Arrhythmias

M. LaCombe
MDFMR/UNECOM
July 22, 2009
Let’s start with an easy one:
 Sinus rhythm with 2:1 AV heart block. The ECG shows a
bradyarrhythmia with non-conducted sinus P waves alternating with
normally conducted P waves. It is not possible to reliably identify
the point of block (nodal vs. infranodal) from this single ECG with
2:1 conduction. There is no evidence of acute inferior ischemia,
either. The site of block could be proximal (in the AV node) or more
distal, in the His-Purkinje system. In general, with 2:1 block,
involvement of the AV node is favored by a narrow QRS complex
and a prolonged PR interval, or by the presence of intermittent AV
Wenckebach. Block (infranodal) in the His-Purkinje system would
be favored by a concomitant bundle branch block and/or with a PR
interval of 160 ms or less. A possibly useful bedside diagnostic test
for chronic 2:1 block (in the absence of active ischemia) would be
to increase the sinus rate (mild exercise). A resumption of 1:1
conduction favors AV node block while worsening of block strongly
favors infranodal disease. Pacemaker placement is indicated for
symptomatic 2:1 block without reversible cause (e.g., drug effect)
and generally for asymptomatic 2:1 block due to infranodal disease.
Intracardiac His bundle electrogram would definitively identify the
site of block. This patient had intermittent 3:2 AV Wenckebach at
other times, and then resumed 1:1 conduction on subsequent
ECGs, consistent with AV node disease
Put this one together for me:
 Sinus rhythm with AV Wenckebach with 4:3 conduction in the
setting of an acute inferior wall infarction. The ECG demonstrates
Q waves and ST elevation in leads 2, 3, and aVF. There are also
reciprocal ST segment depressions in leads 1, aVL and V2-3. The
rhythm is Wenckebach showing progressive prolongation of the PR
intervals, shortening of the R-R intervals and block of every fourth
P wave. The presence of "group" beating is easily recognized and
characteristic of Wenckebach and is often associated with high
vagal tone or nodal ischemia in the setting of an inferior wall
myocardial infraction (MI). The block is at the level of the AV node
You’ve seen this one before, but now,
let’s focus on the rhythm
 Atrial fibrillation with a rapid ventricular response. Right axis deviation.
Intraventricular conduction delay. Right ventricular hypertrophy (RVH).
This patient has severe mitral stenosis with pulmonary congestion,
pulmonary hypertension, and right heart failure. A qR in lead V1 is one of
the most specific signs for right ventricular hypertrophy. Other causes of a
qR in V1 include a right bundle branch block (RBBB) in patients with an
anterior myocardial infarction or normal patients who have a QS in V1 and
subsequently develop a RBBB. This patient has right axis deviation in
addition to the qR in V1 which suggests RVH. Given atrial fibrillation and
RVH one should strongly consider mitral stenosis. Additional note on
differentiating right ventricular hypertrophy (RVH) from lateral MI: In some
cases of severe (RVH) with marked right axis deviation, leads I and aVL
may show rS or even QS waves, simulating lateral MI. In this case, lead
V1 notably shows a narrow qR complex (not just a tall R wave) strongly
suggestive of RVH, rather than posterior-lateral MI. Also, the lateral
precordial leads here show rS type complexes, not QR waves. Physical
examination, echocardiogram and other imaging modalities also provide
important information about RVH vs. lateral MI in cases where the ECG is
ambiguous.
 The tracing shows sinus rhythm with complete heart block and an
A-V junctional type escape rhythm. The P-P interval surrounding an
individual QRS complex is narrower (shorter) than the P-P interval
between two QRS complexes. Sinus rate variation with complete
heart block is called ventriculophasic sinus arrhythmia. The patient
has congenital complete heart block. This entity is usually
idiopathic but may be secondary to placental transfer of anti-Ro
and La antibodies from the mother. The spectrum of disease
ranges from patients who are born with severe bradycardia and
require pacemakers in infancy to patients who live full life spans
without artificial pacemakers. The overall infant mortality is 15%.
The escape rhythm in this instance is proximal in the conduction
system and a pacemaker is not required at this time.
Ventricular paced rhythm with underlying complete heart block (P
waves march through). Most important is superimposed current of
injury with hyperacute ST-T changes inferiorly and laterally with
reciprocal change V1-V3 consistent with acute infero-postero-
lateral ischemia/ myocardial infarction (MI). Pacemaker patterns,
like left bundle branch block (LBBB), often mask acute or chronic
MI. But sometimes, as in the present case, the ischemic changes
"show through."
 Acute infero-lateral and probably posterior myocardial infarction
(MI) with inferior Q waves and hyperacute ST-T complexes
inferiorly and laterally with reciprocal ST depressions V1-V3. Tall
initial R waves in V1-V3 with right bundle branch block. There is
second degree AV block (Type 1) with 2:1 block initially and then
3:2 AV Wenckebach with underlying sinus rate of about 85/min.
Left axis deviation is present. However, since this is an inferior MI,
a pacemaker is not usually indicated: block here is in the AV node
usually due to ischemia and increased vagal tone. In contrast, new
right bundle with left axis with acute anterior-septal MI would be
indication for prophylactic pacemaker. AV block in that setting is
due to Type II mechanism associated with severe involvement of
His-Purkinje system and carries ominous prognosis with high risk
of complete heart block with slow (or no) escape rhythm.
We used to see this more often,
back in the day…
Be careful here. This may look superficially like sinus but if you look
in V1, you can see P waves just before the QRS (there is right
bundle branch block (RBBB) and also P waves in the T wave
(halfway in between) which are partly hidden. Atrial rate is about
150, ventricular rate 75. This is atrial tachycardia with 2:1 block
(paroxysmal atrial tachycardia) "PAT with block" if it occurs
paroxysmally) which may be due to digoxin toxicity, atrial disease,
etc. If you got this right, PAT yourself on back; if you choked on it, a
more forceful interscapular blow may be indicated.
The major finding is narrow complex tachycardia with atrial rate of
about 300 indicating atrial flutter and slightly variable ventricular
response (2:1 conduction, some 3:1 and probably some
Wenckebach). Atrial flutter is sometimes mistaken (by housestaff at
other institutions) for sinus tachycardia. Look, for instance, at V1
where the flutter waves are hard to see vs. lead II where they are
more apparent. If only a V1 type lead were available, the
mechanism could be readily mistaken.
Sinus tachycardia with 2:1 block (hidden P waves in T waves, e.g.
leads V2 and V3) and left bundle branch block (LBBB). This most
likely is type 2 block given its occurrence with sinus tachycardia
and presence of LBBB. Patient was referred for evaluation for
pacemaker. Remember the "meet me halfway" rule: always look
halfway in between obvious P waves for hidden ones.
This one is tricky.
Be careful.
 Note there is evidence here of mitral valvular disease: ECG is
highly suggestive of biventricular hypertrophy with left ventricular
hypertrophy (LVH) type pattern in precordial leads and QRS axis of
about +90 degrees. This combination is common with Rheumatic
Heart Disease with MS/MR +/- aortic disease. Rhythm is junctional
with retrograde P waves with relatively long RP interval in lead II,
V1, etc. with single ventricular premature beat.

