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CONTINUING PROFESSIONAL DEVELOPMENT
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ECG interpretation
multiple choice
questionnaire
Page 59
Read Laura Demmen’s
practice profile on care
after death
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Guidelines on how to
write a practice profile
An introduction to electrocardiogram
interpretation:part 1
NS520 Woodrow P (2009) An introduction to electrocardiogram interpretation: part 1.
Nursing Standard. 24, 12, 50-57. Date of acceptance: July 24 2009.
Summary
Introduction
This article describes how to interpret the single-lead
electrocardiogram (ECG). The author also describes cardiac
electrophysiology and how this is represented by ECG graphs.
Part 2 of this article, to be published next week, will describe
12-lead ECGs and acute coronary syndromes.
Cardiac changes can be sudden and devastating,
and while some changes may not always be
preventable or treatable, patients in acute hospitals
experience significant morbidity and mortality that
is avoidable (National Institute for Health and
Clinical Excellence (NICE) 2007). ECGs are the
most common cardiovascular diagnostic procedure
(Kligfield et al 2007). Nurses who are able to
recognise abnormal ECGs are well placed to initiate
early action to improve patient outcomes.
ECGs contain much information in relatively
little space. A framework is provided in this
article for systematic interpretation and applied
to normal sinus rhythm and the most commonly
encountered dysrhythmias. Once the nurse is
confident with the core aspects, his or her
knowledge and skills can be developed further
through more advanced texts and resources.
Normal sinus rhythm is also described,
together with common conduction problems
and treatments.
Tracings (views) of cardiac electrical activity
taken from electrodes are called ‘leads’;
however, in daily language ‘lead’ is usually
used to describe a wire. In this article, leads are
used to describe views of electrical activity and
‘electrodes’ to identify sites on the body from
which wires transmit electrical information to
ECG machines. Bedside monitors usually only
display one or sometimes two leads, so this
article describes limb lead II, the usual default
lead displayed on monitors, and the usual
‘rhythm strip’ on 12-lead ECGs, which should
be recorded when there are specific concerns.
More information can be found on 12-lead
ECGs in Part 2 of this article, which also
describes acute coronary syndromes.
Author
Philip Woodrow, practice development nurse in critical care,
Intensive Therapy Unit, Kent & Canterbury Hospital, Kent.
Email: [email protected]
Keywords
Atrial fibrillation, atrioventricular blocks, dysrhythmias,
electrocardiograms
These keywords are based on subject headings from the British
Nursing Index. This article has been subject to double-blind review.
For author and research article guidelines visit the Nursing Standard
home page at nursingstandard.rcnpublishing.co.uk. For related
articles visit our online archive and search using the keywords.
Aims and intended learning outcomes
This article aims to improve the reader’s ability
to interpret single-lead electrocardiogram (ECG)
monitoring. After reading this article and
completing the time out activities you should
be able to:
Explain normal cardiac conduction.
Identify components of the normal sinus
rhythm complex and what they signify.
Recognise atrial fibrillation and
atrioventricular blocks.
Use a systematic approach to ECG
interpretation.
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An ECG is a time/voltage graph of electrical
activity in the heart. Cardiac muscle conducts
can also generate electrical impulses. Usually,
muscular contraction, which creates the pulse,
follows electrical activity. There are many
factors that can influence cardiac function, but
measuring the time of electrical conduction and
viewing the voltage involved usually indicate
function, while different parts of the ECG
complex represent different stages of conduction
(Houghton and Gray 2008). ‘Normal’ healthy
adult time ranges are suggested, but as with other
observations and vital signs, what is normal
for each individual patient may vary slightly.
Names of abnormalities sometimes vary
between texts and practitioners so, where
appropriate, this article includes variants –
the nurse should therefore be able to recognise
whatever terms he or she encounters in practice.
This article uses the term dysrhythmias for
abnormal (non-sinus) rhythm rather than the
more commonly used term arrhythmias.
While ECGs may contain abnormal (ectopic)
beats, initial interpretation should focus on the
underlying rhythm.
