electrocardiogram basic

ECG

CES-1

DR.NILESH KATE.M.D.ASSOCIATE PROFESSOR,DEPARTMENT OF PHYSIOLOGY,ESIC MEDICAL COLLEGE, SEDAM ROAD, GULBARGA.

OBJECTIVES.

ANATOMIC CONSIDERATION

MECHANISM OF ORIGIN OF RHYTHMIC CARDIAC IMPULSE

SPREAD OF CARDIAC IMPULSE

ELECTROCARDIOGRAPHY

RECORDING OF ECG

NORMAL ECG

VECTORIAL ANALYSIS OF ECG AND VECTOR CARDIOGRAPHY

CONCEPT OF LEADS (UNIPOLAR/BIPOLAR)

WAVES, SEGMENTS – DURATION & VOLTAGE.

CLINICAL APPLICATION OF ECG

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Cardiac Anatomy

CES-3

Atrial muscle

Sinoatrial (SA)A node Left atrium

Descending aortaInferior

vena cava

Ventricluar

Pulmonary

veins

Superior

vena cava

Tricuspid valve

Mitral valve

Atrioventricular (AV) node

Purkinje

fibers

muscle

Internodal

conductingtissue

ORIGIN AND SPREAD

OF CARDIAC

IMPULSE.

CES-4

Flow of Cardiac Electrical Activity

CES-5

SA node Atrial muscle

AV node (slow)

Purkinje fiber

conducting systemVentricular muscle

Internodal

conducting

fibers

Atrial muscle

Conduction in the Heart

CES-6

0.12-0.2 s approx. 0.44 s

SA

Atria

Purkinje

Ventricle

node

nodeAV

INTRINSIC CONDUCTION SYSTEM

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Function: initiate & distribute impulses so heart depolarizes & contracts in orderly manner from atria to ventricles…….

SA node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

The ECG/EKG

Def:- Extracellular recording of the summed up

electrical events of all the cardiac muscle fibers

generated with each heart beat.

Can record a reflection of cardiac electrical activity on

the skin- EKG

The magnitude and polarity of the signal depends on

what the heart is doing electrically

○ depolarizing

○ repolarizing

○ whatever

the position and orientation of the recording electrodes

CES-8

Electrocardiography is based on the principle of BIOELECTROMAGNETISM, a discipline that examines the electric, electromagnetic, and magnetic phenomena which arise in biological tissues.

An ECG is a representation of depolarization & Repolarization waves in the myocardium.

Genesis of the ECG

HISTORY

WILLIAM EINTHOVEN

-- Dutch physiologist

developed techniques of

ECG

Awarded NOBEL PRIZE

in 1924

Father of modern

electrophysiology.

ECG trace

taken by

WALLER

IN 1887

INTRODUCTION

Electrocardiography

(ECG or EKG)

An electrical picture of

the functioning of the

heart.

Etymology:

electro- electricity

cardio[Gr.]- heart

graph[Gr.]- to write

THE HEART

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is a pump has

electrical activity

(action potentials)

generates electrical

current that can be

measured

on the skin surface

(the EKG)

CURRENTS AND VOLTAGES

At rest, Vm is constant

No current flowing

Inside of cell is at

constant potential

Outside of cell is at

constant potential

CES-14

++++++++++++++++++

------------------------------

A piece of cardiac muscle

outside

inside

0 mV

+-

CURRENTS AND VOLTAGES

During AP upstroke, Vm

is NOT constant

Current IS flowing

Inside the cell is NOT

at constant potential

Outside the cell is NOT

at constant potential

CES-15

++++------------------------------++++++++++++++


outside

inside

Some positive

potential+-

current

AP

An action potential propagating

toward the positive ECG lead

produces a positive signal

MORE CURRENTS AND

VOLTAGES

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outside

current

+-

A negative voltage reading

------++++++++++++++

inside

++++------------------------An action potential propagating

Away from the positive ECG lead

produces a negative signal

More Currents and Voltages

CES-17

current

-------------------------------

A piece of totally depolarized

cardiac muscle

outside

inside

+++++++++++++++++++

Vm not changing

No current

No ECG signal

+++++++-------------------


outside

inside

------------+++++++++++

During Repolarization

+-Some negative potential

Repolarization spreading toward

the positive ECG lead produces

a negative response

Electrophysiology of a Cardiac Muscle

DEPOLARISATION REPOLARISATION RESTORATION OF

IONIC BALANCE

• When a DEPOLARISATION Wave moves

towards a positive electrode a positive signal is

generated and when it moves towards a negative

electrode a negative signal is generated.