But don’t stop there: of note is long Q-T with prominent U waves
raising question of drug effect/toxicity or hypokalemia. Patient was
on a phenothiazine here. The ST-T changes are consistent with
hypertrophy, drug effect, ischemia, etc. Patient was also on digoxin
with low therapeutic level.
 Atrial flutter.

Don't miss hidden atrial (F) wave just after QRS. This is atrial flutter
with 2:1 conduction. Note that with atrial flutter there aren't P waves
per se but atrial waves. So if you talk about atrial flutter do not say
"the P waves...." since once you say P wave, the informed listener
will probably assume it's not atrial fibrillation or atrial flutter. On the
other hand, depending on whom you are talking to, this may not be
an issue. Also note left ventricular hypertrophy (LVH) and left axis
with possible prior inferior wall myocardial infarction (MI) here. Note
that typical flutter waves have negative polarity in lead II, as is the
case here.
 This is highly suggestive of Parkinson's disease.

The ECG shows the classic pseudo atrial flutter/fib type waves
associated with Parkinsonian tremor. The marked amplitude of the
waves, absence of an irregular ventricular rate and subtle hidden
true P waves in selected leads (lead 2, intermittently, aVR) indicate
the diagnosis. Refer to neurology not cardiology.
 This is sinus rhythmn.

This is a case of pseudo-flutter waves due to artifact (probably

Parkinsonian tremor). Some leads show clear sinus P wave, e.g.
V2, V3. So, remember, look at all the leads.
 AV nodal reentrant tachycardia (AVNRT). This tracing
demonstrates a REGULAR narrow complex tachycardia at a rate of
150. The differential diagnosis of this supraventricular tachycardia
includes: sinus tachycardia, AVNRT, automatic atrial tachycardia,
atrio-ventricular reentrant tachycardia (AVRT), involving retrograde
conduction over a "concealed" bypass tract, or atrial flutter with 2:1
block. If P waves can be located it can be helpful in determining the
mechanism of the tachycardia. In this tracing P waves can be
located at the end of the QRS in lead II and aVF, producing a
"pseudo S" wave. Absence of P waves or a "pseudo S" pattern in
II, III, or aVF, or a "pseudo R prime" pattern in V1 is characteristic
of AVNRT due to near simultaneous activation of the atrium and
the ventricle from the AV node. If the diagnosis is still in doubt,
adenosine may be useful in slowing conduction in the AV node.
Reentrant rhythms (AVNRT or AVRT) may "break" abruptly,
converting to sinus; the ventricular response of other atrial
tachcyardia or atrial flutter will slow often revealing underlying atrial
activity. (Note: the final wide complex waveform is either an artifact
or a ventricular premature beat.)
A Pause, for understanding...
Here is another AVNRT, with those pseudo-S waves:
But AVNRT gets confused with the less common AVRT:
AVRT is the consequence of the WPW-type congenital
bypass tracks
The short PR and Delta Wave of WPW
A “classical” 12-lead EKG of WPW
So, what’s this?
Pre-admission testing showed pre-excitation, with subtle (very, very subtle
if you missed it) Wolff-Parkinson-White (WPW) pattern. Note shortish PR
and delta wave, best seen in V5 as slurring of initial QRS, with tall R
(positive delta wave) in V1, negative in aVL, compatable with lateral
bypass tract. What is differential diagnosis of tall R in V1? You should
consider 1) normal variant, esp children, but also some adults, or lead
placement; 2) funny chest/mediastinal configuration with heart more
rightward; 3) posterior myocardial infarction (MI) (inferior/lateral
ischemia/MI usually also seen); 4) right ventricular hypertrophy (usually
right axis); 5) WPW with posterior or lateral bypass tract; 6) right
ventricular conduction abnormality; 7) hypertrophic cardiomyopathy (HCM)
with or without obstruction; 8) Duchenne muscular dystrophy (due to
postero-basal fibrosis).
 Atrial fibrillation with the Wolff-Parkinson-White (WPW) syndrome,
with conduction down the bypass tract. This is for the most part a
wide complex tachycardia with a rate of about 230 beats/min. The
differential diagnosis includes 1) ventricular tachycardia, 2)
supraventricular tachycardia with aberrancy, and 3) WPW with
conduction down the bypass tract. The major clues include the
"irregularly irregular" rhythm and the extremely rapid rate.
Ventricular tachycardia may be mildy irregular but this degree of
irregularity would be unusual at this very fast rate. The short
refractory period of certain bypass tracts can allow extremely rapid
heart rates, especially during atrial fibrillation. A correct diagnosis is
very important because drugs that slow AV conduction (verapamil,
beta blockers, digoxin, adenosine) are contraindicated. These
drugs can facilitate preferential conduction down the bypass tract
and the atrial fibrillation can degenerate to ventricular fibrillation.

