ECG Interpretation

Dr S. A. Medway

SCGH ED CME Thursday 12/03/2015

Original Presentation Credit to Dr. James Wheeler

Resources

• Original Presentation – Dr James Wheeler

• Erics Medical Lectures –YouTube

• LITFL

• emin5.com

• Time on the floor

What is an ECG?

• Graphical representation of the electrical activity of the myocardium over

time

• Standard 12 lead ECG assesses this in various planes (coronal & transverse)

to give a roughly 3D view of the heart

– 3 biploar leads I, II, III

– 9 unipolar leads aVR, aVL, aVF, V1-V6

– Can consider other unipolar lead placements

– V1-6R – look at RV

– V7-9 – look at post LV wall

Lead placement

Anatomical relationship

ANATOMICAL RELATIONSHIP OF LEADS

Considerations

• Methodical systematic approach– “More is missed by not looking than by not

knowing"[Thomas McCrae, 1870-1935]• Consider patients clinical condition• Obtain previous ECG’s for comparison• Limitations of ECG – Electrical activity, not

contractility etc…• The “ normal” ECG

– All normal ECG’s do not look the same– But they do have features in common

ECG helps in detection of:

– Ischaemic heart disease, acute or chronic

– Dysrrhythmias

– Electrolyte disturbances

– Conduction abnormalities (HB, BBB)

– CAD (exercise stress test)

– Cardiac structural abN (LVH, RVH)

– Cardiac manifestations of non-cardiac disease (PE, metabolic disorders, lung disease…)

COMPONENTS OF ECG• Rate• Rhythm / Regularity• Cardiac Axis• Waveform (axis, amp, duration)

– P wave– QRS complex– T wave– U wave

• Intervals– PR interval– QT interval– RR interval

• Segments– PR segment– ST segment

ECG systematic evaluation• Calibration / Speed

– N = 10mm/1mV, 25mm/sec

• Rhythm

– Regularity / QRS width / Rate

• Axis

– N / LAD / RAD

• P wave

– ?presence / relationship to QRS

– Axis

– Amp: RAA / LAA

• PR interval

– Duration / HB / Pre-excitation

• PR segment

– Depression

• QRS

– duration / amplitude / morphology

– Q waves

– R wave

• ST segment

– Depression / elevation / morphology

• T wave

– Axis / morphology / duration

• QT interval

• U wave

• Other waves (delta, osborne, epsilon, pacing

spikes, artifacts)

• ?other leads (V4R, V7-9, Lewis)

Normal ECG

ECG Rhythm

• Rate

– N / tachy / brady

• Regularity

– Regular / reg irreg / irreg irreg

• QRS morphology

– Narrow / wide (120ms)

• P waves

– Absent

– Present / morphology / relationship QRS / PR interval

ECG Rhythm

• Is it normal sinus rhythm (NSR)?

– Can you identify P waves

– P waves preceding all the QRS complexes

– QRS complexes after every P wave

– Normal PR interval

– Regular

• P waves most easily seen in II & V1

• If not – it’s not Sinus Rhythm. What is it??

Arrhythmias - Causes

• Abnormal impulse generation

– SA node

– Outside of the SA node

• Abnormal impulse conduction

– Damaged conduction pathways

– Re-entrant pathways

Note: there are many potential pacemaker sites in the heart!

AXIS (Coronal Plane)• Axis of any ECG depolarisation or repolarisation

• QRS axis in the coronal (frontal) plane as determined by the limb leads :– bipolar (I, II, III) &

– unipolar (aVR, aVL, aVF)

• Normal axis determined largely by the relative size of both the RV & LV, and the position of the heart– may change in various pathological conditions

Determining QRS axis

• Normal QRS coronal axis

is (??) -30 to +90

degrees:

Both I & aVF +ve = normal

Both I & aVF -ve = EAD

lead I -ve & aVF +ve = RAD

lead I +ve & aVF -ve

lead II +ve = normal

lead II -ve = LAD

N

RAD

LADEAD

Normal ECG

Right axis deviation

Causes of RAD

• RVH (most common)

• Acute RH strain - Pulmonary embolus

• Dextrocardia

• Normal in children and tall thin adults

• Chronic lung disease even without pulmonary hypertension

• Left posterior hemiblock

• Lateral / apical AMI

• WPW syndrome - left sided accessory pathway

• Atrial septal defect

• Ventricular septal defect

Left axis deviation

Causes of LAD

• ?LVH

• Left anterior hemiblock

• LBBB

• Q waves of inferior myocardial infarction

• Artificial cardiac pacing

• Emphysema

• WPW syndrome - right sided accessory pathway

• Tricuspid atresia

• Ostium primum ASD

Causes of extreme axis deviation

• Emphysema

• Hyperkalaemia

• Lead transposition

• Artificial cardiac pacing

• Ventricular tachycardia

Transverse axis of QRS / Rotation

• Normal transverse axis is leftward and posterior:– Hence usually a progression in R wave height from V1 to

