diagnosi & therapie shock pusbankes 118 compatibility mode]
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7/18/2019 Diagnosi & Therapie Shock Pusbankes 118 Compatibility Mode]
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DIAGNOSIS & TERAPIDIAGNOSIS & TERAPI
SHOCK HYPOVOLEMIK SHOCK HYPOVOLEMIK
PUSBANKES 118PUSBANKES 118
PERSI DIY PERSI DIY
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TUJUAN PELATIHAN :
1. Difinisi & Klasifikasi Shock 2. Menenali Tan!a & Tinka"an Sock
. ena as en$e a oc. Melak'kan Penananan Shock
(. Melak'kan )es'si"asi *ai+an
,. Moni"o+ )es-on Pasien
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Aliran darah yang tidak Adekwat untuk memenuhi
Kebutuhan Jaringan
1. DIFINISI SHOCK
Gangguan perfusi & oksigenasi jaringan akibat
gangguan sirkulasi.
Jika tidak ditangani dengan baik akan berkembangmenjadi Gagal Multi Organ dan akhirnya Kematian.
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1. KLASI/IKASI SH0*K :
1. Shock H$-ooleik : Shock o.k : enurunan !olume intra!askuler3 isal : -e+!a+ahan3 !ehi!+asi
2. Shock Ka+!ioenik :
#. Shock 0%s"+'k"if : Shock o.k : "ambatan aliran darah yg kembali kejantung 4 eno's +e"'+n 53 isal :
Ta-ona!e 6an"'n3 kons"+ik"if -e+ika+!i"is3 "ension -ne'o"ho+aks
. Shock Dis"+i%'"if : Shock o.k : Gangguan !asomotor enaki%a"kan "'+'nn$a S7) !iik'"i *'+ah Jan"'n $an"i!ak a!ek8a" isal : Se-"ic3 S-inal3 Ne+oenic shock.
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#. $anda $anda %hok
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$anda tanda %hok :'edution of (lood )olume
%ymphateti 'edution
'elease )enous*atheolamin 'eturn
+nrease $ahyardia eriperial Arterial
*ardial $ahypnoea )asoonstri "ypotension*ontratility
+nrease 'edution $issue
*ardial O,ygen erfusion
Anaerobi Metabolisme
Myoardial -ailure Aidosis MOF / DEATH
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Tanda / Gejala Shock :
• Gejala Karakteristik Shock :- Takikardi dengan denyut nadi yang lemah-
Penurunan vol. intravaskuler mengakibatkan tidak adekuatnya alirandarah ke Organ Vital yang mencetuskan Hypoksia Jaringan
Summary
- Pucat, kulit dingin dan lembab- Haus yang ekstreem- Urin Output yang menurun( Oligourie )
- Gangguan Kesadaran Transien- Tachypnoea dengan hiperventilasi
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$anda $anda %hok
1. Takikardia
2. Akral dingin
3. Kesadaran ↓
4. Takipnea
5. Tensi ↓
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. Mengatasi enyebab%hok
1. Shock H$-ooleik :
. oc a+ oen :
#. Shock 0%s"+'k"if :
. Shock Dis"+i%'"if :
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Syok ?????? :
• Hypovolumik Shock – Masalahnya : VOLUME Darah
• – Masalahnya : POMPA Jantung
• Distributif Shock [septic; anaphylactic; neurogenic]
– Masalahnya : Pembuluh darahnya
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&. Penananan Shock
1. Penenalan ;an'an Pe+f'si2. Pen enalan De+a a" Shock
#. Penananan Shock
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a. engenalan Gangguan erfusi :
Ini"ial /ormal - 0 *O 1 2 %) "' ' 2 %)'
P = F x R
+mpaired erfusion 2 4O 5 6O* 5 Aidosis5 3eath
3O# 2 *O , *aO# 0 "b , %at , 758 9 a# , 5 1*ompensatory phase 2 3O# ; )O#
3eompensatory phase 2 3O# < )O# = *O , * 0 a>! 1 # ?