Polarisation Muscular electrical activity occurs
through the movement of ions (sodium, calcium,
potassium) across cell membranes. Ion movement
changes the cell membrane’s charge from its
resting –90 millivolts (mV), so polarity is lost
and the cell becomes electrically excitable
(depolarisation). When normal ion balance
and cell membrane polarity are then restored,
electrical excitability ceases (repolarisation).
To summarise:
Depolarisation = electrical activity.
Repolarisation = end of electrical activity.
Higher control Heart rate is regulated by
the cardiac centre, one of the vital centres in the
brainstem. The cardiac centre sends signals via
the sympathetic and parasympathetic fibres of
the autonomic nervous system. Sympathetic
stimulation increases the heart rate, while
parasympathetic stimulation decreases it.
Most nerve impulses that reach the heart are
parasympathetic, slowing down intrinsically
fast heart rates (Marieb and Hoehn 2007).
Parasympathetic impulses travel through a
branch of the vagus nerve, the tenth cranial
nerve. Therefore, stimulating the vagus nerve in
another part of the body can slow the heart rate
(vagal stimulation). This can be exploited
therapeutically, using carotid massage, but this
should only be attempted if users have been
trained to perform it safely. Vagal stimulation
can occur unintentionally. For example,
people who are constipated and strain when
passing a stool might induce bradycardia and
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myocardial infarction by stimulating vagal
nerve fibres in the gut.
Conduction pathway Impulses are conducted
through a specialised pathway (Figure 1). If one
pacemaker fails, the next part of the conduction
pathway might initiate impulses to fill the gap.
This is referred to as an escape ectopic/rhythm
(Hampton 2008).
Sinoatrial node Normally, the sinoatrial (SA)
node is the pacemaker – it initiates electrical
impulses and sets the heart rate. Any rhythm not
originating from the sinoatrial node is therefore
not sinus. Sometimes the term ‘sinus rhythm’ is
used incorrectly to describe a rate between 60 and
100 beats per minute (bpm), which is a normal
heart rate for adults.
Impulses from the SA node spread out across
atrial muscle, conducted from one muscle cell
to the next. Without specialised conduction
pathways, this makes conduction across the
atria relatively slow.
Atrioventricular node The atrioventricular (AV)
node acts like a gateway into the ventricular
conduction system, delaying impulses
for approximately 0.1-0.2 seconds (Marieb and
Hoehn 2007). This creates a short period of
electrical standstill between the end of atrial
depolarisation (P wave) and ventricular
depolarisation (QRS wave), limiting the number
of impulses that can be conducted by the AV node
to approximately 230bpm (Ganong 2005).
If the AV node does not receive impulses,
it might become the pacemaker, typically with
rates of 50-60bpm (Marieb and Hoehn 2007).
FIGURE 1
Conduction pathway
Sinoatrial node
Atrioventricular node
Bundle of His
Left bundle
branch
Right bundle
branch
Purkinje fibres
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Ventricular conduction Impulses travel
quickly from the AV node through specialised
conduction pathways: the bundle of His, which
splits into the left and right bundle branches.
The left bundle branch further splits into anterior
and posterior fasicles. From the three fasicles
(right bundle branch, left anterior hemibranch,
left posterior hemibranch) impulses spread into
the ventricular muscle mass through the Purkinje
fibres (Hampton 2008).
This conduction tissue enables rapid
transmission from the AV node to ventricular
myocytes – normally no more than 0.1 seconds
(the minimum AV node delay) (Marieb and Hoehn
2007). If no impulses are received from the AV
node, the ventricular conduction pathway can
become the pacemaker, but its rate is often about
30bpm, which is likely to compromise the patient’s
blood pressure and might lead to cardiac arrest.
Time out 1
Think of some patients you have cared for
and list the reasons why bedside cardiac
monitors have been used.
