Ebook Starting to read ECGs: Part 2

(BQ) Part 2 book Starting to read ECGs has contents: Arrhythmia, acute coronary syndrome, genetic cardiac condition, the pediatric ECG, patent ductus arteriosus, coarctation of aorta, treatment for myocardial infarction.

© 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_6

Chapter 6

Keywords Tachycardia • Fibrilation • Supraventricular • Rhythm • Arrhythmia •

Ectopic Premature beat Polymorphic Bigeminy Trigeminy Flutter Reentry

triggered activity, abnormal/enhanced automaticity, reentry and conduction

delays These mechanisms are discussedin more detai below withthe exception

of conduction delays, which are discussedin detaiin Chap 5 As many arrhy

th-mias are caused by or sustained by ectopic focitis necessaryto gain an

under-standing of ectopy

Premature Beats

Theterm premature beat more accurately describes ectopic beats Premature beatscan originate from the atrial, junctional or ventricular regions of the heart The most salient feature of a premature beatis a beatthat occurs earlierthan expected

in the cardiac cycle and has a different morphology to the normal underlying rhythm (Fig.6.1 ) The morphological changes arethe key way ofidentifyingthe

origin of a premature beat The main differences between the different types of premature beat are summarisedin Table.1

Prema ture Bea t Or ig in

There arethree primary mechanismsthat are consideredto bethe cause of ture beats,they consist of:

prema-• Enhanced automaticity

Changes in the cellular threshold level increasing diastolic depolarization leadingto premature beat formation

• Triggered activity

Damage to the myocardium can result in oscilation of the transmembrane

potential Leakage of posiiveionsintothe cel creates after depolarizationsleadingto premature beats Arrhythmias seenin Digoxintoxicity andlong QTsyndromes arethoughtto be caused bytriggered activity

• Reentry circuits/circus movement

Discussedin more detailaterinthe chapter

F ig 6 1 A ven tr icu lar

prema ture bea t

Tab le 6 1 The pr imary fea tures of prema ture bea ts

A tr ia l prema ture bea t

(APB) (JPB)Junctional premature beat Ven(VPB)tricular premature beat

Norma l bea t A tr ia l prema ture bea t

Inver ted p wave

A bea t occurr ing ear l ier than

expec ted w i th a P wave

morpho logy d if fer ing from

pa t ien ts norma l P wave

A bea t occurr ing ear l ier than expec ted w i th no v is ib le P wave A l terna t ive ly the P wave may appear inver ted and may occur before or af ter the QRS comp lex

A bea t occu r ing ea r ie r than expec ted w i th a w ide b iza r re QRS comp lex The T wave is usua l ly in the oppos i te

d rec t ion to the te rm ina l

po r ion o f the QRS comp lex

Compensa tory and Non-compensa tory Pauses

Compensatory pauses are temporary interruptions of sinus rhythm by a ‘gap’ or

‘pause’ with a durationthatis a muliple ofthe normal cardiac cycle To measure acompensatory pause,takethree consecutive PQRST complexes from an otherwiseregular rhythm Measurethe distance betweenthe start ofthe fi rst P wave ofthe fi rstbeat to the start of the P wave of the third beat Next measure the same distance

starting withthe start ofthe P wave fromthe normal beat beforethe premature beatand ending withthe start ofthe P wave ofthe normal beat followingthe prematurebeat Ifthis distanceisthe same asthe previous one,the pauseis a complete com-pensatory pause Ifthe start ofthe P wave onthethird beat occurs earlier,the pause

is termed an incomplete or non-compensatory pause Ventricular premature beats are often followed by a complete compensatory pause Thisis because atrial depo-larization usually occurs as normal An exceptiontothis areinterpolated prematurebeats, which are ventricular premature beatsthat occur exactly betweentwo normal

sinus beats and don’t have any compensatory pause Atrial premature beats howeverusually produceincomplete compensatory pauses

The majority of ventricular premature beats are benign and require notreatment

Patients can be advisedtoimi alcoholtobacco and caffeineintake, occasionally

beta blockers may be used There are however some patterns of ventricular ture beatthat canleadto more serious arrhythmias, such as VT and VF These pat-ternsincludetwo or more ventricular premature beats occurringtogether (Table.2 ) Most ventricular premature beats are unifocal, occurring from the same place and sharingthe same morphology Sometimes ventricular premature beats can be

prema-mulifocal and originate from different areasinthe ventricle The presence of mu

l-tifocal VPBs canindicate serious heart disease Mulifocal VPBs can beidentifi ed

inthe same way as ventricular premature beats withthe exceptionthatthey differinmorphology from one another (Fig 6.2 )

B igem iny and Tr igem iny

A regular repeating pattern of premature beats Bigeminy can be identified by a repeating pattern of normal beat followed by premature beat Trigeminyisidentifi ed

by a repeating pattern of premature beat following every two intrinsic beats Ventricular bigeminy/trigeminyis another pattern of ventricular premature beatthat

Tab le 6 2 Pa tho log ica l pa t terns

of ven tr icu lar prema ture bea t Couple toge venthertricular premature beats occurring

T r ip le ven tr icu lar prema ture bea ts occurr ing

toge ther

Sa lvos ven tr icu lar prema ture bea ts occurr ing

toge ther Prema ture Bea ts

can predisposeindividualsto dangerous arrhythmias, such as VT/VF An example ofventricular bigeminy/trigemniny and atrial bigeminy can be seenin Figs.6.3 and.4

Supraventr icu lar Tachycard ia

Or SVT is a tachycardia that originates from above the ventricles (Fig 6.5 ).Therefore SVTis alanketterm for many different forms oftachycardia (Table 6.3 ).Theterm SVTis often used whenthe specifi c rhythm can not beidentifi ed SVTsusually manifest with rapid narrow QRS complexes, withthe caveat of aberrancy,

whichis discussedlaterinthe chapter

ST depression and T waveinversion (signs ofischemia) are often associated withSVT The rateis usually between 100 and 250 BPM Asthe electricalimpulsetrav-

elsthroughthe AV node, drugs such as Adenosine can be usedtoiniiate atransient

AV block This can reveal the underlying rhythm making a diagnosis possible

Aternatively the rhythm may be terminated completely if it caused by a reentry

pathwaythat utizesthe AV node Another option often usedtoterminate or reveal

an underlying rhythmisthe use of vagal maneuvers Some ofthese maneuvers caneven betaughtto patientsto helpthem deal with future episodes of SVT

F ig 6 2 Mu l ifoca l /mu l iform ven tr icu lar prema ture bea ts

F ig 6 3 Top ) Ven tr icu lar b igem iny , ( bo t tom ) ven tr icu lar tr igem iny

