ECG

Dr. Bernhard Arianto Purba, M.Kes., AIFO

ECG

Textbooks• Guyton, A.C & Hall, J.E. 2006. Textbook of Medical

Physiology. The 11th edition. Philadelphia: Elsevier-Saunders: 918-930, 961-977.

• Brooks, G.A. & Fahey, T.D. 1985. Exercise Physiology. Human Bioenergetics and Sts Aplications. New York : Mac Millan Publishing Company: 122-143.

• Foss, M.L. & Keteyian, S.J. 1998. Fox’s Physiological Basis for Exercise and Sport. 4th ed. New York : W.B. Saunders Company: 471-491.

• Astrand, P.O. and Rodahl, K. 1986. Textbook of Work Pysiology, Physiological Bases of Exercise. New York : McGraw—Hill.

• Braunwald, Pauci, et al.2008. Harrison's PRINCIPLES OF INTERNAL MEDICINE. Seventeenth Edition. New York : McGraw—Hill: Chapter 332, 333, 338.

• Jardins, Terry Des. 2002. Cardiopulmonary Anatomy & Physiology. The 4th edition. USA: Delmar, A Division of Thomson Learning Inc.

ELECTROCARDIOGRAPHY

(ECG)

A Brief introduction to ECG

• The electrocardiogram (ECG) is a time-varying signal reflecting the ionic current flow which causes the cardiac fibers to contract and subsequently relax. The surface ECG is obtained by recording the potential difference between two electrodes placed on the surface of the skin. A single normal cycle of the ECG represents the successive atrial depolarisation/repolarisation and ventricular depolarisation/repolarisation which occurs with every heart beat.

• Simply put, the ECG (EKG) is a device that measures and records the electrical activity of the heart from electrodes placed on the skin in specific locations

What the ECG is used for?

• Screening test for coronary artery disease, cardiomyopathies, left ventricular hypertrophy

• Preoperatively to rule out coronary artery disease• Can provide information in the precence of metabolic

alterations such has hyper/hypo calcemia/kalemia etc.• With known heart disease, monitor progression of the

disease• Discovery of heart disease; infarction, coronal

insufficiency as well as myocardial, valvular and cognitial heart disease

• Evaluation of ryhthm disorders• All in all, it is the basic cardiologic test and is widely

applied in patients with suspected or known heart disease

Each small box = 1 mm = .04 Sec.5 small boxes = 1 large box = 0.2 Sec.

MEASURING ECG ECG commonly measured via 12

specifically placed leads

Lead Configurations for ECG Measurement

Bipolar Leads Augmented Leads Chest (V) Leads

Bipolar Leads: lead I

+ _

vo+

_

Bipolar Leads: lead II

+ _

vo+

_

Bipolar Leads: lead III

+ _

vo+

_

ECG Limb Leads

Augmented Leads: aVR

+ _

vo+

_

Augmented Leads: aVL

+ _

vo+

_

Augmented Leads: aVF

+ _

vo+

_

ECG Augmented Limb Leads

Unipolar Chest Leads

v1 v2

v3

v4

v5 v6

v1: fourth intercostal space, at right sternal margin. v2: fourth intercostal space, at left sternal margin. v3: midway between v3 and v4. v4: fifth intercostal space, at mid clavicular line. v5: same level as v4, on anterior axillary line. v6: same level as v4, on mid axillary line.

Unipolar Chest Leads (cont.)

+ _ +

_

ECG Precordial Leads

Current Lead Placement Conventions(22 Electrodes)

V3R

V4RV5RV6R

E

H

I

3R

5R

V9V8

V7

I

E

M

6R

Current clinical conventions may use 22 different leads

ECG Lead Color Codes

C (brown)

LA (black)

LL (red)RL (green)

RA (white)

Surface Cardiac Potentials

taken at t = to suggests an equivalent dipole located within the heart

Eindhoven’s Triangle-very crude solution to inverse problem using bipolar limb leads:

RA LA

LL

_

_

+

_

++

lead II

lead I

lead III

NORMAL HEARTBEAT AND ATRIAL ARRHYTHMIA

Normal rhythm Atrial arrhythmia

AV septum

Ventri-culardepola-rization

Ventri-culardepola-rization(cont’d)

++

++

++

++ + +

++

++

++

++

++

--

--

--

- ---

--

-

--

--

--

--

--

-

Ventri-cularrepola-rization

Lead I

Lead II

Lead III

LimbLeads(bipolar)

Lead I

Lead II

Lead III

aVR

aVL

aVF

Uni-polarLead

Normalvalues

PR interval0.12-0.20”

P wave00.8-0.11”

QRS duration0.06-0.10”

Intrinsicoid deflection

< 0.05”

