medreg+1 bhuva ecgs

Developing people for health and healthcare

ECG workshop: the common and the dangerous

Anish BhuvaCardiology Academic Clinical FellowThe Heart Hospital

Developing people forhealth and healthcare

Objectives

Acute coronary syndroms

Risk stratification

Management

MimicsSVTAFBroad 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 infusionTemporary 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 7Less ‘resistance’/ non responsiveness ISAR- CHOICE OASIS

7No excess hazard (with fibrinolysis)Improved pharmacokinetics ARMYDA-2

Ticagrelor 180mg loading: PLATOTicagrelor > ClopidogrelCI: moderate hepatic dysfunction, previous haemorrhagic stroke

Prasugrel TRITONCI: age >75; low body weight; previous TIA/Stroke


Admission ECG Scenario 3


a)Blue light, this is a primary!b)Observec)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 elevation2. Peaked asymmetrical T waves with steeper descending element than ascending

Also:1. Variability with heart rate2. 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 WarDerval 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 CASINOIABP

IABP- SHOCK IILVADReperfusion

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 myocardialinfarction 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


NSTEACS


Non ST Elevation Myocardial infarction


NSTEACS


50 year old femaleHR 75Moderate COPDTroponin riseSBP 120/80Creat 75No 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 management



NICE: NSTEACS guidance


Risk scores

Risk Stratification (for NSTEACS)

Other models:• TIMI• ACC/AHA


…may help with triage for invasive management



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


ESC guidelines


Left main stem ischaemia

ST elevation in aVR onlyInfero-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 elevatedNo established infarction

A sign of impending LAD occlusion and requires urgent intervention


Scenario 4


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


LVH + strain

Scenario 4


Scenario 5


HCM

Scenario 5


RV infarction

Scenario 6


Life in the fast lane.com


RV infarction

V1 ST elevation V2 ST depressionIII>II ST elevation


RV infarction: management

Maintain RV pre loadReduce afterload Restore A-V synchrony

Avoid nitrates! Cautious ACEi introduction


Scenario 7


THIS IS A STEMI!


Posterior myocardial infarction

Scenario 7


Posterior infarction

This is a STEMI

Dominant R in V1/2Anterior ST depression with upright T waves

Diagnosis: V7-9


Pick up booklet 3


Arrhythmia management

5 minutesRead through the next few scenarios and come up with a diagnosis and

management


Would you:IV metoprololPO metoprololAmiodaroneFlecainide 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 FibrillationBraunwald’s Heart DiseaseESC 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 DCCVDCCV at 6 hoursVerapamilBetablockadeFlecainide


SVT

Sinus tachycardiaAtrial tachycardiaAVNRTAVRTParoxysmal junctional tachycardia


AVNRT


AVNRT

Stepwise approach:VagalAdenosineVerapamil 5-10mg IV [successful in 2 minutes in 90%]Betablockade less used as less effective but fineDigoxin possible with repeat vagal maneuvresDCCV should be used over flecainide etc.


Would you:a) Adenosineb) DCCV c) Bisoprolold) 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 monomorphicDrugsElectrolytesIschaemia


VT storm

Betablockade

Single most effective treatmentAmiodarone

LignocaineSedation


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:AdmitOP follow upDischarge after observation


Sinus bradycardia with VEQRS 120, Normal axis1st degree heart block


ESC guidelines: syncope 2009


How would you manage him?a) Ignoreb) Bisoprololc) Dual antiplatelet therapyd) 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 withventricular 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: [email protected].


How to look with VT

Hx IHD (95% specificity)+ AVR (80% specificity)Capture beats [sinus beat]Fusion beats [hybrid complexes]Discordant P wavesConcordant complexes


Discordant QRS complexesNegative aVRBut…• Capture beats• Fusion beats


+ AVRConcordant


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 ACSInterpret ischaemic ECGsUnderstand pharmacokinetics on anti-arrhythmicsLook good identifying VT


Acknowledgement

Patients from UCLH and the Heart Hospital

Lifeinthefastlane.com


Thank you

[email protected]

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