Ebook Starting to read ECGs: Part 1

(BQ) Part 1 book Starting to read ECGs has contents: Cardiac anatomy and electrophysiology, calculating electrical axi, chamber abnormalitie, conduction blocks and cardiac pacin, ECG interpretatio.

tar t ing to Read ECGs

A lan Dav ies • A lwyn Sco t

A Comprehens ive Gu ide

to Theory and Prac t ice

ISBN 978-1-4471-4964-4 ISBN 978-1-4471-4965-1 (eBook)

DOI 10 1007 /978-1-4471-4965-1

Spr inger London He ide lberg New York Dordrech t

L ibrary of Congress Con tro l Number : 2014956281

© Spr inger -Ver lag London 2015

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Spr inger is par t of Spr inger Sc ience+Bus iness Med ia ( www spr inger com)

A lan Dav ies

Schoo l of Compu ter Sc ience

Un ivers i ty of Manches ter

Manches ter

UK

A lwyn Sco t Card io logy H igh Dependency Un i Papwor th Hosp i ta l NHS Founda t ion T rus t Cambr idge

UK

Th is book is ded ica ted to the memory o f

Bruce N ige l Dav ies

1953–2013

The authors have also endeavoredtointroduce several newtopicsincluding an

introductiontothe pediatric ECG and genetic cardiac condiionsin an attempttodeepen readers’ awareness of some ofthe broader clinicalissues

This book can be read as a standalone book bythose who already possess somebasic ECG knowledge and wishto deepen and expandtheir knowledge base or bythose who have readthe fi rst bookinthe series and wishto consolidate and expand

on whatthey have already read

The book uses lots of diagrams, tables summarizing key points, and practical examplesto reinforcelearning and summarizeinformation succinctly We hope you

wl fi ndthis book a useful addiionin your continuingjourneyto masterthe ECG

routine and emergency angiogramsincluding primary PCI Alan has also assistedinpacemaker/AICDinsertion,transoesopheageal echo (TOE), cardioversion and elec-trophysiological studies Alanis currently a PhD student combining his knowledgeandinterestsin computer science and electrocardiograms by carrying out research

into capturing expertisethroughthe observation of visual behaviour and using trackingtechnologytoimprove aspects of human and computer ECGinterpretation

eye-lwyn Scott graduated from Birmingham University and has workedinthe NHS

since 1995 Heis currently employed as senior staff nurse forthe Cardiology HighDependency Department at Papworth Hospitalin Cambridgeshire His roleis pre-dominantly that of working with patients who are in acute stages of having heart

atacks both pre- and post-primary PCI Alwynis also heavilyinvolvedin staff

edu-cation Alongside specialist knowledgein acute cardiac nursing and ECGin

terpre-tation, Alwyn also has a vast experiencein emergency care, workingin accident andemergency departments and alsointhe frontine forthe ambulance service respond-ingto 999 calls

