Marathon-related ECG Exasperation

The following two ECGs were taken from a 36-year old marathon runner presenting to the
ED with acute gastroenteritis. He was completely asymptomatic at the time the ECGs were
taken, with normal blood pressure and no chest pain, palpitations or dizziness. Electrolytes
were normal.
What are the ECG findings?

ECGs findings include:

Accelerated idioventricular rhythm (AIVR) at around 60 bpm

Multiple sinus capture beats

Isorhythmic AV dissociation:
Sinus P waves are buried in the QRS complexes and T waves at a similar rate
to the ventricular rhythm best seen in the rhythm strip in ECG # 2

Sinus arrhythmia, with variation in the PP interval of up to 0.2 s

Summary

Competing sinus and idioventricular pacemakers are present. There is

underlying sinus arrhythmia, with sinus capture occurring when the sinus rate
exceeds the idioventricular rate.

Definitions

Accelerated idioventricular rhythm:

An ectopic ventricular rhythm consisting of three or more ventricular
complexes occurring at a rate of 50-110 bpm. The rate differentiates AIVR
from ventricular escape rhythms (rate < 50 bpm) and VT (> 110bpm).

Isorhythmic AV dissociation:
AV dissociation with sinus and ventricular complexes occurring at similar
rates, unlike 3rddegree heart block where the atrial rate is usually faster than
the ventricular rate. Isorhythmic AV dissociation is usually due to functional
block at the AV node from retrogradely conducted ventricular impulses
(interference-dissociation), which leaves the AV node refractory to the
anterograde sinus impulses.

Sinus arrhythmia:
Sinus rhythm in which the PP interval varies by 0.16 s or more.

Q2. What is the mechanism of this arrhythmia?

The likely mechanism of the AIVR in this patient is enhanced automaticity of

an ectopic pacemaker in the ventricles coupled with sinus bradycardia and sinus
arrhythmia due to athletic training.

There are pacemaker cells at various sites throughout the conducting system, with
each site capable of independently sustaining the heart rhythm. The rate of
spontaneousdepolarisation of pacemaker cells decreases down the conducting
system:

SA node (60-100 bpm)

Atria (< 60 bpm)

AV node (40-60 bpm)

Ventricles (20-40 bpm)

Under normal conditions, subsidiary pacemakers are suppressed by the more rapid
impulses from the sinus node. AIVR occurs when the rate of an ectopic ventricular
pacemaker exceeds that of the sinus node.

Athletic training leads to changes in the autonomic nervous system, with increased
resting vagal tone and decreased sympathetic tone. This hypervagotonic state
causes suppression of impulse generation by the SA node and propagation by the
AV node. As a result, athletic individuals will commonly exhibit sinus bradycardia and
low-grade AV blocks (e.g. 1st degree heart block, Mobitz I).

AIVR is most commonly seen during the reperfusion phase of

an acute myocardial infarction.
It is also seen with:

Drug toxicity, especially digoxin, cocaine and volatile anaesthetics such as

desflurane

Electrolyte abnormalities

Cardiomyopathy

Congenital heart disease

Myocarditis

Following return of spontaneous circulation in the post-cardiac-arrest period

What other ECG abnormalities are common in athletes?

The following abnormalities may be present, due to autonomic conditioning

(enhanced vagal tone, decreased sympathetic tone) and ventricular hypertrophy:

Sinus arrhythmia

Sinus bradycardia

Junctional or ventricular escape rhythms

 1st degree heart block

Wenckebach phenomenon

Left ventricular hypertrophy

Axis deviation

Incomplete RBBB

Management

AIVR is a benign rhythm in most settings and does not usually require
treatment.

Administration of anti-arrhythmics may cause precipitous haemodynamic

deterioration and should be avoided.

Treat the underlying cause:

o correct electrolytes

o restore myocardial perfusion

o give Digibind in the case of digoxin toxicity.

Patients with low-cardiac-output states (e.g. dilated cardiomyopathy)

may benefit from restoration of AV synchrony to restore atrial kick in
this case atropine may be used to increase sinus rate and AV
conduction

An Electrocardiographic Exigency

A 23 year-old man is brought in by paramedics after an episode of syncope at home.