Time out 2
Continue reading and focus on the section on
regularity. Use the methods described to calculate
the heart rate in the ECG below. Find at least one
ECG in a patient’s notes and calculate his or her
heart rate at the time it was taken.
failure to detect electrical activity, such as poor
electrode contact (Houghton and Gray 2008).
Electrical activity causes a vertical deflection
from the isoelectric line. Deflections above the
baseline are described as positive, while
deflections below the baseline are described as
negative. Positive and negative deflections are
discussed further in the second article.
ECGs measure voltage, detected in mV.
Standard calibration is 1mV = 10mm (two large
squares) in height. Some monitors or machines
display voltage by a calibration box (either on the
far left or far right), and often add: 10mm/mV.
Voltage is described in more detail in the second
article.
Regularity Normal sinus rhythm is regular, but
some regular rhythms can be abnormal and
life-threatening, such as ventricular tachycardia.
Irregular rhythms are usually abnormal, although
slight variations can be caused by breathing and
other factors (Houghton and Gray 2008).
Staff should know whether or not patients have
regular heart rates by checking the pulse, but
ECG interpretation should begin by assessing
whether or not the rhythm is regular.
Regularity can be assessed by seeing if the
distance between R waves (peaks of complexes) is
constant. The easiest way to do this is usually by:
Placing some paper over a printout so that only
R waves are visible.
Marking a few consecutive R waves.
Moving the paper along a few complexes.
If the distance between R waves remains
(approximately) constant, then the ECG is regular.
If not, it is irregular (Houghton and Gray 2008).
Provided the ECG is recorded using the
standard speed of 25mm/second, heart rate can
be calculated either by (Jevon 2009):
Counting the number of R waves in six seconds
(30 large boxes) and multiplying by ten.
Putting it on paper The ECG is a time/voltage
graph. Time is represented horizontally, and
voltage vertically. In the UK, ECG machines
(including bedside monitors) run at a standard
speed of 25mm/second. ECG graph paper is
divided into millimetre squares, with larger
squares each measuring 5mm. Twenty five small
squares (or five large squares) pass each second.
So on the horizontal axis, each large square
represents 0.2 seconds, and each small square
represents 0.04 seconds. Many screens and
printouts display the time in words: 25mm/s.
If no electrical activity is detected, machines
display a horizontal line, called the isoelectric
line. Asystole will usually produce a slightly wavy
line, so a straight line is more likely to indicate
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Counting the number of large squares between
two consecutive R waves and dividing 300 by
that number.
If ECGs are irregular, then assess whether or
not a pattern can be seen to the irregularity,
for example regularly missed beats. If there is
a pattern, it may be called regularly irregular.
If there is no pattern, it is irregularly irregular.
With irregular rhythms, the first method
suggested above is usually better, although it
may be difficult. The second method is usually
easier for calculating regular rhythms (Houghton
and Gray 2008).
Normal adult heart rates are between 60 and
100bpm – rates below 60bpm are known as
bradycardias, while those above 100bpm are
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tachycardias. Mild tachycardias (up to about
130bpm) are usually compensatory and seldom
compromise blood pressure (Hinds and Watson
2008), so treatments should focus on the
underlying causes. However, faster tachycardias
(more than 130bpm at rest) may become
imminently life-threatening and require urgent
treatment. Treatment of supraventricular
tachycardia (originating above the ventricles) and
ventricular tachycardia is (usually) different, so
rapid identification may be life saving. They can be
distinguished by the width of the QRS complex
(Davey 2008):
Narrow complex tachycardias are
supraventricular.
Broad complex tachycardias are usually
ventricular.
FIGURE 2
Sinus rhythm complex
Atria
2
Ventricles
RR interval
Millivolts (mV)
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R
1
S-T
segment
T
P
0
Q S
Q-T interval
P-R interval = 0.16 sec
–1
0
0.2
0.4
0.6
0.8
1.0
1.2
BOX 1
P wave.
A systematic approach to ECG interpretation
PR interval.
Regularity
Is the rate regular? If not, is the rate:
Regularly irregular – is there a pattern?
