1

Kitty Chan

School of Nursing,The Hong Kong Polytechnic University

Email: hskittyc@inet.polyu.edu.hk

Date: 2005

2

Upon completion of the session, the students

should:

have developed a basic understanding of anatomy and

of the physiology of cardiac conduction in relation

to ECG interpretation;

have developed a systematic and pragmatic approach

to ECG interpretation;

appreciate the clinical significance of ECG

interpretation.

Objectives

3

■ Wiegand, L-M D. J. & Carlson, K. K. (Eds.) (2005). American Association of Critical-Care Nurses AACN Procedure Manual for Critical Care. (5th ed.). Philadelphia: W B Saunders.Section 8

■ Huszar, R. J. (2002). Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.

Indicative Readings

4

The electrocardiogram [ECG] is a helpful in diagnosing cardiac & non-cardiac illnesses. It is also used to monitor the effects of therapeutic treatment. Cardiac monitoring, or telemetry provides a continuous and real-time observation of the client’s cardiac rhythm. A single-strip ECG gives a prompt identification of life-threatening rhythms. In addition, abnormalities that are detected can serve as a basis for 12-Lead ECG or other investigations.12-Lead ECG imparts more information, such as ischaemia and myocardial infarction. The above two aspects will be the main focus of this module.Of course, interpreting axis deviation & hypertrophies or other abnormalities is highly recommended.

Introduction

5

Electrical activities produce current that transmit through the heart conduction system. This is sensed and transformed into ECG waveforms. Depolarization and repolarization occurs in a precise sequence. Normally, mechanical heart contraction follow to generate the cardiac output.However, when disturbances arise, cardiac contraction may not be effective, and there may even be no contractions.Therefore, always match the ECG rhythm with the patients’ clinical manifestation and complains.Before we start interpreting ECG, the anatomy, cardiac cycle and electrophysiology are reviewed

Introduction

6

Five Phases of the Depolarization-Repolarization CyclePHASE Response and Action Potential

0 Rapid Depolarization

A current is conducted from adjacent cells.In response to a stimulus from connecting cells, a sodium channel opens There is a rapid influx of Sodium into the cells Calcium moves slowly into the cells The cell membrane charge moves from -90mv to +20-+30mv

1 Early Repolarization

Sodium channels closeThe cells begin to return to a negative state

2 Plateau The Calcium channels open Slow influx of Calcium Outflow of Potassium Cell membrane potential is around 0mv

3 Rapid Repolarization

The Calcium channels close Rapid outflow of Potassium Cell membrane potential drops rapidly back to it resting membrane potential [RMP]

4 Resting The Sodium pump is reactivated (* It depends on an adequate amount of Magnesium & Phosphate). Normal electrolytes distribution restored: The Cell membrane is impermeable to Sodium Potassium inside the cell & sodium outside the cell The Resting Membrane Potential -90mv

7

Myocardial Transmembrane PotentialsPotential milivolts

0

Resting State

Rapid Depolarization

Early Repolarization

Rapid Repolarization

Absolute Refractory

Period

Absolute Refractory

Period

Restoration of

Balance

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

Sodium Pump

KK++

Na+

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

Relative Refractory

Period

Relative Refractory

Period

Cardiaccell

Cellmembrane

Cellmembrane

Outside cell

Outside cell

+ + + + +

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

KK++

Na+Ca++

Na+ K+

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

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

- - - - - - - - - - -

Mechanical Contractio

n

Action Potentials

Threshold Potentials

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

+ + + + + + + + + + + + + +Fast

Sodium Influx

Slow Calcium channel open Plateau

Plateau

8

Properties of Cardiac CellsTerm Electrophysiological Properties

Automaticity

Spontaneous Depolarization (Pacemaker Potential):Cardiac cells initiate their own action potential WITHOUT a stimulus from another cellA cell membrane allows Na+ & Ca++ ions to move in & prevents K+ from diffusing out. A NET build-up of positive ions inside the cell enables it to reach a threshold (TP) & depolarizeThe slope of the pacemaker potential (i.e., the time it takes to reach TP) determines the automaticity of the cells

Excitability Ability of a cell to depolarize in response to a stimulus:The more negative the Resting Membrane Potential

The LESS excitable is the cell; The FASTER the conduction velocity

Conductivity

Ability of a cardiac cell to transmit an impulse

Refractoriness

The state of a cardiac cell: Regardless of the intensity of the stimulus (much stronger than normally required) to initiate repolarization

9

Automaticity of Cardiac CellsCardiac

CellsElectrophysiological Properties

SA Node Main Pacemaker:Intrinsic firing at a rate of 60-100 times/minuteImpulse generation is fastest & dominantImpulse transmission follow specific path

AV Node Slow Node:Depolarizes at a rate of 40-60 times/minuteDelays impulses from the SA node by 0.04 secondsGenerates impulses when the impulse generation function of the SA node pulse impairs

His-Purkinje Fibres

The Left & Right Bundle Branch conduct impulses at different speeds to synchronize the depolarization of the Left & Right VentriclesPurkinje fibres are usually not activated unless the pulse transmission is blocked or not generated from higher pacemakersGenerates impulses & serves as a pacemaker at a rate of 20-40 bpm or slowerThe impulse transmission is chaotic

10

Time (Second) 0 1.