F ig 6 4 A tr ia l b igem iny

Vaga l Maneuvers

The human autonomic nervous system encompassesthe sympathetic and

parasym-pathetic divisions The autonomic nervous system regulates organs and glands at asubconsciouslevel Stimulating vagal efferent discharge hasthe effect ofinducingtransient AV nodal block Thisinturn hasthe effect ofterminatingtachycardiasthatsubsist on AV conduction, such as AVNRT and AVRT Other SVTs may be moreeasily diagnosed by stimulation ofthe vagus nerve The vagus nerve can be stimu-

lated by using vagal manoeuvres Table.4 ists some ofthese vagal manoeuvres

Atr ia l F ibr i lat ion

The single most commonly encountered arrhythmia increases the annual risk of

stroke by around 4–5 % Theincidence of Atrial fi brilation (AF)increases with age

AFis also often seenin patients following cardiac surgery

AFis characterised onthe ECG by anirregularlyirregular rhythm (Fig 6 ) bestseen in the rhythm strip of an ECG There is no pattern to the irregularity and a

AV node reen try tachycard ia (AVNRT)

AV rec iproca t ing tachycard ia (AVRT)

A tr ia l F ibr i la t ion

chaotic baseline consisting of fibrilatory waves, termed ‘f’ waves is usually observed The other salient feature of AFisthe complete absence of P waves, bestseeninleads II and V1 AFis caused bythe presence of muliple ectopic fociinthe

atria, usuallylocated nearthe pulmonary veins These foci act astriggersincreasingthe atrial rate The AV node however preventsthe majority ofimpulses being con-ductedtothe ventricles Ifthis was notthe casethe outcome would be catastrophic

AF with a ventricular rate <100 BPM is termed ‘controlled AF’, whereas >100 BPMis referredto as ‘uncontrolled’ or ‘fast’ AF Fibrilation ofthe atria reducescardiac output by more than 20 % via loss of ‘atrial kick’ The atrial kick is the contribution made bythe atria priorto ventricular systole It hasthe effect of boost-ingthe effi ciency of ventricular ejection

AFis often detectedthrough manual pulse palpation When GPs record manual

pulses during routine visitsleadingtothe detection of AF,thereis a reductionintheincidence of stroke Unfortunately duethe use oftechnology manual pulse palpa-

tionis not being carried out as frequently as once was Most machines usedtotake

F ig 6 6 A tr ia l fi br i la t ion

Tab le 6 4 Vaga l manoeuvres

Vaga l manoeuvre Procedure

Va lsa lva F o rced exp i ra t ion aga ins t alosed g lo t is Th is can be done by c los ing the

pa t ien ts mou th and ge t ing them to p inch the ir nose The pa t ien t then exha les

as if b low ing up a ba l loon A l terna t ive ly a 10 m l syr inge may be used Ask the pa t ien t to b low in to the ip of the syr inge and try to move the p lunger Müe l ler Forced insp ira t ion aga ins t alosed g lo t is Essen t ia l ly the oppos i te of the

va lsa lva manoeuvre

D iv ing refl ex Of ten used w i th ch i ldren An ice co ld bag is app l ied to the face Th is

reduces the r isk of asp ira t ion assoc ia ted w i th submerg ing the face in ice

co ld wa ter Caro t id s inus

massage Ro10 sta Pationat ienl pressurets shou ld beis app monliedi toredtothe ( inc righludt caroing ECGtid ar andtery BP) for be durtweening 5 and

procedure Doc tors w i of ten is ten for a caro t id bru i w i th ate thoscope as

th is is good ind ica tor of caro t id ar ter ia l s tenos is Caro t id s inus massage is con tra ind ica ted in pa t ien ts w i th :

H is tory of TIA or s troke in las t 3 mon ths Myocard ia l infarc t ion

Occ lus ion of caro t id ar tery

H is tory of VT or VF Prev ious adverse reac t ion to s inus massage Ocu lar pressure Con tra ind ica ted due to the r isk of re t ina l de tachmen t

Cough ing No t techn ica l ly a manoeuvre bu t can be used to s t imu la the vaga l nerve

Encourage the pa ten t to cough hard

patients observations do however displaythe patients pulse Ifthe pulseis ‘jumpingaround’ onthe machinein anirregular mannerthen manual palpation should be car-

ried out Ifthe pulse appearsto beirregular a 12-lead ECG should be carried out

Ifthe arrhythmia persists,iniial electrical remodeling ofthe atriaissubsequently

followed by structural remodeling, whichinturn helpsto maintainthe arrhythmia

Atrial remodeling refersto any persisting changeinthe structure or function ofthe

atria Atrial remodeling makes it more likely that ectopic or reentry activity wil occur Structural changesinduced by AF occur at a cellularlevel andinclude manyfactors, such as: anincreasein myocyte cel size, myolysis, changestothe shape of

mtochondria, changesto structural proteins and fragmentation ofthe sarcoplasmic

reticulum Both electrical and structural remodeling maintainthe arrhythmia,thelonger a patient has AF,the moreikelythese changes areto occur

Atrial fi brilation can be further classifi ed as:

• Paroxysmal Atrial Fibrilation

Terminates spontaneously, usuallyinlessthan 7 days

• Persistent Atrial Fibrilation

Does notterminate spontaneously andlastslongerthan 7 days

• Permanent Atrial Fibrilation

Notterminated orreverted

Patients presenting with AF who have beenin fi brilation forlongerthan 48 hrequire anticoagulation priorto direct current cardioversion (DCCV) Thisis duetothe possibitythatintramuralthrombus may accumulateinthe atria, often aroundtheleft atrial appendage Whenthe normal motion ofthe atriumis recommenced,thereis a riskthatthethrombus may migrate causing a stroke To miigate against

this anticoagulationis given for weeks before and afterthe cardioversion Ifthisis

not possible dueto hemodynamic compromise requiringimmediatetreatment IVheparin can be administered priortothe cardioversion

Patients with a prior history of AF suffering a newincidence of AF forlessthan

48 h can suffer from remodeling of the atria caused by the previous episodes of

AF Inthis casethere may be anincreased riskinvolvedin DCCV To be surethatthere are no intramural thrombi present the patient may have a transoesophageal echocardiogram (TOE) Thisinvolves passing an ultrasound sensorintothe oesoph-agusto better viewthe chambers ofthe heart