Irregularly irregular – is there no pattern?
QRS complex.
ST segment.
T wave, and sometimes a U wave.
Following this sequence using a structured
framework, such as the one shown in Box 1,
helps interpretation. Normal timings, described
in each section, are summarised in Table 1.
Whereas timings should apply to all ECG
leads, the shapes often differ, so the descriptions
below are for limb lead II.
P wave The P wave represents atrial
depolarisation. P waves are relatively broad
and shallow. The normal P wave timing is
0.08 seconds (two small squares) (Marieb and
Hoehn 2007). P waves are often difficult to see,
but should have a rounded (hump-back bridge)
shape. P wave abnormalities indicate atrial (that
is, supraventricular) abnormalities (Hampton
2008). Common P wave abnormalities are listed
in Table 2.
If P waves are missing, other atrial activity may
be seen, for example:
Fibrillation waves (a wavy baseline, which
may be coarse or fine) – atrial fibrillation is
discussed below.
Flutter waves (sharp upstroke – ‘saw-tooth’
or ‘sharks tooth’ (Figure 3)).
Pacing spikes – vertical lines, indicating an
artificial pacemaker (temporary or
permanent); pacing is not discussed further
in these two articles.
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1.6
Time (s)
Normal ECG complex The normal sinus rhythm
complex comprises (Figure 2) :
Q wave.
1.4
P wave
Does the P wave appear before the QRS?
Is there one P wave before every QRS?
Is the shape normal?
Are P waves missing? Check to see if they are replaced by pacing spikes,
for example.
PR interval
Does the PR interval cover three to five small squares?
QRS complex
Is the QRS width within three small squares?
Is the QRS positive or negative?
Is the axis normal?*
Does the QRS look normal?
ST segment
Does the isoelectric line return between the S and the T?
If not, is it:
Elevated (>1mm above the isoelectric line)?
Depressed (<0.5mm below the isoelectric line)?
T wave
Does the T wave look normal?
Is the QT interval less than half the preceding R-R interval, with a
maximum length of 0.4 seconds?
Tachycardia (>100 beats per minute)
Narrow complex (usually with P waves) = atrial (supraventricular).
Wide complex (without P wave) = ventricular.
*The QRS axis is discussed in Part 2 of this article.
(Reproduced with permission from Moore and Woodrow 2009)
Atrial conduction, and therefore contraction,
precedes ventricular activity. Stroke volume
– the amount of blood ejected from a ventricle
when it contracts – is reduced by 20-30% if
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atrioventricular synchronisation is lost (Novak
et al 2002), so making pulses weaker. Therefore,
any rhythm lacking atrial-ventricular
synchronisation, that does not have P waves
preceding ventricular depolarisation, may result
in smaller stroke volumes. Unless compensatory
mechanisms such as increased right-sided filling
(preload) or tachycardia occur, blood pressure
will be compromised.
PR interval The PR interval is measured from the
start of the P wave to the Q wave (the first negative
deflection) (Guyton and Hall 2006) or, in the
absence of Q waves, to the start of the R wave. So it
includes the P wave and the period of electrical
standstill created by impulses crossing the AV node.
Normal PR time is 0.12-0.2 seconds (three to five
small squares, or no more than one large square)
(Hampton 2008).
TABLE 1
Normal timings of the electrocardiogram (ECG) complex
Time
Width*
P wave
0.08 seconds
Two small squares
PR interval
0.12-0.2 seconds
Three to five small squares
(no more than one large square)
QRS
Maximum 0.12 seconds
Maximum three small squares
ST segment
Not significant
T wave
0.16 seconds
QT interval
< half preceding R-R interval
Four small squares
*If ECG speed is 25mm/second
TABLE 2
Common P wave abnormalities
Shape
Likely cause
Peaked
Right atrial enlargement, from lung disease, for example
chronic obstructive pulmonary disease.
Broad or notched
Left atrial enlargement, from left-sided strain, for example
left ventricular failure, mitral valve disease.
Inverted
From an ectopic pacemaker.