A drug of choice is IV procainamide and if this is unsuccessful, DC

cardioversion should be performed promptly.
 Ectopic atrial (non-sinus) tachycardia with 2:1 block and 3:2 AV
Wenckebach (beats 4 and 5). Note the negative P waves in lead II
indicating a non-sinus pacemaker. Other important abnormalities:
right bundle branch block, left anterior fascicular block and a
markedly prolonged QT(U) interval. This patient was on digoxin
and quinidine. The evidence for quinidine toxicity (assuming the
serum potassium is normal and no other factors prolonging
ventricular repolarization are identifiable) is the very long QT(U)
interval best seen in V2-V5. This finding predisposes to torsade de
pointes and may occur with "therapeutic" or "subtherapeutic" levels
of quinidine or other class 1A antiarrhythmic drugs. Atrial
tachycardia with Mobitz I block also strongly raises the question of
digitalis toxicity. With pure 2:1 AV block, it may be impossible from
the surface ECG to tell if the non-conducted beats are due to nodal
or infranodal block. The clue here centers on beats 4 and 5 where
3:2 Wenckebach is evident, indicating block in the AV node.
 It's only NSR if that stands for Not Sinus Rhythm. Note that there
are two P's for every QRS (see V1) and that atrial activity at
176/min is negative in lead 2. This is atrial (not sinus) tachycardia
with 2:1 block (conduction). Block is almost certainly at AV node
level (Type 1 mechanism). Always exclude digitalis excess with this
arrhythmia (not present here). ECG also shows low limb lead
voltage, left ventricular hypertrophy (LVH) by precordial voltage and
slow R wave progression
 There is a wide-complex tachycardia with right bundle branch and left axis
deviation (RBBB/LAD) pattern (old per hx). The rhythm is NOT sinus but
atrial flutter with subtle flutter waves (aVR, II, V1). Note the negative
polarity of atrial waves in lead II, characteristic of typical atrial flutter. Atrial
flutter with 2:1 conduction is among most commonly missed major rhythms
(often called sinus tachycardia by housestaff-- at other institutions, of
course). Sustained atrial flutter is likely the major contributor, if not the
precipitant of congestive heart failure syndrome here in this elderly man.
Note that patients with atrial flutter may be candidates for ablation
treatment to interrupt reentrant wave that underlies this rhythm.
 Sinus rhythm with AV Wenckebach (Type 1 AV block) is present
with 3:2 and 2:1 conduction. Notice progressive PR prolongation in
3:2 cycles with non-conducted sinus P wave followed by normal PR
interval. Etiologies include drugs (beta-blockers, digitalis, calcium
channel blockers), inferior ischemia, intrinsic AV node disease,
Lyme disease, etc. In healthy young adults with high vagal tone
(e.g. athletes) AV Wenckebach during sleeping hours is not
uncommon. This patient's ECG also shows left ventricular
hypertrophy (LVH), left atrial abnormality (LAA) (biphasic P wave
with broad negative component in V1) and infero-lateral T wave
inversions raising question of ischemia.
 Atrial flutter with 2:1 conduction. Don't overlook subtle
"extra" atrial wave (it's NOT a true P wave, but a flutter
wave) in the early ST segment. Atrial flutter with 2:1
conduction (block) is often mistaken for sinus
tachycardia or paroxysmal supraventricular tachycardia
(PSVT)
There is a wide-complex tachycardia. The QRS shows
a classic left bundle branch block (LBBB) pattern. If you
look carefully, you will see atrial activity in the limb
leads, with negative polarity in lead II, at rate of
320/min. Hence, atrial flutter with 2:1 conduction and
LBBB.
 It may look like sinus tachycardia, but look
again in V1: There are two atrial waves for each
QRS, so the atrial rate is 260. This is another
case of atrial flutter with 2:1 conduction, one of
the most commonly mistaken arrhythmias! This
case is particularly tough because of low
voltage in limb leads.
 ECG shows sinus rhythm at 75/min but with 2:1 AV
block. There is also left atrial abnormality (LAA).
Conducted QRS complexes show right bundle branch
block (RBBB) with left axis deviation, most c/w left
anterior fascicular block. Minuscule R waves in II, III,
aVF also raise question of prior inferior myocardial
infarction (MI). The normal PR interval in conducted
beats and the RBBB favor an infranodal location of
block. Aficionados may also note the ventriculophasic
sinus arrhythmia (P-P interval with QRS in-between is
shorter than P-P without intervening QRS due to vagal
tone fluctuations). Treatment: pacemaker.
 Narrow complex tachyardia at 180/min with probable
subtle retrograde P waves just after the QRS (may need
to print this out to see in lead aVR and II). Therefore,
likely diagnosis is AV nodal reentrant tachycardia
(AVNRT); although, concealed bypass tract tachycardia
or atrial tachycardia not excluded. This is, of course,
NOT sinus and is also NOT atrial flutter (no flutter
waves and ventricular rate is too fast for flutter with 2:1
conduction).
 The underlying rhythm is atrial fibrillation (AF) with a
slow regularized ventricular response (45/min)
consistent with complete heart block (CHB) with a
junctional escape mechanism. The QRS complexes
show an intraventricular conduction delay (IVCD) with
left axis and left ventricular hypertrophy (LVH) and there
is Q-T(U) prolongation. Etiologic differential diagnosis
includes intrinsic conduction disease, rule out drug
toxicity or metabolic factors. The long QT here is
against digitalis as sole factor (digitalis shortens the
QT). Hypokalemia or relevant drug effects, such as
sotalol or amiodarone, should be excluded. Treatment:
If no reversible causes, patient will likely require an
implanted ventricular pacemaker, as well as
anticoagulation for AF.
 Atrial tachycardia with 2:1 block and ventricular
premature complexes (VPBs). Check out lead V1 if you
missed this. The atrial rate is 200. (Points against atrial
flutter are the atrial rate and discrete-appearing P
waves, upright in lead 2). Also present: left ventricular
hypertrophy (LVH) with intraventricular conduction
defect (IVCD) (incomplete left bundle branch block-
LBBB) and poor R wave progression (cannot rule out
prior anterior myocardial infarction (MI); but this could
be due to LVH/IVCD alone); also non-specific ST-T
changes. The patient was not digitalis toxic.
 Major Segue!

