Case 1

Middle-aged patient presenting with chest pain and diaphoresis.

BP dropped to 80/50 following sublingual nitrates.
General:

Sinus rhythm, rate 84bpm.

Normal axis.
Borderline 1st degree AV block (PR 220ms).

Signs of inferior STEMI:

STE in inferior leads II, III, aVF.

Reciprocal STD in lateral leads I, aVL, V6.

Signs of associated right ventricular infarction:

STE in III > II.

STE in V1-2.

This patient also had STE in V4R, confirming the diagnosis of RV infarction:

Clinical Pearls
RV infarction typically occurs in the context of inferior STEMI due to RCA occlusion.
These patients are preload sensitive and may have an exaggerated hypotensive response to
nitrates.
 Case 2
20-year old female presenting with palpitations and presyncope, BP
75/50.DEscribe her ECG.
Main Abnormalities: •
Irregularly irregular broad complex tachycardia.
Extremely rapid ventricular rates — up to 300 bpm in places (RR intervals as short as 200ms or
1 large square).
Beat-to-beat variability in the QRS morphology, with subtle variation in QRS width.
Explanation of ECG Findings:
Irregularly irregular rhythm is consistent with atrial fibrillation.
There is a left bundle branch block morphology to the QRS complexes.
However, the ventricular rate is far too rapid for this to be simply AF with LBBB.
The rates of 250-300 bpm and the variability in QRS complex morphology indicate the existence
of an accessory pathway between the atria and ventricles.
Diagnosis:
These findings indicate atrial fibrillation in the context of Wolff-Parkinson-White syndrome.
Clinical Pearls:
Broad complex irregular tachycardia at very rapid rates? -> Suspect AF with WPW!
These patients can rapidly become haemodynamically unstable.
The options for chemical cardioversion are very limited, favouring DC cardioversion.
I would recommend immediate DC cardioversion in this patient. My approach would be to fluid
load (0.5 – 1L crystalloid bolus), add in a push-dose pressor to elevate the BP (e.g. metoraminol
0.5 – 1mg IV) sedate with something that has minimal effects on BP (e.g. fentanyl or ketamine
in cautious doses), and then shock at 200j biphasic. Consider using an AP pad position for
maximal 1st shock success.
 Case 3
Middle-aged diabetic patient presenting with shortness of breath. Clinical evidence of
pulmonary oedema. Describe the ECG
Main Abnormal Findings
• Severe bradycardia of 36 bpm.
• Rhythm is difficult to ascertain — appears irregular (?slow AF) although there are some small-
voltage P waves seen in V1-2.
• Broad QRS complexes with an atypical LBBB morphology.
• Subtle symmetrical peaking (“tenting”) of the T waves in V2-5.

Diagnosis
• The combination of bradycardia, flattening and loss of P waves, QRS broadening and T wave
abnormalities is highly suspicious for severe hyperkalaemia. This patient had a potassium of 8.0 in
the context of anuric renal failure.

Clinical Pearls : When you see the combination of…

• Bradycardia
• Blocks — e.g. AV block, bundle branch blocks
• Bizarre QRS complexes
…. think hyperkalaemia!
 Case 4
20 year old male presenting with seizures. BP 80/50. Describe the ECG.
Main Abnormalities
• Broad complex tachycardia, rate ~ 130 bpm.
• The rhythm is likely sinus tachycardia with a 1st degree AV block — note the “camel hump”appearance to the T waves indicating a
hidden P wave.
• Interventricular conduction delay (QRS duration > 100ms, not typical LBBB / RBBB morphology)
• Right axis deviation.
• Secondary R’ wave in aVR > 3 mm.
Diagnosis
• In the context of a patient presenting with seizures and hypotension, the combination of…
• QRS broadening > 100 ms
• R’ wave in aVR > 3 mm
• … is highly suggestive of poisoning with a sodium-channel blocking agent — e.g. tricyclic antidepressant.
• The sinus tachycardia may be due to the anticholinergic effects of the TCA.
Clinical Pearls
• In the context of sodium channel blockade:
• A QRS duration > 100 ms is predictive of seizures.
• A QRS duration > 160 ms is predictive of cardiotoxicity.
• This patient is already manifesting life-threatening toxicity and needs aggressive resuscitation, including:
• Serum alkalinisation with NaHCO3 to reverse pH-dependent toxicity.
• Intubation and hyperventilation aiming for alkaline arterial pH (e.g. 7.45 to 7.55).
• Seizure management with benzodiazepines.
• BP management with fluid boluses +/- pressors.
 Case 5
This following sequence of ECGs is taken from a middle-aged patient presenting with chest
pain and diaphoresis. Can you interpret each ECG tracing in the context of the patient’s
symptoms?
ECG 5a – Chest pain and diaphoresis (time = zero)
ECG 5a- Chest pain and diaphoresis (time= zero)

Reveal Answer

This ECG demonstrates an anterolateral STEM!

• ST elevation in V2-6, I and aVL

• Reciprocal ST depression in Il l and aVF
• Pathological Q waves in V2-3
• Hyperacute T waves in V2-4

This pattern of changes in consistent with acute occlusion of the left anterior descending artery
ECG 5b – Resolution of chest pain (t+20 mins)
ECG 5c – Recurrence of chest pain (t+25 mins)
•

•
ECG 5d – Ongoing chest pain and diaphoresis (t+35 mins)
-
 Case 6
30-year old patient presenting with generalised weakness. Describe and interpret the ECG.
• Main Abnormalities
• The ECG shows widespread ST segment abnormalities.
• There is a biphasic appearance to the ST segments and T waves, with
initial negative deflection (= ST segment depression / T wave inversion)
followed by a terminal positive deflection (= U wave).
• All these waves merge into each other and it is difficult to tell where one
wave ends and the other begins.
• There is gross prolongation of the QU interval (= time from onset of QRS
complex to end of T/U wave).
Diagnosis
The combination of…
•Widespread ST depression / T wave inversion
•Prominent U waves
•Long QU interval (> 500 ms)
…. is highly suggestive of severe hypokalaemia.
This patient had a serum K of 1.7 mmol/L in the context
of decompensated Conn’s syndrome (primary aldosteronism).
Clinical Pearls
• Biphasic T waves may be seen with both myocardial ischaemia
(Wellens’ syndrome) and hypokalaemia.
• The main differentiating factor (apart from the clinical picture) is the
direction of the T waves:
• Wellens’ biphasic T waves go UP then down.
• Hypokalaemic T waves go DOWN then up.
 Case 7
70-year old patient presenting with chest pain, dyspnoea and dizziness. BP 90/50. SaO2 83%
RA. Describe the ECG.
Main Abnormalities
•Sinus tachycardia ~ 100 bpm.
•Anterior T wave abnormalities: inverted in V1-3, biphasic in V4.
•Inferior T wave abnormalities: biphasic in III, aVF.
•Subtle ST elevation in III and aVF.
Significance of ECG Findings
This pattern of T wave inversions in the right precordial leads V1-4 plus the inferior leads (especially the rightward-
facing lead III) is referred to as the right ventricular strain pattern. It is a marker of right ventricular hypertrophy or
dilatation.
Diagnosis
In a patient presenting with acute shortness of breath, the combination of…
•Sinus tachycardia
•RV strain pattern in V1-4 (+/- lead III)
… is highly suggestive of acute cor pulmonale due to massive pulmonary embolism.
However, these ECG changes are not specific to PE and may be seen in other conditions associated with pulmonary
hypertension and RV enlargement including:
•Chronic lung disease (COPD, lung fibrosis) with chronic cor pulmonale
•Right ventricular hypertropy — e.g. due to congenital causes, valvular heart disease
•Arrhythmogenic right ventricular cardiomyopathy
Clinical Pearls
Other ECG findings associated with pulmonary embolism include:
•New right axis deviation
•New right bundle branch block
•New dominant R wave in V1
•Non-specific ST segment changes
The oft-quoted SI QIII TIII pattern (deep S wave in lead I, Q wave in III, inverted T wave in III) is neither
sensitive nor specific for PE and is infrequently seen (20% of cases).
Similarly, sinus tachycardia is not as ubiquitous in PE as people seem to think (< 50% of cases), and certainly
should not be relied up to exclude PE.
 Case 8
70-year old patient presenting with severe chest pain, diaphoresis and syncope. BP 65/40.
Main Abnormalities
•Widespread ST depression affecting multiple precordial
(V2-6) and limb leads (esp. I, II, avF).
•To some extent this is masked by an indistinct J point,
upsloping (rather than horizontal) ST depression and
some baseline wander of the ECG.
•There is~3 mm ST elevation in aVR.

Diagnosis
In the context of ischaemic chest pain and cardiogenic shock, the combination of…
Widespread ST depression•
ST elevation in aVR > 1 mm•
ST elevation in aVR > V1•
… is extremely concerning for left main coronary artery occlusion.
However, this pattern is not entirely specific for LMCA occlusion. It may be seen whenever there is diffuse
severe subendocardial ischaemia, e.g.
Severe triple vessel disease•
Severe anaemia or hypoxaemia•
Following resuscitation from cardiac arrest•
This patient developed progressive cardiogenic shock complicated by runs of ventricular tachycardia. He
was taken for immediate angiography where he was found to have a complete ostial occlusion of his left
main coronary artery.
Pitfalls

A similar ECG pattern of diffu se ST depression with ST elevati on in aVR may also be seen
with supraventricular tachycardias (AVNRT I atrial flutter). This rate-related change is usually benign and
resolves with resolution of the SVT

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Rate-related change due to SVT

 Case 9
55-year old patient presenting with chest pain. Describe the ECG
This ECG is an example of hyperacute anterolateral STEMI:
•There are markedly peaked, asymmetrical T waves (= hyperacute T waves) in V2-5.
•The associated loss of R wave height (analogous to early Q wave formation) causes the enlarging precordial T
waves to tower over the diminishing R waves.
•There is also some subtle ST elevation in aVL, indicating LAD occlusion proximal to the D1.
•There are frequent ventricular ectopic beats, which are concerning in this context as they suggest underlying
myocardial irritability and a risk of deterioration to malignant ventricular dysrhythmias such as VF or VT.
Serial ECGs of this patient showed evolving anterolateral ST elevation (V1-6, I, aVL) with development of inferior
reciprocal change (lead III).
 Case 10
90-year old patient found on the floor at home. Describe what his ECG shows.
This ECG demonstrates all the classic features of hypothermia:
•Bradycardia
•Osborne waves (J waves) = notching at the J point seen in V4-6
•Long QT interval (~ 600 ms)
•Shivering artefact
The rhythm is probably sinus bradycardia — mapping out the RR intervals reveals a regular rhythm despite the
obliteration of the baseline by the shiver artefact.
 Case 11
Middle aged female presenting with dyspnoea. Previous mastectomy for breast carcinoma.
What does the ECG show?.
Main Abnormalities
•Sinus tachycardia
•Low QRS voltages — Multiple limb lead QRS complexes < 5 mm in amplitude.
•Electrical alternans — There is a beat-to-beat variation in the QRS complex height. Taller complexes
alternate with shorter ones.
The triad of tachycardia, low QRS voltages and electrical alternans is extremely suspicious for massive
pericardial effusion.
Given the clinical history, I would be concerned about the presence of a malignant pericardial effusion
causing tamponade. The diagnosis can be rapidly confirmed on bedside echo (watch these videos
from The Ultrasound Podcast to learn how: Part 1, Part 2). There may also be clinical evidence of pulsus
paradoxus.
 Case 12
Young male found collapsed at home, apparently intoxicated. What does the ECG show?
Main Abnormalities
•Giant T-wave inversions in multiple leads, most prominent in V2-6
•Marked QT prolongation > 600 ms

