The ECG is one of the most common investigations in the ED and one of the most useful diagnostic tools. Recognising what appears 'different' or atypical or unusual is problematic as variations occur due to physical training and ethnic variations and some drugs cause changes which are consequential vs dangerous.

• P wave
• PR interval
• QRS
• QTc interval
• ST seg
• T waves
• Other waves
• ECG axis

P wave
peaked P	• R atrial hypertrophy eg. Pulmonary hypertension, tricuspid stenosis
broad and bifid P	• L atrial hypertrophy eg. Mitral stenosis

PR interval
1O HB	• >200ms, may be normal variant • hyperkalaemia, ↑vagal tone, drugs, myocarditis • no Rx required
2O HB	Mobitz I, (Wenckebach) • progressive prolongation of PR until non-conducted P • assoc with some drugs eg β blockers, Ca blockers, Digoxin • usually benign
2O HB	Mobitz II (Hay block) • intermittent non-conducted P waves • PP remains constant • RR constant multiple • structural damage
WPW	• short PR, delta wave
LGL	• short PR, narrow QRS, ?real diagnosis
PR segment	• depression or elevation associated with MI indicates atrial involvement and carries a poor prognosis • suggests atrial ischaemia/infarction

QRS complex
LBBB	• QRS>120ms • dominant S-V1, broad R-V6 • Sgarbossa criteria for STEMI with LBBB
RBBB	• QRS>120ms • RSR' V1-3; wide, slurred S lat leads • does not affect MI interpretation criteria
Epsilon wave	• small positive deflection (‘blip’ or ‘wiggle’) buried in the end of QRS complex. • caused by post-excitation of the myocytes of RV • also described in post MI; RV infarction; infiltration disease, and sarcoidosis. • the most characteristic finding in arrhythmogenic RV dysplasia (ARVD/C)
Hyperkalaemia	• The only condition that causes the QRS complex to be ≥ 0.24 sec is hyperkalemia • regardless of the rhythm or the presence of an underlying intraventricular conduction delay • the hyperacute T waves are also consistent with hyperkalemia

QTc interval
Long QT syndrome	• QT>450ms • life threatening

Causes of long QT

• Hypokalaemia.
• Hypomagnesaemia.
• Hypocalcaemia.
• Hypothermia.
• Myocardial ischemia.
• ROSC Post-cardiac arrest.
• Raised intracranial pressure.
• Congenital long QT syndrome.

Drug related causes of long QTc

many drugs are associated with long QTc but some common ones include:

anti-arrhythmics	amiodarone, disopyramide, procainamide, quinidine, sotalol, dofetilide, ibutilide
anti-psychotics	chlorpromazine, clozapine, haloperidol, quetiapine, risperidone, thioridazine
anti-depressants	amitryptiline, citalopram, desipramine, doxepin, fluoxetine, impramine, nortriptyline, paroxetine, sertraline, venlafaxine
anti-emetics	ondansetron, prochlorperazine
antibiotics	azithromycin, ciprofloxacin, clarithromycin, erythromycin, fluconazole, ketoconazole, levofloxacin, moxifloxacin, ofloxacin, trimethroprim

ST segment
ST depression	• usually needs to horizontal or downsloping to be relevant • ≥0.5mm at J pt in ≥2 contiguous leads suggests ischaemia • greater depression → worse prognosis • upsloping ST depression with de Winter T waves = highly specific for LAD occlusion • upsloping ST depression = non-specific
ST elevation	• MI - can be convex, concave or obliquely upsloping. Usually with reciprocal ST depression in electrically opposite leads • pericarditis, Benign Early repolarisation, LBBB, LVH & Brugada
	subtle ant MI vs normal variant ST elevation
Brugada Syndrome	• Coved ST: V1-V3 • tendency to VF
Early repolarisation	• ST sharply rising, usually concave upwards with large symmetrical T • present in ≤50% Caucasian athletes and ≤90% Afro-Caribbean athletes • T amplitude should be >4x ST elevation
Pericarditis	• ST concave upwards in most leads except aVR • no reciprocal ST depression except aVR