Homework Assignment for the

interns:
Ten signs or symptoms with
names derived from mythology.
Back to work:
This does indeed look like atrial flutter or coarse atrial
fibrillation with regularized response. However, if you
look closely, (V4; also lead 2 rhythm strip at end) you
can see true P waves buried in baseline artifact. So,
probable tremor artifact.
 Atrial flutter with 2:1 block. Note that there are 2 atrial
waves for each QRS in lead V1. The atrial rate is about
240; therefore, this could easily be misread as sinus
tachycardia or paroxysmal supraventricular tachycardia
(PSVT) variant--not by you of course. ECG also shows
left ventricular hypertrophy (LVH) and possible prior
antero-septal myocardial infarction (MI), along with non-
specific ST-T changes.
 Atrial fibrillation with an extremely rapid ventricular
response (overall average about 204 beats per minute).
There is intermittent right bundle branch block (RBBB)
aberrancy (note QRS morphology in V1/V6, especially),
associated with the very fast rates. In all, there are 10
consecutive beats with RBBB aberrancy, during which
the ventricular response rate is up to 240 beats per
minute
 This looks like sinus bradycardia at a rate of 43 bpm,
BUT... if you look more closely, there are P waves partly
hidden in T waves. So this is actually pure sinus with
blocked atrial premature complexes (APBs) in a
bigeminal pattern. As a result the effective sinus rate is
very slow. There are also non-specific T wave
inversions noted in V1-V3.
The rhythm is sinus with long, atypical AV Wenckebach
cycles (e.g., probable 6:5 block). The reason for the
type 1 second degree AV block is apparent from the
rest of the tracing which shows classic findings of an
acute inferior/right ventricular myocardial infarction,
consistent with proximal to mid-occlusion of the right
coronary artery (RCA). The finding of ST elevation in
lead III>II, as present here, is also consistent with this
finding.
The rhythm is sinus with ventricular bigeminy and late
diastolic premature ventricular complexes (PVCs) that
come just after the second sinus P waves. The PVCs
have a right bundle branch block (RBBB) morphology,
but this is not intermittent RBBB or Wolf-Parkinson-
White Syndrome (WPW).
The rhythm is sinus (or possibly atrial) tachycardia with
a P wave rate of about 120/min with AV Wenckebach.
There is an evolving inferior (posterior) myocardial
infarction (MI) pattern with Q waves and T wave
inversions in 2, 3, aVF, and a tall R in V2. The AV
conduction disturbance is likely related to the MI. There
is also low voltage and non-specific lateral ST-T
changes.
Normal sinus rhythm with artifact in V4-V6, simulating
premature ventricular complexes (PVCs). Note that
simultaneous lead II (bottom) does not show this, and
normal rhythm is not affected by the spurious "beats."
 Classic Wolff-Parkinson-White (WPW) pre-excitation
pattern, with triad of short PR, wide QRS and Delta
waves. Note the polarity of the delta waves (most
positive in lead 2 and lateral chest leads) consistent
with a right-sided bypass tract. Patients with WPW may
not only have atrio-ventricular reentrant tachycardia
involving the bypass tract, but also AV nodal reentrant
tachycardia, as well as atrial fibrillation (AF), etc.
One other segue -- here is WPW in reverse:

That is, White-Parkinson-Wolff

 Sinus with 5:4 AV Wenckebach. Low voltage
(consistent with obesity, Chronic Obstructive Pulmonary
Disease (COPD), and/or myocardial infarction (MI) with
extensive cardiac muscle necrosis) makes identification
of the very broad, low amplitude P waves difficult! Note
subtle changes in T-wave morphology due to
superimposed atrial activity. (Right axis deviation here
could be due to COPD, lateral extension of infarct, or
left posterior fascicular block.)
Normal sinus rhythm with a marked prolonged PR ("1st
degree AV block"). The P waves, partly obscured by the
T waves of the preceding sinus beats, are more clearly
evident after the premautre ventricular complexes
(PVCs), (beats 3 and 9, and the last beat). In addition,
there is an intraventricular conduction delay (IVCD),
borderline left axis deviation, and lateral ST-T wave
changes associated with a history of multiple non-Q
wave myocardial infarctions. The QT appears long in
part because of the superimposed P wave deflection at
the terminal portion of the T wave.
 Sinus rhythm with atrial bigeminy (this pattern starts
after the 4th sinus beat). In addition, there are voltage
criteria for left ventricular hypertrophy (LVH), possible
left atrial abnormality, and poor R-wave progression in
V1-V3. The latter finding could be due to LVH,
underlying anterior myocardial infarction (MI), lead
placement; or could be a physiologic variant. The
seventh QRS complex exhibits aberrancy, with a left
anterior hemiblock morphology.
This is most likely atrioventricular reentrant tachycardia
(AVRT), one of the "short R-P" tachycardias. Note the
inverted P waves in leads II, III, and F; with upright P
waves in aVR, consistent with retrograde activation of
the atria from the region near the AV node and septum.
Therefore, the descending limb of this reentrant rhythm
is down the AV node, and the ascending limb is up a
bypass tract located close to the septum. The
differential diagnosis also includes AV nodal reentrant
tachycardia (AVNRT) with a somewhat prolonged
retrograde (fast pathway) limb, or, less likely, atrial
tachycardia coming from low in the atria, with a very
prolonged PR interval.
 At first glance this might appear to be "sinus tachycardia."
However, a second look reveals two interesting findings. Note the
unusual P wave axis (negative in I and aVL) and the short PR
interval (or very long RP interval). One possible explanation for
these findings is that this is an atrial tachycardia with either 1) a
rapidly conducting ("slick") AV node, or 2) an "atrio-His" bypass
tract with fast conducting properties. This would account for the
short PR interval in the presence of an atrial tachycardia. Another
possibility for this non-sinus tachycardia is that it represents a "long
RP tachycardia" involving a left lateral bypass tract which is slowly
conducting (to account for the long RP interval). In this latter case,
the reentrant circuit would involve antegrade (orthodromic
conduction) down a rapidly conducting AV node and through the
ventricular myocardium, with retrograde conduction up the slowly
conducting bypass tract, and then across the atria back to the AV
node.Note that resting heart rates above 140 beats/min are rarely
due to sinus tachycardia in the very elderly.
 The rhythm is atrial fibrillation with a rapid ventricular
response (irregular rate at about 120 beats/min). There
is an extremely wide QRS of left bundle branch block
morphology; the QRS duration of over 200ms is
suggestive of drug effect or hyperkalemia. Flecainide is
a class Ic (Na+ channel blocking) drug, which exhibits
"use dependency": at faster rates with less time for
dissociation of the drug from the channel, Na+ channels
are increasingly saturated with the drug. This increases
the degree of QRS prolongation, and may be mistaken
for ventricular tachycardia.
 Ventricular tachycardia (VT) at rate of 170. The right
bundle branch block morphology is atypical
(monomorphic R, rather than rSR', in V1), and the R:S
ratio is less than 1 in V6, both suggestive of ventricular
tachycardia. Although the most common underlying
diagnosis in adult North American patients with
sustained monomorphic VT is coronary heart disease
status post myocardial infarction (MI)s, this patient had
a non-ischemic cardiomyopathy. The morphology of the
VT is suggestive of origin from the left side of the heart,
near the base (right bundle branch block with
inferior/rightward axis). As with any wide complex
tachycardia that is hemodynamically tolerated, the most
important data to obtain is the 12-lead ECG, as this can
direct possible radiofrequency ablation at the time of
electrophysiology study.
(This is quite difficult, but worth it.)
Atrial flutter (negative atrial waves in II, positive in V1) with an atrial
rate of approximately 230 BPM with subtle group beating. On close
inspection, there are groups of two ventricular beats followed by
pauses, with more atrial waves than there should be for simple 3:2
AV Wenckebach conduction pattern. This pattern is attributable to
dual levels of block (multilevel block) in the AV node: in this case
2:1 AV conduction "above" 3:2 AV Wenckebach conduction. If you
said atrial flutter (or raised question of flutter vs.rapid atrial
tachycardia) along with Wenckebach variant, give yourself four out
of five stars.
 This is most consistent with accelerated idioventricular
rhythmn (AIVR), originating from the left ventricle and
therefore accounting for the atypical RBBB morphology.
ST elevations in the precordial leads are likely due to
the injury current from and underlying acute myocardial
infarction (MI). AIVR may be marker of reperfusion
following acute MI. The rate of about (83 per minute) is
too slow for ventricular tachycardia and too fast for
complete heart block.
 This is relatively slow bi-directional ventricular
tachycardia (VT). Note the sinus P waves (sinus
tachycardia) at a rate of about 110 beats/min (most
visible in the lead II rhythm strip toward end of
recording) with apparent atrioventricular (AV)
dissociation and a wide complex tachycardia at about
100 beats/min. The QRS complex alternates between
two morphologies. This arrhythmia should always raise
suspicion of digitalis toxicity (not present in this patient
with a recent myocardial infarct).