U wave

ST segmentStd: > 1mmPre : > 2mm

T wave

QT segmentMen < 0.39”Wo < 0.40”

Pre-cordialleads

V1 V2V4

V5

V3

V6

Hori-zontalvsVerti-cal heart

Clock-wisevsCounterclock-wiserotation

Viewed from below the heart looking towards the apex in vertical heart

13

24

13 24

13

24

1

3

24

P wave

V1

AtrialEnlargement

V1

P mitralWide and notch

Biphasic with(-) terminalcomponent

Left atrialenlargement

AtrialEnlargement(cont’d)

V1

Tall and peakedP wave

Right atrialenlargement

Tall and peakedP wave

Elec-tricalaxis

Lead I

aVF

qRS = +3

qRS = +1

TheQRS

Bundle of His

LBB

Anterosuperiordivision

Posteroinferiordivision

RBB

TheQRS

13

2

V1

V6

4

QRS vectors:• Initial depolarization• Terminal depolarization• S-T segmen• Re-polarization

Myo-cardial injury

Electrical forces are directed away from a injured area

A B C D E

Normal Minimal Subendocard Transmural Subepicard

Myo-cardial injury

A B C D E

Normal Minimal Subendocard Transmural Subepicard

ST segment deviated towards the surface of injured tissue

Myo-cardialinfarction

Zones of myocardial infarction:• Necrosis• Injury• Ischaemia

2

13 1

2

34

12

3

4

Myo-cardialinfarction(cont’d)

ECG parameters of myocardial infarction:• Necrosis• Injury• Ischaemia

13

V1

V6

24


Phases of myocardial infarction:

• Hyperacute phase- Slope elevation of the ST sement- Tall widened T wave- Increased ventr. activation time

• Fully evolved phase- Pathological Q wave- Coved, elevated ST segment- Inverted symetrical T wave

• Old infarction- Pathological Q wave- ST segment and T wave return to normal


Localization of infarcted areas

2

13

II, III, aVF

IaVLV4 V5

V6

V1 V2

V3

Rightventricularhypertrophy

12

V1

V6

4

3

Leftventricularhypertrophy

12

V1

V6

4

3

Diatolic overload

Leftventricularhypertrophy

12

V1

V6

4

3

Systolic overload

RBBB

12

V1

V6

4

3

LBBB

1a2

V1

V6

43

1b

QTinterval

QTc= QT

R-R

Prolonged QTc• Hypocalcemia• Acute rheumatic carditis

Shortened QTc

• Hypercalcemia• Digitalis effect• Hyperthermia• Vagal stimulation

Normal QT does not exclude the diagnosis of

• Acute myocardial infarction• Acute myocarditis of any causes• Sympathetic stimulation• Procain effect

AtrialSeptalActiva-tion

Sinus rhythms• Sinus arrythmia• Sinus tachycardia• Sinus bradycardia

AV nodal rythms• AVn extrasystole• Paroxysmal AVn tachycardia• Idionodal tachycardia

Ectopic atrial rythms• Atrial extrasystole• PAT• Atrial fibrilation• Atrial flutter

Ventricular rhytms• V-extrasystole• V-tachycardia• V-flutter• V-fibrilation• Idioventricular tachycardia

Disturbances of impulse formation

Arrhythmias

Disturbances of impulse conduction

S-A blockA-V block

WPW syndrome(Wolf-Parkinson-White)LGL syndrome(Lawn-Ganong-Levin)