Treatment for AF focuses on either rate control or rhythm control Rate control

aimsto reduce symptoms associated withthe high heart rates andto prevent cardmyopathy secondarytothetachycardia Rhythm control onthe other hand aimstoterminatethe underlying rhythm Generally paroxysmal AFistreatediniially withrhythm control Permanent AF alternativelyis usuallytreated with rate control strat-

io-egies Persistent AF can betreated with either Inthese patients rhythm controlis

oftentried firstifthey are younger, symptomatic or have congestive heart failure

Rate controlis attempted fi rstin older patients (>65 years), unsuitable for cardiover

-sion ortreatment with antiarrhythmic drugs or with coronary artery disease If either

ofthe options attempted fi rst failsthe patient may be considered forthe alternative

strategy Figures.7 and.8 showthetreatment algorithms recommended by NICE

A tr ia l F ibr i la t ion

intheir management of atrial fi brilation guidelines for both rhythm and rate control(2014) The symptoms and causes of AF areistedin Tables.5 and.6

Rhythm control optionsinclude:

• Direct current cardioversion

• Chemical/pharmacological cardioversion

Rhy thm con tro l s tra teg ies

O fer atandard be ta-b locker or a ra te im i ing caium channe l b locker as in i ia l mono therapy

to peop le w i thtr ia l ibr i la t ion who need drug trea tmen t as par t o f a ra te con tro l s tra tegy Base the cho ice o f drug on the person ’s symp toms , hear t ra te , comorb id i ies and pre ferences when cons ider ing drug trea tmen t

I mono thrapy does no t con tro l symp toms , and

i con t inu ing symp toms are through to be due

to poor ven tr icu lar ra te , cons ider comb ina t ion therapy w i th any 2f the fo l low ing :

• a be talocker

• d i iazem

• d igox in

O fer rhy thm con tro l to peop le w i thtr ia l ibr i la t ion :

• Whose a tr ia l ibr i la t ion has a revers ib

cause

• Who have hear t fa i lure though t to be pr imar i ly

caused by a tr ia l ibr i la t ion

• W i thtr ia l lu t ter whose cond i ion is

cons idered su i tab le for an ab la t ion s tra tegy

to res tore s inus rhy thm

• For whom a rhy thm cpn tro l s tra tegy wou ld be

more su i tab le based on c l in ica l judgemen t

• W i th new-onse t a tr ia l ibr i la t ion

Cons ider d igox in mono therapy for peop le w i th non-paroxysma l a tr ia l ibr i la t ion on ly they are seden tary (do no or very le phys ica l exerc ise)

Do no t o f fer am iodarone for long- term

ra con tro l

I symp toms are no t con tro l led

I symp toms are no t con tro l led

Is pa t ien t

e igle for a rhy thm con tro l

s tra tegy?

Go tolgor i thm 4 : Abt ion s tra teg ies No

Ye

F ig 6 7 Ra te con tro l s tra teg ies adap ted from NICE , (2014) gu ide l ines on the managemen t of AF

Pers is ten t AF Paroxysma l AF

Assess the need for drug therapy for long term rhy thm con tro l

Cons ider atandard

be b locker Pinthe pocket

Fa i led trea tmen t

Go tolgor i thm 4 : Abt ion s tra teg ies

A lgor i thm 3 : Rhy thm con tro l s tra teg ies

Cons ider o ther drug accord ing to co-morb id i ies :

• Cons ider am iodarone for peop le w i th le f ven tr icu lar impa irmen t or hear t fa i lure

• Dronedarone in accordance w i th TA 197

• Do no t o f fer c lass 1c an t iarhy thm ic drugs such

as leca in ide or propa fenone to peop le w i th known ischaem ic or s truc tura l hear t d isease

echocard iog raphy

gu ided and /or

am iodarone therapy pre and pos t)

D izz iness Loss of consc iousness

Tab le 6 6 Causes of AF Cardiac surgery

Hyper tens ion ick S inus Syndrome (SSS) Hyper thyro id ism

Rheuma t ic va lve d isease

A lcoho l Ischem ic hear t d isease Pre-exc i ta t ion syndromes Acu te infec t ion

Pu lmonary Embo l ism (PE)

P leura l ef fus ion

A tr ia l Sep ta l Defec t (ASD) Card iomyopa thy

A tr ia l F ibr i la t ion

Atr ia l F lutter

Is caused by a macroreentrant circui andis usually paroxysmal Atial fl utter usually

oiginatesromtheight atium Atial fl utter and atial fi brlation are closelyinkedand may alternate in individuals The symptoms and causes of atial fl utter are the same asthosefor AF A prolonged atial fltter often convertstselinto atial fi brla-

tion Figure 6.9 shows a typical macroreentrant circuit seen in the right atium, the

arows showthe directionthe pathway sustainingthe fltter The AV node cannot conductimpulses atthese highratestothe venticles as a degree of hear block develops

-lutter can beidentifi ed onthe ECG byts classic ‘sawtooth’ike appearance,seen bestinlead II, III and aVF As with Atrial Fibrilationthere are no P waves, butinstead prominent Flutter ‘F’ waves (Fig 10 ) Itis also worth notingthat fltterwavesinlead V1 canlookike P waves The atrial rate of atrial fl utteris often around

300 and usually between 200 and 400impulses per minute

There are different conduction ratios between the atrial and ventricular rates These ratios usually remainthe same but can sometimes manifest with a variable

AV block Theterm AV block when usedin relationto atrial fltteris notthe same

T icusp id

annu lus

M tra l annu lus

thing as AV blockinterms of heart block asthe AV nodeis functioning normallyin

fl utter,tisjust respondingto rapid atrial rates by being unableto conduct althe

atrialimpulses dueto refractory periods

Atrial fl utter should be considered when presented with any SVT at a rate of 150BPM This could well be an atrial fl utter with a 2:1 block Vagal manoeuvres or Adenosine can be potentially usedto revealthe underlying rhythm as discussed pre-

viously Common degrees of block relatingtothe heart rate can be seenin Table.7 There aretwo primarytypes of atrial fl utter,type I andtype II Type I fltteris

also referredto astypical or common atrial fl utter There aretwo further subdivision

oftype I atrial fltter; clockwise and counterclockwisetype I atrial fl utter

The reentry pathway usually takes an counterclockwise direction as seen in

Fig 6.9 and can be differentiated from clockwise fltter onthe ECG byinverted fl uter wavesintheinferiorleads II, III and aVF Clockwise fltter onthe other handisthe exact opposite (uprightin II, III and aVF) Type II atrial fl utter, also called uncom-mon or atypical atrial fl utteris more diffi cultoidentify It usually occurs at higher

t-atrial rates (340–440 BPM) and does not fulfithe criteria oftypical atrial fl utter

