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
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
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)
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
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
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
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
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:
Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
Make the point about V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
V1-V3 showing reciprocal changes due to infarct on opposite wall influencing the local ECG.
Note that a raised trop T with chest pain may be a PE
If patient has LBBB then rest of ECG uninterpretable