Diagnosis
This ECG pattern is characteristic of raised intracranial pressure and is classically seen in the context
of massive intracranial haemorrhage, particularly:
•Aneurysmal subarachnoid haemorrhage
•Haemorrhagic stroke

Similar ECG patterns have also been reported in patients with raised ICP due to:
•Large-territory ischaemic stroke causing cerebral oedema (e.g. MCA occlusion)
•Traumatic brain injury
The differential diagnosis for widespread T-wave inversions and QT prolongation includes myocardial
ischaemia (e.g. Wellen’s syndrome) and electrolyte abnormalities (e.g. hypokalemia). However,
neither condition would cause the gigantic “cerebral T waves” seen here.
 Case 13
Middle-aged patient presenting with palpitations and dizziness. What does the ECG show?
Diagnosis
This ECG shows a regular broad complex tachycardia with an RSR’
pattern in V1.
The differential diagnosis could include:
•Ventricular tachycardia.
•SVT with aberrant conduction — either due to RBBB or WPW.
On closer inspection, the ECG demonstrates some classic features
of ventricular tachycardia:
•Northwest axis — QRS is positive in aVR, negative in I and aVF.
•The taller left rabbit ear sign — There is an atypical RBBB pattern
in V1, where the left “rabbit ear” is taller than the right.
•Negative QRS complex (R/S ratio < 1) in V6.
These findings indicate VT rather than SVT with aberrancy.

Clinical Pearls
Other factors that increase the likelihood of VT in patients presenting with regular
broad complex tachycardia include:
Age > 35 (positive predictive value of 85%).•
Structural heart disease — e.g. IHD, CCF, cardiomyopathy.•
Family history of sudden cardiac death or arrhythmogenic conditions such •
as HOCM, Brugada syndrome or ARVC that are associated with episodes of VT.
In any patient with a broad complex rhythm, also consider the possibility of toxic /
metabolic conditions such as hyperkalaemia or sodium-channel blockade.
 Case 14
Middle aged patient presenting with central chest pain. What does the ECG show?
Evidence of inferolateral STEMI
•ST elevation in the inferior leads (II, III, aVF)
•ST elevation in the lateral leads (I, V5, V6)
Evidence of posterior STEMI
•Horizontal ST depression in V1-4 (maximal in V2-3)
•Dominant R wave in V2 (R/S ratio > 1)
•Upright T wave in V2
This pattern of infero-postero-lateral STEMI is most likely
caused by occlusion of a dominant left circumflex artery.
Tips for spotting posterior infarction
Look specifically at lead V2 for the combination of
•Horizontal ST depression.
•Tall, broad R wave (>30ms wide, R/S ratio > 1) —
this is a Q-wave equivalent.
•Upright T wave — particularly the terminal portion of the T wave.

One common trick is to turn the ECG over, hold it up to

the light and look through it from behind. This inverts lead
V2, which then takes on the appearance of a classic
STEMI.
Look for evidence of posterior involvement in any patient with an inferior or lateral STEMI.
Sometimes it can be difficult to determine whether ST depression in V2-3 is due to posterior
STEMI or simply subendocardial ischaemia affecting the anteroseptal wall. The diagnosis can be
confirmed by recording posterior leads V7-9.
 Case 15
Middle aged patient presenting with central chest pain. Posterior leads V7-9. What does the
ECG show?
(same patient as ECG 014)
Posterior leads confirm the presence of posterior wall infarction by demonstrating typical STEMI
morphology:
•ST elevation in V7-9
•Q waves in V7-9
•Inversion of the terminal portion of the T wave (“U wave inversion“) in V7-9

How To Record Posterior Leads

Simply move the V4-6 electrodes around to the back in the same horizontal plane as V6. Annotate
the ECG accordingly.
Approximate positions for V7-9 are:
•V7 – posterior axillary line
•V8 – tip of scapula
•V9 – left paraspinal region
 Case 16
20-year old patient with sudden onset of palpitations. What does the ECG show?
Main Abnormalities
•Narrow complex tachycardia at ~ 150 bpm.
•Right axis deviation = just rightward of +90 degrees.
•Pseudo-R’ waves in V1-2 = retrograde P waves
superimposed on the terminal QRS causing peaking of
the J-point.
•No clear sinus P waves or flutter waves seen.

Differential Diagnosis
When you see a regular narrow complex tachycardia at 150 bpm, you
should think of four main diagnoses:
Atrial flutter with 2:1 block (especially in elderly, IHD, CCF)•
AV-nodal reentry tachycardia (“SVT”)•
Orthodromic AV reentry tachycardia in WPW•
Sinus tachycardia — should see P waves but may be hidden in the T •
waves (e.g. with concurrent 1st degree AV block). There should also be
some HR variability compared to the other 3 rhythms.
The patient’s young age and presence of retrograde P waves (pseudo
R’ waves) suggest a paroxysmal reentry tachycardia involving the AV
node — either AVNRT (“SVT”) or orthodromic AVRT.
The next step is a therapeutic trial of vagal maneouvres and/or
adenosine… (see Quiz ECG 017).
 Case 17
20-year old patient with sudden onset of palpitations. What does the rhythm strip demonstrate?
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Case 18
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Case 19
Main Abnormalities

o ST depression in V2-5, which slopes upwards and joins the ascending limb of the T wave.
o Prominent, "rocket-shaped" T waves in the precordial leads V2-5.
o Subtle ST elevation in aVR

Diagnosis

o This combination of ST depression with rocket-shaped T waves in the precordial leads V1-6 is
referred to as the De Winter ECG pattern or "De Winter's T waves".
o It is becoming increasingly recognised as an anterior STEMI equivalent (-2% of LAD
occlusions).
o Some authors are now recommending that this ECG pattern be treated identically to anterior
STEM I, with urgent PCI or thrombolysis. V3
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'JYpical De Winter's T wave
Case 20
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Case 21
This ECG demonstrates many of the features of chronic pulmonary disease:

• Rightward QRS axis (+90 degrees)

• Peaked P waves in the inferior leads> 2.5 mm (P pulmonale).
• Rightward P-wave axis (inverted in aVL)
• "Clockwise rotation" of the heart with a delayed R!S transition point (transitional lead = V5).
• Absent R waves in the right precordial leads (SV1-SV2-SV3 pattern)
• Low voltages in the left-sided leads {I, aVL, V5-6)

Tachycardia may be due to dyspnoea, hypoxia or beta-agonist treatment This ECG pattern is a
common finding in patients with COPD. The vertical axis (+90 degrees) is due to hyperinflation of
the lungs causing vertical orientation of the heart.

Ve rtic~l he~rt ori ~nt. tion in COPO

 Case 22

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 Case 23
Elderly patient with accidental overdose of sotalol. Describe the ECG.

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Main Abnormalities This ECG demonstrates the key features of sotalol toxicity:
QT Interval Nomogram
• Sinus bradycardia (42 bpm) 600
• Very long QT interval (-600 ms). 550
u.,., 500

Sotalol is a beta blocker with additional class Ill effects (potassium channel blockade), so it causes
both bradycardia and QT prolongation in overdose.
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400
450

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Risk of Torsades 0
250
200
• In comparison to the previous case, this patient is at significant risk of TdP. 20 40 60 80 100 120 140 160
• The combination of bradycardia and significant QT prolongation means that this patient plots Heart Rate (bpm)

well above the "at risk" line on the QT nomogram.

• Prophylaxis ofTdP in this case would include correction of QT-dependent electrolytes (K, Mg,
Ca) to the high-normal range and positive chronotropy (e.g. with isoprenaline) to move the
patient below the at-risk line.
 Case 24

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Case 26
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Case 27
Main Abnormalities

• Bizarre appearing complexes.

• Marked T wave peaking in V2-6.
• Gross QRS prolongation (-200 ms).
• Some leads (1, aVR) are starting to take on a sine wave appearance.

Diagnosis

The combination of...

• Bizarre complexes
• QRS prolongation
• Peaked T waves
• Sine wave appearance

... are all strongly suggestive of severe hyperkalemia.

This patient had a serum K of 9.2 mmolll!

In this elderly paLent with multiple medical problems, causes could include renal failure (e.g. due to
d1uret1cs. N~AI Us, Intercurrent Illness) or treatment w1th AGI::-lnh1b1tors. sp1ronalactone or
K-supplements.
Case 28
ECG FindingsThe patient is in sinus rhythm with no evidence of dysrhythmia or AV block.

The QT interval is normal and there is no evidence of WPW syndrome, HOCM or ARVC.

There is a characteristic pattern of abnormalities in V1 -2:

• RSR' pattern I partial RBBB .

• ST elevation with a ucoved" morphology.
• Inversion of the terminal portion of the T wave.

In a patient presenting with syncope, this ECG is diagnostic of the Brugada syndrome.
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Classic appearance of Brugada syndr ome in V2

 Case 29
Asymptomatic 40-year old patient. Describe the ECG.

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Main Findings

o Irregular narrow-complex rhythm (overall rate = 72 bpm).

o Normal sinus P waves are seen (upright in lead II), indicating a sinus origin of the rhythm.
o QRS complexes cluster in groups, separated by non-conducted P waves.
o The PR interval progressively prolongs within each group
o The PR prolongation can be appreciated by comparing the first and last PR interval of each
group

Diagnosis

o This is the typical appearance of 2nd degree AV block with Mobitz I conduction (Wenchebach
phenomenon)

Clinical Significance

In comparison to patients with Mob1tz II, who typically require a pacemaker for prophylaxis of
complete heart block and ventricular standstill, patients with Mobilz I do not necessarily need any
intervention. This is provided that they are asymptomatic with a normal BP, and that reversible
causes such as drug toxicity (beta-blockers, digoxin), hyperkalaemia and myocardial ischaemia
have been excluded. The risk of progression to haemodynamically unstable AV block in these
patients is very low.
Case 30
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 Case 31
Young adult patient presenting with syncope History of eating disorder. Describe the ECG.

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Case 32
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Example 1: Benign Early Repolarisation
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• ST segment height = 1 mm • ST segment height = 2 mm
• T wave height =6 mm • T wave height = 4 mm
• ST I Twave ratio = 0.16 • ST IT wave ratio = 0.5
• The ST I T wave ratio < 0.25 is consistent with BER. • The ST I T wave ratio> 0.25 IS consistent with pancarditis.
Case 33
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Case 34
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Case 35
On first glance this ECG cou ld easily be mistaken for an example of Mobitz II AV block - there are
intermittent non-conducted P waves with a constant PR interval. However, regular pacing spikes
can be seen following the P waves in leads V3-6.

Th is is an example of pacemaker malfunction, with intermittent failu re to capture:

• Regular P waves are seen at - 65 bpm.