On arrival he is in severe respiratory distress, extremely pale and dripping with
sweat. BP is 125/70, HR is 80bpm, RR 40, SaO2 95% on 15L O2 via NRB. Portable
CXR in resus is normal.

His ECG is presented below:

Q1. Describe the ECG

Sinus rhythm at 80 bpm

Left axis deviation (-70 degrees)

RBBB with wide QRS (150ms), tall R wave in V1, RSR complexes in leads
V1-3

Right ventricular strain pattern with deep T wave inversions in V1-3

Widespread ischaemic changes with 1-2mm ST elevation and early Q

waves in the anterior leads (V2-5) and 1-2 mm ST depression in inferior leads
(II, III and aVF). There is also significant ST elevation in leads aVR and aVL
with formation of Q waves.

Q2. What is your interpretation of the ECG findings given the clinical context?

The combination of new RBBB with signs of right ventricular strain (deep T
wave inversions in V1-3) in a patient presenting with dyspnoea and syncope
is strongly suggestive of acute pulmonary hypertension secondary
to massive PE.

Widespread myocardial ischaemia/infarction is likely related to severe global

tissue hypoxia from obstructive shock (VBG in this patient showed venous
saturations of 10%, venous PO2 10mmHg with a lactate of 8mmol/L).

Left axis deviation may represent left anterior fascicular block.

Shortly after this ECG was taken, the patient lost consciousness and had
a PEA arrest from which he was unable to be resuscitated. Bedside
echocardiogram performed during the resuscitation attempt showed a
grossly dilated right ventricle and partially collapsed left ventricle with
deviation of the interventricular septum to the left. Post-mortem
examination confirmed a large saddle pulmonary embolus with complete
obstruction of the pulmonary trunk. Previous hospital notes showed a
history of thrombophilia and two previous episodes of venous
thromboembolism
Q3. What other ECG changes may be seen in this condition?

ECG changes are all fairly insensitive for the diagnosis of PE, and in most patients
with PE the ECG will be normal.
The following ECG changes may be seen in acute pulmonary embolism:

Sinus tachycardia

SI QIII TIII deep S wave in I, Q wave in III, inverted T wave in III

Complete or incomplete RBBB

Right axis deviation

Right ventricular strain pattern: T wave inversions in V1-3, sometimes

extending to V4

Simultaneous T wave inversions in the inferior (II, III, aVF) and right precordial
leads (V1-3).

Right atrial enlargement (P pulmonale): peaked P wave in lead II > 2mm in

height

Clockwise rotation: shift of the R/S transition point towards V6, persistent S
wave in V6

Atrial tachyarrhythmias: AF, flutter, atrial tachycardia

Extreme right axis deviation may occur, with axis between zero and -90 degrees, giving the
appearance of left axis deviation (pseudo left axis). Simultaneous T wave inversions in the
inferior and right precordial leads is the most specific finding for PE, with reported
specificities up to 99% in one study. Check out Amal Mattu and William Bradys
excellent ECGs for the Emergency Physician books for some great examples of this.

ECG changes in PE are related to:

 dilation of the right atrium and right ventricle with consequent shift in the
position of the heart

right ventricular ischaemia

increased catecholamine levels (which drives the tachyarrhythmias)

Accelerated Junctional Rhythm

Background

Accelerated junctional rhythm (AJR) occurs when the rate of an AV

junctional pacemaker exceeds that of the sinus node.

This situation arises when there is increased automaticity in the AV node

coupled with decreased automaticity in the sinus node.

Causes

Digoxin toxicity (= the classic cause of AJR)

Beta-agonists, e.g. isoprenaline, adrenaline

Myocardial ischaemia

Myocarditis

Cardiac surgery

Terminology

Junctional rhythms are arbitrarily classified by their rate:

Junctional Escape Rhythm: 40-60 bpm

Accelerated Junctional Rhythm: 60-100 bpm

Junctional Tachycardia: > 100 bpm

They may also be classified by their aetiology:

Automatic Junctional Rhythms (e.g. AJR) = Due to enhanced

automaticity in AV nodal cells
 Re-entrant Junctional Rhythms (e.g. AVNRT) = Due to re-entrant loop
involving AV node

ECG Features of AJR

Narrow complex rhythm; QRS duration < 120ms (unless pre-

existing bundle branch block or rate-related aberrant
conduction).

