ECG interpretation

Leads

• Bipolar – I, II, III
  • Measure difference between two leads expressed in Einthoven’s triangle
  • Detect electrical forces in frontal plane
• Augmented unipolar leads – aVF, aVL, aVR
  • Compare lead potential with centrepoint of Einthoven’s triangle
  • Augmented to increase amplitude
• Praecordial leads
  • Detect electrical forces in horizontal plane

Lead misplacement

• V leads
  • Minor displacement of V leads of minimal significance
  • If V1/2 too high – Inverted p wave in V2
  • Swapping of V leads results in interruption of normal R wave progression from V1-6
• Limb leads
  • Results in significant axis changes
  • Reversal of RA and LA
    • Most common
    • Negative p wave and negative QRS in I
    • Extreme axis deviation
    • Upright p wave and QRS in aVR
  • Reversal of RA and LL
    • All leads upside down except aVL
  • Reversal of RL with any other lead
    • Flat line in one of the limb leads
  • Reversal of LA and LL
    • Not easily recognisable
    • Consider if unexplained dynamic changes compared to old ECG

Normal ECG

• T wave
  • Normally inverted or flat in v1 and aVR
  • Inversion in V1-3 occurs in 0.5% of normal Caucasians and has no significance if no associated ST changes
• U wave
  • Due to slow repolarisation of papillary muscles

Normal conduction system

• SA node
  • At junction of SVC and right atrium
  • Sinus node artery off RCA in 55% and left circumflex in 45%
  • Normal rate 60-100
• Anterior, middle and posterior internodal tracts
• AV node
  • Under surface of right atrial endocardium
  • RCA supply in 90% and left circumflex in 10% (hence common AV nodal block in inferior MI)
  • Junctional escape rhythms will occur from cells around the AV node with automaticity at sinus rates <60 (escape rate 40-60)
• Bundle of His (made up of Purkinje fibres)
• RBBB and LBBB with left dividing into left anterior superior fascicle and left posterior inferior fascicle

Normal ECG

• Sinus rhythm (every QRS preceded by P wave)
• Rate 60-100bpm (300/RR interval)
• Axis -30 to +90
• PR interval 0.12-0.20s (start of P to start of QRS)
• QRS <0.10s (>0.12s required for BBB or ventricular rhythm diagnosis – LITFL)
• Bazett’s QTc = QT/(sq.r R-R)
  • Include large incorporated U waves
  • Exclude separate U waves
  • Should be <0.44s in men and 0.46s in women. If >0.50s = increased risk of TdeP

Measuring the QT

• Measure in Lead II or V5/6
• Maximal interval used from successive beats
• Large U waves >1mm fused to T wave should be included
• Maximum slope method used to define end of T wave
• Bazett’s overcorrects at HR >100 and undercorrects at HR <60
• If QRS >0.12s, subtract (QRS – 0.12) from QT

QT nomogram

• Utilised to ascertain risk of TdeP in drug-induced states
• If plotted above line = risk of TdeP
• 97% sensitive for predicting TdeP in poisoning; 99% specific

Left axis deviation

• > -30 degrees
• LVH, LAFB, Inferior AMI, WPW (mimics inferior MI), pregnancy, elderly, paced rhythm

Right axis deviation

• > 90 to 120 degrees
• RBBB
• PE
• Cor pulmonale
• LPFB
• RVH
• Lateral MI
• WPW
• Dextrocardia

Wide QRS

• >120ms
• BBB
• Hyperkalaemia
• Sodium channel blockade
• Accessory pathway
• Profound hypothermia

Mechanisms of conduction disturbance

• Bradyarrhythmia
  • Depression of sinus nodal activity or conduction system blocks with subsequent subsidiary pacemaker cells taking over at slower rates than sinus node
• Tachyarrhythmia
  • 1) Increased automaticity in normal or ectopic site
  • 2) Re-entry in a normal or accessory pathway
  • 3) After depolarisations causing triggered rhythms

Increased automaticity

• Ectopic pacemakers can be due to:
  • Increased automaticity of subsidiary pacemaker cells i.e. accelerated junctional escape rhythm OR
  • Abnormal automaticity of myocardial cells that do not normally have pacemaking activity
• Either way, tends to be gradual in onset and termination vs. re-entry abrupt

Re-entry arrhythmias

• Requires delayed conduction with subsequent depolarisation reaching initial limb once refractory period complete
• Can be around anatomically defined circuit e.g. AVRT/AVNRT or may be disorganised through a syncytium of myocardial tissue e.g. AF or VF

