electrocardiography : an introduction to the ecg

7/28/2019 Electrocardiography : An Introduction to the ECG

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ELECTROCARDIOGRAPHY

maranducliff


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Introduction

The electrocardiogram (ECG) is a graphic

recording of electric potentials generated by

the heart

The signals are detected by means of metalelectrodes attached to the extremities and

chest wall and are then amplified and recorded

by the electrocardiograph. ECG leads actuallydisplay the instantaneous

differences in potential between these

electrodes


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The Clinical Utility of the ECG

immediately available as a noninvasive,

inexpensive, and highly versatile test

used in detecting arrhythmias, conduction

disturbances, and myocardial ischemia

may reveal other findings related to

life-threatening metabolic disturbances

(e.g.hyperkalemia) or increased susceptibilityto sudden cardiac death (e.g., QT prolongation

syndromes).


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Electrophysiology- Basic

Review

Depolarization of the heart is the initiating

event for cardiac contraction.

The electric currents that spread through the

heart are produced by three components:cardiac pacemaker cells, specialized

conduction tissue, and the heart muscle itself


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Important

The ECG, however, records only the

depolarization (stimulation) and repolarization

(recovery) potentials generated by the atrial

and ventricular myocardium


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The Cardiac ConductionSystem


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The Cardiac Conduction

System

The depolarization stimulus for the normal

heartbeat originates in the sinoatrial (SA)

node, a collection of pacemaker cells.

These cells fire spontaneously; that is, theyexhibit automaticity.

The firstphase of cardiac electrical activation

is the spread of the depolarization wavethrough the right and left atria, followed by

atrial contraction.


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The Cardiac Conduction

System Next, the impulse stimulates pacemaker and

specialized conduction tissues in theatrioventricular (AV) nodal and His-bundle areas;

The bundle of His bifurcates into the right and left

bundles, which rapidly transmit depolarizationwavefronts to the right and left ventricularmyocardium by way of Purkinje fibers.

The main left bundle bifurcates into a left anteriorfascicle and a left posterior fascicle.

The depolarization wavefronts then spreadthrough the ventricular wall,from endocardium toepicardium, triggering ventricular contraction


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Normal Activity of Pacemaker Cells

Sinus node automaticity is typically fastest and therefore determines

the normal heart rate and rhythm


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Vector Algebra!!

Since the cardiac depolarization and

repolarization waves have direction and

magnitude, they can be represented by

vectors. Vector analysis illustrates a central concept of

electrocardiographythat the ECG records

the complex spatial and temporal summation

of electrical potentials from multiple myocardial

fibers conducted to the surface of the body


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Limitations of the ECG

The principle of vectors accounts for inherentlimitations in ECG:

sensitivityactivity from certain cardiac regions may becancelled out or may be too weak to be recorded

specificitythe same vectorial sum can result from either aselective gain or a loss of forces in opposite

directions


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ECG Waveforms andIntervals


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Just a Few Lines of Orientation

The ECG waveforms are labelled

alphabetically, beginning with the P wave,

which represents atrial depolarization

The P wave is produced by atrialdepolarization, the QRS complex by

ventricular depolarization, and the T wave by

ventricular repolarization.

The U wave is an inconstant finding, believed

to be due to slow repolarization of the papillary

muscles


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ECG Waves and Intervals


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TQRS complex represents ventricular

depolarization,

ST-T-U complex (ST segment,T wave, and U

wave) represents ventricular repolarization.

J point is the junction between the end of QRS

complex and the beginning of ST segment.

Atrial repolarization is usually too low inamplitude to be detected, but it may become

apparent in e.g acute pericarditis oratrial

infarction


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The QRS-T waveforms of the surface ECG

correspond in a general way with the different

phases of simultaneously obtained ventricular

action potentials, the intracellular recordingsfrom single myocardial fibers


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The rapid upstroke (phase 0) of the action potentialcorresponds to the onset of QRS.

The plateau (phase 2) corresponds to the isoelectric STsegment

Active repolarization (phase 3) corresponds to the inscription

of the T wave. Factors that decrease the slope of phase 0 by impairing the

influx of Na+ (e.g., hyperkalemia, or drugs such as flecainide)tend to increase QRS duration.

Conditions that prolong phase 2 (use of amiodarone,

hypocalcemia) increase the QT interval. Shortening of ventricular repolarization (phase 2), as by

digitalis administration or hypercalcemia, abbreviates the STsegment.


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EEG is ordinarily recorded on special graph

paper which is divided into 1 mm2 gridlike

boxes.