Au thors

x i

Contents

1 Cardiac Anatomy and Electrophysiology 1

Background 1

Anatomy ofthe Heart 1

Chambers 1

Valves 2

Chordae Tendineae 3

Fossa Ovalis 3

Trabeculae Carneae 3

Papilary Muscle 3

Coronary Sinus 3

The Great Vessels 4

Heart Wal 4

Circulatory Function ofthe Heart 4

Coronary Arteries 5

tarling’s Law ofthe Heart 6

Preload and Afterload 6

Cardiac Output 7

Blood Pressure 8

Electrophysiology 9

Understanding Depolarization and Repolarization 10

Absolute and Relative Refractory Periods 12

The Conduction System Relatedtothe Electrocardiogram 12

Summary of Key Points 13

Quiz 14

2 ECG Interpretation 17

Background 17

ECG Paper 18

Basic Checks 19

Artefact 19

Calibration 19

x iv

R Wave Progression/Lead aVR 22

Determinethe Rhythm 23

inus Arrhythmia 25

Rate Calculation 25

Automated Rate Determination 25

The 1,500 Method 27

The 300 Method 27

The Sequential Method 28

The 30 Square Method 28

Converting Time Between Seconds and Miiseconds 29

The ECG Waveform 30

Wave 31

Ta Wave 32

PQ/PR Interval 33

QRS Complex 33

Q Wave 35

R Wave 35

QRS Axis 35

T Wave 35

U Wave 35

ST Segment 37

QT Interval 38

TP Interval 39

RR Interval 39

Why Dothe Waveforms Look Differentin Different Leads? 40

Normal Sinus Rhythm 40

Summary of Key Points 41

Quiz 42

3 Calculating Electrical Axis 45

Background 45

How Is This Useful? 45

Normal Axis 45

Axis Deviation 46

Categories of Axis Deviation 47

Calculatingthe Cardiac Axis 48

Einthoven’s Law 48

Bipolar and Unipolar Leads 49

Method 1 53

Method 2 55

Method 3 57

Summary of Key Points 59

Quiz 59

Con ten ts

4 Chamber Abnormalities 61

Background 61

Atrial Abnormalty 61

Abnormalty or Enlargement? 62

Right Atrial Abnormalty 63

Left Atrial Abnormalty 64

Bilateral Atrial Abnormalty 65

Left Ventricular Hypertrophy 65

Athlete’s Heart/Physiological LVH 65

Intrinsicoid Defl ection/Ventricular Activation Time (VAT) 66

Ventricular Hypertrophy Evaluation Methods 67

Left Ventricular Hypertrophy Evaluation 68

Right Ventricular Hypertrophy 68

Right Ventricular Hypertrophy Evaluation 69

Biventricular Hypertrophy 70

Cardiomyopathies 70

Dilated Cardiomyopathy (DCM) 70

Hypertrophic Cardiomyopathy (HOCM/HCM) 71

Takotsubo Cardiomyopathy 72

Arrhythmogenic Right Ventricular Dysplasia/ Cardiomyopathy (ARVD/C) 73

Heart Failure 74

Cardiac Resynchronization Therapy (CRT) 75

Summary of Key Points 76

Quiz 78

5 Conduction Blocks and Cardiac Pacing 81

Background 81

Bundle Branch Blocks 81

Right Bundle Branch Blocks 81

Left Bundle Branch Blocks 83

Rate Dependent/Transient Bundle Branch Blocks 84

Features and Criteria for Identifying Left and Right Bundle Branch Blocks 85

Wiiam Morrow/Wiiam Marrow 85

Hemiblocks 85

Trifascicular Block 86

Atrioventricular Nodal Blocks 86

1st Degree AV Block 87

nd Degree AV Block 87

rd Degree AV Block 90

rd Degree AV Block and Atrial Fibrilation 91

Con ten ts

xv i

inoatrial Block 92

t Degree SA Block 92

nd Degree SA Block 92

rd Degree SA Block 93

ick Sinus Syndrome 94

Cardiac Pacing 95

Understanding Pacing Codes 96

ingle Chamber Pacemakers 98

Dual Chamber Pacemakers 99

Biventricular Pacemakers 100

Pacemakers andthe ECG 100

Pacemaker Problems Visible onthe ECG 101

Summary of Key Points 101

Quiz 103

6 Arrhythmias 107

Background 107

Premature Beats 107

Premature Beat Origin 108

Compensatory and Non-compensatory Pauses 109

Bigeminy and Trigeminy 109

Supraventricular Tachycardia 110

Vagal Maneuvers 111

Atrial Fibrilation 111

Atrial Flutter 116

Atrial Tachycardia 117

Mulifocal Atrial Tachycardia 118

inus Tachycardia 119

inus Arrhythmia 120

Junctional Tachycardia 120

Reentry 120

Pre-excitation 122

Wolff-Parkinson-White Syndrome (WPW) 123

Orthodromic and Antidromic 124

Wolff-Parkinson-White Syndrome and Atrial Fibrilation 125

Lown-Ganong-Levine Syndrome (LGL) 126

Cardioversion 127

Electrophysiology Studies (EPS) 127

Ablation 129

Ventricular Tachycardia (VT) 130

Fusion Beats 131

Capture Beats 132

AV Dissociation 132

Rhythm Regularity 132

Concordance 132

Cardiac Axis 133

Con ten ts

xv i

Cardiac Arrest Rhythms 135

Pulseless VT 136

Ventricular Flutter 136

Ventricular Fibrilation 136

Asystole 137

Pulseless Electrical Activity 137

Summary of Key Points 138

Quiz 138

7 Acute Coronary Syndromes 141

Background 141

Atherosclerosis 144

Angina 145

table Angina 146

Unstable Angina 146

Prinzmetal’s Angina 146

Digitalis Effect 148