Triggered arrhythmias

• Due to oscillations of transmembrane potential during or after repolarisation (afterpotentials)
• At specific rates, afterpotentials may reach threshold causing complete depolarisation (afterdepolarisation), which may then be self-sustaining
• Triggered arrhythmias associated with early afterpotentials are enhanced by slow heart rates while those associated with late afterpotentials are enhanced by rapid heart rates

ECG Rhythms

• Rate
• Pattern – Regular, irregular (regularly or irregularly)
• Narrow or wide
• P waves absent or present
  • Sinus p waves must be upright in I,II and aVF and inverted in aVR
  • Retrograde p waves are always inverted in inferior leads as the vector is from the AV junction upwards
• AV association, dissociation or intermittent
• Abrupt or gradual onset
  • Abrupt – Re-entrant vs. Gradual – Automaticity
• Response to vagal manoeuvre
  • Sinus tachy, ectopic atrial tachycardia – gradual slowing but resumes
  • AVNRT or AVRT – Abrupt stop or no effect
  • AF or flutter – Gradual slowing
  • VT – No response

Sinus node and atria

Sinus node physiology

• P wave morphology can change with sinus arrhythmia
  • At fast rates the P wave in inferior leads is taller and the PR interval longer as the pacemaker is higher in the sinus node
  • At slow rates, the P wave in inferior leads is shorter and PR interval shorter as the pacemaker is higher toward the tail of the sinus node
  • As long as the pacemaker is within the sinus node, the P waves will be upright in I, II, V5 and V6
  • In reality, changes in P wave morphology may be due to shift of pacemaker within sinus node, differences in atrial propagation or respiratory variations, making the term ‘wandering atrial pacemaker’ not useful
• Sinus arrhythmia
  • PP interval varies >0.16s
  • May be respiratory driven (normal) or non-respiratory-driven (often associated with heart disease in the elderly)
  • Ventriculophasic sinus arrhythmia
    • Patients with AV block show have shorter PP intervals when they contain a QRS complex

Sinus node dysfunction

• Intrinsic causes
  • Idiopathic fibrosis
  • Ischaemia
  • Cardiomyopathy
  • Infiltrative e.g. sarcoidosis/amyloidosis
  • Congenital
• Extrinsic causes
  • Drugs (e.g. Dig, CCB, Beta-blocker)
  • Autonomic dysfunction
  • Hypothyroidism
  • Hyperkalaemia

• ECG changes
  • Can be variable and intermittent
  • Usually ventricular rate is slow
  • Sinus bradycardia
  • Sinus arrhythmia
  • Sinoatrial exit block
  • Sinus pauses
  • Sinus arrest (pause >3 sec)
  • AF with slow ventricular response
  • Tachy-brady syndrome
• Sinus bradycardia
  • Clinically significant if <50/min
  • If <40/min consider sinoatrial block
  • Common in acute inferior MI
• Sinus node extrasystoles
  • P wave morphology unchanged
  • Post-extrasystolic interval is equal to the sinus cycle
• Sinus node reentry and reentrant tachycardia
  • Abrupt onset and offset sinus tachycardia
  • Not a manifestation of sinus node dysfunction as such
• Sinus pause and arrest
  • Result of transient failure of impulse formation or propagation from sinus node
  • Sinus arrest is a pause >3 seconds
  • Differential
    • SA block – Will show a long cycle that is a multiple of the baseline PP interval
    • Sinus arrhythmia – Lengthening of the PP interval is gradual and phasic
    • Blocked PAC – Usually seen as distortions of previous T wave
    • Suppression of sinus activity after conducted premature complexes
    • Overdrive suppression after ectopic tachycardia

• Sinoatrial exit block
  • The sinoatrial node continues to depolarise normally
  • Some sinus impulses are blocked leading to intermittent failure of atrial depolarisation (dropped P waves)
  • The relationship between impulse generation and transmission must be inferred from the P-P interval
  • First-degree SA block
    • Not detectable on ECG
  • Second-degree, type I (Wenckebach)
    • Progressive lengthening of interval between impulse generation and transmission until failure of transmission occurs
    • Successive P waves get closer together as the transmission intervals lengthens
    • Get clumping of P-QRS complexes with pauses at the end of each group
    • Easily mistaken for sinus arrhythmia due to the clumping then pause pattern
  • Second-degree, type II block
    • Intermittent dropped P waves with constant interval between impulse generation and transmission
    • No clustering of P-QRS
    • The pause surrounding a dropped P wave is an exact multiple of the preceding P-P interval
  • Third-degree SA block
    • Complete absence of P waves
    • Rhythm often maintained by junctional escape but NOT always
    • Indistinguishable from sinus arrest
  • SA block is often accompanied by escape rhythms from subsidiary foci
    • When the sinus rhythm is slightly slower than the AV junctional escape rhythm, a bigeminal rhythm known as ‘escape capture bigeminy’ can occur

