EKG #1
Significant findings on this EKG
ST depression.
T wave inversion.
Prominent U waves.
Long QU interval.
1. What does the circle indicate?
U wave
2. What is the test you want to confirm this diagnosis?
Potassium levels
3. What is the next step in management?
Replete K+ level
Effects of hypokalemia on the ECG
Changes appear when K+ falls below about 2.7 mmol/l
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Increased amplitude and width of the P wave
Prolongation of the PR interval
T wave flattening and inversion
ST depression
Prominent U waves (best seen in the precordial leads)
Apparent long QT interval due to fusion of the T and U waves (= long QU interval)
With worsening hypokalaemia:
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Frequent supraventricular and ventricular ectopics
Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de
Pointes
T wave inversion and prominent U waves in hypokalaemia
Handy tips
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Hypokalaemia is often associated with hypomagnesaemia, which increases the risk of
malignant ventricular arrhythmias
Check potassium and magnesium in any patient with an arrhythmia
EKG #2
This ECG displays many of the features of hyperkalaemia:
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Prolonged PR interval.
Broad, bizarre QRS complexes — these merge with both the preceding P wave and
subsequent T wave.
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Peaked T waves.
1. What is the diagnosis?
Hyperkalemia
2. What is the next step in management?
Talk about Insulin + dextrose, albuterol nebs in addition to kayexalate and Lasix.
Teaching topics:
Effects of hyperkalaemia on the ECG
Serum potassium > 5.5 mEq/L is associated with repolarization abnormalities:
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Peaked T waves (usually the earliest sign of hyperkalaemia)
Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:
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P wave widens and flattens
PR segment lengthens
P waves eventually disappear
Serum potassium > 7.0 mEq/L is associated with conduction abnormalities and bradycardia:
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Prolonged QRS interval with bizarre QRS morphology
High-grade AV block with slow junctional and ventricular escape rhythms
Any kind of conduction block (bundle branch blocks, fascicular blocks)
Sinus bradycardia or slow AF
Development of a sine wave appearance (a pre-terminal rhythm)
Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:
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Asystole
Ventricular fibrillation
PEA with bizarre, wide complex rhythm
Handy Tips
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Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially
patients with renal failure, on haemodialysis or taking any combination of ACE inhibitors,
potassium-sparing diuretics and potassium supplements.
EKG #3
1. What is the rate in this EKG?
160 (count # in a 6 sec strip and x by 10.
2. How do you differentiate this from AVNRT (Hint: test/maneuver)
Vagal Maneuvers + Adenosine
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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.
EKG #4
Findings in this EKG
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Irregular ventricular response.
No evidence of organized atrial activity.
Fine fibrillatory waves seen in V1.
1. Diagnosis?
Atrial Fibrillation
2. If this patient has a HR of 140 (You are cross cover!), Next step?
Talk about rate control
3. Any other Pharmaceutical intervention to consider in a patient with this rhythm?
Discuss anticoagulation – CHADSVASC score and HASBLED Score
Introduction
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Atrial Fibrillation (AF) is the most common sustained arrhythmia.
Lifetime risk over the age of 40 years is ~25%.
Causes of Atrial Fibrillation
There are multiple causes of AF, including:
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Ischemic heart disease
Hypertension
Valvular heart disease (esp. mitral stenosis / regurgitation)
Acute infections
Electrolyte disturbance (hypokalemia, hypomagnesemia)
Thyrotoxicosis
Drugs (e.g. sympathomimetics)
Pulmonary embolus
Pericardial disease
Acid-base disturbance
Pre-excitation syndromes
Cardiomyopathies: dilated, hypertrophic.
Pheochromocytoma
Classification of Atrial Fibrillation
Classification is dependent on the presentation and duration of atrial fibrillation as below:
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First episode – initial detection of AF regardless of symptoms or duration
Recurrent AF – More than 2 episodes of AF
Paroxysmal AF – Self terminating episode < 7 days
Persistent AF – Not self terminating, duration > 7 days
Long-standing persistent AF – > 1 year
Permanent (Accepted) AF – Duration > 1 yr in which rhythm control interventions are not
pursued or are unsuccessful
EKG #5
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Atrial rate is ~ 60 bpm.
Ventricular rate is ~ 27 bpm.
None of the atrial impulses appear to be conducted to the ventricles.
There is a slow ventricular escape rhythm.
1. What is the diagnosis?
3rd degree heart block
2. What is the treatment for this condition?
Pacemaker
Definition
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In complete heart block, there is complete absence of AV conduction – none of the
supraventricular impulses are conducted to the ventricles.
Perfusing rhythm is maintained by a junctional or ventricular escape rhythm.
Alternatively, the patient may suffer ventricular standstill leading to syncope (if selfterminating) or sudden cardiac death (if prolonged).