Atr ia l Tachycard ia

Is characterized bythe presence ofthree or more atrial premature beats, and an atrial

rate of between 140 and 250 BPM (Fig 11 ) P waves, best seeninleads II or V1

are sometime present and usually hiddeninthe preceding T waves The rhythmisregular Atrial Tachycardia can also causeloss of ‘atrial kick’ and a reduced cardiac

outputif sustained

a

b

F ig 6 10 A tr ia l fl u t ter seen in lead II rhy thm s tr ip

Tab le 6 7 Degree of b lock re la ted to hear t

ra based on fl u t ter wave ra te of 300 BPM Hear 150t rate (BPM) Degree 2:1 of block

F ig 6 11 A tr ia l tachycard ia

A tr ia l Tachycard ia

Thetachycardia usually originates from an ectopic fociinsidethe atrium but notfrom the sinoatrial node The arrhythmia is usually sustained by an atrial reentry

circui The P waves,ifthey can be seen usually have a different morphologytothe

patients normal P wave Atrialtachycardiais rarely sustained andis usually xysmal Table.8 shows causes of atrialtachycardia

Mu l ifoca l A tr ia l Tachycard ia

Or MAT as it is sometimes referred is quite rare and is therefore possibly under-

diagnosed It may often be mistaken for AF as also manifests with anirregularlyirregular rhythm at a ventricular rate >100 BPM There are however P waves pres-

ent but asthey are duetothree or more ectopic focithe P wave morphologies wivary from one another (Fig.6.12 ) MATtendsto occurin verylindividuals withsevereinfection and/or respiratory failure, such as COPD and CHF It can also becaused by hypoxia, severe pulmonary disease, atrial dysfunction orischemic heart

disease MAT carries a poor prognosis, with death occurring usually as a resul ofthe underlying condiion rather than the arrhythmia As such MAT tends to be

Tab le 6 8 Causes of a tr ia l tachycard ia Caffeine and other stimulants

Phys ica l /emo t iona l s tress Hypox ia

E lec tro ly te imba lance Card iomyopa thy MI

F ig 6 12 MAT [L ife in the Fas t Lane ( h t tp : l ife in thefas t lane com /educa t ion /procedures / pos i ion ing / /CC BY -SA 4 ( h t tp : /crea t ivecommons org / icenses /by-sa /4/

lead-mostly seeninintensive care or high dependency units A mulifocal atrialtachycar

-dia with a rate <100 BPMis referredto as wandering atrial pacemaker andis caused

by other pacemaker sites in the atria or junctional region temporarily taking over duetoincreased vagaltone

S inus Tachycard ia

A sinus rhythm with a rate greaterthan 100 BPMis defi ned as a sinustachycardia(Fig 13 ) Sinustachycardia may resul frominfection, use of stimulants, such astobacco and caffeine and various other medical condiions summarised in Table 6.9

F ig 6 13 inus tachycard ia [L ife in the Fas t Lane ( h t tp : l ife in thefas t lane com /educa t ion dures / lead-pos i ion ing / /CC BY -SA 4 0 ( h t tp : /crea t ivecommons org / icenses /by-sa /4 0 /

T ab le 6 9 Causes of s inus

tachycard ia Overs Anxietimuty/palaintion ofthe sympathetic nervous system

PE Per icard i is Anaem ia Hear t fa i lure Pregnancy

S t imu lan ts Infec t ion hyper thyro id ism Hypo tens ion

S inus Tachycard ia

S inus Arrhythm ia

The presence of normal intrinsic PQRST waves but with an irregular rhythm (Fig 14 ) A 10 % varianceinthe Pto P cycle (the distance betweentwo consecutive

P waves)is considered normal A variation above 10 % pointstowards sinus arrhy

th-mia The rhythmis essentially caused byirregular rates of sinus nodeimpulse

genera-tion The rhythm usually causes no symptoms and requires notreatment Iftreatment

is requiredthen Atropine or exercise are often usedtoterminatethe arrhythmia.The rhythmis alsoinkedtothe respiratory cycle withinspiration reducingtheP-P cycle increasing the heart rate Sinus arrhythmia can be caused or seen in

patients with: diabetes, alcoholic cardiomyopathy, raisedintracranial pressure andthosetaking Digoxin

Junct iona l Tachycard ia

A tachycardia can also originate from the junctional region (Fig 6.15 ) P waves when visible are often seen after the QRS complex and activate the atria

retrogradely

Reen try

Istriggered by animpulse returningto depolarize previously depolarizedissue asecondime Forthisto occurthere needsto be atriggering stimulus and a potentialreentry pathway Patients withischemic disease or congenital accessory pathwaysare proneto arrhythmias

F ig 6 14 inus arrhy thm ia [L ife in the Fas t Lane ( h t tp : l ife in thefas t lane com /educa t ion dures / lead-pos i ion ing / /CC BY -SA 4 0 ( h t tp : /crea t ivecommons org / icenses /by-sa /4 0 /

A premature beat caniniiate atachycardiain patients with a reentry circuiSometimes the impulse can travel down both limbs of a circuit (Fig 6.16a )

Aternatively one limb of a ring of cardiac tissue is more refractory than the

other the impulse then proceeds slowly down the pathway and then back up through the once blocked section (Fig 6.16b ) Finally the impulse can travel very slowly along one pathway andthen backtrack backthroughthe otherimb(Fig 16c )

There are several types of reentry circuits that can trigger a supraventricular tachycardia,theseinclude:

• SA nodalreentry

• AV nodalreentry

• AV nodal bypassreentry

SA nodal reentryis classifi ed as a macroreentranttachycardia and occurs withinthe sinoatrial nodetself (Fig 17 ) These fast and slow pathways can also existinthe AV node (Fig 6.18 ) andis referredto as AV nodal reentrytachycardia (AVNRT).AVNRT is also the most commonly encountered AVNRT is seen on the ECG as

F ig 6 15 Junc t iona l tachycard ia

F ig 6 16 Arrhy thmogen ic mechan isms

Junc t iona l Tachycard ia

regular, fast rhythm with a rate usually above 130 BPM Retrograde P waves are

also often present appearing atthe end ofthe QRS complexes A smal secondary

R wave similartothe one seenin RBBB but withoutthe widened QRSis also oftenseen, asis a RPinterval of <100 ms The other mechanism for reentryis an extra

pathwaythat bypassesthe AV node entirely allowingimpulsesto go back upthrough

this pathway creating a sustainedloop (Fig 18 )

Pre-exc itat ion

Referstothe activation ofthe ventricles by a congenital accessory pathway WolfParkinson- White syndromeis an example of pre-excitation