ECG paper speed is generally 25 mm/s,

The smallest (1 mm) horizontal divisions

correspond to 0.04 (40 ms), with heavier lines

at intervals of 0.20 s (200 ms). Vertically, the ECG graph measures the

amplitude of a given wave or deflection (1 mV

= 10 mm withstandard calibration


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Limb Leads

Unipolar LeadsBipolar Leads

Precordial Leads

3-D View

ECG LEADS


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ECG Leads


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ECG Leads

The 12 conventional ECG leads record the

difference in potential between electrodes

placed on the surface of the body

These leads are divided into two groups: sixlimb (extremity) leads and six chest

(precordial) leads.


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Limb Leads

The six limb leads are further subdivided into

three standard bipolar leads (I, II, and III) and

three augmentedunipolar leads (aVR, aVL,

and aVF). Each standard leadmeasures the difference in

potential between electrodes at two

extremities:

lead I = left arm right arm voltages,

lead II = left leg right arm,

lead III = left legleft arm.


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Unipolar Leads

The unipolar leads measure the voltage (V) at onelocus relative to an electrode (the central terminalorindifferent electrode) that has approximatelyzero potential.

aVR = right arm, aVL = left arm,

aVF = left leg (foot).

The lowercase a indicates that these unipolarpotentials are electrically augmented by 50%.

The right leg electrode functions as a ground.

The spatial orientation and polarity of the sixfrontal plane leads is represented on the hexaxialdiagram


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Precordial Leads

The limb leads record potentials transmitted onto the frontal plane and

the chest leads reco rd potent ialstransmitted onto the horizontal

plane


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Precordial Leads

The six chest leads are unipolar recordingsobtained by electrodes in the followingpositions:

lead V1,fourth intercostal space, just to the rightof the sternum

lead V2, fourth intercostal space, just to the left ofthe sternum

lead V3, midway between V2 and V4

lead V4, midclavicular line, fifth intercostal space

lead V5, anterior axillary line, same level as V4

lead V6, midaxillary line, same level as V4 and

V5.


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Precordial Leads


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3-D View!!!

Together, the frontal and horizontal planeelectrodes provide a three-dimensionalrepresentation of cardiac electrical activity.

Each lead can be likened to a different cameraangle looking at the same eventsatrial andventricular depolarization and repolarizationfrom different spatial orientations.

The conventional 12-lead ECG can besupplemented with additional leads underspecial circumstances.


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3-D View!!!


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Configuration of Leads

The ECG leads are configured so that a

positive (upright) deflection is recorded in a

lead if a wave of depolarization spreads

toward the positive pole of that lead, and anegative deflection if the wave spreads toward

the negative pole.

If the mean orientation of the depolarization

vector is at right angles to a given lead axis, a

biphasic (equally positive and negative)

deflection will be recorded.


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P Wave

QRS Complex

QRS Complex: The Two Vectors Theory

Normal ECG from a Healthy Subject

Axis DeviationT and U Waves

Genesis of the Normal ECG


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P Wave

The normal atrial depolarization vector is

oriented downward and toward the subjects

left, reflecting the spread of depolarization

from the sinus node to the right and then theleft atrial myocardium.

This vector points toward the positive pole of

lead II and toward the negative pole of lead

aVR

Therefore the normal P wave will be positive in

lead II and negative in lead aVR.


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P Wave

By contrast, activation of the atria from an

ectopic pacemaker in the lower part of either

atrium or in the AV junction region may

produce retrograde P waves (negative in leadII, positive in lead aVR).

The normal P wave in lead V1 may be

biphasic with a positive component reflecting

right atrial depolarization, followed by a small

(


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QRS Complex

Normal ventricular depolarization proceeds as

a rapid, continuous spread of activation

wavefronts.

This complex process can be divided into twomajor, sequential phases, and each phase can

be represented by a mean vector

QRS C l Th T V t


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QRS Complex: The Two Vectors

Theory

The first phase is depolarization of theinterventricular septum from the left to

the right and anteriorly (vector 1)


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QRS Complex

Therefore, a right precordial lead (V1) will record this biphasicdepolarization process with a small positive deflection (septalr wave) followed by a larger negative deflection (S wave).

A left precordial lead, e.g.V6, will record the same sequencewith a small negative deflection (septal q wave) followed by a

relatively tall positive deflection (R wave). Intermediate leads show a relative increase in R-wave

amplitude (normal R-wave progression) and a decrease in S-wave amplitude progressing across the chest from the right toleft.

