BASIC
ECG INTERPRETATION
The following is a basic primer in interpretation of the ECG
(EKG). It is intended solely for teaching purposes, and should not be relied
upon in clinical decision making. As an aside,
here's a note on
Brugada's algorithm, and we also have
a note on antiarrhythmic drugs
(and mechanisms of arrhythmia).
An Approach
ECGs can be very confusing, and there are dozens of
different methods of interpretation. It's perhaps best if everyone works out
their own individual approach, but here's just one approach you can build upon:
- Sit back and look -
identify the patterns, and write down what you see!
- Go through the ECG
systematically;
- Correlate ECG and
clinical findings, and if necessary, go back and do a complete rethink;
- Try and invalidate
your assessment --- look for holes!
|
Of the
above steps, the fourth seems counter-intuitive and unnecessary. In fact, it's
the most important. As in all medicine, complacence is dangerous. Avoid it!
Now,
let's sketch out a systematic approach. Ours is:
- Check the patient details
- is the ECG correctly labelled?
- What is the rate?
- Is this sinus
rhythm? If not, what is going on?
- What is the mean frontal
plane QRS
axis (You may wish at this stage to glance at the P and T wave axes
too)
- Are the P
waves normal (Good places to look are II and V1)
- What is the PR interval?
- Are the QRS
complexes normal? Specifically, are there:
- Are the ST segments
normal, depressed or elevated? Quantify abnormalities.
- Are the T waves
normal? What is the QT interval?
- Are there abnormal U waves?
Before
we move through the systematic approach outlined above, we will outline a few
basics. More advanced readers may wish to skip
these basics, and move on to the systematic part of the tutorial.
How
the ECG works
When
cell membranes in the heart depolarise, voltages change and currents flow.
Because a human can be regarded as a bag of salt water (with baad attitude), in
other words, a volume conductor, changes in potential are transmitted
throughout the body, and can be measured. When the heart depolarises, it's
convenient (and fairly accurate) to represent the electrical activity as a dipole
--- a vector between two point charges. Remember that a vector has both a size
(magnitude), and a direction. By looking at how the potential varies
around the volume conductor, one can get an idea of the direction of the
vector. This applies to all intra-cardiac events, so we can talk about a vector
(or axis) for P waves, the QRS complex, T waves, and so on.
In the
above picture, the schematic ECG lead on the right `sees' the (red) vector
moving towards it, shown as a positive deflection in the ECG trace; the lead at
90 degrees to this sees nothing!
Various
events
We
assume some knowledge of heart anatomy. Note that the normal heart has,
electrically speaking, only two chambers, an atrial and a ventricular
`chamber'. Propagation of electrical activity spreads freely between atria and
ventricles, but communication between these two chambers is limited to the AV
node. Everyone knows that the P wave corresponds to atrial depolarisation, the
QRS complex to ventricular depolarisation, and the T wave to repolarisation of
the ventricle.
The
ECG (EKG)
In
order to be able to record myocardial activity, the electrocardiograph needs to
be able to detect tiny changes in potential on the body surface. We are talking
about signals that are often around 1mV, and may be smaller. In addition, we
need some reference point to which we relate the potential changes.
The
12-lead ECG
Over
the years, we have evolved several systems that go to make up the 12-lead ECG.
These are:
- Bipolar leads: the
reference point is on one limb, the `sensing' electrode (if you wish) is
on another limb. The leads are termed I, II, and III.
- Unipolar leads: The
reference point is several leads joined together, and the sensing lead is
on one limb. These leads are conventionally augmented, in that the
reference lead on the limb being sensed is disconnected from the other
two.
- The V leads, which extend
across the precordium, V1 in the fourth right interspace, V2 4th left, V4
at the apex (5th interspace, midclavicular line), V3 halfway in between V2
and V4, and V5 & V6 in the 5th interspace at the anterior and mid
axillary lines respectively.
We can
visualise the directions of the various leads --- I points left, and aVF points
directly down (in a 'Southward' direction). The other leads are arranged around
the points of the compass --- aVL about 30o more north of I, II down
towards the left foot, about 60o south of I, and III off to the
right of aVF. aVR `looks' at the heart from up and right, so effectively it's
seeing the chambers of the heart, and most deflections in that lead are
negative.
(a net
positive vector in AVR is unusual, and suggests that lead placement was
incorrect. If the leads were correctly sited, then think dextrocardia, or some
other strange congenital abnormality).