60.8

2.4

+ + 10mV10mV

--90mV90mV

Membrane Potential

Threshold Threshold PotentialPotential

Action Action PotentialPotential

Resting Resting Membrane Membrane PotentialPotential

-60mV-60mV

Pacemaker Action Potentials & Automaticity

Automaticity in cardiac muscles:

a gradual in K+ permeability resting potential Transmembranous Potential [TMP] reaches a threshold Spontaneous depolarization occurs

SA node - shortest phase 4 dominates impulse generation

Pacemaker Potential: Pacemaker Potential: Spontaneous Depolarization

11

Time (Second) 0 1.

60.8

2.4

+ + 10mV10mV

--90mV90mV

Membrane Potential

Threshold Threshold PotentialPotential

Action Action PotentialPotential

Resting Resting Membrane Membrane PotentialPotential

-60mV-60mV

Pacemaker Action Potentials & Automaticity

Steeper Slope: Automaticity

Increase

Pacemaker Potential: Pacemaker Potential: Spontaneous Depolarization

12

Time (Second) 0 1.

60.8

2.4

+ + 10mV10mV

--90mV90mV

Membrane Potential

Threshold Threshold PotentialPotential

Action Action PotentialPotential

Resting Resting Membrane Membrane PotentialPotential

-60mV-60mV

Pacemaker Action Potentials & Automaticity

Slope Decreases : Automaticity Decreases

Pacemaker Potential: Pacemaker Potential: Spontaneous Depolarization

13

Time (Second) 0 1.

60.8

2.4

+ + 10mV10mV

--90mV90mV

Membrane Potential

Threshold Threshold PotentialPotential

Action Action PotentialPotential

Resting Resting Membrane Membrane PotentialPotential

-60mV-60mV

Effect of Change in RMP

RMPRMP

TPTPBigger Difference

RMP Decreases (More Negative):

Cells are less excitable Stronger stimulus required for depolarization contractility weakens

This occurs in HYPOKalaemia

14

Time (Second) 0 1.

60.8

2.4

+ + 10mV10mV

--90mV90mV

Membrane Potential

Threshold Threshold PotentialPotential

Action Action PotentialPotential

Resting Resting Membrane Membrane PotentialPotential

-60mV-60mV

Effect of Change in RMP

RMPRMPTPTP

RMP Increases (Less Negative):

Cells are easily excitable Depolarization occurs with a very weak stimulus contractility slow & ineffective

This occurs in HYPERKalaemia

Closer to TP

15

Time (Second) 0 1.

60.8

2.4

+ + 10mV10mV

--90mV90mV

Membrane Potential

Threshold Threshold PotentialPotential

Action Action PotentialPotential

Resting Resting Membrane Membrane PotentialPotential

-60mV-60mV

Effect of Change in TP

TP Decreases:

Closer to RMP, the cells are more excitable Depolarization occurs with a very weak stimulus contractility slow & ineffective

This occurs in HYPOCalaemia

HYPERCALCAEMIA is a Positive Inotrope since it sustains & strengthens cardiac contractions

TPTP

Closer to RMP

RMPRMP

16

Electrical Conduction System

Sinoatrial (SA) Node

Atrioventricular (AV) Node

Bundle of His

Left Bundle Branch

Left posterior fascicle

Left anterior fascicle

AV Junction

Purkinje fibresRight Bundle Branch

Interatrial conduction tract(Bachmann Bundle)

Internodal atrial conduction tract

17

Wave Deflection & Current Direction

Current Direction-ve

+ve

Electrical Waveform

Deflection

Toward the Lead

UPRIGHTUPRIGHT

Away from the Lead

DOWNWADOWNWARDRD

Perpendicular to the Lead

BIPHASICBIPHASIC

18

11

4433

22 RR

Cardiac Depolarization & Electrical Current

11. Atrial Depolarization

2. Septal vector

3. Apical vector & both ventricles

4. Remainder of the left ventricle

RR. Resultant Cardiac Vector. Resultant Cardiac Vector

A positive deflection (upstroke) Λ is recorded as depolarization proceeds towards the particular electrode & vice versa.

19

Limb Leads: Frontal Plane of the HeartStandard Bipolar Leads

Inferior

Lead ILead I+

+

Lead IILead II

Lead IIILead III

+

Einthoven’s Equilateral Triangle

20

Limb Leads: Frontal Plane of the HeartThe Augmented Unipolar Leads

Lead Lead aVLaVL

Lead Lead aVFaVF

Lead Lead aVRaVRLead Lead aVRaVR

xNull Null ReferencReference Pointe Point

Null Reference Point: the negative reference for leads aVR, aVL, aVF & the precordial leads V1 - V6

(calculated from the right & left arm and right & left leg electrodes)

21

Hexaxial Reference Circle

aVR -1500

+300

aVL-300

+1500

I 00

+1800

II +600

-1200

aVF +900

-900

III +1200

-600

LADLAD

RADRAD

NORMALNORMAL

IndeterminatIndeterminatee

For determining frontal plane axis deviation

22

12-Lead Electrode Placement

Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

i.e., Electrode Placement at V6 equivalent of MCL6

✼Precordial Leads are useful in detecting ST

Changes & Aberrant Ventricular Conductions

Septal Septal LeadsLeads

Anterior Anterior LeadsLeads

Lateral Lateral LeadsLeads

V1 to V6: Corresponding sites for monitoring of MCL1 to MCL6

V2V2V1V1V6V6

V4V4V5V5V3V3

Mid-Clavicular Mid-Clavicular LineLine

Anterior Axillary LineAnterior Axillary Line

Mid-Axillary LineMid-Axillary Line

23

Right-sided Chest Electrode Placement

V2V2RR

V3V3RR

V5V5RRV6V6RR

V4V4RR

Mid-Clavicular LineMid-Clavicular Line

Anterior Axillary LineAnterior Axillary Line

Mid-Axillary LineMid-Axillary Line

24

Posterior Chest Electrode Placement

Mid-Axillary Mid-Axillary LineLine

Posterior Axillary LinePosterior Axillary LineLeft Paraspinal LineLeft Paraspinal Line

V9V9V7V7V6V6 V8V8

Wiegand & Calrson, 2004, p. 426

25

Cardiac Monitoring & Lead Placement

3-Lead-Wire system:

limited to leads I, II, III &

modified chest leads (MCL1-6)

For single-lead ECG monitoring, unless a specific part of the heart is under scrutiny, Lead II is usually chosen since both the positive & negative vectors are travelling in the same direction of cardiac impulse conduction, producing upright P & QRS complexes.

