ECG

Dr. Sumit Kr. GhoshAsst. Professor

Department of MedicineMedical College & Hospital,

Kolkata

INTRODUCTION

Graphic representation of electrical activities of heart

Resting ECG

Exercise ECG / TMT

24-hr ECG / Holter

READING ECG

• Rate

• Rhythm

• Axis

• Lie & Rotation

• Voltage

• Waves & Intervals

• Abnormalities

ECG PAPER

STANDARDISATION

• 1mv will produce deflection of 10 mm / 1 cm

• Stylus should have an appropriate pressure

WAVES & INTERVALP Q R S T > 5mmq r s < 5mm

PQRSTUJ-pointJδPRQRSSTQTTPPP & RR

LEADSLead = paired electrode

12 leads

Limb leads Precordial leads Frontal or Coronal plane leads Horizontal plane leads Bipolar unipolar (low EP) unipolar I, II, III aVR, aVL, aVF v1, v2, v3, v4, v5, v6 rt side septum lt sideI, avL, v5, v6 : lateral wall II, III Avf : inferior wall

Long leadsV7, v8, v9V1r – v9r3v1 – 3v9Esophageal leads

Resultant vector

• Towards lead : positive / upward deflection

• Away from lead : negative / downward deflection

• Perpendicular to lead : equiphasic deflection

RATE

Ventricular rate vs Atrial rate

Rate = 1500/ no of small square = 300/no of large square

Depends on speed of ECG paper

Usual speed = 90m/hr =1.5m/min

No of QRS complex in 1 min = HR

RHYTHM

• Regular :~ Sinus ~ Nodal~ Idioventricular

• Irregular :~ Regularly irregular~ Irregularly irregular

AXIS• Normal axis : 0 to +90 degree (most cases +40 to +60 degree)• LAD : 0 to -90 degree (slight LAD : 0 to -30 degree

marked LAD : -30 to -90 degree ) • RAD : +90 to ± 180 degree• Inderminate / NW axis : -90 to ± 180 degree

an expression of : - marked RAD - marked LAD - discharge of ectopic ventricular pacemaker

AXIS DETERMINATION• Lead I,II & III• Pairs of perpendicular leads• Perpendicular to the lead where R=S• In degree

I II III

↑ ↑ ↑ Normal

↑ ↑ ↓ ↓ LAD

↓ ↑ ↑ RAD

+

+

_

_ I

aVF

0± 180

- 90

+ 90

NORMAL AXIS RAD LAD INDETERMINATE AXIS

EASY TO REMEMBER

I (left) aVF (right)

↑ ↑ Normal

↑ ↓ LAD

↓ ↑ RAD

↓ ↓ Indeterminate

LAD

• LAHB• LBBB

• Inf wall MI• Pacing from apex of RV/LV• WPWIsolated LVH does not cause

LAD

RAD

• RV dominance - acq. Rt heart disease : pulm embolism chr. Cor pulmonale - cong. heart disease : TOF• Anterolateral MI• LPHB• WPW

LIE & ROTATION• LIE : in frontal plane [ vertical (90 degree) to horizontal (0 degree )

• Rotation : in horizontal plane~ Clockwise – persistent S waves in v5, v6~ Anti-clockwise – R waves in v2

P - WAVE

• Atrial activity (RA earliar than LA)• Best seen in lead II & v1• Normal duration : 0.08 s – 0.1 s (not > 0.11 s)• Normal amplitude : not > 2 mm ( max – 2.5 mm)• Diphasic in v1• Inverted in aVR (normally), wrong electrode placement,

dextrocardia, retrograde atrial activation• Absent : Atrial fibrillation, nodal rhythm, hyperkalemia• P-pulmonale : tall & peaked (amplitude > 2.5 mm) » » RAH• P-mitrale : wide & notched (duration > 0.11 s) » » LAH• P-tricuspidale

QRS COMPLEX

• Ventricular depolarisationQ-wave : initial negative deflection septal depolarisation :: from left to rightR-wave : depolarisation of venticular muscle massS-wave : depolarisation of postero-basal part of left

ventricle, superiormost part of ventricular septum• High amplitude : RVH / LVH• Low amplitude : Low voltage complex

(< 5 mm in limb leads & < 10 mm in precordial leads)

Standardisation is important• Taller in v5 than v6

QRS COMPLEXQRS in precordial leads

T-WAVE

• Ventricular repolarisation

• Blunt apex with 2 asymerical limbs : proximal limb shallower than distal

• Tall –peaked : hyperkalemia

• Tall- wide : hyperacute stage of MI

• Inverted : IHD, Ventricular strain, CVA

• Flat : thick chest wall, emphysema, pericardial effusion, hypokalemia

U-WAVE

• Positive deflection after T & before P of next cycle

• Slow repolarisation of Purkinje’s fibres, septum, papillary muscles but uncertain

• Mid-precordial leads – v2 to v4

• Prominent : hypokalemia

• Inverted / absent : diastolic overload / myocardial dysfunction

P-R INTERVAL

• Beginning of P-wave to beginning of QRS complex

• Intra-atial, AV nodal & His-Purkinje coduction• Normal duration : 0.12 – 0.20 s• Prolonged : Acute rheumatic fever, 1st degree

