Rate 1

Although at this stage we are concerned primarily with measuring heart rate on the
ECG, heart rate is closely interrelated with heart rhythm in many ways, and the
two, in turn, involve a consideration of the cardiac arrhythmias, so that this will be
a good point to introduce—
‘Arrhythmia’ is a term used to imply an abnormality either in electrical impulse
formation or electrical impulse conduction within the heart. Consequently most of
the arrhythmias produce some abnormality either in the rate of the heart beat or the
rhythm of the heart beat, or both. However, some arrhythmias may not affect heart
rate or regularity but can produce an abnormality of conduction, which may be
manifested only on the ECG tracing and may have no clinical symptoms or signs.
Disturbances of impulse formation cause arrhythmias due either to
(1) Escape of impulses. Or
(2) Ectopic impulse formation.
‘Escape’ occurs when there is a sufficietit pause in the dominant rhythm for some
subsidiary tissue to assert its own inherent automaticity or discharge of impulses.
This can be due to either suppression of the sino-atrial (SA) node itself—as, for
example, in sinus bradycardia or sinus arrest—or to defective conduction of a sinus
impulse as may happen in sino-atrial or atrioventricular block. Either way there is a
need for a subsidiary pacemaker to take over or else the heart would stop beating.
It is an important concept that the various pacemaking tissues in the heart compete
with one another in an attempt to govern, and that the one with the fastest rate of
discharge tends to dominate. A dominant pacemaker ‘governs’, so to speak, by
suppressing the as yet incompletely formed impulses of the subsidiary pacemaking
cells (unless the subsidiary pacemaker is ‘protected. in some way, i.e. unless there
is some sort of blockage to conduction of impulses into it).
Escape may take the form either of single ‘escape beats’, or of a series of three or
more beats in an ‘escape rhythm’. An example of an escape rhythm would be the
generation of atrioventricular (AV) junctional rhythm arising as a result of
complete atrioventricular block (see Figs. 34, ~35). Escape rhythms are usually
slower than sinus rhythm because the inherent rate of electrical discharge that each
tissue possesses slows as we ‘pass down the conducting pathways, from the SA
node towards the ventricles.
Fig. 34. No P waves or other evidence of atrial activity is visible, so that this is an
example of complete sino-atrial block (see p. 66). The QRS complexes must
therefore represent an escape rhythm and, since they appear to he normal, they are
unlikely to he arising from ventricular tissue and, in fact, represent AV junctional
escape rhythm at a rate of 50 heats per minute.
Each of the various tissues within the heart which has the property of automaticity
gives ‘rise to its own escape rhythm, so that we may have:
a. Atrial escape, which is characterized by a P’ wave which arrives late in the
cycle (late insofar as it arrives later than the sinus P wave should have arrived).
The P’ wave is different in shape from the sinus P waves, because it arises from
a different pacemaking focus and it is associated with a different (usually
shorter) P’—R interval. Once the escape impulse arises, its subsequent
conduction has the same possibilities as that of other atrial ectopic beats, so it’s
worth reading the section on p. 134 at this stage. Most often, intraventricular
conduction follows the conventional pathways so that the ensuing QRS
complex is. likely to be normal unless we have phasic aberrant ventrical
conduction (see p. 238).
b. AVjunctional escape, which is characterized by the appear~ nce of a QRS
complex arriving late in the cycle and which is preceded or followed by a
retrograde inverted F’ wave with a very short P’—R or R—P’ interval.
Sometimes no P’ wave can be seen because it is sitting within the QRS
complex. Since AV junctional escape beats have many of the characteristics of
other AV junctional ectopic beats, it’s worth reading this section on p. 143 now.
c. Ventricular escape, which is characterized by the appearance of a widened
and bizarre QRS complex arriving late in the cycle and with many of the
characteristics of other ventricular ectopic beats, so read the section on p. 147
d. Wandering pacemaker, which is characterized by the appearance of a number
of supraventricular impulses which arrive late in the cycle and which have
varying F’ wave shapes and F’—R intervals due to their multifocal origin from
various sites within the atria and the AV junction.
Remember that escape beats and rhythms always arise secondary to some
defect in a higher pacemaker, or to subsequent defective .conduction of the
impulse once it leaves the higher pacemaker.
So the diagnosis of an escape beat or rhythm is not complete without a description
of the primary cause.
