Reviewof

Circulatory
System
CARDIOVASCULAR
EMERGENCIES
An Introduction

dr. David D Ariwibowo, Sp.JP

Fakultas Kedokteran
Universitas Tarumanagara
2011

CardiovascularEmergencies
1.
2.
3.
4.

AcuteCoronarySyndrome.
CardiacArrhythmias
CardiacTamponade
AcuteHeartFailure
a.
b.
c.
d.

5.
6.
7.
8.

HypertensiveHeartFailure(HypertensiveEmergency)
AcutePulmonaryEdema
RightVentricularFailure
CardiogenicShock

CardiorespiratoryArrest
Aorticdissection
AcuteLimbIschemic
Etc.

AcuteCoronarySyndrome
1. UnstableAnginaPectoris(UAP)
2. AcuteNonSTElevationMyocardialinfarction

(NSTEMI)
3. AcuteSTElevationMyocardialinfarction(STEMI)

Patophysiology
Atherosclerosis Timeline
Foam
cells

Fatty
streaks

Intermediate
lesion

Atheroma

Fibrous
plaque

Complicated
lesion rupture

Endothelial Dysfunction
From First Decade

Growth mainly by lipid accumulation

Smooth
muscle and
collagen

Thrombosis
hematoma

Deni9on
Normal

Fatty
streak

Fibrous
plaque

Atherosclerotic
plaque

Plaque
rupture/
fissure &
thrombosis

Unstable
angina

NSTEMI
STEMI
Ischemic
stroke/TIA

Clinically silent
Stable angina
Intermittent claudication

Critical leg
ischemia
Cardiovascular
death

Increasing age

Atherothrombosis: a Generalized and Progressive Process

Epidemiology

106
MurrayCJ,LopezAD.Lancet1997;349:12691276

Diagnosis
Presentation
WorkingDx

IschemicDiscomfort
AcuteCoronraySyndrome

ECG

NoSTElevation

Cardiac
Biomarker

UA NSTEMI

FinalDx

UA

NQMI

STElevation

QwMI

Presenta9on
Anginaklasik
Rasa9daknyaman/nyerididaerahsternal>20menit.
Menjalarkelengankiri,leher,rahang,punggung.
Dapatbersifattajam(ditusuk,terbakar)atautumpul(seper9ditekan,diperas).
Disertaikeringatdingin,mual/muntah,kesulitanbernapas,berdebardebar.

AnginaEquivalent
Tidakadanyeri/rasa9daknyamandidadayangkhas.
Gejalagagaljantungmendadak(sesaknapas).
Aritmiaventrikular(palpitasi,presinkop,sinkop)

Presenta9on
FaktorRisiko:
Usia:Tua>Muda
Gender:Lakilaki>Perempuan
RiwayatKeluarga(PJK)
Hipertensi
DiabetesMellitus
PeningkatanKadarKolesterolTotaldanLDL
KadarKolesterolHDLRendah
Obesitas
KurangAk9vitasFisik
Diet:TinggiLemakJenuhdanKolesterol
Merokok

Dieren9alDx
Cardiac

1. Stable Angina
2. MVP
3. Aortic Stenosis
4. Hypertrophic cardio

myopathy
5. Pericarditis

Lungs
1. Lung Emboli
2. Pnemonia
3. Pneumothorax
4. Pleuritis

Gastrointestinal
1.Reflux esofagus
2.Ruptur esofagus
3.Gall bladder disease
4.Peptic Ulcer
5.Pancreatitis

Vascular
1.Aortic dissection

Others
1.Musculoskeletal
2.Herpes zoster

ECG
Todetectischaemicchangesorarrhythmias.
InitialECGhasalowsensitivityforACS.
AnormalECGdoesnotruleoutACS.
ECGisthesoletestrequiredforemergency

reperfusionselection(brinolyticorprimaryPCI).

ECG
AectingallECGfeaturingventricles

ECG
Twavechanges
A.InvertedT
Padaiskemianamunkurang

spesik
PerubahanakhirpadaSTEMI,
terjadisetelahSTelevasikembali
kenormal

C.HyperacuteT
PerubahanawalpadaSTEMI

ECG
STSegmentchanges

A. Withacutesubendocardialischemiatheelectricalforces(arrows)responsiblefortheST
segmentaredeviatedtowardtheinnerlayeroftheheart,causingSTdepressioninV5,which
facestheoutersurfaceoftheheart
B. Withacutetransmural(epicardial)ischemia,electricalforcesaredeviatedtowardouterlayerof
theheart,causingSTelevationintheoverlyinglead.