+rre!ersible phase 2 3O# @ )O# 0 $issue "ypo,ia5 Met. Anaerobik56atate Aid 5 MO- 1
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TREATMENT CONCEPT OF SHOCKTREATMENT CONCEPT OF SHOCK
ENHANCING PERFUSION / OXYGEN DELIVERYENHANCING PERFUSION / OXYGEN DELIVERY
CardiacCardiacout utout ut
Arterial OArterial O22contentcontent
DO2 = CO x CaO2
ScvO2
Oxygen delivery/DOOxygen delivery/DO22 == HR X SVHR X SV XX Hb X S0Hb X S022 X 1.39 + 0.03 X PaOX 1.39 + 0.03 X PaO
FluidsFluidsTransfuseTransfuse PartiallyPartially
dependent ondependent onFIOFIO22 andand
pulmonarypulmonarystatusstatus
Inotropes :Inotropes :••DopaminDopamin
••DobutaminDobutamin
••NorepinephrinNorepinephrin
••EpinephrinEpinephrin
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4 Kelas shock :
1. Kelas 1 : <15% EBV
Tensi N
%. engenalan 3erajat %hok
. e as : 15- %
3. Kelas 3 : 30-40% EBV
4. Kelas 4 : > 40 % EBV
EBV = Estimate Blood Volume70-100 CC/Kg bb
Tensi
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KLAS / DERAJAT SYOK
I II III IVDarah hilang /
(cc)
< 750 750-1500 1500-2000 >2000
Darah hilang / % BV < 15 15 -30 30 - 40 > 40
Nadi <100 >100 >120 >140
TD N N ↓↓↓↓
16
Pulse Pressure NRespirasi 14 - 20 20 - 30 30 - 40 >35
Pruduksi
urin/cc
> 30 20 - 30 5 - 15 tak ada
Kesadaran agak gelisah gelisah gelisah &bingung
bingung &letragi
Cairan
pengganti
Kristaloid Kristaloid Kristaoid
+darah
Kristaloid +
darah
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Klas I
750 mL BVL750 mL BVL
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Klas II 750750 –– 1500 ml BVL1500 ml BVL
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Klas III15001500 –– 2000 ml BVL2000 ml BVL
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Klass IV Perdarahan≥ 2000 ml ≥ 2000 ML BVL≥ 2000 ML BVL
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. enanganan %yok : A < Ai+8a$ = ce+ical con"+ol
> < >+ea"hin = 0ksienasi
* < *i+c'la"ion = K0NT)0L PE)DA)AHAN
21
D < Disa%ili"$ E < E?-os'+e
@ N;T3 ka"e"e+
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Penanganan Shock :
Tindakan Utama dalam pengobatan Shock :
•A = Jalan nafas terjaga dan fraktur servikal tersingkirkan
Summary
• B = Memelihara Ventilasi Adekwat Kontrol Perdarahan
• C = Pergantian Volume cairan Segera & Adekwat
• D = Restorasi perfusi jaringan dengan melihat LOC
• E = Buka & Cari sumber / cedera lain= Penanganan penyakit dasar atau cedera yang mendasari= Pasang NGT, Kateter Urin
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rinsip enanganan1.1.KenaliKenali shockshock
2.2. SebabSebab shock :shock :hemorrhagichemorrhagic
non hemorrhagicnon hemorrhagic
3.3. TerapiTerapi ::
== stop bleeding !stop bleeding !== perbaikanperbaikan volumevolume yangyang hilanghilang
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Terapi shock : Stop bleeding
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enanganan "ypo!olemik %hok:
0ksien : Meani-'lasi 2 !i-lasa.
In"+aasc'la+ : Meninka"kan 7ol. Si+k'lasi Eleasi kaki # B Meninka"kan 7eno's )e"'+n
.
K+is"aloi! 1 2 l C 11( . 4In"+aasc'la+</5
*ai+an A!ek8a".
Moni"o+in H)3 *i+c'la"ion -e+i-he+al3 >P C (1 3
Ka"e"e+ U+in
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$ujuan akir terapi :
'espon asien :
"' ; bermakna dibanding (
!aluasi erfusi : @ 4O5
@ %irkulasi eriper5
@
Metaboli : @ Aidosis Metaboli
@6atate
$)% : reload. !aluasi : *O5*+56A5 AO56)%)B+
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SHOCK PHASE
5. RESUSITASI CAIRAN PADA SHOCK
Pergantian cairan pada shock merupakan hal yang esensial / penting untukpemulihan Sirkulasi dan Stabilisasi hemodinamik. Karena pada difisit yang
melebihi 20 % dapat dengan mudah berakir sebagai shock progresif
Hypovolemik shock Segera diganti volume Adekwat dan Cepatsebagai terapi kausatif.