It's
usual to group the leads according to which part of the left ventricle (LV)
they look at. AVL and I, as well as V5 and V6 are lateral, while II, III and
AVF are inferior. V1 through V4 tend to look at the anterior aspect of
the LV (some refer to V1 and V2 `septal', but a better name is perhaps the
`right orientated leads'). Changes in depolarisation in the posterior aspect of
the heart are not directly seen in any of the conventional leads, although
"mirror image" changes will tend to be picked up in V1 and V2.
Paper
ECG
paper is traditionally divided into 1mm squares. Vertically, ten blocks usually
correspond to 1 mV, and on the horizontal axis, the paper speed is usually
25mm/s, so one block is 0.04s (or 40ms). Note that we also have "big
blocks" which are 5mm on their side.
Always
check the calibration voltage on the right of the ECG, and paper speed. The
following image shows the normal 1mV calibration spike:
Damping
Note
that if the calibration signal is not "squared off" then the ECG
tracing is either over or under-damped, and should not be trusted.
Knowing
the paper speed, it's easy to work out heart rate. It's also very convenient to
have a quick way of eyeballing the rate, and one method is as follows:
- Remember the sequence:
300, 150, 100, 75, 60, 50
- Identify an R wave that
falls on the marker of a `big block'
- Count the number of big
blocks to the next R wave.
If the
number of big blocks is 1, the rate is 300, if it's two, then the rate is 150,
and so on. Rates in between these numbers are easy to `interpolate'.
But
always remember that in the heart, because we have two electrically `isolated'
chambers, the atria and ventricles, that we are really looking at two
rates --- the atrial and ventricular rates! It just so happens that in the
normal heart, the two are linked in a convenient 1:1 ratio, via normal
conduction down the AV node. In disease states, this may not be the case.
Conventionally,
a normal heart rate has been regarded as being between 60 and 100, but it's
probably more appropriate to re-adjust these limits to 50 -- 90/min. A sinus
tachycardia then becomes any heart rate under 90, and bradycardia, less than
50. Note that you have to look at the clinical context -- a rate of 85 in a
highly trained athlete may represent a substantial tachycardia, especially if
their resting rate is 32/minute! One should also beware of agressively trying
to manage low rates in the presence of good perfusion and excellent organ
function.
Sinus
bradycardia
Apart
from fit, but otherwise normal individuals, there's a long list of situations
where sinus bradycardia occurs, including:
- hypothermia;
- increased vagal tone (due
to vagal stimulation or e.g. drugs);
- hypothyroidism;
- beta blockade;
- marked intracranial
hypertension;
- obstructive jaundice, and
even in uraemia;
- structural SA node
disease, or ischaemia.
Sinus
tachycardia
Always
consider pain as a possible cause of tachycardia. There's a long list, however:
- Any cause of adrenergic
stimulation (including pain);
- thyrotoxicosis;
- hypovolaemia;
- vagolytic drugs (e.g.
atropine)
- anaemia, pregnancy;
- vasodilator drugs,
including many hypotensive agents;
- FEVER
- myocarditis
If the
rate is almost exactly 150, always make sure that you are not mistaking atrial
flutter with a 2:1 block for sinus tachycardia. A common error.
Sinus
arrhythmia and heart rate variability
There
is normally a slight degree of chaotic variation in heart rate, called sinus
arrhythmia. Sinus arrhythmia is generally a good thing, and loss of this
chaotic variation is of ominous prognostic significance. Post myocardial
infarction, a metronome-like regularity of the heartbeat is associated with an
increased likelihood of sudden death, and just before the onset of ventricular
tachycardia (or fibrillation), variability is lost! Absence of any sinus
arrhythmia suggests an autonomic neuropathy.
Atrial
extrasystoles
These
arise from ectopic atrial foci. Commonly, the ectopic beat always arises at
about the same time after the sinus beat!
The
ectopic beat usually discharges the SA node, so subsequent beats of SA origin
are not in synchrony with the previous sinus rhythm.
If the
extrasystole occurs early on, it may find the His-Purkinje system not quite
ready to receive an impulse, and a degree of block may be seen. This is termed
`aberration'.
Distinguish
between an atrial extrasystole, and an atrial escape beat, where the SA
node falters, and a subsidiary pacemaker takes over:
(Parenthetically,
we didn't draw the P waves very well in the above strip. Don't let this put you
off from indentifying the underlying rhythm).