• The reverse happens in

case of

REPOLARISATION

Waves

The Normal EKG

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P

Q

R

S

T

Right Arm

Left Leg

QTPR

0.12-0.2 s approx. 0.44 s

Atrial muscle

depolarization

Ventricular muscle

depolarization

Ventricular

muscle

repolarization

“Lead II”

Action Potentials in the Heart

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AV

Purkinje

Ventricle

Aortic artery

Left atrium

Descending aortaInferior

vena cava

Ventricluar

Atrial muscle

Pulmonary

veins

Superior

vena cava

Pulmonary artery

Tricuspid valve

Mitral valve

Interventricular

septum

AV node

SA node

ECG

QTPR

0.12-0.2 s approx. 0.44 s

SA

Atria

Purkinje

fibersmuscle

Specializedconducting

tissue

ECG Graph Paper

Recording ECG

Speed of paper – 25 mm/sec

Recording ECG

ISOELECTRIC LINE: Tracing following the T Wave & preceding the next P Wave.

HEART RATE: The frequency of:

• P Wave gives Atrial Rate &

• QRS Complex gives Ventricular Rate

Calculation of HR=

Speed of paper 25

mm/ sec

So in 1 min = 1500

mm

So HR / MIN

= 1500/ RR Interval

THE INFORMATION CONTENT OF

THE 12-LEAD SYSTEM

Leads

Bipolar

I,II,III

Unipolar

Precordial

( Chest leads )

V1,v2 ,V3,V4,V5,V6

Augmented limb leads

aVR,aVL,aVF

Standard limb leads

LEADS USED IN ECG

Einthoven's

assumption

body – homogenous

plate

Both shoulders &

pubic region corners

of equilateral triangle.

With heart in centre.

Einthoven’s Triangle Hypothesis

He was awarded the Nobel

Prize in Medicine for his

work on ECG.

This Hypothesis states that if

the electrical potentials of 2

limb leads are known, the 3rd

can be determined by simply

summing up the two.

wiki/Nobel_Prize_in_Medicine

Electrode Electrode Placement

RA On the right arm, avoiding bony

prominences.

LA Same as RA, but on the left arm this

time.

LL On the left leg, avoiding bony

prominences.

NOTE: The right leg is used as earth

to minimize interference.

Positioning of Electrodes

Standardlimb lead

RA LA

LL

l

ll lll ll lll

l

LL

RA LA

+ +

+-

- -

RECORDING THE CARDIAC ELECTRICAL SIGNAL

Standard bipolar limb leads

THE INFORMATION CONTENT OF

THE 12-LEAD SYSTEM

Leads

Bipolar

I,II,III

Unipolar

Precordial

( Chest leads )

V1,v2 ,V3,V4,V5,V6

Augmented limb leads

aVR,aVL,aVF

Standard limb leads

Position of Precordial Leads

http://butler.cc.tut.fi/~malmivuo/bem/bembook/15/15x/1508x.htm

http://butler.cc.tut.fi/~malmivuo/bem/bembook/15/15x/1508x.htm

E.C.G. Recording of Precordial

Leads

Augmented Unipolar Limb Leads

Precordial Leads

Summary of Leads

Limb Leads Precordial Leads

Bipolar I, II, III(standard limb leads)

-

Unipolar aVR, aVL, aVF (augmented limb leads)

V1-V6

Arrangement of Leads on the EKG

Anatomic Groups(Septum)

Anatomic Groups(Anterior Wall)

Anatomic Groups(Lateral Wall)

Anatomic Groups(Inferior Wall)

Anatomic Groups(Summary)

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ECG Deflection Waves

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(Pacemaker) Atrial repolarization

ECG

P wave

CONFIGURATION –

○ Positive ( upright deflection)

CAUSE -- Atrial depolarization

DURATION -- < 0.1 sec

AMPLITUDE – 0.1- 0.12 mv

CLINICAL SIGNIFICANCE

. If the Waves are normal in

morphology & the P Wave is regularly

followed by a QRS Complex,

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ECGs, Normal & Abnormal

No P waves

ECGs, Abnormal

CES-48

Arrhythmia: conduction failure at AV node

No pumping action occurs

QRS complex

QRS complex

Configuration –

○ Q wave small negative wave.

○ R wave tall positive.

○ S wave small negative wave.

Cause -- Ventricular Depolarization.

Duration --Q < 0.08 sec

Amplitude

Q – 0.1- 0.2, R wave – 1mv, S wave – 0.4 mv.

Clinical significance.