Sick sinus syndrome

• Types
  • Persistent, severe, unexplained sinus bradycardia
  • Sinus arrest, brief or sustained, with an escape atrial or AV junctional rhythm
  • Prolonged sinus arrest with failure of subsidiary pacemaker -> Total cardiac asystole
  • Chronic AF with slow ventricular response not due to medications
  • Inability of the heart to resume sinus rhythm post-cardioversion for AF
  • Tachy-brady syndrome
• Tachy-brady
  • Conglomerate of multiple arrhythmias and responses to these
  • Tachycardia may be paroxysmal nodal reentry or AF commonly
  • Mechanisms
    • Tachycardia initiated by bradycardia
      • e.g. AV junctional or atrial ectopic during sinus pause is transmitted retrogradely to atria resulting in reciprocating AV nodal tachycardia
    • Bradycardia initiated by tachycardia
      • Long pauses commonly seen after SVT, A flutter or A fib due to depression of sinus node pacemaker and concomitant failure of escape pacemakers
    • Brady- and tachycardia resulting from common mechanism
      • Drugs e.g. digoxin, electrolyte disturbance, endocrine
    • Coexisting brady- and tachycardia from unrelated mechanisms

Premature atrial impulses

• Premature atrial complexes
  • Arise from ectopic foci in the atria
  • P wave morphology differs from sinus P waves
  • May be early, superimposed on ventricular complex or may be late occurring just before the next sinus impulse (can result in atrial fusion complexes)
  • May be unifocal or multifocal
  • May appear at random intervals or after 1-3 sinus complexes (bigeminal/trigeminal/quadrigeminal)
  • If near to AV junction, P wave is inverted in inferior leads
  • Generally the QRS morphology is unchanged, but not uncommonly it will show a RBBB pattern owing to the relatively longer refractory period of the right bundle branch
• Post-extrasystolic pauses
  • The ectopic atrial impulses that reach the SA node will reset it -> Cycle length longer than basic sinus cycle
  • Not usually fully compensatory (unlike PVC’s)

Ectopic atrial rhythm

• Atrial rate <100/min with normal PR and abnormal P wave morphology

Accelerated atrial rhythm

• Atrial rate faster than normal sinus rate for patient but still <110

Automatic ectopic atrial tachycardia

• May be transient, recurrent, sustained (>30s) or incessant
• Often arise during sinus bradycardia
• Most common type of paroxysmal supraventricular arrhythmia
• Also known as benign slow paroxysmal atrial tachycardia as tends to be <150/min
• In patients with recurrent automatic atrial tachycardias, the tachycardia is usually initiated by a late atrial premature impulse during sinus rhythm with a normal PR interval
• P waves remain visible throughout
• DO not respond to vagal stimulation but 80% respond to adenosine
• The PR interval can lengthen owing to incomplete AV node recovery in a rapid atrial rate
  • In extreme cases this results in PAT with block
• The P wave morphology remains the same from the initiated atrial ectopic complex throughout the tachycardia
• Illustrates ‘warm-up’ where PP interval gets shorter with time

Intra-atrial reentry tachycardia

• Requires two functionally distinct pathways with different conduction velocities and refractory periods within the atria
• The tachycardia is induced by a PAC but then the P wave morphology changes during the tachycardia
• Does not show ‘warm-up’ phenomenon

Paroxysmal atrial tachycardia with block

• Increased automaticity of an ectopic atrial focus associated with impaired AV conduction
• Often mistaken for AV nodal reentrant tachycardia, atrial tachycardia without block or sinus tachycardia owing to P waves often being superimposed on ventricular complexes
• If the block is variable, the irregular ventricular rhythm is often mistaken for AF
• Atrial flutter resembles this the most
  • A flutter is NOT caused by digoxin toxicity, while PAT with block IS
  • The atrial rate in A flutter is usually >250/min unlike PAT with block (atrial rate normally 150-250)

Non-conducted P waves

• Differential
  • Blocked premature atrial complex (PAC)
    • Lonely P wave occurs earlier than it should
  • Mobitz I
    • Regular P-P interval with prolonging P-R
  • Mobitz II
    • Regular P-P interval with regular P-R interval
  • Complete heart block/3rd degree
    • Regular P-P interval with random P-R interval

AV node

Conduction block

• Can be divided into nodal and infranodal block
• AV nodal blocks are usually due to reversible depression of conduction, self-limited and have a stable infranodal escape pacemaker
  • Good prognosis
• AV infranodal blocks are usually due to organic disease of the conducting system, with irreversible damage
  • Generally slow, unstable ventricular escape rhythm with serious prognosis

