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HEART ATTACK
dr. Dea Prista Agatha
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What is it?
Heart Attack or Myocardial Infarctionis a sudden blockage of blood ow toa portion of the heart which reducethe oxygen levels.
As a result so!e of the heart !usclebegins to die.
"ithout early !edical treat!ent thisda!age can be per!anent.
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What causes a heartattack?
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#he heart is a !uscular pu!p that needs a continuoussupply of oxygen. It gets oxygen fro! the blood whichows to the heart !uscle through arteries on the heart$ssurface. #hese arteries are called the coronary arteries.
#he !ost co!!on cause of heart attack is coronay heartdisease %&HD' ( the slow build)up of fatty deposits on theinner wall of the arteries that supply the heart !uscle withblood. #hese fatty deposits called plague gradually clogthe inside channel of the arteries causing the! to narrow. Itis a process that begins early in life and continues over theyears.
A heart attack usually begins when an area of pla*uecracks. +lood cells and other co!ponents of the blood stickover the da!aged area and for! a clot that suddenly andco!pletely blocks the blood ow to the heart !uscle. If theartery re!ains blocked the lack of blood ow through thatartery per!anently da!ages the area of heart !uscle thatit supplies blood to.
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Signs and Symptoms
Pain in the chest
Pain spreading
Disco!fort in theupper body
Di,culty breathingnausea or vo!iting
a cold sweat or afeeling of beingdi--y or lightheaded.
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Heart attack sy!pto!s vary. ot all heartattacks begin with a sudden crushing painthat is often shown on #/ or in the !ovies. #hewarning signs and sy!pto!s of a heart attackaren$t the sa!e for everyone. Many heartattacks start slowly as !ild pain or disco!fort.0o!e people don$t have sy!pto!s at all %thisis called a silent heart attack'.
#he sy!pto!s usually last for at least 12!inutes and you !ay experience !ore thanone of the heart attack sy!pto!s below.
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Pain in the chest
#he !ost co!!on sy!pto! of heart attack is chest pain or disco!fort. #hepain so!eti!es starts slowly or !ay co!e on suddenly or develop over afew !inutes. Most heart attacks involve disco!fort in the center of the chestthat lasts for !ore than a few !inutes or goes away and co!es back. It !ayfeel like tightness pressure heaviness fullness or s*uee-ing. #he feeling has
been described as3 4like a steel band tightening around !y chest4 4like anelephant sitting on !y chest4 or 4like a red hot poker in the centre of !ychest4. #he pain can range fro! severe to !oderate or even !ild. Heartattack pain can so!eti!es feel like indigestion or heartburn
Pain spreading
#he chest disco!fort !ay spread to the neck and throat 5aw shoulders the
back either or both ar!s and even into the wrists and hands. Discomfort in the upper body
0o!e people do not get any chest pain )only disco!fort in parts of the upperbody. #here !ay be a choking feeling in the throat. #he ar!s !ay feel 4heavy4or 4useless$.
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Other symptoms6ften there !ay also be di,culty breathing nausea or vo!itinga cold sweat or a feeling of being di--y or light)headed.
#he sy!pto!s of angina can be si!ilar to the sy!pto!s of aheart attack. Angina is pain in the chest that occurs in people
with coronary artery disease usually when they$re active. Anginapain usually lasts for only a few !inutes and goes away with rest.Angina that doesn$t go away or that changes fro! its usualpattern %occurs !ore fre*uently or occurs at rest' can be a sign ofthe beginning of a heart attack and should be checked by adoctor right away.
"o!en4s !ost co!!on heart attack sy!pto! is chest pain ordisco!fort. +ut wo!en are so!ewhat !ore likely than !en toexperience so!e of the other co!!on sy!pto!s particularlyshortness of breath nausea7vo!iting and back or 5aw pain.
