MedReg+1 Bhuva ECGs

Developing people for health and healthcare
ECG workshop: the
common and the
dangerous
Anish Bhuva
Cardiology Academic Clinical
Fellow
The Heart Hospital

Developing people for
health and healthcare
Objectives
Acute coronary syndroms
Risk stratification
Management
Mimics
SVT
AF
Broad complex tachycardia

Format
3 ECG Booklets
ST segment elevation
NSTEACs
Arrhythmia
Brief small group discussion of each booklet followed by answers

Pick up booklet 1

Booklet 1
Decide whether to
Blue light, this is a primary!
Leave until the post-take round
Observe for now
5 minutes for 10 scenarios

STEACS: diagnosis

Inferior STEMI
Blue light to nearest PCI centre! Scenario 1

Inferior STEMI
20% associated with CHB
Stablise prior to transfer!
Narrow QRS, Rate > 50 is safer
Will one dose atropine last an LAS transfer?
Isoprenaline infusion
Temporary pace + escort?

Anterior STEMI
Blue light to nearest PCI centre! Scenario 2

Medication in primary PCI

Novel antiplatelet agents
Clopidogrel 600mg:
Better outcomes only in PCI OASIS 7
Less ‘resistance’/ non responsiveness ISAR- CHOICE OASIS 7
No excess hazard (with fibrinolysis)
Improved pharmacokinetics ARMYDA-2
Ticagrelor 180mg loading: PLATO
Ticagrelor > Clopidogrel
CI: moderate hepatic dysfunction, previous haemorrhagic stroke
Prasugrel TRITON
CI: age >75; low body weight; previous TIA/Stroke

Admission ECG Scenario 3

a)Blue light, this is a primary!
b)Observe
c)Discharge

Repeat at 20 minutes

Scenario 4

High take off
Scenario 4

High take off
This patient was taken to the cath lab
Normal coronaries
Fixed ECG changes on repeat at 24 hours

Scenario 5

Early repolarisation

Early repolarisation
1. J point elevation + concave ST elevation
2. Peaked asymmetrical T waves with steeper descending element than
ascending
Also:
1. Variability with heart rate
2. Young, male, Afro-Caribbean
History and clinical context (Pre test probability) important if unsure
(Provide copy of ECG on discharge)
Definition of Early Repolarization: A Tug of War
Derval et al Circulation 2011 Scenario 5

Scenario 6

Pericarditis

Scenario 9

Scenario 7

Scenario 7
LV Aneurysm

Scenario 8

Q wave infarction
Scenario 8

“Pain was worst two hours ago”
Assume this was the index episode
Candidate for emergency reperfusion
Extent of R wave voltage
“No chest pain, but I am breathless”
Cardiogenic shock

Cardiogenic shock
Inotropes CASINO
IABP
IABP- SHOCK II
LVAD
Reperfusion SHOCK
..ECMO
Is myocardium viable?
• History
• ECG
• Echo
• Clinical context
Escalate early: these are the difficult
decisions balancing high risk and mortality

Scenario 10

Sgarbossa criteria
Look for concordant ST Elevation!
Sgarbossa et al Electrocardiographic diagnosis of evolving acute myocardial
infarction in the presence of left bundle-branch block. N Engl J Med 1996;334:481–487.

Myth- busting
You can’t interpret a paced rhythm

Truth
You can observe for dynamic changes
Use Sgarbossa’s criteria

Pick up booklet 2

Practice scenarios
Decide on the important diagnostic features and key management steps in
the next ECG booklet
5 minutes for 9 scenarios

NSTEACS
Scenario 1

Would you:
a) Discharge after 48 hours ACS Rx;
b) Refer for angiography;
c) Organise stress imaging.

NSTEACS

Troponin

Cardiac troponin I (cTnI) levels in a healthy reference population and in an acute coronary
syndrome (ACS) population.
Mahajan V S , and Jarolim P
Circulation. 2011;124:2350-
2354
Copyright © American Heart Association,
Inc. All rights reserved.

How to use hs-Trop
Diagnosis
>99th centile at 3hours:
• Sensitivity = c. 99%
<99th centile at 3 hours:
• NPV > 95%
Risk stratification
Any level of + troponin is associated with a poor prognosis
BUT we are now picking it up in patients without an acute coronary syndrome

“When troponin was a lousy assay it was a
great test, but now that it's becoming a
great assay, it's getting to be a lousy test.”
Jesse RL. On the relative value of an assay versus that of a test: a history of
troponin for the diagnosis of myocardial infarction. J Am Coll Cardiol.
2010;55:2125–2128

Non ST Elevation Myocardial infarction

50 year old female
HR 75
Moderate COPD
Troponin rise
SBP 120/80
Creat 75
No ST changes

Risk scores
Risk Stratification (for NSTEACS)
Other models:
• TIMI
• ACC/AHA
http://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html
…may help
with triage
for invasive
managemen
t

NICE: NSTEACS guidance

Take home message
High sensitivity assays may give borderline false positive results
Risk scores are influenced by epidemiological as well as patient specific
factors

Scenario 2

health and healthcareESC guidelines

Left main stem ischaemia
ST elevation in aVR only
Infero-lateral ST depression
“Whilst this does not qualify for primary PCI this patient, I am worried that
this is main stem ischaemia”

S
Scenario 8

Wellen’s syndrome
Scenario 3

Wellen’s syndrome
Chest pain (often intermittent)
Characteristic ECG:
Anterior T wave inversion
Bifid T waves
Normal Trop/Mildly elevated
No established infarction
A sign of impending LAD occlusion and
requires urgent intervention

Would you:
a) Discharge;
b) Refer for angiography;
c) Organise stress imaging.