Supraventricular
tachyarrhythmias (SVT)
Irregular
SVT
By far
the commonest cause of irregular SVT is atrial fibrillation, where the atrial
rate is in the region of 450 to 600/min, and the atria really do not contract
rhythmically at all. The atrium "fibrillates", writhing like a bag of
worms. The conventional view of the pathogenesis of AF is that there are
multiple re-entrant `wavelets' moving through the atrial muscle, but recent
evidence suggests that much AF actually arises from ectopic activity in the
muscular cuff surrounding the pulmonary veins where they enter the left atrium.
AF is thought to beget further AF through "electrical remodelling"
--- electrophysiological changes that are induced in atrial myocytes due to
fast rates and the consequent calcium loading.
Note
that in the above tracing of AF, the ventricular response rate seems rather
slow, so we suspect that AV block has been increased using pharmacological
manipulation. In uncontrolled AF, rates of about 130 or more are common.
Other
causes of irregular SVT are:
- Frequent atrial
extrasystoles;
- Multifocal atrial tachycardia,
where there are three or more distinct atrial foci, combined with
tachycardia. There is often severe underlying disease (e.g. chronic
obstructive airways disease), and in the ICU setting, MAT has a poor
prognosis.
- "Atrial flutter with
variable block".
Although
it looks like atrial fibrillation, the above image actually shows multifocal
atrial tachycardia. Note how there are at least three different P wave
configurations!
Regular
SVT
Atrial
flutter is
common. The atrial rate is commonly 300/min, and there is usually a 2:1 block,
resulting in a ventricular response rate of 150/min. Other ratios are possible,
and sometimes the ratio varies. This rhythm is often unstable, and the heart
may flip in and out of sinus rhythm, or there may be runs of atrial
fibrillation.
In the
above ECG the clue is the rate. A rate of 150 should always engender the
suspicion of atrial flutter with 2:1 block.
Probably
the commonest cause of regular SVT is AV nodal re-entrant tachycardia.
Here, there are generally two ways that electrical depolarisation can enter the
AV node from the atrium, a slow and fast `pathway'. A re-entrant circuit can be
set up, with impulses moving in a circular fashion, and causing depolarisation
of the ventricles at fast rates (up to 200/min or even more).
Other
causes of regular SVT include:
- ectopic atrial
tachycardia, due to repetitive discharges from an ectopic atrial focus;
- AV re-entrant tachycardia,
via an accessory pathway, discussed next.
Accessory
pathways
Abnormal,
congenital extra pathways between the atria and ventricles are common, and can
perforate the electrically insulating fibrous ring that normally separates the
atrial `chamber' and the ventricular one. The most well-characterised is the
Wolff-Parkinson-White syndrome. Reasonable (WHO) criteria for the WPW pattern
on ECG are:
- PR interval under 0.12s
- A delta wave
- QRS duration of 0.12s (or
more)
- A normal P-wave axis
Because
depolarisation moves `antegrade' from atria to ventricles, part of the
ventricle depolarises prematurely, and this is responsible for the slurred,
initial delta wave. It should be clear that the PR interval will therefore be
short, and the QRS duration should be prolonged. Note however that not everyone
with an accessory pathway will conduct all of the time down that pathway.
Accessory pathways are common, estimated to occur in one to three individuals
in every thousand. Symptomatic pathways are far less common.
The
WPW syndrome is a combination of the WPW pattern, and tachycardias. The
tachycardias may be due to impulse conduction down via the AV node and back up
the accessory pathway (commonest, called orthodromic tachycardia), the
other way around (down accessory pathway, up AV node, termed antidromic
tachycardia), or even related to atrial fibrillation. This last cause is
ominous, as if the accessory pathway is able to conduct impulses at fast rates,
the ventricle may be driven at rates in excess of 200/min, causing collapse or
even death.
Distinguishing
causes of SVT
A few
pointers are in order. The important thing to look for is the P wave:
- If the P is inscribed
before the QRS, it's probably an ectopic atrial tachycardia;
- If the P is after the QRS,
consider orthodromic AV re-entrant tachycardia;
- If the P is not seen (and
probably lost within the QRS) it's likely to be AV nodal re-entrant
tachycardia.
A few
other hints:
- The baseline ECG is
invaluable (may show WPW, for example);
- It's useful if you can
capture onset or termination of the arrhythmia.