Myocardial Infarction 149

Doorto Needle or Balloon Time 150

ST Elevation 151

Waves 152

STEMI 153

Ventricular Aneurysm 155

Tombstoning 155

Reciprocal Changes 156

MI Regions/Territories 156

Posterior and Right Ventricular MI 158

LBBB and Chest Pain 161

NSTEMI 161

Cardiac Biomarkers 161

Treatment for Myocardial Infarction 162

Summary of Key Points 165

Quiz 167

8 Genetic Cardiac Conditions 171

Background 171

Brugada Syndrome 173

Treatment 175

Lev’s Disease 176

Duchenne Muscular Dystrophy 176

Long QT Syndromes 177

Romano-Ward Syndrome 178

Jervel and Lange-Nielsen Syndrome 178

Arrhythmogenic Right Ventricular Dysplasia/ Cardiomyopathy (ARVD/C) 179

Summary of Key Points 179

Quiz 179

Con ten ts

xv i

9 The Pediatric ECG 181

Background 181

tages of Myocardial Development 181

Patent Foramen Ovale 185

Patent Ductus Arteriosus (PDA) 185

Tetralogy of Fallot 186

Atrial Septal Defect (ASD) 188

Ventricular Septal Defect (VSD) 189

Coarctation of Aorta 189

Ebstein’s Anomaly 190

Transposiion ofthe Great Arteries 190

Dextrocardia 191

Isolated Dextrocardia/Dextrocardia of Embryonic Arrest 192

Dextrocardia Situs Inversus 192

Technical Dextrocardia 192

Congenital Accessory Pathways 193

Normal Child ECG Values 193

Axis 194

Intervals/ST Segment 196

Summary of Key Points 197

Quiz 197

Index 199

Con ten ts

© Spr inger -Ver lag London 2015

A Dav ies , A Sco t S tar t ing to Read ECGs: A Comprehens ive Gu ide

to Theory and Prac t ice , DOI 10 1007 /978-1-4471-4965-1_1

Chapter 1

Keywords Anatomy • Physiology • Electrophysiology • Action potential • Depolarization • Repolarization • Cardiac output • Blood pressure • Circulatorysystem

Background

The human heartis an organthat has both mechanical and electrical components

Both knowledge of basic cardiac anatomy and physiology, as wel as electrophys

i-ologyis necessaryto fully understandthe basics ofthe electrocardiogram (ECG).Understanding and awareness of these elements in the normal heart is essential before building a more complete picture ofthe pathological heart

We wi start with an overview ofthe basic anatomy and physiology ofthe heartbefore looking more specifically at the electrophysiological components of the heart’s function Finally we wilook at howthe mechanical and electrical systems

ofthe heartinteract with each otherin a healthyindividual

Anatomy of the Heart

Figure.1 displaysthe main anatomical features ofthe human heart A brief descr

ip-tion of some ofthe primary anatomical features follows

Chambers

The heart consists of four chambers,two smal chamberslocated superiorly, calledtheleft and right atrium andtwolarger chamberslocatedinferiorly calledtheleftand right ventricle Theleft ventricleislargerthanthe right as hasto pump blood

tothe majority ofthe body, whereasthe right ventricle pumps bloodintothelungs.The atria and ventricles are separated from one another bytheinteratrial septum andtheinterventricular septum respectively

Va lves

The heart also has four valves Thetricuspid and mitral valves, known asthe atrventricular valves as they sit between the atria and ventricles allowing access for

io-bloodto pass fromthe atriatothe ventricles The othertwo valves arethe aortic and

pulmonary valves, and are referredto asthe semilunar valves whichleadtothe aortaandthe pulmonary artery The principle purpose ofthe valvesisto prevent regurgi-

tation of blood from the ventricles back into the atria The valves open when the pressureinthe chamber filed with blood exceedsthe pressureinthe area pastthe

valve For example whenthe pressureinthe right atrium exceedsthe pressureinthe right ventricle,the valve opens andthe blood passes from atriumto ventricle.The valves have fl aps that are sometimes referred to as leafl ets or cusps The

tricuspid valve hasthree such fl aps or cusps The mitral valveis also referredto asthe bicuspid valve and hastwo cusps

Brach iocepha l ic ar tery

Chordae Tend ineae

M tra l va lve

Le f a tr ium

Pu lmonary ve ins

Pu lmonary ar tery Aor ta

Le f subc lav ian ar tery

Le f common caro t id ar tery

F ig 1 1 Bas ic ana tomy of the hear t

1 Card iac Ana tomy and E lec trophys io logy

Chordae Tend ineae

The chordae tendineae are fi brous tendon like cords that connect to the tricuspid

valveinthe right ventricle andthe mitral valveintheleft ventricle Whenthe valves

closethe chordaetendineae preventthe cusps from swinging upwardsintothe atrialcavity

