Seizure CVA

Toxic and Metabolic

Drugs (e.g. verapamil in patients with AF+WPW) Drug-induced QT prolongation with torsades de pointes Environmental

Electrical shocks, drowning, hypothermia Sepsis

Tension pneumothorax Pulmonary embolism Primary pulmonary hypertension Sleep apnoea Bronchospasm Aspiration

Myocardial ischemia / infarction Cardiomyopathy (dilated, hypertrophic, restrictive) Channelopathies e.g. Long QT (acquired / congenital) causing TdP –> VF and Brugada syndrome Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis)

Premature ventricular contractions (PVCs) ST changes R on T phenomenon Sinus pause QT prolongation Ventricular tachycardia Supraventricular arrhythmias Sinus tachycardia

Ventricular Tachycardia SVT with aberrant conduction due to bundle branch block SVT with aberrant conduction due to the pre-excitation syndromes Pace-maker mediated tachycardia Metabolic derangements e.g. hyperkalaemia Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants)

Occurs due to early or late after-depolarisations Examples include Torsades de Pointes and digitalis toxicity

Monomorphic Polymorphic VT Torsades De Pointes (Polymorphic with QT prolongation) Right Ventricular Outflow Tract Tachycardia Fascicular Tachycardia Bidirectional VT Ventricular Flutter Ventricular Fibrillation (VF)

Ischaemic Heart Disease Dilated cardiomyopathy Hypertrophic cardiomyopathy Chaga’s Disease

Severe sinus bradycardia Sinus arrest Sino-atrial exit block High-grade second degree AV block Third degree AV block Hyperkalaemia Drugs: beta-blocker, calcium-channel blocker or digoxin poisoning

Digoxin toxicity (= the classic cause of AJR) Beta-agonists, e.g. isoprenaline, adrenaline Myocardial ischaemia Myocarditis Cardiac surgery

Severe sinus bradycardia Sinus arrest Sino-atrial exit block High-grade second degree AV block Third degree AV block Hyperkalaemia Drugs: beta-blocker, calcium-channel blocker or digoxin poisoning

Ischaemic heart disease Hypertension Valvular heart disease (esp. mitral stenosis / regurgitation) Acute infections Electrolyte disturbance (hypokalaemia, hypomagnesaemia) Thyrotoxicosis Drugs (e.g. sympathomimetics) Alcohol Pulmonary embolus Pericardial disease Acid-base disturbance Pre-excitation syndromes Cardiomyopathies: dilated, hypertrophic. Phaeochromocytoma

Anxiety Sympathomimetics Beta-agonists Excess caffeine Hypokalaemia Hypomagnesaemia Digoxin toxicity Myocardial ischemia

PVCs arising from the right ventricle have a left bundle branch block morphology (dominant S wave in V1) PVCs arising from the left ventricle have a right bundle branch block morphology (dominant R wave in V1)

Anxiety Sympathomimetics Beta-agonists Excess caffeine Hypokalaemia Hypomagnesaemia Digoxin toxicity Myocardial ischaemia

Sick sinus syndrome Increased vagal tone (athletes) Vagal stimulation (surgery, pain) Inferior myocardial infarction Myocarditis Drugs: digoxin, beta-blockers, calcium channel blockers, amiodarone

Ventricular tachycardia Accelerated idioventricular rhythm Ventricular escape rhythm Ventricular-paced rhythm

Brugada syndrome – localised QRS widening in V1-2 with RBBB morphology. Arrhythmogenic right ventricular dysplasia (AVRD) – localised QRS widening in V1-2 plus epsilon waves and variable signs of right ventricular hypertrophy

Wolff-Parkinson-White syndrome – wide QRS plus delta waves.

Sodium-channel blocker toxicity (e.g. TCA overdose) – wide QRS plus positive R’ wave in aVR.

Hyperkalaemia

Left ventricular hypertrophy Right ventricular hypertrophy Biventricular enlargement Dilated cardiomyopathy

Left anterior fascicular block Left posterior fascicular block Left bundle branch block Right bundle branch block Bifascicular block Trifascicular block

Hyperkalaemia Tricyclic antidepressant poisoning.

Ischaemic heart disease (40-60%) Structural heart disease (50-80% association) Aortic stenosis Anterior MI Lenègre-Lev disease Congenital heart disease Hyperkalaemia (resolves with treatment) Digoxin toxicity

Ischaemic heart disease (40-60% cases) Structural heart disease (50-80% association) Aortic stenosis Anterior MI (occurs in 5-7% of acute AMI) Lenègre-Lev disease Congenital heart disease Hyperkalaemia (resolves with treatment)

Right axis deviation (RAD) (> +90 degrees) rS complexes in leads I and aVL qR complexes in leads II, III and aVF Prolonged R wave peak time in aVF

Left axis deviation (usually -45 to -90 degrees) qR complexes in leads I, aVL rS complexes in leads II, III, aVF Prolonged R wave peak time in aVL > 45ms