The name, bi-directional VT, is confusing, as are many

terms generated by cardiologists, who in the main, are
poorly literate in my estimation. It refers to alternating
right-and left- BBB conduction of the ectopic ventricular
focus. “Ventricular remodeling” is another term that
drives me crazy; it evokes images of rearranging the
furniture in the LV chamber.
 Atrial fibrillation with a very rapid ventricular response
(average 160-170/min).Other Findings: Low limb
voltage, minor RV conduction delay with rsr' (or possibly
Qr) in V1 complex, and non-specific ST-T changes (on
digoxin).
 Coarse atrial fibrillation (not flutter) is present with a
slow ventricular response. There is an atypical left
bundle branch block (LBBB) pattern. The rsR' in lateral
leads (e.g., V6 here) is highly suggestive of severe left
ventricular (LV )dysfunction, often associated with a
ventricular aneurysm (El-Sherif sign). A QR or rsR'
complex is also present in I and aVL. Left axis deviation
and a long QT are noted, as well. The patient had heart
failure due to prior silent infarction.
Atrial tachycardia (NOT sinus tachycardia) with variable block. Also
left ventricular hypertrophy (LVH) and left axis deviation are
present. This is not complete heart block either. Note that the rate
is not slow and regular. Instead, the changing PR is due to variable
AV block. This patient has a history of rheumatic heart disease
(mitral and aortic regurgitation) and underwent a cardiac
electrophysiology procedure with ablation of the ectopic atrial site
that was the source of the tachycardia. Always exclude digoxin
excess (not present here) in cases of atrial tachycardia with block
as well. (Note: the subtle variation in QRS morphology, e.g., in
leads II,IIII and aVF, which is due to varying degrees of
superposition of the P waves on the QRS complexes and also,
possibly, to slight changes in QRS conduction at different rates.
This nonspecific finding should be distinguished from 2:1 electrical
alternans patterns.)
Now let’s cover some
ventricular issues:
Causes of wide-QRS tachycardia
Brugada algorithm
 Differential criteria considering the QRS
morphology in leads V1 and V6 in case of right
bundle branch block (RBBB) or left bundle branch
block (LBBB) aspect.
 Our first unknown.

Rapid SVT or V. Tach? Makes a difference, right?

We’ll start with the Brugada algorithm
Are there any RS complexes
in the V leads?

Absence of any RS complex

in the precordial leads V1..V6
is 100% specific for VT, but is
insensitive (26%).
 Here’s the tracing once again.

So, is there an RS in any of the precordial leads?

 Yes, V2 has an RSR’.

So let’s go to the next step of the

Brugada Algorithm...
Brugada algorithm
In any of these RS complexes,
is the interval from start of R
to nadir of S > 100ms ?
Look at V2, and specifically at the fifth complex there...

The R wave starts on a solid line, and the nadir of the S wave
is only two small boxes or .08 secs (80 msecs) out.
So we need to go to the next step
in the algorithm...
Is there AV dissociation, or
are there fusion or capture
beats?

{A capture beat QRS looks normal because a

conducted sinus beat transiently captures the
ventricles; fusion beat's QRS is
intermediate between normal and the VT
complex}
 Well, what do you think?

I think I can see P waves. Can you?

So, if we are correct, then according to
the algorithm this is V. Tach, because
there are P waves not associated with
any QRS’s. But let’s suppose we
aren’t sure.

Let’s go to the next step of the B.A.,

that is examining morphology. (This
is tedious, but productive.)

Is the QRS complex in V1

predominantly positive?
No it isn’t. So this doesn’t help us.

Let’s move on...

The RS interval is over 60 ms., so...
 Next look at V6. Is there a
monophasic R , or a QR ,
or an R:S ratio < 1 , or a
QS?