Conduction block

• First degree AV block: PR >0.20s
  • Causes: Increased vagal tone, athletic, inferior MI, hypokalaemia, AV node blockers (beta-blockers, CCB, dig, amiodarone), rheumatic heart disease, infective endocarditis
  • No difference in mortality if no organic heart disease
• Second degree AV block
  • Mobitz I (Wenckebach): Progressive prolongation. Same causes as above but usually benign. Normal property of cardiac tissue
    • Usually transient and seen in acute inferior MI, digoxin toxicity, myocarditis or after cardiac surgery
    • Most common block in AMI (and portends bad prognosis)
    • Ratios can be variable. If always 2:1 cannot tell Mobitz I or II
  • Mobitz II: P waves march through with intermittent non-conducted ones
    • Typically have pre-existing LBBB or bifascicular block with subsequent failure of third fascicle) 
    • Typically structural problem and causes include anterior MI (septal), fibrosis, cardiac surgery, rheumatic fever, SLE, amyloid, hyperkalaemia and nodal blocking drugs)
    • Typically wide QRS due to infranodal escape rhythm
    • If 2:1 cannot differentiate between Mobitz Type I and II but if QRS is wide, more likely infranodal block
    • If QRS narrow (Bundle of His origin) indicates more severe disease

Conduction block

• Advanced (high-grade) second-degree AV block
  • 3:1 or greater. If narrow QRS = Type I = Nodal block (20-25%). If broad QRS = Type II = Infranodal block (75-80%
• Complete AV block – Can be end point of Mobitz I or II. Causes include inferior MI and AV nodal blocking drugs
  • Can have nodal or infranodal complete block with narrow or wide QRS complex accordingly
  • Junctional escape usually 40-60/min; Ventricular escape usually 20-40/min
  • Most common ‘unstable’ rhythm in AMI

Risk

• Risk of complete HB in MI
  • 1 point for each:
    • First-degree AV block
    • Mobitz type I 2^nd degree HB
    • Mobitz type 2 2^nd degree HB
    • LAFB
    • LPFB
    • RBBB
    • LBBB
• Score
  • 0 = 1.2%; 1= 7.8%, 2= 25%, 3= 36.4%

Conduction block

• AV dissociation
  • Separate and independent pacemakers drive atria and ventricles
  • Passive
    • Impulse fails to reach AV node due to sinus node failure or block
    • Escape rhythm takes over and paces ventricles
    • When sinus node recovers, atrial activity resumes but there is often a period of independent atrial and ventricular pacing
    • Occurs if sinus node falls due to sinus bradycardia, sinus arrhythmia, SA block or sinus pause
    • Causes include IHD (acute inferior MI), myocarditis, digoxin and vagal stimulation and athletes
  • Active
    • Slower pacemaker accelerates to usurp the sinus node to capture the ventricles with ongoing visible sinus P waves unrelated to ventricular QRS. VT is the classic example
    • Causes: Myocardial ischaemia, digoxin

Bundle branch block

Left bundle branch block

• Ventricular activation via RBBB, from right to left and inferior to superior
• QRS >0.12
• Loss of septal Q waves in I, V5,6
• Small R wave with deep S wave in II, III, aVF, V1-V3
• Broad monophasic R wave in I, aVL, V5, V6 = delayed ventricular activation time in V6 (VAT)
• LAD
• Poor R wave progression
• Appropriate discordance: ST and T waves always go in opposite direction to main QRS vector
• Causes: Aortic stenosis, IHD, HTN, dilated CM, anterior MI, hyperkalaemia, dig toxicity, RV pacing

Sgarbossa criteria (NEJM 1996)

• Used to diagnosis STEMI in LBBB and right ventricular paced rhythms
• Dynamic changes are most important = serial ECG
• Three criteria
  • Concordant STE >1mm in leads with positive QRS (5)
  • Concordant ST depression >1mm in V1, V2, V3 (3)
  • Excessively discordant ST elevation >5mm in leads with negative QRS (2)
• Score of 3 or more = 90% specific for MI
• Validation studies have shown sensitivity of 35% but specificity of 99%

Modified Sgarbossa Criteria (Smith et al. Ann. Emerg. Med 2012)

• Criteria
  • Concordant ST elevation >=1mm in any lead
  • Concordant ST depression >=1mm in V1, V2 or V3
  • Discordant ST elevation >25% of depth of preceding S wave
• Internally validated
• External validation (BARCELONA trial) showed sensitivity of 67% and specificity of 92%

BARCELONA Criteria

• Criteria
  • Concordant ST elevation >=1mm in any lead
  • Concordant ST depression >=1mm in any lead
  • Discordant ST elevation or depression >=1mm when major R or S is <= 6mm
• Sensitivity 95%; Specificity 90%
• Not externally validated as yet