Summary
Cardiogenik shock Penggantian cairan dibawah pengawasanketat
Venovasodilatory shock Penggantian volume adekwat, terapi vasopressor
(septic, neurogenic,anaphylactic types)
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Peranan terapi cairan :
• Primer Penggantian volume
• Preload Mengisi Intra vascular
• Balanced ( CIS , CES )
• Ter antun OP & Permiabelitas
• Crystalloid Isotonic (metabolism cell ? )
• Colloid ( + / - )
• Balances Approach = 1000 cc crystalloid + 500 cc colloids
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'esusitasi airan : )olume
In"+aeno's line -akai $an %esa+ < 2 6al'+ @ a%il sa-le !a+ah *+oss Ma"ch
@ anak : in"+aoseo's
29
*ai+an !-" !ihana"kan < ) L C D(F C Na*l 3GF Kece-a"an -e%e+ian < '$'+3 %isa !i'lan
T+ansf'si :
@ !e+ 2 .. M'nkin @ !e+ # .. Pas"i
@ !e+ .. M'"lak3 ha+'s
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BLO
OD
RL
RA
NaCl 0.9 %
NaCl 3 %
Albumin
Plasma
Dextran
Gelatin
HES
COLLOIDCRYSTALLOID
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Mau diganti seberapa ?
Crystalloid = 4.1 x hilangnya darah
• Colloid = 1.4 x hilangnya darah
Jika kehilangan darah ~1,400mLPikirkan Ganti Darah
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Volume darah : 7% BB (70 cc/kgBB)Volume darah : 7% BB (70 cc/kgBB)
Penderita 70 kg, shock, tensi sudah turun :
- Vol. Darah= 70 X 70
= 4900 cc
- Kehilangan darah minimal =
30% X 4900 cc = ± 1500 cc
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Profil kompartment :
• Hypovolaemic shock :• Absolute dehydration
#C
.:
+ntra!a
• Septic shock
• Intra vascular <
• Interstitial >• Intracellular > :
C
7:
7C
/ormal
s&
+ntersti
siil
+ntrasel
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Akses )ena :
Akses !ena : bisa langsung pasang # jalur
@ ena -e+ife+
@ ena seksi 4 eno's c'"!o8n 5
35
@ in"+a ose's 4 , "h 5 @ ena sen"+al 4 J''le+3 /eo+al3 S'%claia 5
*airan :
@ )ine+ Lak"a" C Na*l 3GF
@ 1 2 li"e+ 4 2 cc k >> 5
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Terapi shock : Akses vena
Vena periferVena perifer
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Terapi shock : Akses vena
Vena perifer (v. jugularis eksterna)Vena perifer (v. jugularis eksterna)
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Terapi shock : Akses vena
IntraIntra--oseusoseus
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Terapi shock : Akses vena
Vena SectieVena Sectie
VenoVeno--clysisclysis
Venous utVenous ut--downdown(VC)(VC)
Di depanDi depan
Mall.medialisMall.medialis
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Terapi shock : Akses vena
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Terapi shock : Akses vena
V.SubklaviaV.Subklavia
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Terapi shock : Akses vena
V.Jugularis internaV.Jugularis interna
6 MONITOR
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6. MONITOR
RESPON PASIEN :
PENGARUH PENGGANTIAN CAIRAN PADA
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PENGARUH PENGGANTIAN CAIRAN PADA
PERFUSI JARINGAN DAN FUNGSI ORGAN
cardiacoutput
tissueperfusion
bodycontrol
O2 supply
Summary
volume
replacement
metabolism
diuresisSHOCK PHASES
Respon thd resusitasi cairan
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Respon thd resusitasi cairan
(RL 2000cc/20-0cc per K!""# $0-$%&'
Responcepat
Respontransient
Responnegatif
Tanda vital kembalinormal
Perbaikansementara
tetapburuk
Darah 10 - 20 % 20 - 40 % 40 %
45
ang er angsung
!ebutuhancairantambahan
"arang sering sering
Transfusi "arang sering#perlu segera$perasi mungkin mungkin
sekalisangatmungkin
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ResponRespon CepatCepat
Bila kehilangan darah <20 %
Respon terhadap resusitasi cairan
RESPON TERAPI
Konsultasi Bedah
Tetap dilanjukan monitor
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RESPON TERAPI ResponRespon SementaraSementara
Bila kehilangan darah 20% -40%
Evaluasi, Konsultasi Bedah
Resusitasi Cairan lanjut, pikirkan darah
Perdarahan berlanjut : Operasi !!!!!!!!!
