiac conditions and, inconvenience of a hospital Dr Mike Knapton
We have also highlighted potential problems, as these articles demon- clinic appointment, and BHF Medical Director
and explained how they can be recognised
and avoided. We have set out several simple
therapy of the European Society of Cardiology
methods for axis determination that can be References (ESC). Developed in collaboration with the
used at the bedside, or in the clinic room. Adamson DL, Nelson-Piercy C (2007) Managing
European Heart Rhythm Association (EHRA).
We hope to have provided readers with a palpitations and arrhythmias during pregnancy.
Eur Heart J 34(29): 2281–329. doi: 10.1093/
Heart 93(12): 1630–6 eurheartj/eht150. http://tinyurl.com/gwmufpy
working knowledge of this important topic Aehlert B (2011) ECGs Made Easy. 4th edn. (accessed 18 March 2016)
which, though challenging, provides further Mosby Elsevier, Maryland Heights Burns E (2014) ECG Axis Interpretation. http://
insight into the 12-lead ECG. Next month, Bennett DH (2013) Bennett’s Cardiac Arrhythmias: lifeinthefastlane.com/ecg-library/basics/axis/
we review our progress so far by revisiting Practical notes on interpretation and treatment. (accessed 18 March 2016)
our 12-lead ECG interpretation tool. We 8th edn. Hodder Arnold, London Chow GV, Marine JE, Fleg JL (2012)
Brignole M, Auricchio A, Baron-Esquivias G et al Epidemiology of arrhythmias and conduction
also tackle another important subject in (2013) 2013 ESC Guidelines on cardiac pacing disorders in older adults. Clin Geriatr Med
12-lead ECG interpretation—the signs of and cardiac resynchronization therapy: the Task 28(4): 539–53. doi: 10.1016/j.cger.2012.07.003
chamber enlargement. BJCN Force on cardiac pacing and resynchronization Crawford J, Doherty L (2008) Recording a

Professions. 3rd edn. Blackwell Publishing,

Chichester: 56–69
Key Points Nielsen JB, Strandberg SE, Pietersen A, Graff C,
w QRS axis represents the net direction of depolarisation within the ventricles, and is Holst AG; Copenhagen ECG Study (2014) Left
anterior fascicular block and the risk of
measured using the limb leads. A normal axis lies between -30 and +90˚; anything
cardiovascular outcomes. JAMA Intern Med
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jamainternmed.2014.578
w Axis deviation may be a normal variant, but is often the result of structural or Oxborough D (2008) A practical approach to
electrical heart disease. Incorrect limb lead placement also affects axis, and should transthoracic echocardiography. British Journal
be suspected when other unusual features such as P-wave inversion and a positive of Cardiac Nursing 3(4): 163–9. doi: 10.12968/
QRS in aVR are seen bjca.2008.3.4.28922
Pappano AJ, Wier WJ (2013) Cardiovascular
w Axis is calculated by most ECG machines. This is usually highly accurate, but Physiology. 10th edn. Elsevier/Mosby,
Philadelphia
practitioners should be able to verify axis manually, in case of machine error.
Rose L, Kuhn L (2009) ECG interpretation part 2:
Several methods can be used, including the quadrant approach and identification of determination of bundle branch and fascicular
the isoelectric lead blocks. J Emerg Nurs 35(2): 123–6. doi:
10.1016/j.jen.2008.03.009. Epub 2008
w If all other causes of axis deviation have been excluded, a diagnosis of fascicular Sampson M (2016a) Understanding the ECG. Part
block may be made. This has important prognostic implications, especially in the 4: Conduction blocks. British Journal of Cardiac
patient with co-existing right-bundle branch block and first-degree AV block. In these Nursing 11(2): 71–9. doi: 10.12968/
bjca.2016.11.2.71
individuals, careful evaluation must be made for higher degrees of AV block. If they Sampson M (2016b) Understanding the ECG. Part
are found, a pacemaker should be implanted 5: Pre-excitation. British Journal of Cardiac
Nursing 11(3): 123–30. doi: 10.12968/
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Davies A (2007) Calculating cardiac axis on a Boca Raton 10.12968/bjca.2015.10.11.548
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Surawicz B, Childers R, Deal BJ, Gettes LS et al
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Answer to ECG of the month

The first ECG shows normal sinus rhythm, rate 66 beats per not been present on the first ECG.
minute, otherwise normal-looking ECG. The team is concerned On further comparison of the ECGs, there appears to be trans-
about the inferior leads on the second ECG, which appear differ- position of the limb leads. AVL and AVF are direct opposites of
ent from the first, with Q-waves and T-wave inversion that had each other, leading to the transposition of leads I and II as well.


Part 7: Chamber enlargement
E
nlargement of the cardiac enlargement, and examine the sensitivity The first step in structured assessment of
chambers is common, and results and specificity of published criteria. the ECG is to evaluate heart rate, rhythm,
from diseases affecting the heart and conduction intervals. Box 1 suggests
and lungs (Houghton and Gray, 2014). Structured ECG interpretation the key questions that we need to ask when
The growth in chamber size or wall By now, regular readers of this series will evaluating rate and rhythm, while Table 1
thickness reflects disease progression, appreciate that the 12-lead ECG contains a outlines normal conduction intervals
and is associated with increasing great deal of information (Garcia, 2015). (Sampson and McGrath, 2015). If heart
morbidity and mortality (Haddad et al, In the second article in this series, we dis- rate, rhythm or intervals are abnormal,
2008; Artham et al, 2009). Although cussed the use of a structured approach to further analysis should be made to deter-
echocardiography or magnetic resonance interpretation, and highlighted its value in mine the cause. Common causes for abnor-
imaging (MRI) is required to confirm ensuring that important information is not malities include sinus bradycardia or tach-
chamber enlargement, the overlooked (Sampson and McGrath, 2015). ycardia, arrhythmias and conduction
electrocardiogram (ECG) often reflects We proposed the use of the RPQRST sys- blocks (Sampson, 2016a; 2016b).
these changes, and is a more widely tem, which is shown in Figure 1 (Gregory, Remember that a prolonged QT interval
performed test (Rautaharju and Soliman, 2006). Let’s take a few moments now to suggests inherited or acquired long
2014). An abnormal ECG may therefore revisit this tool, and to briefly review the QT syndrome, and is associated with an
provide the first evidence of an ground that we have covered so far. increased risk of ventricular arrhythmias
underlying disease process, and a need (Mizusawa et al, 2014).
for further investigation and treatment The second step is to search for signs of
(Hampton, 2013a). Because of this, a R Rate, rhythm & intervals
pre-excitation on the ECG. These include a
search for the signs of chamber short PR interval, a wide QRS, and a delta
enlargement should be included in any P Pre-excitation wave (Mark et al, 2009). We need to
structured assessment of the 12-lead remember that pre-excitation alters the
ECG (Garcia, 2015). Q QRS axis electrical activation of the ventricles and,
Recognising chamber enlargement is therefore, the shape of the QRS complexes
also important from a broader diagnostic R Right or left bundle branch block (Maden et al, 2015). Pre-excitation can
viewpoint (Houghton and Gray, 2014). alter normal R-wave progression, and
On the ECG, chamber enlargement may Scan each lead: cause axis deviation (Sampson, 2016c).
alter the size and shape of the QRS com- S Patients with pre-excitation need specialist
plex, and result in ST-segment depres- evaluation because of an increased risk of
sion and T-wave inversion (Hancock et arrhythmias and sudden cardiac death
al, 2009). A failure to recognise the cause T Translate findings
(Obeyesekere et al, 2012).
of these changes could lead to misdiag- The third step is to evaluate QRS axis
nosis, particularly in the setting of sus- Figure 1. System of interpretation. Adapted using the limb leads (Table 2). The normal
pected myocardial ischaemia (Edhouse with kind permission from Gregory (2006) axis lies between -30 and +90 degrees, with
et al, 2009).
In this seventh part of our ECG series,
Box 1. Rhythm evaluation questions
we briefly revisit our structured ECG
interpretation tool before turning our 1. Is the rhythm regular?
attention to chamber enlargement. We
discuss why chamber enlargement occurs,
and describe how it can be recognised on
the ECG using a variety of criteria. We
also consider the limitations of using the
ECG to screen patients for chamber

Table 1. Normal conduction intervals important, abnormalities on the 12-lead

ECG (Gregory, 2006). There are, however,
many others that we have not discussed
(Hampton, 2013b). So, how do we evaluate
the ECG for these other abnormalities?
The answer is that we examine, or scan,
each of the 12 leads of the ECG to evaluate
whether the waveforms and segments
Table 2. Polarity of limb leads in normal and abnormal axis appear normal (Gregory, 2006). This
Lead I Lead aVF Lead II should be done in a methodical fashion to
+ + ensure that every lead is looked at in turn
+ (Aehlert, 2011). Any abnormality detected
+ should be evaluated in the light of the sur-
rounding leads. In other words, we should
ask whether this is an isolated finding (and
therefore more likely to be a normal vari-
ant), or part of a larger pattern of abnormal
any value outside this range referred to as lar depolarisation, and therefore widens findings that suggests an underlying dis-
axis deviation (Surawicz et al, 2009). Axis the QRS complex (Sampson, 2016b). ease process (Garcia, 2015). Houghton and
deviation results from numerous condi- Bundle branch block should be suspected Gray (2014) suggest that we should look
tions including fascicular blocks, ventricu- if the QRS is wide despite a normal rhythm. for the following features:
lar hypertrophy, pre-excitation, and myo- Because the pattern of ventricular activa- w P-waves that are too tall, or too wide
cardial infarction (Burns, 2014). It may tion is altered, characteristic changes in the w Pathological Q-waves
also be a normal variant, especially in peo- appearance of the QRS complexes are seen, w QRS complexes that are too small, or too
ple who are particularly tall and thin according to whether the right or left bun- large
(right-axis deviation), or short and broad dle is blocked (Aehlert, 2011). These w QRS complexes that have an abnormal
(left-axis deviation). A finding of axis devi- changes are compared in Figure 2. Bundle shape
ation should trigger thorough evaluation of branch blocks suggest underlying cardio- w ST segments that are depressed, or ele-
the 12-lead ECG to determine the cause, vascular disease, and can result from acute vated
and further investigations if necessary myocardial infarction, so warrant clinical w T-waves that have an abnormal shape, or
(Sampson, 2016d). evaluation (Kumar et al, 2013). are inverted.
The final step that we have covered so far Although there are many conditions that
is consideration of bundle branch block. Scanning each lead can cause these types of changes, among
Failure of conduction through either the These first four steps in our system will the most common are chamber enlarge-
left or right bundle branch delays ventricu- identify many of the most common, and ment and myocardial ischaemia or infarc-
Figure 2. Characteristic changes seen in the chest leads when bundle branch block is present. In right-bundle branch block, there is an
RSR in V1/V2, and a wide S-wave in V6. In left-bundle branch block, there are deep S-waves in V1–V3, and a stumpy, notched
R-wave in V6

tion (Hampton, 2013a). In this article we siderable force. To move blood out of the 2009). Another common cause is dilated
will discuss chamber enlargement, turning heart, the left ventricle must push blood cardiomyopathy (DCM), in which case the
to ischaemia and infarction in the next through the aortic valve, and overcome primary problem is diseased heart muscle.
article in the series. Let’s start by discuss- the diastolic pressure in the aorta, typi- DCM is often an inherited disorder, but
ing left ventricular hypertrophy (LVH), cally 80 mmHg in a healthy individual can also be caused by ischaemic heart dis-
the most common type of chamber (Marieb and Hoehn, 2015). Consequently, ease, alcohol abuse, and viral myocarditis
enlargement encountered in clinical prac- the LV has thick, muscular walls that can (Jefferies and Towbin, 2010).
tice (Hancock et al, 2009). generate the necessary pressure (Tortora On the ECG, it is not possible to deter-
and Nielsen, 2014). mine whether chamber enlargement is a
Left-ventricular enlargement If pressure within the aorta is increased, result of hypertrophy or dilatation (Garcia,
The left ventricle (LV) is responsible for or there is an obstruction to blood flow, the 2015). Current clinical guidelines
pumping blood into the systemic circula- LV must work harder, and its walls thicken acknowledge this, but suggest using the
tion (Klabunde, 2012). This requires con- to cope with the additional work load using the term hypertrophy when describ-
(Pappano and Wier, 2013). This process is ing ECG changes owing to LV enlarge-
referred to as hypertrophy (Kenney et al, ment (Hancock et al, 2009). In this article,
Predominant direction of depolarisation
2015). LVH commonly occurs in response we will use the same convention.
to systemic hypertension, but can also be a
Right Left result of aortic stenosis, or coarctation of Voltage criteria for LVH
V6
the aorta (Houghton and Gray, 2014; The ECG changes that occur in LVH can be
Porthon et al, 2015). Hypertrophic cardio- divided into two categories; voltage and
V5
myopathy (HCM) also causes LVH, non-voltage criteria (Edhouse et al, 2009).
although the mechanism is proliferative Voltage criteria refers to an increase in the
V4 disease rather than pressure overload size of the QRS complexes (Houghton and
V1 V2 V3 (Elliot, 2010). Gray, 2014). This occurs because the
Enlargement of the LV without wall enlarged ventricle has more myocytes, and
Transition complex
thickening is also possible if the chamber therefore produces more electricity
walls become stretched (Klabunde, 2012). (Garcia, 2015). So which QRS complexes
This is referred to as dilatation, and may are affected?
Figure 3. Leads facing the right ventricle occur secondary to volume overload in Broadly speaking, all of the QRS com-
have deep S-waves, while those facing the conditions such as chronic kidney disease, plexes may be affected; however, the pat-
left ventricle have tall R-waves or aortic regurgitation (Artham et al, tern seen reflects the orientation of the
Figure 4. Left-ventricular hypertrophy (LVH). In this example, the R-waves are especially tall in leads I, V4 and V5. S-waves are
abnormally deep in V2 and V3