Right ventricular hypertrophy / cor pulmonale Pulmonary embolus Ischaemic heart disease Rheumatic heart disease Congenital heart disease (e.g. atrial septal defect) Myocarditis Cardiomyopathy Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting system

Aortic stenosis Ischaemic heart disease Hypertension Dilated cardiomyopathy Anterior MI Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting system Hyperkalaemia Digoxin toxicity

Inferior myocardial infarction AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin) Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease), causing true trifascicular block

Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone Increased vagal tone (e.g. athletes) Inferior MI Myocarditis Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair

Increased vagal tone Athletic training Inferior MI Mitral valve surgery Myocarditis (e.g. Lyme disease) Electrolyte disturbances (e.g. Hyperkalaemia) AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone) May be a normal variant

PR interval > 200ms (five small squares)

Inappropriate Sinus Tachycardia

Regular Atrial

Sinus tachycardia Atrial tachycardia Atrial flutter Inappropriate sinus tachycardia Sinus node reentrant tachycardia Irregular Atrial

Atrial fibrillation Atrial flutter (variable block) Multifocal atrial tachycardia Regular Atrioventricular

AVRT AVNRT Automatic junctional tachycardia

Drugs e.g. digoxin, beta-blockers, calcium channel blockers. Autonomic dysfunction. Hypothyroidism. Electrolyte abnormalitites — e.g. hyperkalaemia

Exercise Pain Anxiety Hypovolaemia Hypoxia, hypercarbia Acidaemia Sepsis, pyrexia Anaemia Pulmonary embolism Cardiac tamponade Hyperthyroidism Alcohol withdrawal

Sinus bradycardia may be indistinguishable from type II sino-atrial block

Beta-blockers Calcium-channel blockers (verapamil & diltiazem) Digoxin Central alpha-2 agonists (clonidine & dexmedetomidine) Amiodarone Opiates GABA-ergic agents (barbiturates, benzodiazepines, baclofen, GHB) Organophosphate poisoning

Normal during sleep Increased vagal tone (e.g. athletes) Vagal stimulation (e.g. pain) Inferior myocardial infarction Sinus node disease Hypothyroidism Hypothermia Anorexia nervosa Electrolyte abnormalities – hyperkalaemia, hypermagnesaemia Brainstem herniation (the Cushing reflex) Myocarditis

Frequent premature atrial contractions Second-degree AV block, Mobitz I (Wenckebach phenomenon) Type I Sinoatrial Exit Block

Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children) Each QRS complex is preceded by a normal P wave Normal P wave axis: P waves upright in leads I and II, inverted in aVR The PR interval remains constant QRS complexes < 100 ms wide (unless co-existent interventricular conduction delay present

Pulmonary hypertension Mitral stenosis Pulmonary embolism Chronic lung disease (cor pulmonale) Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis) Arrhythmogenic right ventricular dysplasia (ARVD)

Right axis deviation Dominant R wave in V1 Dominant S wave in V5 or V6

Pulmonary hypertension Mitral stenosis Pulmonary embolism Chronic lung disease (cor pulmonale) Congenital heart disease (e.g. Tetralogy of Fallot, pulmonary stenosis) Arrhythmogenic right ventricular cardiomyopathy

Right bundle branch block (complete or incomplete

Right bundle branch block produces an RSR’ pattern in V1 and deep slurred S waves in the lateral leads. Left bundle branch block produces a dominant S wave in V1 with broad, notched R waves and absent Q waves in the lateral leads. Hyperkalaemia is associated with a range of abnormalities including peaked T waves Tricyclic poisoning is associated with sinus tachycardia and tall R’ wave in aVR Wolff-Parkinson White syndrome is characterised by a short PR interval and delta waves Ventricular pacing will usually have visible pacing spikes Hypothermia is associated with bradycardia, long QT, Osborn waves and shivering artefact

Bundle branch block (RBBB or LBBB) Hyperkalaemia Poisoning with sodium-channel blocking agents (e.g. tricyclic antidepressants) Pre-excitation (i.e. Wolff-Parkinson-White syndrome) Ventricular pacing Hypothermia Intermittent aberrancy (e.g. rate-related aberrancy

Myocardial ischaemia / NSTEMI Reciprocal change in STEMIPosterior MI Digoxin effect Hypokalaemia Supraventricular tachycardia Right bundle branch block Right ventricular hypertrophy Left bundle branch block Left ventricular hypertrophy Ventricular paced rhythm

Pulmonary embolism and acute cor pulmonale (usually in lead III) Acute aortic dissection (classically causes inferior STEMI due to RCA dissection) Hyperkalaemia Sodium-channel blocking drugs (secondary to QRS widening) J-waves (hypothermia, hypercalcaemia) Following electrical cardioversion Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease

Acute myocardial infarction Coronary vasospasm (Printzmetal’s angina) Pericarditis Benign early repolarization Left bundle branch block Left ventricular hypertrophy Ventricular aneurysm Brugada syndrome Ventricular paced rhythm Raised intracranial pressure Takotsubo Cardiomyopathy

Hypocalcaemia Hypomagnesaemia Hypothermia Raised intracranial pressure Left ventricular hypertrophy Hypertrophic cardiomyopathy

Bradycardia Severe hypokalaemia.