SAN reen try

F ig 6 17 SA noda l reen try

Wo lf f-Park inson-Wh i te Syndrome (WPW)

Isthe most common form pre-excitation and was named afterts discoverers Afoetal abnormalty resultsin a pathwaythat connectsthe atria and ventricles The

atria and ventricles are electricallyisolated bythe atrioventricular ring, allowingimpulsesto onlytravel between atria and ventricles bythe conduction pathway

This extra pathway is referred to as the bundle of Kent and allows impulses totravel viathe bundle Impulses can alsotravel back uptothe atria fromthe ven-

tricles creating a sustainedtachycardia WPW normally occursinthe young andadults aged 20–35 years of age Most people with this condiion seek medical

atention due to the frequent occurrence of supraventricular tachyarrhythmias Becausethereis no AV nodeto slowtheimpulseinthe accessory pathwaythe PR

AV noda l reen try

AV noda l bypass reen try

F ig 6 18 AV noda l reen try

Pre-exc i ta t ion

intervalis short Theimpulseisthen slowerto activatethe ventricles as is notpassingthroughthe normal conduction system Thisleadstothe formation of a

‘delta wave’ onthe ECG The short PRinterval and delta wave arethe key ECGfeatures of this syndrome Figures 6.19 and 6.20 shows the slurred upstroke termed a delta wave and short PRinterval withthe P wavelocated very closely

tothe QRS complex

There aretwo subtypes of WPW calledtype A andtype B WPW These subtypescan beidentifi ed bylooking atthe defl ection of QRS complexesin V1

• Type A – QRS complexes are posiively defl ectedin V1

• Type B – QRS complexes are negatively defl ectedin V1

Or thodrom ic and An t idrom ic

The direction the impulse takes through the accessory pathway is referred to as

orthodromic or antidromic and can distinguished onthe ECG by broad or narrowQRS complexes (Table 6.10 )

De l ta wave

F ig 6 19 The de l ta wave

and shor t PR in terva l

assoc ia ted w i th WPW

Wo lf f-Park inson-Wh i te Syndrome and A tr ia l F ibr i la t ion

Atrial fibrilation or less commonly flter can occur in patients with WPW (Fig 6.21 ) The accessory pathway allows impulses to bypass the AV node and

A tr ioven tr icu lar

r ing

R igh t a tr ium

S inoa tr ia l node (SAN)

Impu lse trave ls down AV node and back up

through the accessory pa thway D isp lays a

narrow QRS comp lex

Impu lse trave ls down accessory pa thway and back up through the AV node D isp lays a broad QRS comp lex

Pre-exc i ta t ion

conductthe ventricles rapidly Thereis also a possibitythe rhythm wi degenerate

to VT or VF Adenosineis contraindicatedin WPW with atrial fi brilation as mayleadto 1:1 conduction Other drugsthat should not be administered are showninTable 6.11 DC cardioversionis however safe and effective

Lown-Ganong-Lev ine Syndrome (LGL)

More common in the young and women, patients also present with tachyarrhy

th-mias Like WPW was also named afterthe people who discoveredthe syndrome.The main ECG fi ndings are a short PRinterval no delta wave and episodes of reen-tranttachycardia (Fig 22 ) The exact mechanisms precipitatingthis syndrome are

not fully understood Some experts believed in the past that accessory pathways, such as James fi bres or Brechenmacher fi bres allowedimpulsesto bypass al or part

ofthe AV node Enhanced AV nodal conductionis now consideredto bethe primarymechanism Electrophysiological studies have shownthatthere are often differentarrhythmic mechanisms at workin so called LGL syndrome andthatthelabel ofLGLis usedto describe a short PRinterval with normal but accelerated AV nodalconduction caused by various different arrhythmogenic mechanisms

F ig 6 21 WPW and AF [L ife in the Fas t Lane ( h t tp : l ife in thefas t lane com /educa t ion dures / lead-pos i ion ing / /CC BY -SA 4 0 ( h t tp : /crea t ivecommons org / icenses /by-sa /4 0 /

T ab le 6 11 Con tra ind ica ted drugs for trea tmen t

of WPW and AF IV Verapam Adenosiine

D igox in

D i iazem

Card iovers ion

Direct current cardioversion (DCCV)is used when an arrhythmialeadsto dynamic compromise or for routine planned cardioversion of an arrhythmia Ifthe

haemo-patient has no cardiac outputthen unsynchronised defi brilationis carried out DCCVis usedtotreat cardiac arrhythmias by depolarizingthe cells ofthe myo-cardium Thisis done via an electrical current deliveredthrough defi brilator padsappliedtothe patient Itis hopedthat following depolarization ofthe heart normalrepolarization wi occur andthe cardiac arrhythmia wi beterminated

Synchronised cardioversion can be used if R waves are visible on the ECG Modern defi brilators havethe abityto synchronizethe electrical discharge

20 ms (0.02 s) afterthe R wave Thisis doneto applythe currenttothe myocardium

a a point whenthe cells arein a state of depolarization Ifthe current wereto be

discharged duringthe relative refractory period (Fig.6.23 )t couldtrigger ‘R on T’phenomenon, which can precipitate VF and polymorphic VT The relative risks andbenefits of DCCV can be seen Table.12

E lec trophys io logy S tud ies (EPS)

Catheters can be placedinthe heart via a vein or artery (Fig 24 ) usuallyinthegroin The catheters are placed by x-ray The procedure allows detailed examination

ofthe heart’s electrical systemto be carried out Electrodes can also be usedto pacethe heartto stimulate arrhythmias sothe source can be detected

F ig 6 22 LGL syndrome

Pre-exc i ta t ion

4 R

P

Q S

Shock de l ivered 20 ms

a ter peak o f R wave

F ig 6 23 Synchron ized

card iovers ion

Tab le 6 12 R isks and benefi ts of DCCV

Ab la t ion

Oncethe source ofthe arrhythmia has beenlocated ablation may be offered Ablation

is a method of destroying cellsthat are supporting an arrhythmia Radiofrequency

ablationis often usedto burn cells Cryoablationis also utizedin some centres and

alows cells to be destroyed using extreme cold The advantage of cryotherapy is that cells can be frozento seetheir effect onthe arrhythmia beforethey are perma-nently destroyed Ifthe wrong cells aretargetedthey can potentially recover

H IS purk in je

H is bund le

ca the ter

Le f ven tr ic le

Le f

a tr ium

R igh t ven tr icu lar

apex ca the ter

As mentioned previously the ectopic foci in AF are usually sited around the

pulmonary veins Ablation can be used as atreatment option for AF Some elecphysiologists use 3D electroanatomic mapping systems (Fig 6.25 ) to map the

tro-intended ablation sites Ablation of ectopic foci around the pulmonary veins is