AV block• Progressive prolongation : Mobitz type-I (2nd

degree AV block) » » Wenckebach phenomenon• Shortened : WPW syndrome, AV nodal rhythm

QRS INTERVAL• Total ventricular depolarisation• Beginning of Q-wave ( beginning of P-wave,

if no Q-wave present) to termination of S-wave

• Normal duration : usually not > 0.09 sec (range 0.05-0.11 s)

• Prolonged : Intaventricular conduction defect or BBB ≥ 0.12 sec » » complete BBB

• Intrinsicoid deflection / ventricular activation time : time taken for an impulse to traverse myocardiumVAT normally not > 0.02 s in v1, v2 & not > 0.04 s in v5, v6

ST SEGMENT

• End of QRS complex to beginning of T• Normal ST segment merges smoothly & imperceptibly with

proximal limb of T : difficult to separate• Time interval between ventricular depolarisation &

repolarisation• Isoelectric to TP segment• Elevated :

~ with upward convexity : AMI, coronary spasm, LV Aneurysm~ with upward concavity : acute pericarditis

• Depressed :~ oblique/plane/sagging : CAD~ mirror image of correction mark : digitalis effect~ upward convexity : strain pattern

• End of QRS complex & beginning of ST segment : J point

QT INTERVAL

• Beginning of Q to end of T• Ventricular depolarisation + repolarisation• Corrected QT or QTc : as QT changes with heart rate• Bazett’s formula : QT interval √RR intervalIt should be ≤ 0.44 sProlonged : acute rheumatic carditis, hypokalemia,

hypocalcemia, drugsShortened : hypercalcemia, digitalis, hyperthermia

QTc =

PP & RR INTERVAL• PP interval : distance between 2 successive P waves

- reflects atrial rate

• RR interval : distance between 2 successive R waves - reflects ventricular rate

• Normally PP = RR

Atrial hypertrophy :LAH : P-mitrale RAH : P- pulmonaleBi-atrial hypertrophy

Ventricular hypertrophy :LVHRVHBi-ventricular hypertrophy

LVH• Voltage criteria :

~ Sv1 + Rv6 > 35~ Sv1 / Rv6 ≥ 20~ Rv6 ≥ Rv5~ RI ≥ 15~ RaVL ≥ 11~ Rall(12) > 175

• Horizontal heart • VAT in v5/v6 > 0.04 s• Strain pattern in I, aVL, v5, v6

LAD is not a criteria for isolated LVH

• Pressure overload LVH • Volume overload LVH

RVH• Voltage criteria :

~ R > S~ Rv1 > 5 mm~ persistent Sv5 / Sv6

• Usually RAD (most common & at times only manifestation); but axis may be normal

• Vertical heart• VAT in v1 > 0.02 s• Strain pattern in v1, Avr• Associated P-pulmonale may be there

BIVENTRICULAR HYPERTROPHY

• LVH + RAD• LVH + Clockwise rotation • Tall Rv6 + tall Rv1 ( R > S)

CORONARY INSUFFICIENCY

• Impaired coronary blood flow : present all the time : absolute

• Increased demand : present time to time : relative• ST depression : horizontality, upward sloping, plane,

downward sloping• ST elevation : coronary vasospasm

more severe than ST depression • T wave :

~ symmetrical limbs with sharp vertex : coronary insufficiency~ asymmetrical limbs with blunt vertex : strain, digitalis effect

• Inverted U

MYOCARDIAL INFARCTION

ECG CHANGES• Hyperacute phase

~ increased amplitude of R wave~ increased VAT~ slope elevation of ST segment~ tall & wide T

• Fully evolved phase

~ pathological Q~ ST elevation with upward convexity~ symmetrical T inversion

• Chronic stabilized phase

~ pathological Q~ ST segment & T may be normal or point towards coronary insuffiency

Indicative & reciprocal changes

AMI

LV RVv1 & v4R

Anterior wall

Extensive anterior wallI, aVL, v1 to v6

Anterolateral wallI, aVL, v4 to v6

Anteroseptal walv1 to v4

Apical wallV5,V6

Inferior wallII, III, aVF

Posterior wallmirror-image change

in v1 to v3, esp v2

PATHOLOGICAL Q• Present in indicative leads• 0.04s in duration• >4 mm deep• >1/4th of R wave magnitude

Physiological Q• Septal depolarisation from left to right• Present in lateral leads I, aVL, v5,v6

Loss of Q : early feature of LBBB

Deep Q with giant negative T : HOCM

• Sinus rhythm : 60-100 beats/min• Sinus arrythmia (sinus node rate can change with

inspiration/expiration, especially in younger people variation of the P-P interval from one beat to the next by at least 0.12 seconds

• Sinus tachycardia : regular sinus rhythm with sinus node rate > 100/min

• Sinus bradycardia : regular sinus rhythm with sinus node rate < 60 / min

Similarities :Premature

EctopicEtiology

Dissimilarities :

