BASICS IN ELECTROCARDIOGRAPHY

Dr. NAGULA PRAVEEN

MD,DM (CARDIOLOGY)

ELECTROCARDIOGRAPHY

BASICS

INTRODUCTION

• ECG is the common diagnostic tool essential in the evaluation

of patient presenting with cardiac complaints.

ARTHUR D.WALLER

• Recorded first electrical activity from the human heart

WILLEM EINTHOVEN (1860-1927)

Received Nobel prize for the year 1924

Named Electrocardiography

Waves obtained by A.D.

Waller (top);

waves obtained by Einthoven

with his improved capillary

electrometer (middle);

Electrocardiographic tracing

by use of the string

galvanometer (bottom).

EMANNUEL GOLDBERGER

• Augmented limb leads : Extremity leads are of low electric potential and

are therefore instrumentally augmented,these augmented extremity leads

are thus prefixed by letter A.

• All unipolar leads are termed V leads.– V being used after voltage.

WILSON

• Wilson central terminal

•SIR THOMAS LEWIS

LEWIS LEADS

Helps in delineation of atrial waves

The reformed triangle focuses only on atria

BASIC CARDIAC PHYSIOLOGY

• Cardiac cells are internally negative.

• They lose the negativity on propagation of electrical impulse – depolarization.

• Propagates from cell to cell – wave of depolarization through entire heart – T tubule system.

• Wave of depolarization is actually flow of electric current – detected by electrodes on the surface of the body.

• Restoration of resting polarity – repolarization

ACTION POTENTIAL – MYOCARDIAL CELL

• Different phases of the action potential relate directly to the waveforms,

intervals and segments that constitute a cardiac cycle on the ECG.

• Each phase is distinguished by an alteration in cell membrane

permeability to sodium, potassium and calcium ions.

• Helpful in learning ECG features associated with conduction

abnormalities, drug toxicities, and electrolyte disturbances.

• Action potential of the myocardial cell is divided into five phases.

• Phases (0-4)

PHASES

PHASE Channels ECG

0 Ventricular depolarization Sodium entry

Fast gated sodium

channels

QRS complex

1 Early Ventricular

repolarization

Opening of

potassium channels

J point

2 Plateau Ventricular

repolarization

Balancing potassium

efflux with the

sustained entry of

calcium ions

ST segment

3 Rapid Ventricular

repolarization

Continued potassium

efflux

Closure of calcium

ions

T wave

4 Resting membrane potential Continued potassium

efflux

Na/K ATPase

TQ segment

ACTION POTENTIAL OF A PACEMAKER

CELL

• Spontaneously depolarize and initiate action potentials

• Three phases (0,3,4)

• Upsloping phase 4 potential differentiates it from myocardial cell.

• Slow inward sodium current results in the gradual rise of the membrane

potential toward its threshold potential.

• Current responsible for phase 4 depolarization phase is also called as

funny current (If).

• Calcium channels open to depolarize the cell during phase 0.

• Phase 3 – opening of potassium channels and closure of calcium

channels

• No early repolarization and plateau phase.

PACEMAKER CELLS

• They have ability of spontaneous depolarization.

• Dominant pacemaker is SinoAtrial node – 70 /min

• AV node - 40-60 /min

• Ventricles - 30-40 /min

MYOCARDIAL CELLS (CONTRACTILE

MACHINERY)

ECG LEADS,CALIBRATION

EINTHOVEN TRIANGLE

GENERAL APPROACH TO ECG INTERPRETATION

• Clinical history

• Calibration

• Date

• Patient name

• Rate

• Rhythm

• Axis

• Wave morphologies

• P wave

• QRS complex

• T wave

• U waves

• QRS voltage

• QRS width

• Intervals

• PR interval

• QT interval

• Signs of ischemia

• ST segment

• T waves

• Pathologic Q waves

• Conclusion

• Differentials

Always compare with an prior ECG if possible.

STANDARDIZATION

• Normal standardization – speed at 25 mm/sec, with 10 mm deflection for each

1mv of calibration signal .

• Half standardization – speed at 25 mm/sec, with 5 mm spike for each 1mv of

calibration signal.

