influence of time-to-treatment on the odds ratio (or) of mortality

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