Fossa Ova l is

The fossa ovalis is the remains of what was once a hole (foramen) that existed

betweentheleft atrium andthe right atrium,locatedinthe atrial septum This hole

alows bloodto bypassthelungsin a developing fetus when fetal oxygen supplyisprovided viathe placenta, asthe fetallungs are undeveloped

Trabecu lae Carneae

Thetrabeculae carneae are muscular columns ofirregular shapethat existin bothventricles Intheleft ventriclethey are smooth and fi ne when comparedtothoseinthe right ventricle It is believed that the function of the trabeculae carneae is to prevent suction that could impair the pumping action of the ventricles that could

otherwise occurifthe ventricles were smooth Whenthetrabeculae carneae contracttheyinturn pul onthe chordaetendineae

Pap i lary Musc le

Atype oftrabeculae carneaethat are connectedto ventricular surface at one end and

athe othertothe chordaetendineae

Coronary S inus

The coronary sinus allowsthe cardiac veins carrying deoxygenated bloodto drain

intothe right atrium

Ana tomy of the Hear t

The Grea t Vesse ls

Incorporatethe vena cava, pulmonary artery/veins andthe aorta Inthe rest ofthebody oxygenated blood is found in arteries and deoxygenated blood in the veins

This general rule does not applytothe heart which sometimes causes confusion.The pulmonary artery carries deoxygenated bloodintothelungs andthe pulmonary

veins carrythe resuling oxygenated bloodintotheleft atrium The aortatrifurcates

intothree other branches; brachiocephalic,left common carotid andleft subclavian

arteries which supply the upper portion of the body with blood The descending aorta bifurcatesintothe commoniac arteries supplyingthelegs with blood

Hear t Wa l

The wal ofthe heart (Fig 2 )is made up of severallayers Theinnermostlayeristhe endocardium, followed by the thicker myocardium that makes up the cardiac muscle and consists of cardiomyocytes, which are cardiac muscle cells The outerlayer ofthe heart walis known asthe epicardium Directly followingthe epicar-

diumis a gap calledthe pericardial cavitythat separatesthe heart fromthe pericar

-dium The pericardial cavity contains pericardial (serous) flid The pericardiumis

a protective membranethat coversthe heart and also envelopsthe roots ofthe greatcardiac vessels The principle functions ofthe pericardium (Fig.1.3 ) areto anchorthe heartin place preventing excess movement act as a barrierto protectthe heartfrominternalinfection from other organs andtolubricatethe heart

C ircu latory Funct ion of the Heart

Deoxygenated bloodis emptiedintothe right atrium viathe vena cava Theinferiorvena cava returns blood fromthelower portion ofthe body asthe superior vena cava

Ep icard ium

Myocard ium

Endocard ium

Par iel per icard ium

F irbous layer

Per icard ia l cav i ty

F ig 1 2 Layers of the hear t

from ou ts ide to ins ide

1 Card iac Ana tomy and E lec trophys io logy

returns blood fromthe higher portion Bloodisthen pumpedthroughthetricuspid

valveintothe right ventricle andintothelungs viathe pulmonary artery whereisoxygenated Oxygenated blood then returns from the lungs into the left atrium where can be pumpedtothe rest ofthe body bytheleft ventricle, viathe aorta.The circulatory system hastwo divisions;the systemic and pulmonary circulatorysystem (Fig.1.4 ) The pulmonary systemis responsible for circulating blood fromthe right ventricletothelungs and backintotheleft atrium The systemic system asthe nameimplies pumps blood viathe aortato every other part ofthe body Thisiswhytheleft ventricleislarger and more powerfulthanthe right as hasto pump

blood over greater distances Thisis also whyleft ventricular pressureis higherthan

right ventricular pressure

Coronary Ar ter ies

In addiiontothe heart pumping bloodtothe rest ofthe body,the hearttself requires

its own blood supplyin orderto function as an organ As bloodis pumped viatheaortatothe rest ofthe body,t also passesintothe coronary arteriesthat arelocated

at the aortic root There are two main coronary arteries, called the left and right coronary arteries respectively (Fig.1.5 ) Theleft coronary artery bifurcatesintothe

circumflex andleft anterior descending arteries Deoxygenated bloodis returnedtothe right ventricle by coronary veins viathe coronary sinus The coronary arteriesare discussedin more detaiin Chap 7

F ig 1 3 The per icard ium

C ircu la tory Func t ion of the Hear t

S tar l ing’ s Law of the Hear t

The Frank Staringlaw essentially statesthat anincreasein end diastolic volume corresponds with anincreaseinthe heartstroke volume To putt another waythe greaterthedegree of stretch to the cardiac muscle in diastole (relaxation of cardiac muscle), the