QRS complex

< 0.10 s 0.10-0.12 s > 0.12 s

NormalIncomplete bundle

branch block

Bundle branch block

PVC

Ventricular rhythm

Remember: If you have a BBB determine if it is a right or left BBB.

3rd degree AV block

with ventricular

escape rhythmIncomplete bundle branch block

ECG Deflection Wave Irregularities

CES-51

Enlarged

QRS =

Hypertrophy

of ventricles

T wave

Configuration – last positive dome shaped

deflection

Cause – ventricular repolarization.

Duration – approx 0.27 sec

Amplitude – 0.3 mv

Clinical significance.


CES-53

Elevated T wave :

Hyperkalemia


CES-54

Flat T wave :

Hypokalemia

or ischemia

U wave

Configuration – small round positive wave

Cause – slow repolarization of papillary muscles.

Duration – approx 0.08 sec

Amplitude – 0.2 mv

Clinical significance. – rarely seen normally

Prominent in hypokalemia.

Axis of three bipolar and three

unipolar leads

AXIS.

Axis refers to the mean QRS axis (or vector) during ventricular depolarization. As you recall when the ventricles depolarize (in a normal heart) the direction of current flows leftward and downward because most of the ventricular mass is in the left ventricle.

Axis

The QRS axis is determined by overlying a circle, in the frontal plane.

By convention, the degrees of the circle are as shown.

The normal QRS axis lies between -30o and +110o.

0o

30o

-30o

60o

-60o-90o

-120o

90o120o

150o

180o

-150o

A QRS axis that falls between -30o

and -90o is abnormal and called left

axis deviation.

A QRS axis that falls between +90o

and +150o is abnormal and called

right axis deviation.

Axis

Causes of left axis deviation include:

Left ventricular hypertrophy

Inferior wall MI

Left bundle branch block

Left anterior fascicular block

Horizontal heart

0o

-90o

90o

180o

• Causes of right axis deviation include:

– Right ventricular hypertrophy

– Lateral wall MI

– Right bundle branch block

– Pulmonary hypertension

– Vertical heart

Intervals

It is the duration between two specific ECG

events. For example:

PQ/PR Interval

It is from the beginning of the P wave to the beginning of the QRS complex

Time duration:

0.16 second

QT Interval

It is from the beginning of the QRS complex (ventricular depolarization) to the end of the T wave (ventricular repolarization).

0.35 second

Intervals

PR interval

< 0.12 s 0.12-0.20 s > 0.20 s

High catecholamine

states

Wolff-Parkinson-White

Normal AV nodal blocks

Wolff-Parkinson-White1st Degree AV Block

Intervals

QT interval

The duration of the QT interval is

proportionate to the heart rate. The faster

the heart beats, the faster the ventricles

repolarize so the shorter the QT interval.

Therefore what is a “normal” QT varies

with the heart rate. For each heart rate you

need to calculate an adjusted QT interval,

called the “corrected QT” (QTc):

QTc = QT / square root of RR interval

Intervals

QTc interval

< 0.44 s > 0.44 s

Normal Long QT

A prolonged QT can be very dangerous. It may predispose an individual to a type of

ventricular tachycardia called Torsades de Pointes. Causes include drugs, electrolyte

abnormalities, CNS disease, post-MI, and congenital heart disease.

Torsades de Pointes

Long QT

Segments

A segment is the length between two specific points on the ECG which are supposed to be at the baseline amplitude .

ST Segment The ST segment connects the QRS complex and the T wave

TP Segment The portion of the ECG from the end of the T wave to the beginning of the P wave.

PR Segment portion of the ECG from the end of the P wave to the beginning of the QRS complex.


CES-66

60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute


CES-67

1st

Degree

Heart

Block =

P-Q

interval

longer

than 0.2

seconds.

60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute


CES-68

Prolonged QT

Interval =

Repolarization

abnormalities

increase chances

of ventricular

arrhythmias.

Rhythm Summary

Rate 90-95 bpm

Regularity regular

P waves normal

PR interval 0.12 s

QRS duration 0.08 s

Interpretation?

Normal Sinus Rhythm

Normal Sinus Rhythm (NSR)

Etiology: the electrical impulse is formed in

the SA node and conducted normally.

This is the normal rhythm of the heart; other

rhythms that do not conduct via the typical

pathway are called arrhythmias.

NSR Parameters

Rate 60 - 100 bpm

Regularity regular

P waves normal

PR interval 0.12 - 0.20 s

QRS duration 0.04 - 0.12 s

Any deviation from above is sinus tachycardia,

sinus bradycardia or an arrhythmia

Arrhythmia Formation

Arrhythmias can arise from problems in the:

• Sinus node

• Atrial cells

• AV junction

• Ventricular cells

SA Node Problems

The SA Node can:

fire too slow

fire too fast Sinus Bradycardia

Sinus Tachycardia

Sinus Tachycardia may be an appropriate

response to stress.