Hypertrophic Cardiomyopathy is associated with deep T wave inversions in all the precordial lead

Poisoning with sodium-channel blocking drugs (e.g. TCAs) Dextrocardia Incorrect lead placement (left/right arm leads reversed) Commonly elevated in ventricular tachycardia (VT)

Causes of Dominant R wave in V1

Normal in children and young adults Right Ventricular Hypertrophy (RVH) Pulmonary Embolus Persistence of infantile pattern Left to right shunt Right Bundle Branch Block (RBBB) Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9) Wolff-Parkinson-White (WPW) Type A Incorrect lead placement (e.g. V1 and V3 reversed) Dextrocardia Hypertrophic cardiomyopathy Dystrophy Myotonic dystrophy Duchenne Muscular dystrophy

(1) PR interval

The PR interval is normally between 0.12-0.20 seconds (3-5 small squares). A prolonged or changing (esp lengthening) PR interval indicates heart block. Shortened PR intervals can be because of WPW or LGL syndromes, or a junctional rhythm. (2) QRS width (“QRS-interval”)

The QRS-interval is normally less than 0.12 seconds (3 small squares). A widened QRS width indicates some sort of conduction defect with the left or right bundle branches. (3) ST segment (“ST-interval”)

This is probably the most important thing to look at. …then look at it a 2nd and 3rd time. Look for sloping (especially downsloping) or flattening of the ST segments. (4) QT interval

The QT interval is the time from the start of the Q wave to the end of the T wave

(1) P wave

Lead II is usually the best lead place to look at the P wave morphology. Observe the P-wave morphology e.g. in particular P pulmonale or P mitrale. (2) QRS complexes (or QRS “waves”)

Look in ALL leads for the presence of Q waves. Observe the QRS amplitude and look for QRS progression through the chest leads. (3) T waves

Look in ALL leads for T waves. Look for T wave inversion, T wave concordance or discordance with QRS and the presence of T wave flattening. (4) U waves

Are U waves present or not?

Extreme Axis Deviation

Ventricular rhythms – e.g.VT, AIVR, ventricular ectopy Hyperkalaemia Severe right ventricular hypertrophy

. Right Axis Deviation

Right ventricular hypertrophy Acute right ventricular strain, e.g. due to pulmonary embolism Lateral STEMI Chronic lung disease, e.g. COPD Hyperkalaemia Sodium-channel blockade, e.g. TCA poisoning Wolff-Parkinson-White syndrome Dextrocardia Ventricular ectopy Secundum ASD – rSR’ pattern Normal paediatric ECG Left posterior fascicular block – diagnosis of exclusion Vertically orientated heart – tall, thin patient Left Axis Deviation

Left ventricular hypertrophy Left bundle branch block Inferior MI Ventricular pacing /ectopy Wolff-Parkinson-White Syndrome Primum ASD – rSR’ pattern Left anterior fascicular block – diagnosis of exclusion Horizontally orientated heart – short, squat patient

P WAVES ABSENT

Narrow complex: Junctional escape rhythm Broad complex: Ventricular escape rhythm

1. Not every P wave is followed by a QRS complex (= AV node dysfunction)

AV block: 2nd degree, Mobitz I (Wenckebach) AV block: 2nd degree, Mobitz II (Hay) AV block: 2nd degree, “fixed ratio blocks” (2:1, 3:1) AV block: 2nd degree, “high grade AV block” AV block: 3rd degree (complete heart block)

1. Every P wave is followed by a QRS complex (= sinus node dysfunction)

Sinus bradycardia Sinus node exit block Sinus pause / arrest

IRREGULAR

Ventricular fibrillation Polymorphic VT Torsades de Pointes AF with Wolff-Parkinson-White syndrome Any irregular supraventricular tachycardia with aberrant conduction — e.g. due to bundle branch block, rate-related aberrancy.

REGULAR BCT

Ventricular tachycardia Antidromic atrioventricular re-entry tachycardia (AVRT). Any regular supraventricular tachycardia with aberrant conduction — e.g. due to bundle branch block, rate-related aberrancy.

ATRIOVENTRICULAR

Atrioventricular re-entry tachycardia (AVRT) AV nodal re-entry tachycardia (AVNRT) Automatic junctional tachycardia

ATRIAL – IRREGULAR

Atrial fibrillation Atrial flutter with variable block Multifocal atrial tachycardia

ATRIAL – REGULAR

Sinus tachycardia Atrial tachycardia Atrial flutter Inappropriate sinus tachycardia Sinus node re-entrant tachycardia