• Double standardization – speed at 25 mm/sec, with 20 mm spike for each 1 mv of

current passed.

• 50 mm/sec speed for Arrhyhthmias.

RATE

• 1500/ small squares – 25 small squares *60

• 300/ large squares --- 5 big squares *60

• R-R intervals in 6 sec = no in 30 small squares *10

RHYTHM

• Sinus rhythm

• Junctional rhythm

• Ectopic rhythm

• Ventricular rhythm

• Pacemaker rhythm

AXIS

• Normal axis is from -10 to 90 degrees

• Left axis deviation is from -30 to -90

• Right axis deviation is from 90 to 180

• Indeterminate axis is from -90 to -180

• Lead I is to AVF (0 - 90 )

• Lead II is to AVL ( 60 - -30)

• Lead III is to AVR ( 120 - -150)

DETERMINATION OF AXIS

• Hexaxial Reference system

• Each lead axis is differentiated by 30ᵒ

• Upper half - negative

• Lower half - positive

• Three ways of determining axis

• 1.Standard Lead technique

• Lead II = Lead I + lead III

• 2.Hexaxial Perpendicular axis method

• 3.Quadrant method

• 1.If a vector is perpendicular to an lead axis – the net impression on that lead is

nil. the deflexion in that lead is usually small and equiphasic so that the positive

and negative deflexion , so to speak cancel each other.

• 2.If a vector is parallel to an lead axis – the net impression on that lead is high.

and based on the direction of the vector relative to the lead axis to either positive

terminal or negative terminal – the deflection in that lead will be positive or

negative.

Rule

• Determine the QRS which is equiphasic on ECG

• See the lead perpendicular to it.

• Determine the direction of QRS complex in that lead

• The mean QRS axis is determined accordingly

Lead I = POSITIVE

Lead II = POSITIVE

aVF = POSITIVE

This puts the axis in the left lower quadrant

(LLQ) between 0° and +90° – i.e. normal

axis

Lead aVL is isoelectric, being biphasic

with similarly sized positive and negative

deflections (no need to precisely measure

this).

From the diagram above, we can see

that aVL is located at -30°.

The QRS axis must be ± 90° from lead

aVL, either at +60° or -120°

With leads I (0), II (+60) and aVF (+90) all

being positive, we know that the axis must

lie somewhere between 0 and +90°.

This puts the QRS axis at +60° –

i.e. normal axis

Lead I = NEGATIVE

Lead II = Equiphasic

Lead aVF = POSITIVE

This puts the axis in the left lower

quadrant, between +90° and +180°,

i.e. RAD.

Lead II (+60°) is the isoelectric lead.

The QRS axis must be ± 90° from lead II, at

either +150° or -30°.

The more rightward-facing leads III (+120°) and

aVF (+90°) are positive, while aVL (-30°) is

negative.

This puts the QRS axis at +150°.

Lead I = POSITIVE

Lead II = Equiphasic

Lead aVF = NEGATIVE

This puts the axis in the left upper

quadrant, between 0° and -90°, i.e. normal

or LAD.

Lead II is neither positive nor negative

(isoelectric), indicating physiological LAD.

Lead II (+60°) is isoelectric.

The QRS axis must be ± 90° from lead II,

at either +150° or -30°.

The more leftward-facing leads I (0°) and

aVL (-30°) are positive, while lead III

(+120°) is negative.

This confirms that the axis is at -30°

Lead I = NEGATIVE

Lead II = NEGATIVE

Lead aVF = NEGATIVE

This puts the axis in the upper right

quadrant, between -90° and 180°,

i.e. extreme axis deviation

The most isoelectric lead is aVL (-30°).

The QRS axis must be at ± 90° from aVL at

either +60° or -120°.

Lead aVR (-150°) is positive, with lead II

(+60°) negative.

This puts the axis at -120°.

This is an example of extreme axis

deviation due to ventricular tachycardia.

Lead I = isoelectric.

Lead aVF = positive.

This is the easiest axis you will ever have

to calculate. It has to be at right angles to

lead I and in the direction of aVF, which

makes it exactly +90°!