leads in relation to the LV (Hampton, Box 2. The Sokolow-Lyon and Cornell voltage criteria for LVH
2013a). On the normal ECG, the LV domi- Sokolow-Lyon
nates the shape of the QRS complex
because of its larger mass (Sampson,
2016b). As a result, leads that face away Cornell
from the LV (V1 and V2) have deep
S-waves, while those facing the LV (I, aVL,
V5 and V6) have tall R-waves (Garcia, criterion was found to be accurate at pre- words, in many cases, the ECG will fail to
2015) (Figure 3). In LVH, this pattern is dicting echocardiographic LVH, and has detect LVH; although when it does, the
exaggerated by the increased LV voltages the advantage of being simple to assess on likelihood of a correct diagnosis is high. A
(Hampton, 2013a). The S-waves in leads the ECG. The disadvantage of this single- study by Porthan et al (2015) found that
V1 and V2 are therefore deeper than nor- lead approach is demonstrated in Figure 4. using the Sokolow-Lyon and Cornell crite-
mal, while the R-waves in leads I, aVL, V5 On this ECG, the R-wave in aVL is only ria together increased sensitivity, and this
and V6 are unusually tall (Figure 4). 8 mm tall, suggesting that LVH is not is an approach that has also been suggested
present. This seems unlikely, given the by clinical guidelines (Hancock et al, 2009).
How much is too much? large QRS complexes in other leads. In short, the more criteria you use, the
You might be wondering how tall the Use of different criteria to evaluate this more likely that LVH will be detected.
R-waves, or how deep the S-waves, need to ECG produces very different outcomes. Further considerations when evaluating
be in order to diagnose LVH. This is a very The Sokolow-Lyon and Cornell criteria are the ECG for LVH are age, athletic training,
good question that unfortunately does not widely used in clinical practice, and use and lead placement. QRS voltages are often
have a simple answer. Various voltage crite- more than one lead in assessing the ECG higher in young people, despite normal
ria have been published, most of which are for LVH (Sokolow and Lyon, 1949; Casale hearts. Voltage criteria for LVH are there-
based on comparison of the ECG with et al, 1985; Hancock et al, 2009) (Box 2). fore inaccurate in individuals below the age
LV mass measured at autopsy or by According to both of these criteria, the of 36 years, and should not be used
echocardiogram (Rautaharju and Soliman, ECG in Figure 4 is consistent with LVH. (Hancock et al, 2009). Voltages are also
2014). Some of these criteria are quite sim- This demonstrates a widely recognised increased in athletes, whose hearts are
ple, while others are more complex. limitation of the ECG diagnosis of LVH, enlarged as a result of cardiovascular train-
The simplest criterion is the evaluation namely that sensitivity of individual crite- ing (Corrado et al, 2010). Finally, lead
of a single lead, for example an R-wave in ria is low, despite a high specificity placement must also be considered. In one
aVL that is greater than 11 mm (Garcia, (Hancock et al, 2009; Hampton, 2013a; study, voltages varied by as much as 25%
2015). In a study by Gosse et al (2012), this Rautaharju and Soliman, 2014). In other owing to daily variation in lead placement
Figure 5. LVH with strain. This ECG meets multiple voltage criteria for LVH (the patient was a 68-year-old woman). There are second-
ary ST-T abnormalities in all of the left-sided leads

increased LV burden, such as HCM. it harder for the left atrium to eject blood
Current guidelines therefore suggest that into the ventricle. As a consequence, the left
the term ‘secondary ST-T abnormalities’ is atrium enlarges (Douglas, 2003). A recent
more appropriate (Hancock et al, 2009). meta-analysis demonstrated a strong asso-
In LVH, secondary ST-T abnormalities ciation between left-atrial enlargement
are seen in those leads that face the LV; in (LAE) and LVH (Cuspidi et al, 2013). LAE
particular, leads I, aVL, V5 and V6 also occurs in mitral valve disease and left-
(Hampton, 2013a) (Figure 5). Typically, the ventricular dysfunction, and is associated
ST segment is down-sloping and depressed, with an increased risk of adverse cardiovas-
Ischaemia
and the T-wave asymmetrically inverted cular outcomes including atrial fibrillation,
Figure 6. In typical LVH with strain there (Hampton, 2013a). This appearance has stroke and death (Patel et al, 2009).
is down-sloping ST depression and asym- been compared to a ‘reverse tick’, and is On the ECG, LAE causes widening of the
metrical T wave inversion. T wave inver- unlike the symmetrical T-wave inversion P-wave and changes in waveform mor-
sion due to myocardial ischaemia is more typically seen during myocardial ischaemia phology (Bayes de Luna et al, 2012). The
often symmetrical. (Garcia, 2015) (Figure 6). This is an impor- normal duration of the P-wave is less than
tant distinction to make in clinical prac- 0.12 s (Houghton and Gray, 2014). In LAE,
tice. Changes to the ST segments and this duration is extended to 0.12 s or more
T-waves are pivotal in the evaluation of (Garcia, 2015). The traditional explanation
patients with acute chest pain (Steg et al, for this is that the wave of depolarisation
2012). A failure to recognise LVH with has further to travel in an enlarged atrium
strain can result in a misdiagnosis of myo- (Edhouse et al, 2009). This view has been
cardial ischaemia (Hampton, 2013a). In challenged by Bayes de Luna et al (2012)
Lead ll Lead V1 the case of patients with known LVH, sec- who argue that conduction delay or block
ondary ST-T abnormalities can mask within the atria may be responsible for the
Figure 7. Left atrial abnormality. There is a
ischaemic changes, and make it more dif- P-wave changes seen in LAE.
bifid P wave in lead II, with more than one
ficult to diagnose myocardial infarction Changes in P-wave morphology are seen
small square separating the peaks. In lead
(Edhouse et al, 2009). Evaluation of previ- in the inferior leads, and lead V1 (Hampton,
V1, the negative component is greater than
ous ECGs is essential in these cases. 2013b). The P-wave is produced by depo-
one small square wide and deep
From a prognostic perspective, ST-T larisation of first the right, and then the left
(Farb et al, 1990). Lead placement should abnormalities are associated with more atrium. The two waveforms created are
therefore be considered if unexpected advanced disease, and a greater risk of superimposed on each other to produce
results are seen. adverse cardiovascular events (Rautaharju the single waveform that we call the P-wave
and Soliman, 2014). In the PIUMA study, (Garcia, 2015). In LAE, delayed depolarisa-
Non-voltage criteria for LVH for example, patients whose ECG met the tion of the left atrium causes a separation
The increase in LV size that occurs in LVH Sokolow-Lyon or Cornell criteria for LVH of these two waveforms, producing a bifid
does not merely increase the number of were found to have approximately twice or ‘M-shaped’ P-wave in the inferior leads
cells, and therefore the voltage of QRS the risk of adverse cardiovascular events (Hancock et al, 2009). A slightly notched
complexes. A range of additional electrical compared with patients without LVH on P-wave may be a normal variant, so
effects is seen, including changes to depo- the ECG (Verdecchia et al, 1998). For those Edhouse et al (2009) suggest that a distance
larisation, repolarisation, and mean QRS individuals with a strain pattern, the risk of one small square (40 ms) between the
axis (Edhouse et al, 2009). Left-axis devia- was nearer five-fold. In trials of anti-hyper- two peaks of the P-wave is necessary to
tion is one non-voltage criterion for LVH tensive drugs, a regression of the ECG diagnose LAE with confidence (Figure 7).
(Garcia, 2015). The other important crite- markers of LVH has been demonstrated In lead V1, a similar separation of right-
ria are secondary ST-T abnormalities, and following control of blood pressure, with a and left-atrial components occurs. The
left atrial enlargement (Hancock et al, corresponding fall in cardiovascular risk P-wave in lead V1 is often biphasic, with
2009; Garcia, 2015). (Verdecchia et al, 2003; Okin et al, 2004). the first (positive) part representing right-
atrial depolarisation, and the terminal
Secondary ST-T abnormalities Left-atrial enlargement (negative) part representing activation of
As the LV enlarges, progressive change In the normal heart, the LV distends as the left atrium (Hampton, 2013a). In LAE,
may occur in the ST segment and T-wave blood fills it during diastole (Marieb and the terminal portion of P-wave becomes
(Schocken, 2014). The ST segment shifts Hoehne, 2015). This stretching of the heart wider and deeper than normal (Houghton
downwards, and the T-wave flattens and allows it to accommodate increased venous and Gray, 2014). A width and depth of at
ultimately inverts (Garcia, 2015). This pat- return during exercise, and stimulates con- least 1 small square has been suggested as
tern is commonly referred to as ‘strain’ tractility via the Frank-Starling mechanism the criteria for LAE (Kitvungvan and
from its early association with increased (Klabunde, 2012). In LVH, the ventricle is Spodick, 2009; Garcia, 2015).
LV afterload (Hancock et al, 2009). We less compliant, so stretches less readily In the past, the P-wave associated with
now know that a strain pattern is also seen (Artham et al, 2009). This stiffening of the LAE was referred to as ‘P mitrale’ because
in conditions that do not result from chamber increases filling pressures, making of its association with mitral valve disease

Box 3. The Romhilt-Estes scoring system for LVH. A score of Houghton and Gray, 2014; Garcia, 2015).
four indicates that LVH is probable, a score of 5 or more is ST-T abnormalities also have a prognostic
role, given their association with increas-
diagnostic for LVH. ing cardiovascular risk (Schocken, 2014).
Criteria Points Various diagnostic tools have been pro-
OR OR 3 posed that use non-voltage as well as volt-
age criteria, the best known of which is
3 Romhilt-Estes scoring system (Romhilt-
1
Estes, 1968) (Box 3). Despite its increased
complexity, a recent study using MRI to
3 validate ECG criteria suggests that its sen-
duration sitivity is no better than simpler criteria
2 such as Sokolow-Lyon or Cornell, with a
1 similar specificity (Jain et al, 2010).
1
Right-ventricular enlargement
(Burns, 2011). Although widely known as LAE should be called ‘interatrial block’ Right-ventricular enlargement results from
and understood, this name is not appropri- instead. Current practice guidelines pressure or volume overload in much the
ate to our modern understanding of the acknowledge the place of electrical disease same way as left-ventricular enlargement
ECG. Mitral valve disease is not the most in P-wave abnormality, but recommend the (Haddad et al, 2008). The principal cause is
common cause of LAE, and LAE is not the term ‘left-atrial abnormality’ as it encom- pulmonary hypertension, although it also
only cause of this P-wave appearance. passes both structural and electrical causes occurs in pulmonary valve stenosis, and
Bayes de Luna et al (2012) suggest that of ECG change (Hancock et al, 2009). pulmonary embolism (Hampton, 2013a).
atrial conduction block, in the absence of On the ECG, it is usually referred to as
LAE, is a more common cause of P-wave Combining voltage and non- right ventricular hypertrophy (RVH)
widening and morphology change. This is voltage criteria (Hancock et al, 2009). RVH is much less
supported by a study by Tsao et al (2008) Although non-voltage criteria are often common than LVH, and its ECG features
that compared ECG and MRI findings in seen in LVH, the low specificity of left- have been less well studied (Whitman et al,
people with and without LAE. Only 35% of atrial and ST-T abnormalities means that 2014). Both voltage and non-voltage crite-
people with abnormal P-waves had LAE at they are not considered diagnostic without ria have been identified; however, all are
MRI, suggesting that the ECG has poor voltage changes (Hancock et al, 2009). limited by poor sensitivity and specificity
specificity for LAE. In light of this, Nonetheless, they are widely appreciated as (Harrigan and Jones, 2009).
Kitvungvan and Spodick (2009) suggest additional diagnostic clues that help to The principal voltage criteria in RVH is a
that the ECG findings typically described confirm a diagnosis (Hampton, 2013a; dominant R-wave in lead V1 (Houghton
Figure 8. RVH with strain. Note the dominant R-waves in V1–3, and the deep S-waves in V4–6. There are secondary ST-T abnormali-
ties in leads V1–4, and right-axis deviation