Mechanism
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Complete heart block is essentially the end point of either Mobitz I or Mobitz II AV block.
It may be due to progressive fatigue of AV nodal cells as per Mobitz I (e.g. secondary to
increased vagal tone in the acute phase of an inferior MI).
Alternatively, it may be due to sudden onset of complete conduction failure throughout
the His-Purkinje system, as per Mobitz II (e.g. secondary to septal infarction in acute
anterior MI).
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The former is more likely to respond to atropine and has a better overall prognosis.
EKG #6
1. What is the rhythm?
Regularized atrial fibrillation. (Coarse atrial fibrillation with 3rd degree AV block
and a junctional escape rhythm.)
2. What is the etiology of this rhythm?
Digoxin toxicity
Clinical features
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GI: Nausea, vomiting, anorexia, diarrhoea
Visual: Blurred vision, yellow/green discolouration, haloes
CV: Palpitations, syncope, dyspnoea
CNS: Confusion, dizziness, delirium, fatigue
Electrocardiographic Features
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Digoxin can cause a multitude of dysrhythmias, due to increased automaticity (increased
intracellular calcium) and decreased AV conduction (increased vagal effects at the AV
node)
 The classic dysrhythmia associated with digoxin toxicity is the combination of
a supraventricular tachycardia (due to increased automaticity) with a slow ventricular
response (due to decreased AV conduction), e.g. ’atrial tachycardia with block’.
Other arrhythmias associated with digoxin toxicity are:
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Frequent PVCs (the most common abnormality), including ventricular bigeminy and
trigeminy
Sinus bradycardia or slow AF
Any type of AV block (1st degree, 2nd degree & 3rd degree)
Regularized AF = AF with complete heart block and a junctional or ventricular escape
rhythm
Ventricular tachycardia
EKG #7
This ECG shows MAT with additional features of COPD:
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Rapid, irregular rhythm with multiple P-wave morphologies (best seen in the
rhythm strip).
 Right axis deviation, dominant R wave in V1 and deep S wave in V6 suggest right
ventricular hypertrophy due to cor pulmonale.
1. Diagnosis?
Multifocal atrial tachycardia
2. Name some risk factors that lead to this condition?
i.e. COPD, Hypoxia, PAH, theophylline, chronic renal failure
Definition
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A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria.
Most commonly seen in patients with severe COPD or congestive heart failure.
It is typically a transitional rhythm between frequent premature atrial complexes (PACs)
and atrial flutter / fibrillation.
Electrocardiographic Features
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Heart rate > 100 bpm (usually 100-150 bpm; may be as high as 250 bpm).
Irregularly irregular rhythm with varying PP, PR and RR intervals.
At least 3 distinct P-wave morphologies in the same lead.
Isoelectric baseline between P-waves (i.e. no flutter waves).
Absence of a single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent
PACs).
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Some P waves may be nonconducted; others may be aberrantly conducted to the
ventricles.
There may be additional electrocardiographic features suggestive of COPD.
Clinical Relevance
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Usually occurs in seriously ill elderly patients with respiratory failure (e.g. exacerbation of
COPD / CHF).
Tends to resolve following treatment of the underlying disorder.
The development of MAT during an acute illness is a poor prognostic sign, associated
with a 60% in-hospital mortality and mean survival of just over a year. Death occurs due
to the underlying illness; not the arrhythmia itself.
EKG #8
Typical example of pericarditis with:
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Widespread ST elevation and PR depression
Reciprocal ST depression and PR elevation in V1 and aVR
1. What is the diagnosis?
Pericarditis
2. Name two common etiologies for this condition?
Post CABG, Viral pericarditis
3. What is the most specific finding on EKG for this condition?
PR depression is more specific that ST elevation
Introduction
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Inflammation of the pericardium (e.g. following viral infection) produces characteristic
chest pain (retrosternal, pleuritic, worse on lying flat, relieved by sitting forward),
tachycardia and dyspnoea.
There may be an associated pericardial friction rub or evidence of a pericardial effusion.
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Widespread ST segment changes occur due to involvement of the underlying epicardium
(i.e. myopericarditis).
How To Recognise Pericarditis
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Widespread concave ST elevation and PR depression throughout most of the limb leads
(I, II, III, aVL, aVF) and precordial leads (V2-6).
Reciprocal ST depression and PR elevation in lead aVR (± V1).
Reciprocal PR elevation and ST depression in aVR
Causes of Pericarditis
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Infectious – mainly viral (e.g. coxsackie virus); occasionally bacterial, fungal, TB.
