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).
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:
1. First degree block:
simply slowed conduction. This is manifest by a prolonged PR interval;

2. 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 I second degree heart
block)*.
*{Footnote: Thanks to the reader who pointed out the typo}


3. 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!
Bundle branch blocks
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:
1. Tall R' in V1;
2. 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. atrial septal defect), ischaemic heart disease, cardiomyopathy, or
even acute right heart strain.
LBBB
Diagnose this as follows:
1. No RBBB can be present;
2. QRS duration is 0.12s or more;
3. 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 -45
o
) 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 30
o
C.
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):
1. increased VAT
2. increased R wave amplitude (!)
3. ST elevation which is sloped upwards!
4. 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:
1. prominent Q waves;
2. elevated ST segments;
3. 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:
QT
c
= QT
measured

---------------------
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.