Ventricular rate usually 60 100 bpm.

Retrograde P waves may be present and can appear before,

during or after the QRS complex.

Retrograde P waves are usually inverted in the inferior leads

(II, III, aVF), upright in aVR + V1.

AV dissociation may be present with the ventricular rate

usually greater than the atrial rate.

There may be associated ECG features of digoxin

effect or digoxin toxicity.

ECG Example
junctional Tachycardia

Narrow complex tachycardia at 115 bpm.

Retrograde P waves inverted in II, III and aVF; upright in V1 and

aVR.

Short PR interval (< 120 ms) indicates a junctional rather than atrial
focus.

Atrial Flutter
Background

Atrial flutter is a type of supraventricular tachycardia caused by a re-

entry circuit within the right atrium.

The length of the re-entry circuit corresponds to the size of the right
atrium, resulting in a fairly predictable atrial rate of around 300 bpm
(range 200-400).
 Ventricular rate is determined by the AV conduction ratio (degree of AV
block).

The commonest AV ratio is 2:1, resulting in a ventricular rate of ~150

bpm.

Higher-degree AV blocks can occur usually due to medications or

underlying heart disease resulting in lower rates of ventricular
conduction, e.g. 3:1 or 4:1 block.

Atrial flutter with 1:1 conduction can occur due to sympathetic

stimulation or in the presence of an accessory pathway especially if
AV-nodal blocking agents are administered to a patient with WPW.

Atrial flutter with 1:1 conduction is associated with severe

haemodynamic instability and progression to ventricular fibrillation.

typical anticlockwise re-entry circuit within the right atrium

Classification

This is based on the anatomical location and direction of the re-entry circuit.

Typical Atrial Flutter (Common, or Type I Atrial Flutter)

Involves the IVC & tricuspid isthmus in the reentry circuit. Can be further classified
based on the direction of the circuit:

Anticlockwise Reentry. This is the commonest form of atrial flutter (90% of

cases). Retrograde atrial conduction produces:

Inverted flutter waves in leads II,III, aVF

Positive flutter waves in V1 may resemble upright P waves

Clockwise Reentry. This uncommon variant produces the opposite pattern:

Positive flutter waves in leads II, III, aVF

Broad, inverted flutter waves in V1

Atypical Atrial flutter (Uncommon, or Type II Atrial Flutter)

Does not fulfil criteria for typical atrial flutter.

Often associated with higher atrial rates and rhythm instability.

Less amenable to treatment with ablation.

ECG Features

General Features

Narrow complex tachycardia

Regular atrial activity at ~300 bpm

Flutter waves (saw-tooth pattern) best seen in leads II, III, aVF
may be more easily spotted by turning the ECG upside down!

Flutter waves in V1 may resemble P waves

Loss of the isoelectric baseline

Fixed AV blocks

Ventricular rate is a fraction of the atrial rate, e.g.

2:1 block = 150 bpm

3:1 block = 100 bpm

 4:1 block = 75 bpm

Variable AV block

The ventricular response is irregular and may mimic AF

On closer inspection, there may be a pattern of alternating 2:1, 3:1 and

4:1 conduction ratios

Atrial flutter with a 3:1 block

Handy Tips For Spotting Flutter

Rapid Recognition

Narrow complex tachycardia at 150 bpm (range 130-170)? Yes ->

Suspect flutter!

Turn the ECG upside down and scrutinise the inferior leads (II, III + aVF)
for flutter waves.

Vagal Manoeuvres + Adenosine

Atrial flutter will not usually cardiovert with these techniques

(unlike AVNRT), although typically there will be a transient period of
increased AV block during which flutter waves may be unmasked.