Ectopy, on the other hand, usually occurs when some focus other than the SA
node fires off impulses, either as single beats or as a series of beats which are often
at a faster rate than that of the SA node or, in addition, to the basic
rhythm—whatever that rhythm may be. An example of this would be paroxysmal
ventricular tachycardia (see’ Figs 92, 93), or isolated ectopic beats (see Figs
Usually an ectopic focus with a relatively slow rate of discharge would be
dominated by a pacemaker situated higher (anatomically) in the heart. However,
sometimes an ectopic pacemaker is able to maintain its inherent slow rate. This
suggests that it must be protected from being suppressed by the dominant rhythm.
The mechanism whereby it is protected is called ‘entrance block’ and it implies
that the impulses coming down from the SA node are blocked or prevented from
entering (and thus suppressing) the ectopic pacemaker.
Similarly, stimuli from this same ectopic focus can be prevented from affecting
surrounding tissues because for some reason the impulse fails to emerge from its
site of origin. This is termed ‘exit block’. The disturbance occurs in the area
between the pacemaking focus and the myocardium around it.
Remember that in order to become manifest on the electrocardiogram, the
impulse must have left its focus of origin, passed through the
electrophysiologically silent area between its pacemaking focus and the
surrounding myocardium, and to have actually reached the myocardium.
Therefore exit block can’t actually be seen on the ECG and can only be inferred,
either by a sudden change in pacemaker rate or rhythm when exit block
commences or ends, or because of the presence of some type of second degree
such as Wenckebach or 3 :2 exit block. (See p. 72.)
Another manifestation of exit block occurs in parasystole (see p. 128), when
calculation of cycle length may reveal that, even though the ectopic pacemaker
discharges at the right time in the refractory cycle, no impulse appears on the ECG.
This implies an exit block from the ectopic focus.
Disturbances of impulse conduction mostly occur because of some abnormality
in the normal conducting pathway. However, sometimes conduction fails with no
actual conduction defect being present, but simply because a tissue is unable to
respond to an impulse. This occurs for instance in very rapid supraventricular (SV)
tachyarrhythmias when the ventricles are just not capable of responding to each
impulse because they have not had enough time to recover from the effect of
previous impulses, i.e. they are still refractory, so that some subsequent impulses
are blocked and we have a faster supraventricular than ventricular rate.
This understanding of electrophysiology forms the basis for a classification of the
arrhythmias, which will be discussed at various stages throughout the book.
1. Due to some Abnormality of Impulse Formation
1. In the SA node.
a. Sinus bradycardia.
b. Sinus tachycardia.
c. Sinus arrhythmia.
d. Sinus arrest.
2. In the atria.
a. Atrial extrasystoles.
b. Atrial parasystole.
c. Atrial tachycardia.
d. Atrial flutter.
e. Atrial fibrillation.
f. Wandering pacemaker.
3. In the AV junction.
a. AV junctional extrasystoles.
b. AV junctional escape beats.
c. AV junctional parasystole.
d. AV junctional rhythm.
e. AV junctional tachycardias.
4. In the ventricles.
a. Ventricular extrasystoles.
b. Ventricular escape beats.
c. Ventricular parasystole.
d. Idioventricular rhythm.
e. Paroxysmal ventricular tachycardia.
f. Idioventricular tachycardia.
g. Ventricular flutter.
h. Ventricular fibrillation.
Due to some Abnormality of Impulse Conduction
1. SA block-complete.
2. lntra-atrial block.
3. AV block—
incomplete—first degree.
—second degree.
Mobitz type I.
Mobitz type II.
complete—third degree
4. Intraventricular block—
Bundle-branch block—left.
Bifascicular block.
Trifascicular block.
5. Phasic aberrant conduction.
6. Dissociation.
Even after careful examination of an ECG, it is easy to be misled about the
regularity of the rhythm and the components of the various waves.
I find that a pair of calipers is extremely helpful. Also it often simplifies things
to mark off P waves and/or QRS complexes on a piece of blank paper partially
superimposed over the ECG (see Fig. 36).
Fig. 36. Mapping Out the P waves.
The use of iaddergrams’ often helps to clarify what’s happening to the impulse.
To draw a laddergram we draw some horizontal parallel lines to represent the
areas of the atria, AV junction and ventricles (see Fig. 37). If it’s relevant to the
particular ECG we’re looking at, we can also add an area to represent the SA node
or an ectopic site.
Fig. 37. Normal sinus rhythm with normal atrjoventrjcular and intraventricular
Fig. 38. Impaired AV conduction.
