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By Laurence Sharifi
ISCHAEMIC CHANGES ON THE
ECG
Some theory if you’re interested
ECGs and acute coronary syndromes
ECGs and stable angina
WHAT WE WILL BE COVERING
WHY THE HEART PRODUCES AN
ECG SIGNAL
The heart contracts because of
the cardiac conduction system
A wave of depolarisation
spreads across the myocardium
in a co-ordinated way, making
the heart contract in the right
way through every heart beat
HOW THE HEART BEATS
67 year old man, obese, HTN, DM
Retrosternal pain, tight, radiating to
arm and jaw lasting past 30 minutes
Not relieved with GTN spray, now
sweating and distressed
Time to take an ECG!!
CASE 1: ACS
WHY THE ECG LOOKS THE WAY
THAT IT DOES
Don’t think of an ECG lead as the
bit of wire stuck on the chest – this
isn’t what it is
An ECG lead is actually a calculated
voltage difference between two
electrodes– not REALLY vital to
know about the details
Think of a lead as a “photo” of the
heart taken at a particular orientation
ECG LEADS
=
ECG LEADS ARE “VIEWS”
Think of the ECG leads as photographs of the heart taken at different angles. This slide
illustrates this concept using the limb leads
=
V5
V1
V6
This slide illustrates the same concept but on the chest
leads. Cheryl remains the same, we just look at her from
different directions
The ECG leads all look at the heart from different angles:
ECG LEADS ARE VIEWS
Each lead is looking at a different part of
the heart’s surface
Depolarisation travels
from the endocardium
through to the
epicardium (in to out)
Repolarisation goes from
the epicardium to the
endocardium (out to in)
HOW THE HEART BEATS
• Causes a positive deflection
in ECG if travelling towards
lead
• Causes a negative deflection
if travelling away from lead
Depolarisation
• Causes a negative deflection
in ECG if travelling towards
lead
• Causes a positive deflection
if travelling away from lead
Repolarisation
RULES ABOUT ECG LEADS
THE CORONARY CIRCULATION –
WHEN IT ALL GOES WRONG
• The myocardium is adequately perfused
• The conduction system works
The heart pumps properly when:
• Left Main coronary artery. Branches:
• Left anterior descending artery
• Circumflex artery
• Right coronary artery. Branches:
• Acute marginal branch
• AV node branch
• Posterior descending artery
Key vessels are:
THE CORONARY ARTERIES
Ischaemic tissue
• Myocytes are still working – still
get an ECG signal from the
tissue
• Signal is different though as
anaerobic cells behave differently
Infarcted tissue
• Tissue is dying/dead– no ECG
signal from the tissue
• Heart is beating abnormally due
to presence of dead tissue
• ECG signal looks different
ISCHAEMIC TISSUE BEHAVES
DIFFERENTLY TO INFARCTED TISSUE
The blood supply can become compromised in:
• Stable angina
• Acute coronary syndrome (ACS)
Coronary artery
lumen becomes
narrowed
Partly
(NSTEMI)
Tissue becomes
ischaemic
Tissue dies
slowly
Wholly
(STEMI) Tissue becomes
extremely ischaemic
(transmural)
Tissue dies
quickly
ACUTE CORONARY SYNDROME
K+ channels open earlier in ischaemic
tissue
Repolarisation normally causes a positive
deflection if moving away from lead
(think T wave)
Ischaemic tissue repolarises early so you
get a positive deflection earlier, otherwise
known as ST ELEVATION
ST Elevation often means SEVERE
TRANSMURAL ISCHAEMIA
ISCHAEMIC CELLS REPOLARISE
FASTER
+20
-100 100ms
membpotl(mV)
Red = normal cardiac action potential
Blue = ischaemic tissue action potential
ECG in suspected ACS is used to
• Confirm or refute the diagnosis
• Guide therapy
• Estimate prognosis
Consider ECG alongside:
• Major cardiovascular risk factors (fat, old, DM, HTN)
• The description of the pain (central, crushing >20 min, at rest)
• History of cocaine indulgence
• How the patient looks. Are they sweaty, grey and breathless? Beware the
“silent MI” however – a patient may be having a heart attack but look
entirely normal. Diabetic patients are particularly susceptible to this
THE ECG IN ACS
ECG and ACS Therapy
• ST elevation MI will benefit from thrombolysis /
PCI
• Other ACSes need aggressive anti-platelet therapy
ECG and ACS prognosis
• Assess ACS using risk scoring tools
• Resting ECG changes are important variables
THE ECG IN ACS
Our patient has had
a series of ECGs
What could they
show?