If any of these morphologic criteria exist,

it’s likely to be V tach. What’s your call?
 So by morphology, and because we think
We see A-V dissociation as well, we can say:
This is a rapid monomorphic ventricular tachycardia
(VT), 280 beats per minute, associated with
hemodynamic collapse. This tracing was obtained
from a patient with severe ischemic cardiomyopathy
during an electrophysiologic (EP) study. The rhythm
later converted to sinus with a single external
shock. This patient had an atrial rate of 72 beats per
minute (measured with intracardiac electrodes, not
shown). Although ventriculoatrial dissociation
(faster V rate than A rate) is diagnostic of VT, the
surface ECG findings are only present
approximately 20% of the time. In this tracing, the
ventricular rate is simply too fast for P waves to be
observed. VT with cycle lengths from 200-240 ms is
often termed ventricular flutter.
 But here’s an important point:
if there is hemodynamic collapse,
shoot first and ask questions
later:

Often the best 'drug' is in fact

electricity, as sustained VT
often deteriorates into VF if
left unmanaged.
 Okay, next case:

Is this supraventricular, or
nonsustained V. Tach?
If we use the algorithm...
 You will readily see that two
sensitive criteria for V. Tach are
met:

There is A-V dissociation, and in

V1, the interval from the start of
the R wave to the nadir of the S
wave is > 100 msec.
Can you see the P waves, without corresponding
QRS’s? (A-V dissociation)

And in V1, the first complex starts on a solid

Line and the nadir of the S wave is at least 2.5
boxes later (i.e. .10 sec. or 100 msec)
 So this is repetitive monomorphic ventricular
tachycardia (VT) from an asymptomatic 45-year-old
female wind surfer. This patient has a structurally
normal heart. This ECG pattern is typical for a form
of idiopathic VT arising from the right ventricular
outflow tract. Unlike ischemic VTs, this form of VT
is often provoked by exercise and suppressed by
beta blockade or verapamil. The prognosis for these
patients is good, with the following 2 exceptions: (1)
occasionally, this form of VT is associated with
right ventricular dysplasia, which is associated with
sudden death, and (2) occasionally, patients with
incessant VT develop congestive heart failure due
to tachycardia-induced cardiomyopathy. The
cardiomyopathy generally resolves when the
tachycardia is treated.
What’s this one?
You might be tempted to jump to
“atrial fibrillation with an
aberrated ventricular conduction”
but let’s use the algorithm first.
Brugada algorithm
 There are RS’s in the precordial
leads, so that criteria is not met,
those are very broad S waves (not
to be confused with inverted
broad ST/T segments) so the RS
interval is certainly greater than
100 msec.
 Agree?

Also, look at V4-6. Remind you of

anything?
 Polymorphic V. Tach
This ECG shows a relatively regular, wide complex
polymorphic ventricular tachycardia, rate 150 bpm,
that is most likely a type of torsade(s) de pointes.
See leads V4-V6 for classic “turning of the points”
morphology. Intermittent ventricular fusion beats
may be present. Causes of this life-threatening
arrhythmia include a variety of drugs and specific
electrolyte abnormalities (especially hypokalemia
and hypomagnesemia) associated with long QT (U)
intervals, as well as hereditary long QT syndromes
due to “channelopathies.”Admission laboratory
testing revealed a serum potassium of 2.2 (normal
range 3.5-5.3 mEq/L), sodium of 143 (range 135-148
mEq/L), bicarbonate of 16 (normal 21-30mEq/L),
phosphate 1.0 (range 2.7-4.5 mg/dL) and
magnesium 2.5 (range 1.6-2.6 mg/dL.)
This one should be easy for you now...
 Because there are RS waves in
the precordial leads, that criteria
is not met, but the RS interval is
huge.

Let’s use that other table of

criteria on this one, just for fun...
 Differential criteria considering the QRS
morphology in leads V1 and V6 in case of right
bundle branch block (RBBB) or left bundle branch
block (LBBB) aspect.
Do you agree that this looks RBBB-like?
 Differential criteria considering the QRS
morphology in leads V1 and V6 in case of right
bundle branch block (RBBB) or left bundle branch
block (LBBB) aspect.

So, the tracing has a RBBB like

appearance, and V1 has a qRSR’.
 So this one is monomorphic V. Tach

The ECG shows a relatively regular, very wide-

complex tachycardia with a heart rate of 130/min
and a QRS duration of about 180 ms. The QRS
morphology is that of a right bundle branch block
(RBBB) with a qRSR′in V1, rS in V6 and a marked
rightward axis. Underlying atrial activity is hard to
discern with certainty but may be sinus with AV
dissociation. These factors indicate ventricular
tachycardia which was confirmed at cardiac
electrophysiology study. A left ventricular
tachycardia intramyocardial focus (associated with
this ECG pattern) localized below the anterior
papillary muscle was successfully eliminated with
radiofrequency ablation.
A wide-complex tachycardia.
V. Tach?
Let’s start with this again...
There are RS’s in the precordial
leads, so that’s out.

The RS interval is not greater

than 100 msec. so that’s out too.
Is there A-V dissociation?

Actually, there is A-V association;

Look at lead III
So now we have to go through all those laborious
morphologic criteria:
Is the QRS complex in V1 predominantly
positive?
Yes it is.

So:
V1 is a QR

So, next look at V6...

Ans.: none of the above, so this is
SVT, but...
A close look at V5 gives us
another way to attack this...
 So this is not V. Tach. This is

Atrial flutter with 2:1 conduction and RBBB

This ECG shows subtle atrial flutter with 2:1 block,

right bundle branch block and right axis deviation.
The atrial rate is about 260 bpm (see upright flutter
waves in lead V1) with a ventricular response rate of
about 130 bpm. The right axis deviation here, in the
absence of clinical evidence of right ventricular
hypertrophy or lateral infarction, likely represents
left posterior fascicular block.The patient had
persistent atrial flutter with variable block or atrial
fibrillation at other times.
Here’s a three-fer. Careful.
This ECG shows underlying coarse atrial fibrillation
(AF) with (right) ventricular demand pacing at a rate
about 78 bpm with a relatively wide QRS complex
(left bundle branch block morphology) at about 180
milliseconds. Two PVCs are seen (2nd and 6th
beat).There are no sinus P waves or flutter waves
and no atrial spikes to indicate dual chamber
pacing.

You don’t need algorithms for this one.

What is this?
Back to the algorithm...
My problem is knowing where
the baseline is in the precordial
leads, and therefore defining R,
S, and Q waves.

So we’ll need to do the

morphology thing again.

Or use that other chart...