Ventricular
extrasystoles
Because
these arise within an ectopic focus within the ventricular muscle, the QRS
complex is wide, bizarre, and unrelated to a preceding P wave. There is usually
a constant relationship (timing) between the preceding sinus beat and a
subsequent ventricular beat, because the preceding beat influences the ectopic
focus.
The
ventricular beat is not usually conducted back into the atria. What happens to
the atrial beat that occurred, or was about to occur when the VE happened?
Usually, this is blocked, but the subsequent atrial beat will occur on time,
and be conducted normally.
Rarely,
the ventricular beat may be conducted retrogradely and capture the atrium
(resulting in a P wave after the QRS, with an abnormal morphology as conduction
through the atrium is retrograde). The atrial pacemaker is now reset! In the
following rather complex tracing, we have a ventricular rhythm (a bit faster
than one might expect, perhaps an accelerated idioventricular rhythm) with
retrograde P waves, and something else --- some of the P waves are followed by
a normal looking `echo' beat as the impulse is conducted down back into the
normal pathways).
Because
the intrinsic rate of an ectopic focus often tends to be slow-ish,
extrasystoles will tend to arise more commonly with slower rates. In addition,
if the rate is varying, extrasystoles will tend to `squeeze in' during long RR
intervals. Some have called this the "rule of bigeminy".
Couplet
Two
VE's are termed a couplet.
Fusion
beat
Occasionally,
a VE occurs just after a sinus beat has started to propagate into the
His-Purkinje system. This results in a `fusion beat', which combines the
morphology of a normal sinus beat and that of the extrasystole.
Parasystole
Rarely,
the ectopic focus is protected from other influences, and does its own merry
thing. This is termed `parasystole', and is detected by noting the unvarying
coupling between extrasystoles, and the lack of coupling between the
extrasystole and sinus beats! In the following trace, note the fusion beats as
the normal rhythm and parasystolic rhythm transiently coincide...
We've
put in the above unusual ECG more as a mnemonic than for any other reason. We
want you to remember that even with extrasystoles, there is flow of information
from the normal rhythm to the ectopic focus. The ectopic focus is therefore
modulated by the normal rhythm, and usually occurs at about the same interval
from the normal events. Parasystole is unusual.
Ventricular
tachycardia
Three
or more ventricular extrasystoles are a bad sign, and are termed ventricular
tachycardia (VT). There is usually severe underlying myocardial disease.
Sustained VT (more than about 30 beats) often degenerates into ventricular
fibrillation, resulting in death.
The
above strip shows several `characteristic' features of VT. Apart from the
regular fast rate and wide complexes, we have a few more clues ... clearly, the
atrial rate is different from the ventricular rate, and there is dissociation
between atria and ventricles --- the P waves occur at any time in relation to
the QRS complexes. Even more characteristic of VT is the presence of a fusion
beat at the start of the trace --- a QRS complex which is something in between
the VT morphology and normal morphology. There is also a capture beat
later on, where the P wave has managed to sneak through and transiently take
over, resulting in a normally-shaped QRS complex and T wave.
VT
vs SVT+aberration
Distinguishing
between VT, and SVT with aberration is tricky. When in doubt, one should apply
synchronised DC countershock, and agonize later. This is especially the case if
the patient is haemodynamically unstable. If the patient is haemostable, the
rate is slowish (under about 150), then one may have more time. A variety of
algorithms have been proposed - Brugada's approach may have merit --- you can explore
a web-based version of his algorithm here.
Ventricular
fibrillation
This
is a chaotic ventricular rhythm that rapidly results in death. It is often
precipitated by a critically timed extrasystole, that occurs during the
relative refractory period of the myocardial fibres. Conventional wisdom has it
that this results in chaotic, unco-ordinated wavelets of depolarisation moving
through the ventricular mass.
VF is
a dire emergency. If unsynchronised DC countershock is applied within 30s of
the onset of VF, there is an approximately 97% chance that sinus rhythm will be
restored, and the person will survive. Survival decreases exponentially
thereafter, with every minute of delay.
Ventricular
flutter
Ventricular
'flutter' is a bizarre sine-wave like rhythm, and usually degerates into
ventricular fibrillation. You won't see it often (or for long).
Axis
The
peculiar system we use in electrocardiography is non-Cartesian, and rather
arbitrary! We measure the direction of vectors in degrees, and zero is indeed
facing `East', but +90o is South, instead of North as it
would be in a Cartesian system. You can work out that ± 180o is
'West', and that minus 90o is 'North'.