a dominant R-wave in the right-sided pre- Right-atrial abnormality

cordial leads. Because the amount of Right-atrial abnormality refers to changes
hypertrophy needed to alter the predomi- in the size and shape of the P-wave that
nant vector is large, many people with mild occur in diseases affecting the right side of
RVH will have a normal ECG, and hence the heart (Houghton and Gray, 2014). It is
sensitivity of the ECG for RVH is low commonly associated with RVH, and often
(Whitman et al, 2014). reflects enlargement of the right atrium
In addition to poor sensitivity, specificity owing to increased filling pressures in the
is also an issue with this ECG finding. A RV (Haddad et al, 2008). This may occur
tall R-wave in lead V1 is a normal variant, acutely in pulmonary embolism, or over a
and is also seen in other conditions includ- longer period in chronic disease such as
Figure 9. Right-atrial abnormality in ing posterior myocardial infarction, pre- pulmonary hypertension and chronic
lead II. The P-wave is tall (almost 3 mm) excitation, and right-bundle branch block obstructive pulmonary disease (Hampton,
and peaked. Note the ST-T abnormality, (Hampton, 2013a; Houghton and Gray, 2013a). Other causes of right-atrial
which also suggests RVH 2014). Additional ECG features must enlargement include congenital heart dis-
therefore be sought when making a diag- ease, and tricuspid stenosis, although these
and Gray, 2014). By dominant, we mean nosis of RVH. These include (Harrigan and are less common (Harrigan and Jones,
that the R-wave is greater than the S-wave Jones, 2009; Hampton, 2013b): 2009).
(Hampton, 2013a). This can also be w QRS duration less than 0.12 s (to exclude The characteristic finding in right atrial
expressed as an R:S ratio of greater than 1 right-bundle branch block) abnormality is a tall, peaked P-wave in the
(Garcia, 2015). This is an unusual finding w Right-axis deviation ≥110˚ anterior and inferior leads (Harrigan and
on the ECG, as lead V1 commonly has a w Deep S-waves in leads V5 and V6 Jones, 2009) (Figure 9). In the inferior leads
small R-wave, and a deep S-wave. w Secondary ST-T abnormalities (strain) (II, III and aVF), the height of the P-wave
Lead V1 sits over the right ventricle (RV) w Right-atrial abnormality. is greater than or equal to 2.5 mm (Garcia,
(Houghton and Gray, 2014). In the normal The secondary ST-T abnormalities that 2015). P-wave duration is usually normal
heart, left-to-right depolarisation of the develop in RVH are similar to those in unless there is congenital heart disease
septum moves towards this lead, creating a LVH in that the typical pattern is down- (Hancock et al, 2009). In older texts, the
small R-wave. The subsequent depolarisa- sloping ST depression, with asymmetrical term ‘P pulmonale’ is often used, reflecting
tion of the ventricles is dominated by the T-wave inversion (Hancock et al, 2009). In the association between right-atrial
thicker-walled LV, so the predominant vec- RVH, however, the strain pattern is seen in enlargement and chronic lung disease
tor moves away from lead V1, causing a the right-sided precordial leads (V1 to V3), (Hampton, 2013a). As with left-atrial dis-
deep S-wave (Hampton, 2013a). In severe and often the inferior leads (Hampton, ease, the preferred terminology today is
RVH, the RV mass may exceed that of the 2013b). This is because these are the leads right atrial abnormality, reflecting the fact
LV, shifting the predominant vector of overlying the hypertrophied RV (Garcia, that both electrical and structural factors
depolarisation to the right and towards 2015). Figure 8 illustrates many of the key can influence P-wave morphology
lead V1 (Hancock et al, 2009). This creates features of RVH. (Hancock et al, 2009).
Biventricular enlargement
BHF Resources In advanced heart disease, both ventricles
may be enlarged (Klabunde, 2012). Because
voltages on both sides of the heart will be
prevent heart disease devastating people’s lives. increased, these changes may cancel each
Visit bhf.org.uk other out to a certain extent (Garcia, 2015).
The ECG therefore has particularly poor
w Cardiac arrhythmias
sensitivity and specificity in this situation
w Heart valve disease (Hancock et al, 2009). The ECG features
w Congenital heart disease that might be seen are voltage criteria for
w Cardiomyopathies. LVH plus features of RVH such as deep
S-waves in V5 and V6, right-axis deviation,
and right-atrial abnormality (Hancock et
al, 2009).
The same principles apply to bi-atrial
and family
enlargement, in which case features of both
left- and right-atrial abnormality may be
present. In the inferior leads, for example,
the P-wave is wide and broadly bifid, but
Join today at bhf.org.uk/alliance also has a peaked initial component that is
at least 2.5 mm high (Garcia, 2015).

Conclusion
Enlargement of all four chambers of the Key Points
heart may be reflected in the 12-lead ECG w Many important cardiovascular and respiratory diseases cause enlargement of the
(Garcia, 2015). LVH is more common and,
as a result, has been more widely studied
and defined (Rautaharju and Soliman, reducing the usefulness of the ECG as a screening tool
2014). Numerous voltage criteria for LVH
have been proposed, although they are w
only diagnostic in adults over 35 years old
who are non-athletes (Hancock et al, 2009).
In this population, all of the published cri-
teria are highly specific but lack sensitivity,
suggesting a limited role for the ECG in w
population screening (Hampton, 2013a).
Of the available criteria, the Sokolow-Lyon
and Cornell are widely used, and in combi-
nation may increase sensitivity (Hancock
et al, 2009). They should be combined with
w
a search for non-voltage criteria such as
left-axis deviation, secondary ST-T abnor-
malities, and left-atrial abnormality
(Houghton and Gray, 2014).
RVH is less common, and does not affect w
the ECG unless disease is severe (Harrigan
and Jones, 2009). Consequently, sensitivity
of the ECG for RVH is poor (Hampton,
2013a). The principal sign of RVH, a dom-
w
inant R-wave in lead V1, has poor specifi-
city because of multiple differentials. A
diagnosis of RVH must be supported by
associated changes such as deep S-waves in
leads V5 and V6, right-axis deviation, ST-T hypertrophy: development and prospective 30(5): 990–6. doi: 10.1097/
abnormalities, and right-atrial abnormali- validation of improved criteria. J Am Coll Cardiol HJH.0b013e3283524961
6(3): 572–80 Gregory J (2006) An analysis tool for 12-lead ECG
ty. The QRS must be narrow, as a wide QRS Corrado D, Pelliccia A, Heidbuchel H et al (2010) interpretation. British Journal of Cardiac Nursing
suggests that ECG changes are owing to Recommendations for interpretation of 12-lead 1(5): 216–21. doi: 10.12968/bjca.2006.1.5.21118
right-bundle branch block. electrocardiogram in the athlete. Eur Heart J Haddad F, Doyle R, Murphy DJ, Hunt SA (2008)
31(2): 243–59. doi: 10.1093/eurheartj/ehp473. Right ventricular function in cardiovascular
Next month we turn our attention to the Epub 2009 disease, part II: pathophysiology, clinical
signs of myocardial ischaemia and infarc- Cuspidi C, Rescaldani M, Sala C (2013) Prevalence importance, and management of right ventricular
tion, examining the ECG changes that take of echocardiographic left-atrial enlargement in failure. Circulation 117(13): 1717–31. doi:
hypertension: a systematic review of recent 10.1161/CIRCULATIONAHA.107.653584
place, and placing them in the context of clinical studies. Am J Hypertens 26(4): 456–64. Hampton JR (2013a) The ECG in Practice. 6th edn.
coronary artery anatomy and the patho- doi: 10.1093/ajh/hpt001 Churchill Livingstone, London
physiology of coronary heart disease. BJCN Douglas PS (2003) The left atrium: a biomarker of Hampton JR (2013b) The ECG Made Easy. 8th edn.
chronic diastolic dysfunction and cardiovascular Churchill Livingstone, London
disease risk. J Am Coll Cardiol 42(7): 1206–7 Hancock EW, Deal BJ, Mirvis DM et al (2009) AHA/
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British Journal of Cardiac Nursing May 2016 Vol 11 No 5


Part 8: myocardial ischaemia
and infarction (part A)
Michael Sampson, BHF Arrhythmia Nurse Specialist, St George’s Hospital, and Senior Lecturer, School of Health
D
espite advances in medical Because of the size of the subject, it will gen and a poor capacity for anaerobic
treatment and improvements in be addressed in two parts. In this first part, metabolism (Ramanathan and Skinner,
public health, myocardial ischaemia we examine the coronary circulation, the 2005). To meet its high demand for blood
and infarction remain common causes of pathophysiology of CHD and the diagnosis flow, the heart has a dedicated supply in the
hospital admission worldwide (Nabel and and treatment of ST elevation MI (STEMI). form of the coronary circulation (Kim et
Braunwald, 2012). The most common In the second part, to be published next al, 2006).
cause is coronary heart disease (CHD), a month, we will complete our discussion of The coronary circulation consists of a
condition in which the coronary arteries STEMI, before moving on to non–ST ele- branching network of arteries, veins and
supplying blood to the heart muscle are vation MI (NSTEMI) and unstable angina. capillaries (Grech, 2011). The left and right
narrowed or blocked (Marshall, 2011). In coronary arteries arise from the base of the
the UK, CHD consumes a large part of the The coronary circulation aorta, just above the aortic valve, and run
NHS budget, and is the cause of death in Every cell in the human body requires oxy- across the epicardial surface of the heart in
15% of men and 10% of women (British gen to maintain its normal function the first part of their course (Marieb and
Heart Foundation (BHF), 2015). Although (Marieb and Hoehn, 2015). Although Hoehn, 2015) (Figure 1). Both arteries give
mortality rates have fallen over the past many cells can function for brief periods off important branches that also run on the
four decades, prevalence of the disease is without oxygen, a sustained loss of blood outer surface of the heart, with smaller
rising, and increasing numbers of patients supply results in cellular dysfunction and, sub-branches diving down into the myo-
are seen in both primary and secondary ultimately, cell death (Pappano and Wier, cardium to feed an extensive capillary net-
care (Bhatnagar et al, 2015). 2014). The heart is especially vulnerable to work (Tortora and Nielsen, 2014). A net-
Given the scale of the problem, the diag- ischaemia, having a high demand for oxy- work of cardiac veins returns blood to the
nosis and management of CHD is a prior-
©Peter Lamb
ity in all healthcare settings (National
Institute of Health and Care Excellence
(NICE), 2010). The 12–lead ECG plays an
important role in this process, and is espe-
cially important in the diagnosis of acute
ischaemic events (Hampton, 2013).
Changes in the QRS complex, ST segment,
and T-wave occur during ischaemia, and Left coronary artery
are combined with patient history and Circumflex
blood results when making a diagnosis
(Houghton and Gray, 2014). Of particular Right coronary Obtuse marginal
importance is the identification of persist- artery
ent ST segment elevation, which has the
Diagonals
strongest association with acute myocar-
dial infarction (MI) (Thygesen et al, 2012). Acute marginal
This eighth instalment of this ECG series Left anterior
will examine the ECG changes that occur
descending
during myocardial ischaemia and infarc-
Posterior descending
tion, and place them in the context of
underlying pathophysiology and clinical
management. Figure 1. Typical coronary artery anatomy
290 British Journal of Cardiac Nursing June 2016 Vol 11 No 6