 Differential criteria considering the QRS
morphology in leads V1 and V6 in case of right
bundle branch block (RBBB) or left bundle branch
block (LBBB) aspect.
The rSR’ in V1 suggests a RBBB
...and the QS in V6 gives it away...
 This is monomorphic ventricular tachycardia at a
rate of about 140 bpm with a very wide (QRS
duration about 0.20 second) with a right bundle
branch block and superior axis deviation
morphology. The previous ECG done on this
patient the same day showed an extensive
anterolateral ST elevation acute myocardial
infarction . There is suggestion of ST elevation here
in V5 and V6 which is difficult to interpret with the
wide QRS here.
An easy one...
 This ECG shows sinus rhythm with
ventricular bigeminy (every other beat is a
ventricular premature beat or complex (VPB
or VPC, for short) of the same morphology
in each lead.Note also the minimal diffuse
ST elevations (with non-specific T wave
inversions). These repolarization changes
are consistent with sub-clinical
perioperative pericarditis, a ECG common
finding after coronary artery bypass graft
(CABG) surgery.
Try this:
 The problem here is that it’s
impossible for me to fit this into
a BBB category (and use the
table), and I can’t really define
the baseline well enough to use
the Brugada algorithm.

So let’s see if we can dissect this

out...
This ECG shows a very wide-complex (between 160-200 msec)
tachycardia at a rate about 180 bpm with a bundle branch (BBB)
morphology.
The diagnosis of monomorphic ventricular tachycardia is strongly
supported by the following criteria:

1) Wide QRS (greater than 140 ms) in the absence of drugs or

hyperkalemia (the QRS here is extremely wide);

2) wide monophasic R wave in lead V1 (or RS or QR complex in

that lead (or whatever we choose to call it).
3) QR complexes in the inferior leads with extreme axis
deviation;
4) rS or QS waves in V6.

It’s the rS in V6 that makes me worry

about V. tach.
A resting rate of 180 bpm excludes sinus tachycardia, especially in
this age group. There is no evidence of atrial flutter or atrial
tachycardia, and, as described, the QRS morphology here is
strongly against aberrant supraventricular conduction.

This patient had a complicated cardiac history of coronary artery

disease, status post bypass graft surgery and prior inferior
infarction. He had recurrent ventricular tachycardia, likely
originating the area of the prior inferior infarct. An echocardiogram
revealed showed a dilated left atrium and left ventricle, extensive
thinning with an akinetic scar of the inferior base and moderately
severe mitral regurgitation. Estimated left ventricular ejection
fraction was 35%.
This is a great tracing. I hope you’re saving these.
Let’s see if our algorithm works for this one:
There are RS complexes in the precordium, but
the RS interval is quite long, much greater than
100 msec, so that criteria is fulfilled for V. Tach
Now let’s use the table. Is this more RBBB or
LBBB?
LBBB type. Here’s the table:

The R in V1 is
not greater than
30 ms, and V6
has an RS, so
neither criteria is
fulfilled here for
V tach.
 So we have conflicting algorithms. Is there
anything else that helps us here? Think outside
the box:
 The first 4 beats of this ECG show termination of a run of wide-complex
tachycardia at rate about 150 bpm. The 5th and the 6th beats
supraventricular conduction with underlying atrial fibrillation now apparent.
The conducted supraventricular beats suggest underlying inferior
myocardial infarction with prominent Q waves in leads II and aVF and a
borderline intraventricular conduction delay (QRS=110 msec). Starting with
the 7th beat and continuing to the end, the wide-complex ventricular
tachycardia resumes. The wide-complex tachycardia (QRS about 160
msec) has left bundle branch block morphology, with an inferior QRS
axis.This ECG shows two features strongly favoring ventricular tachycardia
over supraventricular tachycardia with left bundle aberrancy, namely: 1) a
broad R wave (40 msec or more in duration) in leads V2, and 2) a delayed
intrinsicoid deflection great than 70 msec in V1-V2 measured from the
initial onset of the QRS to the nadir of the S wave. (The absence of these
findings does not exclude ventricular tachycardia, however.)This patient
ruled in for a small acute myocardial infarction with an elevated troponin,
but normal creatine kinase. Echocardiogram showed a major infero-lateral
wall motion abnormality consistent with prior myocardial infarction as well.
He had recurrent episodes of ventricular tachycardia and underwent
successful ablation of an ectopic focus in the crest of the interventricular
septum, under the left coronary cusp, consistent with the monomorphic
ventricular tachycardia seen here with a left bundle branch block, inferior
QRS axis morphology.
New case: what do you think?
For the sake of brevity, I will tell you that neither
the Brugada algorithm nor the table work for this
one. That is to say, both will tell us that this is
SVT.

Well then, what kind of SVT? It’s not flutter.

There are no flutter waves. Nor are there any
atrial fibrillatory waves. It’s not WPW; there are
no delta waves. There are no reentrant atrial
waves seen, although after some of the ventricular
complexes, one can see P waves.

Sometimes the algorithms mislead us. That is

why you need to think for yourself. This is hard
stuff, but no one can fault you for saying:
“I’m still worried about V. Tach.”
 This ECG shows sinus rhythm (normal QTc) with runs of non-
sustained monomorphic ventricular tachycardia (starting 2nd
beat, rate 170 bpm). The ventricular beats have a left bundle
branch block pattern and inferior/borderline rightward QRS
axis raising consideration of repetitive monomorphic
ventricular tachycardia arising from the right ventricular
outflow tract (RVOT). Isolated premature ventricular
complexes (PVCs) and two ventricular couplets are also
present with the same morphology.Atrial tachycardia is
excluded as there are no premature P waves prior to the runs.
The P waves associated with the wide complex beats appear
to be retrograde consistent with ventricular-atrial conduction.
No atrial flutter waves are seen. There is no delta wave to
suggest Wolff-Parkinson-White pattern.The patient had an
idiopathic cardiomyopathy with global mild ventricular
hypokinesis. Previous attempts at ablation in the RVOT region
had been attempted. At the time of repeat cardiac
electrophysiologic study, the arrhythmia was not inducible,
despite intensive programmed electrical and pharmacologic
stimulation. The diagnosis was monomorphic ventricular
tachycardia of unknown mechanism, possibly arising from the
superior portion of the interventricular septum.
Trouble?
 This is a classic ECG obtained during a ventricular
fibrillation (VF) cardiac arrest. The findings are
typical of ventricular fibrillation with more organized
ventricular electrical activity in the second half of
the strip consistent with ventricular flutter.There is
no evidence of any atrial activity ruling out atrial
fibrillation with Wolff-Parkinson-White (WPW ) or
atrial flutter with a bundle branch block. The
characteristic, systematic variation in QRS axis of
torsade is not seen here (although torsade may
degenerate terminally into ventricular fibrillation.)
This is one for the table:
The tracing has a classic RBBB
configuration