V6

• Transitional lead (where R = S)– usually V3 or V4

• Displacement of transition:– Right (V1, V2) = counterclockwise rotation

– Left (V5, V6) = clockwise rotation

Normal ECG

WAVE MORPHOLOGY

• Shape

• Axis

• Duration

• Amplitude

• Progression

P wave - Normal

• Normal P wave– Represents atrial depolarisation

– Axis 0 – 75 deg

– Upright monophasic I, II, III and AVF

– Inverted in AVR

– Biphasic in V1 (RA bf LA)

– <2.5mm (0.25mV) in height limb leads

– <1.5mm in praecordial leads

– <3mm (120ms sec) in width

Lead II

Normal ECG

P wave - Abnormalities

• Morphology• RAH (Pulm HTN) increased amplitude• LAH (MS, HTN) notched in I & II, deep -ve in V1• A Fib/Flut no clear P waves / sawtooth• Hyperkalaemia reduced amplitude• Ectopic atrial rhythm

• Axis• Retrograde• Dextrocardia right displacement• Pulmonary disease inferior displacement• Congenital heart disease left displacement

• Rhythm• Ectopic atrial rhythm• A Fib / flutter• Multifocal atrial tachycardia• SVT (retrograde P waves)

P wave – RAE / LAE

PR Interval - Normal

• Start of the P wave - start of the QRS

• Normal = 120 – 200ms

= 3 - 5 small squares

• Increases with age

• Is rate dependent

• Delay at AV node

» Protect ventricles

» Allow for ventricular filling

PR interval - Abnormal

• Short– Preexcitation of ventricles (WPW) & other SVT’s– AV junctional rhythm– Exercise induced tachycardia

• Long– AV Block– Hyperkalaemia– CHD– Drugs (Digoxin, B-Blockers, Quinidine)– Hypothermia– Hypothyroidism

PR segment• Normally isoelectric using the TP (not ST) segment as a

baseline

• Abnormal:

– Elevation

• Myocarditis (aVR, V1)

• Atrial infarction

– Depression

• Myo/pericarditis

• Atrial infarction

• Exercise induced tachycardia

QRS parameters

• Q waves

– ?abnormal Q’s

• R wave

– Progression

– Dominant R wave in aVR / V1

• QRS amplitude

• QRS duration (<100ms)

QRS waveform nomenclature

R r qR qRs Qrs QS

Qr Rs rS qs rSr’ rSR’

QRS complex – Q waves

• Normal Q waves– Due to rightward septal depolarisation

– May occur in I, II,III, aVR, aVF, aVL, V4-V6

– Size <0.4mV (4 squares) or 25% of R wave height

– Duration <0.03sec (under 1 square)

– May be slightly greater in III & aVR (normal variant)

– No Q waves in V1-V3

• Abnormal Q waves– >0.4mV (4 squares) or 25% of R wave height

– >0.03sec (ie. 1 square or greater)

– Presence in V1-3

– Suggest: evolved AMI / ventricular enlargement / rotation of heart / HOCM / abnormal conduction / lead misplacement

Normal ECG

QRS – R wave Abnormalities• Dominant R wave V1

– normal in children / young adults / persistent juvenile pattern

– RVH / PE / L to R shunt

– RBBB

– Post AMI (= Q wave)

– WPW type A

– Dextrocardia

– HOCM

– Muscular dystrophy

– Incorrect lead placement

• Dominant R wave aVR (>3mm, or R/S ratio >0.7)

– Na channel blockade

– Dextrocardia

– RVH

– Incorrect lead placement

• Poor R wave progression– Prior anteroseptal AMI / LVH / incorrect lead placement / dextrocardia / normal variant

QRS abnormal amplitude:• Increased

• LVH (S in V1 + R in V5 or V6 >35mm sensitive but not specific)

• BER• Hyperthyroidism• Normal / athletes

• Decreased (<5mm limb leads, <10mm precordial)

• Pericardial / Pleural effusion• Hypothyroidism• Pneumothorax• Restrictive cardiomyopathy• COPD• Haemochromatosis

• Fluctuating / Electrical alternans

QRS prolonged duration:

• Causes– BBB (may be rate related)

