Deep dive into interpretation of ECG covering ischaemia and arrhythmias. Targeted at the critical care physician.

1. ECG
Interpretation
Dr Andrew Crofton
Emergency Registrar
Disclaimer: https://criticalcarecollaborative.com/disclaimer/

2. 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

3. 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

4. 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

5. 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

6. 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

7. 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

8. Measuring the QT
Prolonged ST portion (Phase 2) = Much lower risk of TdeP vs.
Prolonged T wave (Phase 3) = Much higher risk of TdeP

9. 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

10. Left axis deviation
❖ > -30 degrees
❖ LVH, LAFB, Inferior AMI, WPW, pregnancy

11. Right axis deviation
❖ > 90 to 120 degrees
❖ RBBB
❖ PE
❖ Cor pulmonale
❖ LPFB
❖ RVH
❖ Lateral MI
❖ WPW
❖ Dextrocardia

12. Wide QRS
❖ >120ms
❖ BBB
❖ Hyperkalaemia
❖ Sodium channel blockade
❖ Accessory pathway
❖ Profound hypothermia

13. 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

14. 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

15. 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

16. 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

17. ECG Rhythms
❖ Rate
❖ Pattern - Regular, irregular (regularly or irregularly)
❖ Narrow or wide
❖ P waves absent or present
❖ 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

18. Conduction block
- AV 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

19. 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)
❖ 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)
❖ 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
❖ 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
❖ Most common ‘unstable’ rhythm in AMI

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

21. 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

22. 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

23. LBBB

24. Sgarbossa criteria
❖ 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 V1-3 (3)
❖ Excessively discordant ST elevation >5mm in leads with negative
QRS (2)
❖ Score of 3 or more = 90% specific for MI

25. Modified Sgarbossa Criteria
❖ 1 or more leads with >=1mm concordant ST elevation
❖ 1 or more leads of V1-3 with >=1mm of concordant ST
depression
❖ 1 or more leads with >=1mm and proportionally
excessively discordant ST elevation (>=25% of depth of
preceding S wave)

26. 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

27. RBBB

28. 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

29. Ashman phenomenon

30. 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

31. 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

32. Left anterior fascicular block

33. 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)

34. Left posterior fascicular block

35. Bifascicular block
❖ RBBB + LAFB = RBBB with left axis deviation
❖ RBBB + LPFB = RBBB with right axis deviation
❖ 1% per year progress to complete heart block

36. Trifascicular block
❖ Bifascicular + 1st degree AV block (most common)
❖ RBBB + LAD/RAD + 1st degree AV block
❖ Bifascicular + 2nd degree AV block
❖ RBBB + LAD/RAD + Mobitz I/II/2:1/3:1
❖ RBBB + Alternating LAD/RAD
❖ Complete = Bifascicular + 3rd degree AV block
❖ Complete heart block with RBBB + LAD/RAD

37. 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

38. STEMI 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

39. STEMI and STEMI
equivalents
❖ LBBB with Sgarbossa criteria (concordance!)
❖ Posterior MI: Anterior ST depression
❖ 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

40. Anatomy Lesson

41. Anatomy Lesson

42. Anatomy Lesson

43. 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

44. Infarct localisation
❖ Posterior MI
❖ Posterior myocardium not visualised, so need
reciprocal changes in V1-3
❖ Horizontal ST depression (=ST elevation)
❖ Tall, broad R waves
❖ Upright T waves (= TWI)
❖ Dominant R wave in V2 (= Q wave)

45. Infarct localisation
❖ Posterior MI (ST depression V1,2) - RCA and LCX
occlusion
❖ Look for posterolateral (STE I, aVL, V5, V6)
❖ Look for inferoposterior (STE II, III, aVF, ST
depression V1,2)

46. 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

47. Left main coronary artery
occlusion

48. DeWinters

49. Hyperacute T waves
❖ Broad, asymmetrically
peaked T waves
❖ Early STEMI

50. Wellen’s syndrome

51. 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

52. 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

53. 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)
❖ ST elevation <25% of T wave height in V6 (>25% suggests
pericarditis)
❖ No reciprocal ST depression (except in aVR)
❖ No dynamic changes

54. 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

55. 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

56. VT vs. SVT with aberrancy
❖ 3 possibilities:
❖ VT/SVT with BBB/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 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)

57. WPW
❖ Short PR <0.12s
❖ Broad QRS
❖ Delta wave

58. Brugada
❖ Phase 0 Sodium channelopathy
❖ High incidence of sudden death with structurally normal hearts
❖ Need ECG Brugada sign + Clinical to make diagnosis
❖ Coved ST elevation >2mm in 2 or more of V1-3 followed by negative T wave
❖ Clinical
❖ Documented VF or polymorphic VT
❖ FHx of sudden cardiac death <45yo
❖ Coved-type ECG in family
❖ Inducible VT
❖ Syncope
❖ Nocturnal agonal respiration
❖ Brugada type 2 and 3 are non-diagnostic
❖ Type 2 = >2mm of saddleback shaped ST elevation
❖ Type 3 = Morphology of type 1 or 2 criteria but not >2mm

59. Brugada example

60. 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

61. 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

62. 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

63. Hypercalcaemia
❖ Less diastolic relaxation – eventually stops in systole
❖ Shortened QTc (<350ms)
❖ Bradycardias relatively common
❖ Broad-based tall peaked T waves
❖ Wide QRS
❖ Low amplitude R waves/p waves

64. Hypocalcaemia
❖ Prolongs ST and QT intervals
❖ Narrowed QRS
❖ Shortened PR
T wave flattening and inversion
❖ ST depression

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

66. Drug-induced prolonged QT
Drug group Drug
Antipsychotics Chlorpromazine
Haloperidol
Droperidol
Quetiapine
Olanzapine
Amisulpride
Thioridazine
Type IA anti-arrhythmics Quinidine
Procainamide
Disopyramide
Type IC anti-arrhythmics Flecainide

67. Drug-induced prolonged QT
Class III Anti-arrhythmics Sotalol
Amiodarone
TCA Amitryptiline
Doxepine
Imipramine
Nortryptiline
Desipramine
Other anti-depressants Citalopram
Escitalopram
Venlafaxine
Bupropion
Moclobemide
Antihistamines Diphenhydramine
Loratadine
Terfanadine
Other Chloroquine
Hydroxychloroquine
Quinine
Macrolides - Erythromycin,
Clarithromycin
Organophosphates

68. Long QT syndrome
❖ QTc > 470 in men and 480 in women
❖ Increased susceptibility to torsades de pointes
❖ Consider in syncope

69. Short QT
❖ Causes
❖ Hypercalcaemia
❖ Congenital short QT
❖ Digoxin effect

70. 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

71. Preterminal rhythms
❖ 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)

72. Preterminal rhythms
❖ 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

73. 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

74. 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

75. 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