This is referred to as a “vertical axis” and is seen in patients with emphysema who

typically have a vertically orientated heart.

WAVES,SEGMENTS,INTERVALS

P WAVE

• Atria are typically activated in a right to left direction as the electrical impulse

spreads from the sinus node in the right atrium to the left atrium.

• First half of the P wave represents activation of the right atrium.

• Second half – left atrium

• In normal sinus rhythm, P waves should be upright in the inferior leads (reflecting

the superior to inferior direction of the impulse from sinus to AV node)

• P wave in V1 is upright or biphasic.

QRS COMPLEX

• Represents rapid ventricular depolarization

• Phase 0 of action potential

• Widened by delay in intraventricular conduction system and ventricular

hypertrophy.

• Zone of transition is at V3 or V4

• If at V2 or V1 – counter clockwise rotation, q waves in lead II,III,aVF

• If at V5 or V6 - clockwise rotation , q waves in Lead I,aVL

• Normal QRS complex duration is 0.08sec to 0.10 sec (2 small boxes to 2

½ small boxes)

T WAVE

• Phase 3 of the action potential

• Repolarization of epicardium followed by endocardium

• Axis of the T wave should parallel that of the QRS wave when

depolarization is normal

U WAVE

• May be absent in the normal electrocardiogram

• The U wave is a small (0.5 mm) deflection immediately following the T

wave

• U wave is usually in the same direction as the T wave.

• U wave is best seen in leads V2 and V3

• The source of the U wave is unknown.

• Three common theories regarding its origin are:

1. Delayed repolarisation of Purkinje fibres

2. Prolonged repolarisation of mid-myocardial “M-cells”

3. After-potentials resulting from mechanical forces in the ventricular wall

NORMAL U WAVE

• The U wave normally goes in the same direction as the T wave

• U -wave size is inversely proportional to heart rate: the U wave grows

bigger as the heart rate slows down

• U waves generally become visible when the heart rate falls below 65 bpm

• The voltage of the U wave is normally < 25% of the T-wave voltage:

disproportionally large U waves are abnormal

• Maximum normal amplitude of the U wave is 1-2 mm

PROMINENT U WAVE• U waves are prominent if >1-2mm or 25% of the height of the T wave.

• Note that many of the conditions causing prominent U waves will also cause a long QT.

Drugs that may cause prominent U

waves:

Digoxin

Phenothiazines (thioridazine)

Class Ia antiarrhythmics (quinidine,

procainamide)

Class III antiarrhythmics (sotalol,

amiodarone)

Prominent U waves seen in:

Bradycardia (MC cause)

Hypokalemia (severe)

Hypocalcemia

Hypomagnesemia

Hypothermia

Raised intracranial pressure

LVH

HCM

INVERTED U WAVE

• U-wave inversion is abnormal (in leads with upright T waves)

• A negative U wave is highly specific for the presence of heart disease

The main causes of inverted U waves are:

Coronary artery disease

Hypertension

Valvular heart disease

Congenital heart disease

Cardiomyopathy

Hyperthyroidism

In patients presenting with chest pain, inverted U waves:

Are a very specific sign of myocardial ischaemia.

May be the earliest marker of unstable angina and evolving myocardial infarction

Have been shown to predict a ≥ 75% stenosis of the LAD / LMCA and the presence

of left ventricular dysfunction

INTERVALS

• PR interval :

• Represents the time for an impulse to travel from the atria to the ventricles

including the time it takes to travel through the AV node and bundle of His.

• PR prolongation most often results from delayed conduction within the AV

node.

• PR shortening classically occurs when an impulse travels from atrium to

ventricle through an accessory pathway that bypasses the delay in

conduction that occurs in the AV node.

QT INTERVAL

• Represents ventricular depolarization and repolarization, corresponding to

phase 0 to 3 of the action potential and ventricular systole.

• QT prolongation often results from delay in repolarization.

R-R INTERVAL

• Corresponds to complete cardiac cycle.

ST SEGMENT

• The ST segment is the flat, isoelectric section of the ECG between

the end of the S wave (the J point) and the beginning of the T wave. It

represents the interval between ventricular depolarization and

repolarization.