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Primary ManagementTechniques Heart Attack Treatment
First you must conduct a primary survey of the casualty;
A primary survey consists of following the DRABCD procedure, this involves;
D = DANGE ! "f " find a heart attac# casualty " should chec# for any surrounding
danger to myself first and for the casualty and others
= esponse ! " should asses whether the person is conscious or unconscious using
the $%&' procedure; ($an you hear me, (%pen your eyes, (&hat is your name,(')uee*e my hand+
A = Airways ( After response if the casualty is unconscious " should then chec# the
airways for any ostructions or loc#ages and if there is a loc#age turn the victim onto
his-her side and clear the airway+
. = .reathing ! /he ne0t step if the patient is unconscious is to chec# for signs of life+
$hec# for reathing y using loo#, listen and feel techni)ue+ "f reathing place the
casualty in recovery position, if not give 1 rescue reaths and+++
$ = $ompressions ( "f the casualty is unconscious with no reathing, start compressions
immediately2 Give 34 compressions+ At a rate of 544 compressions per minute 6appro0 1
compressions per second7+ At 5-3 depth of the casualty8s chest+
D = Defirillation ( "f availale use a defirillator on the casualty as soon as possile+
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"f the casualty is conscious attempt to sit him-her in a
comfortale position and encourage rela0ation and steady
reathing until emergencies arrive+
"t is also vital that the lood flow to your heart is )uic#ly
restored+ /his is usually achieved in one of the following ways9 Fibrinolysis
involves the use of special clot(dissolving medications which
are administered directly into the lood stream+
Angioplasty and stent implantation $oronary angioplasty is a heart attac# treatment that aims to
restore lood flow to the heart y using a special alloon to
open a loc#ed artery from the inside
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Bypass surgery $oronary Artery .ypass Graft 'urgery is an operation in
which lood flow is redirected around a narrowed area,allowing lood to flow more freely to the heart muscle+
Implantable cardiac defibrillators (ICDs) After recovering from a heart attac#, some people may
develop, or e at high ris# of developing, anormal heartrhythms 6arrhythmias7 which could e life(threatening+ "n
some cases, a small device can e implanted in thechest and connected to the heart in order to treat suchan arrhythmia if it occurs+ /his device is called animplantale cardiac defirillator 6"$D7+
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Heart Attack Recovery :odern treatments, along with healthy lifestyle choices, can assist
in recovering from a heart attac# and greatly reduce the ris# offurther heart prolems and relieve or control symptoms such asangina+
/he most important things you can do to reduce your ris# and aidheart attac# recovery are9 /a#e medications as prescried y a doctor .e smo#e free Enoy healthy eating .e physically active $ontrol lood pressure Achieve and maintain a healthy ody weight "f the person affected has diaetes, they should also aim to #eep
their lood glucose levels within the normal non(diaetic range+
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Cardiac rehabilitation /he
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A spectru! of clinical diagnoses co!prisingunstable angina on)0#8MI and 0#8MI thatshare si!ilar pathological features involvingintracoronary thro!bosis
Acute Coronary Syndromes
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ACS: Definition
From:Braunwalds Heart Disease
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Pathophysiology atherosclerosis with superimposed coronary thromosis
'lowly growing high(grade stenoses can progress to completeocclusion ut do not usually precipitate acute '/E:" d-t
collateral circulation
During development of pla)ues, arupt transition can occur,
resulting in
latelet activation /hromin generation
/hromus formation
.lood flow occlusion leads to imalance etween supply and
demand and could lead to myocardial necrosis
ts with non(transmural infarction more li#ely to have more
significan stenosis in "A
>ess severe stenosis with lipid(laden pla)ues and fragile caps
more li#ely to rupture and causing thromsis and '/E:"
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PathophysiologyStable Angina Progressive
narrowing of
coronary lumen Stable fibrous cap
Unstable Angina Progressive
narrowing Acute worsening
of coronary lumen
due to thrombus
formation
NSTEMI Acute worsening ofcoronary lumen due
to thrombus
formation Sub-occlusive/
transient coronary
thrombus withmyocardial necrosis
STEMI inimal prior
narrowing of
coronary lumen Acute rupture of
thin fibrous cap !cclusive
thrombus
formation Acute in"ury
pattern
yocardialnecrosis
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ACS Ea!uation
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Angina Definition: Discomfort in the chest/ choking,
that characteristically comes on with e#ertion$
relieved by rest and/or %&'Favors Ischemic
Origin
Against
Ischemic Origin
Character ConstrictingS(uee)ing
*urning
+eaviness
Dull ache
,nife-lie$ sharp
.abs
Pleuritic
Location SubsternalAnterior thora#
Arms$ shoulders
%ec$ teeth$
nterscapular
0eft submammary area
0eft hemithora#
ProvokingFactors
1#ertion
1#citement
Cold$ meals$ stress