• Each P wave is following by a pacing spike (best seen in V3-6, subtle pacing spikes also
~lai ii.J~ ltll .
present in I, aVR, V1) This indicates that atrial sensing is intact. NB. Pacing spikes will
typically not be seen in all 12 leads. Failure to Captu re
• Some of the pacing spikes are followed by typical ventricular-paced complexes. The LBBB
Thr. prohlm-~ h r. ~ i:-. fr-lilurr: ni rhr. p.lt.cm;;k~r tn "rapture·• (d~r>ol;; rr:.r.) thn v~ntrir.u1 .1r mynrAlrr1ium
morphology indicates that the pacing lead is in the right ventricle -the heart depolarises from
Causes of L1is iochJCe:
right to left in the same way as LBBB. Also note the negative concordance in V1-6 (all QRS
• Pu:.:tllluk~l lt:!tld II~C(Uit! Of l llliJitl t OU {tt.g . ~U~ lo '.rYic..kllet'~ symJIOI I ~f.
complexes are negative). Th is is often quoted as a feature of ventricular tachycardia, but
• Refractory m~rocard ium due to clcctrol;r.c abnormality (c~p. h)rpcrkalacmta} or myocardial
simply indicates that the rhythm is arising from the anterior surface of the right ventricle- the I ~C.hNWni.:.

heart is depolarising away from the Vt-6 e lectrodes.

• Several of the P waves I pacing spikes are not followed by QRS complexes, producing a
ventricular rate of- 40 bpm.
• Quite worryingly, there does not seem to be any native ventricular activity kicking in when the
~@aQI'~te-:9r.qQS, ,T,~e second half of the rhythm strip shows two sequential non-conducted P
s hu.JW..av..e.s Jllli.1ih DO. ~dence of any escape rhythm . This suggests the presence of underlying
complete heart block with inadequate escape mechanisms and significant risk of ventricu lar
Case 36
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Case 37
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 Case 38
15-year old patient presenting with rapid palpitations and dizziness. Symptoms recur in ED.
Describe the ECG.

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 Main Abnormalities

o Very rapid, regular broad-complex tachycardia (- 200 bpm).

o LBBB morphology (dominantS wave in V1)
o No clear atrial activity - no flutter waves or fibrillatory waves.
o No obvious diagnostic features for VT.

Differential Diagnosis

In a patient presenting with a regular broad-complex tachycardia and no evidence of atrial activity,
the main diagnostic considerations are:

o Ventricular tachycardia.
o SVT with aberrant conduction due to bundle brach block.
o SVT with aberrant conduction due to WPW.

Although diagnostic criteria exist to aid in differentiation of these rhythms, none of them have 100%
sensitivity or specificity - leading many authors to recommend treating as VT if uncertain.
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• However;-el it:li~aLco.ntext is everything

This patient has two strong indicators of SVT with aberrancy

o Young age - the vast majority of BCTs in children are SVT with aberrancy
o Evidence of WPW on previous EGGs.
 Diagnosis

This is an example of antidromic AV reentry tachycardia - a reentrant SVT seen in WPW where
the impulse travels from atria to ventricles via the accessory pathway, recycling backwards through
the AV node (hence "antidromic"). Activation of the ventricles via the accessory pathway produces a
broad complex that may be indistinguishable from VT. This is in comparison to orthodromic SVT,
where the impulse travels forwards through the AV node producing a normal-looking, narrow QRS

This patient reverted back to sinus rhythm with vagal maneouvres. The WPW pattern was once
again visible on his sinus rhythm EGG.

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AVRTwith orthodromic (left ) and
antidromic (right) AV nodal conduction
Case 39
• II II
•

• II
•
 Case 40

n
<
 NB. Fusion and capture beats are often discussed in the context of VT. They are not specific to VT,
but rather can be seen with any ventricular rhythm, including paced rhythms and AIVR.

Explanation

• Competing sinus and ventricular pacemakers are present There is underlying sinus
arrhythmia, with sinus capture occurring when the sinus rate exceeds the idioventricular rate.
• This patient was a fit athlete with presumably high resting vagal tone that suppressed his
sinus node output and allowed an ectopic ventricular pacemaker to emerge

Definition s

• 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)
• lsorhythmic AV dissociation
AV dissociation with sinus and ventricular complexes occurring at similar rates, unlike
3'ddegree heart block where the atrial rate is usually faster than the ventricular rate.
\fsorR'ythrmcl;t.w...(J.fssociation is usually due to functional block at the AV node from
)WS .b.,LMJFetrt>§ra(lely-·eof.ldtlcted ventricular impulses ("interference-dissociation"), which leaves the AV

node refractory to the anterograde sinus impulses.

 Case 41

I
Th~ II r
Case 42
Main Abnormalities

This is a typical example of atrial fl utter with 21 AV block

• Narrow complex tachycardia at 150 bpm.

• Sawtooth flutter waves are seen in the inferior leads II, Ill, aVF.
• Upright flutter waves in V1 appear either as pseudo-P waves or as notches in the T wave.
• There is a clear 2 1 relationship between the flutter waves (300 bpm) and QRS complexes
(150 bpm)

::'...:J:•'II·:. . II .• :. : 1• ..I' . '.

. . '. .
'I .'I·. II . I : : .. I, .. .: . ·, ..... ,
::·:l i;:: .
·:
I . l

~t; ::: -:~ :r-·~-:-:-l :<I ~-~:-,-.·J :-:-:-1 Tips for Spotting Atrial Flutter
:~L- ··· ~.:... _ +-_j -· L_··t
. . · I. . : .: - ·. l : I.
.! · · • Suspect flutter with 2:1 block in any patient with a regular NCT at 150 bpm
• Scrutinise leads II and V1 for flutter waves.
• Flutter waves are typically sawtooth in lead II and resemble P waves in V1.
• Try turning the ECG upside down - this can make the flutter waves in lead II easier to see.

Inverted f l utter waves i n lead II.

Inverting the ECG makes f lutter waves i n lead II easier to see

Upright flutter waves in V1.

- I •. • •
Case 43
•
•
•

•
•

)
I
• II-
Case 44
 II .
• (
Clinical Pearls

o Sarcoidosis should always be considered as a differential diagnosis in younger patients

presenting with complete heart block, particularly if other manifestations of sarcoidosis are
present such as bilateral hilar lymphadenopathy or cutaneous lesions (erythema nodosum,
lupus pernio).
o One of the most common reversible causes of complete heart block is severe hyperkalaemia
-always get an urgent K+ (e.g run a VBG) on patients presenting with CHB. You look a bit
silly inserting an unnecessary pacing wire when you could have corrected the problem with
some calcium gluconate!

Causes of Complete Heart Block

o AV nodal blocking drugs (e g.calcium-channel blockers, beta-blockers, digoxin)

o Severe hyperkalaemia.
o Inferior myocardial infarction - due to increased vagal tone.
o Anterior myocardial infarction -due to septal necrosis.
o Idiopathic fibrosis of the conducting system (Lenegre's or Lev's disease)
o Cardiac surgery (especially surgery occurring close to the septum, e.g. mitral valve repair)
o Infiltrative mypcardial disease (amyloidosis, haemochromatosis, sarcoidosis)
o Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease).
o Autoimmune (SLE, systemic sclerosis)
Case 45
This ECG shows a ventricular paced rhythm with positive Sgarbossa criteria:

• There is concordant ST depression in V2-5. This violates the expected pattern

of discordance for a V-paced rhythm and is a marker of superimposed myocardial infarction.
• The morphology in V2-5 is reminiscent of posterior STEM I, with horizontal ST depression and
prominent upright T waves.
• Multiple non-conducted P waves are seen, indicating the presence of underlying high-grade
AV block (probably the indication for pacemaker insertion) However, the fusion complex (beat
#5 on rhythm strip) suggests that P waves are occasionally transmitted, arguing against
complete heart block.

This patient did indeed have an isolated posterior infarction, due to complete occlusion of a
posterolateral branch of the RCA She was successfu lly treated with PCI.

Sgarbossa Criteria
These criteria allow for detection of myocardial infarction in patients with LBBB and V-paced
rhythms (previously thought to be "impossible")
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rhythms (previously thought to be "impossible"). Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Normal Pattern in LBBB I VPR
Jaundice

• The expected finding in patients with uncomplicated LBBB I V-paced rhythm is discordance Feed Me
- i.e. the ST segments and T waves point in the opposite direction to the QRS complex.
LITFL Review 323

Discordant
ST-Segments and T-Waves
OSCE Resources
___
............................................................................................................

B. •

t
•
Nonnal for LBBB and paced rhythm

Image reproduced from ECGMedicaiTraining.com with permission.

How To Spot Superimposed Ml

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How To Spot Superimposed Ml

Superimposed myocardial infarction is suspected if there is either:

• Loss of the usual pattern of discordance - i.e. concordant ST changes.

• Excessi ve discordant ST elevation - i.e. out of proportion to what would be expected for
LBBB I paced rhythm .

Sgarbossa's Criteria
LBBB I Poc:ed Rhythm

_, J.
VI,V2,V3

t·L- I
Image reproduceafrom£CGMedica/Training.com with permission.
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-- ---- - --- -- -

Sgarbossa Criteria

Diagnosis of Ml in LBBB I VPR requires at least one of the following criteria to be present:

• Concordant ST depression > 1 mm in V1-3.

• Concordant ST elevation > 1 mm in any lead.
• Excessively discordant ST elevaUon in any lead >5 mm (original Sgarbossa criteria) or >25%
of the corresponding S-wave depth (modified Sgarbossa criteria = more specific).

Changes only have to be present in a single lead to be diagnostic of MI.

Read more about Sgarbossa criteria here.

More ECG Clinical Cases...

« PREV MENU NEXT» Last update: [last-modified]

Case 46
Jiz ECG 046 • LITFL • Life in t X ~ Quiz ECG 046 • LITFL · Life in t ; X

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This EGG contain

• Regular bro.
• Very broad <
• Northwest a
• Brugada's s
• Josephson·~ RECENT POSTS

Northw est Axis

Medmastery: Mitral regurg

Tropical Travel Trouble 00:

Jaundice

Feed Me

LI TFL Review 323

OSCE Resources
B rugada's sign (red callipers) and Josephson 's sign
(blue arrow)

'C>J .. , .
Also note the presence of morphology criteria favouring VT over RBBB:
~
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• Tall
• Don

Monophasic R wave in V1 with VT

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6
IV -4--f+l.lll.IH
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w
Dominant S wave in V6 with VT
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This pattern in V1 and V6 is very different from the expected morphology in RBBB.

RSR' pattern in V1 with RBBB

Dominant R wave with wide slurred S wave in V6

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Tips for Spotting VT when RBBB morphology present

[NB. RBBB morphology = QRS > 120ms with dominant R wave in V1)

Suspect VT in any patient with a regular broad complex tachycardia (especially if > 160 ms wide).

Look ataVR

Look at V1

Look atV6

If sllll uncertain. scrutm1se the EGG for·

For more tips on spotting VT, read th1s art1cle.

More ECG Clinical Cases...

 Case 47

I Middle-aged patient presenting with palpitations Describe the ECG

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vr or non vr general practitioner -

Reveal Answer whitsundays
Australia,Oueensland
An excellent opportunity has arisen in Whitsun

This is another example of ventricular tachycardia, this time with a LBBB morphology (compare this
perth - gp - permanent vr general
with ECG 046) practitioner
Australia,Western Australia

• Regular broad complex tachycardia at- 160 bpm Charterhouse Medical are currently worKing in

• Features of VT in V1 • Initial R wave > 30 ms wide, RS interval > 70 ms (= Brugada sign).