26

Cardiac Monitoring & Lead Placement

5-Lead-Wire system:

4 standardized electrodes corresponding to limbs leads I, II, III, aVR, aVL & aVF

placement of 5th chest leads provides 7 precordial lead options

V1-V6 (1 at a time)

27*Sweep speed of ECG & paper dispense @ 25mm per second

1 1 Large Large

SquareSquare

5mm across = 0.2

second

1mm across

= 0.04 second

1mm tall = 0.1mV of amplitude

1 1 Small Small

SquarSquar

ee

55 Large Large Squares Squares

= = 11 SecondSecond

28

Normal ECG/EKG Waveform

PPTT

UU

RR

QQSS

ST ST SegmentSegment

PR PR IntervalInterval

QT QT IntervalInterval

Lead II

P

PR Interval

Q

R

S

TU

ST Segment

QT Interval

29

Normal ECG Waveforms & ConfigurationsWavefor

mConfiguration & Duration (second) Leads

Amplitude Duration

P Rounded & SymmetricalAmplitude 0.5-2.5cm

0.06-0.10

I, II, aVF, V4-V6

PR Interval

0.12-0.20

QRS Q: Small & Non-significant 0.06-0.12

I, II, III, aVL, V4-V6

R: progressively higher in amplitude –

limb leads > 5mmchest leads > 10mm

V2-V5, gradually diminish in V5-V6

ST Curves gently into the proximal limb of the T waveIsoelectric in ALL Leads

Elevation < 1mm & Depression < 0.5mm

J Point Junction of QRS complex & the ST segment

T wave Rounded & Symmetrical, amplitude:limb leads< 5mm & chest leads < 10mm

Positive in I, II, V3-V6

Inverted in aVR

QT (<½ preceding RR)

U wave Delayed depolarization of the purkinje system

30

P

PR INTERVAL

P wave: Atrial Depolarization

P:P:

•rounded & symmetrical

• 0.06- 0.10 sec

•amplitude: 0.5-2.5mm

•positive in Lead I, II, aVF & V4-V6

PR Interval:PR Interval:

•0.12-0.20 sec

Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

31

QRS: Ventricle Depolarization

P

QRS

QRS: QRS:

•Q waves is small &

nonsignificant in leads I, II, III,

aVL, V4-V6

•R wave progressively higher

in amplitude from V2-V4/V5

gradually diminish to V6

•0.06- 0.12 sec

•amplitude: >5mm in limb

leads; >10mm in Chest leadsPaul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

32

P

QRS

ST:ST:

•Curves gently into the proximal limb of the T wave

•Isoelectric in ALL Leads

•elevation <1mm

•depression <0.5mm

J Point:J Point:

•The junction of QRS complex & the J point of the ST segment

•deviates from the isoelectric line if an ST elevation/

depression exist

ST SEGMENT

ST Segment: Isoelectric Line

Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

J Point

33

T: T: •slightly rounded & symmetrical

•positive in leads I, II, V3-V6

•inverted in aVR

•amplitude <5mm in limb leads & <10mm in chest leads

QT: QT: ventricular refractory period

•0.30-0.44sec

•*0.12-0.20 sec (<½ preceding RR)

U wave:U wave: delayed repolarization of the purkinje

system

T

QRS

P

QT

T wave: Ventricular Repolarization

Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

34

Sinus Rhythm

Rhythm Atrial Rate

Ventricular Rate

P wave PR Interval

QRS P:QRS Ratio

Normal Sinus Rhythm

regular 60-100 Before every QRS (Normal Configuraton)

Normal 1:1

Sinus Tachycardia

regular >100 usu. < 160

Before every QRS (Normal Configuraton)

Normal 1:1

Sinus Bradycardia

regular < 60

Before every QRS (Normal Configuraton)

Normal 1:1

Sinus Dysrhythmia

irregular 60-100 ✼ inspiration expiration

Before every QRS (Normal Configuraton)

Normal 1:1

Sinus Rhythm

35

Normal Sinus Rhythm [NSR]

P P P PPP P P

66 SecondsSeconds

Total in 6 seconds

Characteristics

P Waves: 7 Upright & amplitude 1mm

PR Interval 0.12 second

Each P is followed by a QRS

QRS Complex 7 (HR=70bp

m)

Normal (0.12 second)

RR Interval Regular

36

Sinus Bradycardia

P PPP P6 6 SecondsSeconds

QRS QRS ComplexComplex

Total in 6 seconds

Characteristics

P Waves: 5 Upright & amplitude 1mm

PR Interval 0.12 second

Each P is followed by a QRS

QRS Complex 5 (HR=50bp

m)

Normal (0.12 second)

RR Interval Regular

37

Sinus DysrhythmiasSinus

DysrhythmiasCharacteristics

Sinus Pause dropped P wave & SR resumed subsequently

Sinus Arrest /Sinoatrial Exit Block

SA node fails to initiate an impulse for 3 seconds

Sick Sinus Syndrome (SSS):