Fig. 39. Second degree sino-atrial block (see p. 64) showing non-conduction of the
second sinus impulse out of the SA node, with subsequent omission of a complete
Fig. 40. Normal sinus rhythm with a premature beat arising from an ectopic ventricular site, and showing no retrograde AV conduction.
Fig. 41. There is no evidence of sinus or other atrial impulses. so that we have
complete sino-atrial block (see p. 66). This gives rise to AV junctional heats
showing earlier anterograde than retrograde AV conduction.
Fig. 42. Progressive slowing of AV con duction until finally a sino-atrial impulse
isn’t conducted at all—Wenckebach con duction (see p. 64)
We mark the site of origin of our impulse by placing a dot in the relevant
representative area, and then we represent conduction by drawing a line from the
site of origin, in the direction of conduction. The rate of conduction is represented
by the length of the line.
A blockage to conduction is represented by terminating the line with a short
transverse bar. Abnormal intra ventricular conduction is represented by two
diverging lines (see Figs 37—42).
When analysing arrhythmias, especially those which appear confusing look at the
arrhythmia in stages:
Look at all the P waves, F’ waves, or P wave substitutes. If the P
wave is normal, it is likely to be arising from the SA node or from a
fairly high ectopic atrial focus.
If the P wave is deformed in shape but still upright, then it’s likely
to be arising from somewhere in the atria (providing that it’s not a P
mitrale or P pulmonale, see p. 182/183). In general the shorter the
P—R interval, the lower down in the atria is the ectopic focus likely
to be.
If the P wave is inverted in leads in which we would expect it to be
upright, then the impulse must be arising from low down in the atria,
the AV junction, or from the ventricles, whence it is being conducted
upwards towards the SA node in a retrograde fashion.
When P waves are seen, whether anterograde or retrograde,
remember to note the rate, and to comment on the presence of
bradycardia or tachycardia.
Often P wave substitutes are seen, as in atrial flutter or fibrillation
but if no P waves or P wave substitutes are visible, we may have sinus
arrest or complete SA block.
Measure and assess the P—P (or P’—P’) intervals. This indicates the
supraventricular rate. Measure all the P—P intervals. Progressive
shortening of the P—P intervals implies sino-atrial Wenckebach
conduction (see p. 64). Sudden shortening may be due to an atrial
premature beat. Sudden lengthening may be due to third degree
sino-atrial block or sinus arrest.
Examine each of the QRS complexes. If they are normal then they are
likely to have resulted from an impulse, which arose in a
supraventricular site such as the SA node, an atrial ectopic focus, or
the AV junction.
If the QRS complexes are bizarre in shape then they may be arising
from an ectopic ventricular focus, or they may be arising from a
supraventricular site and are being conducted down via a blocked
bundle of His (see p. 222) or via aberrant ventricular pathways (see p.
Check the numerical relationship between the P waves and QRS
complexes. If there are more P or F’ waves than QRS complexes then
there may be some blockage to conduction across the AV junction,
such as occurs with blocked atrial premature beats, or second and third
degree AV block. Alternatively, more QRS complexes may mean that
more ventricular beats may be being formed as occurs in ventricular
Examine the time relationship between the P waves and QRS
complexes, i.e. the P—R intervals.
Short P—fl intervals may suggest A—V junctional beats or rhythm,
or the Wolff—Parkinson—White syndrome, whereas a long P—fl
interval suggests first degree AV block.
If the P—P interval varies then we must consider such things as
wandering atrial pacemaker, Wenckebach conduction, dissociation,
and complete AV block.
Of course, if F’ waves follow the QRS complexes then we must
measure and examine the R—P’ intervals in the same way as the
P’—R interval.
Examine the relationship in position between the P waves and the
QRS complexes. If the P wave precedes the QRS complex then it is
likely that the impulse originates in the SA node or the AV junction
and is being conducted downwards in an anterograde direction.
However, if this preceding P wave is inverted, then it implies
retrograde conduction from a low atrial or AV junctional focus and it
also tells us that this retrograde conduction occurs earlier than the
anterograde conduction which gives rise to the ensuing QRS complex.
If the P wave follows the QRS complex, then either the QRS
complex arose first and was conducted retrograde, as may occur with
ventricular ectopic beats and rhythms, or the impulse arose as an AV
junctional ectopic beat or rhythm, and the anterograde conduction
proceded at a faster rate than retrograde conduction.