CASE 1: ACS
ECG CHANGES IN STEMI
0
• No ECG
changes
1
• Hyper-
acute T
waves
2: Infarction
• ST
elevation
3: Fibrosis
• ST normal
• T wave
inversion
• Q wave
development
4
• Re-
inversion
of
inverted
T waves
5
• Late loss
of Q
waves
Onset
Lasts a
few
minutes
Minutes
to hours
Hours to
days
Days to
weeks
Years to
decades
STEMI PATTERNS
• I
• II
• aVL
• V1-5/6
Leads
showing ST
elevation
• Anterolateral
Infarct
description
• Proximal
LAD (left
anterior
desciending)
Artery
occluded
STEMI PATTERNS
• II
• V1-3/4
Leads
showing ST
elevation
• Anteroseptal
Infarct
description
• Left anterior
descending
Artery
occluded
STEMI PATTERNS
• II
• III
• aVF
Leads
showing ST
elevation
• Inferior
Infarct
description
• Right
coronary if
ST  II>III
• Circumflex if
ST  III>II
Artery
occluded
STEMI PATTERNS
• I
• II
• V5/6
Leads
showing ST
elevation
• Lateral
Infarct
description
• Diagonal branch
LAD
• Obtuse marginal
branch
circumflex
Artery
occluded
STEMI PATTERNS
• V1 - 3
Leads
showing ST
depression
• Posterior
Infarct
description
• Circumflex
Artery
occluded
This happens because the ST elevation on
the posterior wall causes a RECIPROCAL
change on the opposite side. Confirm by
doing a posterior ECG
Patient has had a posterior
STEMI
ST depression in V1-3
We would see ST elevation
in posterior chest leads
CASE 1: ACS
CASE 1: ACS
74 year old lady, Hx of HTN, PC:
chest pain at rest
Normal ECG but raised Trop T 12
hours later – ischaemic damage to
myocardium highly likely
Sounds like ACS, so why normal
ECG?
CASE 2: ACS
Normal ECG is possible in NSTEMI
• Only small coronary artery affected
• Posterior infarct
• Diagnosis is made clinically and with TropT
NSTEMI ECG Changes
• T wave flattening
• T wave inversion – follows the coronary artery distribution
• ST depression – ominous sign, high predictor of mortality
NSTEMI ECG PATTERNS
NSTEMI ECG PATTERNS
Inverted T waves
ST depression
45 year old man, smoker,
sedentary lifestyle
Chest pain on mild inclines,
relieved by sitting still again
ECG to confirm stable
angina
CASE 3: ANGINA
ECG changes in stable angina:-
• Normal when resting (unless evidence of a previous MI
like Q waves)
Exercise ECG:-
• Treadmill (Bruce protocol) gradually getting harder
• ST depression and developing symptoms
• Exercise test isn’t 100% though
STABLE ANGINA ECG
STABLE ANGINA EXERCISE ECG
ST depression
ECG leads look at the heart from lots of different directions
and give information about the conduction system and
myocardial contraction
ECGs are key investigative tools helping delineate the acute
coronary syndromes and their correct interpretation influences
management dramatically
Stable angina is more of a clinical diagnosis but exercise ECG
can assist where there is uncertainty
SUMMARY

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Acute Coronary Syndrome and the ECG

  • 1. By Laurence Sharifi ISCHAEMIC CHANGES ON THE ECG
  • 2. Some theory if you’re interested ECGs and acute coronary syndromes ECGs and stable angina WHAT WE WILL BE COVERING
  • 3. WHY THE HEART PRODUCES AN ECG SIGNAL
  • 4. The heart contracts because of the cardiac conduction system A wave of depolarisation spreads across the myocardium in a co-ordinated way, making the heart contract in the right way through every heart beat HOW THE HEART BEATS
  • 5. 67 year old man, obese, HTN, DM Retrosternal pain, tight, radiating to arm and jaw lasting past 30 minutes Not relieved with GTN spray, now sweating and distressed Time to take an ECG!! CASE 1: ACS
  • 6. WHY THE ECG LOOKS THE WAY THAT IT DOES