Table 1. Areas of the heart typically supplied by each artery which the PDA arises from the LCx, mak-
Coronary artery Area of the heart supplied ing this vessel likely to be the culprit vessel
in an inferior MI (Houghton and Gray,
Right coronary artery (RCA) RA, RV, sinus node, AV node, inferior LV
2014). In the remaining 7–8% of the popu-
Left anterior descending (LAD) Anterior LV, apex, interventricular septum lation, the coronary circulation is co-dom-
Left circumflex (LCx) LA, lateral LV, posterior LV inant; the inferior LV is perfused by
branches arising from both the RCA and
right atrium via the coronary sinus between coronary arteries and cardiac ter- the LCx (Rinta-Kiikka et al, 2014).
(Pappano and Wier, 2013). ritory is summarised in Table 1.
The right coronary artery (RCA) runs in Pathophysiology of CHD
the groove between the right atrium (RA) Individual variation As with all arteries, those in the coronary
and right ventricle (RV), before coursing Although the arrangement described circulation are composed of three layers;
down the right side of the heart towards above is common, there can be signifi- an outer tunica adventitia, a middle tunica
the apex (Tortora and Nielsen, 2014). It cant variation in the branching pattern of media and an inner tunica intima (Marieb
gives off important branches including the the coronary circulation (Marieb and and Hoehn, 2015) (Figure 2). The adventi-
sinus node, RV and acute marginal branch- Hoehn, 2015). tia is composed of tough connective tissue,
es (Kim et al, 2006). In one third of people, the LCA trifur- the media of smooth muscle cells, and the
In most people, it also gives rise to the cates after the LMS to form three major intima of endothelial cells (Tortora and
posterior descending artery (PDA), which branches instead of two (Rinta-Kiikka et al, Nielsen, 2014).
supplies the inferior wall of the left ventri- 2014). The additional artery is referred to When the demand for blood flow is high,
cle (LV) (Cademartiri et al, 2008). Broadly as the ramus intermedius, and supplies an for example during exertion, the smooth
speaking, the RCA supplies blood to the area equivalent to the first diagonal branch muscle in the media relaxes, dilating the
RA, RV, proximal conduction system and (Jowett and Thompson, 2007). Other peo- vessel lumen and increasing blood flow
inferior LV (Jowett and Thompson, 2007). ple are born with a single coronary artery (Marieb and Hoehn, 2015). This process is
Occlusion of the RCA is associated with supplying the entire heart, or have arteries regulated by the release of vasoactive hor-
inferior MI, often with RV involvement with highly unusual origins or courses mones from the endothelial cells of the
(Ondrus et al, 2013). Because the RCA (Cademartiri et al, 2008). intima (Ramanathan and Skinner, 2005).
supplies the proximal conduction system, A second area of variation is in collateral The endothelial lining also provides a
AV block is common in this type of MI circulation. Collaterals are vessels that link smooth, non-stick surface to the inside of
(Aehlert, 2011). coronary arteries together via anastomo- the artery, promoting blood flow and
The left coronary artery (LCA) runs in ses, helping to improve blood supply across resisting the adhesion of white blood cells
the left atrioventricular groove (Marieb the heart (Tortora and Nielsen, 2014). A (Libby et al, 2011).
and Hoehn, 2015). Following a short initial growth in collateral circulation is seen in CHD occurs when the endothelial lining
section referred to as the left main stem people who exercise regularly, and also in of the coronary artery becomes damaged
(LMS), the artery divides to form the left individuals with chronic CHD (Klabunde, by oxidative, haemodynamic or biochemi-
anterior descending (LAD) and left cir- 2012). Research suggests that one in four cal processes (Nabel and Braunwald, 2012).
cumflex (LCx) arteries (Cademartiri et al, people with CHD has sufficient collateral Common causes of damage include ciga-
2008). The LAD runs down the front of the circulation to prevent ischaemia during rette smoking, hypertension and high lev-
heart, giving off diagonal branches that brief coronary artery occlusion (Seiler et al, els of glucose or cholesterol in the blood
supply the anterior wall of the LV, as well as 2013). This has a protective effect during (Yusef et al, 2004). Further risk factors for
perforators that penetrate and supply the acute ischaemic events, and is associated CHD development are detailed in Box 1.
interventricular septum (Tortora and with decreased morbidity and increased Damage to the endothelium triggers a
Nielsen, 2014). survival (Regieli et al, 2009).
Of the three major coronary arteries, the This variation in coronary anatomy
©Peter Lamb
LAD provides the greatest proportion of means that there is not always a direct rela-
blood to the LV (Rinta-Kiikka et al, 2014). tionship between ECG findings and the
Blockage of this vessel therefore has the location of ischaemic events in the heart
greatest effect on LV function, and is asso- (Rinta-Kiikka et al, 2014). One of the most
ciated with increased morbidity and mor- important confounders to be aware of is
tality (Lee et al, 1995). the source of the PDA, and therefore the
The LCx continues around the left side of blood supply to the inferior LV (Jowett and Tunica intima
the heart in the atrioventricular groove Thompson, 2007). In 85% of people, the Tunica media
(Marieb and Hoehn, 2015). Its major circulation is said to be right dominant,
branches are the obtuse marginals, which meaning that the PDA arises from the RCA Tunica adventitia
supply blood to the lateral wall of the LV (Kim et al, 2006). In these people, an infe-
(Cademartiri et al, 2008). It also supplies rior MI is the result of RCA occlusion
the left atrium (LA) and posterior wall of (Hampton, 2013). In contrast, 7–8% of
the LV (Kim et al, 2006). The relationship people have a left dominant circulation, in Figure 2. Arterial wall layers
British Journal of Cardiac Nursing June 2016 Vol 11 No 6 291

timing of events, the affected artery and the

Box 1. Risk factors for coronary artery disease (Kennedy, 2008)
amount of myocardium at risk, which will
Modifiable risk factors Non-modifiable risk factors inform a potential treatment strategy (Steg
Smoking Age et al, 2012).
Alcohol intake Male gender Where possible, comparison should be
Lack of physical exercise Family history of premature CHD made with previous ECGs as previous
Low consumption of fruits and Ethnicity ischaemic events or chronic changes may
vegetables confound diagnosis (Houghton and Gray,
Hypertension 2014). ECG evaluation should also be
Hypercholesterolaemia made in the light of patient history, physi-
Diabetes cal examination, and the level of biochemi-
Abdominal obesity cal markers, ideally troponin I or T
Psychosocial factors (Hampton, 2013).
Depending on the findings of a clinical
chronic inflammatory process in which 2012). Unlike stable angina, ACS is typi- evaluation, ACS can be classified as one of
white blood cells and lipids accumulate in fied by chest pain that is persistent, unre- the following:
the intimal layer of the artery wall (Libby et lieved by rest or nitrates, and often associ- w ST elevation MI (STEMI)
al, 2011). Over time, the lesion is swelled ated with nausea, vomiting and sweating w Non–ST elevation MI (NSTEMI)
by the migration of smooth muscle cells (NICE 2010). ACS is a medical emergen- w Unstable angina.
from the media, and the formation of a cy, warranting emergency assessment and At initial presentation, the focus is on
fibrous cap (Stone et al, 2011). treatment (Marshall, 2011). confirming or excluding the presence of
As the lesion grows, the lumen of the STEMI because treatment guidelines rec-
vessel becomes progressively narrower, The 12–lead ECG in ACS ommend immediate reperfusion therapy
although significant impairment of blood During the early minutes of an ACS, the in these patients (NICE, 2013; Steg et al,
flow may not occur until 60–70% of the 12–lead ECG may be entirely normal 2012). Troponin levels are not needed
lumen is obstructed (Gould, 2009). At this despite severe symptoms (Morris and before starting treatment in STEMI,
point, ischaemia may occur during Brady, 2009). Serial ECGs should therefore although they are essential to the manage-
increased demand, resulting in predictable, be performed, ideally at 15–30 minute ment of NSTEMI and unstable angina
exertional symptoms described as stable intervals or using continuous computer- (Marshall, 2011).
angina (Grech, 2011). The classical symp- assisted recording (Thygesen et al, 2012).
tom of stable angina is retrosternal chest Serial ECGs will also capture dynamic ST elevation MI
pain that is provoked by exertion and changes, providing information about the STEMI results from the acute occlusion of
relieved by rest or short-acting nitrates
(Nabel and Braunwald, 2012). The pain is
©Peter Lamb
often described in terms of pressure, tight-
ness or weight on the chest, and may radi-
ate to the shoulders, neck, jaw, back or
arms (Fox et al, 2006). It is rarely severe, Thrombus formation
and usually does not last more than 15 Platelet
minutes (NICE, 2010). If there is a well-
developed collateral circulation, individu-
als may have few or no symptoms despite Lipid core Fibrous cap rupture
high-grade stenosis or even complete ves-
sel occlusion (Seiler et al, 2013).
In contrast, unpredictable or severe
symptoms are usually related to sudden
rupture of a cap covering a lesion
(Marshall, 2009). This exposes the lipid-
rich contents to the circulating blood,
triggering platelet aggregation, blood clot
formation and vasoconstriction (Libby et
al, 2011) (Figure 3). This may completely
or partially occlude the vessel, resulting in
severe ischaemia or infarction of the area
supplied by the artery (Steg et al, 2012).
These sudden, life-threatening thrombot-
ic events are described as acute coronary Figure 3. Rupture of the cap covering an atherosclerotic lesion, resulting in platelet
syndromes (ACS) (Arbab-Zadeh et al, aggregation and blood clot formation (adapted from Libby et al, 2011)

an epicardial coronary artery, and is associ-

ated with transmural ischaemia of a sig-
Table 2. Contiguous leads in STEMI diagnosis. Probable culprit
nificant area of the heart (Wei et al, 2013). artery is based on a typical right dominant circulation
If ischaemia is not relieved, infarction of ECG leads Anatomical area Probable culprit artery
the affected area may ensue within an hour, II, III, aVF Inferior LV wall Right coronary artery
with progressive tissue damage as further V1–V4 Anterior LV wall Left anterior descending
time elapses (Rinta-Kiikka et al, 2014).
I, aVL, V5, V6 Lateral LV wall Left circumflex
Following early identification of STEMI,
reperfusion of the affected area limits inf-
©Peter Lamb
arction size and decreases complications
and mortality (McNamara et al, 2006).
STEMI can be identified by a patient his-
tory of typical symptoms, in association Normal
with ST elevation in at least two anatomi-
cally contiguous leads—in other words,
two ECG leads looking at the same area of
the heart (Steg et al, 2012). For the purpose Peaked T wave
of contiguous leads, the ECG can be divid-
ed into three groups of leads, each of which
corresponds approximately with an ana- Degrees of ST
tomical region, and the blood supply from segment evelavtion
a major coronary artery (Morris and Brady,
2009) (Table 2).
Although ST elevation is the key diag- Q wave formation
nostic feature in STEMI, a number of asso- and loss of R wave
ciated ECG changes are commonly seen
(Hampton, 2013). These appear in a
sequential fashion, creating a dynamic T wave inversion
ECG pattern that is characteristic of STEMI
(Thygesen et al, 2012). These dynamic
changes help to differentiate STEMI from
other causes of chest pain, although not Figure 4. Evolution of a STEMI
every feature is seen in every patient
©Peter Lamb
(Houghton and Gray, 2014). Typical fea-
tures, which we will examine individually
in turn, include (Garcia, 2015) (Figure 4):
w Hyperacute T-waves
w ST segment elevation
w Q-wave formation
w Loss of R-wave height ST segment
w T-wave inversion
w Reciprocal ST-segment depression
T wave
Hyperacute T-waves
Hyperacute T-waves are the first ECG sign
of an evolving STEMI, and appear within
5–30 minutes of artery occlusion (Morris
and Brady, 2009) (Figure 4). Because of the
time that usually elapses between symptom J point
onset and the recording of an ECG, they
may not be seen, making ST elevation the TP segment
first detected ECG change (Houghton and
Gray, 2014). Hyperacute T-waves are taller, Figure 5. The ST segment (in red) starts at the J point, and is isoelectric with the
more symmetrical, and more peaked than TP segment
normal (Garcia, 2015). They appear in the
ECG leads overlying the ischaemic area of Comparison with previous ECGs may be ST segment elevation
the heart, and tend to be more prominent needed to confirm their presence (Morris The ST segment is the short section of
in the chest leads (Hampton, 2013). and Brady, 2009). baseline that joins the end of the QRS

©Peter Lamb
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure 6. Inferior STEMI. There is >1mm of ST elevation in leads II, III and aVF. The ST depression in lead aVL is a reciprocal change
complex to the T-wave (Figure 5). This hours of ischaemia (Houghton and Gray, young men (Hampton, 2013). This phe-
segment is normally isoelectric, which 2014) (Figure 6 ). The initial rise may be nomenon is often referred to as ‘high
means it is at the same level as the TP small but a progressive increase in the take-off ’ or an ‘early repolarisation pat-
segment (Aehlert, 2011). height of the ST segment often occurs tern’ (Garcia, 2015) (Figure 8 ). The degree
Elevation of the ST segment follows (Garcia, 2015). The ST segment may merge of ST elevation required to diagnose
hyperacute T-waves in the evolution of with the T-wave, with complete loss of the STEMI is therefore greater in these leads,
STEMI, and occurs within the first few ST-T angle (Morris and Brady, 2009). If the and greater in men than women (Thygesen
ST segment reaches the top of the QRS as et al, 2012) (Table 3).
well, a single monophasic waveform
results, commonly referred to as a ‘tomb- Q-wave formation and loss of
stone’ (Hampton, 2013). Figure 7 illustrates R-wave height
different degrees of ST elevation. A Q-wave refers to any downward deflec-
ST segment elevation is measured at the tion preceding an R-wave (Aehlert, 2011).
J–point (Houghton and Gray, 2014). This Small, narrow Q-waves are a normal find-
Figure 7. Degrees of ST elevation. In the is the point where the QRS complex tran- ing in the leads facing the LV, and reflect
example on the right, the ST segment has sitions into the ST segment (Figure 5). left to right depolarisation of the interven-
almost entirely merged with the QRS and T– Elevation of the J-point is a normal vari- tricular septum (Hampton, 2013). These
wave to form a single ‘tombstone’ complex ant in leads V2 and V3, especially in ‘septal Q-waves’ are normally seen in leads
I, aVL, aVF, V4, V5 and V6 (Thygesen et al,
2012) (Figure 9 ). A Q-wave is also a normal
finding in lead aVR, and is a normal vari-
ant in leads V1 and III (Houghton and
Gray, 2014).
Abnormal or pathological Q-waves may
develop as a STEMI evolves, and usually
appear while the ST-segment is still elevat-
ed (Houghton and Gray, 2014). They are
caused by a loss of viable myocardium
below the recording electrode, and are
therefore a marker of tissue necrosis
(Garcia, 2015). They are often accompa-
nied by a loss of R-wave height in the same
leads (Aehlert, 2011) (Figure 10).
The explanation for Q-wave appearance
is simple. Infarcted myocardium is electri-
cally inert—it does not produce electricity,
Figure 8. High take-off in leads V2 and V3. The patient was a fit, healthy young man and is therefore invisible to the ECG
attending for routine health screening. There is isolated T–wave inversion in lead III, (Hampton, 2013). An ECG electrode
which is a normal variant placed over an area of dead tissue therefore

