EKG Spot diagnosis

Pictures Findings and Diagnosis

• Left axis deviation
• Small Q waves with tall R waves
(= ‘qR complexes’) in leads I and aVL
• Small R waves with deep S waves
(= ‘rS complexes’) in leads II, III, aVF

Left Anterior Fascicular Block

• Right axis deviation

• Small R waves with deep S waves
(= ‘rS complexes‘) in leads I and aVL
• Small Q waves with tall R waves
(= ‘qR complexes‘) in leads II, III, aVF

Left Posterior Fascicular Block

• Coved ST segment elevation in V1-V3

followed by negative T wave

Brugada Type 1

• > 2mm of saddleback shaped ST

elevation in V1-V2

Brugada Type 2
• Normal sinus rhythm
• PR interval 260 ms

1st degree AV block

• The PR interval progressively increases

• 5 P waves : 4 QRS complexes
• P-P interval is relatively constant despite
the irregularity of the QRS complexes

2nd degree AV Block Mobitz I

• Intermittent non-conducted P waves

• No progressive prolongation of the PR
interval
• The PR interval remains constant
• The P waves constant rate

2nd degree AV Block Mobitz II

• 4 P waves : 1 QRS complexes

• Atrial rate is approximately 140 bpm.
• Ventricular rate is approximately 35

2nd degree AV Block Fixed Ratio 4:1

(High grade block);
High grade means> 3:1
• Atrial rate ~ 60 bpm.
• Ventricular rate ~ 27 bpm.
• None of the atrial impulses appear to be
conducted to the ventricles.
• There is a slow ventricular escape
rhythm

Complete Heart Block

Bidirectional ventricular tachycardia

• Large precordial voltages.

• Deep narrow Q waves < 40 ms wide in
the lateral leads I, aVL and V5-6

Classic HCM
• Large precordial voltages.
• Giant T inversions in precordial leads
• Inverted T waves are also seen in the
inferior and lateral leads.

Apical HCM

• Upsloping ST depression in the

precordial leads (> 1mm at J-point).
• Peaked anterior T waves (V2-6)
ascending limb of T commencing below
the isoelectric baseline
• Subtle ST elevation in aVR > 0.5mm.

De Winter T waves
• “sagging” ST segments and T waves
taking on the appearance of “Salvador
Dali’s moustache“.

Digoxin effect

• Marked shortening of the QT interval

(260ms).

Hypercalcaemia
• Osborn J waves

Severe hypercalcaemia

• Long PR segment
• Wide, bizarre QRS

Hyperkalaemia

• Tall, symmetrically peaked T waves

Hyperkalaemia
• Osborn J waves

Severe hypothermia

• Tachycardia (~ 110 bpm)

• Probably sinus tachycardia, with P
waves embedded in each T wave
• Broad QRS complexes (120 ms)
• Positive R’ wave in lead aVR

Tricyclic antidepressant
(or another sodium-channel blocking agent)

• Sinus tachycardia (~120 bpm)

• Low QRS voltages
• Electrical alternans ( alternating tall and
short QRS complexes)

Massive pericardial effusion

• ST elevation in aVR and V1 of similar

magnitude (V1>aVR)
• Widespread ST depression (V3-6, I, II,
III, aVF)

Proximal LAD occlusion

• ST horizontal / downsloping ST
depression in multiple leads (V3-6, I, II,
aVL)
• ST elevation in aVR > V1

LMCA/3VD

• There is concordant ST depression in

V2-5 (= Sgarbossa positive)
• The morphology in V2-5 is reminiscent
of posterior STEMI, with horizontal ST
depression and prominent upright T
waves

Positive Sgarbossa criteria in a patient

with a ventricular paced rhythm

• Sinus tachycardia
• Widespread concave STE and PR
depression (I, II, III, aVF, V4-6).
• Reciprocal ST depression and PR
elevation in V1 and aVR

Acute Pericarditis
• Sinus rhythm, very short PR (< 120 ms)
• Broad QRS complexes with delta wave
• Dominant R wave in V1 —bknown as
“Type A” WPW and is associated with
a left-sided accessory pathway
• Tall R waves and inverted T waves in
V1-3 mimicking right ventricular
hypertrophy — these changes are due
to WPW and do not indicate RVH
• Negative delta wave in aVL simulating
the Q waves of lateral infarction — this is
referred to “pseudo-infarction” pattern.

Type A” WPW
• Sinus rhythm with inverted T waves
• Prominent U waves
• Long QU
• A premature atrial complex lands on the
end of the T wave, causing ‘R on T’
phenomenon and initiating a paroxysm
of polymorphic VT
• Because of the preceding long QU
interval, this can be diagnosed as TdP.

TdP secondary to hypokalaemia

• Biphasic T waves in V2-3

Wellens Syndrome (Type A Pattern)

• Deep, symmetrical T wave inversions

throughout the anterolateral leads
(V1-6, I, aVL)

Wellens Syndrome (Type B Pattern)