ECG
A. STdepresion

Bermaknabila>1mmdibawah

garisdasarPTdi99kJ
Ti9kJadalah99kakhirkompleks
QRSdanpermulaansegmenST
BentuksegmenST:
A.

B.

C.

Horizontal
Spesikuntukiskemia.
Downsloping
Palingspesik.
Upsloping
Tidakspesik

ECG
B. STelevation
Occursintheleads
facingtheinfarctionin
theearlystages
SlightSTelevationmay
benormalinV1orV2

ECG
Qwave
Qwavedurationofmorethan0.04seconds(1mm)
Qwavedepthofmorethan1/3ofensuingRwave

ECG
R

R
T

ST

ST

Q S

1minuteafteronset

1hourorso

Afewhours

R
P

ST

P
T

Adayorso

ST

P
T

Laterchanges

Afewmonths

SequenceofchangesinevolvingSTEMI

ECG

ECG
I

aVR

III

aVL

INFERIOR

V4

SEPTAL

LATERAL
II

V1

aVF

AnatomiKoroner&EKG12sandapan
V1&V2menghadapseptalareaLV.
V3&V4menghadapdindinganteriorLV
V5&V6+I&avLmenghadapdindinglateralLV
II,III&avFmenghadapdindinginferiorLV

V2

V3

ANTERIOR
V5

LATERAL
V6

Laboratorium
100

CardiacBiomarkersinSTEMI
Mul9plesofthe
URL

50

Cardiactroponinnoreperfusion

20

Cardiactroponinreperfusion

10

CKMBnoreperfusion
CKMBreperfusion

5
2

Upperreferencelimit

1
0

DaysAherOnsetofSTEMI

URL=99th%9leof
ReferenceControlGroup

Alpertetal.JAmCollCardiol2000;36:959.
Wuetal.ClinChem1999;45:1104.

Penjelasanslidesebelumnya
CardiacbiomarkersinSTelevationmyocardialinfarction(STEMI).Typical

cardiacbiomarkersthatareusedtoevaluatepatientswith
STEMIincludetheMBisoenzymeofCK(CKMB)andcardiacspecic
troponins.Thehorizontallinedepictstheupperreferencelimit(URL)
forthecardiacbiomarkerintheclinicalchemistrylaboratory.TheURListhat
valuerepresentingthe99thpercentileofareferencecontrolgroupwithout
STEMI.ThekineticsofreleaseofCKMBandcardiactroponininpatientswho
donotundergoreperfusionareshowninthesolidgreenandredcurvesas
multiplesoftheURL.NotethatwhenpatientswithSTEMIundergo
reperfusion,asdepictedinthedashedgreenandredcurves,thecardiac
biomarkersaredetectedsooner,risetoahigherpeakvalue,butdeclinemore
rapidly,resultinginasmallerareaunderthecurveandlimitationofinfarct
size.ModiedwithpermissionfromAlpertetal.JAmCollCardiol
2000;36:959andWuetal.ClinChem1999;45:1104.

DiagnosisNomenclature
1. Timingatpresentation:
Acute(07days)

Recent(714days)
Old(>14days)

2. Infarctlocation
Septal,anterior,anteroseptal,anterolateral,anteriorextensive
Inferior,inferolateral,lateral
Posterior,rightventricularinfarct

Example
UAP
AcuteNSTEMI
AcuteAnteriorSTEMI
RecentinferolateralMCI
OldInferiorMCI

AcuteAnteriorSTEMI
Anteriorinfarction

IIIIII

Left
coronary
artery

aVRaVLaVF

V1V2V3

V4V5V6

Penjelasanslidesebelumnya
Location of infarction and its relation to the ECG: anterior infarction
As was discussed in the previous module, the different leads look at different aspects

of the heart, and so infarctions can be located by noting the changes that occur in
different leads. The precordial leads (V16) each lie over part of the ventricular
myocardium and can therefore give detailed information about this local area. aVL,
I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often
show similar appearances to each other. II, aVF and III record the inferior part of the
heart, and so will also show similar appearances to each other. Using these we can
define where the changes will be seen for infarctions in different locations.
Anterior infarctions usually occur due to occlusion of the left anterior descending
coronary artery resulting in infarction of the anterior wall of the left ventricle and the
intraventricular septum. It may result in pump failure due to loss of myocardium,
ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I,
aVL, and V26, with ST depression in II, III and aVF are indicative of an anterior
(front) infarction. Extensive anterior infarctions show changes in V16 , I, and aVL.