  • 7. Don’t think of an ECG lead as the bit of wire stuck on the chest – this isn’t what it is An ECG lead is actually a calculated voltage difference between two electrodes– not REALLY vital to know about the details Think of a lead as a “photo” of the heart taken at a particular orientation ECG LEADS
  • 8. = ECG LEADS ARE “VIEWS” Think of the ECG leads as photographs of the heart taken at different angles. This slide illustrates this concept using the limb leads
  • 9. = V5 V1 V6 This slide illustrates the same concept but on the chest leads. Cheryl remains the same, we just look at her from different directions
  • 10. The ECG leads all look at the heart from different angles: ECG LEADS ARE VIEWS
  • 11. Each lead is looking at a different part of the heart’s surface
  • 12. Depolarisation travels from the endocardium through to the epicardium (in to out) Repolarisation goes from the epicardium to the endocardium (out to in) HOW THE HEART BEATS
  • 13. • Causes a positive deflection in ECG if travelling towards lead • Causes a negative deflection if travelling away from lead Depolarisation • Causes a negative deflection in ECG if travelling towards lead • Causes a positive deflection if travelling away from lead Repolarisation RULES ABOUT ECG LEADS
  • 14. THE CORONARY CIRCULATION – WHEN IT ALL GOES WRONG
  • 15. • The myocardium is adequately perfused • The conduction system works The heart pumps properly when: • Left Main coronary artery. Branches: • Left anterior descending artery • Circumflex artery • Right coronary artery. Branches: • Acute marginal branch • AV node branch • Posterior descending artery Key vessels are: THE CORONARY ARTERIES
  • 16. Ischaemic tissue • Myocytes are still working – still get an ECG signal from the tissue • Signal is different though as anaerobic cells behave differently Infarcted tissue • Tissue is dying/dead– no ECG signal from the tissue • Heart is beating abnormally due to presence of dead tissue • ECG signal looks different ISCHAEMIC TISSUE BEHAVES DIFFERENTLY TO INFARCTED TISSUE The blood supply can become compromised in: • Stable angina • Acute coronary syndrome (ACS)
  • 17. Coronary artery lumen becomes narrowed Partly (NSTEMI) Tissue becomes ischaemic Tissue dies slowly Wholly (STEMI) Tissue becomes extremely ischaemic (transmural) Tissue dies quickly ACUTE CORONARY SYNDROME
  • 18. K+ channels open earlier in ischaemic tissue Repolarisation normally causes a positive deflection if moving away from lead (think T wave) Ischaemic tissue repolarises early so you get a positive deflection earlier, otherwise known as ST ELEVATION ST Elevation often means SEVERE TRANSMURAL ISCHAEMIA ISCHAEMIC CELLS REPOLARISE FASTER +20 -100 100ms membpotl(mV) Red = normal cardiac action potential Blue = ischaemic tissue action potential
  • 19. ECG in suspected ACS is used to • Confirm or refute the diagnosis • Guide therapy • Estimate prognosis Consider ECG alongside: • Major cardiovascular risk factors (fat, old, DM, HTN) • The description of the pain (central, crushing >20 min, at rest) • History of cocaine indulgence • How the patient looks. Are they sweaty, grey and breathless? Beware the “silent MI” however – a patient may be having a heart attack but look entirely normal. Diabetic patients are particularly susceptible to this THE ECG IN ACS
  • 20. ECG and ACS Therapy • ST elevation MI will benefit from thrombolysis / PCI • Other ACSes need aggressive anti-platelet therapy ECG and ACS prognosis • Assess ACS using risk scoring tools • Resting ECG changes are important variables THE ECG IN ACS
  • 21. Our patient has had a series of ECGs What could they show? CASE 1: ACS