T waves
peaked T waves	• hyperkalaemia • normal variant • occasionally ischaemia • hypertrophy • in general, T changes are non-specific and therefore best assessed 'in context'
Wellens Syndrome	• deeply inverted (most common) or biphasic T in V1,2 • impending extensive MI with LAD occlusion
de Winter T waves	• rare - ~2% prox LAD occlusions • upsloping ST depression in precordial leads • peaked symmetrical T waves starting from below isoelectric baseline • subtle ST elevation aVR - may appear later • highly predictive of acute LAD occlusion

inverted T waves

• inverted T waves is a normal finding in leads III, aVR, aVL, and V1 in adults • T waves changes are grouped into lead groups: anterior (V2, V3, V4), lateral (I, aVL, V5, V6), and inferior (II, aVF) • Lateral T-wave inversion is associated with increased risk of mortality and CHD. T-wave inversion in anterior lead group is independently associated with the risk of CHD, but not mortality. T-wave inversion in the inferior lead group probably benign. Prognostic Sig of T inversion 2021 • Global inversion refers to T inversion in all std leads except aVR. Seen in: • L main coronary artery or equivalent MI • Takotsubo cardiomyopathy • Kounis syndromeclose simultaneous appearance of ACS with anaphylaxis or anaphylactoid reaction. Probably secondary to vasospastic mediators released during such allergic and hypersensitivity reactions https://www.medintensiva.org/en-kounis-syndrome-articulo-S2173572712000872 • apical hypertrophic cardiomyopathy • acute pericarditis • acute cerebrovascular event, electrolyte abnormalities, phaeochromocytoma • pulmonary embolism, and pulmonary edema The significance of inverted T waves beyond V1,2 is debatable. Inf/lat does requires Ix. Consider: • ARVD • congenital coronary micro-fistulae and other cardiomyopathies • T inversion cases

other waves
Q	• QS complex in V1 is normal
U	• same direction as T wave • prominent U seen with ↓(Mg, Ca, K, temp) • <25% of T wave height • inverted usually related to myocardial ischaemia
J	hypothermia

using isoelectric method find lead with equal +ve and -ve QRS deflection axis is 90deg to that lead in the direction of the lead with greatest +ve
R axis deviation	QRS is POSITIVE (dominant R wave) in Lead II, Lead III and aVF RS is NEGATIVE (dominant S wave) in Lead I
L axis deviation	QRS is POSITIVE (dominant R wave) in Lead I QRS is NEGATIVE (dominant S wave) in leads II, III and aVF

• a combination of the presence of a congenital accessory pathway and episodes of tachyarrhythmia
• associated small risk of sudden death

presentation can be varied, with variation depending also on age:

• chest pain, palpitations, SOB
• irritability, pallor
• exercise intolerance

• PR interval <120ms
• Delta wave – slurring slow rise of initial portion of the QRS
• QRS prolongation >110ms
• ST, T wave discordant changes – i.e. in the opposite direction to the major component of the QRS complex

• a pre-excitation rhythm
• in the setting of tachycardia normal/narrow complex QRS with short PR interval (<0.12s) - there is no Delta wave seen in WPW
• no increased mortality risk
• some suggestion that this is not really a syndrome at all.

• Intermittent non-conducted P waves without progressive prolongation of the PR interval
• PP interval remains constant while RR maintains constant multiple
• usually as a result of structural damage vs Mobitz I which is more functional (drugs, vagal tone etc)
  • MI, fibrosis, inflammatory and autoimmune destruction
• more likely to become haemodynamically unstable, severe brady and progress to Complete Heart Block
• risk of asystole 35% per year

• A pattern of deeply inverted or biphasic T waves in V2-3. Unusually, and atypically, the ECG changes appear after pain has resolved
• may be pain free at time ECG is taken and have normally or minimally elevated cardiac enzymes
• extremely high risk for extensive anterior wall MI within the next few days to weeks.

Diagnostic criteria:

• Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6)
• Isoelectric or minimally-elevated ST segment (< 1mm)
• No precordial Q waves
• Preserved precordial R wave progression
• Recent history of angina
• ECG pattern present in pain-free state
• Normal or slightly elevated serum cardiac markers

Two patterns of T-wave abnormality in Wellens syndrome:

• Type A – Biphasic, with initial positivity and terminal negativity (25% of cases)
• Type B – Deeply and symmetrically inverted (75% of cases)

Type A

Type B

Left Ventricular Hypertrophy ECG Criteria

References include:
https://litfl.com/pre-excitation-syndromes-ecg-library/
https://rebelem.com/five-ecg-patterns-you-must-know/
BMJ ECG danger
BMJ - international criteria for ECGs in athletes 2017
https://reference.medscape.com/features/slideshow/ecgs-life-threatening#page=1
https://litfl.com/killer-ecg-patterns/
https://www.aliem.com/cant-miss-ecg-findings/
Circulation: Arrhythmia and electrophysiology 2012
Early repolarisation syndrome - cause of sudden death 2015
https://litfl.com/benign-early-repolarisation-ecg-library/
Healio: LVH review
ECG blog
4th universal definition of Myocardial infarction 2018
Heart Rhythm J: variability of Epsilon wave assessment review 2016
World J Cardiol: cardiac and non cardiac causes of T wave inversion
Euro Heart J suppl. Inverted T waves - when to worry
Medscape ECG challenge - hyperkalaemia