A complete description of any beat or arrhythmia must include comments about:
1. The site of origin of each impulse, e.g. SA node, ectopic atrial focus, AV
junction or ventricle.
2. The sequence of impulse discharge, e.g. sinus rhythm, bradycardia, tachycardia,
flutter or fibrillation.
3. The conduction sequence between the site of origin of the impulse and the
surrounding tissues, e.g. normal conduction, first degree, second degree or
complete block.
4. When there is a secondary rhythm, this too must be described, e.g. atrial
fibrillation with complete AV block and subsequent idioventricular escape
5. Intra-atrial conduction.
6. A—V conduction.
7. Subsequent intraventricular conduction.
8. Remember also to look at the conduction sequence of the secondary rhythm.
What we are in fact doing is to follow and carefully analyse everything that
happens to every impulse from the instant it is formed, all the way down its
passage along the conducting system and until it reaches its end point.
Every time you look at an electrocardiogram examine it with this sequence of
events in mind.
So that, for example, a full description of an arrhythmia might be ‘sinus
tachycardia with regular 2:1 AV block conducted with phasic aberrant ventricular
conduction and complicated by ventricular ectopic beats with retrograde AV
Since the ECG paper usually moves through the machine at a rate of 25mm per
second, each millimetre represents 1/25 (or 0.04 of a second) and each of the heavy
lines (which are 5 mm apart) represents a time interval of 5 x 0.04 see, i.e. 0.20 or
1/5 of a second.
That is, each large square represents (horizontally) 1/5 of a second, so 5 large
squares pass by the writing stylus each second and 300 large squares pass the
writing stylus each minute.
Therefore, to measure ventricular rate we count the number of large, i.e. 5-mm,
squares between corresponding waves of adjacent ORS complexes and divide this
number into 300. It is easiest to take either the peaks of adjacent P waves or the
troughs of the S waves as these are usually the most prominent. This gives the rate
per minute (Figs 43, 44).
Fig. 43. There are 46 large squares between consecutive P waves, so that the sinus
rate is 300/4.6 or 65 beats per minute.
Atrial rate is measured by considering the number of large (5-mm) squares
between consecutive P waves and dividing this number into 300 (Fig. 44).
Fig. 44. There are 7•5 large squares between adjacent R waves so the ventricular
rate is 300/7.5 or approximately 40 beats per minute. However, there are only 32
large squares between adjacent P Waves so that the atrial rate is 300/3.2 or
approximately 94 per mInute. This is an example of sinus rhythm with complete
AV block and idioventricular escape rhythm (see p. 60).
Alternatively, measuring the fl—P (or P—F, F—F or f—f) interval in seconds
and dividing this into 60 gives us the rate per minute. For example, an fl—fl
interval of 0~8 seconds represents a rate of 60/0.8 or 75 beats per minute.
If the rhythm is irregular, then we can either take a fairly average R—R or P—P
interval to measure the approximate rate or, more accurately, we can take the
shortest and longest R—R or P—P intervals and measure the extremes of rate,
reporting on the rate as ranging, for example, between say 60 and 90 beats per
If the rate is normal, e.g. between 60 and 100 beats per mm, progress to Stage II.
If the rate is slow, consider the possible causes:
1. Sinus bradycardia.
2. Wandering pacemaker (or idio-atrial or atrial escape rhythm).
3. AV junctional rhythm.
4. Idioventricular rhythm.
5. Complete AV block.
6. SA block.
7. Atrial arrhythmias with high grades of AV block.
8. Ventricular standstill.
Sinus bradycardia is the rhythm which occurs when the SA node ~harge its
impulses at an arbitrarily chosen, slower than normal rate.
Apart from the fact that the sinus rate is slow, i.e. less than 60 beats per min, the
ECG complexes are completely normal in every respect (see figs 45, 46).
Remember that in sinus rhythms we are concerned with the P-P intervals. If the
rate is less than 40 per minute and the ECG appears to be otherwise normal, we
should consider the possibility of SA block rather than sinus bradycardia,
especially if the rate is completely regular.
Fig. 45. The ventricular rate is 50 per mm. P waves. P—R intervals, and QRS
complexes are normal. Sinus bradycardia.
Fig. 46. The P—P intervals range from 112 to 128 seconds which represents a
sinus rate of 47 to 53 beats per minute, so that we have sinus bradycardia with
sinus arrhythmia.