•
•
Features of VT in V6 Dominant S wave in V6, absence of typical LBBB morphology.
Abnormal axis with positive aVR, although does not quite meet criteria for northwest axis. VIeW all jObS on ~vocortex
NB. Note that a positive Brugada sign only requires an RS interval of> 70 ms when LBBB
morphology is present, compared to >100 ms when RBBB morphology is present.

RECENT POSTS

W ndows b.!··:·~~·; Medmastery Mitral regurgitation

.W nCICJWS b ... ,,,'-')~~ uu J;u,
Tropical Travel Trouble 005 RUQ Pain and
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RECENT POSTS

Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jaundice

Feed Me

LITFL Review 323

OSCE Resources

c
A : > 30 ms FAVOURS VT
B: NOTCHING, SLURRING FAVOURS VT
C: > 70 ms FAVOURS VT
WId .I: Vl' - appear ance in V1. Reproduced f rom Wellens (2001 ).
Jiz ECG 047 • LITFL • Life in t X

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COLLECTIONS ECG LIBRARY

.
TOX LI BRARY

. . .
B: NOTCHING, SLURRING FAVOURS VT
~
CCC PART ONE CASES TOP 100

C: > 70 ms FAVOURS VT
VT- appearance in V1. Reproduced from Wellens (2001 ).

VT- appearance in V6.

Again, these features are very different to the expected pattern in LBBB, which has:

• Dominant S wave in V1 , but with an RJS interval < 70 ms and minimal initial R wave.
• Dominant R wave in V6 (often slurred).
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v, 'W'

LBBB- appearance in V1.

'M'

LBBB- appearance in V6.

Tips for Spotting V T when LBBB morphology present

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Tips for Spotting VT when LBBB morphology present

[NB. LBBB morphology = QRS > 120ms with dominant S wave in V1]

Suspect VT in any patient with a regular broad complex tachycardia (esp if> 160 ms wide).

Look at aVR

Look atV1

Look atV6

If still uncertain, scrutinise the ECG for:

• AV dissociation - P waves randomly deforming the QRS complexes and T waves.

• Fusion and capture beats

. . . .... : . . . . .
.':'"t ·: . ..:. :]··.. ..:..:.:..·.1.......... . .. ...
• • 0 : • • • • • ••• : • :
:. :.: .~ .:.:
·:·;·~- • 0 .. . ..
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.• . . . .. . . . . . . . . . . : .
-·r·- · ·· ·-_ ·1

AV dissociation: superimposed P waves at a differe nt rate to the QRS complexes

The first of the narrower complexes is a fusion beat, the next two are capture beats.

For more tips on spotting VT, read th1s art1cle.

 Case 48
30-year old female presenting with sudden onset of palpitations. Normally well. Describe the EGG.

..
.·I•••
I .
'I !
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On first glance this would appear to be SVT with LBBB as there is: Chartemouse Medical are currently working in...

~VQCOrtex
• Regular broad-eomplex tachycardia.
• No atrial activity seen. VIeW all JObS on
• Typical LBBB morphology in aVR, V1 and V6.
• No obvious diagnostic features for VT- compare this with EGG 047.

However, there is one feature here that is unusual for LBBB, can you spot it?

Reveal Answer

RECENT POSTS
• There is an inferior axis (+90 degrees), which is atypical for LBBB.
• LBBB normally has a leftward axis.
Medmastery: Mitral regurgitation
This combination of... Tropical Travel Trouble 005 RUQ Pain and
Jaundice
• Broad complex tachycardia with typical LBBB morphology
• Inferior axis (+90 degrees). Feed Me

LITFL Review 323

... is suggestive ora specific type ofVT known as right ventricular outflow-tract tachycardia (RVOT).
OSCE Resources
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RVOT is a relatively common form of right ventricular VT, occurring in two main groups:

• Patients with structurally normal hearts (= 70% of idiopathic VT).

• Patients with arrhythmogen1c nght ventricular cardiomyopathy.

It may be very difficult to differentiate RVOT from SVT with LBBB.

[NB. Left bundle branch block morphology simply indicates that the heart is depolarising from right
to left. Hence, similar QRS patterns are seen with LBBB, RVOT and RV-pacing]

lips for Spotting RVOT

• Suspect RVOT when you see LBBB morphology + inferior axis.

• Record a long rhythm strip looking for fusion and capture beats.

I have diagnosed this only a couple of times in the past Each time I had to stand by the monitor
with my finger on the "print• button waiting for a fusion or capture beat to appear before anyone
would believe me!

u
Case 49
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' .. . . ..
Australia,Western Australia
Charterhouse Medical are currently worKing in .. .
• Broad complex tachycardia at- 120 bpm.
• Pacing spikes precede each QRS complex.
• LBBB morphology {dominantS wave in V1-2) indicates a pacing electrode in the right
ventricle.
VIeW all jObS On ~vocortex
• Negative concordance is seen in V1-6 (all precordial leads show negative complexes) This is
an often-cited feature of VT, but also occurs with paced rhythms. It simply indicates that
ventricular depolarisation is spreading from anterior to posterior (away from V1 -6), e.g due
to a pacemaker electrode stimulating the anterior wall of the RV.

These features are consistent with a pacemaker malfunction resulting in a rapid ventricular-paced
rhythm. RECENT POSTS

Differential Diagnosis Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

The differential diagnosis of this rhythm includes:
Jaundice

• Pacemaker-mediated tachycardia Feed Me

• Wl~ei~u~filaghycard ia
LI TFL Review 323
.w nctcJws b.A.Atriabtaebyc_ardla.(e g sinus, AF) driving the pacemaker to its maximum rate- may be
appropriate response to exercise, shock, sepsis, etc. OSCE Resources
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- "' 1' .. , .

• Atnal tachycardia (e.g. s1nus, AF) dnvmg the pacemaker to 1ts mruomum rate- may be
appropriate response to exercise, shock, sepsis, etc. OSCE Resources

Pacemaker Mediated Ta chycardia (PMT)

This is a re-entrant rhythm involving the pacemaker circuit. It behaves very much like
the atrioventricular re-entry tachycardia (AVRT) seen with WPW syndrome, except that in this case
the ·accessory pathway" is formed by the pacemaker circuit. PMT is triggered when ventricular
impulses pass retrogradely through the AV node and depolarise the atria. This retrograde P wave is
sensed by the pacemaker, which then immediately paces the ventricles. This is followed by another
retrograde P wave that maintains the circus movement. This rhythm can be terminated by activating
magnet mode (which switches off sensing), or by reprogramming the pacemaker box (e.g.
increasing the refractory period to "block out'' the retrograde P waves)
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Pacemaker Mediated Tachycardia

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Pacemaker Mediated Tachycardia

Activation of magnet mode terminates PMT and switches

to AV sequential pacing (no sensing).

Sensor Induced Tachycardia (SIT)

• Modern pacemakers are programmed to allow increased heart rates in response to

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Sensor Induced Tachycardia (SIT)

• Modem pacemakers are programmed to allow increased heart rates in response to

physiological stimuli such as exercise, tachypnoea, hypercapnia or acidaemia.
• Sensors may "misfire• in the presence of distracting stimuli such as vibrations, loud noises,
fever, limb movement, hyperventilation or electrocautery (e.g. during surgery).
• This misfiring leads to pacing at an inappropriately fast rate.
• The ventricular rate cannot exceed the pacemaker's upper rate limit.
• Similar to PMT, these may also terminate with application of a magnet, or with removal of the
inciting stimulus.

Tips for Dealing w ith Rapid Paced Rhyt hms

• If the patient is attached to critical care monitoring, ensure that you switch off respiratory
impedence monitoring mode (where the monitor senses respiratory rate via the ECG
electrodes). This gives off an electrical signal that is known to interfere w1th pacemakers. If
this doesn't work, try changing monitors to one that does not use respiratory impedance
technology.
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Tips for Dealing with Rapid Paced Rhythms

• If the patient is attached to critical care monitoring, ensure that you switch off respiratory
impedence monitoring mode (where the monitor senses respiratory rate via the ECG
electrodes). This gives off an electrical signal that is known to interfere w1th pacemakers. If
this doesn't work, try changing monitors to one that does not use respiratory impedance
technology.
• Apply a magnet to the pacemaker box. This activates magnet mode, which resets the
pacemaker to provide temporary asynchronous pacing (AOO, VOO or 000).
• Arrange for an urgent pacemaker check. A pacemaker technician may be able to adjust the
settings to terminate the dysrhythmia and prevent its recurrence.
• If a pacemaker technician is not readily available, then a trial of AV nodal blocking drugs
(e.g. beta blockers, verapamil) may be successful in terminating PMT.

More ECG ClinicalLCases...

Last update: [last-modified)

 Case 50
Elderly patient presenting with collapse C linically dehydrated. Describe the ECG.
J
-,. ' • ".j. 1

RKYlt<H STRIP, II
ZS -m/t:~c. ; J u/tr~V

-rt
Jiz ECG 050 • LITFL • Life in II X

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. . . .. - . .- . .- . .
This is a classic sine wave ECG of cntical hyperkalaemia practitioner
Auslralia,Westem Australia
Charterhouse Medical are currently working in...
• Bradycardia (- 55 bpm).
• Bizarre-looking QRS complexes.
•
•
Gross QRS prolongation(> 300 ms).
Massively peaked T waves.
VIeW all jObS on ~vocortex
This patient had a K+ of 9.9 mmoVL!

Clinical Pearls

Any time you see an ECG that is ...

RECENT POSTS
• Blocked (AV block, bundle branch block)
• Bradycardic (sinus brady, slow AF, junctional bradycardia) Medmastery: Mitral regurgitation
• Bizarre in appearance
Tropical Travel Trouble 005 RUQ Pain and
Jaundice
... consider hyperkalaem1a and check the K+ urgently!
Feed Me
_-
......................................................................................................
LITFL Review 323
- - - -
or
 Case 51

2-year old boy presenting with febrile seizure. Interpret the ECG.
 This is a normal paediatric ECG, displaying multiple age-appropriate features:

o Heart rate of 110 bpm (normal for age)

o Dominant R waves in V1-3.
o Partial RBBB (RSR' pattern in V1)
o Juvenile T-wave pattern (T wave inversion in V1-3).

Any of the following findings may be normal on the paediatric ECG:

Heart rate and rhythm

o Heart rate >100 beats/min.

o Marked sinus arrhythmia.

Right-sided predominance

o Rightward QRS axis > +90•

o Dominant R wave in V1
o ~Sf}~ttESrlt:J q ,Y,l;
1115 b~ ..T.w_§ye.J~ves§fo~in V1 -3 ("juvenile T-wave pattern")
Jiz ECG 051 • LITFL • Life in II X

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• T wave inversions in V1 -3 ("juvenile T-wave pattern")

LITFL Review 323

P waves OSCE Resources

• Slightly peaked P waves (< 3mm in height is normal if $ 6 months)

Intervals

• Short PR interval(< 120ms) and QRS duration {<80ms)

• Slightly long QTc (s 490ms in infants$ 6 months)

Pseudo-infarction patterns

• Q waves in the inferior and left precordial leads.

More ECG Clinical Cases...