Paroxysmal or alternating sinus bradycardia & atrial tachycardia (brady-tachy syndrome)Failure to HR to meet body demand

38

Atrial Dysrhythmias

Rhythm Atrial Rate

Ventricular Rate

P wave PR Interval QRS P:QRS Ratio

Premature Atrial Complexes (PACs)

Irregular Depends on underlying rhythm

Early Morphology varies

Varies Normal 1:1

Wandering Atrial Pacemaker

Irregular 60-100 Before every QRS

Some variations

Normal 1:1

Atrial Flutter Regular/ irregular

240-340 Depends on AV conduction

Saw-toothed flutter wave

Not measurable

Normal P QRS

Atrial Fibrillation

Irregular 350 varies Coarse or fine fibrillatory waves

Not measurable

Normal P QRS

39

Atrial Flutter

66 SecondsSeconds

Total in 6 seconds

Characteristics

P Waves: Varies Saw-Tooth

QRS Complex 9 (HR=90bp

m)

Normal

RR Interval IRREGULAR

Identical undulating SAW-TOOTH FLUTTER WAVES

F F F F F F F F F F QRS QRS ComplexComplex

QRS QRS ComplexComplex

40

Atrial Fibrillation [Fine AF]

Total in 6 seconds

Characteristics

P Waves: Varies FIINE Fibrillatory Waves

QRS Complex HR 50-60 bpm

Normal

RR Interval IRREGULAR6 6 SecondsSeconds

41

Atrial Fibrillation [Coarse AF]

Total in 6 seconds

Characteristics

P Waves: Varies Coarse Fibrillatory Waves

QRS Complex

HR 80bpm

Normal

RR Interval IRREGULAR6 6 SecondsSeconds

42

Atrial Dysrhythmias

P’ P’ P’ P’ P’

MAT (multifocal atrial tachycardia)•Various P morphologies originate from multiple atrial ectopic foci

*(3 or more pacemaker sites)

•Rate = 160-240bpm

43

Juntional Rhythm

6 6 SecondsSeconds

Total in 6 seconds

Characteristics

P Waves: 0

QRS Complex 6(HR=60bp

m)

Normal

RR Interval 0.98 second

REGULAR

QRS QRS ComplexComplex

44

Junctional Dysrhythmias1o pacing from the AV node

Rhythm Atrial Rate Ventricular Rate

P waves QRS PR Interval P:QRS Ratio

AV Junctional Rhythm

Regular Indeterminate 40-60 Inverted Before /After/Being Buried in QRS

Normal 0.2 sec if P precedes QRS

P QRS

Junctional Tachycardia

Regular Indeterminate 100-250 Inverted Before /After/ Being Buried in QRS

Normal Indeterminate P QRS

Paroxysmal Supraventricular Tachycardia (PSVT)

Regular Present or absent

160-240 *begins abruptly & last from a few seconds to many hours

Inverted Before /After/ Being Buried in QRS

Usually normal

0.2 sec if P precedes QRS

P QRS

45

Non-uniform recovery from refractory period leading to re-entry circuit:

1. Slow conduction of impulses at a refractory zone

→ Unidirectional Block→ Detouring of Impulse

2. Activation & transmission of impulse via accessory pathway

3. Subsequent activation of impulse through the previously refractory zone (now recovered)

4. The reentry & activation of new impulses occur in a circuitry manner

Re-Entry Phenomenon [1]

46

Unidirectional Block & Delayed Conduction within the circuit

→Original impulse emerges & reenters the adjacent tissue (just recovered)

→ Recycles within the circuit

Unidirectional Block & Delayed Conduction within the circuit

→Original impulse emerges & reenters the adjacent tissue (just recovered)

→ Recycles within the circuit

Normal Impulse NOT yet fired from SAN ∴ AV Node NOT Reactivated

Normal Impulse NOT yet fired from SAN ∴ AV Node NOT Reactivated

Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implications for patient care. Philadelphia: Saunders.

Re-Entry Phenomenon [2]

47

AVNRT (AV Node Re-entry Tachycardia)Micro-Circuits: At cellular level within the AV node with unidirectional block & the Purkinje fibers

Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

Ventricular Pre-excitation

48Paul S & Hebra J D 1998 The Nurse’s Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders

AVRT (AV Re-entry Tachycardia)-

Macro-Circuits: Antegrade travel through the AV node & retrograde across an accessory pathway

Classic Ventricular Pre-excitation

Wolf-Parkinson-White Syndrome:pre-excitation via a Bundle of Kent without delay at the AV node

Depolarization occurs with AV impulse after normal delay

delta wave(slurred upstroke)

49

PSVT (Paroxysmal Supraventricular Tachycardia)

*It is useful to capture the beginning of the PSVT to

identify the re-entry loop, especially when aberrant

conduction occurs & a wide bizarre QRS exists

50

Atrioventricular Blocks(Heart Block)

Rhythm Atrial Rate Ventricular Rate

P Wave PR Interval QRS P:QRS Ratio

1o Heart Block regular 60-100 Precedes each QRS

Prolonged ( 0.2s)

Normal 1:1

2o Heart Block (Wenkebach, Mobitz Type I)

irregular ventricular rate

sinus rate Precedes each QRS EXCEPT a non-conducted P (regular)

Cycles of Progressive lengthening until non-conduction

Normal 1:1

2o Heart Block (Mobitz Type II)

irregular ventricular rate

Depends on degree of block

Periodic non-conducted P wave (dropped beat)