Pain after completionof e#ercise
Pain with movement
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NormalNormalElevated cardiac /n", /n/
or $?(:.Cardiac
Marker
/ wave flattening or
inversion in leads with
dominant wave
Normal E?G
Fi0ed @ waves
Anormal '/ segments or
/ waves not documented to
e new
New or presumaly new,
transient '/ segment
deviation 64+4BmC7 or /
wave inversion 64+1mC7with symptoms
EKG
$hest discomfortreproduced y palpation or
respiration
E0tracardiac vasculardisease
/ransient :, hypotension,diaphoresis, pulmonary
edema or rales
Exam
roale ischemicsymptoms in asence of
the intermediate li#elihood
characteristics
ecent cocaine use
$hest or left arm pain ordiscomfort as chief
symptom
Age 4
:ale gender
Diaetes mellitus
$hest or left arm pain ordiscomfort as chief
symptom reproducing prior
documented angina
?nown history of $AD,
including :"
History
LowIntermediateHig!eat"re
Like#iood tat signs $ sym%toms re%resent an AC& secondary to CAD
.raundwald 5 A
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Chest Pain Classification
Substernal
1#ertional
2elieved with rest
nterpretation! &ypical Angina: 3 criteria from above
! Atypical Angina: 4 criteria from above!%on-Anginal Chest Pain: 5 or less criteria from
above
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Classification of Angina
S&A*01 vs 6%S&A*01
CCS Classification for S&A*01 Angina
! : %o symptoms$ or angina with strenuous e#ertion
! : Slight limitation of ordinary physical activity 7aling more than two blocs$ climbing more than one
flight of stairs brings on angina
! : ared limitation of ordinary physical activity
7aling less than two blocs$ climbing less than oneflight of stairs
! 8: Any physical activity brings on angina9 angina
at rest
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9A70#8MI#H:88 P:I&IPA; P:808#A#I6
2 !inutes
ew)onset Angina ew)onset angina of at least &&0&las III severity
Increasing Angina Previously diagnosed angina thathas beco!e distinctly !orefre*uent longer in duration orlower in threshold %i.e. increased
by = 1 &&0' class to at least &&0&lass III severity
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6S/%S&1 2#
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anagement of 6A/%S&1
medication !#ygen ASA $ clopidogrel Anticoagulant: 6F+$ 07+ %itrates for pain
! %itropatch ;
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Platelet nhibitors in the ACS
@A platelet 'pb/a receptor antagonist
should be administered$ in addition to ASA
and 6F+$ to patients with continuing ischemia
or with other high ris featuresB
@0evel of the evidence: AB
ACC/AA !"i#eline Circ"lation
$%%%&'%$('')*+'$%)
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A%&P0A&101& 2#
C#ass I
De'inite AC& wit contin"ing(ossi)#e AC& Like#y*De'inite AC& Iscemia or +ter Hig,Risk
!eat"res or %#anned (CI
As%irin As%irin As%irin-- --
&")c"taneo"s LM.H I/ e%arinor
I/ e%arin I/ %#ate#et G( II)*IIIa antagonist
--
ACC Slide
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1#ercise Stress &esting
! Positive response: hori)ontal 5mm S& depressionand symptoms
! +igh ris response: Deep S& depression Poor e#ercise tolerance: unable to e#ercise past stage 4 E mins
1#ercise induced hypotension and dysrhythmias! 6ninterpretable:
0*** Digo#in 08+
! Contra-indications: Severe Aortic stenosis Aortic dissection /ACS within 4= h P1
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Angiography
'old standard! Defines anatomy: 58D$ 48D$ 38D$ 0! Assesses 08 function! 'uides treatment: PC$ CA*' or medical therapy
ndications! 6A/post with ongoing pain$ S& depresssion! +emodynamic instability! C+F$ ventricular arrhythmias! Previous PC$ CA*'
! +igh ris non-invasive test! 1merging as the strategy of choice for initial evaluation of mostACS with elevated troponins or 1,' changes
*ased on F2SC $ &AC&CS trials
Strateg, nee#s to be in#ivi#"ali-e#.
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ndications for nvasive 2is Stratification
Strategy in 6A/%S&1
Class ! 2ecurrent ischemia at rest despite medical 2#! 1levated troponin or &!%ew S& depression
! +igh ris findings on non-invasive testing! Depressed 08 function! +emodynamic instability! Sustained 8&! PC within E months! Prior CA*'
n the absence of the above$ either non-invasive orinvasive strategy can be followed mg to allow for buccal absorption
Pain control
! &ry to decrease sympathetic activity! Analgesics! %itrates
Coronary vasodilation$ decrease preload by increasing venouscapacitance
Avoid if suspect 28 infarct
! *eta blocers 2educe +2$ decrease myocardial o#ygen demand 2educe pain 2educe the need for analgesics 2educe infarct si)e
! !#ygen
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S&1 - 2eperfusion
@&ime is muscleB ncreased mortality with delay in reperfusion
regardless of strategy
0ess time:! 2ecovery of 08 systolic f#n! mproved diastolic dysf#n! 2educed mortality
! Post ischemic contractile dysf#n can occur afterreperfusion
! yocardial stunning
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S&1 - 0ytics
*enefits! 2ecanali)e thrombotic occlusion
! 2estores coronary flow
! 2educe infarct si)e! mproves myocardial function
! mproves survival
! ay result in microvascualr damage andreperfusion in"ury
! S&2 strong predictor of reperfusion
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S&1 - lytics
'SS first trial to demonstrate benefit ofstreptoinase
!ther fibrinolytics
! Alteplase t-PA '6S&!