RR intervals

In atrial flutter with variable block the R-R intervals will be multiples of
the P-P interval e.g. assuming an atrial rate of 300bpm (P-P interval
of 200 ms), the R-R interval would be 400 ms with 2:1 block, 600 ms
with 3:1 block, and 800 ms with 4:1 block.
 Look for identical R-R intervals occurring sporadically along the rhythm
strip; then look to see whether there is a mathematical relationship
between the various R-R intervals on the ECG.

In contrast, atrial fibrillation will be completely irregular, with no patterns

to be discerned within the R-R intervals.

ECG Examples

Example 1

Atrial Flutter with 2:1 Block

There are inverted flutter waves in II, III + aVF at a rate of 300 bpm (one per
big square)

There are upright flutter waves in V1 simulating P waves

There is a 2:1 AV block resulting in a ventricular rate of 150 bpm

Note the occasional irregularity, with a 3:1 cycle seen in V1-3

This is the classic appearance of anticlockwise flutter.

Example 2

Atrial Flutter with Variable Block

Inverted flutter waves in II, III + aVF with atrial rate ~ 300 bpm

Positive flutter waves in V1 resembling P waves

The degree of AV block varies from 2:1 to 4:1

The diagnosis of flutter with variable block could be inferred here from the R-R
intervals alone (e.g. if flutter waves were indistinct) note how the R-R intervals
during periods of 4:1 block are approximately double the R-R intervals during 2:1
block.
Example 3

Atrial flutter with 4:1 block

There are inverted flutter waves in II, III + aVF at a rate of 260 bpm.

There are upright flutter waves in V1-2 (= anticlockwise circuit).

There is 4:1 block, resulting in a ventricular rate of 65 bpm.

The relatively slow ventricular response suggests treatment with an AV nodal

blocking agent.
Example 4

Atrial Flutter with Variable Block

The block varies between 2:1 and 4:1

The presence of positive flutter waves in lead II suggests a clockwise re-entry

circuit (= uncommon variant).

Example 5
Atrial Flutter with High-Grade AV Block

There is anticlockwise flutter with marked AV block (varying from 5:1 up to

8:1).

The very low ventricular rate suggests treatment with AV nodal blocking drugs
(e.g. digoxin, beta-blockers). Other possibilities could include intrinsic
conducting system disease (true AV block) or electrolyte abnormality (e.g.
hyperkalaemia).

Tip: The combination of new-onset atrial flutter with high-grade AV block is very
suspicious for digoxin toxicity.

Example 6
Atrial Flutter with 1:1 Block?

There is a very rapid, regular narrow-complex tachycardia at 250-300 bpm.

Flutter waves are not clearly seen, but there is an undulation to the baseline in
the inferior leads suggestive of flutter with a 1:1 block.

Alternatively, this may just be rapid SVT (AVNRT / AVRT) with rate-related ST
depression.

With ventricular rates as rapid as this, spending any further time evaluating the ECG
is unwise! Resuscitation is the priority This patient will almost certainly be
haemodynamically unstable, requiring emergent DC cardioversion.

Example 7
Atrial Flutter with 2:1 Block

There is a narrow complex tachycardia at 150 bpm.

There are no visible P waves.

There is a sawtooth baseline in V1 with flutter waves visible at 300 bpm.

Elsewhere, flutter waves are concealed in the T waves and QRS

complexes.

The heart rate of 150 bpm makes this flutter with a 2:1 block.

Remember

Suspect atrial flutter with 2:1 block whenever there is a regular narrow-
complex tachycardia at 150 bpm particularly when the rate is extremely
consistent.

In contrast, the rate in sinus tachycardia typically varies slightly from beat to
beat, while in AVNRT/AVRT the rate is usually faster (170-250 bpm).

To tell the difference between these rhythms, try some vagal manoeuvres or
give a test dose of adenosine AVNRT/AVRT will often revert to sinus
rhythm, whereas slowing of the ventricular rate will unmask the underlying
atrial rhythm in sinus tachycardia or atrial flutter.
Flutter waves unmasked by adenosine

AVNRT reverts to sinus rhythm after an adenosine bolus

Example 8

Atrial flutter with 3:1 Block

Negative flutter waves at ~ 300bpm are best seen in the inferior leads II,
III and aVF (= anticlockwise pattern).