Normal or constantly prolonged

Normal P QRS

3o Complete Heart Block

regular ventricular rate

60 Regular No relationship

٪ P & QRS

Normal or 0.12 sec

P QRS

51

PR Interval: Constant

RR Interval: Constant

P:QRS Relationship -1:1

Heart Block

1o HB11oo

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

P P P P

52

Heart Block

Type I 2o HB (Wenkebach)

22oo

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

PR Interval: Progressive lengthening

P P P P P

Non-conduction

Absence of QRS complex after P

53

Heart Block

22oo

Advanced AV Block

3:1 Block

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

PR Interval: Constant

Type II 2o HB sudden drop beat

PR Interval: Constant RR Interval: Constant Regular drop beat(s)

54

NO Relationship between P & QRS complex

Heart Block

33oo

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

3 o HB

P-P Interval Constant

P-P Interval Constant

R-R Interval Constant

R-R Interval Constant

55

Third Degree Heart Block & A-V Dissociation

Sinus Dysrhythmias, AV Conduction distrubances or Junctional/Ventricular Tachycardai may result in complete Atrioventricular (AV) Dissociation

Differentiate 3o HB & AV Dissociation:

3o HB Atrial Rate > Ventricular Rate

AV Dissociation Atrial Rate ≈ Ventricular Rate (slightly faster)

RARELY the Primary Problem

56

Right Bundle Branch Block

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

rSR’ pattern Wide S wave

✼ RBBB: QRS 0.12 secT wave Inversion in V1 is common

rR’

Late abnormal electrical vector leading to depolarization of right ventricle > (R’)

RBBB

57

Left Bundle Branch Block

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

LBBB

Impulse activates across the septum from Right to LeftDelayed & prolonged electrical vector toward the eft ventricle → notched R wave

✼LBBB: QRS 0.12 secElevated ST is common in V1-V4

V1

QS WAVE: Wide negative QRS

V6

Large notched R wave

T wave inversion

58

Hemi-/ Fascicular Blocks

Left Anterior Fasicular Block (LAFB)

Left Anterior Fasicular Block (LAFB)

Left Posterior Fasicular Block (LPFB)Left Posterior Fasicular Block (LPFB)

Block Characteristics LAFB Left axis deviation

Prolonged QRS

Q1S3 syndrome

(Q in Lead I; Deep S in Lead III) LPFB Right axis deviation

Prolonged QRS

S1Q3 syndrome

(S in Lead I; Q in Lead III)

59

Ventricular Dysrhythmias

Rhythm Atrial Rate Ventricular Rate

P wave

PR Interval

QRS P:QRS Ratio

Premature Ventricular Complexes (PACs)

irregular indeterminate Depends on the underlying rhythm

unidentifiable Bizzare ( 0.12s) 1:1

Ventricular Tachycardia

Slightly irregular

indeterminate 150-250 unidentifiable Bizzare ( 0.12s) QRS

Ventricular Fibrillation

Irregular indeterminate rapid unidentifiable Fibrillatory waves

none

Idioventricular Rhythm

Regular or irregular

none 40 None or retrograde

Bizzare ( 0.12s) none

Accelerated Idioventricular Rhythm

Usually regular

none 40 - 100 None or retrograde

Bizzare ( 0.12s) none

Ectopic foci

60

Premature Ventricular Contractions

(PVCs)

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

Group Beats Couplet Ventricular Tachycardia

R-on-T

Bigeminy

Trigeminy

61

Ventricular Dysrhythmias

Ventricular tachycardia (monomorphic)

Torsades de pointes

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

62

Ventricular Dysrhythmias

Coarse V F

Fine V F

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

63

Ventricular Dysrhythmias

1. EMD (electromechanical dissociation):*apparently normal ECG but no cardiac output/pulse generated

2. PEA (pulseless electrical activity)

3. Asystole

PEA

Asystole

64

Atrial & Ventricular Hypertrophies

P wave characteristics Associated Conditions Right Atrial Enlargement

Leads II, III aVF: P pumonale Tall Peaked P 2.5mm Lead V1: Biphasic P

COPD Tricuspid valve disease Pulmonary valve disease Pulmonary hypertension

Left Atrial Enlargement

Leads I, II & V4-V6: P Mitrale Leads V1 & V2: Diphasic P 1mm

Left ventricular failure Mitral valve disease Aortic valve disease Systemic hypertension

Right Ventricular Hypertrophy

Lead V1: Tall R wave ( S wave) Inverted T

Lead V6: Deep S wave Right axis deviation

COPD Mitral valve disease Pulmonary stenosis Ventricular septal defect Pulmonary hypertension

Left Ventricular Hypertrophy

Lead I – R wave + Lead III- S wave 25mm Precordial Leads:

V1 – S wave + V5 or V6 - R wave 35mm ST depression

Left axis deviation

SVR Aortic stenosis or insufficiency Mitral insufficiency

65

P Pulmonale in Leads II, III & aVF :Direction: Upright Amplitude: ≥ 2.5mm

4mm

Right Atrial Hypertrophies

66

Left Atrial Hypertrophies

P-Mitrale in Lead I, II, V4-6

Biphasic P: duration > 0.10 second

67

Left Ventricular Hypertrophies

S wave in Lead V1 : 12mmR wave in Leads V5 & 6: 45 & 39mm, respectivelyS [V1] + R [V5] = 41mm (Fit criteria ≥ 35mm)

R wave in Lead I : 20mmS wave in Lead III: 20mm R [I] OR S [III] = 20mm (Fit criteria ≥ 20mm) R [I] + S [III] = 40mm (Fit criteria ≥ 25mm)

68

Normal 12-Lead Electrocardiogram

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

69Totora G J & Grabowski S R 2003 Principles of Anatomy and Physiology. 10th ed. New York: John Wiley & Sons.