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 Case 52

Middle-aged patient presenting with central chest pain. Now asymptomatic. Interpret the ECG.

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

• This is classic ECG of Wellens' syndrome, demonstrating characteristic biphasic T waves in whitsundays
Australia,Oueensland
V1-3.
An excellent opportuni1y has arisen in Whitsun
• This ECG pattern is highly predictive of a significant occlusive lesion of the LAD.
• The biphasic T waves are a marker of reperfusion and may occur after an aborted anterior perth - gp - permanent vr general
STEM I. practitioner
Australia,Western Australia
• Despite often being pain free and having normal cardiac enzymes at presentation, these
Charterhouse Medical are currently worKing in .. .
patients are at risk of sudden LAD re-occlusion leading to massive anterior STEM I and are
best managed with early angiography and PCI / CABG.

VIeW all jObS On ~vocortex

RECENT POSTS

Medmastery: Mitral regurgitation

W ndows b.!··;·"·;
··./ 11 0 s h_!"ll'· .__,.:, .l.Lt' U'-'~ Jji.u Tropical Travel Trouble 005 RUQ Pain and
Jiz ECG .052 • LITFL • Life in t X

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Tropical Travel Trouble 005 RUQ Pain and

Jaundice

Feed Me

LI TFL Review 323

Biphasic T w aves in Wellens' syndrome OSCE Resources

Ol
- -
Jiz ECG 052 • LITFL • Life in II X

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Biphasic Twaves in Wellens' syndrome OSCE Resources

Clinical Pearls

Biphasic T waves may be seen with both Wellens' syndrome and hypokalaemia.

The main differentiating factor (apart from the clinical picture) is the direction of the T waves:

• Wellens' biphasic T waves go UP then down.

• Hypokalaemic T waves go DOWN then up.

Wellens' Syndrome
Jiz ECG .052 • LITFL • Life in t X

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COLLECTIONS ECG LIBRARY TOX LIBRARY CCC PART ONE CASES TOP 100

Wellens' Syndrome

Hypokalaemia
 Case 53

Elderly patient presenting with nausea and palpitations. Interpret the ECG.
Jiz ECG 053 • UTFL • Life in t ' X

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• I . . • I • • . I

This rhythm is frequently misidentified as atrial fibrillation. However, note in this case An excellent opportunity has arisen in Whitsun

• Well.defined sawtooth waves in II, Ill, aVF with regular rate (-300bpm ) and consistent
perth - gp - permanent vr general
practitioner
morphology. Australia,Western Australia
• Positive flutter waves ("pseudo.P waves") in V1.2. Charterhouse Medical are currently worKing in.. .
• The rhythm is not irregularly irregular There are repeating patterns of identical R·R intervals

~vocortex
that crop up throughout the rhythm strip, corresponding to AV conduction ratios of either 2 1 or
41 . VIeW all jObS On

This is atrial fl utter with a variable block.

RECENT POSTS

Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

.W nCICJWS h_!"ll'· .__,.:, .l.L~ Jaundice
Jiz ECG 053 • LITFL • Life in I I X

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Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Recurring RR intervals in flutter with v ariable block
Jaundice

Feed Me

UTFL Review 323

Clinical Pearl s
OSCE Resources

• Misidentifying this rhythm as AF is not normally a big problem as both conditions are managed
similarly - i.e. rate control, anticoagulation.
• However, flutter Will card1overt w1th lower energy than AF - e g. 50 j compared with 100-200 j.

More ECG Clinical Cases ...

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 Case 54
Elderly patient presenting with nausea and visual disturbance. Interpret the ECG.
I
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~~ ·. ili~l~.
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.
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~
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..

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,...
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T· .I ~ ... I'-
I=
r
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:•1•
I= -+ +-: H·
'"'
~

·r I .l ~-, . .. l
v I•'• --o=
1~
j- L. .rl .....1... 1.
. 1•,: I I
;I ........... .....
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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

- --. . . . . . . . . . .
This is a tricky ECG!
vr or non vr general practitioner -
There is evidence of atrial fibrillation, as evidenced by the irregular baseline w ith fibrillatory waves
whitsundays
Australia,Oueensland
most prominent in V1-2. An excellent opportunity has arisen in Whitsun

NB. Fibrillatory waves are characteristically seen in V1-2 (which overlie the atria), as opposed to perth - gp - permanent vr general
tremor artefact which may be in seen in multiple leads without a predominance for V1-2. practitioner
Australia,W estern Australia
Charterhouse Medical are currently worKing in .. .
However, the ventricular rhythm is regular. How can this be? AF is irregular by definition .. .

This is an example of "regularised AF" due to digoxin toxicity VIeW all jObS On ~vocortex
o The underlying rhythm is AF, wh ich is being treated w ith digoxin.
o There is complete heart block, prevent atrial impulses from reaching the ventricles.
o There is an accelerated junctional rhythm maintaining cardiac output

If th is all seems like too much of a coincidence, then consider the pathophysiology of digoxin
toxicity .. .
RECENT POSTS

Medmastery: Mitral regurgitation

Jiz ECG 054 • LITFL • Life in I I X

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Mechanisms of Digoxin Toxicity

Tropical Travel Trouble 005 RUQ Pain and
Jaundice
Digoxin toxicity produces a wide variety of dysrhythmias, due to:
Feed Me

• Increased automaticity of atrial, junctional and ventricular tissues - via actions at the Na/K UTFL Review 323
and Na/Ca exchangers causing increased intracellular calcium and therefore increased
OSCE Resources
spontaneous depolarisation of cardiac pacemaker cells.
• Decreased AV conduction -via increased vagal tone at the AV node.

Digoxin toxicity therefore usually produces some combination of:

• Increased atrial automaticity - especially atrial tachycardia, but also atrial ectop1cs, AF ,
flutter.
• Increased junctional automaticity - especially accelerated junctional rhythms.
• Increased ventricular automaticity - frequent VEBs and bigeminy, polymorphiC VT.
• AV blocks - including 1st, 2nd and 3rd degree AV block.

Characteristic EGG patterns include:

• Atnal tachycardia w1th high-grade AV block (= the classic dig-toxic rhythm).

• Regulansed AF = AF with complete heart block + accelerated junctional escape rhythm,
Jiz ECG 054 • LITFL • Life in I I X

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Characteristic EGG patterns include:

• Atnal tachycardia~ 'h lugh-grade AV block (= the classic dig-toxic rhythm).

• Regulansed AF = AF with complete heart block + accelerated junctional escape rhythm,
producing a paradoxically regular rhythm.
• B1d1rectlona1 VT = polymorphic VT with QRS complexes that alternate between left- and right-
axis-deviation, or between LBBB and RBBB morphology

NB. Digoxin toxicity should not be confused with digoxin effect (= "sagging• ST depression and
T-wave inversion in patients on therapeutic doses of digoxin; not predictive of toxicity).

Clinical Pearls

• Check for tremor artefact before you start diagnosing regularised AF!
• If the ECG pattern appears genuine and the clinical picture is compatible with digoxin toxicity
(GI upset, xanthopsia, current digoxin treatment), then check an urgent digoxin level.

More ECG Clinical Cases...

 Case 55

Middle-aged patient presenting with drowsiness. BP 85/50. Pupils dilated. Interpret the ECG.
Jiz ECG 055 • UTFL • Life in t • X

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whitsundays
Australia,Oueensland
Main Abnormalities An excellent opportunity has arisen in Whitsun

This is a classic ECG of tricyclic antidepressant toxicity, demonstrating multiple characteristic perth - gp - permanent vr general
practitioner
abnormalities. Australia,Western Australia
Charterhouse Medical are currently worKing in
Signs of sodium-channel blockade

o Broad QRS complexes (120 ms, or 3 small squares) VIeW all jObS on ~vocortex
o Positive R' wave in lead aVR > 3 mm.
o Prolonged PR interval (240 ms).
o Long QT interval (> 1/2 the RR interval)
o Brugada-like pattern in V1 .

Signs of anticholinergic toxidrome

RECENT POSTS
o Sinus tachycardia (- 11 0 bpm), with P waves embedded in each T wave.

Medmastery Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jiz ECG .055 • LITFL • Life in t X

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Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jaundice

Feed Me

UTFL Review 323

Positive R' wave in aVR > 3mm

OSCE Resources
__
·- ·- _______..________________............................ .. ..
Jiz ECG .055 • LITFL • Life in t X

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-- --
P w aves visible in V2 with long PR interval

Pseudo-Brugada pattern in V1

This patient had taken a life-threatening overdose of dosulepin (a TCA)

How to Spot Sodium-Channel Blockade

• QRS prolongation(> 100ms or 2.5 small squares), typically measured in lead II.
• A terminal or secondary R wave (R' wave) in aVR > 3 mm.
• An R'/S ratio in aVR > 0.7.

Prognostic Value of the ECG

Jiz ECG 055 • LITFL • Life in I I X

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This patient had taken a life-threatening overdose of dosulepin (a TCA).

How to Spot Sodium-Channel Blockade

• QRS prolongation(> 100ms or 2.5 small squares), typically measured in lead II.
• A terminal or secondary R wave (R' wave) in aVR > 3 mm.
• An R'/S ratio in aVR > 0.7.

Prognostic Value of the ECG

In patients with TCA overdose, the degree of QRS prolongation correlates with the degree of clinical
toxicity

• QRS width > 100 ms is predictive of seizures.

• QRS width > 160 ms is predictive of cardiotoxicity (e.g broad-complex dysrhythmias,
hypotension).

Clinical Pearls
Jiz ECG 055 • LITFL • Life in I I X

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• QRS width > 160 ms is predictive of cardiotoxicity (e.g. broad-complex dysrhythmias,

hypotension}.

Clinical Pearls

• The combination of PR prolongation and sinus tachycardia with TCA overdose often makes
the P waves difficult to see, and may lead the rhythm to be incorrectly identified as VT. This
patient needs bicarbonate and hyperventilation, not electricity and amiodarone!
• The clinical significance of a TCA-Induced Brugada ECG pattern remains controversial- i.e.
is it purely a manifestation of severe sodium-channel blockade, or does it represent
"unmasking" of underlying Brugada syndrome? These issues are discussed here.

More ECG Clinical Cases...

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 Case 56

Middle-aged patient presenting with drowsiness. Brief seizure in ED. BP unrecordable. Interpret the
ECG.

T 73
Jiz ECG 056 • UTFL • Life in t • X

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g p
+ Reveal Answer whitsundays
Australia,Oueensland
An excellent opportunity has arisen in Whitsun

This is a repeat ECG of the previous patient with massive TCA overdose, taken a short while later.
perth - gp - permanent vr general
practitioner
o There is now evidence of advanced sodium-channel blockade, with grossly prolonged QRS Australia,Western Australia

and QT intervals and further evolution of the R' wave in aVR. Charterhouse Medical are currently worKing in

o The ECG is beginning to take on bizarre morphology and a sine wave appearance

~vocortex
reminiscent of severe hyperkalaemia
o In some leads (II, Ill, aVF), the QRS morphology resembles ventricular tachycardia. VIeW all jObS on

These features are all due to sodium-channel blockade, and resolved following aggressive
treatment with IV bicarbonate, intubation and hyperventilation.