>90 % effective fortreating AF, howeverthereis good chancethe AF wi return

wthinthe fi rst year followingtreatment (30–50 %)

Another optionisto use ablationto deliberately destroythe patients AVjunction

This creates a complete conduction block preventing rapid ventricular activation The patientthen has a permanent pacemakerimplanted and becomestotally pace-maker dependent To reducethe need fortemporary pacing priorto permanent pace-makerinsertion, a pacemaker may beimplanted several weeks beforethe ablation

Figure.26 displaysthe NICE algorithm forleft atrial ablation

is also often possibleto use ablationtotreat atrial fltter Thisis done by scar

-ringissueinthe path ofthe circui causingthe fl utter

Ventr icu lar Tachycard ia (VT)

VTis a broad complextachycardia with a rate≥120 BPM Four or more ventricularpremature beats consttutes a run of VT Sustained VTis defi ned as VTthatlasts formorethan 30 s It can be challengingto differentiate between a ventriculartachycar-

dia and a supraventriculartachycardia with aberration

Aberrant conductionis essentially conduction of animpulse from supraventrlar regiontothe ventriclesin a signifi cantly different way from normal conduction

Thisis especially possiblein patients with a bundle branch block or WPWsyndrome.

Ifthe rateis rapid andthe aberrant conduction causesthe appearance of wide QRScomplexes, an SVT canlookike a VT Distinguishing betweenthetwo can be veryimportant as AV blocking agents that work well for terminating SVT can cause haemodynamicinstabityif givento a patient with VT Fortunately DC cardiover-

sionis a safe and effective option for both VT and SVT

Telingthe difference between VT and SVT with aberrancy can be done by tematic examination to look for supporting evidence of a ventricular tachycardia The more evidencethe moreikely isto be a VT Firstly VTis more commonlyencounteredthan SVT with aberrancy Cluestothe presence of ventricular ectopyinclude:

Fus ion Bea ts

Caused byimpulses from differentlocations occurring simultaneouslyinthe sameregion ofthe heart (Fig.6.27 ) The beat canterallylookikethe merging oftwo

different beatstogether

O fer le f a tr ia l surg ica l abt ion a t the same ime

as o ther card io thorac ic surgery to peop le w i th symp toma t ic a tr ia l

f ibr i la t ion

A lgor i thm 4 : Le f a tr ia l ab la t ion s tra teg ies

I drug trea tmen t has fa i led to con tro l symp toms o f

a tr ia libr i la t ion or is unsu i tab le :

• O f fer le f a tr ia l ca the ter ab la t ion to peop le w i th

paroxysma l a tr ia l ibr i la t ion

• D iscuss the r isks and bene f ts w i th the person

• Cons ider ca the ter or le f a tr ia l surg ica l ab la t ion

for peop le w i th pers is ten t a tr ia l ibr i la t ion

Cons ider le f a tr ia l ca the ter ab la t ion be fore pac ing

and a tr ioven tr icu lar node ab la t ion

Le f a tr ia l ab la t ion-cons idered for pa t ien ts w i th

symp toma t ic AF or AF caus ing hear t fa i lure

Card iac surgery

Reassess the need for ab la t ion a f ter pac ing and op t im isa t ion o f drug therapy Ye

F ig 6 26 Ab la t ion s tra teg ies a lgor i thm adap ted from NICE gu ide l ines for AF (2014)

Ven tr icu lar Tachycard ia (VT)

Cap ture Bea ts

Are caused bytemporary reassertion ofthe SA node overthe ventriclesleadingto asubsequent QRS complex of normal duration (Fig.6.28 )

AV D issoc ia t ion

Regularly occurring P waves may be seen onthe ECG but have no relationshiptothe QRS complexes (Fig 29 )increasingtheikelihood ofthe rhythm being VT

Rhy thm Regu lar i ty

If the rhythm is markedly irregularly irregular it may suggest atrial fi brilation

which would make probablethatt was a SVT not a VT Some smalirregularity

is also commonin VT

Concordance

Referstothe defl ection of complexesinleads V1to V6 beingthe same Ifthey arepredominantly defl ectedinthe same directionthen concordance exists and providesaddiional evidence forthe presence of VT Ifthereis no concordance howevercould stl be VT Concordance can be either posiive or negative

F igure 6 28 A cap ture bea t

Card iac Ax is

The QRS axis wi be differenttothe axis ofthe normal sinus rhythm (Fig 30 )

This also favors a VT diagnosis

There are several subtypes of VT,including:

• Monomorphic/unifocal VT

Right ventricular outfl owtract VT (RVOT)

Fascicular VT

Fascicular tachycardia is another monomorphic VT that is characterised by a RBBB pattern with axis deviation (Table 6.13 ) Fascicular tachycardia originates fromthe posterior or anterior fascicle oftheleft bundle branch

Polymorphic VT is a form of VT where there are muliple ventricular ectopic foci Polymorphic VTis often seeninthe context of myocardialinfarction The axisand ampltude ofthe QRS complexes vary Torsades de pointesis a French name for

twisting about points (Fig 33 ) Thisis atype of polymorphic VTthatis associated

wth along QTinterval unlike other forms of polymorphic VT which occur with anormal QTinterval

Idioventricular rhythmis also referredto as slow VT andis a reperfusion arrhy

th-mia associated with myocardial infarction Idioventricular rhythm is discussed in more detaiin Chap 7

F ig 6 32 R igh t ven tr icu lar ou tfl ow trac t tachycard ia (RVOT)

Tab le 6 13 Defi n ing ECG fea tures of

pos ter ior and an ter ior fasc icu lar VT FascPostericior De RBBBtails pattern withleft axis deviation

An ter ior RBBB pa t tern w i th r igh t ax is dev ia t ion

F ig 6 33 Torsades de po in tes

Card iac Arrest Rhythms

A cardiac arrest occurs whenthe heart failsto pump enough blood aroundthe body

to sustainife Loss of consciousness occurs duetolack of oxygen and glucosetothe brain A cardiac arrestis a medical emergency and requiresimmediateinterven-

tion to prevent death Prompt CPR and defi brilation (if the rhythm is shockable) should be applied as soon as possible Delaysin receiving prompttreatment canlead

to death or a degree of brain damage Chest compressions (Fig 34 ) provided bycardiopulmonary resuscitation (CPR) areinstrumentalin providing a fl ow of oxy-genated bloodtothe brain and other organs delaying permanentissue death Thereare certain causes of cardiac arrestthat havethe potentialto betreated andterminatethe arrest These factors are referredto asthe reversible causes and are summarised

in Table 6.14 Attempts to identify these causes should be made whilst providing immediate/advancedife support The principle cardiac arrest rhythms comprise of:

• Pulseless ventriculartachycardia

• Ventricular fi brilation

Of the four primary arrest rhythms, only VF and VT are ‘shockable’ rhythms (respond favorablyto defi brilation) Both VT and VF have better outcomesthanthe

other arrest rhythms

Pu lse less VT

The same as VT but sustained and not producing suffi cient cardiac outputto gener

-ate a pulse Inthis case defi brilationis usedto attemptto restore sinus rhythm

Ven tr icu lar F lu t ter

A form of VT with a very rapid rate (250–350 BPM) presenting with a monomor

-phic sine waveike appearance (Fig.6.35 ) Ventricular flter normally rapidly gressesto ventricular fi brilation

Ven tr icu lar F ibr i la t ion

Rapid irregular electrical activity producing no cardiac output There are no dcernable waveforms orintervals VF can appear coarse or fi ne (Fig.6.36 ) Fine VF

is-follows coarse VF and reduces the chance of successful treatment as myocardial

Tab le 6 14 The po ten t ia l ly

revers ib le causes of card iac

arres t

Hypox ia Hypovo laem ia Hypo /hyperka lem ia and o ther me tabo l ic Hypo therm ia

Tens ion pneumo thorax Tamponade

Tox ins Thrombos is (e i ther card iac or pu lmonary)

F ig 6 35 Ven tr icu lar fl t ter

Absence of any ventricular or atrial activity (Fig 37 ) Thereis no cardiac output

in this rhythm and unless reversible causes are present the outlook is extremely poor Sometimes P waves may be present (termed P wave asystole),these patientsmay be suitable for pacing Itis alsoimportantto checkthe gain onthe monitor as

fi ne VF can sometimes be missed as it can look like asystole if not set properly (1 mV per cm) A complete fl atine on a monitoris anindicationthat one ofthemonitoringleads may not be connected properly

Pu lse less E lec tr ica l Ac t iv i ty

Usedto be called electromechanical dissociation Essentially coordinated electricalimpulse generation is taking place but there is no cardiac output This is another reason to remember the old adage about treating the patient not the rhythm The

patient wi be unconscious and not breathing but a rhythmthat should produce a

pulseis seen onthe monitor Defi brilationis not appropriate astheissueis caused

bylack of responseto electricalimpulses ratherthantheimpulsesthemselves

Summary of Key Po ints

• Atrial fi brilationisthe most commonly encountered cardiac arrhythmia

• There are various patterns of premature ventricular beats that can predispose individualsto dangerous arrhythmias such as VT and VF

• SVTis a blanketterm for arrhythmias occurring abovethe ventricles

• VT and VF arethe only arrest rhythmsthats respondto defi brilation

• Cardioversionis a safe and effectivetreatment for both SVT and VT

• Torsades de pointesis a polymorphic VTthat can only be diagnosedin patients

wth QT prolongation

• An SVT with a regular rate of 150 BPM may be atrial fltter

• Vagal manoeuvres or Adenosine can be potentially usedto reveal an arrhythmia

in patients with SVT

Qu iz

Q1 Occasional ventricular premature beats

(A) Should betreated as a medical emergency

(B) Do not usuallyrequire anytreatment

(C) Alwaysrequire monitoring

Q2 Anirregularlyirregular rhythm with no P wavesis

Q6 The main mechanisms of arrhythmogenesis are

(A) Triggered activity, abnormal/enhanced automaticity andreentry

(B) Triggered activity, abnormal/enhanced automaticity and bigeminy (C) Activated activity, ventricular automaticity andjunctionalreentry

Interpretthe following ECGs

Q7

Q8

Qu iz

Q9

Q10

Answers: Q1 = B, Q2 = C, Q3 = A, Q4 = B, Q5 = A, Q6 = A, Q7 = WPW, Q8 = AF,Q9 Atrial fl utter, Q10 = Ventriculartrigeminy

© 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_7

Chapter 7

Keywords ACS • STEMI • NSTEMI • Angina • ST elevation • ST depression • Myocardialinfarction Biomarkers Reciprocal changes

Background

Acute coronary syndromes are a group of condiions precipitated by a reduction orcessation of blood fl owthroughthe coronary arteries An acute coronary syndrome(ACS)is a medical emergency requiringimmediateintervention ACS encompassesany narrowing or obstruction ofthe coronary arteriesleadingto acute symptoms.Acute coronary syndromesinclude:

• ST elevation myocardialinfarction (STEMI)

• Non ST elevation myocardialinfarction (NSTEMI)

• Unstable angina

To better understandthese syndromesis necessaryto gain an awareness of howthe coronary arteries function and their anatomy There a two principle coronary

arteries, the left and right coronary arteries (Fig 7.1 ) The left further subdivides

intotheleft anterior descending and circumfl ex arteriesthat supply bloodtotheleft

side and front of the heart The right coronary artery divides into the posterior descending and acute marginal arteries, supplying bloodtothe right atrium, rightventricle, SAN and AV node and some part oftheleft ventricle (Fig.7.2 )

The coronary arteries arise fromthe aorta and supplythe heart muscle with bloodand oxygen The artery that supplies the posterior descending artery and one or more posterolateral branchesis referredto asthe dominant vessel The right coro-nary artery is the dominant vessel in 80–85 % of cases, other people have a left dominant or codominant systems

Any narrowing or blockage to these arteries can reduce or prevent blood fl owreaching portions ofthe heart pastthe area of narrowing or blockage,leadinginturn

to an acute coronary syndrome ACS often presents as chest pain, orightness/dcomfort ofthe chest Pain may be accompanied by sweating and nausea The pain

is-may spreadto other areasincludingthe back, shoulders, neck,jaw and arms Thereason painis felin areas otherthanthe chest such asthe arm andjawis duetothebrain’s inabity to distinguish between visceral and somatic sensory distribution Somatic pain originatesin deepissues and skin, whereas visceral pain derives from

internal organs This confusion originates fromthe factthatthe visceral and somaticnerves fromthe heart and spinal nerves enterthe spinal cord atthe same point caus-ingthe braintointerpretthe pain as originating fromthe somatic regions When a

patient presents with chest painisimportantto rule out any other causes (Table.1 )and ask appropriate questionsto ascertainthetype of painthe patientisexperiencing