Table 3. Degree of ST elevation needed to diagnose STEMI. Assumes normal calibration of the
ECG (10 mm = 1 mV), and the absence of LVH or LBBB
ECG leads Population ST elevation considered diagnostic
All leads except V2/V3 All patients ≥1 mm
V2/V3 Women ≥1.5 mm
V2/V3 Men ≥40 years old ≥2 mm
V2/V3 Men <40 years old ≥2.5 mm
‘sees’ through the infarcted area to the

healthy wall on the opposite side of the
heart. Because depolarisation starts at the
endocardium and moves outwards through
the heart wall, the electrical vector that the
lead sees is moving away from it, and
therefore a negative deflection is recorded
(Jowett and Thompson, 2007).
The timing of pathological Q-wave for-
mation is variable; it may occur within the
first few hours, or not until 24 hours have
elapsed (Morris and Brady, 2009). Because
of this, Q-wave development does not
accurately predict the timing of ischaemic
events, nor does it indicate a completed MI
(Marshall, 2009). Q-waves often persist as a
permanent marker of MI, although, in Figure 9. Septal Q-waves. There are small, narrow Q-waves in leads I, II, aVL, aVF, V4–V6
smaller infarcts, contraction of scar tissue
during healing can result in their disap-
pearance (Rinta-Kiikka et al, 2014).
Pathological Q-waves are usually wide
and/or deep, and may occur in leads where
Q-waves are not normally seen (Marshall,
2009). Houghton and Gray (2014) suggest
that the features of abnormal Q-waves are
w Width >1 small square, and/or
w Depth >2 small squares/>25% of the
subsequent R-wave height.
T-wave inversion
With further evolution of the STEMI, the
ST segment starts to return towards baseline Figure 10. Anterior STEMI. Note the ST elevation in leads V1–V6, and deep, wide
and the T-waves begin to invert (Garcia, Q-waves in leads V1–V4
2015) (Figure 11). It may take several weeks
for the ST segment to completely normalise;
T-wave inversion may persist for months, or
even remain as a permanent marker of inf-
arction (Morris and Brady, 2009).
Persistent ST elevation is suggestive of an
LV aneurysm, although it is not a reliable
indicator (Hampton, 2013) (Figure 12).
Houghton and Gray (2014) suggest that this
late complication of MI occurs in around
10% of survivors.
Reciprocal ST depression
Reciprocal ST depression refers to changes
that are seen in leads remote from the Figure 11. The same patient as Figure 10, following primary PCI. The ST segments are
region of the infarct (Houghton and Gray, returning towards baseline and the T-waves are inverting

bolysis could be given (NICE, 2013). If the

delay is likely to be greater than 120 min-
utes, thrombolysis is the preferred option.
There are several caveats to this guidance.
First, PCI is recommended in patients with
cardiogenic shock, even if treatment delay is
likely to exceed two hours. Second, the
guidance applies only if the patient has pre-
sented within 12 hours of symptom onset. If
presentation is later than this, PCI is not
recommended unless there is evidence of
ongoing ischaemia (NICE, 2013). This rec-
ommendation is based on research, includ-
ing the large Occluded Artery Trial that
failed to show a benefit of delayed PCI com-
Figure 12. The same patient, 12 months post MI. The ST segments are still slightly elevated. pared with medical treatment (Hochman et
Echocardiography excluded LV aneurysm. Note the Q–waves, loss of R–wave height and al, 2006).
inverted T–waves National audit data for England in 2013–
14 shows that 98.5% of eligible STEMI
2014) (Figure 6 ). It is often described as a and early 1990s (Nabel and Braunwald, patients received PCI, and only 1.5% throm-
‘mirror image’ change—in other words, the 2012). Although thrombolysis improves bolysis (Myocardial Ischaemia National
ST depression seen reflects ST elevation outcomes in most patients, it is unsuccess- Audit Project, 2014). Other acute interven-
occurring on the other side of the heart ful in 20–30% of cases (Department of tions for STEMI are listed in Table 4; how-
(Garcia, 2015). Reciprocal ST depression is Health (DH), 2008). It is also associated ever, their delivery should not delay reper-
seen in around 70% of inferior and 30% of with a risk of acute bleeding, and causes fusion (NICE, 2010).
anterior STEMI (Morris and Brady, 2009). It haemorrhagic stroke in 1% of recipients
has a high positive predictive value for (NICE, 2013). It can, however, be adminis- Conclusion
STEMI, and is therefore useful in support- tered rapidly in any healthcare setting, Although ACS presents in a variety of
ing a diagnosis when ECG features or symp- including local healthcare facilities or the ways, persistent ST elevation has the
toms are atypical (Hampton, 2013). back of an ambulance (Gershlick et al, strongest association with acute myocar-
The cause of reciprocal ST depression is 2013). It may be the only viable option in dial infarction, and is an indication for
uncertain; it may represent ischaemia remote locations with poor access to a large emergency reperfusion (Steg et al, 2012).
remote from the site of the infarction or be hospital (Redberg, 2012). During a STEMI, various ECG changes
a benign electrical phenomenon (Morris In contrast, PCI requires admission to a may be seen, including hyperacute T-waves,
and Brady, 2009). Recent research suggests hospital equipped and staffed to perform ST segment elevation, pathological
that persistent reciprocal ST depression cardiac catheterisation (Nabel and Q-waves, loss of R–wave height and T-wave
after STEMI is associated with increased Braunwald, 2012). This limits treatment to inversion (Houghton and Gray, 2014).
infarct size and a higher risk of adverse car- specialised centres, usually in large, regional These progressive changes are seen in con-
diovascular events in the future (Reinstadler hospitals (DH, 2008). Coronary angiogra- tiguous leads, and provide information
et al, 2015). phy is performed to identify the blocked about the location of the infarct, its progress
artery, and balloon angioplasty to reopen it and the area of myocardium at risk
Treatment of STEMI (Cooper, 2015). A stent is usually deployed (Thygesen et al, 2012).
The treatment priority for patients present- to prevent reocclusion (Stefanini and Although ECG changes during STEMI
ing with STEMI is to reopen the occluded Holmes 2013). Other techniques such as are characteristic, they must be correlated
artery and reperfuse the ischaemic area of clot aspiration may also be used to maxim- with patient history and physical examina-
the heart (Steg et al, 2012). One half of ise vessel patency, and to minimise compli- tion in reaching a diagnosis (Hampton,
potentially salvageable tissue may be lost cations such as downstream embolization of 2013). Care should also be taken to exclude
within the first hour of ischaemia, and two micro-emboli (Lam, 2015). PCI is associat- normal variants such as early repolarisa-
thirds by three hours (Reimer et al, 1977). ed with fewer complications than throm- tion or septal Q-waves (Garcia, 2015).
Time is therefore of the essence (Lassen et bolysis, and improved outcomes provided Once diagnosis is confirmed, reperfusion
al, 2013). that it is delivered in a timely fashion by PCI is the preferred option, although
Reperfusion can be achieved by one of (Asseburg et al, 2007). thrombolysis is an alternative if a treat-
two methods—thrombolysis or primary The speed with which reperfusion can be ment delay of more than two hours is
percutaneous coronary intervention (PCI) delivered is the key discriminator in decid- anticipated (NICE, 2013).
(Jowett and Thompson, 2007). ing between thrombolysis and PCI Aspirin, analgesia and continuous moni-
Thrombolysis uses intravenous drugs to (Gershlick et al, 2013). Current national toring are also important while reperfusion
dissolve the clot blocking the artery and guidance recommends PCI if it can be deliv- is arranged, but should not delay definitive
was the treatment of choice in the 1980s ered within 120 minutes of when throm- treatment (NICE, 2010).

Table 4. Interventions during acute STEMI

Intervention Rationale/notes
Aspirin 300 mg orally To inhibit further platelet aggregation
Sublingual or buccal nitrates To relieve pain and reduce cardiac work; pain increases sympathetic tone, making the
(e.g. GTN spray) and intravenous heart work harder and use more oxygen
opiates (usually morphine)
Intravenous anti-emetic To relieve nausea and vomiting, which is a common side effect of opiates, as well as
a common symptom of STEMI
Supplemental oxygen, if indicated Only if SpO2 falls below 94%. Target SpO2 is
w 94–98% in most adults
w 88–92% in people with chronic obstructive pulmonary disease, when there is a
risk of hypercapnic respiratory failure
Continuous monitoring of ECG and vital To detect hypoxia, hypotension and arrhythmias. Hypotension may result from STEMI,
signs or the administration of nitrates/opiates. Arrhythmias are common in acute STEMI,
especially AV blocks and VT/VF, and may be life threatening
Serial ECGs To detect dynamic ECG changes
Emergency pacing/defibrillation Should be available in the event of life-threatening arrhythmia
Information and reassurance STEMI is a frightening experience for both patient and relatives. Simple information
giving and appropriate reassurance can reduce anxiety
Source: NICE, 2010; Steg et al, 2012
the effectiveness of primary angioplasty compared Statistics 2015. www.bhf.org.uk/research/heart-