Immunological – SLE, rheumatic fever
Uraemia
Post-myocardial infarction / Dressler’s syndrome
Trauma
Following cardiac surgery (post pericardiotomy syndrome)
Paraneoplastic syndromes
Drug-induced (e.g. isoniazid, cyclosporin)
Post-radiotherapy
EKG #9
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RBBB
Extreme right axis deviation (+180 degrees)
S1 Q3 T3
T-wave inversions in V1-4 and lead III
Clockwise rotation with persistent S wave in V6
1. Name the classic EKG finding seen on this EKG?
S1Q3T3
2. Which condition leads to these findings on EKG?
PE (Right Heart Strain)
Electrocardiographic Features
The ECG changes associated with acute pulmonary embolism may be seen in any condition that
causes acute pulmonary hypertension, including hypoxia causing pulmonary hypoxic
vasoconstriction. These findings include:
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Sinus tachycardia – the most common abnormality; seen in 44% of patients.
Complete or incomplete RBBB – associated with increased mortality; seen in 18% of
patients.
 Right ventricular strain pattern – T wave inversions in the right precordial leads (V1-4) ±
the inferior leads (II, III, aVF). This pattern is seen in up to 34% of patients and is
associated with high pulmonary artery pressures.
 Right axis deviation – seen in 16% of patients. Extreme right axis deviation may occur,
with axis between zero and -90 degrees, giving the appearance of left axis deviation
(“pseudo left axis”).
 Dominant R wave in V1 – a manifestation of acute right ventricular dilatation.
 Right atrial enlargement (P pulmonale) – peaked P wave in lead II > 2.5 mm in height.
Seen in 9% of patients.
 SI QIII TIII pattern – deep S wave in lead I, Q wave in III, inverted T wave in III. This
“classic” finding is neither sensitive nor specific for pulmonary embolism; found in only
20% of patients with PE.
 Clockwise rotation – shift of the R/S transition point towards V6 with a persistent S wave
in V6 (“pulmonary disease pattern”), implying rotation of the heart due to right
ventricular dilatation.
 Atrial tachyarrhythmias – AF, flutter, atrial tachycardia. Seen in 8% of patients.
 Non-specific ST segment and T wave changes, including ST elevation and depression.
Reported in up to 50% of patients with PE.
Simultaneous T wave inversions in the inferior (II, III, aVF) and right precordial leads (V1-4) is the
most specific finding in favour of PE, with reported specificities of up to 99% in one study.
Compared to findings of Acute Coronary Syndrome
While T wave inversions are commonly associated with acute coronary syndromes, there are
several findings associated with pulmonary embolism that differentiate this diagnosis from ACS.
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ACS is rarely associated with tachycardia
Both ACS and PE will present with elevated troponin
Ultrasonography may be useful in differentiating the two
Kosuge et al have shown that simultaneous inversion in III and V1 are diagnostically
significant:
“negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared
with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive
predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%,
99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads
III and V1 allows PE to be differentiated simply but accurately from ACS in patients with
negative T waves in the precordial leads.”
Clinical Usefulness
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The ECG is neither sensitive nor specific enough to diagnose or exclude PE.
Around 18% of patients with PE will have a completely normal ECG.
However, with a compatible clinical picture (sudden onset pleuritic chest pain, hypoxia),
an ECG showing new RAD, RBBB or T-wave inversions may raise the suspicion of PE and
prompt further diagnostic testing.
EKG #10
Typical ECG of TCA toxicity demonstrating:
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Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best
seen in V1-2).
Broad QRS complexes.
Positive R’ wave in aVR.
45 yo male with New Mexico Found Down Syndrome.
1. What is the likely causative agent?
TCA
2. What is your next step in management?
Talk about serial EKG ‘S and administering bicarb if QRS is prolong
Background
The ECG is a vital tool in the prompt diagnosis of poisoning with sodium-channel blocking
medications such as:
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Tricyclic antidepressants (= most common)
Type Ia antiarrhythmics (quinidine, procainamide)
Type Ic antiarrhythmics (flecainide, encainide)
Local anaesthetics (bupivacaine, ropivacaine)
Antimalarials (chloroquine, hydroxychloroquine)
Dextropropoxyphene
Propranolol
Carbamazepine
Quinine
The two main adverse effects of sodium-channel blocker poisoning are seizures and ventricular
dysrhythmias (due to blockade of sodium channels in the CNS and myocardium)
Handy tip: An ECG should be taken in all patients who present with a deliberate self-poisoning
(or altered GCS of unknown aetiology) to screen for TCA overdose.
Electrocardiographic Features of Sodium-Channel Blockade
Features consistent with sodium-channel blockade are:
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Interventricular conduction delay — QRS > 100 ms in lead II
Right axis deviation of the terminal QRS:
 Terminal R wave > 3 mm in aVR
 R/S ratio > 0.7 in aVR
Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to
muscarinic (M1) receptor blockade.
Tricyclics mediate their cardiotoxic effects via blockade of myocardial fast sodium channels
(QRS prolongation, tall R wave in aVR), inhibition of potassium channels (QTc prolongation) and
direct myocardial depression. Other toxic effects are produced by blockade at muscarinic (M1),
histamine (H1) and α1-adenergic receptors.