! 2eteplace rtPA '6S&! e(uivalence
! &enecteplase &%, ASS1%& e(uiv with t-PA
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1vidence for Fibrinolysis: 'SS
n K55$;;;
A22: 4I
222: 5I
Circ+ --.
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ASS1%& 4
%L 5EQ=Q
Design: non-inferiority
&rend toward decrease in bleeding
mprove ease of use with *olus infusion
Combination with heparin 8
Lancet5; 01235H(11
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&ime to 2#
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Choosing a Fibrinolytic
Patients in whom t-PA is proven superior to S,:
! Age R>
! Anterior $ presenting within = hours
! +igh ris/e#tensive at other site within = hours
! Cardiogenic shoc
! Previous S, e#posure
&%, L rtPA K tPA
! 1asy administration
! 0ower chance of med error
! 0ess non-cerebral bleeds
Patients in whom S, appears to be e(uivalent to t-PA:! nferior$ posterior or lateral
! at any site after E hours
! Age K R> years
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*leeding complications with 0ytics
a"or bleeding ;-4I
inor bleeding: 5;-4; I
ntracranial hemorrhage: ;-4I
anagement:
! D/C thrombolytic! Cryoprecipitate fibrinogen enriched
! f heparin$ give protamine sulfate
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ndications for Primary PC
Class
! Alternative to thrombolytic if erformed in a timel* fashion 0* skilledindi1iduals
! Patients within 3E hours of A$ with cardiogenic shoc$ R> years
Class a
! Contraindication to thrombolysis Class b
! %S&1 within 54 hours$ with less than & flow in infarctrelated artery
Class
! 1lective PC of non-2A at time of A! *eyond 54 hours of symptoms$ no evidence of ischemia
! Successful thrombolysis
2rom ACC/AHA Guidelines, &'''
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S&1 -PC
eta analyis shows improved clinical
endpoints favoring PC
! Factors to consider
&ime to treatment
2is of S&1
Cardiogenic shoc
,ilip class KL
2is of bleeding
&ime to transport to silled PC center
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S&1 M !ther 2#
ASA! SS-4
&hienpyridines! Clopidogrel
C0A2&G! &iclopidine nhibit binding to adenosine diphosphate receptor
'Pb/a inhibitors! Abci#imab! &irofiban
! 1ptifibatide
'6S&! 8! rtPA vs 5/4rtPA and abci#imab! similar efficace endpoints but increased bleeds with b/a
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ASA: SS 4
3ancet, -..
n K 5R$ ;;;
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S&1 M !ther 2#
+eparin
! reduces reinfarction$ stroe$ P1
! reduces mortality in pts receiving lytic
07+
! ASS1%& showed benefit over 6F+ in pts
receiving &%,
!thers! *ivalirudin +&&
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Post- S&1 2#
** AC1i
! Prevents ventricular remodeling! mproved hemodynamics
! 2educes C+F! Selected population: long-term$ started day 3-5E
SA81 A21 &2AC1
! 6nselected pop short term$ started early 'SS 3 S01 SS-= CCS-5
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Post- S&1 2#
A2*
! !P&AA0 losartan
! 8A0A%& valsartan
Aldasterone antagonists
! 1P+1S6S acute $ 08 dysf#n$ +F
! 2eduction in mortality
Statins! P2!81-&
h i l C li i f
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8ariable 8SD Free 7all2upture
Papillaryuscle 2upture
Age E3 EQ E>
Days$ post 3-> 3-E 3->
Anterior EEI >;I 4>I
%ew urmur Q;I 4>I >;I
&hrill Ges %o 2are
Previous 4>I 4>I 3;I
1cho: 8SD Pericardial1ffusion
Flail leaflet
2
PA catheter: !4 step-up2A-28
1(uali)ation ofdiastolic press;I
Q;I
H
Q;I
=;-Q;I
echanical Complications of
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!ther Complications
Arrhythmias! 1lectrical instability
8P*
8&
8F A82
! Pump failure/inc symp drive Sinus tachy
AFib/Flutter
S8&
! *rady/conduction Sinus brady
.unctional escape
A8*
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!ther Complications
2ecurrent chest pain
! Distinguish reinfarction from recurrent ischemia
from non-ischemic chest pain
Pericarditis
08 aneurysm
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2is Stratification
survival after S&1 depends on
! 08 f#n
Stress/pharma 1cho$ P1&
! 2esidual potentially ischemic myocardium Subma#imal 1&&
! Susceptibility to vent arrhythmias
2i St tifi ti
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2is Stratification
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Discharge Planning
usually > days post S&1
counseling
! ambulation but avoid heavy lifting
! graded activity symptom limited
! 2ehabilitation