We can
talk about the `axis' of any ECG depolarisation, but most people when they are
talking 'axis' are referring to the mean frontal plane QRS axis. There
is a number of ways of determining this, but the following method has the merit
of simplicity:
- Estimate the overall
deflection (positive or negative, and how much) of the QRS in standard
lead I;
- Do the same for AVF;
- Plot the vector on a
system of axes, and estimate the angle, thus:
Note
in the above picture that the (abnormal) axis illustrated is negative
("towards the left") because AVF is negative.
People
tend to faff quite a lot about QRS axis deviations, but they are a fairly
blunt-edged tool. Marked right axis deviation (e.g. +150o) may signify
significant `right-sided' heart disease. Left axis deviation is not uncommon in
inferior myocardial infarction, and if this is absent, the most likely
`diagnosis' is left anterior hemiblock. (There are several other cause of left
or right axis deviation, for example depolarisation via accessory pathways).
Where
the axis is up and to the left (eg. -135o), this is termed a
"north west axis". It is commonly seen in congenital heart disease,
dextrocardia, and sometimes in severe chronic obstructive airway disease.
The T
wave axis is much neglected, and may be of value. If the T wave axis is
more than about 45 to 60o different from the QRS axis, this is
abnormal. Schamroth gives a super mnemonic --- "the T-wave axis moves away
from the `region of mischief'".
Even
the P-wave axis is of use. The normal axis is about +40 to +60o,
moving right with chronic obstructive disease. The axis may move left with
congenital heart disease, even up to -30o (especially Ebstein's
anomaly). One can also spot an ectopic atrial focus low down in the atrium
(`coronary sinus rhythm') due to the `northern' shift in axis.
The
P wave
Normal
atrial activation is over in about 0.10s, starting in the right atrium. A good
place to look at P waves is in II, where the P shouldn't be more than 2.5mm
tall, and 0.11 seconds in duration.
A tall
P wave (3 blocks or more) signifies right atrial enlargement, a widened bifid
one, left atrial enlargement:
In V1,
another good place to look, depolarisation of the right atrium results in an
initial positive deflection, followed by a vector away from V1 into the left
atrium, causing a negative deflection. The normal P wave in V1 is thus
biphasic. It's easy to work out the corresponding abnormalities with left or
right atrial enlargement:
There
are a few other tips:
- A qR in V1 suggests right
atrial enlargement, often due to tricuspid regurgitation! (Observed
by Sodi-Pallares). [qv]
- If the overall QRS
amplitude in V1 is under a third of the overall QRS amplitude in V2, there
is probably RA enlargement! (Tranchesi).
- A P wave originating in
the left atrium often has a `dome and dart' configuration.
The
PR interval (and PR segment)
The PR
interval extends from the start of the P wave to the very start of the QRS
complex (that is, to the start of the very first r or q wave). A normal value
is 3 to 5 `little blocks' (0.12 to 0.20 seconds). It's convenient at this point
to discuss blocks...
SA
node block
This
is a diagnosis of deduction, as no electrical activity is seen. An impulse that
was expected to arise in the SA node is delayed in its exit from the node, or
blocked completely. A second degree SA block can be `diagnosed' if the heart
rate suddenly doubles in response to, say, administration of atropine.
If the SA node is blocked, a subsidiary pacemaker will (we hope) take over, in the
atrium, AV node, or ventricle!
AV
nodal blocks
There
are three "degrees" of AV nodal block:
- First degree block:
simply
slowed conduction. This is manifest by a prolonged PR interval;
- Second degree block:
Conduction
intermittently fails completely. This may be in a constant ratio (more
ominous, Type II second degree block), or progressive (The Wenckebach
phenomenon, characterised by progressively increasing PR interval culminating
in a dropped beat --- this is otherwise known as Mobitz Type II second degree
heart block).
- Third degree block:
There
is complete dissociation of atria and ventricles.
Clearly
a bad thing, requiring temporary or even permanent pacing.
The
QRS complex
The
nomenclature is mildly arcane --- small deflections are reflected using lower
case, and larger deflections UPPER CASE. An initial downwards deflection is a Q
(or q), any negative deflection after this is an S. An upward deflection is an
R. Note that we refer to a second deflection in the same direction by adding a
prime, so we have R', R'', S' and so on. We might thus refer to an rSR' morphology,
or whatever.