(Jowett and Thompson 2007)
FIGURE 3
Atrial flutter
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The only possible PR abnormalities are that
the intervals are too long or too short. Short PR
intervals are fairly rare and are usually caused by
abnormal conduction pathways such as that of
the bundle of Kent, an extra conduction pathway,
which causes Wolff-Parkinson-White syndrome
(Hampton 2008). Long PR intervals, caused by
prolonged delay at the AV node, are more
common. Prolonged PR intervals are variously
called first-degree block, first-degree heart block
or first-degree AV node block – all terms mean
the same thing.
Q wave The Q wave, the first negative deflection,
is caused by depolarisation through the septum
(muscle wall) that separates the left and right
ventricles, and through which the ventricular
conduction pathway passes. Q waves are usually
small or absent, depending on the electrical view
(or lead used). Deep Q waves (bigger than
0.2 small squares) often indicate myocardial
infarction (Meek and Morris 2008). However,
deep Q waves do not always appear following
infarction, so a diagnosis of infarction cannot be
excluded if deep Q waves are not present.
Generally it is more useful to look at the QRS
complex in its entirety.
QRS complex The QRS complex represents
ventricular depolarisation. Much voltage is
needed for ventricular depolarisation, making
the QRS the tallest part of these complexes.
However, the specialised conduction pathway
(bundle of His, bundle branches and
hemibranches, and Purkinje fibres) ensures
that impulses travel quickly from the AV node
to ventricular muscle. Normal QRS width is
within 0.12 seconds (three small squares)
(Jevon 2009) and is often half this width.
In limb lead II (the lead most often shown
on single-lead ECGs), and in most other leads,
the QRS is normally positive. This is discussed in
more detail in Part 2.
Wide QRS complexes indicate ventricular
abnormalities (Jevon 2009). Although there are
also other less frequent causes, likely causes of
wide QRS complexes include (Hampton 2008):
Bundle branch block (discussed in Part 2 of
this article).
Ventricular ectopics or rhythms.
Artificial pacemakers.
ST segment After a negative deflection at the
S wave, the QRS should return to the isoelectric
line quickly, followed by some electrical standstill
(horizontal isoelectric line) before the T wave.
Timing of the ST segment is not significant.
What is important is that there is no elevation
or depression (Hampton 2008). Although ST
abnormality may be suspected from a single-lead
ECG, a 12-lead ECG is necessary to confirm the
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abnormality. ST elevation and depression,
and acute coronary syndromes are discussed
in Part 2.
T wave The T wave represents ventricular
repolarisation, the end of the cardiac conduction.
The normal T wave time is 0.16 seconds (four
small squares) (Marieb and Hoehn 2007).
However, height is more important than T wave
length. Jowett and Thompson (2007) suggested
that normal T wave height is less than 5mm, but
Houghton and Gray (2008) suggested there is no
normal height. It should be taller than the P wave.
T wave abnormalities are non-specific, which is
usually all the information given by machine
diagnosis. Although there may be various causes
for T wave abnormalities, a common cause is
abnormal potassium levels in blood (Houghton
and Gray 2008):
High T wave = (probably) high potassium levels.
Low T wave = (probably) low potassium levels.
T wave inversion is usually abnormal (unless QRS
complexes are negative). T wave inversion can
also have various causes, including hypertrophy,
but a newly inverted T wave may be the result of
ischaemia or infarction (Hampton 2008).
QT interval The QT interval from the beginning of
the Q wave to the end of the T wave represents total
ventricular depolarisation and repolarisation time.
It should be less than half the time of the preceding
R-R interval (Jevon 2009). Prolonged QT intervals
represent delayed repolarisation, which may cause
tachydysrhythmias (dysrhythmias with rates over
100bpm, and often considerably faster than this)
and sudden cardiac death (Straus et al 2006).