• CAD is suggested by horizontality, plane depression or sagging of the

ST segment – Lead II,V5 andV6.

• Digitalis effect

• Strain pattern

• Hyperacute phase of MI

TQ SEGMENT

• Isoelectric line

• Diastole

ARTIFACTS

• AC interference – describes the type of electricity we get from the wall.

• When an ECG machine is poorly grounded or not equipped to filter out this

interference, you can get a thick looking ECG line.

• If one were to look at this ECG line closely, he would see 60 up-and-down wave

pattern in a given second (25 squares).

MUSCLE TREMOR /NOISE :

• The heart is not the only thing in the body that produces measurable

electricity. When skeletal muscles undergo tremors, the ECG is

bombarded with seemingly random activity.

• The term noise does not refer to sound but rather to electrical

interference.

• Low amplitude muscle tremor noise can mimic the baseline seen in atrial

fibrillation.

• Muscle tremors are often a lot more subtle than that shown in

WANDERING BASELINE

In wandering baseline, the isoelectric line changes position. One possible

cause is the cables moving during the reading. Patient movement, dirty lead

wires/electrodes, loose electrodes, and a variety of other things can cause

this as well.

LIMB LEAD REVERSAL

RA RL REVERSAL

With reversal of the RA and RL(N) electrodes, Einthoven’s triangle collapses to

very thin “slice” with the LA electrode at its apex.

The RA and LL electrodes now record almost identical voltages, making the

difference between them negligible (i.e, lead II = zero).

Lead aVL runs within this thin slice, facing approximately opposite to lead III.

Displacement of the neutral electrode renders leads aVR and aVF mathematically

identical, such that they appear exactly alike (but different to the baseline ECG).

Lead I becomes an inverted lead III.

Lead II records a flat line (zero potential).

Lead III is unchanged.

Lead aVL approximates an inverted lead III.

Leads aVR and aVF become identical.

As the neutral electrode has been moved, the

precordial voltages may also be distorted.

LA/RL(N) reversal

• With reversal of the LA and RL(N) electrodes, Einthoven’s triangle collapses to very

thin “slice” with the RA electrode at its apex.

• The LA and LL electrodes now record almost identical voltages, making the difference

between them negligible (i.e. lead III = zero).

• Lead aVR runs within this thin slice, facing approximately opposite to lead II.

• The displacement of the neutral electrode renders leads aVL and aVF mathematically

identical, such that they appear exactly alike (but different to the baseline ECG).

Lead I becomes identical to lead II.

Lead II is unchanged.

Lead III records a flat line (zero potential).

Lead aVR approximates to an inverted lead II.

Leads aVL and aVF become identical.

As the neutral electrode has been moved, the

precordial voltages may also be distorted.

Bilateral Arm-Leg Reversal (LA-LL plus RA-RL)

• If the electrodes on each arm are swopped with their corresponding leg electrode (LA

with LL, RA with RL), Einthoven’s triangle collapses to a very thin slice with the LL

electrode at its apex.

• The RA and LA electrodes (now sitting on adjacent feet) record almost identical

voltages, which makes the difference between them negligible (i.e. lead I = zero).

• Leads II, III and aVF all become identical (equivalent to inverted lead III), as they are

all now measuring the voltage difference between the left arm and the legs.

• The displacement of the neutral electrode renders leads aVL and aVR mathematically

identical, such that they appear exactly alike but different to the baseline ECG

ECG features:

•Lead I records a flat line (zero potential).

•Lead II approximates an inverted lead III.

•Lead III is inverted.

•aVR and aVL become identical.

•aVF looks like negative lead III

LL/RL(N) reversal

With reversal of the lower limb electrodes, Einthoven’s triangle is

preserved as the electrical signals from each leg are virtually identical.

Thank You

REFERENCES

1. Leo Schamroth An Introduction to Electrocardiography

2. Rapide Interpretation of ECGs in Emergency Medicine A visual Guide –

Jennifer L.Mandale

3. Dr.Smith ECG BLOG

4. Lifeinthefastlane