And is triphasic both in V1 and V6

There is a classic right bundle branch block (RBBB)
morphology (rsR' in V1) making VT unlikely. No
definite atrial activity is seen (P waves or flutter
waves). The very regular rate at 150/min excludes
AF. Therefore, the rhythm is most consistent with
paroxysmal supraventricular tachycardia (PSVT),
most likely AV nodal re-entrant tachycardia
(AVNRT), although AV re-entrant tachycardia or
atrial tachycardia (with hidden P waves) are not
excluded.
An easy one...
 There are fixed coupled premature
ventricular compexes (PVCs) in a bigeminal
pattern. Note the onset of each VPC comes
just after a (non-conducted) sinus P wave,
giving the appearance of a short PR.The
sinus beats show probable left atrial
abnormality, borderline left axis deviation,
and a minor right ventricular (RV)
conduction delay.
Why the wide-complex rhythmn?
Both atrial and ventricular pacemaker
spikes are seen, for example, in lead II,
before each P wave and QRS,
respectively. The patient has a dual
chamber rate responsive pacemaker
(DDDR) pacemaker.
A difficult one...
 Complex ECG showing:

1) Underlying atrial fibrillation;

2) Long Q-T(U);
3) Ventricular pacing with intermittent
sensing failure; and
4) Run of torsade de pointes-type of
polymorphic ventricular tachycardia
(second half of record).
Very tough. Be careful.
Hint: I showed you this one to illustrate the A-V
dissociation criteria of the Brugada algorithm

Do you see the A-V dissociation?

 There is a wide complex tachycardia at
about 165/min with an right bundle branch
block (RBBB) morphology. Underlying sinus
tachycardia at about 136/min and AV
dissociation are noted, confirming the
diagnosis of ventricular tachycardia (VT).
(Note the clear sinus P waves, e.g., just after
5th QRS.) The QRS morphology and axis are
consistent with origin of the VT from the
posterior septum. The patient had had a
prior large inferior-posterior myocardial
infarction (MI). (Of additional note here is the
relatively low limb lead voltage and sinus
tachycardia).
Thoughts?
 What helps me here is V6. I get an idea of where the
baseline is, and the RS interval here clearly exceeds 100

msecs.
Ventricular tachycardia (VT) at rate of 170. The right
bundle branch block morphology is atypical
(monomorphic R, rather than rSR', in V1), and the
R:S ratio is less than 1 in V6, both suggestive of
ventricular tachycardia. Although the most common
underlying diagnosis in adult North American
patients with sustained monomorphic VT is
coronary heart disease status post myocardial
infarction (MI)s, this patient had a non-ischemic
cardiomyopathy. The morphology of the VT is
suggestive of origin from the left side of the heart,
near the base (right bundle branch block with
inferior/rightward axis). As with any wide complex
tachycardia that is hemodynamically tolerated, the
most important data to obtain is the 12-lead ECG, as
this can direct possible radiofrequency ablation at
the time of electrophysiology study.
Is this ventricular tachycardia?
 No. The rhythm is atrial fibrillation with a rapid
ventricular response (irregular rate at about 120
beats/min). There is an extremely wide QRS of left
bundle branch block morphology; the QRS duration
of over 200ms is suggestive of drug effect or
hyperkalemia. Flecainide is a class Ic (Na+ channel
blocking) drug, which exhibits "use dependency":
at faster rates with less time for dissociation of the
drug from the channel, Na+ channels are
increasingly saturated with the drug. This increases
the degree of QRS prolongation, and may be
mistaken for ventricular tachycardia.

The take-home message here, for this impossible

case, is to ask what meds the patient is on. Even if I
were told “flecainide for A. Fib” I would not send
this patient home.
Is this polymorphic V-tach?
 No. This is atrial fibrillation with an
extremely rapid ventricular response
(overall average about 204 beats per
minute). There is intermittent right bundle
branch block (RBBB) aberrancy (note QRS
morphology in V1/V6, especially),
associated with the very fast rates. In all,
there are 10 consecutive beats with RBBB
aberrancy, during which the ventricular
response rate is up to 240 beats per minute

(Both the algorithm and the table work well

on this one.)
DC countershock immediately?
No. This is a ventricular paced rhythm with
underlying complete heart block (P waves
march through). Most important is
superimposed current of injury with
hyperacute ST-T changes inferiorly and
laterally with reciprocal change V1-V3
consistent with acute infero-postero-lateral
ischemia/ myocardial infarction (MI).
Pacemaker patterns, like left bundle branch
block (LBBB), often mask acute or chronic
MI. But sometimes, as in the present case,
the ischemic changes "show through."
Think this one through with me.
Forget about algorithms.
 Atrial fibrillation with the Wolff-Parkinson-White (WPW) syndrome,
with conduction down the bypass tract. This is for the most part a
wide complex tachycardia with a rate of about 230 beats/min. The
differential diagnosis includes 1) ventricular tachycardia, 2)
supraventricular tachycardia with aberrancy, and 3) WPW with
conduction down the bypass tract. The major clues include the
"irregularly irregular" rhythm and the extremely rapid rate.
Ventricular tachycardia may be mildy irregular but this degree of
irregularity would be unusual at this very fast rate. The short
refractory period of certain bypass tracts can allow extremely rapid
heart rates, especially during atrial fibrillation. A correct diagnosis is
very important because drugs that slow AV conduction (verapamil,
beta blockers, digoxin, adenosine) are contraindicated. These
drugs can facilitate preferential conduction down the bypass tract
and the atrial fibrillation can degenerate to ventricular fibrillation.
Call EP fellows stat! A drug of choice is IV procainamide and if this
is unsuccessful, DC cardioversion should be performed promptly.
 Summary:

Many of these are very difficult.

The algorithms are hard to
commit to memory.
For family medicine practitioners
who see this stuff infrequently,
this can be an impossible
situation,
unless you remember this axiom:
 Always assume the patient has the worst
treatable condition you can do something
about, and proceed from there.

In the case of wide-complex tachycardias,

to say: “This is probably just SVT with
aberrated conduction” and send the patient
home, is to court disaster.
 You do not have to know
everything to be a great doctor.

You just have to think.