The degree of QRS broadening on the ECG is correlated with adverse events:
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QRS > 100 ms is predictive of seizures
QRS > 160 ms is predictive of ventricular arrhythmias (e.g. VT)
Management of Significant Tricyclic Overdose (> 10mg/kg) with Signs of Cardiotoxicity (ECG
changes)
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Patients need to be managed in a monitored area equipped for airway management and
resuscitation.
Secure IV access, adminster high flow oxygen and attach monitoring equipment.
Administer IV sodium bicarbonate 100 mEq (1-2 mEq / kg); repeat every few minutes
until BP improves and QRS complexes begin to narrow.
Intubate as soon as possible.
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Hyperventilate to maintain a pH of 7.50 – 7.55.
Once the airway is secure, place a nasogastric tube and give 50g (1g/kg) of activated
charcoal.
Treat seizures with IV benzodiazepines (e.g. diazepam 5-10mg).
Treat hypotension with a crystalloid bolus (10-20 mL/kg). If this is unsuccessful in
restoring BP then consider starting vasopressors (e.g. noradrenaline infusion).
If arrhythmias occur, the first step is to give more sodium bicarbonate. Lidocaine
(1.5mg/kg) IV is a third-line agent (after bicarbonate and hyperventilation) once pH is >
7.5.
Avoid Ia (procainamide) and Ic (flecainide) antiarrhythmics, beta-blockers and
amiodarone as they may worsen hypotension and conduction abnormalities.
Admit the patient to the intensive care unit for ongoing management.
EKG #11
Inferior STEMI:
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ST elevation in II, III and aVF.
Q-wave formation in III and aVF.
Reciprocal ST depression and T wave inversion in aVL
ST elevation in lead II = lead III and absent reciprocal change in lead I (isoelectric ST
segment) suggest a circumflex artery occlusion
1. What is the diagnosis?
Inferior STEMI
2. Where is the causative lesion?
RCA
Which Artery Is the Culprit?
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The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right
coronary artery (RCA).
Less commonly (around 18% of the time), the culprit vessel is a dominant left circumflex
artery (LCx).
EKG #12
Monomorphic VT:
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Classic monomorphic VT with uniform QRS complexes.
Indeterminate axis.
Very broad QRS (~200 ms).
Notching near the nadir of the S wave in lead III = Josephson’s sign.
1. Rhythm?
Monomorphic V tach
2. What is shown by the circle?
CAPTURE beat
3. What is shown by the square?
FUSION beat
Monomorphic ventricular tachycardia
Clinical Significance
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Ventricular tachycardia may impair cardiac output with consequent hypotension,
collapse, and acute cardiac failure. This is due to extreme heart rates and lack of
coordinated atrial contraction (loss of “atrial kick”).
 The presence of pre-existing poor ventricular function is strongly associated with
cardiovascular compromise.
 Decreased cardiac output may result in decreased myocardial perfusion with
degeneration to VF.
 Prompt recognition and initiation of treatment (e.g. electrical cardioversion) is required in
all cases of VT.
Classification of Ventricular Tachycardia
Ventricular tachycardia can be classified based on:
1. Morphology
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Monomorphic
Polymorphic VT
Torsades De Pointes (Polymorphic with QT prolongation)
Right Ventricular Outflow Tract Tachycardia
Fascicular Tachycardia
Bidirectional VT
Ventricular Flutter
Ventricular Fibrillation
2. Duration
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Sustained = Duration > 30 seconds or requiring intervention due to hemodynamic
compromise.
 Non-sustained = Three or more consecutive ventricular complexes terminating
spontaneously in < 30 seconds.
3. Clinical Presentation
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Hemodynamically stable.
Hemodynamically unstable — e.g hypotension, chest pain, cardiac failure, decreased
conscious level.
Electrocardiographic Features of Ventricular Tachycardia
Ventricular tachycardia can be difficult to differentiate from other causes of broad complex
tachycardia. The following characteristics aid in the identification of VT.
Features common to any broad complex tachycardia
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Rapid heart rate (> 100 bpm).
Broad QRS complexes (> 120 ms).
Features suggestive of VT
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Very broad complexes (>160ms).
Absence of typical RBBB or LBBB morphology.
Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I +
aVF.
AV dissociation (P and QRS complexes at different rates).
Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in
the midst of AV dissociation, to produce a QRS complex of normal duration.
Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid
complex of intermediate morphology.
Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show
entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.
Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the Swave is > 100ms.
Josephson’s sign – Notching near the nadir of the S-wave.
RSR’ complexes with a taller “left rabbit ear”. This is the most specific finding in favour of
VT. This is in contrast to RBBB, where the right rabbit ear is taller.