Some people are genetically susceptible to long QT
syndrome, and need to avoid drugs that might
aggravate the problem – this is an extensive list,
but it includes many commonly used drugs such as
salbutamol, many psychotropic drugs and
paradoxically many cardiac drugs such as beta
blockers. As high heart rates decrease the QT
interval, cardiologists might calculate the QTc
– the QT interval corrected to what it would be if
the heart rate was 60bpm (Davey 2008).
Time out 3
Ask your ward or department
pharmacist which drugs, that
are commonly used in your
clinical area, patients with long
QT syndrome should avoid.
(Hampton 2008). Unless staff are very skilled at
ECG interpretation, U waves are usually best
forgotten about.
Atrial fibrillation So far this article has focused on
the normal sinus rhythm. However, ECGs are
generally recorded because of cardiac
abnormalities or concerns. Many ECGs seen in
practice are abnormal. The most common
abnormal rhythm is atrial fibrillation (AF) (Royal
College of Physicians (RCP) and NICE 2006). AF
affects about 5% of people over the age of 65 in the
UK, and incidence increases with age, to about 9%
in people over the age of 80 years (RCP and NICE
2006). AF causes chaotic atrial activity, with no
co-ordinated conduction or contraction occurring
in the atria (Jevon 2009). There will therefore be no
P waves, but some erratic atrial activity may appear
as a ‘wavy’ isoelectric line (Figure 4).
AF may be ‘fine’ (little or no activity is seen
between T waves and QRS complexes) or ‘coarse’
(chaotic activity is visible between T waves and
QRSs) (Jevon 2009).
Consensus classification (RCP and NICE
2006) defines AF as one of the following:
An initial event.
Paroxysmal: spontaneous termination,
recurrent, for less than seven days, and often
for less than 48 hours.
Persistent: not self-terminating.
Permanent (accepted): not terminated.
The first three groups are sometimes termed acute
AF, while permanent AF is sometimes called
chronic AF. Acute AF often occurs in response to a
trigger, such as illness or surgery. Treatment aims
for acute AF are to control heart rate and restore
sinus rhythm, using drugs such as amiodarone
and/or electrical cardioversion (Zimetbaum 2007,
Musco et al 2008). With sinus rhythm, atria
contract before ventricles, causing active flow
of blood into ventricles. AF lacks this active part
to atrial bloodflow, leaving only passive flow,
which may result in thrombi and therefore emboli
that may cause strokes. Anticoagulants may
therefore be needed to the reduce the risk of
stroke. Permanent or chronic AF cannot be cured,
but should be controlled (RCP and NICE 2006).
As with acute AF, the two aspects that should be
controlled are heart rate and coagulation.
FIGURE 4
Atrial fibrillation
U wave While U waves are frequently described in
texts, they are seldom seen in practice. Often they
are not present. If they are present they are often
too small to see on ECGs, and may be a sign of
good health or problems (often hyperkalaemia)
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Time out 4
Ask your medical team what
drugs they prescribe to control
heart rate and coagulation. Also
discuss what alternative drugs
they might use, and factors that
would influence their choice.
AF usually causes tachycardia. The target
for heart rate control is usually below 100bpm.
Although the RCP and NICE (2006) suggest that
amiodarone or other rhythm-control drugs are
preferable to the rate-control drug digoxin,
established AF is still often treated with digoxin.
Passive blood flow through the atria increases
the risk of thrombi, and therefore strokes and
other thrombotic events (Hart et al 2003).
Anticoagulation, usually with warfarin (Mant
et al 2007, Waldo 2008), reduces stroke risk by
60% (Shannon 2009), and is usually given to
achieve a target international normalisation ratio
of 2-3 (RCP and NICE 2006). Warfarin has a
narrow therapeutic range, so serum levels need to
be monitored frequently.
ECGs (and pulses) where the rate is
irregularly irregular (no pattern) are usually
caused by AF or a mixture of various rhythms
(one of which may be AF). Erratic times between
pulses cause variable ventricular filling times,
and so variable pulses. Some pulses may be too
weak to be felt at the peripheries, which causes
an apex-radial deficit. Digoxin, or other heart
rate control drugs, should usually be omitted
if the heart rate is below 60bpm. Recorded
observations usually measure the brachial pulse
rate (from automated blood pressure monitors).