LVH + strain
Scenario 4

HCM
Scenario 5

RV infarction
Scenario 6

Life in the fast lane.com

RV infarction
V1 ST elevation
V2 ST depression
III>II ST elevation

RV infarction: management
Maintain RV pre load
Reduce afterload
Restore A-V synchrony
Avoid nitrates!
Cautious ACEi introduction

health and healthcare Scenario 7

THIS IS A STEMI!

Posterior myocardial infarction
Scenario 7

Posterior infarction
This is a STEMI
Dominant R in V1/2
Anterior ST depression with upright T waves
Diagnosis: V7-9

Pick up booklet 3

Arrhythmia management
5 minutes
Read through the next few scenarios and come up with a diagnosis and
management

Would you:
IV metoprolol
PO metoprolol
Amiodarone
Flecainide
Shock

Acute control
Drug Time to rhythm
control/hrs
Time to rate
control/hrs
Chance of
cardioversion
Metoprolol 5 mins 13%
Sotalol 10-15%
Digoxin 2-6 hours 5%
Verapamil 0.5 5 mins 6-14%
Flecainide 1 67-92% at 6hrs
Amiodarone 6-24 6-8 hours 40-60% at 24 hrs
MgSO4 5-15 mins OR 1.6 (1.07-2.4)
Expect 50% conversion at 15-120minutes ESC Guidelines: Atrial Fibrillation
Braunwald’s Heart Disease
ESC textbook of cardiology

Flecainide
Better than amiodarone for <24 hours duration of AF
Contraindicated in abnormal LV function and ischaemic heart disease
Risk of ‘paradoxical’ rate increase

Tip
Echo for LV function useful prior to giving flecainide

Would you:
Urgent DCCV
DCCV at 6 hours
Verapamil
Betablockade
Flecainide

SVT
Sinus tachycardia
Atrial tachycardia
AVNRT
AVRT
Paroxysmal junctional tachycardia

AVNRT

AVNRT
Stepwise approach:
Vagal
Adenosine
Verapamil 5-10mg IV [successful in 2 minutes in 90%]
Betablockade less used as less effective but fine
Digoxin possible with repeat vagal maneuvres
DCCV should be used over flecainide etc.

Would you:
a) Adenosine
b) DCCV
c) Bisoprolol
d) Flecainide

Atrial Flutter

Take home message
Easy to DCCV flutter (50J)
Difficult to rate control

Broad complex tachycardia
If ischaemic heart disease, think:
VT
VT
VT
95% specificity

VT storm
>3 episodes in 24 hours
Cf. Incessant VT
1 episode of hours duration

VT storm
Treat cause
More likely due to scar substrate than acute ischaemia if monomorphic
Drugs
Electrolytes
Ischaemia

VT storm
Betablockade
Single most effective treatment
Amiodarone
Lignocaine
Sedation

Pacing and VT
Appropriate shocks:
Device action can promote cardiac dysfunction
– > further arrhythmia
Inappropriate shocks:
Get a magnet [resus trolley]
Cause?
• eg. Lead migration/fracture (effusion?)
Reprogramme/control SVT

78 year old male. History 3 previous MI, NIDDM, BPH. He presents with
syncope and subsequent head injury. Normal CT head.

Would you:
Admit
OP follow up
Discharge after observation

Sinus bradycardia with VE
QRS 120, Normal axis
1st degree heart block

health and healthcare ESC guidelines: syncope 2009

How would you manage him?
a) Ignore
b) Bisoprolol
c) Dual antiplatelet therapy
d) Amiodarone

NSVT
Can be found in structurally normal hearts
Ask yourself what is the cause

Post MI, Cardiomyopathy groups:
Suppression of ambient arrhythmia is not a therapeutic target
ACC/AHA/ESC 2006 guidelines for management of patients with
ventricular arrhythmias and the prevention of sudden cardiac death

VT or not VT?

Three hundred and forty-eight VTs and 170 SVTs with aberrant conduction were included in
the comparison: Brugada criteria.
Alzand B S , and Crijns H J Europace 2011;13:465-472
Published on behalf of the European Society of Cardiology. All rights reserved. © The Author
2010. For permissions please email: journals.permissions@oup.com.

How to look with VT
Hx IHD (95% specificity)
+ AVR (80% specificity)
Capture beats [sinus beat]
Fusion beats [hybrid complexes]
Discordant P waves
Concordant complexes

Discordant QRS complexes
Negative aVR
But…
• Capture beats
• Fusion beats

+ AVR
Concordant

No positive criteria for VT
• LBBB
• Sharp initial downstroke
SVT + LBBB aberrancy?
VT- not ruled out

Preexcited AF

Preexcited AF
AF in the context of an accessory pathway
Variable QRS length
High risk to degenerate into VF
AV Nodal agents contraindicated

Artefact

Summary
Identify high risk ACS
Interpret ischaemic ECGs
Understand pharmacokinetics on anti-arrhythmics
Look good identifying VT

Acknowledgement
Patients from UCLH and the Heart Hospital
Lifeinthefastlane.com

Thank you
Anish.bhuva@nhs.net

MedReg+1 Bhuva ECGs

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