Le f an ter ior descend ing

ar tery (LAD)

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

C ircum f lex

ar tery

Sep ta l branches

D iagona ls

Ob tuse marg ina ls

Sp ine

Le f coronary ar tery seen in

r igh t an ter ior ob l ique v iew

Sp ine

SA noda l

Conus branch

R igh t ven tr icu lar branch

Acu te marg ina ls Pos ter ior le f

ven tr icu lar branch

Pos ter ior descend ing

ar tery

R igh t coronary ar tery seen in

r igh t an ter ior ob l ique v iew

F ig 7 2 Lef t and igh t coronary ar tery ana tomy

143 Tab le 7 1 Ches t pa in

d if feren t ia l d iagnos is Per Tamponadeicardiis/myocardiis

Ang ina

D issec t ing aor t ic aneurysm Oesophagea l pa in Muscu loske lel pa in

Pu lmonary embo l ism

T rauma Pan ic a t tack Arrhy thm ia

P leur isy Mas t is (seen in breas tfeed ing women)

Tab le 7 2 Ches t pa in

h is tory ques t ions When Where d dididthethe pa painin s startart?t?

Wha t were do ing a t the ime?

Does the pa in spread anywhere e lse?

How wou ld you descr ibe the pa in?

Does the pa in come and go or is cons tan t?

Have you had pa in ike th is in the pas t?

Is there any th ing tha t makes the pa in be t ter or worse?

On a sca le of 0–10 , 0 be ing no pa in and 10 be ing the wors t pa in imag inab le , wha t score wou ld you g ive the pa in a t the momen t?

Do you fee l shor t of brea th?

Have you had any nausea or vom i ing?

Do you have a h is tory of hear t a t tack and /or ang ina?

(Table.2 ) andif is cardiacin origin Patients presenting with acute chest painsuspect of ACS should havethe following assessments carried out

• 12-lead ECG on admission followed by serial ECGs as required

• Haemodynamic assessment

• Complete medical history and history of presenting complaint

• Bloodtest for cardiac biochemical markers

Suspected MI patients should have accessto defi brilation, high fl ow oxygen andanalgesia, usually an opiate given with an antiemetic Cyclizineis not recommendedduets potential hemodynamic effects Antiplatelet aggregators, such as Aspirin are

often given to impair platelet aggregation around the clot Low molecular weight heparins are also often usedin ACS patientsto reduce coagulation ofthe blood The

authors do notinclude muchinformation about specifi c drugs andtheir doses delerately asthis differsin certain countries and setings Instead we recommendthatthe reader is famiiar with their own local policies and procedures for the pharmacological management of patients

Background

Atherosc leros is

Is a process where arteries become hardened by plaques made up of fatty substances,such as cholesterol andtriglycerides The hardening and narrowing ofthe arteriescan reducethe fl ow of blood and oxygentothe heart muscle causing coronary heart

disease In other arteriesthe process can cause stroke or peripheralarterial disease

If a plaque ruptures (Fig 3 )t canleadtothe formation of a blood clot known

as a thrombus This clot can then block subsequent blood fl ow to portions of the heart supplied bythe blocked artery (Fig.7.4 ) An enzyme namedthrombin causes

fi brinto be formed from fi brinogen (Fig 5 ) This mesh of fi brintraps blood cellsand platelets Platelet aggregationistriggered bythe damagetothe vessels endothe-

lium caused bythe rupture The platelets attachtothe exposed collagen by binding

to von Wilebrand’s factors

The risk factors for coronary heart disease can be splinto modifi able and modifi able risk factors (Table.3 ) Modifi able risk factorsincludethingsthat can bechanged or better managed by patients, usually by making certainifestyle changes.Nonmodifi able risk however are beyondthe control orinfl uence ofthe patient such

non-as gender and genetic makeup

Norma l cu t-sec t ion o f ar tery

Tear in ar tery wa l

Fa t ty ma ter ia l depos i ted in vesse l wa l

Narrowed ar tery becomes b locked by a b lood c lo t

F ig 7 3 A therosc leros is

lead ing to coronary thrombus

forma t ion

Ang ina

The extent of the arterial occlusion can cause symptoms of angina or other acute coronary syndromes Nitrates, such as; glyceryltrinitrate (GTN),isosorbide mono-

ntrate (ISMN) andisosorbide dinitrate (ISDN) are often usedto relieve symptoms

of angina Nitrates work by dilating the coronary arteries and increasing blood/oxygen fl ow to the heart, whilst simultaneously reducing preload by dilating the systemic veins Duetothe mechanism of action and side effects of nitrates, patients

F ig 7 4 The occ lus ion in the

r igh t coronary ar tery can be

c lear ly seen Th is pa t ien t had

a co l la tera l vesse l a l low ing

b lood to bypass the b lockage

na tura l ly

Thrombogen ic ma ter ia l ( from p laque)

Thromb in Pro thromb in

F ibr in

Occ lus ive c lo t

Myocard ia l in farc t ion

F ibr inogen

F ig 7 5 Thrombus

forma t ion lead ing to

myocard ia l infarc t ion

Ang ina

can develop tachycardia, feel dizzy, have headaches and develop postural hypotension There are several differenttypes of angina,including:

• Stable angina

• Unstable angina

• Prinzmetal’s/variant angina

S tab le Ang ina

table angina pectoris(Fig 6 )is caused by atherosclerotic plaque(s)in one or more

othe coronary arteriesreducing blood fl owtothe hear Thereduced blood fl owis not

normally noticed during routine activiies; but during situations requiing increased myocardial demand, angina symptoms become apparent Painis oftenfelinthe chestneck,jaw or arms andis essentially caused by demandfor blood and oxygen being

greaterthan supply Exercise and emotional stress canigger an angina attack

Uns tab le Ang ina

Unlike stable angina, symptoms can also occur during rest Thereis signifi cant narrowing ofthe arteriallumen substantially reducing coronary blood fl ow (Fig 7 )

Pr inzme ta l’ s Ang ina

Also known as vasospastic or variant anginais a form of anginathatis not caused

by narrowing ofthe vessel dueto plaques butinstead by contraction ofthe smooth

Tab le 7 3 Mod ifi ab le and

nonmod ifi ab le coronary hear t

d isease r isk fac tors

Nonmod ifi ab le Mod ifi ab le

Race H igh b lood cho les tero l Sex H igh b lood pressure Gene t ics Obes i ty and inac t iv i ty

D iabe tes

Lumen Med ia

Endo the l ium Adven t ia

A therosc lero t ic

p laque

Necro t ic cen tre

F ig 7 6 tab le ang ina

pec tor is