Next month with thrombolysis and its relationship to time delay: a statistics (accessed 24 May 2016)
Despite the usefulness of the ECG in the Bayesian evidence synthesis. Heart 93(10): 1244–50 Cademartiri F, La Grutta L, Malagò L et al (2008)
diagnosis of STEMI, it does have some Bhatnagar P, Wickramasinghe K, Williams J, Rayner M, Prevalence of anatomical variants and coronary
Townsend N (2015) The epidemiology of anomalies in 543 consecutive patients studied with
weaknesses (Steg et al, 2012). cardiovascular disease in the UK 2014. Heart 64–slice CT coronary angiography. Eur Radiol 18(4):
First, a number of non-ischaemic condi- 101(15): 1182–9 781–91
tions produce ST elevation on the ECG, British Heart Foundation (2015) Cardiovascular Disease Cooper D (2015) The use of primary PCI for the
some of which also cause chest pain
(Houghton and Gray, 2014). This can result
in diagnostic uncertainty, or misdiagnosis
Key Points
w Acute coronary syndromes (ACS) are life threatening events associated with
(Edhouse et al, 2009).
coronary artery lesion rupture and thrombus formation. Symptoms include
Second, the right ventricle and posterior
persistent chest pain that is not relieved by rest or nitrates, nausea and vomiting,
wall of the heart are not ‘seen’ by the stand-
and sweating
ard ECG leads, making infarction of these
regions harder to diagnose (Wei et al, w ACS can be divided into STEMI, NSTEMI and unstable angina, depending to ECG
2013). Additional ECG leads are often nec- appearance and the result of biochemical markers such as troponin. Persistent ST
essary (Garcia, 2015). segment elevation has the strongest association with myocardial infarction (MI), and
Third, new left bundle branch block is a is an indication for immediate thrombolysis or percutaneous coronary intervention
STEMI equivalent and an indication for (PCI). Confirmation of troponin rise is not needed to initiate reperfusion in STEMI
reperfusion (Thygesen et al, 2012). It may
w In the standard ECG leads, the diagnostic criteria for STEMI is ST elevation of 1 mm
also be longstanding problem with a non-
or more in two contiguous ECG leads, although the cut-off is increased in leads V2
ischaemic aetiology, making diagnosis
and V3. The diagnostic level in these two leads depends on age and gender
problematic (Kumar et al, 2013).
Next month, we complete our examina- w During STEMI, ST elevation is often accompanied by progressive change in the ECG
tion of STEMI by considering these diffi- that includes Q wave formation, loss of R wave height, and T wave inversion.
culties. We also turn our attention to the Hyperacute T waves may precede ST elevation, but are often not seen. Dynamic
other two ACS presentations, NSTEMI and change in the ECG strengthens the diagnostic certainty of STEMI, as does reciprocal
unstable angina, and consider the role of ST depression
the ECG in their management. BJCN
w Delay in achieving reperfusion is associated with larger infarct size and increased
mortality. NICE guidance recommends PCI if it can be performed without excessive
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Available online at bhf.org.uk or on DVD, there are three films covering ECG: Acute Management. NICE, London. www.nice.org.
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Part 9: Myocardial ischaemia
and infarction (part B)
and Social Care, London South Bank University, and BHF Alliance member, London.
M
yocardial ischaemia and Differential diagnosis often accompanied by reciprocal
infarction are common causes of of ST elevation ST depression in other areas of the ECG
mortality, morbidity and hospital Diagnosing STEMI quickly ensures that (Morris and Brady, 2009). ECG changes
admission (Nabel and Braunwald, 2012). suitable patients are offered reperfusion are usually dynamic; serial ECGs will
They are usually caused by coronary heart therapy, limiting infarct size, and reducing reveal changes in the degree of ST eleva-
disease (CHD), a progressive, complications and mortality (McNamara tion, as well as the development of Q-waves
inflammatory condition that results in et al, 2006). It is important, however, to and T-wave inversion (Steg et al, 2012).
narrowing or blockage of the coronary ensure that misdiagnosis is not made, as Symptoms are also characteristic. Patients
arteries (British Heart Foundation (BHF), this can result in inappropriate treatment typically present with chest pain that is
2015). In last month’s instalment of our (Edhouse et al, 2009). In a study carried substernal, heavy or crushing, and unre-
ECG series, we examined the anatomy of out in the emergency department of a uni- lieved by nitrates, posture or breathing
the coronary circulation, and outlined the versity hospital, only 15% of patients pre- (Marshall, 2011). This is often accompa-
areas of the heart supplied by the three senting with chest pain and ST elevation nied by nausea, vomiting, and sweating
main coronary arteries. We also discussed on the ECG were diagnosed with STEMI (Resuscitation Council UK (RCUK), 2016).
the pathophysiology of CHD, and related (Brady et al, 2001). A range of other cardi- STEMI is more likely in patients who are
this to patient presentation with stable ac and non-cardiac diagnoses were made older, and who have risk factors for CHD
angina or acute coronary syndromes in the remaining 85%. (Yusef et al, 2004). These include hyperten-
(ACS). We completed our initial Determining the cause of ST elevation sion, diabetes and hypercholesterolaemia,
examination of this topic by discussing the on the ECG can be difficult in clinical prac- as well as lifestyle issues such as poor diet,
role of the ECG in the diagnosis of ST tice (Wang et al, 2003). Although many excessive alcohol, cigarette smoking and
elevation myocardial infarction (STEMI), causes of ST elevation are associated with lack of exercise (Kennedy, 2008). Males
and briefly considering current treatment characteristic ECG features, these are not and individuals with a family history of
recommendations. conclusive, and may not be present in premature cardiovascular disease are also
In this penultimate article in our ECG every patient (Hampton, 2013). The ECG is at higher risk of STEMI, and tend to
series, we return to STEMI to answer the therefore only one part of the diagnostic present at a younger age (Yunyun et
following questions: picture, and must be considered alongside al, 2014).
w Firstly, what are the differential diag- patient symptoms, age and medical history
noses for ST elevation on the 12-lead (O’Donovan, 2013). Physical examination, Acute pericarditis
ECG? and the results of additional diagnostic In acute pericarditis, ST elevation is typi-
w Secondly, how can we detect STEMI tests are also important (Houghton and cally widespread, and does not correspond
affecting the right ventricle (RV) or pos- Gray, 2014). To illustrate this point, the with coronary territories as it does in
terior wall of the left ventricle (LV), diagnostic features of some of the common STEMI (Hampton, 2013). The appearance
given that they are poorly seen by the causes of ST elevation are discussed in the of the ST segment is also different, usually
standard ECG leads (Garcia, 2015)? next section; a full list of common differen- having a concave or saddle-shaped appear-
w Thirdly, how does left-bundle branch tials can be found in Table 1. ance (Porela et al, 2012). There may be
block (LBBB) affect the diagnosis of PR segment depression in the same leads,
acute myocardial infarction? STEMI and reciprocal ST depression in leads aVR
We also turn our attention to non-ST During STEMI, ST elevation typically has a and V1 (Snyder et al, 2014) (Figure 2). The
elevation MI (NSTEMI) and unstable flat, up-sloping or convex shape, and is pain of pericarditis is typically sharp and
angina, and evaluate the role of the ECG in seen in contiguous leads that reflect the pleuritic; it is worse on inspiration, and
the diagnosis and management of these territory of one or more coronary arteries relieved by sitting forwards (Houghton
conditions. (Thygesen et al, 2012) (Figure 1). This is and Gray, 2014). A pericardial friction rub
332 British Journal of Cardiac Nursing July 2016 Vol 11 No 7

Table 1. Common causes of ST elevation male (Snyder et al, 2014). In two studies
looking at patients undergoing angiogra-
Condition Diagnostic features
phy for suspected ACS, pericarditis was the
STEMI w Upsloping or convex ST elevation in a coronary territory most common diagnosis reached when the
w Dynamic ECG changes coronary arteries were found to be normal
w Reciprocal ST depression may be present (Widimsky et al, 2006; Gu et al, 2008).
w Crushing central chest pain, unaffected by posture or
breathing
Left-ventricular aneurysm
LV aneurysm is a late complication of
LV aneurysm w Persistent ST elevation over the affected area of the heart STEMI, and occurs in around 10% of sur-
w Recent history of acute MI vivors (Houghton and Gray, 2014). The
w Aneurysm visible on echocardiogram characteristic finding is persistent ST ele-
Acute pericarditis w Widespread ST elevation and PR depression vation in one or more coronary territories;
although unlike acute STEMI, there are no
w ST elevation is usually concave
dynamic changes on serial ECGs (Garcia,
w There may be reciprocal ST depression in aVR/V1 2015). Most commonly, the anterior and
w Sharp, pleuritic chest pain apical LV are affected; ST elevation is
Aortic dissection w ‘Tearing’ chest pain, radiating to the back therefore seen in the anterior chest leads
(Wang et al, 2012). Patients may present
w Different blood pressure in each arm
with chest pain, heart failure or arrhyth-
w Neurological/pulse deficits, aortic regurgitation mias, and will have a recent history of
w Mediastinal widening at chest X-ray myocardial infarction (Houghton and
Prinzmetal’s w ECG appearance mimics STEMI Gray, 2014). Aneurysm can be confirmed
(vasospastic) w Transient—ST segments return to baseline if spasm is
by echocardiography, which also has an
angina relieved
important role in assessing the degree of
LV dysfunction (Wang et al, 2012). If this is
Left-ventricular w Tall QRS complexes in leads facing the LV, deep S-waves in severe, surgical treatment to repair the
hypertrophy V1/V2 aneurysm and restore normal LV geome-
w ST elevation seen in V1/V2, with ST depression/T-wave try may be necessary (Antunes et al, 2005).
inversion in V5/V6. T-wave inversion is asymmetrical
Left-bundle branch w Typical pattern of deep S-waves in right-sided precordials, Aortic dissection
block and monophasic, notched R-wave in V6/lead I If the coronary arteries are disrupted by
w ST elevation is a normal feature in leads V1–V3 acute dissection of the aorta, a STEMI-like
ECG can result (Houghton and Gray,
Benign-early w Mild ST elevation in the precordial leads, with tall T-waves
2014). It may be impossible to differentiate
repolarisation w The ST segment is concave, and there may be notching at the two conditions from the ECG alone;
the J-point however, other characteristic features are
w Common in young men often present. Unlike STEMI, the chest
w There is no reciprocal ST depression pain associated with aortic dissection tends
to be sharp, tearing or ripping, and often
Ventricular-paced w The QRS is broad, often with a left-bundle branch pattern
radiates to the back (Hampton, 2013). Pain
rhythm w Pacing spikes will be visible on the ECG onset is abrupt, and immediately severe,
Brugada w Right-bundle branch pattern lacking the build-up that may be reported
syndrome w Coved ST elevation ≥2 mm and T-wave inversion in leads in STEMI (Thrumurthy et al, 2011).
V1–V3 Physical examination may reveal neuro-
Hyperkalaemia w Wide QRS complexes with down-sloping ST elevation logical or pulse deficits, a difference in
blood pressure between the arms, or the
w Tall, peaked T-waves
murmur of aortic regurgitation (RCUK,
w P-waves low amplitude or absent 2016). Mediastinal widening may be seen
Raised-intracranial w ST elevation is widespread and concave, similar to at chest X-ray, although more advanced
pressure (e.g. pericarditis imaging such as computed tomography
cerebral bleed) w Reciprocal change is seen only in aVR and V1 (CT) angiography is required to confirm
dissection, and guide management
w Neurological symptoms will be present

(Golledge and Eagle, 2008).
is a common finding at physical examina- STEMI patient, individuals presenting with Benign early repolarisation
tion, occurring in up to 85% of patients pericarditis are usually below the age of 50 In benign early repolarisation (BER),
(Snyder et al, 2014). Unlike the typical years; although, like STEMI, they are often ST elevation is usually mild (<5 mm) and is
British Journal of Cardiac Nursing July 2016 Vol 11 No 7 333

Figure 1. Anterior STEMI. There is upsloping ST elevation in the anterior chest leads, suggesting acute occlusion of the left-anterior
descending artery. Reciprocal ST depression can be seen in leads III and aVF
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure 2. Acute pericarditis. There is widespread concave ST elevation, and PR depression. Note the reciprocal ST depression in
lead aVR
seen in the precordial leads, typically V2– vation such as left-ventricular hypertrophy Prinzmetal’s angina (Houghton and Gray,
V4 (Houghton and Gray, 2014). As in peri- (LVH) (Brady et al, 2001). 2014). A thorough evaluation of symp-
carditis, the ST segment is usually upward- In summary, the shape and distribution toms, history, physical findings and test
ly concave, and there may be ‘fish-hook’ of ST elevation is characteristic in STEMI, results will help to differentiate between
notching of the J-point (Burns, 2016) and contrasts with that seen in conditions these conditions (Steg et al, 2012). Careful
(Figure 3). The T-wave in affected leads such as pericarditis and BER (Garcia, patient evaluation will also provide clues to
may be unusually tall; reciprocal ST depres- 2015). Additional features such as recipro- support a suggested ECG diagnosis; for
sion is absent (Garcia, 2015). BER is com- cal ST depression and dynamic change are example, an ECG showing widespread,
mon in young men, less pronounced in also useful diagnostic markers (Morris and concave ST elevation is more likely to be
women, and rare in the elderly (Wang et al, Brady, 2009). Even in the presence of these pericarditis in a young man with pleuritic
2003). Although it does not cause symp- typical features, however, diagnosis cannot chest pain and no risk factors for CHD
toms, BER may be mistaken for STEMI in be made from the ECG alone (Hampton, (Snyder et al, 2014). Equally, it should be
patients who present with non-cardiac 2013). A STEMI-like ECG may be seen in remembered that most chest pain does not
chest pain, as may chronic causes of ST ele- LV aneurysm, aortic dissection and have cardiovascular cause. ST elevation on

lar, V3R and V4R (Steg et al, 2012)

(Figure 5). Because voltages are typically
smaller in the RV, the diagnostic threshold
in these leads is lower. In men below the
age of 30 years, 1 mm of ST elevation is
diagnostic of RV infarction; in all other
individuals, only 0.5 mm is required
(Thygesen et al, 2012).
Diagnosing RV infarction is important
for several reasons. Firstly, RV infarction is
associated with a greater incidence of ven-
tricular arrhythmias, complete heart block
and cardiogenic shock than simple inferior
STEMI, owing to the larger area of dam-
V4 aged myocardium (Somers et al, 2003).
Secondly, a significant number of patients
with an RV infarct present with hypoten-
Figure 3. Lead V4 from an individual with benign early repolarisation. Note the concave sion and jugular venous distension as a
ST segment elevation and ‘fish-hook’ notching of the J-point result of acute right heart failure (Ondrus
et al, 2013). Failure to diagnose RV infarc-
the ECG may be unrelated to patient pres- (Ondrus et al, 2013). Current guidelines tion as the cause may result in inappropri-
entation, as in BER, ventricular hypertro- suggest evaluating all patients with inferior ate haemodynamic management
phy and bundle branch blocks (Brady et al, STEMI for associated RV infarction (Steg (Hampton, 2013). In patients with an
2001). et al, 2012). LV infarct, acute heart failure is managed
On the ECG, RV involvement is sug- by withholding intravenous (IV) fluid, and
Right-ventricular infarction gested by several features during inferior using vasodilators and diuretics to offload
Because the right ventricle is poorly seen infarction. Inferior STEMI is characterised fluid and reduce LV preload (Whitlock and
by the 12 standard ECG leads, infarction of by ST elevation in leads II, III and aVF MacInnes, 2014). This relieves back pres-
the right ventricle (RV) may be overlooked (Hampton, 2013). When the RV is also sure on the pulmonary circulation, caused
(Hanna and Glancy, 2011). In most indi- involved, ST elevation may be greater in by LV systolic dysfunction, and reduces
viduals, the right coronary artery (RCA) lead III than lead II, and there may be addi- pulmonary oedema (Serrano-Gomez and
supplies the inferior surface of the LV, as tional ST elevation in lead V1 (Somers et Thompson, 2009). In an RV infarct,
well as the RV (Cademartiri et al, 2008). In al, 2003) (Figure 4). Although these find- LV function is often preserved; hypoten-
consequence, up to half of inferior STEMI ings are highly suggestive, RV infarction sion is caused by low LV filling pressures
are complicated by RV involvement, can only be confirmed by recording leads secondary to RV systolic dysfunction, and
although isolated RV infarction is rare placed over the right ventricle; in particu- pulmonary oedema is absent (Houghton
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Figure 4. Inferior STEMI with RV involvement. The ST elevation is greater in lead III than in lead II, and there is ST elevation in V1.
Lead V4R was subsequently recorded, and showed ST elevation of 3 mm

