1. No category

ECG interpretation for
beginners – 2
Axel en Luc De Wolf
RZ Tienen
UZ Leuven
3
INFLUENCE OF TIME-TO-TREATMENT ON
THE ODDS RATIO (OR) OF MORTALITY
80
The “golden hour”: 65 lives are saved for every
1,000 patients treated when the treatment is
initiated within the first hour of symptom onset!
ABSOLUTE BENEFIT PER
1,000 TREATED PATIENTS
60
PATHOPHYSIOLOGY
+ EPIDEMIOLOGY
THROMBOLYSIS IN
CLINICAL TRIALS
AND REGISTRIES
NEW TRIALS/
REGISTRIES
40
MANAGEMENT
OF ACUTE MI AND
THE RATIONALE
FOR EARLY
REPERFUSION
20
CLINICAL
QUESTIONS
METALYSE
(+ PRESCRIBING
INFORMATION)
0
0
3
6
9
12
15
18
21
24
COSTS
REFERENCES
TREATMENT DELAY IN HOURS
Boersma et al. Lancet 1996; 348: 771–775.
SYSTEM
REQUIREMENTS
IMPRESSUM
A heart
• Blood circulates, passing near
every cell in the body, driven by this
pump
• …actually, two pumps…
• Atria = turbochargers
• Myocardium = muscle
• Mechanical systole
• Electrical systole
Excitation of the Heart
Excitation of the Heart
Cardiac Electrical Activity
A system
 Quality of ECG?
 Rate
 Rhythm
 Axis








P wave
PR interval
QRS duration
QRS morphology
Abnormal Q waves
ST segment
T wave
QT interval
A system
 Quality of ECG?
 Rate
 Rhythm
 Axis








P wave
PR interval
QRS duration
QRS morphology
Abnormal Q waves
ST segment
T wave
QT interval
P wave
• Are there P waves….?
– Pointy = P pulmonale (RA hypertrophy)>2,5mm
– Bifid = P mitrale (LA hypertrophy)>2,5mm
• Not very accurate or useful….
PR interval
 Start of P wave to start of QRS
 Normal = 0.12-0.2s
 Too short – can mean WPW syndrome (ie. an
accessory pathway), or normal!
 Too long –means AV block (heart block) 1st/2nd/3rd degree
A system
 Quality of ECG?
 Rate
 Rhythm
 Axis








P wave
PR interval
QRS duration
QRS morphology
Abnormal Q waves
ST segment
T wave
QT interval
QRS complex
• Should be <0.12s duration
• >0.12s = BBB (either LBBB or RBBB)
• ‘Pathological’ Q waves can mean a previous
MI (? territory)
• >25% size of subsequent complex
• Q waves are allowed in V1, aVR and III
BBB
Look at V1 and V6
W I LL ia M = LBBB
M a RR o W = RBBB
QRS complex
 Is there LVH?
 Sum of the Q or S wave in V1 and the biggest R
wave in V5 or V6 >35mm
 (R wave in aVL >11mm)
 Not actually very useful….
A system
 Quality of ECG?
 Rate
 Rhythm
 Axis