Rhythm #1

30 bpm• Rate?

• Regularity? regular

normal

0.10 s

• P waves?

• PR interval? 0.12 s

• QRS duration?

Interpretation? Sinus Bradycardia

Rhythm #2

130 bpm• Rate?


normal

0.08 s

• P waves?


• QRS duration?

Interpretation? Sinus Tachycardia

Rhythm #3

70 bpm• Rate?

• Regularity? occasionally irreg.

2/7 different contour

0.08 s

• P waves?

• PR interval? 0.14 s (except 2/7)

• QRS duration?

Interpretation? NSR with Premature Atrial

Contractions

Premature Atrial Contractions

Deviation from NSR

These ectopic beats originate in the atria (but not

in the SA node), therefore the contour of the P

wave, the PR interval, and the timing are different

than a normally generated pulse from the SA

node.

Etiology: Excitation of an Atrial cell forms an impulse that is

then conducted normally through the AV node and ventricles.

AV Junctional Problems

The AV junction can:

fire continuously

due to a looping re-

entrant circuit

block impulses

coming from the SA

Node

Paroxysmal

Supraventricular

Tachycardia

AV Junctional Blocks

Ventricular Cell Problems

Ventricular cells can:

fire occasionally from 1 or more foci

fire continuously from multiple foci

fire continuously due to a looping re-entrant circuit

Premature Ventricular

Contractions (PVCs)

Ventricular Fibrillation

Ventricular Tachycardia

Rhythm #4

60 bpm• Rate?

• Regularity? occasionally irreg.

none for 7th QRS

0.08 s (7th wide)

• P waves?


• QRS duration?

Interpretation? Sinus Rhythm with 1 PVC

PVCs

Deviation from NSR

Ectopic beats originate in the ventricles resulting in wide and bizarre QRS complexes.

When there are more than 1 premature beats and look alike, they are called “uniform”. When they look different, they are called “multiform”.

Etiology: One or more ventricular cells are depolarizing and the impulses are abnormally conducting through the ventricles.

Ventricular Conduction

NormalSignal moves rapidly

through the ventricles

AbnormalSignal moves slowly

through the ventricles

Rhythm #5

100 bpm• Rate?

• Regularity? irregularly irregular

none

0.06 s

• P waves?

• PR interval? none

• QRS duration?

Interpretation? Atrial Fibrillation

Atrial Fibrillation

Deviation from NSR

No organized atrial depolarization, so no normal P waves (impulses are not originating from the sinus node).

Atrial activity is chaotic (resulting in an irregularly irregular rate).

Common, affects 2-4%, up to 5-10% if > 80 years old

Rhythm #6

70 bpm• Rate?


flutter waves

0.06 s

• P waves?


• QRS duration?

Interpretation? Atrial Flutter

Atrial Flutter

Deviation from NSR

No P waves. Instead flutter waves (note “sawtooth” pattern) are formed at a rate of 250 -350 bpm.

Only some impulses conduct through the AV node (usually every other impulse).

Etiology: Reentrant pathway in the right atrium with every 2nd, 3rd or 4th impulse generating a QRS (others are blocked in the AV node as the node repolarizes).

Ventricular Arrhythmias



Rhythm #8

160 bpm• Rate?


none

wide (> 0.12 sec)

• P waves?


• QRS duration?

Interpretation? Ventricular Tachycardia


Deviation from NSR

Impulse is originating in the ventricles (no P waves, wide QRS).

Etiology: There is a re-entrant pathway looping in a ventricle (most common cause).

Ventricular tachycardia can sometimes generate enough cardiac output to produce a pulse; at other times no pulse can be felt.

Rhythm #9

none• Rate?

• Regularity? irregularly irreg.

none

wide, if recognizable

• P waves?


• QRS duration?

Interpretation? Ventricular Fibrillation


Deviation from NSR

Completely abnormal.

Etiology: The ventricular cells are excitable and

depolarizing randomly.

Rapid drop in cardiac output and death occurs if not

quickly reversed

AV Nodal Blocks

1st Degree AV Block

2nd Degree AV Block, Type I

2nd Degree AV Block, Type II

3rd Degree AV Block

Rhythm #10

60 bpm• Rate?


normal

0.08 s

• P waves?


• QRS duration?