-greatertheforce of contractionin systole(contraction of cardiac muscle) What goesincomes out Problems can occurfthe hearis continually maximally stretchedfor along

period ofime, as occursin hearfailure Like an elastic band,ftis continually maxi

mally stretched wi become weak,lose elasticity andfaitoreturnto’ original shape. Pre load and Af ter load

The heart’s preload and afterload are important factors in determining the stroke

volume Preload referstothe amount of musculartension whenthe ventricle tracts atthe end of diastoleto ejectthe blood fromthe filed ventricle Afterloadisthereforethe systemic vascular resistancetheleft ventricle pushes againstin order

con-to expelthe blood during systole (Fig 6 )

In fer ior vena cava

R igh t ven tr ic

Super ior vena cava

Deoxygena ted b lood Oxygena ted b lood

Aor ta

Le f

a tr ium

Le f ven tr ic

Genera l body

F ig 1 4 Schema t ic d iagram of the c ircu la tory func t ion of the hear t

1 Card iac Ana tomy and E lec trophys io logy

Card iac Ou tpu t

Cardiac outputisthe blood volume pumped fromthe heartintres per minute Theaverage male pumpsjust over fi veters a minute whilethe average female pumpsjust under fi vetres per minute at rest The formula for cardiac outputis:

CO SV HR= ×

Le f an ter ior descend ing

ar tery (LAD)

C ircum f lex (cx) branch o f (LCA)

F ig 1 5 Coronary ar ter ies

F ig 1 6 le f Pre load , ( igh t ) af ter load

C ircu la tory Func t ion of the Hear t

Wth SV beingthe stroke volume and HR beingthe heart rate The stroke volumeis

calculated by subtractingthe end systolic volume (ESV) fromthe end diastolic voume (EDV):

l-SV EDV El-SV= −Various condiions can reduce cardiac output A reduction in cardiac output may meanthatinsuffi cient blood and oxygenis availableto perfusetheinternal organs

Blood pressureis also dependent on cardiac output

B lood Pressure

Is the pressure of the blood against the arterial walls, and is usually measured in

mlimeters of mercury (mmHg) Thetop number representsthe systolic pressure,

wththe bottom number representingthe diastolic pressure Blood pressure variesamongstindividuals andis differentthroughoutthe course ofthe day High bloodpressureis referredto as hypertension whereaslow blood pressureis referredto ashypotension Classifi cations of blood pressurelevels can be seenin Table.1

t is recommended that blood pressure be taken manually in patients with any irregularityin pulse Automated devices for blood pressure measurement may havepoorer accuracylevelsifthe pulseis variable, as seenin patients with atrial fi brila-

tion It is also important to use the appropriately sized blood pressure cuff when taking a patients blood pressure

Blood pressureis determined by muliplyingthe cardiac output bythe systemicvascular resistance (SVR), whichisthetotal resistanceto blood fl ow fromthe vas-

culature in the whole body Sometimes SVR is referred to as total peripheral resistance

BP CO SVR= ×

Tab le 1 1 B lood pressure c lass ifi ca t ions

Ca tegory Sys to l ic BP (mmHg) D ias to l ic BP (mmHg) Hypotens ion <90 <60

Norma l / opt ima l b lood pressure

Therefore a reductionin cardiac output also hasthe effect of reducing blood sure An average blood pressuretaken duringthe period of a cardiac cycle,termedthe mean arterial pressure (MAP) can be determined by muliplying the cardiac

pres-output with the systemic vascular resistance and adding the central venous pressure

MAP CO SVR CVP=( × )+For clinical purposesthe MAP can be approximated as follows:

MAP d≈ia+(sys d− ia)

3(dia = diastolic pressure,sys = systolic pressure)

Ifthe MAPis <60 mmHg, blood pressureis generallyinsuffi cientto perfusetheorgans Some electronic observation machinesthat record blood pressure may also

display the mean arterial pressure An understanding of the relationship between cardiac output, blood pressure and the effect they have on providing suffi cient

blood/oxygen to the organs of the body provides a basis for understanding the

potential problems arising from any reductionin cardiac output dueto pathology

E lectrophys io logy

When the heart is functioning correctly, mechanical aspects of the heart are act

i-vated bythe heart’s electrical system at regularintervals Action potentials gener