Acute Coronary Syndrome & Coronary Circulation

Coronary atherosclerosis poses the

potential risk of plague rupture,

mircroemboli & occlusive thrombus

A spectrum of clinical syndromes will develop due to coronary artery occlusion:

1. Unstable angina

2. Non-Q MI

3. Q wave MI

4. Sudden cardiac arrest

70

Anterior View of Coronary

Arteries

Right

Atrium

Left

Atrium

Arch of Aorta

Ascending Aorta

Pulmonary

Trunk

Right Coronary Artery [RCA]

Left Coronary Artery [LCA]

Circumflex Coronary

Artery [Cx]

Right Ventricle

Left

VentricleAcute Marginal

Artery

Left Anterior Descending

Coronary Artery[LAD]

Posterior Descending Artery [RD]

71

Myocardial Injury: Ischaemia and

Infarction

V5

Acute Transmural Ischaemia

V5

Acute Subendocardial Ischaemia

72

Ischaemic Zone

Injury Zone

Infarction Zone

Infarction significant Q/QS wave*absence of depolarization current from dead myocardial tissue facing lead recorded opposing electrical vector “through” infarcted area

Injury elevated ST

Ischaemia T wave inversion

* Reciprocal Effect on Opposite Leads

Recovery ST & T wave return to normal

Myocardial Injury:Ischaemia and Infarction

Lead I

73Anterior View of Coronary Arteries

InferiorInferior

II, III, aVFII, III, aVF

LateralLateral

I, aVLI, aVL

LateralLateral

V5 & V6V5 & V6

AnteriorAnterior

V3 & V4V3 & V4

SeptalSeptal

V1 & V2V1 & V2

Coronary Circulation & Ischemic Changes

74

Myocardial Infarction & 12-Lead ECGType of Infarction

Coronary Arteries Involved Leads Involved

Possible ECG Changes

Extensive: LCA LAD

I, V1-V4 Anterior

Localized: LAD diagonal branches

V3 & V4

ST elevation T wave inversion Significant Q waves Progressive loss of R wave

Lateral Left Circumflex Marginal branch of left circumflex Diagonal branch of LAD

I, aVL or V5 & V6

ST elevation T wave inversion Significant Q waves Right axis deviation

Inferior RCA II, III & aVF ST elevation T wave inversion Significant Q waves Left axis deviation

Septal LAD (septal perforator branch)

V1 & V2 ST elevation T wave inversion Significant Q waves loss of R wave in V1 Left axis deviation

Posterior Posterior RCA Distal Circumflex

V1 & V2 reciprocal changes in V1-2: R S ST depression Elevated T

75

Anteroseptal Myocardiac Infarction

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

QS waves: V1 & V4*(r waves absent)

ST segment elevation: V1-V4

EARLY ECG CHANGES: 0 - 2 hours

76

Anteroseptal Myocardiac Infarction

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby.

2- 24 hours:•Maximal ST elevation•minimal Q wave formation

24- 72 hours:•QS wave in V1-V4•ST returned to Baseline•T waves inversion

LATE ECG CHANGES

77

ST Changes

Huszar R J 2002 Pocket Guide to Basic Dysrhythmias: Interpretation & Management. 3rd ed. St Louis: Mosby

ST Elevation

Normal ST

Associated conditions:•Myocardial injury or infarction•pericarditis•ventricular fibrosis, aneurysm•ventricular hypertrophy•digitalis effect

ST Depression

Flat Downsloping Upsloping

78

ECG Changes in Hypokalemia

Gradual ST depression

Flattened T wave

Tall U wave

Serum <K+ 3mEq/L

Serum <K+ 2.7mEq/L

Prolonged PR

U wave size increases

Serum <K+ 2.0mEq/L

Widened & Bizarre QRS complex

Marked ST depression

Inverted T

79

ECG Changes in Hyperkalemia

Serum K+ > 5.5 mEq/L

Peaked, narrow, 60-100bpm

Serum K+ progressive 6.5 8.0mEq/L

Loss of P wave & Bizarre QRS

Atrioventricular block, sinus arrest, VF , asystole

Serum K+ progressive 6.5 8.0mEq/L

Loss of P wave & Bizarre QRS

Atrioventricular block, sinus arrest, VF , asystole

80

ECG Changes: Hypocalcemia/Hypercalcemia

Serum Ca++ > 10.5mg/dL

Shortened ST

Shortened QT

Serum Ca++ < 8.5mg/dL

Lengthened ST

Lengthened QT

May cause Torsades de pointes

81

ECG Changes: Hypomagnesemia/ Hypermagnesemia

Serum Mg++ > 2.5mEq/L

Prolonged PR

Lengthened QT

QRS > 0.12sec

Serum Mg++ < 1.5mEq/L

Lengthened QT

Broad & flattened T

often co-exist with hypokalemia

82

Systematic ECG Interpretation

1: Determine Dysrhythmia Calculate HR

Determine the ventricular rhythm

Measure the RR regularity - variance < 0.12 second (use a caliper or the paper-&-pencil method)