Show post-treatment ECG

RECENT POSTS

Clinical Pearls Medmastery Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jiz ECG 056 • LITFL • Life in t ' X

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Show post-treatment ECG

I RECENT POSTS

Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jaundice

Feed Me

LITFL Review 323

OSCE Resources

r +--
...
.. L
Resolvi ng TCA toxicity - QRS complexes narrowi ng and R' wave disappearing with treatment.

VVIII d OWS.{
!0 I b ..•'''"'
Jiz ECG 056 • LITFL • Life in I I X

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.. . . ... . . . . . . . .. .

Clinical Pearl s

• Advanced sodium-channel blockade can resemble either VT or hyperkalaem1a.

• Standard VT treatments such as DC cardioversion and amiodarone are likely to be ineffective
and potentially harmful if the broad complex rhythm is due to sodium-channel blockade.
Consider the clinical context and look for clues of TCA toxicity (e.g ant1cholmerg1c tox1drome).
• In arrested I peri-arrest patients with a broad or bizarre-looking EGG, consider empirical
treatment for both hyperkalaem1a (with calcium) and sodium-channel blockade (with
bicarbonate and hyperventilation).

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''h1951
 Case 57

Middle-aged patient presenting with chest pain and diaphoresis. Becomes unresponsive during
recording of EGG. Interpret the EGG.

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I .. ·il:!
11
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'

111
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Main AbnormalitiesThis is a fascinating EGG with multiple abnormalities:

• The first half or the tracing shows a ventricular paced rhythm with positive Sgarbossa VIeW all JObS on ~VQCQrtex
critena indicating superimposed mferior STEMI.
• There is excess1vely discordant ST elevation (> 25% of Q/S wave depth) in II, Ill and aVF with
reciprocal change in I and aVL.
• A ventricular ectopic (beat #8) occurs at a vulnerable time, resulting in a run of ventricular
flutter (very rapid VT at rates > 200-300 bpm)
• This rapidly degenerates to ventricular fibrillation (seen in the rhythm strip, which is recorded
after the other 12 leads).
RECENT POSTS
• The artefact at the start of the rhythm strip may represent a precordial thump!

Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jaundice
Clinical Pearls
Feed Me
• While most rhythm strips are recorded simultaneously with the 12-lead ECG, some older
LITFL Review 323
machines may record the rhythm strip after the other 12 leads.
• Cons1der this as a possibility if your rhythm strip doesn't seem to "line up" with the rest of the OSCE Resources
EGG.
 Case 58

Elderly patient presenting with chest pain Interpret the EGG.

Jiz ECG 058 • LITFL • Life in II X

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COLLECTIONS ECG LIBRARY TOX LIBRARY CCC PART ONE CASES TOP 100

pe gp pe g
practitioner
This ECG shows changes consistent with an old anterolateral infarction - the sa-called left Ausllalia,Westem Australia

ventricular aneurysm pattern. Charterhouse Medical are currently working in...

•
•
ST elevation in V1 -3 associated with deep Q waves(= LV aneurysm rnorphology).
Pathological Q waves also seen in I, aVL and V4. VIeW all jobs on ~vocortex
• Poor R wave progresSIOn (= R wave height < 3 mm in V3).
• Biphasic I inverted T waves in V1-5, I and aVL.

Clinical Pearls
RECENT POSTS

• The LV aneurysm pattern refers to the combination of residual ST elevation, deep Q waves
and inverted or biphasic T waves seen in patients following an acute myocardial Medmastery: Mitral regurgitation
infarction. This ECG pattern is associated with transmural scarring and paradoxical movement
Tropical Travel Trouble 005 RUQ Pain and
of the LV on wall on echocardiography.
Jaundice
• Around 60% of patients with anterior STEM I develop some degree of chronic ST elevation on
their ECG, which can cause diagnostic confusion.
• If these patients present with chest pain, the safest approach is to take serial ECGs looking for
Feed Me
__
.............................................................................................................
LITFL Review 323
signs of evolving STEMI such as evolving ST elevation or pseudo-normalisation ofT waves.
 Case 59

I 57 -year old man with ROSC following VF arrest Interpret the EGG.
Jiz ECG 059 • UTFL • Life in t ' X

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

perth - gp - permanent vr general

Main Abnormalities practitioner
Australia,Western Australia
Charterhouse Medical are currently worKing in .. .
• Sinus rhythm with frequent ventricular ectopics in a pattern of ventricular bigeminy.
• Grossly prolonged QT interval (> 600 ms)
• "R on T" phenomenon is present, with each VEB falling on the end of the T wave - this EGG
pattern is very high risk for deterioration to torsades de pointes and ventricular fibrillation .
VIeW all jObS On ~vocortex
• Relatively short PR interval and possible delta waves (leads I, II, V6) are suggestive - but not
diagnostic - of WPW syndrome.
• Voltage criteria for left ventricular hypertrophy are present in multiple leads.

This patient had suffered a cardiac arrest in the context of severe hypertrophic cardiomyopathy and
long QT syndrome.
RECENT POSTS
(NB -1 /3 of patients with HOCM will have some evidence of WPW on their EGG)
Medmastery: Mitral regurgitation
Can you guess what happened next?
Tropical Travel Trouble 005 RUQ Pain and
Jaundice
+\ Revea:l>Ms!lrer.u:w
··./ 11 0 s h_!"ll'· .__,.:, .l.Lt' U'-'~ Jji.u
Feed Me
Jiz ECG 059 • UTFL • Life in t ' X

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

This patient had suffered a cardiac arrest in the context of severe hypertrophic cardiomyopathy and
long QT syndrome.
RECENT POSTS
(NB -1 /3 of patients with HOCM will have some evidence of WPW on their ECG)
Medmastery: Mitral regurgitation
Can you guess what happened next?
Tropical Travel Trouble 005 RUQ Pain and
Jaundice
+ Reveal Answer
Feed Me
• The patient had a further TdP cardiac arrest!
LITFL Review 323
• This was treated with IV magnesium and potassium, with restoration of sinus rhythm.
OSCE Resources
This interesting case is discussed in more detail here.

More ECG Clinical Cases ...

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N
 Case 60
16-year old male presenting with syncope. Describe and interpret his EGG.

III I I I I II
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II

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11.J~P' ' £1'' ,; ~
'
1
1A I
II I
~~ J!
u V6
lA I~ :u .~
v I I I I I
Jiz ECG 060 • UTFL • Life in t ' X

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

. .... . . .. .. ' ' .

Main Abnormalities perth - gp - permanent vr general
practitioner
Australia,Western Australia
• Markedly peaked T waves in V2.6. Charterhouse Medical are currently worKing in
• Extremely short QT interval (-240 ms)

In a patient presenting with syncope, this ECG pattern is very suspicious for the short QT VIeW all jObS on ~vocortex
syndrome.

Short QT Syndrome

• This is a recently.described arrhythmogenic cond ition associated w ith paroxysmal atrial and
ventricular fibrillation.
• The hallmark is a significantly shortened QT interval (at least< 360 ms, often < 330 ms) w ith
associated T.wave peaking RECENT POSTS
• SQTS is a genetically.inherited cardiac channelopathy on the same spectrum as other familial
arrhythmogenic diseases such as Long QT Syndrome (LQTS}, Brugada Syndrome Medmastery Mitral regurgitation
and Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT).
Tropical Travel Trouble 005 RUQ Pain and
\j1 '1d 0 rs P..'~l,/, Jaundice
When to Suspec QTS
,s n _! .. " • • .__, .:, .J,i.. t' W'-' ~ ..,jA.J.J
Feed Me
Jiz ECG 060 • LITFL • Life in I I X

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COLLECTIONS ECG LIBRARY TOX LI BRARY CCC PART ONE CASES TOP 100

. ..
.. .. .. .. ,. .. ..... .. .. ... ....... - .. . ~ . .......
and Catecholammerg1c Polymorphic Ventricular Tachycardia (CPVT).
Tropical Travel Trouble 005 RUQ Pain and
Jaundice
When to Suspect SQTS
Feed Me
• Any patient with a QT interval < 330 ms.
UTFL Review 323
• QT interval < 360 ms and convincing symptoms (syncope, cardiac arrest) or family history.
OSCE Resources
Differential Diagnosis

• Peaked T waves and short QT interval may be seen with severe hyperkalaemia.
• A shortened QT interval may also be seen with severe hypercalcaemia.

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 Case 61

Middle-aged patient presenting with an episode of chest pain Currently asymptomatic. Describe
and interpret his EGG

_ L
i I ,
•
' I
II , , I i I
II I 1 I
!-\-+ 1 I
--1---'---1--1-4 I- t .j--:..-H-,-H-+++-1-++ . 1-t-
~~- .,~~-~-~-~~-~-~-~~+~-f . 1- ~-·
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. -- . +-!-+.++-! -h~-H-hH-++
~JI\] + t,l-_++1--1-'+-1-+.+++++-H--H--H-H-t
I I I
I I
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~llt-1' ±t r-v. • t 1 ' ·r'
- f-
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1 I. -+---
'-'-..j +-.. 1._..,_.,.-f-H-1-~+
.!...J-; .......,. ,,_......_w..
I I
Jiz ECG 061 • UTFL · Life in t • X

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

Reveal Answer vr or non vr general practitioner -

whitsundays
Australia,Oueensland
• This pattern of deeply inverted T waves in the anterolateral leads V2-6, I and aVL is characteristic of An excellent opportunity has arisen in Whitsun
Wellens syndrome.
• This ECG pattern is highly predictive of a significant occlusive lesion of the LAD. perth - gp - permanent vr general
• The inverted T waves are a marker of reperfusion and may occur after an aborted anterior STEM I. practitioner
Australia,Western Australia
• Despite often being pain free and having normal cardiac enzymes at presentation, these patients
Charterhouse Medical are currently worKing in .. .
are at risk of sudden LAD re-occlusion leading to massive anterior STEMI and are best managed
with early angiography and PCI / CABG.

Differential Diagnosis
VIeW all jObS On ~vocortex
A similar pattern of deep anterolateral T-wave inversions may also be seen with:

• Apical hypertrophic cardiomyopathy - suspect if associated LVH

• Raised intracranial pressure - patient will be comatose (see Quiz ECG #12)

More ECG Clinical Cases ... RECENT POSTS

.Wnc
« PREV
1nl'':l0 . N
, nwieNu NEXT» Last update: [last-modified]
Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

 Case 62

Middle aged patient presenting with chest pain and diaphoresis. Describe and interpret his ECG
Jiz ECG 062 - UTFL - Life in t ' X

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GP required for a permanent role in well-estab .. .

Reveal Answer

vr or non vr general practitioner -

Main Abnormalities whitsundays
Australia,Oueensland
An excellent opportunity has arisen in Whitsun
• ST depression in V2-6, which slopes upwards and joins the ascending limb of the T wave.
• Prominent, "rocket-shaped" T waves in the precordial leads V2-5.
perth - gp - permanent vr general
• Subtle ST elevation in aVR. practitioner
Australia,Western Australia

Diagnosis Charterhouse Medical are currently worKing in

• This combination of ST depression with rocket-shaped T waves in the precordial leads V1-6 is
referred to as the De Winter ECG pattern or "De Winter's T waves" (also see ECG #19) --,.-~~-r.-1"'!"1'1~~~...,
• It is becoming increasingly recognised as an anterior STEMI equivalent (-2% of LAD occlu! -ii----+~-+...-~..-+--+'----'-1
• Some authors are now recommending that this ECG pattern be treated identically to anteri<
STEM I, with urgent PCI or thrombolysis.