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RESPON TERAPI
ResponRespon Minimal :Minimal : Perdarahan > 40%
a erespon ter a ap resus tas ca ran Segera konsultasi Bedah
Singkirkan Dx Shock Non hemorrhagi Segera operasi eksplorasi
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Reevaluasi Perfusi Organ :
MonitorMonitor Tanda Vital
Perfusi Kulit
UOP
Pulse oximetry
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Evaluasi terhadap ResusitasiProduksiProduksi UrinUrin / jam : / jam :
Tidak adekwatnya UOP berarti
Tidak adekwatnya resusitasi
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Asam Basa Abnormal
Monitor dengan ABGs ( Astruff )
Penyebab Umum
•
adekwatnya PerfusionPerfusion• Anak : Asidosis biasanya disebabkan tidak
adekwatnya VentilationVentilation
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Abnormalitas Asam
Basa
Tx
• Oksigenasi dan ventilasi
•• Stop the bleeding !Stop the bleeding !• Biasanya inadekwat volume restorasi
Bikarbonat bukan indikasi
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Thank youTerima kasih banyaksr_rahardjo @ yahoo.sg
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BENTUK SHOCK YANG SERING :
TIpe Shock Penyebab
Hypovolumic Shock Kehilangan cairan > 20 %
Summary
Cardiogenic Shock
mis : myocardial infarction
Septic Shock Sepsis karena infeksi dan toksin
Neurogenic ShockCedera kepala , Cedera Otak –
Medula Spinalis
Anaphylactic Shock Kontak berulang dengan antigen
Diagnosis :
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KOMPONEN SELULER DARAH
leucocyte
Diagnosis :
Summary
eryt rocyte
thrombocyte
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%umber perdarahan :
)ona Da!a )ona Pe+'"
58
Pelis Pa"ah T'lan Pan6an
Pe+!a+ahan ke-ala < JJJ
"DO)O6M+K %"O*K :
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"DO)O6M+K %"O*K :
• Medical • Cholera • Surgical
• Acute Adrenal Ins.
• Heat Stroke
• ayor trauma
• Mayor burns
• Massive surgery
• Crush Injury
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E.
GAMBARAN KLINIK
GAMBARAN KLINIK
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Faktor Penentu Curah Jantung
PREE LOAD HEART RATE
CVP
CARDIACOUT PUT
AFTER LOADCONTRACTILITY
PAOP
EF
LVSV SVR
F. REAKSI TUBUH TERHADAP
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SHOCK HIPOVOLEMIK :
- Penurunan Sementara TD sebagai respon terhadap kejadian- Stimulasi Simpatis (Terbebasnya Catecholamines )
- Takicardia
I. Fase Inisial atau Kompensasi - Macrosirkulasi.
Summary
-
- Vasokonstriksi Venous return meningkat (Vena > 50% vol. darah )- Meningkatnya Tekanan Diastol
- Manifestasi klinis fase ini :
- Takikardi, Takipnoe, Gelisah, Kulit pucat, dingin
- Pengisian kapiler lambat ( > 2 detik )
Centralization
F. REAKSI TUBUH TERHADAP
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SHOCK HIPOVOLEMIK :II. Fase Decompensasi atau Progresif - Microsirkulasi
Pada stadium ini terjadi kegagalan dari mekanisme kompensasi untukmempertahankan perfusi jaringan
- Vasodilatasi Mengakibatkan turungnya TD
Summary
- Konstriksi Pre- and post-capillary- Penuruanan tekanan Kapiler
- Penurunan outflow cairan
- Peningkatan influks cairan
- Perburukan fungsi Organ Vital
Oncotic effect
F. REAKSI TUBUH TERHADAP
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SHOCK HIPOVOLEMIK :III. Fase Final atau Fase Ireversibel
Pada Fase ini terjadi
- Penurunan Curah Jantung ,
Summary
- Tekanan darah yang bermakna.
- Stagnasi aliran darah
- Pada stadium ini terjadi gagal organ
- Dan diakiri dengan Kematian Organ
PENGARUH PENGGANTIAN CAIRAN
Grafik Hypovolemik Shock yang tidak
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Grafik Hypovolemik Shock yang tidak
mendapatkan penanganan
Bleeding
Heart ratemin
Blood pressure mmHg
•150
•100
Summary
Decompen-sation
Compen-sation
Irreversi-bility
Three Shock phases
• 50
• 0
Bloodpressure
MKA/+%M "OMO%$A%+%
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MKA/+%M "OMO%$A%+%
3"+3'A$+O/ E %"O*K
)EDU*E >0D /LUID 70LUME
%tress +nrease Osmol
Kidney "yphophyse
os eron
'eabsorbsi /a Bater abs.