RBBB

• Ventricular activation via left bundle from left to right
• Usually do NOT get right axis deviation
• ECG criteria
  • QRS >0.12
  • Triphasic QRS complexes RSR’ in lead V1 (Delayed VAT in V1)
  • Wide, slurred S waves in I, V5, V6
  • Normal onset ventricular activation time (VAT) in V6
• Not necessarily deep S wave (W)
• Also get depolarisation issues: ST depression and T wave inversion in right precordial leads (V1-3)
• DDx: Normal variant, Cor pulmonale, PE, IHD, Myocarditis, Congenital HD, Ashman phenomenon, LV pacing

Ashman phenomenon

• Wide QRS complex following a short R-R interval preceded by a long R-R interval
• Seen in AF
• Aberrantly conducted supranodal complex rather than one originating in either ventricle

Unifascicular blocks

• Includes LAFB, LPFB and RBBB
• Causes include ischaemia, cardiomyopathies, valvular (esp. aortic), myocarditis, cardiac surgery, congenital conditions
• Left posterior fascicle is far more broad and disease indicates widespread myocardial involvement

Left anterior fascicle block

• Left axis deviation (-30 to -90 degrees)
• R wave in I > R wave in II and III
• Small q waves with tall R waves in I and aVL
• Small r waves with deep S waves in II, III, aVF
• QRS slightly prolonged (0.08-0.11s – but not >0.12)
• Prolonged time to R wave peak in aVL >0.045s
• Increased QRS voltage in limb leads
  • May meet LVH criteria but will not show left ventricular strain pattern
• Caused by AMI and LVH

Left posterior fascicle block

• Exact opposite of left anterior fascicular block
• Right axis deviation (+110-180 degrees)
• R wave in II and III > R wave in I
• Small r waves with deep S waves in I, aVL
• Small q waves with deep R waves in II, III, aVF
• Slightly prolonged QT
• Prolonged time to peak R wave >0.045s
• Increased QRS in limb leads
• Extremely rare to see this in isolation and is usually part of bifascicular block. LOOK FOR OTHER CAUSES OF RAD (PE, tricyclic, lateral MI, right ventricular hypertrophy)
• Usually associated with RBBB or septal ischaemia (usually inferior)

Bifascicular block

• RBBB + LAFB = RBBB with left axis deviation
• RBBB + LPFB = RBBB with right axis deviation
• 1% per year progress to complete heart block

Trifascicular block

• Incomplete (“impending”)
  • Bifascicular (RBBB + LAFB or LPFB [LAD or RAD]) with either 1st or 2nd degree AV block
    • Impossible to tell if block is in node or fascicle (true “trifascicular”)
  • Fixed RBBB with alternating LAFB/LPFB (LAD/RAD)
• Complete
  • 3rd degree AV block with escape rhythm showing RBBB + LAFB or LPFB (LAD or RAD)

Trifascicular block

• DDx:
  • IHD, HTN, primary conducting system disease (Lenegre-Lev disease), congenital, Hyperkalaemia, digoxin toxicity
• If asymptomatic bifascicular with 1st degree AV block -> Does not warrant pacing
• All others warrant Cardiological opinion but may not require admission
• If symptomatic e.g. syncope -> Definitely admit for Cardiological opinion

Rate-related BBB

• Typically seen in diseased hearts
• Occurs if pacemaker depolarisations reach bundle fibres still in their refractory period
• More likely to occur if prolonged refractory period in conduction pathways i.e. sodium channel blockade

STEMI

Diagnostic criteria

• New LBBB
• >2.5mm STE in V2/3 in males <40
• >2.0mm STE in V2/3 in males >40
• >1.5mm STE in V2/3 in females
• >1.0mm STE in all other leads
• The Fourth Universal Definition of MI recommends >=0.5mm in leads V7-9 as an extension of the STEMI criteria
  • States isolated ST depression in V1-3 “may indicate left circumflex occlusion but is non-specific”
• National Cardiovascular Data Registry guidelines recommend ST elevation in posterior chest leads (V7-9) or ST depression maximal in V1-3, without ST elevation in other leads, is considered a STEMI equivalent and demonstrates posterobasal infarction