-atedinthe cardiac conduction system cause proteinsto contractin contractle cells,leading to mechanical activation of the heart The cells of the cardiac conduction system are imbued with the abity to spontaneously depolarize This qualty is referredto as automaticity Figure.7 displaysthe cardiac conduction system.The atria and ventricles are electrically isolated from each other in the healthy heart This meansthat electricalimpulses can only pass between atria and ventricles

viathe specialized conduction pathways The hearts primary pacemakeristhe s

ino-atrial node (SAN), located in the right atrium The SAN is composed of self- excitatory cells that discharge electrical impulses at a rate of between 60 and 100 beats per minute (BPM)in atypical person The determination ofthe heartbeat bythe sinoatrial nodeis wheretheterm sinus rhythm derives, meaning a rhythm origi-

nating fromthe sinoatrial node After fi ring ofthe SANtheimpulsetravelsto both

atria causingthe atriato depolarize;thisis followed by physical atrial contraction.Theimpulsethen passesthroughthe atrioventricular (AV) node, downthe bundle of

His andintotheleft and right bundle branches and fi nallyterminatinginthe purkinje

fi bres Theleft bundle branchis more complexthanthe right and has an anterior andposterior fascicle Followingthisthe ventriclesthen also depolarize and contract

E lec trophys io logy

If any problems withthe conduction system occur preventing primary pacemakergeneration ofimpulsesthen other parts ofthe conduction system are capable oftak-ing over asthe dominant cardiac pacemaker Thelower downthe conduction systemthe primary pacemakerislocated,the slowerthe heart rate The heart rates related

tothelocation ofthe primary pacemaker can be seenin Table.2

Unders tand ing Depo lar iza t ion and Repo lar iza t ion

Depolarizationis a process where a resting cel changes from being predominantlynegatively chargedto posiively charged Repolarizationisthe reverse ofthis pro-cess withthe cel returningtots resting state and predominantly negative charge(Fig 8 ) The process of depolarizationis accomplished bytheinflux of posiivelycharged extracellularionsintothe cel resulingin an action potential (Fig.1.9 ) The

action potential has various phases (0–4)

S inoa tr ia l

node (SAN)

Bachmanns bund le

A tr ioven tr icu lar

r ing bund le

o H is

Le f bund le branch

An te t ior fasc ic le Pos ter ior fasc ic le Sep ta l branch

R igh t bund le branch

In ternoda l

pa thways

A tr ioven tr icu lar

node

F ig 1 7 The card iac conduc t ion sys tem

1 Card iac Ana tomy and E lec trophys io logy

Phase 0

Representsthe rapid depolarisation effect Phase 0istriggered whenthe cel brane reacheststhreshold (around −70 mV) Rapid entry of sodium (Na+ ) occurs.Phase 1

Representsthe rapid repolarization effect Flow of sodium ceases asthe fast sodiumchannels close Potassium continuestoleavethe cel Asthe posiive charge ofthe cellular membrane decreases

Tab le 1 2 Hear t ra te based on loca t ion of pr imary card iac pacemaker

Loca t ion of dom inan t pacemaker in the conduc t ion

sys tem Hear t ra te (BPM)

S inoa tr ia l node 60–100

A tr ioven tr icu lar node 45–60

Purk in je fi bres 15–30

+ + + +

+++++

+ + + + +

++++

+++++

+ + +

+ + + ++

Repo lar ised

F ig 1 8 Depo lar iza t ion and

repo lar iza t ion

phase 0 phase 2

Phase 3

Representsthe end ofthe repolarisation phase The membrane potential returnsto

its resting state andtheinside ofthe cel startsto become more negative as more

potassium is leaving the cel; than calcium is entering causing the membrane

potentialto become more negative

Phase 4

This represents the gap between one action potential and another During this

timetheinside ofthe celis more negatively charged Excesslevels of sodiumaretransported out ofthe cel with potassium beingtransported backintothe

cel

Abso lu te and Re la t ive Refrac tory Per iods

There is a point after iniiation of an action potential at which cardiac cells are unabletoiniiate another action potential no matter how powerfulthe stimulusis

Thisistermedthe absolute refractory period The relative refractory period howevercantransmiimpulses but with a delay

This can be evidenced in AV nodal blocks where impulses arriving at the AV node in the absolute refractory period are not transmited to the ventricles at al The earlier the impulse arrives during the relative refractory period the longer it

wltaketo gettothe ventricles AV nodal blocks are discussedin more detaiinChap 5

The Conduc t ion Sys tem Re la ted to the E lec trocard iogram

The ECG waveformis made up of various waves,intervals and segments represening a single heartbeat (Fig 10 )