SVPB VPB

Focus in Atrium ( other than SA node)

Ventricle

QRS complex Morphology similar

Narrow

Morphology dissimilar

Wide

ST-T No significant change Usually displaced in opposite direction of QRS

Compensatory pause Incomplete Complete

APC / SVPB vs. VPC / VPB

SUPRAVENTRICULAR TACHYARRYTHMIA

SVTs from a sinoatrial source:• Inappropriate sinus tachycardia • Sinoatrial node reentrant tachycardia (SANRT) SVTs from an atrial source:• Ectopic (unifocal) atrial tachycardia (EAT) • Multifocal atrial tachycardia (MAT) • Atrial fibrillation with a rapid ventricular response • Atrial flutter with a rapid ventricular response

SVTs from an atrioventricular source (junctional tachycardia):• AV nodal reentrant tachycardia (AVNRT) or junctional reciprocating

tachycardia (JRT) • AV reentrant tachycardia (AVRT) - visible or concealed (including

Wolff-Parkinson-White syndrome) • Junctional ectopic tachycardia

PAT / PSVT / AVNRT• A run of rapidly repeated SVPBs ( usually ≥ 3 )• Narrow QRS• Rate around 160-220/ min • Usually 1:1 conduction; sometimes AV block associated

(PAT with block)• Prolonged PR

• Management : carotid sinus massage, adenosine,

verapamil, DC cardioversion

Atrial fibrillation

• Chaotic atrial excitation & contraction• Atrial rate 350-600 / min• No definite P; replaced by ‘f’ wave• Irregularly irregular ventricular rhythm• Narrow QRS• Etiology : • Management :

Atrial flutter• Regular atrial contraction• Atrial rate 220-350 / min• Ventricular rate ½ - ¼ th of atrial rate; may be

irregular; QRS complex : normal morphology • “Saw-toothed” appearance; flutter wave

VENTRICULAR TACHYARRYTHMIA

VT

VFl

VFVPC

Bigeminy : alternate sinus beat & VPC

Trigeminy : 2 sinus beat followed by VPC

Couplets / pairs : 2 successive VPCs

VT : ≥ 3 consecutive VPCs with rate >100

VT

Sustained VT : >30s in duration & symptomatic : generally requires termination by anti-tachycardia pacing techniques

Non-sustained VT : episodes are short (≥3 beats) and terminate spontaneously

Monomorphic VT : regular rate and rhythm and fixed shape or morphology of the ECG trace

Polymorphic VT : irregular in rate and rhythm and has varying shapes or morphologies on the ECG

Monomorphic VT may deteriorate into polymorphic VT to VF

VFl

• High frequency (250- 350/min) beats• The ECG signal looks like sinusoidal or ‘sine-

like wave’ form • High rate of contraction of heart chambers : time

of blood flow into the chamber becomes very small : very little blood flows to body

• The person who is experiencing VFl is close to unconsciousness

VF

• Most dangerous arrythmia• Ventricular rate 350-450/min• Totally uncoordinated : no discriminate waves :

totally irregular, bizarre & deformed deflections of varying width, height & shape

• No audible heart sounds, no palpable pulse• Treatment : immediate electrical defibrillation• If lucky to survive from VT, chance of VF in near

future

ATRIOVENTRICULAR CONDUCTION DEFECTS

• 1st degree

• 2nd degree~ Mobitz type I~ Mobitz type II~ Constant / fixed AV block

• 3rd degree / Complete block

1st degreeProlonged PR interval (>0.2 s)

2nd degreeMobitz type IMobitz type IIConstant / fixed AV block

3rd degree / Complete blockNo SA impulse pass through AV

nodeIdioventricular rhythmNo synchrony between atrial rhythm

& ventricular rhythm

Mobitz type I Mobitz type II

More common Less common

Benign Serious

Inf wall MI Ant wall MI

Proximal to bundle of His

Distal to bundle of His

Prognosis better Prognosis worse

INTERVENTRICULAR CONDUCTION DEFECTS

• Unilateral bundle branch block ( LBBB, RBBB)

• Peripheral block ( LAHB, LPHB, Septal block)

• Bifascicular block

• Trifascicular block

BBB

LBBB• M pattern or M-shaped complexes in lead I, aVL, v5, v6• Absent Q• ST depression with T inversion• QRS interval more or less 0.12s• Usually LAD• Usually VAT prolonged

Most cases have organic heart diseaseRecent onset LBBB : think of AMIPresence of Q in lateral leads : never LBBB

RBBB

• RSR’ pattern in v1, v2, aVR, v3R• ST depression with T inversion • Wide & slurred S in I, aVL, v5, v6• QRS interval more or less 0.12 s• Usually VAT prolonged

Commoner than LBBB, often without any cardiac diseases

LAHB• LAD• qR in I, aVL & rS in II, III, aVF

LPHB• RAD• qR in II, III, aVF

Bifascicular block• RBBB + LAHB

• RBBB + LPHB

• LAHB + LPHB

Trifascicular block• LAD + RBBB + Prolonged PR