Normally,
the septum depolarises before other parts of the left ventricle. This is seen
as a small initial vector, which in the `septal leads' (V1 and V2) is a
positive deflection, and in lateral leads (e.g. V6) is seen as a small q. This
observation is of relevance, as in conditions such as left bundle branch block,
where the septum cannot depolarise normally, the lateral (septal) q is
conspicuously missing.
Something
of some importance is the time it takes the ventricle to depolarise, often
termed the ventricular activation time. We can estimate this from the
surface ECG by looking at the time from the onset of the QRS to the sudden
downstroke of the QRS. (The fancy name for this sudden downstroke is the
`intrinsicoid deflection'). In right orientated leads, a normal VAT is 0.02s,
and on the left (e.g. V6) the duration should not exceed 0.04s.
Q
waves - myocardial infarction
|
|
|
Many
people who have had a prior MI will have an ECG that appears normal. There
may however be typical features of previous MI, and the most conspicuous of
these is Q waves. A simplistic explanation of these prominent Q waves is that
an appropriately placed lead "sees through" the dead tissue, and
visualises the normal depolarisation of the viable myocardial wall directly
opposite the infarcted area. Because, in the normal myocardium,
depolarisation moves from the chamber outwards, this normal depolarisation is
seen as a Q wave!
Another
feature of previous MI is loss of R wave amplitude. It's easy to imagine that
if muscle is lost, amplitude must be diminished. (Having a pre-infarction ECG
for comparison is invaluable).
|
One
can get some idea of the site of infarction from the lead in which
abnormalities are seen - inferior, lateral, or anterior.
Hypertrophy
and chamber enlargement
Because
of the thin-walled nature of the atria, from an ECG point of view, one cannot
talk about "atrial hypertrophy" but only about enlargement.
Conversely, thickening of the ventricle may result in increased voltages seen
on the surface ECG, and we can then discuss "ventricular
hypertrophy".
Left
ventricular systolic overload/hypertrophy (LVH)
The
absence of LVH on ECG means nothing, as the features are insensitive. If
however they are present, LVH is very likely. Because the criteria were
formulated on white males, they are very insensitive in e.g. black
women.
Systolic
overload results in increased QRS deflections, with the sum of the S in V1 and
the R in V5 or V6 over 35mm indicating hypertrophy. (In the above picture, also
note the predominantly negative deflection of the P wave in V1, suggesting left
atrial enlargement). A host of other criteria have been proposed. Useful are:
- R in I over 15mm
- R in AVL over 11mm
- Sum of all QRS voltages
under 175mm (!)
T wave
axis changes can be predicted knowing Schamroth's rule .
LV
diastolic overload
Features
of LVH may be present (as above). Enormous R waves may be seen in left-sided
leads, especially with aortic or mitral regurgitation. In contrast to systolic
overload, where septal q waves in the lateral leads are often diminished or
absent, in diastolic overload, prominent lateral Qs are noted. Unlike systolic
overload (where the T waves are often inverted), T waves are usually upright,
very symmetrical, and somewhat pointed.
Inverted
U waves in V4-6 suggest either systolic or diastolic LV overload.
RV
hypertrophy
A
number of ECG abnormalities have been associated with right ventricular
hypertrophy. These include:
- right axis deviation;
- A tall R wave (bigger than
the S) in V1;
- A `little something' in V1
(an initial slur of the QRS, a small r, or a tiny q).
- Increased VAT in V1
- left-sided RS or rS
complexes, partial or complete RBBB, or RS complexes in the mid-precordial
leads.
Whenever
you see a tall R in V1, consider the following differential:
- posterior myocardial
infarction
- RV hypertrophy
- Right bundle branch block
- Wolff-Parkinson-White
syndrome (with an appropriately placed accessory pathway)
- Other rare causes such as
dextrocardia, Duchenne muscular dystrophy, and so on
- and, of course, incorrect
lead placement!
A
broadened QRS complex suggests a bundle branch block, although there are other
causes:
RBBB
Diagnostic
criteria for right bundle branch block are somewhat empiric, but useful. Here
they are:
- Tall R' in V1;
- QRS duration 0.12s or
greater (some would say, >= 0.14);
In
addition, there is usually a prominent S in the lateral leads (I, V5, V6).
RBBB
is sometimes seen in normal people, or may reflect congenital heart disease
(e.g. ASD), ischaemic heart disease, cardiomyopathy, or even acute right heart
strain.