Understanding ofthe depolarization and repolarization ofthe heart andt’s

relationshiptothe ECG waveformis necessaryto understandthe relationship

between the electrical and mechanical systems of the heart in a normal person

The P wave on the ECG represents depolarisation of the right and left atria (Fig 11a ) The atriathen repolarize asthe ventricles beginto depolarize fromtheapex ofthe heart upwardsleadingtothe QRS complex onthe ECG (Fig.1.11b, c )

Atrial repolarizationis not normally visible onthe ECG asis masked bythe QRS

1 Card iac Ana tomy and E lec trophys io logy

complex The ventricles then begin to repolarize from the bottom of the heart upwards, represented onthe ECG bythe T wave (Fig.1.11d, e )

Summary of Key Po ints

• The heart has both electrical and mechanical elements

• The sinoatrial nodeisthe dominant pacemaker ofthe heart

• Any reduction in cardiac output can reduce the amount of blood and oxygen availabletothe organs ofthe body

• The circulatory system hastwo main parts, systemic circulation providing blood

tothe majority ofthe body and pulmonary circulation moving blood fromlungs

tothe heart and back again

R

T U P

Isoe lec tr ic base l ine

Q S ST

QT

PR

In terva l

In terva l Segmen t

F ig 1 10 The ECG waveform

Key Wave o f depo lar iza t ion Wave o f repo lar iza t ion

• In healthy peoplethe electrical system correspondsto mechanical activation ofthe heart

Qu iz

Q1 The dominant pacemaker ofthe heartin a healthy personis

(A) The atrioventricular node

(B) The sinoatrial node

(C) The purkinje fi bres

Q2 The absolute refractory periodis

(A) Cellularinabitytoiniiate another action potential no matter how power

-fulthe stimulus

(B) Someimpulses can getthrough,they arejust slower

(C) Depolarization oftheight bundle branch

Q3 The pericardiumis

(A) A collection of cardiomyocytes capable of spontaneous depolarization (B) Thetopleft chamber ofthe heart

(C) A fi brous sacthat surrounds and protectsthe hearts

Q4 Atrial repolarizationis not usually see onthe surface ECG

(A) True

(B) False

Q5 Hypotension refersto

(A) Higherthan normal blood pressure

(B) Lowerthan normal blood pressure

(C) Normal blood pressure

Q6.Thelower downthe conduction systemthe primary pacemakerislocatedthe

slowerthe heart rate

Q8 The P wave onthe ECG represents

(A) Depolarization oftheight andleft ventricle

(B) Repolarization oftheight andleft atrium

(C) Depolarization oftheight andleft atrium

Answers: Q1 = B, Q2 = A, Q3 = C, Q4 = A, Q5 = B, Q6 = A, Q7 = B, Q8 = C

Qu iz

© Spr inger -Ver lag London 2015

A Dav ies , A Sco t S tar t ing to Read ECGs: A Comprehens ive Gu ide

to Theory and Prac t ice , DOI 10 1007 /978-1-4471-4965-1_2

Chapter 2

Keywords WaveformsIntervals Segments Artefact Calibration Rate Rhythm

Background

Interpretingthe ECGis ataskthat requires an underpinning knowledge ofthe waythe ECG is organised, what is being displayed and what the normal ranges and

values ofthe various waveforms,intervals and segments should be In addiionto

this iniial knowledge base practioners should spend as much time as they can looking at real ECGsin context and preferably discussingthese fi ndings with moreexperienced colleagues Like learning to play the piano or developing foreign language profi ciency it requires many hours of practice buit on top of the basic knowledge gained from books,lectures and other sources

There are many ways to interpret an ECG The authors recommend using a systematic approachthatincludesthe following aspects:

• Basic qualty control checks

• Rhythm determination

• Rate calculation

• Examination ofthe morphology and duration ofthe various waves,intervals andsegments

• Determining ofthe QRS axis

• Scanning for any addiional features or abnormalies

We begin bylooking at howthe ECGis organised onthe paper andinleads andmove ontolook atthe normal values forthe various components ofthe ECG wave-form, including different methods of calculating the rate and determining the rhythm