STEMI and STEMI equivalents

• LBBB with Sgarbossa criteria (concordance!)
• Posterior MI: ST depression maximal in V1-4 (Pendell Meyers et al.)
• Left main coronary artery occlusion: STE in aVR and ST depression elsewhere
• DeWinter ST/T wave complex: 1mm ST up-sloping depression in V1-6 with peaked T waves. Represents severe chronic LAD stenosis vs.
• Wellen’s syndrome: Acute LAD occlusion with deep inverted or biphasic T waves in V2-3 (typically from biphasic to deep inverted)
  • Criteria include normal or minimally elevated ST segment, no praecordial Q waves, normal R wave progression, recent hx of angina, ECG pattern present in pain free state and normal or slightly elevated troponin
• Hyperacute T waves
• Aslanger Pattern
  • 13.3% of inferior STEMI reportedly present with this
  • Inferior STEMI in patients with pre-existing multivessel disease without contiguous STE
  • ECG criteria
    • Inferior ST elevation isolated to lead III
    • Concomitant ST depression in any of V4-6 with a positive T wave
    • ST segment in V1 > V2
  • The pre-existing multivessel disease means the vector of ST elevation is a summation of inferior ST elevation + subendocardial ischaemia that is non-localising and causes ST elevation pointed towards aVR -> Aslanger pattern

Anatomy Lesson

Anatomy Lesson

Anatomy Lesson

Infarct localisation

• Inferior (60%) – II, III, aVF. Reciprocal I, aVL. 
  • RCA or LCx
  • ST elevation III > II suggestive of RCA culprit
  • Look for STE in V1 and V4R to rule out RV involvement (40% of inferior MI due to RCA involvement proximal to RV)
  • Look for inferolateral (I, aVL, V5, V6 due to LCx occlusion in left dominance)
  • Look for inferoposterior (ST depression V1,2)
    • Equally present in LCx and RCA culrits

Infarct localisation

• Posterior MI
  • Posterior myocardium not visualised, so need reciprocal ST depression maximal in V1-4
  • Horizontal ST depression (=ST elevation posteriorly)
  • Tall, broad R waves
  • Upright T waves (= TWI)
  • Dominant R wave in V2 (= Q wave)

Infarct localisation

• Posterior MI (ST depression maximal in V1-4 or ST elevation V7-9) – RCA and LCX occlusion
  • Look for posterolateral (STE I, aVL, V5, V6, V7-9)
  • Look for inferoposterior (STE II, III, aVF, ST depression V1,2)

Infarct localisation

• LAD lesions
  • Septal MI: STE V1,2
  • Anterior MI: STE V3,4
  • Lateral MI: STE I, aVL, V5, V6
  • Anteroseptal: V1-4
  • Anterolateral: V3-6
  • Extensive anterior: V1-6

Left main coronary artery occlusion

DeWinters

Hyperacute T waves

• Broad, asymmetrically
  peaked T waves
• Early STEMI

Wellen’s syndrome

Pseudo-normalisation in Wellen’s

• Typical pattern is anterior MI (from LAD) that may not be captured on ECG
• Re-perfusion (natural or pharmacological) results in Wellen’s pattern ECG
• If remains open, biphasic to deep inverted transition occurs
• Re-occlusion results in pseudo-normalisation of T waves and may involve chest pain or precede it
• If remains occluded, get evolving anterior STEMI pattern
• Can have ‘stuttering’ flipping T waves

Pseudo-Wellens

• LVH causes TWI that mimics Wellens’
• In Wellens’, chest pain is usually resolved by the time of ECG
• Wellens’ presents in V2-4 predominantly. If V3-6 TWI, consider LVH or benign TWI

Aslanger Pattern

Benign Early Repolarisation

• Typically young and under 50yo
• Widespread concave ST elevation in V2-5
• Notched/slurred J point
• Prominent, slightly asymmetrical T waves concordant with QRS (descending limb straighter and steeper)
  • Cannot have hyperacute T waves (suggests ischaemia)
• ST elevation <25% of T wave height in V6 (>25% suggests pericarditis)
• No reciprocal ST depression in any leads (except in aVR)
• No dynamic changes
• Should still have S wave in V2/3 (terminal QRS distorsion equates to STEMI

Ventricular hypertrophy

LVH criteria

• 25% sensitive and 85% specific
• Very unreliable if <40yo
• QRS width must be <120ms
• Voltage criteria + Non-voltage required
• Voltage criteria
  • Sokolov-Lyon criteria = S wave depth in V1 + R wave height in V5/6 >35mm
• Non-voltage criteria
  • Increased R wave peak time in V5/6 (like LAFB/LPFB)
  • ST depression and TWI in left lateral leads (LV strain pattern)
• Other changes seen
  • LA enlargement
  • Left axis deviation
  • ST elevation V1-3 (discordant to deep S waves)
  • Prominent U waves

Right ventricular hypertrophy

• Right axis deviation
• Dominant R wave in V1 (>7mm)
• Dominant S wave in V5/6 (>7mm)
• QRS <0.12s (i.e. changes not due to RBBB)
• Supported by:
  • P pulmonale
  • RV strain (ST depression/TWI V1-4 and II/III/aVF)
  • S1S2S3 = dominant S waves in I, II, III
  • Deep S waves in I, aVL, V5, V6