– Ventricular origin / Ventricular pacing

– Hyperkalaemia

– Na channel blockade

– Pre-excitation

– Hypothermia

ST Segment - Normal• Represents period between depolarisation & repolarisation

(J point to T wave)

• Normally isoelectric with respect to TP & PR segment

• Abnormal if:

– Elevated

– Depressed

Normal ECG

ST segment - Elevation

• Morphology– Concave - some non-AMI causes– Convex - suggestive of AMI

• Distribution– Widespread - ?non- AMI– Localised to anatomically contiguous leads - suggestive of AMI

• Magnitude– Larger suggestive of AMI

• QRS morphology– Large amplitude - consider LVH– Widening - consider BBB or vent. paced rhythm

ST segment elevation causes:• Acute Coronary Syndrome• Acute pericarditis• Benign early repolarisation (BER)• LV aneurysm• LVH• BBB

• Left - R to mid precordial leads• Right - lateral leads

• Cardiomyopathy• Acute myocarditis• Hypothermia• Hyperkalaemia• Myocardial contusion• CNS injury• Brugarda Syn• Paced vent. Rhythms• Post-electrical cardioversion

BER- Prominent, assymetrical, concordant (with QRS) T waves - Widespread concave ST segments V2-5- J point elevation (notching / slurring)- <25% T wave height in V6 (usually <2mm precordial)- No reciprocal ST depression- Stable over time

ST Segment - Depression

• Morphology– Flat or downsloping with ACS

• Distribution• QRS morphology

– Large amplitude - consider LVH– Wide complex - BBB, vent. Pacing, LVH

ST segment depression causes:

• ACS (>1mm depression at J point, diffuse, horizontal or downsloping, not localising)

• AMI (NSTEMI, Post MI, reciprocal)• BBB• LVH• Ventricular pacing• Digoxin effect• Rate related• Myocardial contusion• Metabolic• Post-electrical cardioversion

T wave - Normal

• Magnitude– No clearly defined range (<5mm limb, <15mm precordial)

– General rule - 1/2 the height of preceding QRS

• Axis– Largely dependent on QRS (concordant)

– Positive in I, II, V3-V6

– Negative in aVR, V1

– Variable in III, aVF, aVL, & V2

Normal ECG

T wave - Abnormalities

• Prominent• AMI (hyperacute), Hyperkalaemia, BER, Myopericarditis (concave STE & PR

depression), BBB (esp. LBBB in V1-V3), LVH (similar to LBBB)

• Inverted• ACS (all stages) NB may be flattened

• Wellen’s Syn. (critical prox LAD stenosis without MI) NB may be biphasic

• Past MI• Pericarditis• Children / Persisting juvenile pattern (V1-V3)

• CNS injury/ICH• BBB• PE, RVH, LVH, HOCM, Digoxin, toxic, metabolic

U wave

• Positive deflection that occasionally occurs after T wave

• Most visible at slow HR’s in V1-V4

• The origin is uncertain (repol of the IVS)

• Presence or absence does not signify pathology

• Abnormal if:

– >1/3 preceding T wave height (N 1-2mm)

– Disconcordant with T wave

U wave - Abnormalities

• Increased amplitude• Athletes• Bradycardia• HypoK+ / HypoCa2+ / HypoMg2+• CNS event• Hypertension• Hypothermia• Medications (digoxin, quinidine)

• Inversion• Ischaemia• LV overload• RV overload• PE

QT interval - Normal

• Measured from the start of the QRS to the end of the T wave– Measure in II, V 5-6– use slope– include U waves if continuous with T wave

• Represents the time required for ventricular activation & recovery

• Range 330 - 440ms (460ms women)• Rule of thumb < half RR interval• QT interval corrected to the heart rate

QTc calculation

• Multiple formulas

• Bazett’s

– QTc = measured QT interval

R-R interval

• Hence QTc = QT at HR of 60bpm

QTc - Abnormal Duration• Short

– Hypercalcaemia / Digoxin / Congenital

• Long– lengthened repolarisation time

– ventricle more susceptible to early after depolarisation which can precipitate a variety of potentially fatal arrhythmias (VF, VT, torsades de

pointes)

– Congenital long QT syndromes

– CNS disease

– Metabolic syndromes (HYPO: K+, Ca++, T4)

– Hypothermia

– Drugs:

• erythromycin, cisapride, amiodarone, haloperidol, quinidine…

Overview

• Rate & rhythm

• Axis

• Wave morphology

• Intervals

• Segments

• In the context of:– Look at the patient (hear the story)

– Compare to old ECG’s

– Get a second opinion