ciation with infarction of another cardiac

territory, the greater infarct size results in
higher mortality and a greater incidence of
complications (Rinta-Kiikka et al, 2014). In
studies of isolated posterior STEMI, the
culprit lesion is most commonly in the LCx
(Agarwal et al, 1999; Pride et al, 2010).
On the ECG, the signs of posterior
STEMI are less obvious, because the 12
standard leads of the ECG do not visualise
V2R V1R the back of the heart directly (Garcia,
V6R 2015). ‘Mirror image’ changes can, howev-
V3R
er, be seen in leads V1–V3 (Hampton,
V5R 2013). The principal finding is ST depres-
V4R
sion in these leads, typically with upright
T-waves (Somers et al, 2003) (Figure 6). The
R-waves in the same leads may also become
taller and wider, creating dominant R-waves
in leads V1 and/or V2 (Houghton and
Gray, 2014). These changes are the reverse
of the Q-waves, ST elevation, and T-wave
inversion that would be seen if the elec-
Figure 5. Placement of right precordial electrodes. Positions are a mirror image of the trodes were placed over the posterior wall
normal left-sided electrodes of the heart (Morris and Brady, 2009). As
with RV infarction, posterior STEMI can
and Gray, 2014). In this situation, IV fluids Posterior infarction be confirmed by recording additional ECG
should be given to increase LV preload The posterior wall of the LV is supplied by leads, in this case V7–V9 (Garcia, 2015)
while vasodilators and diuretics should be the RCA or left circumflex artery (LCx) (Figure 7). As with leads V3R and V4R, the
avoided (Morris and Brady, 2009). As with (Cademartiri et al, 2008). Posterior infarc- diagnostic cut-off is ST elevation of 0.5 mm,
all types of STEMI, definitive treatment tion can therefore complicate either inferi- although this is increased to 1 mm in men
remains the opening of the occluded artery or or lateral STEMI, although it occasion- below the age of 40 (Thygesen et al, 2012).
and reperfusion of the ischaemic myocar- ally occurs in isolation (Somers et al, 2003). When posterior infarction occurs in the
dium (Steg et al, 2012). Where posterior STEMI is found in asso- context of inferior or lateral STEMI, there
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure 6. Inferolateral STEMI with posterior involvement. Note the ST elevation in the inferolateral leads, and marked ST depression
in V1–V3. There is a dominant R-wave in lead V2

leads V1–V3, especially when T-waves are

Scapula upright (Steg et al, 2012). Posterior chest
leads (V7–V9) should be recorded in these
individuals (Thygesen et al, 2012). There
may also be some benefit in recording pos-
terior leads when the ECG is non-diagnos-
tic; in a study of 58 such patients, posterior
STEMI was diagnosed in 18 individuals, all
but one of whom went on to receive percu-
taneous coronary intervention (PCI)
(Agarwal et al, 1999).
Left-bundle branch block

The final challenge that we need to con-
V7 V8 V9 sider when diagnosing STEMI is the indi-
vidual presenting with LBBB. New or pre-
sumed new LBBB, in the presence of typi-
cal symptoms, is considered a STEMI
equivalent, and an indication for immedi-
ate reperfusion (Steg et al, 2012). This is
straightforward; the difficulty arises when
the patient has pre-existing LBBB, but
presents with symptoms consistent with
acute MI. We know that in LBBB, abnor-
malities in the ST segment and T-waves are
Figure 7. Posterior electrode placement. V7 is placed in the left-posterior axillary line, a common and normal finding (Garcia,
V8 in the left mid-scapular line, and V9 at the left-paraspinal border 2015). Distinguishing between these nor-
mal findings, and abnormal changes that
is a good chance of correct diagnosis and diagnosis of NSTEMI or unstable angina might indicate acute ischaemia is difficult;
treatment owing to the presence of ST ele- (Khan et al, 2012). This may result in a however, the orientation and magnitude of
vation on the ECG (Hampton, 2013). This failure to offer reperfusion, and impaired the ST segment and T-wave provides useful
is less certain when posterior infarction patient outcomes (Pride et al, 2010). diagnostic information (Houghton and
occurs in isolation; the lack of ST elevation Current European guidelines suggest a Gray, 2014).
and presence of ST depression in the right- high index of suspicion in any patient with To understand the diagnosis of STEMI
sided chest leads may result in an incorrect typical symptoms and ST depression in in LBBB, we need to define the term ‘con-
Figure 8. Left -bundle branch block without acute ischaemia. Note the appropriate discordance; for example, the ST elevation and
upright T-waves in leads V1–V3, and the ST depression and T-wave inversion in leads I, aVL, V5, V6

cordance’. In ECG terms, concordance There is a high rate of false negatives in thrombus may be smaller (Overbaugh,
means that the T-wave follows the same patients taken for coronary angiography; 2009). As a consequence, arterial occlusion
direction as the QRS (Garcia, 2015). So, in in other words, patients with LBBB and is usually incomplete, and the clot may
leads where there is an upright QRS, the chest pain, but no critical coronary artery embolise to block a smaller, more distal
T-wave is also upright. In LBBB, the nor- stenosis (Larson et al, 2007). vessel (RCUK, 2016). This usually results
mal rules of concordance are reversed in subendocardial, rather than transmural,
(Houghton and Gray, 2014). In leads with NSTEMI and unstable angina ischaemia, and permanent tissue damage
negative QRS complexes, such as V1, there NSTEMI and unstable angina are collec- may not occur (Nikus et al, 2010). Persistent
are upright T-waves, as well as ST eleva- tively referred to as non-ST elevation ACS ST elevation is not seen on the ECG
tion. In contrast, QRS complexes that are (NSTEACS) (Marshall, 2011). The inci- (Hampton, 2013). The benefit of immedi-
positive, for example V6, have inverted dence of NSTEACS has risen over recent ate reperfusion in NSTEACS is less clear,
T-waves and ST depression (Hampton, years, while that of STEMI has declined and a decision on treatment is based on
2013) (Figure 8). These normal findings in (Plakht et al, 2016). This is reflected in data several factors including the risk of death,
LBBB are referred to as ‘appropriate dis- from the UK; of 89 724 heart attacks or reinfarction over the coming months
cordance’ (Edhouse et al, 2009). In other reported in 2013–14, 39% were STEMI, (Roffi et al, 2016).
words, the T-waves and ST segments are and 61% NSTEMI (Myocardial Ischaemia
discordant, but that’s normal in this situa- National Audit Project, 2014). Although Diagnosis of NSTEACS
tion. the reasons for this shift are unclear, sev- The diagnosis of NSTEACS is based on
In the patient with chronic LBBB and eral explanations have been proposed. typical symptoms, in association with ECG
acute myocardial ischaemia, the ST seg- Firstly, the demographics of ACS have changes suggesting acute ischaemia
ment or T-wave may become concordant changed, with more elderly, female, dia- (Overbaugh, 2009). The measurement of
(Houghton and Gray, 2014). This is referred betic and obese patients (McManus et al, cardiac biomarkers, usually troponin I or
to as ‘inappropriate concordance’; in other 2011). Secondly, a change in CHD risk T, is also an essential component of the
words, there is now concordance, but it’s profile has been seen in Western popula- diagnostic process (Roffi et al, 2016).
not normal in LBBB. Another change that tion; in particular, a decline in smoking Troponins are cellular proteins that are
suggests acute ischaemia is when discord- and an increased use of statins (Bhatnagar released by dying myocytes, and are there-
ant ST elevation (normal in LBBB) becomes et al, 2015; BHF, 2015). It has been argued fore indicative of cellular necrosis (Shah et
exaggerated (Smith, 2015). These changes that these alterations have contributed to a al, 2013). They are measured by serial
may be more evident over serial ECGs, or change in the predominant pathology blood tests in all patients presenting with
when compared with historical recordings responsible for ACS (Libby and Pasterkamp, suspected ACS (Marshall, 2011). If signifi-
(Edhouse et al, 2009). 2015). cant changes in troponin levels are detect-
The changes that occur in LBBB during In STEMI, coronary artery plaques tend ed, a diagnosis of NSTEMI is made
acute ischaemia are the basis of a scoring to be large, lipid-rich lesions covered by a (Thygesen et al, 2012). In contrast, the
system that predicts the likelihood of thin fibrous cap (Libby and Pasterkamp, signs and symptoms of ACS without tro-
STEMI. This system, developed by 2015). Acute rupture of this cap results in a ponin change suggests that no permanent
Sgarbossa et al (1996), uses three diagnos- thrombus that completely occludes the tissue damage has occurred, and the diag-
tic criteria: coronary artery, resulting in transmural nosis is unstable angina (Roffi et al, 2016).
w Concordant ST elevation of 1 mm or ischaemia and ST elevation on the ECG Although the ECG is useful in making a
more (5 points) (Wei et al, 2013). Unless the occluded diagnosis of NSTEACS, it cannot differen-
w ST depression of 1 mm or more in leads artery is reopened swiftly, permanent myo- tiate between NSTEMI and unstable angi-
V1, V2 or V3 (3 points) cardial damage occurs (Rinta-Kiikka et al, na (Hampton, 2013).
w Discordant ST elevation of 5 mm or 2014). Immediate reperfusion is recom-
more (2 points). mended in clinical guidelines because it The ECG in NSTEACS
According to Sgarbossa et al (1996), a limits infarct size, prevents complications, The typical ECG changes seen during
score of 3 or more has a sensitivity of 78% and improves patient outcomes (Steg et al, NSTEACS are ST segment depression and/
for STEMI, with a specificity of 90%. Smith 2012; National Institute for Health and or T-wave inversion, although transient
(2015) argues that this has similar diagnos- Care Excellence (NICE), 2013). ST elevation may also occur (Nikus et al,
tic accuracy to the criteria used in the non- Vulnerability of the fibrous cap to rupture 2010). In up to a third of cases, no ECG
LBBB ECG (i.e. ST elevation in contiguous has been linked to inflammatory processes changes are detected (Savonitto et al, 1999).
leads). However, others have been critical driven by traditional risk factors such as The classic progression of ECG changes
of the criteria, suggesting that they are smoking and hypercholesterolaemia that occurs in STEMI is absent in
complex and lack diagnostic certainty (Libby, 2012). NSTEACS; however, dynamic changes in
(Shlipak et al, 1999; Tabas et al, 2008). In contrast to STEMI, the plaques associ- the ST segments and T-waves do occur
Current guidelines suggest that concordant ated with NSTEACS tend to be smaller, (Hampton, 2013). Given the possibility of
ST elevation has the best predictive value, with less lipid and a thicker fibrous cap dynamic change, and transient abnormali-
but note that most cases of chest pain with (Libby and Pasterkamp, 2015). Lesion dis- ties, serial ECGs are as important in
LBBB evaluated in the emergency depart- ruption typically occurs through erosion, NSTEACS as in STEMI (Roffi et al, 2016).
ment do not have STEMI (Steg et al, 2012). rather than rupture, and the subsequent A 12-lead ECG should be recorded at regu-