Windows b.!··;,;·;
.W ndOI'oS b!"" '' .....,) .JL~ uv, J.o..,
 Case 63

Elderly patient presenting with reduced level of consciousness, hypothermia and hypotension
refractory to inotropes Describe and interpret his ECG

..__ -<I- -J--

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It ovt. V2 vs

Ill
~
~
.J. J... J,... A,.-
~
I
r I

oYF Y3 V6
J·J I

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j'-- I

Rli'tT~ STRIP ' II

2S.l"m/OPc: I e.>/•V

Vo 'nd"J' S bJI.llll
··owL ...A c.\!.: ,j.c:
Jiz ECG 063 • UTFL • Life in t ' X

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The most stnkmg abnormality on th1s ECG IS extremely low QRS voltage, 1n th1s case due to severe Australia,Western Australia
myxoedema. Charterhouse Medical are currently worKing in

~vocortex
Definition
VIeW all jObS on
The QRS is said to be low voltage when

" • The amplitudes of all the QRS complexes in the limb leads are < 5 mm; or
• The amplitudes of all the QRS complexes in the precordial leads are < 10 mm

RECENT POSTS
Mechanisms
Medmastery Mitral regurgitation
Low voltage is produced by ...
Tropical Travel Trouble 005 RUQ Pain and
Jaundice
" • The "damping" effect of increased layers of fluid, fat or air between the heart and
Feed Me
\A, the ~rew~~~. ~? electrode..
vv 1d0
• Loss o v1a e myocardium. LI TFL Review 323
.W ndOI'oS _.s.,._ U'-' ~
o,._J.J
• Diffuse innltration or myxoedematous involvement of the heart.
OSCE Resources
Jiz ECG 063 • LITFL • Life in tl X

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..::...._....:...__ _ __
... ~ 0
Causes ~ library Gtnesis @ Electronic library. Dow... 0 Ebook Categories· Kic... G) 10 Btst Torrtnts Sites f... ~ TopS Best Torrent Site... ~ imaging of the chest T... B, "High Yitld lma~

Specific causes of low vol ' COLLECTIONS ECG LIBRARY TOX LIBRARY CCC PART ONE CASES TOP 100

• Pneumothorax
" Fluid
Infiltrative I Connective Tissue Disorders
• Pencard1al •
• Pleural effu • Myxoedema
• Infiltrative myocardial diseases - i.e. restnct1ve cardiomyopathy due to
Fat amyloidosis, sarcoidosis, haemochromatosis
• Constrictive pericarditis
• Obesity • Scleroderma

Air Loss of viable myocardium

• Emphysem. • Previous massive Ml

• Pneumotho • End-stage dilated cardiomyopathy

Infiltrative f Con

The most important cause is massive pericard ia! effusion, which produces a triad of:
Jiz ECG 063 • LITFL • Life in I I X

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The most important cause is massive pericardia! effusion, which produces a triad ot

" • Low voltage

• Tachycardia
• Electrical alternans

Patients with this triad need to be immediately assessed for clinical or echocardiographic evidence of
tamponade.

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t'''M95'
 Case 64

Chest pain and diaphoresis. BP 80/50. Describe and interpret his ECG

.... V4

II .... V2 vs

.----...JI.../''-'~/'-----~1-n
v•
.../'-JL ../ -.........Jl-/'.----41.-/'- - -----II /'-J \....1"'-~-ILJl
II

I
~ ~ .AJ~
'-' "" ~ -".
Jiz ECG 064 - UTFL - Life in t ' X

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An excellent opportunity has arisen in Whitsun

Key Abnormalities
perth - gp - permanent vr general
• There is ST elevation in the inferior leads II, Ill and aVF practitioner
• The concave morphology might lead you to suspect pericarditis - however, there is reciprocal Australia,Western Australia
Charterhouse Medical are currently worKing in .. .
change in the high lateral leads I and aVL, confirm ing the diagnosis of inferior STEMI.

There are additional features suggestive of right ventricular infarction

VIeW a ll jObS On ~vocortex
• ST elevation in Ill > II
• lsoelectric ST segment in V1 with ST depression in V2

Other Abnormalities

• There is a break in the rhythm towards the end of the rhythm strip, with what appears to be a non-
conducted P wave, suggesting the development of 2nd degree AV block - e.g a slowly-evolving RECENT POSTS
Wenckbach cycle.
• The 13th QRS complex appears to be a supraventricular ectopic beat (PAC or PJC).
Medmastery: Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

- -
Jaundice
MENU NEXT» Last update: [last-modified]
 Case 65

Chest pain and diaphoresis. BP 80/50. Describe and interpret his ECG

I .... (d;J
------'----n
II ..... V5

Ill

"'--n
II

I
Jiz ECG 065 - UTFL - Life in t • X

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• n
This is a repeat ECG of the previous patient, demonstrating
perth - gp - permanent vr general
practitioner
• Inferior STEMI - STE in II, Ill, aVF with reciprocal change in I and aVL Australia,Western Australia
• Evidence suggesting RV infarction - STE in Ill > II. Charterhouse Medical are currently worKing in .. .
• Evidence confirming RV infarction - STE and hyperacute T wave in V4R.
• Evolving second degree AV block with alternating 2:1 block and 3:2 Wenckebach cycles.
VIeW all jObS On ~vocortex
This ECG pattern is diagnostic of a right coronary artery occlusion.

Rhythm Strip Explanation

1 2 1 2
+
II

+ + +
RECENT POSTS

Medmastery: Mitral regurgitation

• Arrows indicate the position of P waves.
• Black arrrows indicate conducted P waves. Tropical Travel Trouble 005 RUQ Pain and
• Re'cM:irrGWs'ftidlaatiWWn-conducted P waves - some of these are concealed within the preceding T Jaundice
.w ndo s .l::wave,-eauSing-a-small bump at the back of the T wave.
• Complexes cluster together in groups with either 2 1 conduction or as 3:2 Wenckeback cycles, with Feed Me
Jiz ECG 065 • LITFL • Life in II X

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• Arrows 1nd1cate the pos1l1on of P waves.

• Black arrrows indicate conducted P waves.
' . ry ' eg g
Tropical Travel Trouble 005 RUQ Pain and
• Red arrows indicate non-eonducted P waves - some of these are concealed within the preceding T Jaundice
wave, causing a small bump at the back of the T wave.
• Complexes cluster together in groups with either 2:1 conduction or as 3:2 Wenckeback cycles, with Feed Me
prolongation of the PR interval prior to the non-eonducted P wave. UTFL Review 323
• The number above each P wave denotes its position in the sequence.

Bradycardia and AV Block in Inferior STEM I

OSCE Resources
__
............................................................................................................

Up to 20% of patients with inferior STEMI will develop either second- or third degree heart block.

There are two presumed mechanisms for this:

" • Ischaemia of the AV node due to impaired blood flow via the AV nodal artery.
This artery arises from the RCA 80% of the time, hence its involvement in inferior
STEM I due to RCA occlusion.
• Bezold.Jarisch reflex = increased vagal tone secondary to ischaemia.
w
Jiz ECG 065 • LITFL • Life in I I X

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COLLECTIONS ECG LIBRARY TOX LI BRARY CCC PART ONE CASES TOP 100

J: • ue oocc uso .
• ~

• Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia.

• The conduction block may develop either as a step.wise progression from 1st degree heart block via
Wenckebach to complete heart block (in 50% of cases) or as abrupt onset of second or third-degree
heart block (in the remaining 50%).
• Patients may also manifest signs of sinus node dysfunction, such as sinus bradycardia, sinus
pauses, sinoatrial ex1t block and sinus arrest. Similarly to AV node dysfunction, this may result from
increased vagal tone or ischaemia of the SA node (the SA nodal artery is supplied by the RCA in
60% of people).
• Bradyarrhythmias and AV block in the context of inferior STEMI are usually transient (lasting hours
to days), respond well to atropine and do not require permanent pacing

More ECG Clinical Cases ...

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 Case 66

Elderly patient presenting with chest pain and diaphoresis. Describe and interpret his ECG
Jiz ECG 066 - UTFL - Life in t ' X

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- • - ;# - ' -

vr or non vr general practitioner -

whitsundays
This ECG demonstrates an infera-posterior STEMI, as manifest by: Australia,Oueensland
An excellent opportunity has arisen in Whitsun

• Subtle inferior STE and hyperacute T waves (T waves> QRS complexes)

perth - gp - permanent vr general
• ST depression and terminal T-wave positivity in V2-3 = posterior wall involvement
practitioner
Australia,Western Australia
See Quiz EGG 14 for another example of posterior infarction. Charterhouse Medical are currently worKing in .. .

Tips for spotting posterior infarction

VIeW all jObS On ~vocortex
Look specifically at leads V2-3 for the combination of

• Horizontal ST depression
• Tall, broad R wave {>30ms wide, RIS ratio> 1) - this is a Q-wave equivalent
• Upright T wave - particularly the terminal portion of the T wave.

RECENT POSTS

Windows b.!'·;,;·;
Medmastery: Mitral regurgitation
.W ndOI'oS b!"'"' .....,) .JL~ uv, J.o..,
Tropical Travel Trouble 005 RUQ Pain and
Jiz ECG 066 • LITFL • Life in t• X

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

.. t I .. I • ' ' .. '.. I ' ' I ... •4 .. I .. It ' ' .. ''"' ... I I f .. '"'

• Upright T wave - particularly the terminal portion of the T wave.

'

, RECENT POSTS

Medmastery Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jaundice
Typical appearance of posterior infarction
in V2-3 Feed Me

LITFL Review 323

One common trick is to turn the ECG over, hold it up to the light and look through it from behind. This
inverts lead V2, which then takes on the appearance of a classic STEMI.
OSCE Resources

l 3t !1ffi ltJ 1+11 i!

rtl ~
I
.1 •
•
. 1i.• lr. 'c;::
t
:
=-~~ ,;1},f. l.H! : -";n !
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1T -rll4 7
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t
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t . lti l -:1 H ~ \
!I t ~1
r 4 jffl
Inverted ECG- the complexes now
tL :llif
. .' .
:t --'-~
:. :rtr H

resemble a typical STEMI

Jiz ECG 066 • LITFL • Life in t X

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Inverted ECG- t he complexes now

resemble a typical STEM I

In this ECG example, V3 is the most characteristically abnormal lead.

Look for evidence of posterior involvement in any patient with an inferior or lateral STEM I.

Sometimes it can be difficult to determine whether ST depression in V2-3 is due to posterior STEMI or
simply subendocardial ischaemia affecting the anteroseptal wall. The diagnosis can be confirmed by
recording posterior leads V7-9.

More ECG Clinical Cases ...

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 Case 67

Elderly patient with chest pain and diaphoresis. Describe and interpret his ECG

=1 - +

Ill
Jiz ECG 067 • LITFL • Life in I I X

I CD 9} a https://lifeint hefastlane.com/ecg- library/1 00- ecgs/quiz-ecg-067I ••• ~ <:r .J.. Ill\ Ill
orary Genesis @ Electronic library. Dow... 0 Ebook Categories - Kic... m10 Best Torrents Sit es f... ~ Top 5 Best Tarrent Sit o... ~ imaging of tho chost T... Rr "High Yield Imaging C... FREE MEDICAL BOOKS

COLLECTIONS ECG LIBRARY TOX LI BRARY CCC PART ONE CASES TOP 100

Ill
- ~VP
- -
gp requ1recl for permanent role at a
reputable mixed billing practice in
north brisbane
Auslralia,Oueensland
GP required for a permanent role in well-estall...