Identify & examine the P waves morphology

Measure the PR interval

Measure & Examine QRS complex morphology

Examine P:QRS correlation

Look for escape or dropped beats

Look for miscellaneous abnormalities

2: Identify Atrioventricular Block & Aberrant Conduction

3: Identify Axis Deviation & Hypertrophies

4: Determine MI - 12-Lead ECG overview

83

Heart Rate Calculation

1. Six Second Count Method: Number of R-R intervals in a 6sec strip x 10 = HR bpm

2. R-R Interval Method: HR bpm = 300 Number of Large Squares

between the peaks of 2 consecutive R waves

6 second Interval

RR Interval

84

Heart Rate Calculation

3. Conversion table: Number of Small Squares between the peaks of 2 consecutive R waves

4. Heart Rate Calculator Ruler Method:

HEART RATE CALCULATORHEART RATE CALCULATOR

* 3rd Complex from Arrow = bpm

85

P wave•Indeterminat

e

VENTRICULAR DYSRHYTHMIAS

ALGORITHM•P-R normal

SINUS RHYTHM

ALGORITHM

•P-R > 0.2 s

HEART BLOCK

ALGORITHM

•Identifiable

•Normal•P’ present or absent

•QRS normal

•Polymorphic

•Irregular R-R

•Irregular P-R

•160-240 bpm

MULTIFOCAL ATRIAL

TACHYCARDIA

•Fibrillatory baseline

•Irregular R-R

•Flutter waves

•Regular or irregular R-R

ATRIAL FIBRILLATION

ATRIAL FLUTTER

SUPRAVENTRICULAR TACHYCARDIA

•P:QRS = 1:1

•Regular R-R

•Regular P-R

HR40-60

HR>100

HR60-100

HR160-240

ACCELERATED JUNCTINAL

RHYTHM

JUNCTIONAL

RHYTHM

JUNCTINAL THCHYCARDIA

Basic Dysrhythmias Interpretation Algorithms

86

Sinus Dysrhythmias & Heart Blocks Algorithms

P-R interval normal 0.12-0.20sec.

•P:QRS = 1:1

•Regular atrial rhythm

•Regular R-R

HR<60

Sinus Bradycardia

HR100-160

Sinus Tachycardia

HR60-100

Regular Sinus Rhythm

Irregular atrial rhythm

Irregular R-R

Sinus Arrhythmia

•Regular R-R

•P:QRS = 1:1

Progressive PRRegular non-conducted QRS

2o Heart Block

Wenkebach

Morbitz Type I

Constant prolonged PRHR 60-100

1o Heart Block

•Irregular R-R

P > QRS

Constant PRSudden dropped QRS

2o Heart Block

Morbitz Type II

No relationship ./. P & QRS

3o Complete

Heart Block

P-R interval > 0.20sec.

P WAVE NORMAL

87

Ventricular Dysrhythmias Algorithms

•Unidentifiable QRS

•Coarse & or fine fibrillatory waves

Ventricular

Fibrillation

•Narrow-complex QRS ( 0.12 sec)

•HR 160-240 bpm

PSVT

•Wide-complex QRS (>0.12 sec)

•HR = 40-100

Accelerated

Idioventricular

Rhythm

•HR< 40

Idioventricular

Rhythm

•HR: 150-250

Monomorphic

SVT &

Aberrant

Conduction

Polymorphic

Torsade de

Pointes

Ventricular

Tachycardia

P WAVE Indeterminate

88

QRS Axis Determination: Frontal Plane

There are a few methods for determining the

Frontal Plane Axis and identifying any Axis

Deviation. Each has its advantages.

The Quadrant method for locates deviation

quickly & easily, while the Degree Method

gives exact measurements.

Choose the one that is most suitable for you &

practice reading 12-Lead ECG using the same

method.

Once you are familiar with a method, you

might try another one.

89

QRS Axis Determination: Frontal Plane

Quadrant Method:Use Leads I & aVFLocate the Main Deflection of the QRS complex

Axis QRS complex

Lead I Lead aVF

Normal Upright in Both Leads

Left Axis Deviation

UprightPoints

Downward

Right Axis Deviation

Points Downward

Upright

Indeterminate

Points Downward

90

QRS Axis Determination: Frontal Plane

Quadrant Method:

+0o

+90o

-90o

±180o

91

QRS Axis Determination: Frontal Plane

Degree Method:

Use Leads I & aVF

A negative wave (usually an S wave)

is subtracted from the height of the R

wave.

Plot the resultant vector on the

hexaxial reference circle to locate the

axis

92

QRS Axis Determination: Frontal Plane

Degree Method: Step 1

93

QRS Axis Determination: Frontal Plane

Degree Method: Step 2

94

QRS Axis Determination: Frontal Plane

Degree Method: Step 3

95

QRS Axis Determination: Frontal Plane

Null Plane Method:

Identify the equiphasic QRS

Locate the corresponding perpendicular

lead

Map the axis that is parallel to this lead

The axis points to the predominant

direction of either the positive or

negative pole

96

Horizontal Axis Rotation

◈ Dominance of Electrical Vector (Normal):

◈ V3 : R > S

◈ V4 : S > R

(V3 & V4 is the transition zone)◈ Identify the relationship of S-deflection &

R-deflection in V1 to V6

◈ Determine Axis Rotation:

◈ Clockwise Rotation – Shift to V5 & V6

◈ Counter-clockwise Rotation – Shift to V1

& V2

◈ Dominance of Electrical Vector (Normal):

◈ V3 : R > S

◈ V4 : S > R

(V3 & V4 is the transition zone)◈ Identify the relationship of S-deflection &

R-deflection in V1 to V6

◈ Determine Axis Rotation:

◈ Clockwise Rotation – Shift to V5 & V6

◈ Counter-clockwise Rotation – Shift to V1

& V2

97

Clinical Significance of ECG Interpretation

Recognizing Life-threatening dysrhythmias

is extremely important:

prompt interventions for cardiac arrest & cardiac

compromise

restoration of haemodynamic stability

Familiarizing with anti-arrhythmic

medications & life-saving measures are

essential

Further readings:

Advanced Cardiac Life Support (ACLS)

algorithms

98

Medication Indications Adult Dosage Amiodarone Extremely potent & effective:

Ventricular fibrillation and pulseless VT (FIRST CHOICE in newest ACLS guidelines)

SVT Recurrent life-threatening ventricular

arrhythmias

300mg IV push x refractory ventricular arrhythmias

150mg IV bolus over 10 mins for hemodynamically stable ventricular arrhythmias

infusion: 1mg/min for 6 hrs then 0.5mg/min for 18 hrs

maintenance dose 200-600mg/day p.o.

Lidocaine Acute ventricular arrhythmias (second-tier choice)

Stable VT

Loading bolus 1mg/Kg Additional boluses 0.5-1.5mg/kg Q5-

10mins to total 3mg/Kg IV infusion 0.5-4mg/min

Digoxin Narrow toxic-to-therapeutic dose especially with hypokalemia, hypomagnesemia & acid-base abnormalities

Rapid ventricular response in atrial flutter or atrial fibrillation

Beta-blockers: e.g.,

Propanolol Metoprolol Labetolol

Refractory SVT Ventricular arrhythmias associated

with digitalis toxicity Hypertensive crisis

Calcium channel blockers: e.g.

Verapamil Diltiazem

PSVT Narrow complex tachyarrhythmias

Adenosine (ATP) Drug of choice for symptomatic PSVT Arrhythmias due to reentry pathways

involving AV or sinus nodes

6.0mg initially IV PUSH (1-3sec.) repeat at 12mg after 1-2mins & repeat12mg IV push to a total of 30mg

consider alternative therapy for persistent tachyarrhythmias

Antiarrhythmic Therapy

99

References Davis, D. (2001). Quick and Accurate: 12-Lead ECG

Interpretation. (3rd Ed.). Philadelphia: Lippincott.

Huszar, R. J. (2002). Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.

Huszar, R. J. (2002). Pocket Guide to Basic Dysrhythmias: Interpretation & Management. (3rd Ed.). St Louis: Mosby.

Jackson, K. (Ed.). (2002). ECG Interpretation made Incredibly Easy. (2nd Ed.). Springhouse: Springhouse.

Linda, D., Urden, K. & Stacy, M. E. L. (2002). Thelan’s critical care nursing: diagnosis and management. (4th ed.). St Louis: Mosby.

Lewis, K. M. (2000). Sensible ECG Analysis. Albany: International Thomson Publishng Company.

100

References Paul, S. & Hebra, J. D. (1998). The Nurse’s

Guide to Cardiac Rhythm Interpretation: Implication for patient care. Philadelphia: Saunders.

Swearingen, P. L. & Keen, J. H. (2001). Manual of Critical Care Nursing: Nursing Interventions & Collaborative Management. (4th Ed.). St Louise: Lippincott.

1998 12-Lead ECG Interpretation. Baltimore: Williams & Wilkins *CD-ROM

101

Journals Adams-Hamoda, M. G., Caldwell, M. A., Stotts, N. A. &

Drew, B. J. (2003). Factors to Consider When Analyzing 12-Lead Electrocardiograms for Evidence of Acute Myocardial Ischemia. American Journal of Critical Care, 12(1) 9-18.

Hutchisson, B., Cossy, S. & Wheeler, R., (1999). Basic Electrocardiogram Interpretation for the OR Nurse. AORN Journal, 69(1) 221-239.

Henderson, N. (1997). Electrocardiography. Nursing Standard, 11(44) 45-56.

Drew, B. J. (2002). Celebrating the 100th birthday of the electrocardiogram: Lessons learned from research in cardiac monitoring. American Journal of Critical Care, 11(4) 378.

102

Web Resources■ Jenkins, D. & Gerrid, S. (2002). ECG Library. Retrieved July 20, 2005, from

http://www.ecglibrary.com/ecghome.html

■ Mysioki, F. (2003). McGill Medical Informatics. Electrocardiology and Cardiac Arrhythmias. Retrieved July 20, 2005, from McGill Univeristy, Physiology Department Web site: http://sprojects.mmi.mcgill.ca/cardiophysio/

■ SkillStat Learning Inc. (2005). SkillStat Learning Tools. Retrieved July 20, 2005, from http://www.skillstat.com/learn.htm

■ Scheinman, M. M. (n.d.). Supraventricular Tachycardias Tutorial. Retrieved July 20, 2005, from the Electrophysiology Service at UCSF in San Francisco, California Website: http://www.blaufuss.org/SVT/index.html

■ Texas Arrhythmias Institute. (n.d.). Educational Material: Arrhythmias & Heart Failure. Retrieved July 20, 2005, from http://www.txai.org/edu/education.htm

■ Wong, R. (n.d.). Heart Sound Tutorial. Retrieved July 20, 2005, from The Harbor-UCLA Medical Center, Research lab of John Michael Criley, M.D. Website: http://www.blaufuss.org/tutorial/indexTut.html#

■ Yaniwitz, F. G. (2002). ECG Learning Center in Cyberspace. Retrieved July 20, 2005, from University of Utah School of Medicine, ECG Department Web site: http://medlib.med.utah.edu/kw/ecg/index.html