(ody -luid )olume
Osmol
A3"
+nrease 4rine roduti!itas E dilute
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%$A'6+/G -O'* : ergerakan *airan 2 K =0 >ππππ i 1 > 0 i > ππππ 1 ?
K 2 *oefisien Kapiler 2 $ekanan "ydrostatik Kapiler
ππππ i 2 $ekanan Koloid Osmotik +nterstisielππππ 2 $ekanan Koloid Osmotik Kapiler
Artery2 +ntra!asular ke +nterstisiel )ena 2 +nterstisiel ke +ntra!asular
FLUID EXCHANGE
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CAPILLARY BED atau MICROCIRCULATION
Arterioles and arterial
Venules and venouspart of capillaries
par o cap ar es
MlCROCIRCULATION
PERPINDAHAN CAIRAN
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TRANSKAPILERPada kapiler bed (microcirculation) Tek. Darah ( BP ) danTek. Oncotic ( OP ) bekerjasaling berlawanan
OP pada kompartement interstisiel konstan berkisar = 25 mm Hg.BP, akan turun ketika melewati kapiler pada ujung arteri = 35 mmHg
pada awal vena = 15 mm HgPerbedaan tekanan ini meru akan tekanan endoron Net in - and outflow dari
Summary
35 mm Hg 25 mm Hg 15 mm Hg
Arterial end Venous endBlood pressurein the capillarydrops during
passage
net outflow net inflow
cairan antara kapiler dan kompartemen interstisiel.
Gangguan keseimbangan tersebut akan mencetuskan edema atau dehidrasi.
.
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Sympatomimetik Endogen & Eksogen
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y p g g
MACAM OBAT KERJA OBAT
α 1 α 2 β 1 β 2
DOSIS
Katekol Amin Endogen
Epinephrin
Norepinephrin
Dopamin
ν
ν
ν
ν
ν
ν
ν 0,001-0,003mcg/kgBB, > 0,003 α 1 dominan
0,01 -0,02 mcg/kg
2 - 5 mcg renal dose
- mcg no rop
> 10mcg α 1 dominant
Katekol Amin Eksogen
Isoproterenol
Dobutamin
ν
ν
ν ν
ν
ν
ν
0,01 – 0,05 mcg
5-20 mcg, > 10 mcg vasodilatasi
Non Katekolamin
Ephedrin
Phenylephrin
Mathoxyamin
Vasopressin
Angiotensin
ν
ν
ν
ν
ν
ν
ν
ν
ν
ν
ν
ν
ν
ν
Ν
5-50 mg
5-10 mg
5 – 10 IU
%$+* %"O*K :
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%$+* %"O*K :
*a'ses : Infec"ion C Se-"ic
+ + '
o+ *ell'la+ Daae!
A$O-+%+O6OG+* :
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A$O-+%+O6OG+* :
Inc+ease! ca-illa+$ -e+ea%ili"$ /l'i! E?"+aasa"ions
@
@ Hi-e+ol'e : In"e+s"i"ial & In"+acell'la+
Daae *ell : P+ie+ = Sec'n!e+
In"+aasc'la+ /l'i!
PATOFISIOLOGI SEPTIC SHOCK
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PAT0/IS0L0;I SEPTI* SH0*K
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(A*$'+
'6A% M3+A$O' $/- αααα +nterleukin
*ahetine "istamine
ββββ endorphin * omplement
*6+/+*A6 %D/3'OM-e!er )asodilatation ''
( derease5 / inrease
"D'3+/AM+* '%O/%
*+'*46A$+/G "4MO'A6 -A*$O'
MDO*A'3+A6 3'%+O/ -ator
"DO3+/AM+K '%O/
(+)/$'+*46' 3+%-4/*$+O/
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Clinical Presentation Septic Shock
• Two phases:Two phases:Two phases:Two phases:
1. “ Warm ” Shock. ( Early phase )
• yper ynam c response,VASODILATION
2. “ Cold ” Shock. ( Late phase )
• Hypodynamic response• DECOMPENSATED STATE
Clinical Manifestations
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– Massive vasodilatation
– Pink, warm, flushed skin
– Decreased SVR*
– Increased CO & CI
EARLY HYPERDYNAMIC STATE ( COMPENSATION ) “
– Increased Heart Rate Full
bounding pulse – Tachypnoea
– SvO2 will be abnormally
high – Crackles
Clinical Manifestations
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– Vasoconstriction – Skin is pale & cool –
LATE HYPODYNAMIC STATE ( DE COMPENSATION )
– Decreased BP
– Change of LOC
– Increased SVR – Decreased CO – Decreased UOP
– Metabolic & RespiratoryAcidosis with Hypoxemia
SEPSIS
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• Systemic Inflammatory Response (SIRS) to
Infection manifested by two or > of following:
– Temp > 38,5 or < 36 centigrade
– HR > 90 – RR > 20 or PaCO2 < 32
– WBC > 12,000/cu mm or > 10% Bands (immature)
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3iagnosis :1. /ee+ #, o+ #3(