FIGURE 5
Atrioventricular node construction blocks
a) First-degree block
b) Second-degree block
b) Third-degree block
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If the brachial pulse rate is below 60bpm, the
apex rate should be checked before giving any
drugs that slow down heart rate (such as
digoxin), as tachycardia in AF can cause
significant apex-radial deficits, with slow
brachial pulses (Levine 2005).
AV node blocks Electrical impulses will fail to be
conducted through any tissue that is electrically
unexcitable (or blocked). Blocks can occur in any
part of the conduction system, but occur most
often at or near the AV node. A block may be:
A delay where all impulses are conducted,
but more slowly than normal.
Incomplete – some impulses are conducted,
others are not.
Complete – no impulses are conducted.
AV node conduction blocks or AV heart blocks
(Figure 5) are: first degree (delay), second degree
(incomplete) and third degree (complete).
Unless there are other diseases such as congenital
defects or valve disease, blocks are usually caused
by (Riley 2002):
Age-related sclerosis of the AV node.
Myocardial damage or infarction.
Drugs, for example beta blockers.
First-degree block A first-degree block does not
usually cause problems or require treatment.
If there are symptoms such as breathlessness or
chest pain, then they should be treated. If it is
caused by drugs, then the patient’s prescriptions
should be reviewed. If it is symptomatic and
persistent, permanent artificial pacing is
sometimes necessary.
Second-degree block A second-degree or
incomplete block is more likely to cause
symptoms. There are two types of second-degree
block (Jevon 2009): Type 1 (also called
Wenckebach or Mobitz type 1) and Type 2 (also
called Mobitz type 2, and sometimes just Mobitz).
Type 1, with progressively lengthening PR
intervals until a P wave is not conducted, is the
more common and less sinister type (Hatchett
2002). Type 2, where all PR intervals remain
the same length, but some P waves (at regular
intervals) are not conducted, is less common,
but more likely to progress to complete
(third-degree) block or asystole (Houghton
and Gray 2008, Jevon 2009).
Third-degree block A third-degree or complete
block means that whatever happens in the atria is
not conducted to the ventricles. The ventricles are
therefore paced from a focus in the ventricles
themselves, typically causing slow, wide QRS
complexes – often the heart rate is about
30-40bpm (Jevon 2009). If the sinoatrial node is
functional, there will be regular P waves (typically
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60-100bpm) that are unrelated to the ventricular
complexes, and which may be lost in any part
of the QRS, ST segment or T wave. More often,
third-degree blocks develop in patients with
significant cardiac disease, who previously had
established AF. The slow rate usually compromises
cardiac output, causing hypotension and usually
needs urgent pacing (Davey 2008).
Conclusion
ECGs are widely used, and might detect or
confirm various cardiac problems. Some
problems might necessitate urgent action, so
nurses able to interpret ECGs are more likely
to initiate actions or call for help. Interpreting
ECGs is a skill which, like all skills, improves
with practice. This article has provided a
systematic means for interpreting ECGs, and
described core aspects of single-lead normal
sinus rhythm, together with some common
dysrhythmias. Part 2 of this article in next week’s
Nursing Standard will describe 12-lead ECGs
and acute coronary syndromes NS
Time out 5
Using the framework outlined in
Box 1, practise interpreting some
ECGs in your clinical area.
Depending on individual patients,
some aspects might involve advanced
interpretation (not discussed in this article).
Make a list of what you have found and discuss
this list with your colleagues, or check your
answers by using a textbook on ECGs. Make
notes of how any problems were treated. If there
are any treatments you do not understand,
discuss them with more experienced colleagues,
and what alternative treatments or management
might have been used.
Time out 6
Now that you have completed
the article, you might like to
write a practice profile. Guidelines
to help you are on page 60.
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november 25 :: vol 24 no 12 :: 2009 57
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