AcuteInferiorSTEMI
Inferiorinfarction

IIIIII

Right
coronary
artery

aVRaVLaVF

V1V2V3

V4V5V6

Location of infarction and its relation to the ECG: inferior infarction

ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads
are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the
right circumflex coronary arteries resulting in infarction of the inferior surface of the left
ventricle, although damage can be made to the right ventricle and interventricular septum. This
type of infarction often results in bradycardia due to damage to the atrioventricular node.

AcuteLateralSTEMI
Lateralinfarction

IIIIII

Left
circumex
coronary
artery

aVRaVLaVF

V1V2V3

Location of infarction and its relation to the ECG: lateral infarction

Occlusion of the left circumflex artery may cause lateral infarctions.
Lateral infarctions are diagnosed by ST elevation in leads I and aVL.

V4V5V6

Management
TreatmentDelayedisTreatmentDenied

Symptom
Recognition

Callto
MedicalSystem

PreHospital

ED

CathLab

IncreasingLossofMyocytes
DelayinInitiationofReperfusionTherapy

Management
OnsetofSTEMI
Prehospitalissues
Initialrecognitionandmanagement
intheEmergencyDepartment(ED)
Reperfusion

MONA
Morphin 2- 5 q 5 min titrate to response and side

effects.
O2 Nasal cannula 4 L/mnt
Nitrat: ISDN 5 mg SL 3 times
Aspirin 160-320 mg

Op9onsforTransportofPa9entsWith
STEMIandIni9alReperfusionTreatment
Hospitalbrinolysis:
DoortoNeedle
within30min.

NotPCI
capable
Onsetof
symptomsof
STEMI

911
EMS
Dispatch

EMSonscene

Encourage12leadECGs.
Considerprehospitalbrinolyticif
capableandEMStoneedlewithin30
min.

GOALS

5
min.
Patient

Inter
Hospital
Transfer

EMS
Triage
Plan

PCI
capable

8
EMSTransport
min.
EMS

Dispatch
1min.

Prehospitalbrinolysis
EMStransport
EMStoneedle
EMStoballoonwithin90min.
within30min.
Patientselftransport
Hospitaldoortoballoon
within90min.

GoldenHour=rst60min.

Totalischemictime:within120min.

SelectReperfusionTreatment.
Ifpresentationis<3hoursandthereisnodelaytoaninvasivestrategy,
thereisnopreferenceforeitherstrategy.

Fibrinolysisgenerallypreferred
Earlypresentation(3hoursfromsymptom
onsetanddelaytoinvasivestrategy)
Invasivestrategynotanoption
Cathlaboccupiedornotavailable
Vascularaccessdiculties
NoaccesstoskilledPCIlab

Delaytoinvasivestrategy

Prolongedtransport
Doortoballoonmorethan90minutes

>1hourvsbrinolysis(brinspecicagent)now

SelectReperfusionTreatment.
Invasivestrategygenerallypreferred
SkilledPCIlabavailablewithsurgical
backup
Doortoballoon<90minutes

HighRiskfromSTEMI

Cardiogenicshock,Killipclass3

Contraindicationstobrinolysis,

includingincreasedriskofbleedingand
ICH

Latepresentation

>3hoursfromsymptomonset

DiagnosisofSTEMIisindoubt

PercutaneousCoronaryIntervention(PCI)

CoronaryArteryBypassGraft(CABG)
Surgery

Deni9on(acuteheartfailure)

AHFRapidonsetorchangeinthesigns&symptomsofHF.
NeworworseningofpreexistingchronicHF.
TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

Causes&precipita9ngfactorsofAHF
Theseaetiologies&
conditionsoften
interactshouldbe
identied&
incorporatedintothe
treatmentstrategy.

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

Clinicalpresenta9on
Usuallycharacterizedbypulmonarycongestion
cardiacoutput&tissuehypoperfusionmaydominatetheclinicalpresentation
Reectsaspectrumofconditionspresentinoneof6clinicalcategories.
Figuredemonstratesthepotentialoverlapbetweentheseconditions

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

Clinicalpresenta9on

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

Diagnosis
Basedonthepresentingsymptoms&clinicalndings.
Conrmationbythehistory,physicalexamination,ECG,CXR,echocardiography,

laboratoryinvestigation,withbloodgases&specicbiomarkers.