There is a 3:1 relationship between the flutter waves and the QRS
complexes, resulting in a ventricular rate of 100 bpm.

Atrial Tachycardia
AKA paroxysmal atrial tachycardia (PAT), unifocal atrial tachycardia, ectopic atrial
tachycBackground

Atrial tachycardia is a form of supraventricular tachycardia, originating

within the atria but outside of the sinus node.

Both atrial flutter and multifocal atrial tachycardia are specific types of
atrial tachycardia.

Pathophysiology

Usually due to single ectopic focus.

The underlying mechanism can involve reentry, triggered activity or increased

automaticity.

May be paroxysmal or sustained.

Multiple causes including digoxin toxicity, atrial scarring, catecholamine excess,

congenital abnormalities; may be idiopathic.

Sustained atrial tachycardia may rarely be seen and can progress to tachycardia-
induced cardiomyopathy

ECG Features

Atrial rate > 100 bpm.

P wave morphology is abnormal when compared with sinus P wave due to ectopic
origin.

There is usually an abnormal P-wave axis (e.g. inverted in the inferior leads II, III and
aVF)

At least three consecutive identical ectopic p waves.

QRS complexes usually normal morphology unless pre-existing bundle branch block,
accessory pathway, or rate related aberrant conduction.

Isoelectric baseline (unlike atrial flutter).

AV block may be present this is generally a physiological response to the rapid

atrial rate, except in the case of digoxin toxicity where there is actually AV node
suppression due to the vagotonic effects of digoxin, resulting in a slow ventricular
rate (PAT with block).

ECG Example
Ectopic atrial tachycardia:

There is a narrow complex tachycardia at 120 bpm.

Each QRS complex is preceded by an abnormal P wave upright in V1,

inverted in the inferior leads II, III and aVF.

AV Block: 2nd degree, Mobitz II

Definition

Intermittent non-conducted P waves without progressive prolongation of the

PR interval (compare this to Mobitz I).

The PR interval in the conducted beats remains constant.

The P waves march through at a constant rate.

The RR interval surrounding the dropped beat(s) is an exact multiple of the

preceding RR interval (e.g. double the preceding RR interval for a single
dropped beat, treble for two dropped beats, etc).
 Arrows indicate dropped QRS complexes (i.e. non-conducted P waves)

Mechanism

Mobitz II is usually due to failure of conduction at the level of the His-Purkinje

system (i.e. below the AV node).

While Mobitz I is usually due to a functional suppression of AV conduction

(e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due
to structural damage to the conducting system (e.g. infarction, fibrosis,
necrosis).

Patients typically have a pre-existing LBBB or bifascicular block, and the 2nd
degree AV block is produced by intermittent failure of the remaining fascicle
(bilateral bundle-branch block).

In around 75% of cases, the conduction block is located distal to the Bundle
of His, producing broad QRS complexes.

In the remaining 25% of cases, the conduction block is located within the His
Bundle itself, producing narrow QRS complexes.

Unlike Mobitz I, which is produced by progressive fatigue of the AV nodal

cells, Mobitz II is an all or nothing phenomenon whereby the His-Purkinje
cells suddenly and unexpectedly fail to conduct a supraventricular impulse.
 There may be no pattern to the conduction blockade, or alternatively there
may be a fixed relationship between the P waves and QRS complexes, e.g.
2:1 block, 3:1 block.

Causes of Mobitz II

Anterior MI (due to septal infarction with necrosis of the bundle branches).

Idiopathic fibrosis of the conducting system (Lenegres or Levs disease).

Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral
valve repair)

Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).

Autoimmune (SLE, systemic sclerosis).

Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis).

Hyperkalaemia.

Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone.

Clinical Significance

Mobitz II is much more likely than Mobitz I to be associated with

haemodynamic compromise, severe bradycardia and progression to 3rd
degree heart block.

Onset of haemodynamic instability may be sudden and unexpected, causing

syncope (Stokes-Adams attacks) or sudden cardiac death.

The risk of asystole is around 35% per year.

Mobitz II mandates immediate admission for cardiac monitoring, backup

temporary pacing and ultimately insertion of a permanent pacemaker.