The precordial lead where the R and S waves are ofapproximately equal amplitude is referred to as the transitionzone (usuallyV3 or V4

N l ECG f H lth


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Normal ECG from a Healthy

Subject


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The Electrical Axis of the QRS

Describes the mean orientation of the QRS

vector with reference to the six frontal plane

leads

Normally, the QRS axis ranges from 30 to+110


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Left Axis Deviation

An axis more negative than -30

Lies between -30 and -90

Left axis deviation may occur as a normal

variant but is more commonly associated with:

left ventricular hypertrophy,

a block in the anterior fascicle of the left

bundle system (left anterior fascicular blockor hemiblock),

or inferior myocardial infarction


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Right Axis Deviation

Lies between 110 and 180

may also occur as a normal variant (particularly inchildren and young adults)

as a spurious finding due to reversal of the left and

right arm electrodes or in conditions such as right ventricular overload

(acute or chronic),

infarction of the lateral wall of the left ventricle,

dextrocardia, left pneumothorax,

or left posterior fascicular block.


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ECG QRS Voltage

High voltage usually corresponds with ventricularenlargement/hypertrophy

Exception: voltage often abnormal in BBB

Several different criteria for LVE/LVH and

RVE/RVH

Low voltage corresponds with various clinical

states

ObesityHypothyroidism/myxedema

Pericardial effusion

Hyponatremia


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T Wave and U Wave

The normal U wave is a small, rounded

deflection (1 mm) that follows the T wave and

usually has the same polarity as the T wave.

Abnormal increase in U-wave amplitude ismost commonly due to drugs (e.g., quinidine,

procainamide) or hypokalemia.

Very prominent U waves indicate increasedsusceptibility to torsades de pointe type of

ventricular tachycardia

Inversion of the U wave in the precordial leads

is abnormal and may be a subtle sign of


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Cardiac Enlargement and Hypertrophy

Bundle Branch BlockWolff-Parkinson-White Syndrome

Heart Block

Myocardial Infarction and Ischemia

Metabolic Factors and Drug Effects

Major ECG Abnormalities

Cardiac Enlargement and


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Cardiac Enlargement and

Hypertrophy

Right atrial overload (acute or chronic) maylead to an increase in P-wave amplitude (2.5mm)

Left atrial overload typically produces abiphasic P wave in V1 with a broad negativecomponent or a broad (120 ms), oftennotched P wave in one or more limb leads

This pattern may also occur with left atrialconduction delays in the absence of actualatrial enlargement, leading to the more generaldesignation ofleft atrial abnormality.


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Bundle Branch Block

Intrinsic impairment of conduction in either the

right or left bundle system intraventricular

conduction disturbances leads to prolongation

of the QRS interval With complete bundle branch blocks, the QRS

interval is 120 ms in duration; with incomplete

blocks the QRS interval is between 100 and

120 ms.

The QRS vector is usually oriented in the

direction of the myocardial region where

depolarization is delayed


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Important

Prolongation of QRS duration does notnecessarily indicate a conduction delay but maybe due topreexcitation of the ventricles via abypass tract, as in Wolff-Parkinson-White (WPW)

patterns The diagnostic triad of WPW consists of a wide

QRS complex associated with a relatively shortPR interval and slurring of the initial part of the

QRS (delta wave), the latter effect due to aberrantactivation of ventricular myocardium

The presence of a bypass tract predisposes toreentrant supraventricular tachyarrhythmias


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Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White syndrome is characterized by the

presence of an accessory atrioventicular pathway

located between the wall of the right or left atria and the

ventricles, known as the Bundle of Kent. This pathway

allows the impulse to bypass the AV node and activate

the ventricles prematurely. Consequently, an initial slur to

the QRS complex, known as a delta wave may be

observed. The QRS complexes are wide, more than 0.11sec, indicating that the impulse did not travel through the

normal conducting system. The PR is shortened, to less

than 0.12 sec, because the delay at the AV node is

bypassed


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Wolff-Parkinson-White Syndrome


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PR Interval

.2- AV Junctional Rhythms with retrograde atrial

activation (inverted P waves in II, III, aVF):

Retrograde P waves may occurbefore the QRS

complex (usually with a short PR interval), in the

QRS complex (i.e., hidden from view), orafterthe

QRS complex (i.e., in the ST segment).

3- Ectopic atrial rhythms originating near the AVnode (the PR interval is short because atrial

activation originates close to the AV node; the P

wave morphology is different from the sinus P)

4- Normal variant

PR I t l


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PR Interval

.