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

GoalsoftreatmentinAHF

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

Immediategoals
tissueoxygenation&haemodynamicspermit

furtherinterventionsby:

1. Reduceuidvolume&llingpressures.
2. Reducesystemicvascularresistance(SVR)
3. Increasecardiacoutput(CO)

Therapeu9cGoalParameters
Clinical
1.
2.
3.
4.

SBP>90mmHg
Warmextremities
JVP<8cm
Noorthopnea

Hemodynamic
1. SBP
2. SVRI
3. PCWP
4. RAP

>90mmHg
<1200dynescm5
<15mmHg
<8mmHg

Specictreatmentstrategy
basedondistinguishingtheclinicalconditions

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

TwoMinutesAssessmentof
HaemodynamicProle
TheForresterclassicationisbasedonclinicalsigns&haemodynamic

characteristics.
FigurepresentsamodiedfromtheForresterclassication.

Pa9entTreatmentSelec9on

FonarowGC.RevCardiovascMed.2001;2(suppl2):S7S12.

Ini9altreatmentalgorithm

TheEuropeanSocietyofCardiology:Guidelinesforthediagnosisandtreatmentofacuteandchronicheartfailure,2008

AHFtreatmentstrategyaccordingtosystolicBP

TheEuropeanSocietyofCardiology,Guidelinesonthediagnosisandtreatmentofacuteheartfailure,2005

Loopdiure9cs
Inthepresencecongestion&volumeoverload.
ClassI,levelofevidenceB

TheEuropeanSocietyofCardiology,Guidelinesonthediagnosisandtreatmentofacuteheartfailure,2005

Vasodilators

TheEuropeanSocietyofCardiology,Guidelinesonthediagnosisandtreatmentofacuteheartfailure,2005

Inotropicagents

TheEuropeanSocietyofCardiology,Guidelinesonthediagnosisandtreatmentofacuteheartfailure,2005

Syaratdasaruntukhidup
Fungsi
Sirkulasi

Fungsi
Pernapasan

Terganggu

Terganggu

HentiJantung

HentiNapas

Cardiorespiratory arrest
suatu keadaan dimana pasien: tidak sadar, tidak bernafas,
tidak ada denyut nadi

HENTI
NAPAS
HENTI
JANTUNG

Sebab tersering: serangan jantung

Bantuan hidup jantung

Kematian akibat penyakit jantung terutama

disebabkan henti jantung mendadak, dengan

irama terdokumentasi paling sering adalah
ventrikel fibrilasi (VF).
Pertolongan bantuan hidup dasar yang berhasil,
dilakukan dalam 5 menit pertama dengan
bantuan AED
Bantuan hidup jantung merupakan gabungan
pengamatan dan tindakan yang tidak terputus
yang disebut Chain of Survival

Bantuan hidup dasar

Serangkaianusahaawaluntukmengembalikanfungsi
pernafasandanatausirkulasipadaseseorangyang
mengalamihentinaFasdanatauhentijantung.

LANGKAHLANGKAH
Pastikanpenolongdankorbandalamkondisiaman
Tempatkankorbandiatasalasyangkerasdalam

posisitelentang
Lakukanlangkahlangkahalgoritme.

LANGKAH2
Pastikan penolong dan
korban dalam kondisi
aman
Tempatkan korban di atas
alas yang keras dalam
posisi telentang
Lakukan langkah-langkah
algoritme.

CekRespons

Carilahtandatanda

sirkulasi:

Bergerak
Bersuara
Bernapas

Dengancaramenepuk

dengancukupkuat
bahu/dadakorban
sambilmemanggil
korban

AChangeFromABCtoCAB
For adults, children, and infants (excluding the newly born)
The vast majority of cardiac arrests in adults & the highest

survival rates witnessed arrest and an initial rhythm of VF or

pulseless VT.
The critical initial elements chest compressions and early
defibrillation.
In the A-B-C, chest compressions are often delayed while the
responder opens the airway to give mouth-to-mouth breaths,
retrieves a barrier device, or gathers and assembles
ventilation equipment.
In the C-A-B, chest compressions will be initiated sooner and
the delay in ventilation should be minimal (ie, only the time
required to deliver the first cycle of 30 chest compressions, or
18 seconds)

KompresiDada

Tekancepatdankuat
(minimal100x/menit)
(minimaldalamnya5cm)