LBBB
Diagnose
this as follows:
- No RBBB can be present;
- QRS duration is 0.12s or
more;
- There must be evidence of
abnormal septal depolarization. The tiny q waves normally seen in the
left-sided leads are absent. (And likewise for the normal tiny r in V1).
In
addition, the VAT is prolonged, and tall, notched R waves are seen in the
lateral leads (RR' waves). There is usually a notched QS complex in V1 and V2.
Fascicular
blocks
Left
anterior hemiblock
(LAHB) is interruption of the thin anterosuperior division of the left bundle.
Suspect it if there is left axis deviation (past -45o) without
another cause (such as inferior myocardial infarction, or some types of
congenital heart disease or accessory pathways).
Other
features of LAHB include an initial QRS vector which is down and to the
right, a long VAT, and several other minor changes.
LAHB
may indicate underlying heart disease, but is much more worrying when
associated with other abnormalities (such as PR interval prolongation or RBBB).
The
diagnosis of left posterior hemiblock is mentioned only to be avoided!
The
ST segment
The
junction between QRS and ST
Hypothermia
Besides
sinus bradycardia, the most common finding is a prominent J wave.
In
addition, there may be delayed VAT , QRS prolongation, and nonspecific T wave
abnormalities, with QT prolongation. Eventually, blocks, ventricular
extrasystoles, and finally ventricular fibrillation occurs, below 30oC.
Ischaemic
heart disease - ST changes
One
should always remember that more than a quarter of people presenting with an
acute myocardial infarction will have no ECG evidence of ischaemia or
infarction! The ECG on its own is a blunt-edged tool in the detection of
coronary artery disease. Exercise testing to elicit ischaemia is also not very
sensitive in detecting this common disease.
Acute
myocardial infarction --- the `hyperacute phase'
There
are four main features of early myocardial infarction (as per Schamroth): [qv
etc]
- increased VAT
- increased R wave amplitude
(!)
- ST elevation which is sloped
upwards!
- Tall, widened T waves (The
ST segment often merges with these)
Note
that Q waves are not seen early on.
Established
acute myocardial infarction
|
|
|
We
now lay great emphasis on ST segment elevation in diagnosing acute MI (In the
past, Q waves were remarked on, but as noted above, these are often absent,
early on). The features of `full blown' MI may be:
- prominent Q waves;
- elevated ST segments;
- Inverted `arrowhead' T
waves.
Remember
our previous warning, that a significant proportion of people having an acute
MI will have a normal ECG, so do not rely on any of these features to exclude
MI.
|
Posterior
MI
The
trick in diagnosing this is to realise that posterior wall changes will be
mirrored in the leads opposite to the lesion --- V1 and V2. S we'll see a tall
R (corresponding to a Q), ST depression, and upright arrowhead T waves:
Right
ventricular infarction
This
occurs in about 1/3 of patients with inferior MI, but is often missed. It would
be distinctly unusual in the absence of inferior MI. Sensitivity can be
improved by looking at V4R --- V4, but put the lead on the right
side of the chest! Look for ST elevation which is higher than that in V1 -- V3.
Another suggestive feature is lack of ST depression in V1 with evidence
of MI in the inferior leads (look for ST depression in V2 under 50% of the ST elevation
in AVF).
Non-ST
elevation MI
There
are no reliable correlates of "subendocardial" or non-ST elevation
MI, and the diagnosis is based on the combination of clinical and laboratory
criteria (troponin elevation being important). There may be no ECG changes, or
even ST segment depression and/or T wave abnormalities.
Angina
and stress testing
The
most important component of an effort ECG that indicates the presence of
coronary artery disease is where exercise reproduces the patient's chest
discomfort or pain. Other findings may be:
- ST segment depression (It
is customary to apply the Sheffield criteria, that is, 1mm (0.1mV)
ST depression 0.08s after the J point;
- failure of suppression of
ventricular ectopy, or (especially) development of ectopy in the recovery
period;
- Failure of the blood
pressure to rise with exercise (an ominous finding);
- ST segment elevation
- T-wave changes (which may
be rather nonspecific)
- Development of inverted U
waves, which, although subtle, is said to be specific for the presence of
ischaemia!
Did
you notice the ST segment depression in our section on voltage and timing,
above?
Prinzmetal's
angina
The
simple (and possibly even correct) explanation of why you see ST segment
elevation with this variant form of angina is that the predominant area of
ischaemia is epicardial. This disorder is thought to be related to vascular
spasm, and angiography shows coronaries without a significant burden of
atheroma. Many other morphological abnormalities have been described with this
disorder.