Interpretation? 1st Degree AV Block

1st Degree AV Block

Deviation from NSR

PR Interval > 0.20 s

Etiology: Prolonged conduction delay in

the AV node or Bundle of His.

Rhythm #11

50 bpm• Rate?

• Regularity? regularly irregular

nl, but 4th no QRS

0.08 s

• P waves?

• PR interval? lengthens

• QRS duration?

Interpretation? 2nd Degree AV Block, Type I

2nd Degree AV Block, Type I

Deviation from NSR

PR interval progressively lengthens,

then the impulse is completely blocked

(P wave not followed by QRS).

Etiology: Each successive atrial impulse

encounters a longer and longer delay in the AV

node until one impulse (usually the 3rd or 4th)

fails to make it through the AV node.

Rhythm #12

40 bpm• Rate?


nl, 2 of 3 no QRS

0.08 s

• P waves?


• QRS duration?

Interpretation? 2nd Degree AV Block, Type II

2nd Degree AV Block, Type II

Deviation from NSR

Occasional P waves are completely blocked (P

wave not followed by QRS).

Etiology: Conduction is all or nothing (no prolongation of

PR interval); typically block occurs in the Bundle of His.

Rhythm #13

40 bpm• Rate?


no relation to QRS

wide (> 0.12 s)

• P waves?


• QRS duration?

Interpretation? 3rd Degree AV Block

3rd Degree AV Block

Deviation from NSR

The P waves are completely blocked in the AV

junction; QRS complexes originate

independently from below the junction.

Etiology: There is complete block of conduction in the AV

junction, so the atria and ventricles form impulses

independently of each other. Without impulses from the

atria, the ventricles own intrinsic pacemaker kicks in at

around 30 - 45 beats/minute.

Views of the Heart

Some leads get a

good view of the:

Anterior portion

of the heart

Lateral portion

of the heart

Inferior portion

of the heart

MI -- ST Elevation

One way to

diagnose an

acute MI is to

look for

elevation of the

ST segment.

ST Elevation (cont)

Elevation of the ST

segment (greater

than 1 small box) in

2 leads is consistent

with a myocardial

infarction.

Other MI Locations

Now, using these 3 diagrams let’s figure where to look for a lateral wall and inferior wall MI.

Limb Leads Augmented Leads Precordial Leads

Anterior MI

Remember the anterior portion of the heart is best

viewed using leads V1- V4.


Lateral MI

So what leads do you think the lateral portion of the heart is best viewed?


Leads I, aVL, and V5- V6

Inferior MI

Now how about the inferior portion of the heart?


Leads II, III and aVF

Left Ventricular Hypertrophy

Compare these two 12-lead ECGs. What stands out as

different with the second one?

Normal Left Ventricular Hypertrophy

Answer: The QRS complexes are very tall

(increased voltage)


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.


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.

Bundle Branch Blocks

Turning our attention to bundle branch blocks…

Remember normal

impulse conduction is

SA node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

Normal Impulse ConductionSinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers


So, depolarization of the

Bundle Branches and

Purkinje fibers are seen

as the QRS complex on

the ECG.

Therefore, a conduction

block of the Bundle

Branches would be

reflected as a change in

the QRS complex.

Right

BBB


With Bundle Branch Blocks you will see two changes on the

ECG.

1. QRS complex widens (> 0.12 sec).

2. QRS morphology changes (varies depending on ECG lead, and if

it is a right vs. left bundle branch block).


Why does the QRS complex widen?

When the conduction

pathway is blocked it

will take longer for

the electrical signal

to pass throughout

the ventricles.

Right Bundle Branch Blocks

What QRS morphology is characteristic?

V1

For RBBB the wide QRS complex assumes a

unique, virtually diagnostic shape in those

leads overlying the right ventricle (V1 and V2).

“Rabbit Ears”

Left Bundle Branch Blocks

What QRS morphology is characteristic?

For LBBB the wide QRS complex assumes a

characteristic change in shape in those leads

opposite the left ventricle (right ventricular

leads - V1 and V2).

Broad,

deep S

wavesNormal

CHANGES IN IONIC

COMPOSITION OF BLOOD

SODIUM –

Associated with low voltage ECG.

POTASSIUM –

Normal plasma levels 4-5.5 meq/L

HYPERKALEMIA -- > 7 meq/L TALL T WAVE

HYPOKALEMIA -- < 4.5 meq/L LOW VOLTAGE

CALCIUM –

HYPERCALCEMIA – heart stops in systole

(calcium rigor)

HYPOCALCEMIA – prolonged ST segment.

THANK YOU

CES-119

electrocardiogram basic

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