P wave
PR interval
QRS duration
QRS morphology
Abnormal Q waves
ST segment
T wave
QT interval
ST segment
 ST depression
◦ Downsloping or horizontal = abnormal
◦ Ischaemia (coronary stenosis)
◦ If lateral (V4-V6), consider LVH with ‘strain’ or digoxin (reverse
tick sign)
 ST elevation
◦ Infarction (coronary occlusion)
◦ Pericarditis (widespread)
 These are usually in ‘territories’ eg. anterior/lateral/inferior
etc. and will be present in contiguous leads
T wave
• Peaked (hyperkalaemia or normal young man)
• Inverted/biphasic (ischaemia, previous infarct)
• Small (hypokalaemia)
• No pot, no tea!
QT interval
 Don’t worry about too much…
 Start of QRS to end of T wave
 Needs to be corrected for HR
 Various formulae
◦ eg. Bazett’s:
 Computer calculated often wrong
 Long QT can be genetic (long QT sy.) or secondary eg. drugs
(amiodarone, sotalol)
 Associated with risk of sudden death due to Torsades de Pointes
Morfologische afwijkingen
Hypertrofie
Voorkamer en Kamer
K51 – Rechter voorkamerhypertrofie
•
•
•
•
•
Dilatatie van de rechter voorkamer
Hoge spitse P toppen in afl. II & aVF ( 0,25 mV)
Toename initiële P voltage in afl. II, III, aVF & V1
Normale duur P golf
Vaak in combinatie met tekenen van rechter kamerhypertrofie
P pulmonale
K52 - Linker voorkamerhypertrofie
• Dilatatie van de linker voorkamer
• P golf > 120 ms
• Gehaakte P top door toename amplitude terminaal deel van P golf in afl. I,
II, aVL & V6
• Bifasische P golf in afl. V1 met terminaal negatief deel ( 0,1 mV,  40 ms)
Risico op atriale fibrillatie
K53 - Linker kamerhypertrofie
• (R in V5 of V6) + (S in V1 of V2) > 3,5 mV (35 mm)
• ST elevatie concaaf naar boven met hoge positieve
T top in rechtszijdige afleidingen
• ST depressie convex naar boven met asymmetrisch negatieve T top in
linkszijdige afleidingen
• Normale as
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS
complexes?
As the heart muscle wall thickens there is an increase in
electrical forces moving through the myocardium resulting in
increased QRS voltage.
LVH
Increased QRS voltage
ECHOcardiogram
For more presentations
www.medicalppt.blogspot.com
Left Ventricular Hypertrophy
• Criteria exists to diagnose LVH using a 12-lead ECG.
– For example:
• The R wave in V5 or V6 plus the S wave in V1 or V2 exceeds 35
mm.
• However, for now, all
you need to know is
that the QRS voltage
increases with LVH.
For more presentations
www.medicalppt.blogspot.com
K55 – Rechter kamerhypertrofie
•
•
•
•
•
•
Hoge R in V1 (> 0,7 mV) met R/S ratio > 1
Vlakke R progressie
Diepe S in V5-V6 ( > 0,7 mV) met R/S ratio < 1
qR of rSR’ in V1 met hoge spitse R’ (diff. diagnose RBTB)
Hoge, terminale R in aVR
Rechter asdeviatie
(komt overeen met diepe S in I en aVL)
Kliniek van longlijden
Ischemie en Infarkt
K56 - Ischemie
• Wanneer een elektrode geplaatst wordt tegenover een zone van ischemie
betekent
- ST segment depressie:
subendocardiale ischemie
- ST segment elevatie:
transmurale (subepicardiale) ischemie
Characteristic changes in AMI
•
•
•
•
•
ST segment elevation over area of damage
ST depression in leads opposite infarction
Pathological Q waves
Reduced R waves
Inverted T waves
ST elevation
• Occurs in the early stages
R
ST
P
Q
• Occurs in the leads facing the
infarction
• Slight ST elevation may be
normal in V1 or V2
Deep Q wave
• Only diagnostic change of
myocardial infarction
R
ST
• At least 0.04 seconds in
duration
P
T
Q
• Depth of more than 25% of
ensuing R wave
T wave changes
• Late change
R
• Occurs as ST elevation is
returning to normal
ST
P
• Apparent in many leads
T
Q
Bundle branch block
Anterior wall MI
I II III
aVR aVL aVF
Left bundle branch block
V1 V2 V3
V4 V5 V6
I II III
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Sequence of changes in evolving AMI
R
R
R
ST
T
ST
P
P
Q S
P
T
Q
1 minute after onset
Q
1 hour or so after onset
A few hours after onset
R
ST
P
ST
P
T
Q
A day or so after onset
T
P
T
Q
Later changes
Q
A few months after AMI
Anterior infarction
Anterior infarction
I II III
Left
coronary
artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Inferior infarction
Inferior infarction
I II III
Right
coronary
artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Lateral infarction
Lateral infarction
I II III
Left
circumflex
coronary
artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Location of infarct combinations
I
aVR
V1
aVL
ANT
POST
V2
LATERAL
II
V4
ANT
SEPTAL
V5
ANT
V3
III
INFERIOR
aVF
V6
LAT
Diagnostic criteria for AMI
• Q wave duration of more than 0.04
seconds
• Q wave depth of more than 25% of
ensuing r wave
• ST elevation in leads facing infarct
(or depression in opposite leads)
• Deep T wave inversion overlying
and adjacent to infarct
• Cardiac arrhythmias