ECG Paper

12-lead ECGs are usually displayed on special gridded paper (Fig 2.1 ) The 12 leads I, II, III, aVR, aVL, aVF and V 1 –V6 are displayed on the paper under their respective headings The limb leads are found on the left hand side and the chest leads V/C 1–6 onthe right Theleads are separated bylead divider markers whichresemble an elongated punctuation colon ( The gridded area ofthe paperis spl

intolarger boxes with smaller boxesinsidethem Eachlarge box measures 5 mm2

(containing 25 smaller 1 mm2 boxes) Timeis measured alongthe x-axis (hor

izon-tal)in seconds Eachlarge box represents 0.2 s ofime, with each smaller box suring 0.04 s Each lead represents around 3 s of time Most 12-lead ECGs also include a rhythm strip, shown belowthe otherleads This stripis one ofthe existingleads displayed above, shown for around 12 s, usually lead II or V 1 This allows

mea-interpreterstolook for patterns and featuresthat might not otherwise be visibleinshorterime periods Some ECGs have morethan one rhythm stripincluded They-axis (vertical) representsthe ampltude ofthe ECG waveforms, measuredin mil-

livolts Onelarge square represents 0.5 mV, with a smal square measuring 0.1 mV

Large

square

Sma l square

V1 V2 V3

V4 Pre-pr in ted paper gr id

V5 V6

Bas ic Checks

There are several detailsthat should be checked priorto analysingthe waveformsand formulating aninterpretation These checksinclude:

• Ensuringthe ECGis free from artifact and recorded at suffi cient qualtyto enable

a subsequentinterpretation

• Checking R wave progressioninthe chestleads andthe defl ection oflead aVR

• Checkingthe calibration markers/calibration signal boxesto ensurethe ECGisrecorded usingthe standard setings

Artefact

Is any artifiial disturbancethat negativelyimpacts onthe qualty ofthe ECG Thereare many forms ofinterferencethat can affectthe qualty There are however severaltypes of commonly encounteredinterferencethat can be easily recognised and pre-vented or reduced in most cases Table 2.1 shows the most common forms of

interference,including possible causes and solutions

Ca l ibrat ion

tandard ECGsinthe UK, USA and many other parts ofthe world are recorded at

a speed of 25 mm/s and a voltage of 10 mm/mV Thisis usually displayed ontheECG somewhere (often atthe bottom) Thisinformationis also displayed graphi-

callyinthe form of calibration markers, sometimes called calibration signal boxes.These markerslookike rectangles (Fig 2.2 ) and are usually seen ontheleft hand

side ofthe ECG precedingtheleads

Whenthe ECGis set upto record atthe standard 25 mm/s and 10 mm/mV,the

calibration markers should measure 1 cm in height (2 large boxes) by 0.5 cm in

width (1large box) The authors recommendthat practioners recording andinterpreting ECGs always checkthatthe ECG was recordedinthe standard calibrationbefore attempting interpretation Speed and ampltude setings can be altered on most ECG machines,tistherefore possiblethat someone may either deliberately oraccidentally alterthese setings Ifthe recording speed was alteredto 50 mm/s,twould havethe effect of elongatingthe waveforms, and can make appearthatthe

-patient has an extremelylow heart rate and along QTinterval eventhoughtheir

other observations could otherwise be normal Sometimes alteringthese setingsisdone deliberately A patient may have a very rapid heart rate making diffi cultosee P waves This can sometimes be overcome by changingthe recording speed and

elongatingthe waveformsto see featuresthat would otherwise be missed Figure.3 shows a standard calibration marker and onethatis setto 50 mm/s As shownintheimagethe second markeristwice as wide as normal encompassingtwolarge boxes

Ca l ibra t ion

Figure.4 shows a calibration marker at half voltage.

Some machines wil also allow the voltage to be reduced just for the limb or chestleads,leavingthe otherleads at normal voltage Thisis represented by a cali-bration marker with a stepin Ifthe stepis ontheleftt represents a reductionintheimblead voltage only, whereas a step onthe right hand side represents a reduc-

tioninthe voltage ofthe chestleads only (Fig 5 )

Finallythe voltage can be decreased andthe recording speed changed simulously Thisis represented by a smal and wide calibration marker (5 mmin height

and 10 mmin width) Practioners should be famiiar with both normal and adjusted

calibration markers, whatthey represent and whatimpact changingthese setingsmay have on the interpretation of the ECG Even though the calibration markers

wl refl ect any changesistl good practiceto document onthe ECG any changes

tothe normal setings made when recordingto draw other practioners attentiontothese changes explicily

R Wave Progress ion /Lead aVR

R wave progression refers to the defl ection changes that occur in the chest leads (V1 –V6 asthey move from a predominantly negativeto a predominantly posiivedefection (Fig.2.6 )

F ig 2 4 Ca l ibra t ion marker

show ing ½ vo l tage (5 mm /

mV)

F ig 2 5 Reduced imb lead vo l tage on ly ( le f , reduced ches t lead vo l tage on ly ( igh t )

2 ECG In terpre ta t ion