influence of time-to-treatment on the odds ratio (or) of mortality
DESCRIPTION
ECG interpretation for beginners – 2 Axel en Luc De Wolf RZ Tienen UZ Leuven. INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY. 3. 80. - PowerPoint PPT PresentationTRANSCRIPT
ECG interpretation for beginners – 2
Axel en Luc De Wolf
RZ Tienen UZ Leuven
INFLUENCE OF TIME-TO-TREATMENT ON THE ODDS RATIO (OR) OF MORTALITY
Boersma et al. Lancet 1996; 348: 771–775.
ABSO
LUTE
BEN
EFIT
PER
1,
000
TREA
TED
PATI
ENTS
TREATMENT DELAY IN HOURS
0 3 6 9 12 15 18 21 240
20
40
60
80
3
PATHOPHYSIOLOGY + EPIDEMIOLOGY
THROMBOLYSIS IN CLINICAL TRIALS AND REGISTRIES
NEW TRIALS/ REGISTRIES
MANAGEMENT OF ACUTE MI AND THE RATIONALE FOR EARLY REPERFUSION
CLINICAL QUESTIONS
METALYSE (+ PRESCRIBING INFORMATION)
COSTS
REFERENCES
SYSTEM REQUIREMENTS
IMPRESSUM
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!
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 systemQuality of ECG?
RateRhythmAxis
P wavePR intervalQRS durationQRS morphologyAbnormal Q wavesST segmentT waveQT interval
A systemQuality of ECG?
RateRhythmAxis
P wavePR intervalQRS durationQRS morphologyAbnormal Q wavesST segmentT waveQT 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 QRSNormal = 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 systemQuality of ECG?
RateRhythmAxis
P wavePR intervalQRS durationQRS morphologyAbnormal Q wavesST segmentT waveQT 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
W I LL ia M = LBBB
M a RR o W = RBBB
Look at V1 and V6
QRS complexIs 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 systemQuality of ECG?
RateRhythmAxis
P wavePR intervalQRS durationQRS morphologyAbnormal Q wavesST segmentT waveQT interval
ST segmentST 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 intervalDon’t worry about too much…
Start of QRS to end of T waveNeeds to be corrected for HRVarious 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
• 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)
K52 - Linker voorkamerhypertrofie
Risico op atriale fibrillatie
• (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
K53 - Linker kamerhypertrofie
For more presentations www.medicalppt.blogspot.com
Left Ventricular Hypertrophy
Why is left ventricular hypertrophy characterized by tall QRS complexes?
LVH ECHOcardiogramIncreased QRS voltage
As the heart muscle wall thickens there is an increase in electrical forces moving through the myocardium resulting in increased QRS voltage.
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.
• 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)
K55 – Rechter kamerhypertrofie
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
R
P
Q
ST
• Occurs in the early stages• Occurs in the leads facing the
infarction• Slight ST elevation may be
normal in V1 or V2
Deep Q wave
R
P
Q
T
ST
• Only diagnostic change of myocardial infarction
• At least 0.04 seconds in duration
• Depth of more than 25% of ensuing R wave
T wave changes
R
P
Q
T
ST
• Late change• Occurs as ST elevation is
returning to normal• Apparent in many leads
Bundle branch block
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Anterior wall MI Left bundle branch block
Sequence of changes in evolving AMI
1 minute after onset 1 hour or so after onset A few hours after onset
A day or so after onset Later changes A few months after AMI
Q
R
P
QT
STR
P
Q
ST
P
QT
ST
R
P
S
T
P
QT
ST
R
P
Q
T
Anterior infarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary artery
Inferior infarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
Lateral infarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
Location of infarct combinations
aVR V1 V4I
II
III
LATERAL
INFERIOR
ANTPOST ANT
SEPTAL
ANT
LAT
aVL
aVF
V2
V3
V5
V6
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