Prolonged PR: >0.20s

1-First degree AV block (PR interval usually constant)

2-Second degree AV block (PR interval may be normal or prolonged; some P

waves do not conduct)

Type I (Wenckebach): Increasing PR until nonconducted P wave occurs

Type II (Mobitz): Fixed PR intervals plus nonconducted P waves

3-AV dissociation: Some PR's may appear prolonged, but the P waves and QRS

complexes are dissociated .4- Rheumatic fever

5- Digitalis


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First Degree AV Block

Second Degree AV Block (Mobitz


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Second Degree AV Block (Mobitz

I)-Wenckebach


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Heart Block

Atrioventricular block.

For 1st-degree block, conduction is slowed

without skipped beats. All normal P waves are

followed by QRS complexes, but the PRinterval is longer than normal (> 0.2 sec).


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Heart Block

Mobitz type II 2nd-degree atrioventricular

block.

The PR interval remains constant. Beats are

intermittently nonconducted, and QRScomplexes dropped, usually in a repeating

cycle of every 3rd (3:1 block) or 4th (4:1 block)

P wave.


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Myocardial Infarction and


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Ischemia

The ECG is a cornerstone in the diagnosis of

acute and chronic ischemic heart disease

Ischemia exerts complex time-dependent

effects on the electrical properties ofmyocardial cells



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Ischemia

Severe, acute ischemia lowers the resting

membrane potential and shortens the duration

of the action potential

Such changes cause a voltage gradientbetween normal and ischemic zones

As a consequence, current flows between

these regions.



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Ischemia

These currents of injury are represented on

the surface ECG by deviation of the ST

segment


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Metabolic Factors and Drug


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Effects

A variety of metabolic and pharmacologic

agents alter the ECG and, in particular, cause

changes in repolarization (ST-T-U) and

sometimes QRS prolongation. Certain life-threatening electrolyte

disturbances may be diagnosed initially and

monitored from the ECG



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Effects

Hyperkalemia produces a sequence of

changes usually beginning with narrowing and

peaking (tenting) of the T waves

Further elevation of extracellular K+ leads toAV conduction disturbances, diminution in P-

wave amplitude, and widening of the QRS

interval

Severe hyperkalemia eventually causes

cardiac arrest with a slow sinusoidal type of

mechanism followed by asystole


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Effects

Prolongation of the QT interval is also seen

with drugs that increase the duration of the

ventricular action potentialclass 1A

antiarrhythmic agents and related drugs (e.g.,quinidine, disopyramide, procainamide,

tricyclic antidepressants, phenothiazines) and

class III agents



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Effects

Marked QT prolongation, sometimes with

deep, wide T-wave inversions, may occur with

intracranial bleeds, particularly subarachnoid

hemorrhage Systemic hypothermia also prolongs

repolarization, usually with a distinctive convex

elevation of the J point (Osborn wave)


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Computerized


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p

Electrocardiography

Computerized ECG systems are widely used. Digital systems provide for convenient storage

and immediate retrieval of thousands of ECGrecords.

Despite advances, computer interpretation ofECGs has important limitations.

Incomplete or inaccurate readings are most likelywith arrhythmias and complex abnormalities.

Therefore, computerized interpretation (includingmeasurements of basic ECG intervals) should notbe accepted without careful clinician review.

F th R di


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Further Readings..

ASHLEY EA et al:An evidence-based review of the restingelectrocardiogram as a screening technique for heart disease. ProgCardiovasc Dis 44:55, 2001

GOLDBERGER AL: Clinical Electrocardiography: A Simplified Approach,7th ed. St. Louis, Mosby/Elsevier, 2006

GUGLIN MF,THATAI D: Common errors in computer electrocardiograminterpretation. Int J Cardiol 106:232, 2006

KRIGFIELD P, et al: Recommendations for the standardization andinterpretation of the electrocardiogram. Part I: The electrocardiogram andits standardization. J Am Coll Cardiol 49:1109, 2007

MIRVIS DM, GOLDBERGER AL: Electrocardiography, in Braunwalds HeartDisease:A Textbook of Cardiovascular Medicine, 8th ed, P Libbyet al (eds).Philadelphia, Saunders, 2008

SURAWICZ B, KNILANS TK: Chous Electrocardiography in ClinicalPractice, 5th ed. Philadelphia, Saunders, 2001

WAGNER G, et al: Recommendations for the standardization andinterpretation of the electrocardiogram. Part VI: Acute myocardial ischemia.J Am Coll Cardiol 53:1003, 2009

electrocardiography : an introduction to the ecg

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