  • 22. ECG CHANGES IN STEMI 0 • No ECG changes 1 • Hyper- acute T waves 2: Infarction • ST elevation 3: Fibrosis • ST normal • T wave inversion • Q wave development 4 • Re- inversion of inverted T waves 5 • Late loss of Q waves Onset Lasts a few minutes Minutes to hours Hours to days Days to weeks Years to decades
  • 23. STEMI PATTERNS • I • II • aVL • V1-5/6 Leads showing ST elevation • Anterolateral Infarct description • Proximal LAD (left anterior desciending) Artery occluded
  • 24. STEMI PATTERNS • II • V1-3/4 Leads showing ST elevation • Anteroseptal Infarct description • Left anterior descending Artery occluded
  • 25. STEMI PATTERNS • II • III • aVF Leads showing ST elevation • Inferior Infarct description • Right coronary if ST  II>III • Circumflex if ST  III>II Artery occluded
  • 26. STEMI PATTERNS • I • II • V5/6 Leads showing ST elevation • Lateral Infarct description • Diagonal branch LAD • Obtuse marginal branch circumflex Artery occluded
  • 27. STEMI PATTERNS • V1 - 3 Leads showing ST depression • Posterior Infarct description • Circumflex Artery occluded This happens because the ST elevation on the posterior wall causes a RECIPROCAL change on the opposite side. Confirm by doing a posterior ECG
  • 28. Patient has had a posterior STEMI ST depression in V1-3 We would see ST elevation in posterior chest leads CASE 1: ACS
  • 30. 74 year old lady, Hx of HTN, PC: chest pain at rest Normal ECG but raised Trop T 12 hours later – ischaemic damage to myocardium highly likely Sounds like ACS, so why normal ECG? CASE 2: ACS
  • 31. Normal ECG is possible in NSTEMI • Only small coronary artery affected • Posterior infarct • Diagnosis is made clinically and with TropT NSTEMI ECG Changes • T wave flattening • T wave inversion – follows the coronary artery distribution • ST depression – ominous sign, high predictor of mortality NSTEMI ECG PATTERNS
  • 32. NSTEMI ECG PATTERNS Inverted T waves ST depression
  • 33. 45 year old man, smoker, sedentary lifestyle Chest pain on mild inclines, relieved by sitting still again ECG to confirm stable angina CASE 3: ANGINA
  • 34. ECG changes in stable angina:- • Normal when resting (unless evidence of a previous MI like Q waves) Exercise ECG:- • Treadmill (Bruce protocol) gradually getting harder • ST depression and developing symptoms • Exercise test isn’t 100% though STABLE ANGINA ECG
  • 35. STABLE ANGINA EXERCISE ECG ST depression
  • 36. ECG leads look at the heart from lots of different directions and give information about the conduction system and myocardial contraction ECGs are key investigative tools helping delineate the acute coronary syndromes and their correct interpretation influences management dramatically Stable angina is more of a clinical diagnosis but exercise ECG can assist where there is uncertainty SUMMARY

Editor's Notes

  1. ACS are due to thrombus in coronary artery that can transiently or permanently occlude the vessel. They can also break up sending emboli distally. Key feature is chest pain at rest
  2. Phase 0: Onset of MI Phase 1: Hyperacute T waves, mechanism unclear. Lasts a few minutes so often not seen Phase 2: ST elevation is a result of sub-epicardium being more ischaemic than sub-endocardium (the outside is more ischaemic than the inside). Leads to a current flow from inside to outside BEFORE the T wave. Phase 3:
  3. Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
  4. Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
  5. Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
  6. Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
  7. V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
  8. Note that a raised trop T with chest pain may be a PE If patient has LBBB then rest of ECG uninterpretable
  9. T wave inversion and ST depression in leads V2-V6