Reveal Answer
vr or non vr general practitioner -
whitsundays
• This is the same patient as ECG 066. Australia,Oueensland
• Posterior leads V7-9 show subtleST elevation with early Q-wave formation, confirming the An excellent opportunity llas arisen in Wllilsun ...

presence of postenor 1nfarct1on.

perth - gp - permanent vr general
practitioner
More ECG Clinical Cases ... Australia,Western Australia
Charterhouse Medical are currently working in ...
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About Edward Burns

Ed Bums is an Emergency Physician working in Prehospital & Retrieval
Medicine in Sydney, Australia. He has a passion for ECG interpretation and
medical education. Ed is the force behind the LITFL ECG library 1 + Edward
 Case 68

Severe chest pain and hypotension (70/40) in an elderly man. Describe and interpret his ECG 1
Jiz ECG 068 - UTFL - Life in t ' X

CD Y'J a https://liteinthetastlane.com/ecg -library/1 oo-ecgs/quiz-ecg-068/

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

This ECG shows: whitsundays

Australia,Oueensland
An excellent opportunity has arisen in Whitsun
o ST elevation in aVR.
o ST depression in multiple leads (V5-6, I, II, aVL, aVF) perth - gp - permanent vr general
o Evidence of anteroseptal STEM I - ST elevation with Q wave formation in V1 -3. practitioner
Australia,Western Australia
Charterhouse Medical are currently worKing in .. .
In the context of ischaemic chest pain and cardiogenic shock, the combination of..

o
Widespread ST depression
ST elevation in aVR > 1 mm
VIeW a ll jObS On ~vocortex
o ST elevation in V1 -3

... is concerning for proximal LAD occlusion (compare this to the LMCA pattern seen in Quiz ECG 008)

While this pattern of diffuse ST depression with STE in aVR if often referenced as a marker of LMCA I
proximal LAD occlusion, may be seen whenever there is diffuse severe subendocardial ischaemia, e g.
RECENT POSTS
o Severe triple vessel disease
o Severe anaemia or hypoxaemia Medmastery: Mitral regurgitation
o Folfc/~7nrlQ9esbJ2~ from cardiac arrest
. V ndo s h_!ttll'· <-I.) JLt' uv. Jji.u Tropical Travel Trouble 005 RUQ Pain and
Jiz ECG 068 - UTFL - Life in t ' X

CD Y'J a https://liteinthetastlane.com/ecg -library/1oo-ecgs/quiz-ecg-068/

brary Genesis @ Electronic library. Dow... 0 Ebook Categories - Kic... (1l 10 Best Torrents Sites f... !!!!! Top 5 Best Torrent Site... \t imaging of the chest T... llF "High Yield Imaging C... Q FREE MEDICAL BOOKS

COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

... is concerning for proximal LAD occlusion (compare this to the LMCA pattern seen in Quiz ECG 008)

While this pattern of diffuse ST depression with STE in aVR if often referenced as a marker of LMCA I
proximal LAD occlusion, may be seen whenever there is diffuse severe subendocardial ischaemia, e.g.
RECENT POSTS
o Severe triple vessel disease
o Severe anaemia or hypoxaemia Medmastery: Mitral regurgitation
o Following resuscitation from cardiac arrest
Tropical Travel Trouble 005 RUQ Pain and
Outcome Jaundice

Feed Me
This patient actually had severe multi-vessel disease. Angiography demonstrated a chronic total
occlusion of his circumflex artery, with critical stenoses of his proximal LAD, RCA and ramus intermedius. LI TFL Review 323
Surprisingly, in this case the culprit vessel was thought to be the RCA, which had been collateralising his OSCE Resources
chronically occluded circumflex. He went on to receive a CABG x 4.

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.W 1100 S O_! ttll '· <--~.) .lLt' uv. ~
 Case 69

18-year old female with severe traumatic brain injury, ICP 40mmHg. Fluctuating BPs. Describe and
interpret her ECG
Jiz ECG 069 - UTFL - Life in t ' X

CD Y'J a https://liteinthetastlane.com/ecg -library/1 oo -ecgs/quiz-ecg -069/

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COLLECTIONS ECG LI BRARY TOX LIBRARY CCC PART ONE CASES TOP 100

vr or non vr general practitioner -

whitsundays
Australia,Oueensland
Reveal Answer An excellent opportunity has arisen in Whitsun

• The ECG shows diffuse ST elevation. perth - gp - permanent vr general

• The morphology is atypical, there is no clear anatomical predominance for a vascular territory and practitioner
Australia,Western Australia
no obvious reciprocal changes (except the inverted leads V1 and aVR)
Charterhouse Medical are currently worKing in
• This is an example of a pseudo-infarction pattern due to raised intracranial pressure.
• Compare this with Quiz ECG 012 (raised ICP causing giant T wave inversions)

ECG changes with elevated ICP

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Raised ICP is associated with certain characteristic ECG changes:

" • Widespread giant T-wave inversions ("cerebral T waves")

• QT prolongation
• Bradycard ia (the Cushing reflex - indicates imminent brainstem herniation). RECENT POSTS

Wmdows b.!·:·,·;
Medmastery Mitral regurgitation

Tropical Travel Trouble 005 RUQ Pain and

Jiz ECG 069 • LITFL • Life in II X

I CD 9} a https://lifeinthefastlane.com/ecg-library/1 00-ecgs/quiz-ecg-069/ ••• ~ <:r .J.. Ill\ Ill

orary Genesis @ Electronic library. Dow... 0 Ebook Categories - Kic... m10 Best Torrents Sites f... ~ Top 5 Best Tarrent Sito... ~ imaging of tho chost T... Rr "High Yield Imaging C... FREE MEDICAL BOOKS

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Tropical Travel Trouble 005 RUQ Pam and

Other possible ECG changes that may be seen:
Jaundice

Feed Me
" • ST segment elevation I depression - this may mimic myocardial ischaemia or
LITFL Review 323
pericarditis.
• Increased U wave amplitude. OSCE Resources
• Other rhythm disturbances: sinus tachycardia, junctional rhythms, premature
ventricular contractions, atrial fibrillation.

In some cases, these ECG abnormalities may be associated with echocardiographic evidence of regional
ventricular wall motion abnormality - so-called neurogenic stunned myocardium or neurogenic stress
cardiomyopathy. The presumed mechanism is massive release of catecholamines, similar to Takutsubo
syndrome.

This patient developed labile blood pressures and transient wall motion abnormalities plus these ECG
changes during a sustained spike in her ICP The ECG changes and wall motion abnormalities improved
once her /CPs came under control.

More ECG Clinical Cases...

 Case 70
Elderly patient presenting with sudden onset of chest pain and shortness of breath. Hypoxic (Sa02
82% RA) and hypotensive (80/50). Describe and interpret his ECG

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perth - gp - pel"manent VI" genel"al

There are multiple features suggestive of nght ventricular hypertrophy or strain: pl"actitionel"
Ausllalia,Westem Australia
Charterhouse Medical are currently working in...
• Right axis deviation
• Dominant R wave m V1
•
•
Right bundle branch block
Right ventricular stram pattern - T wave inversions in V1-4, lead Ill
VIeW all jObS on ~vocortex
• S1 Om Tm pattern
• Clockwise rotation of the heart, with a persistent S wave in V6

Given the clinical history, the most likely scenario is acute right heart strain due to massive pulmonary
embolism.

A similar ECG pattern may also be seen with chronic cor pulmonale, pulmonary hypertension or RV RECENT POSTS
hypertrophy (e.g. due to congenital heart disease).
Medmastery: Mitral regurgitation
ECG changes in pulmonary embolism include:
Tropical Travel Trouble 005 RUQ Pain and

• Sinus tachycardia -the most common abnormality; seen in 44% of patients.

• Cornplet~ or ihcomp'thle RBBB - associated with increased mortality; seen in 18% of patients.
Jaundice
__
...............................................................................................................................
Feed Me
• "'Right ventricular stram pattern - T wave inversions in the right precordial leads (V1-4) ± the inferior
LITFL Review 323
This pattern
Jiz ECG 070 • LITFL • Life in II X

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COLLECTIONS ECG LIBRARY TOX LIBRARY CCC PART ONE CASES TOP 100

ECG changes in pulmonary embolism include:

Tropical Travel Trouble 005 RUQ Pain and
Jaundice
• Sinus tachycardia - the most common abnormality; seen in 44% of patients.
• Complete or Incomplete RBBB - associated with increased mortality; seen in 18% of patients. Feed Me
• Right ventricular stra1n pattern - T wave inversions in the right precordial leads (V1-4) ±the inferior
UTFL Review 323
leads (II, Ill, aVF). This pattern is seen in up to 34% of patients and is associated with high
pulmonary artery pressures. OSCE Resources
• 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 1n 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.
• 510 111 T111 pattern - deepS wave in lead I, Q wave in Ill, inverted T wave in Ill. This "classic" finding
is neither sensitive nor specific for pulmonary embolism; found in only 20% of patients with PE.
• Clockwise rotation - shift of the RIS 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.

Simu/J.f3neous T wave inversions in the inferior (II, Ill, aVF) and right precordia/leads (V1-4) is the most
specific finding in favour of PE.
 Case 71

Palpitations· Descnbe
. an d Interpret
· this ECG
Jiz ECG 071 • LITFL • Life in t X

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gp required for permanent role at a

reputable mixed billing practice in
north brisbane
Australia,Queensland
GP required for a permanent role in well-estab...

vr or non vr general practitioner -

whitsundays
Reveal Answer Australia,Queensland
An excellent opportunity has arisen in Whitsun ...
QRS alternans - due to AVNRT (i.e. electrical phenomenon), not pericardia! effusion as normal voltages.
perth - gp - permanent vr general
practitioner
More ECG Clinical Cases ... Australia,Western Australia
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About Edward Burns

Ed Burns is an Emergency Physician working in Prehospital & Retrieval
Medicine in Sydney, Australia. He has a passion for EGG interpretation and
 Case 72

Palpitations, chest heaviness

r~tJJJ)J~rlllffi~~r+H+

·~ . rrti~
Jiz ECG 072 - UTFL - Life in t ' X

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Australia,Oueensland
GP required for a permanent role in well-estab .. .

Reveal Answer vr or non vr general practitioner -

whitsundays
Australia,Oueensland
Rate-related ST change with SVT = not necessarily ischaemic. An excellent opportunity has arisen in Whitsun

Mimics appearance of LMCA occlusion. perth - gp - permanent vr general

practitioner
Australia,Western Australia
• Next ECG Charterhouse Medical are currently worKing in
• Previous ECG

~vocortex
• Back to menu
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About Edward Burns

Ed Burns is an Emergency Physician working in Prehospital & Retrieval
~l~icine in Sydney, Australia. He has a passion for ECG interpretation and
.W ndo s
'-"-'. ni~dica l education. Ed is the force behind the LITFL ECG library 1 + Edward
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