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 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.
 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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