VT vs. SVT with aberrancy

• 3 possibilities:
  • VT or SVT with BBB or SVT with WPW
  • In ED, 80% of broad complex tachyarrhythmia is VT
• Increased likelihood of VT
  • Age >35
  • Absence of typical RBBB/LBBB morphology
  • Northwest axis
  • Very broad >0.16s
  • AV dissociation (only seen in 25% of cases) – Evidenced by canon A waves, fusion beats and capture beats
  • Capture beats (normal QRS duration amongst wide complex)
  • Fusion beats (hybrid complex)
  • Positive or negative concordance – All R or all QS complexes across praecordium
  • Brugada’s sign – Onset of QRS to nadir of S wave >0.1s
  • Josephson’s sign – Notching near nadir of S wave
  • RSR’ with tall left rabbit ear (vs. RBBB right rabbit ear taller) – MOST SPECIFIC)

All of the above just make VT more likely, their absence does NOT rule in SVT with aberrancy

Criteria accuracy

• Brugada 89% sensitive for ruling in VT
• Griffith 94% sensitive; 40% specific
• Bayesian 89% sensitive
• Vereckei aVR 87% sensitive
• Lead II RWPT 60% sensitive

Moral is, none of the above are accurate enough to rule in VT and definitely not accurate enough to rule out VT and treat as SVT.

Considering VT is highly fatal, treat it as this and just move on.

Even if baseline ECG shows same BBB pattern, can still be fooled.

WPW

• Short PR <0.12s
• Broad QRS
• Delta wave

Brugada

• Phase 0 Sodium channelopathy
• High incidence of sudden death with structurally normal hearts
• Developing gold standard diagnostic criteria
  • Spontaneous Type 1 BrS-ECG in V1 or V2 or V3
  • Baseline Type 2 or 3 with Type 1 unmasked by fever or sodium-channel blockers and a Shanghai Score of at least 1
• Shanghai Criteria
  • ECG
    • Spontaneous Type 1 = 3.5
    • Fever induced Type 1 = 3
    • Type 2 or 3 that converts with provocative drug test = 2
  • Clinical history
    • Unexplained arrest or documented VF/polymorphic VT = 3
    • Nocturnal agonal respirations = 2
    • Suspected arrhythmogenic syncope = 2
    • Syncope of unclear cause = 1
    • AF/AFib in patient under 30 with no other cause = 0.5
  • FHx
    • 1st or 2nd degree with definite BrS = 2
    • Suspicious sudden cardiac death in first or second-degree relative (fever, nocturnal or Na-channel blocker associated)
    • Unexplained SCD >45yo in first or second-degree relative with negative autopsy
  • Genetic Test Result
    • Probable pathogenic mutation in BrS susceptibility gene = 0.5
• Brugada Type 1 ECG (Coved)
  • J point elevation >= 2mm and terminal ST segment elevation >= 2mm
  • Wider QRS complex
  • Wide and deep S wave in lead I
  • Fractionation in right praecordial leads
• Brugada Type 2 ECG (Saddleback)
  • J point elevation >= 2mm with terminal ST segment elevation >=1mm with positive T wave
  • Less wide and deep S wave in I
  • Less prominent fractionation
• Brugada Type 3 ECG (Saddleback)
  • J point elevation >=2mm with terminal ST segment elevation <1mm
  • Absence of deep S wave in I
  • No fractionation

Brugada example

Disposition of Brugada

• Brugada sign + Clinical = Admit
• Brugada without clinical = Cardiology Consult for consideration of pharmacological induction or EPS studies
• Type 2 or 3 with or without clinical = Cardiology Consult for consideration of pharmacological induction or EPS studies
• Normal ECG with syncope and FHx of sudden cardiac death = Cardiology referral for provocative testing

Electrolyte disturbance

Hyperkalaemia

• Peaked T waves
  • Narrow-based, symmetrical, sharp apex. T >= R amplitude in more than one lead
• Far left axis
• P wave widens and flattens through to paralysis
• PR segment lengthens
• P waves eventually disappear
• Prolonged QRS (highest risk feature)
• High-grade AV block with slow escape rhythms
• Shortened QT
• Conduction blocks
• Sinus bradycardia
• Sine wave
• Asystole
• VF
• PEA

Hypokalaemia

• Increased amplitude of P wave
• Prolonged PR interval
• T wave flattening and inversion
• U wave
• ST depression
• Long QT due to long QU
• Frequent ectopics
• SVT
• VT/VF/TdeP