Other
morphological abnormalities
'Early
repolarisation'
This
is common --- ST segment elevation is conspicuous, often with a prominent J
wave. It has been remarked upon in athletes, particularly. It's important to
relate the ECG to the clinical context, as always, as otherwise one might
inappropriately suspect serious underlying heart disease.
T
waves
T wave
abnormalities are common and often rather nonspecific. T-wave changes that
suggest ischaemia are a very sudden junction between the ST segment and the T
wave, and very symmetrical T waves. A variety of changes may be seen with
cardiomyopathies, intracranial haemorrhage and so on. Symmetrical deep T-wave
changes most prominent in V3 and V4 suggest ischaemia in the territory of the
left anterior descending artery (LAD T0-waves). We should all know the features
of hypo- and hyper-kalaemia.
Hyperkalaemia
Initial
features are tall "tented" T waves. Later, despite the continuation
of sinus rhythm, the P waves disappear, and finally, the QRS complexes broaden
and become bizarre, the ST segment almost vanishes, and the patient dies from
ventricular arrhythmia or cardiac standstill.
For
features of hypokalaemia, see below .
Measures
- QT
This
is the time from onset of QRS to end of T wave. Because QT varies with rate, it
is common to apply a correction, usually using Bazett's formula:
QTc = QTmeasured
---------------------
SQRT (RR interval)
SQRT
refers to the square root. A normal value is about 0.39s ±0.04s (slightly
larger values are acceptable in women). Be particularly concerned if the value
is over 0.5, as may be seen in poisoning with tricyclic antidepressants,
congenital QT syndromes, hypocalcaemia, and toxicity from a variety of other
drugs (quinidine, procainamide, amiodarone, sotalol, erythromycin, etc). Other
cause have been reported, including hypothermia, head injury, acute myocardial
infarction (!), and hypertrophic cardiomyopathy.
U
waves
Hypokalaemia
The T
waves flatten, U waves become prominent (this may be falsely interpreted as QT
prolongation), and there may even be first or second degree AV block.
Several
syndromes
Myocarditis
Common
findings are tachycardia, heart blocks (first degree, LAHB), and increased VAT
. A variety of ST changes may be seen, including those of myopericarditis.
Atrial and ventricular extrasystoles are common.
Myopericarditis
Pericarditis
is usually associated with a degree of contiguous myocarditis. The major
manifestation is widespread ST segment elevation.
There
is also usually sinus tachycardia, and T wave abnormalities are common.
Pericardial
effusion
The
most common finding here is simply diminished amplitude of the ECG deflections.
There may also be T wave inversion, and sometimes one sees electrical alternans
.
Pulmonary
thromboembolism
Apart
from sinus tachycardia, ECG abnormalities are not common. The `classical'
S1Q3T3 syndrome occurs in under 10%. Other features may be those of right atrial
enlargement, RV hypertrophy or ischaemia, RBBB and atrial tachyarrhythmias.
Digoxin
effect
ST
segment changes are pretty characteristic, with their "reverse tick"
conformation. These changes are not indicative of toxicity, but merely the
presence of digitalis. With toxicity, practically any arrhythmia can be seen,
although certain arrhythmias are highly suggestive, for example, the presence
of both increased irritability and AV nodal block (such as paroxysmal
atrial tachycardia with a 2:1 AV nodal block).
Electrical
alternans
Here,
there is no rhythm disturbance, but the QRS amplitude alternates --- tall one
beat, shorter the next (and so on...). At fast rates, this is said to be of
little significance, but at slower rates usually signifies severe heart
disease, or pericardial effusion.
Bibliography
and sources
A good
general reference is Leo Schamroth's An Introduction to Electrocardiography,
published by Blackwell Scientific. (7th Ed., 1990, ISBN 0-632-02411-9). It has
the merits of both clarity, accuracy and depth). Leo was one of the truly great
men of electrocardiography, and a brilliant physician, to boot.
This
primer is still a work in progress, and we anticipate adding a lot of
information, and images, over the next few years. Most of the above images were
painstakingly redrawn (mainly from a variety of mediocre- or worse-quality Web
images), vectorised using the demonstration version of the excellent R2V
program, screen captured into PaintShop Pro, and then further processed. They
are far from perfect!
Date
of First Publication:
2003/7/4
|
Date
of Last Update:
2003/7/4
|
|