Sinus bradycardia occurs in normal people, athletes, hypothyroidism, hypothermia,
SA node disease, uraemia, jaundice, convalescence from infective fevers, raised
intracranial pressure and drugs such as the beta-adrenergic blocking agents,
digitalis and calcium antagonists. Sinus bradycardia is often associated with sinus
arrhythmia and tends to be complicated by escape rhythms (see p. 39).
Fig. 47. Hypothyroidism.
In hypothyroidism, we often see marked sinus bradycardia together with a
prolonged P—R interval and low amplitude QRS complexes. However, the most
sensitive sign is in the T wave, which becomes flattened or even inverted. With
replacement therapy the T waves rapidly recover, and recovery of the other
abnormalities soon follows (see Fig. 47).
This is an uncommon arrhythmia and occurs if either SA node impulse formation is
suppressed or if there is SA block. In either case we could expect a subsidiary
pacemaker to give rise to an escape rhythm, but at a rate slower than the normal
sinus rate.
If the escape rhythm were to arise in an ectopic atrial site, we would see on the
1. A slow rate at about 50 to 60 beats per minute (although it may be even slower).
If it emanates from a single ectropic atrial focus, the rhythm would be regular
because it would have a constant escape interval. However, often there are
multifocal escape sites within the atria and the AV junction so that the rhythm is
far more likely to be irregular. It’s very important to remember that this is an
escape rhythm, i.e. it comes in late in the cycle and at a rate slower than the
normal SA node pacemaker, otherwise it could be confused with the presence of
multiple atrial premature beats.
2. If there is a single escape focus, the P waves will all be identical and the rhythm
will be regular but since there are more often a number of ectopic sites, the P
waves will tend to vary in shape and size and the rhythm is usually irregular
because of varying escape intervals. This gave rise to the concept of a
‘wandering pacemaker’. Although there is some difference of opinion as to the
actual underlying mechanism in the entity of wandering pacemaker, the
essential factor is the slowing in basic manifest sinus rhythm which results in
the atrial (and sometimes AV junctional) escape beats.
3. Since we have P waves arising from different foci, atrial fusion beats are not
uncommon. These are seen as a summation of the characteristics of the pure
sinus P wave and a pure ectopic P wave.
4. There may be evidence of the basic marked sinus bradycardia or sino-atrial
block, which constitutes the primary need for the escape to occur (see Fig. 48).
You may remember that we said on p. 38 that if the normal pacemaker (the SA
node) is suppressed for some reason, or if there is a blockage to conduction out
from it, then a subsidiary pacemaker may ‘escape’ from the dominance of the
usually faster-firing higher pacemaker, and give rise to what is called an escape
rhythm (Fig. 34). Now, AV junctional rhythm is a good example of this and,
because automaticity around the AV junction is about 40—60 beats per mm, AV
junctional rhythm usually runs at this rate (Figs 49, 50, 58, 225).
Sometimes when an idionodal escape rhythm begins, there is a short period of
gradual acceleration until the rate stabilizes. This sort of ‘warming-up’ process is
known as the Treppe phenomenon.
In the past the AV node itself was considered to be the initiating focus and to
have been able to fire off impulses from its higher, mid and lower parts, so giving
rise to ‘high, mid and lower nodal arrhythmias’. However, there is some doubt
now as to whether the AV node itself has pacemaking cells and the area which
contains the AV node, the main bundle of His and the adjacent area is called the
AV junction. Rhythms emanating from this area are now called ‘AV junctional
rhythms’. Also the differences between what were described as upper, mid and
lower nodal rhythms have been ascribed to different rates of conduction so that
these terms also are not in general use now, although the concept was a very
useful one.
On the EGG, AV junctional rhythm has the following characteristics:
1. The rate is a little slower than normal sinus rate, usually 40—60 beats per
minute because of slightly slower automaticity as we pass down the conducting
pathways. The rhythm is usually completely regular.
2. The position of the P wave in relation to the QRS complex depends on the
relative rates of anterograde and retrograde conduction from the AV junctional
focus. Remember that the normal P wave in normal sinus rhythm is upright in
leads I, II, aVF and V3—V6 and is biphasic in Vi and sometimes V2.