Hypercalcaemia

• Less diastolic relaxation – eventually stops in systole
• Shortened QTc (<350ms) due to shortened ST segment
  • Drags the T wave back towards the R wave giving the impression of ST elevation (or ST depression if baseline TWI)
• Bradycardias relatively common
• Broad-based tall peaked T waves
• Wide QRS
• Low amplitude R waves/p waves

Hypocalcaemia

• Prolongs ST and therefore QT intervals
• Narrowed QRS
• Shortened PR
• T wave flattening and inversion
• ST depression

Prolonged QT

• Causes
  • Hypokalaemia
  • Hypomagnesaemia
  • Hypocalcaemia
  • Hypothermia
  • MI
  • Post-cardiac arrest
  • Raised ICP
  • Congenital long QT syndrome
  • Medications: See next slide

Drug-induced prolonged QT

Drug-induced prolonged QT

Long QT syndrome

• QTc > 470 in men and 480 in women
• Increased susceptibility to torsades de pointes
• Consider in syncope

Short QT

• Causes
  • Hypercalcaemia
  • Digoxin (through intracellular hypercalcaemia)
  • Congenital short QT (generally presents in young children with SCD/near-miss

Preterminal rhythms

• Pulseless electrical activity
  • Organised electrical complexes without cardiac output
  • In the setting of cardiac arrest, is due to profound metabolic disturbance of myocardium
  • Associated with hypovolaemia, hypoxia, acidosis, hypo/hyperkalaemia, hypoglycaemia, hypothermia, TCA/digoxin/CCB, beta-blocker, cardiac tamponade, massive PE, tension pneumo/haemothorax, AMI and ventricular wall rupture

• Idioventricular rhythm
  • Ventricular escape rhythma at <40 beats/min
  • Occurs due to complete infranodal AV block, AMI, cardiac tamponade, exsanguinating haemorrhage
  • Treatment is CPR if no output and adrenaline
  • Atropine of no proven benefit (likely due to infranodal escape and no vagal stimulation)

• Agonal ventricular rhythm
  • Very broad and irregular ventricular complexes at a slow rate without associated ventricular contractions
• Cardiac asystole
  • CPR and adrenaline
  • Transthoracic pacing sometimes induces electrical capture but rarely yields effective output

Paced rhythm interpretation

• RV pacing (most common) causes secondary repolarisation abnormalities of opposing polarity to the predominant QRS complex
• Most leads will have predominantly negative QRS complexes followed by ST segment elevation and positive T waves
• In this setting, discordant ST elevation >5mm is most indicative of AMI in leads with predominantly negative QRS complexes
• Any ST elevation concordant with QRS complexes in a predominantly positive QRS complex is highly specific for AMI

Non-ischaemic ST elevation

• Pericarditis
• Benign early repolarisation
• LBBB
• LVH
• Ventricular aneurysm
• Brugada syndrome
• Ventricular paced rhythm
• Subarachnoid haemorrhage or other causes of raised ICP

ST elevation in aVR

• Differential
  • LMCA syndrome
  • Triple vessel disease
  • Proximal LAD
  • Global hypoperfusion e.g. post-ROSC
  • Thoracic aortic dissection
  • Massive PE
  • LBBB
  • LVH
  • Severe atrial tachydysrhythmias

STEMI vs. Pericarditis

• Witting et al. 2020
• What makes STEMI more likely?
  • ST depression aside from V1/aVR – OR 31
  • ST elevation III > II – OR 21
  • Horizontal or convex ST elevation
  • R-T sign – T wave shoots off R wave without gradual transition
• What makes pericarditis more likely?
  • PR depression in multiple leads (but look at above FIRST)
    • Seen in 12% of STEMIs
  • Spodick’s sign – Downsloping T-P segments

Lewis Leads

• Utilised to more closely assess atrial activity
• Useful to differentiate VT vs. SVT with aberrancy or to more definitively diagnose AF/Aflutter/AV block
• Move right arm electrode to the manubrium
• Move left arm electrode to right parasternal 5th ICS
• Move left leg electrode to right costal margin
• Lead I classically used as most sensitive lead but important to look at all leads for atrial activity

Accelerated idioventricular rhythm (AIVR)

• Classically seen post-lysis and termed ‘reperfusion rhythm’
• Occurs when ventricular pacemaker rate exceeds that of the sinus node (and junction)
• Regular, broad-complex rhythm (QRS >120ms) at 50-110/min
• Usually well-tolerated, benign and self-limiting
• If rate is <50 = ventricular escape rhythm
• If rate >110 = ventricular tachycardia
• Other causes include beta-agonists, digoxin toxicity, electrolyte disturbance, myocarditis, post-ROSC and athletic heart (high vagal tone)

Last Updated on August 29, 2024 by Andrew Crofton