Reciprocal rythms

Arrhythmias

2nd disorders of rythms

Atrial escape

Ventricular escape

AVn escape

A-V dissociation

Aberrant ventricular conduction

Arrhythmias

Diagnostic approach

To be continued next weekInsyaa Allah

Arrhythmias

12

V1

V6

4

3

Electrocardiogram

The WavesP wave

atrial depolarization

duration 0.11s

amplitude < 3mm

detects atrial functionSA node

Electrocardiogram

The WavesQRS Complex

ventricular depolarization duration 0.10s

detects ventricular functionQ wave

first downward strokeR wave

first upward strokeS wave

any downward stroke preceded by an upward stroke

T waveventricular repolarization

Intervals and Segments

PR segmentend of P wave to start of

QRSmeasures time of

depolarization through AV node

PR intervalstart of P wave to start of

QRSmeasures time from start of SA conduction to end of

AV node conductionnormal 0.12-0.20s


ST segmentend of QRS complex to start

of T wavemeasures start of ventricular

repolarizationelevated in MI’s

ST intervalend of QRS to end of T waverepresents complete time of

ventricular repolarization

QT intervalstart of QRS to end of T wave

duration of ventricular systole

< 1/2 of the RR interval


Intervalsthe timing for

depolarizations/repolarizations can be interpreted from the EKG

P-R 0.12-0.2 secmeasures the time between the start

of atrial depolarization and the start of ventricular depolarization

a long P-Q interval is a sign of AV node dysfunction

QT interval, about 0.4 secstart of QRS to end of T wave

QRS 0.08-0.1 secwider with ventricular dysfunction

ST segment (don’t worry about time)elevated with acute MI

Electrocardiogram

The wavesmore on the QRS

note that the Q or the R or the S wave is not always

presentname according to direction

of first deflection, second, etcQ waves are often absent

lead V1no Q

small Rlarge S

lead V2no Q

large Rsmall S

Heart Rate

Heart Ratedefined as beats per

minuteeasy way to estimate ratefind an R wave on a thick

linecount off on the thick

lines 300, 150, 100, 75, 60,

50until you reach another

R wave

in our example the middle R wave falls on the dark

linethe next R falls just before the 75, so

estimate about 80 bpm

300

15010075

Normal Sinus Rhythmheart rate between 60-100

bpm pacing by SA node.

QRS after every P waverhythm is regular

Sinus Tachycardiaheart rate > 100 bpm

p wave is there but hidden by the T wave

regular QRS rhythmSinus Bradycardiaheart rate < 60 bpm

QRS after every P waveregular rhythm

Heart Rate

ST segment elevation

ischemia

Q wavein some leads may indicate ischemia and

necrosis

T wave inversionlate sign of

necrosis and fibrosis

Wave Abnormalities

Atrial Fibrillationmultifocal areas in atria firing

no p waves and irregular heart rate

Rhythm Abnormalities

Complete (3rd degree) AV Block AV node cannot conduct impulsep waves and QRS not connected

irregular heart rate


Premature Ventricular Contractionsventricles pace early

early heart beatlarge QRS


Ventricular Tachycardiarapid ventricular pacing

rapid, regular ratewide QRS


Ventricular Fibrillationmultifocal

ventricular beatsirregular

won’t last long


0

+90

180

-90

Axis

QRS AXISanother name for the vector of

depolarizationan axis is measured in degrees the axis is measured by adding

the positive deflection and subtracting the negative

deflectionoverall + is left axis directionoverall - is right axis direction

for lead one most of the QRS is positive, therefore it has a

leftward axisif an MI caused the QRS to be

mostly negative the lead would have a rightward axis

— +

QRS AXISlead II

positive on left legnegative on right arm

looking at the tracing we see that the QRS is

mostly positivewhat does this mean?0

+90

180

-90

—

+

Axis

QRS AXISlead III

positive on left legnegative on left arm

looking at the tracing we see that the QRS is

mostly positivewhat does this mean?0

+90

180

-90

—

+

Axis

QRS AXISlead I

leftward axislead II

downward axisfrom this we can see that a

normal QRS axis lies somewhere in between 0 and +90 degrees

remember that infarction will cause the axis to shift rightward

(>+90) and that hypertrophy will shift the axis upward

(between 0 and -90)

0

+90

180

-90

—

+

+

Axis

The Anatomy of the Heart

The Blood Supply to the Heart• Coronary circulation meets heavy demands

of myocardium for oxygen, nutrients• Coronary arteries (right, left) branch from

aorta base• Anastomoses (arterial interconnections)

ensure constant blood supply• Drainage is to right atrium

• Great, middle cardiac veins drain capillaries• Empty into coronary sinus

• Arteries include the right and left coronary arteries, marginal arteries, anterior and posterior interventricular arteries, and the circumflex artery

• Veins include the great cardiac vein, anterior and posterior cardiac veins, the middle cardiac vein, and the small cardiac vein

Blood Supply to the Heart

SA node activity and atrial activation begin.

Stimulus spreads across the atrial surfaces and reaches the AV node.

There is a 100-msec delay at the AV node. Atrial contraction begins.

The impulse travels along the interventricular septum within the AV bundle and the bundle branches to the Purkinje fibers.

The impulse is distributed by Purkinje fibers and relayed throughout the ventricular myocardium. Atrial contraction is completed, and ventricular contraction begins.

Time = 0

SA node

AV node

Elapsed time = 50 msec


AV bundle

Bundle branches


Elapsed time = 225 msec Purkinje fibers

Coronary Circulation


Figure 20.9a, b


Figure 20.9c, d

HOLTER MONITOR

Technology• 5 electrodes• 2-3 leads• Derived 12 lead available• Digital or analog recording• Digital transmission to analyzer• Requires removal of Holter monitor to

scan recording

Uses:• Patients experiencing daily symptoms• Precise quantification of arrhythmias

Positives:• 24-48 hours full disclosure available• Heart rate and AF burden graphs• Arrhythmia counts (ex., 10 PVCs per

hour)

HOLTER MONITOR

ECG

Documents

Transcript of ECG