Once the impulse is discharged from the AV junction it may be conducted:
a. Retrograde at a faster rate than anterograde so that we will see an inverted
F’ wave before the QRS complex.
b. Anterograde at a faster rate than retrograde so that we will see that the QRS
complex is followed by an inverted F’ wave (see Fig. 49).
c. Anterograde at the same rate as retrograde so that the F’ wave falls within
the QRS complex and may not be visible at all (see Fig. 50).
d. Along normal intraventricular conducting pathways, which have had time
to recover, electrically speaking, so producing a normal QRS complex (see
Fig. 50).
e. With impaired conduction down the bundle branches so that we may see
right or left bundle-branch block or hemiblock (see Fig. 51).
f. With phasic aberrant ventricular conduction if there is marked tachycardia,
and if therefore the premature AV junctional impulse reaches the ventricles
before the intraventricular conducting pathways have had time to recover. In
this case we’ll see the typical widened and bizarre QRS complexes of phasic
aberrant ventricular conduction (p. 238).
g. AV junctional rhythm may occasionally be associated with an unusual type
of aberrant conduction which occurs in association with late escape
impulses. If the impulse arrives late rather than prematurely, the question is,
why should it be conducted aberrantly? There are several theories:
1. The impulse may be conducted down only part of the bundle of His.
Intraventricular conduction may be via some ectopic pathway.
in. The aberrant-looking impulses may in fact be arising in the proximal
part of the bundle branches.
iv. There may be bradycardia-dependent conduction impairment
associated with what is termed phase 4 aberration (see Fig. 52).
h. Antero grade conduction can be affected by AV block. Schamroth4 says that
first degree anterograde AV block out of the AV junction is present if the
P’—R interval is longer than 016 seconds.
Second degree anterograde AV block during AV junctional rhythm is
manifested on the EGG by the presence of solitary F’
Fig. 49. AV junctional rhythm with late retrograde AV conduction—except in the
fourth complex of lead a VL in which the QRS is preceeded by, but dissociated
from (see p. 197), a sinus P wave, and again in the fifth complex, in which no P
wave is visible so that we have anterograde and retrograde conduction proceeding
at equal rates.
Fig 51. There is sinus rhythm at a rate of 88 beats per minute, but the P waves bear
no relationship to the QRS complexes so that we have complete AV block. This
results in AV junctional escape rhythm at a rate of 60 per minute, which is
conducted downwards with this typical right bundle-branch block pattern.
Fig 50. Sinus rhythm with complete A V block. The escape rhythm is A V
junctional rhythm. Anterograde and retrograde conduction from the AV junctional
focus must be proceeding at the same rate because no retrograde P’ waves are
Fig. 52. This is a very peculiar looking ECG, and the first thing we notice is that
there are no normal sinus P waves. Instead, we see inverted retrograde P’ waves at
a rate of about 45 beats per minute (see leads II, III, aVF, and V3 to V6)—so that
we would appear to have either a low atrial ectopic or an AV junctional escape
rhythm due to complete SA block (see p. 66). However, if we look more carefully,
we’ll see that in some leads the QRS complexes are closely followed by P waves
of similar shape and axis to the other P waves so that they must be arising from the
same ectopic focus. In some leads (e.g. aVR) they can be seen very clearly
immediately following the QRS, and in others they are just visible as a notch
deforming the down strokes of the R waves (see leads II, III, aVL, aVF, and Vi).
It’s these second P waves closely following the QRS complexes that start to give
the game away. What we’re looking at then, are QRS complexes due to low atrial
or AV junctional rhythm with anterograde conduction, followed by later retrograde
AV conduction. If we measure these P—P intervals we see that our ectopic
pacemaker rate is about 88 beats per minute, so that we have idionodal tachycardia
(see p. 86). However, it immediately strikes us that for every two retrograde P’
waves, there’s only one anterograde QRS complex so that we must have second
degree 2:1 anterograde AV block. Furthermore, to add to the confusion, if we mark
out the P’—P’ intervals we see that in some places (e.g. the beginning of lead
aVR), we have alternate long—short—long P’—P’ intervals which indicates
retrograde Wenckebach conduction without any dropped beats. As if all this isn’t
enough, we must ultimately comment on the QRS complexes themselves! We can
see that in most leads, although the ORS complexes resemble one another, there
are some obvious variations in morphology due to some aberrancy in
intraventricular conduction (see p. 238). But, since these more bizarre complexes
aren’t premature, why should there be aberrant conduction? This is an example of
a rather atypical aberrancy well recognized as being associated with idionodal
rhythm and is probably due to so-called phase 4 aberration.