sation abnormalities that occur in bundle sic, or ‘pseudonormal’ (T-waves that are
branch blocks and ventricular hypertrophy usually inverted, but have flipped upright
(Garcia, 2015). In these conditions, chang- as a result of ischaemia) (Houghton and
es in the ST segments and T-waves have Gray, 2014)
A B
characteristic features (Hampton, 2013): w Dynamic changes in the ST segment or
w ST depression is down-sloping, with T-waves over serial recordings
asymmetrical ‘reverse tick’ T-wave inver- (Hampton, 2013)
sion (Figure 8) w ECG changes seen in contiguous leads,
w ST depression and T-wave inversion are consistent with the territory of one or
C D discordant to the QRS complex more coronary artery (Edhouse et al,
w In the short term, ST segment and 2009).
T-wave changes are fixed; there is no Figure 10 illustrates some of these fea-
Figure 9. In the normal ST segment (A), dynamic change on serial ECG record- tures. Current guidelines suggest that
the ST segment is isoelectric, and blends ings ST depression of at least 0.5 mm, occurring
seamlessly with the T-wave. Early w ST depression and T-wave inversion in two contiguous leads, is strongly indica-
ischaemia may result in T-wave flattening occur in predictable leads: In leads fac- tive of NSTEACS, while recognising that
(B), with loss of this smooth transition. ing the LV (e.g. I, aVL, V5, V6) in LVH other ECG findings, or a normal ECG are
Ischaemic ST depression may be flat (C) and left-bundle branch block, and in also possible (Roffi et al, 2016).
or down-sloping (D) leads facing the RV (e.g. V1, V2) in right
ventricular hypertrophy and right-bun- Localising NSTEACS
lar intervals, and when there is a change in dle branch block. In contrast to STEMI, there is a poor cor-
reported pain (Overbaugh, 2009). The ECG changes that occur during relation between ECG abnormalities and
As with STEMI, any ECG abnormalities NSTEACS can be difficult to distinguish affected coronary territory during
detected must be distinguished from nor- from these chronic changes; however, there NSTEACS (Hanna and Glancy, 2011). It is
mal variants, or the effects of chronic dis- are a number of ECG characteristics that therefore harder to predict the culprit
ease. T-wave inversion is normal in leads are consistent with acute ischaemia: artery, and to assess prognosis. Despite
aVR and V1, and may be a normal variant w ST depression that is horizontal or down- this, conclusions can be drawn from ECG
in lead III (Houghton and Gray, 2014). In sloping, with an upright T-wave; the in several circumstances.
children, T-wave inversion is normal in all ST segment may be concordant with the Firstly, a number of studies have demon-
of the right-sided precordials (V1–V3), QRS complex (Hanna and Glancy, 2011). strated that outcomes are worse in patients
and this may persist into early adulthood In mild ischaemia, there may be flatten- presenting with ST depression, than with
(Hampton, 2013). This ‘persistent juvenile ing of the ST segment rather than depres- T-wave inversion or a normal ECG
pattern’ is more commonly seen in young sion, resulting in a sharp angle between (Savonitto et al, 1999; Mueller et al, 2004).
women, especially those of African descent the ST segment and T-wave (Channer There is a linear relationship between the
(Hanna and Glancy, 2011). and Morris, 2009) (Figure 9) extent of ST depression (number of leads
T-wave inversion in any other lead is w T-wave inversion that is deep and sym- multiplied by millimetres of ST depres-
considered abnormal, although it is a rec- metrical (Garcia, 2015). Other variants sion) and the risk of death or complication
ognised feature of the secondary repolari- include T-waves that are flattened, bipha- (Savonitto et al, 2005).
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Figure 10. NSTEACS. There is horizontal ST depression with upright T-waves in leads II, III, aVF, and V3–V6

Secondly, although ECG changes in the research by Wellen and colleagues; in their Acute treatment of NSTEACS
inferior and lateral leads often result from study, outcomes were evaluated in patients As with STEMI, immediate treatment pri-
poorly localised subendocardial ischaemia, who did or did not undergo angiography orities include nitrates and opiates to
changes in the anterior chest leads often for ACS (de Zwaan et al, 1982). Of the relieve pain, anti-emetics, oxygen if indi-
reflect disease in the left-anterior descend- patients with Wellen’s syndrome who were cated, serial ECGs, and close monitoring of
ing artery (LAD) (Nikus et al, 2010). In managed without angiography, 75% devel- heart rhythm and vital signs (Marshall et
particular, deep symmetrical or biphasic oped an extensive anterior infarction. This al, 2011). Unlike STEMI, immediate reper-
T-wave inversion in leads V2 and V3, with led the authors to recommend urgent angi- fusion is not indicated unless there is
or without similar change in V1 and V4 to ography in any patient with these charac- deemed to be a high risk of death or
V6, is strongly associated with critical ste- teristic ECG findings. Subsequent studies adverse cardiovascular events (Roffi et al,
nosis of the proximal LAD. In patients with have reached similar conclusions, and have 2016). Current UK guidelines recommend
unstable angina, this ECG pattern is found the features of Wellen’s syndrome in the use of a risk-prediction tool such as the
referred to as Wellen’s syndrome (Hollar et 14% of patients presenting with unstable Global Registry of Acute Cardiac Events
al, 2015). Other ECG features associated angina (Hanna and Glancy, 2011). [GRACE] score (Granger et al, 2003; NICE,
with this syndrome include little or no 2010).
ST elevation, normal precordial R-wave Differential diagnosis The GRACE score predicts the risk of
progression, and an absence of Q-waves As with ST elevation, numerous cardiac death in the next 6 months, and is used to
(Khan et al, 2013) (Figure 11). and non-cardiac conditions can result in place patients in risk categories according
Because individuals with Wellen’s syn- ST depression or T-wave inversion, and to the likelihood of a future adverse cardio-
drome present with unstable angina, car- must therefore be excluded when evaluat- vascular event (NICE, 2010) (Table 3). For
diac biomarkers are typically normal, and ing the ECG for NSTEACS (Hanna and those at intermediate or higher risk, angi-
pain intermittent (Hollar et al, 2015). The Glancy, 2011). As with STEMI, careful ography is recommended within 96 hours,
characteristic ECG pattern described above consideration of the patient, presenting with progression to PCI if necessary
is recorded when patients are pain-free; symptoms, medical history, physical find- (NICE, 2010). Early angiography is also
during pain, there may be transient ST ele- ings, and other diagnostic tests are impor- recommended for patients with ongoing
vation or hyperacute T-waves in the ante- tant, and must be considered alongside the ischaemia, and should be performed
rior chest leads, consistent with brief occlu- ECG (Roffi et al, 2016). Common causes of urgently in individuals who are unstable or
sion of the LAD (Hanna and Glancy, 2011). ST depression and T-wave inversion are at high ischaemic risk (NICE, 2010). Low-
The syndrome was identified during shown in Table 2. risk individuals can be managed conserva-
tively (Roffi et al, 2016).
The other treatment priority for patients
with NSTEACS is the prevention of further
coronary thrombosis (RCUK, 2016). All
patients should be commenced on an
V1 V4 aggressive anti-thrombotic regime to
inhibit clot formation (Marshall, 2011). A
typical protocol includes dual anti-platelet
therapy in the form of aspirin plus a P2Y12-
inhibitor (clopidogrel, prasugrel or ticagre-
lor) (Khan, 2015). Loading doses are given
if the patient is not already established on
these drugs (Overbaugh, 2009). A parenter-
V2 V5 al anticoagulant is also started, usually
fondaparinux, although unfractionated
heparin is preferred in patients with sig-
nificant renal impairment (NICE, 2010).
Conclusion
The ECG plays an important role in the
diagnosis of both STEMI and NSTEACS.
V3 V6 In STEMI, persistent ST elevation indicates
complete occlusion of an epicardial coro-
nary artery, and transmural cardiac ischae-
mia (Wei et al, 2013). Although urgent

Figure 11. Wellen’s syndrome. There is biphasic T-wave inversion in leads V1–V3, and reperfusion is mandated to limit myocar-
deep symmetrical T-wave inversion in lead V4. R-wave progression is preserved, there dial damage, care must be taken to exclude
are no Q-waves, and only minor ST elevation is present. The patient is at risk of an alternative causes of ST elevation such as
extensive anterior STEMI pericarditis, aortic dissection, and BER

Table 2. Causes of ST depression and T-wave inversion (Houghton and Gray, 2014). Careful evalu-
Secondary repolarisation abnormalities ation of the ECG alongside patient age,
history, symptoms and physical findings
w Left- and right-bundle branch block are the key to correct diagnosis (Hampton,
w Left- and right-ventricular hypertrophy 2013).
w Cardiomyopathies Care must also be taken to evaluate the
w Pre-excitation ECG for possible RV or posterior STEMI,
as these are not obvious from the standard
Normal variants
12 leads (Somers et al, 2003). Additional
w T-wave inversion normal in leads aVR, V1 ECG leads should be considered in inferior
w T-wave inversion a normal variant in lead III STEMI, when there is ST depression in
w T-wave inversion normal in V1–V3 in children, and in persistent juvenile pattern V1–V3, or when there are typical symp-
toms but a non-diagnostic ECG (Thygesen
Acute ischaemia
et al, 2012). LBBB should be considered a
w NSTEACS STEMI equivalent if it is new or presumed
w Demand or rate-related ischaemia (e.g. during exercise tolerance testing, to be so; diagnosis of acute infarction in a
arrhythmias) patient with chronic LBBB is more difficult
Wellen’s syndrome but examination of ST segments for exag-
gerated or concordant changes can be use-
w Deep symmetrical or biphasic T-wave inversion in leads V2/V3, +/--V1, V4, V5
ful (Steg et al, 2012).
w Denotes critical LAD stenosis, and high risk of anterior STEMI In NSTEACS, ECG changes are more
Posterior STEMI variable, and have a less direct relationship
w ST depression greatest in V1-–V3 +/- dominant R-waves in V1/V2 with coronary anatomy and prognosis
(Nikus et al, 2010). The degree of ST depres-
w Record additional posterior leads V7–V9 to confirm or exclude
sion is, however, a useful prognostic indi-
Reciprocal change cator, as are the signs of Wellen’s syndrome
w ST elevation will be seen in another coronary territory (Hanna and Glancy, 2011). As with STEMI,
Pulmonary embolism normal variants, chronic changes, and dif-
w T-wave inversion possible in the anterior and/or inferior leads, but various other ferential diagnoses must be considered
presentations also occur, including acute RV-strain pattern (similar to RVH). The when reaching a diagnosis, and thorough
most common ECG finding is sinus tachycardia patient assessment must accompany scru-
tiny of the ECG (Houghton and Gray,
Hypokalaemia 2014). Initial treatment follows similar
w ST depression and T-wave flattening may occur and there may be prominent U-wave lines to STEMI; however, risk assessment is
Digoxin effect used to evaluate the benefit of angiography,
w ST depression and T-wave flattening are seen with therapeutic levels and aggressive anti-thrombotic treatment
is started while assessment takes place
Pericarditis
(NICE, 2010).
w Widespread T-wave inversion may occur following resolution of ST elevation Next month, we complete our examina-
Intracranial haemorrhage tion of the 12-lead ECG by considering
w Giant T-wave inversion may be seen some important presentations that we have
yet to cover during our series. These
T-wave memory
include the patient who is paced, the effect
w T-wave inversion caused by transient ventricular arrhythmia, pacing or bundle- of cardiovascular drugs on the ECG, and
branch block may persist for some time after normal rhythm is restored the changes that occur during common
Source: Hanna and Glancy, 2011 electrolyte disturbances. BJCN
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BHF Resources
ST-elevation myocardial infarction: a literature
review. Ann Noninvasive Electrocardiol 19(6): 509– The British Heart Foundation (BHF) is committed to sharing our knowledge to
23. doi: 10.1111/anec.12210 prevent heart disease devastating people’s lives. We have created a range of
Roffi M, Patrono C, Collet JP et al (2016) 2015 ESC resources that can be used by health professionals to support people with a
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Savonitto S, Ardissino D, Granger C et al (1999) w Electrocardiogram—Your quick guide. A short illustrated leaflet that helps
Prognostic value of the admission adults understand what to expect if they’re having an ECG. It explains the
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bundle-branch block. GUSTO-1 (Global
Utilization of Streptokinase and Tissue The BHF Alliance is a free membership scheme that supports professionals
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What are the steps in the systematic analysis tool for 12-lead ECG interpretation?

What are the steps in the systematic analysis tool for 12-lead ECG interpretation?

What are some conditions that can cause ST segment and T wave changes on an ECG besides acute coronary syndromes?

What are some conditions that can cause ST segment and T wave changes on an ECG besides acute coronary syndromes?

Practical Procedures

An analysis tool for 12-lead

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and Pritchett, 1999). In a normal heart,

6 seconds = 30 large boxes

British Journal of Cardiac Nursing May 2006 Vol 1 No 5 217

Figure 5. Parameters for normal sinus

Axis deviations are common to ventricular

hypertrophy and hemi-blocks as well as

Wolff-Parkinson-White syndrome (Garcia Atrioventricular node

and Holtz, 2001). For this reason, if Wolff-

ventricles. In sinus rhythm, the electrical Posterior fascicle

through the atrioventricular node and into Right bundle branch

heart in the chest, together with the mus-

cular and electrical dominance of the left ax

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British Journal of Cardiac Nursing May 2006 Vol 1 No 5 219

with the baseline, although slight elevation

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often manifested by abnormally tall P waves.

British Journal of Cardiac Nursing May 2006 Vol 1 No 5 221

Understanding the ECG.

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There is considerable interchange

British Journal of Cardiac Nursing November 2015 Vol 10 No 11 549

Myocyte Electrical cell

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British Journal of Cardiac Nursing November 2015 Vol 10 No 11 551

Figure 6. ECG waveforms

duction to the waves recorded on the ECG

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of the U-wave remains uncertain. Some

British Journal of Cardiac Nursing November 2015 Vol 10 No 11 553

To discuss your ideas please contact the editor:

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Understanding the ECG

called the chest or precordial leads. Each

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ECG paper RV V6 lateral

British Journal of Cardiac Nursing December 2015 Vol 10 No 12 589

Large Heart rate

Figure 6. The R-R method of estimating heart rate

Figure 7. The 30-square method of estimating heart rate

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Evaluating heart rate infallible and may miscalculate the heart

the heart rate is to use the figure calculat-