2. Dec+ease L0*#. Tach$-noeC >+a!$-noe
. Tach$ca+!ia
(. H$-o"ension
,. Th+o%oc$"o-enia
O. Le'koc$"e 1( o+ #(. /ocal infec"ion.
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$herapy: *a'sa"ie : /in! & kill "he so'+ce of infec"ion 4 D+ainae30- 5 A--+o-+ia"e! An"i%io"ics
S'--o+"ie : 7en"ila"ion & 0?$ena"ion 4 Ma?. D02 5
/l'i! +es'sci"a"ion
N'"+i"ional S'--o+" *0
P+eloa! : 7ol'e Af"e+ loa! : 7asocons"+ic"ion3 !ila"a"ion
*on"+ac"ili"$ : Ino"+o-ic D+'s : S"e+oi!3 I'nolo%'line *on"+ol co-lica"ion : DI*3M0DS
ENDP0INT OF
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RESUSCITATION
• MACRO CIRCULATION.• Relief COMPENSATION State.
• Reverse NORMAL.
• MICRO CIRCULATION.• Decrease Lactate concentration
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COLLABORATIVE MANAGEMENT
• Prevention !!!
• Find and kill thesource of the
• Maximize O2 deliverySupport
• Fluid Resuscitation• Vasoconstrictors
• Inotropic drugs
• Nutritional Support
• Comfort & Emotionalsupport
In summary,
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Treatment of Septic Shock
• Identify the patient at high risk for shock
• Control or eliminate the cause
•
perfusion• Correct acid base imbalance
• Treat cardiac Arrhythmia
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CARDIOGENIC SHOCK
• Causes : Heart Diseases – SBP < 90 mmHg
–
• OUP < 20 cc/h ( 1/2 cc/kg/h )• Coronary BF⇒ Arrhythmia⇒ Heart Lactate
• Others Stress responses
• Others Shock sign
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*auses :
*oon *a'ses MI 4 1( F < 5 )isk /ac"o+ : Ae3 0%ese3 MI
a+ oen c oc :
@ M$o-a"h$ *S :
AMI3 Hea+" Dila"e!3 MD/ on Se-"ic shock
@ Mechanical *S :
M)3 7SD3 Ane'+$s 7en"+icle3 Lef" 7en"+icle/lo8 o%s"+'c"ion
C di i Sh k
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Cardiogenic Shock
• Decreased Contractility
• Increased Filling Pressure
• ecrease
• Decreased LV Stroke Work
• Increased SVR ( Compensatory )
3i i
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3iagnosis : Ne'+oho+ones +es-onse :
@ H) 3TD 3 *on". 3 *M)2 3 *on" 3 *0 3 *S
*I 13 lCQC23 S7)
E!ea L'n : P*RP3 L7EDP
M0D3 Me". Aci!osis3 H$-o"he+ic3 *oa3.
@ D$s-noe3 *$anosis3 c+e-i"a"in
@ EP 4 5 :
)a!iolo$ L'n E!ea ⇒ P*RP
Hi-ooloia. P*RP 2 H
$h i
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$herapies :
Inc+ease! f'nc"ion Lef" 7en"+icle
S'--o+"ie : Pain 3 Me"a%olic3 Elec"+ol$"e3 A++h$"hias3 )es-. S'-
a es aeo $na c
Ma?ialisasion 2 S'--l$ Dean!$oca+!ial
Cardiogenic Shock
M t
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Management
• Treat Arrhythmias
• Diastolic dysfunction may require increase fillingpressure
• Vasodilators if not hypotension.
• Vasopressor if hypotension to raise diastolicpressure
• Inotrope administration
• Mechanical assistance
• Consultation
"3 M t
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"3 Management :
Inasie oni"o+in3 A+essiel$ "he+a-ies.
P*RP 1 H: 3
D+'s : Dec+ease! P+eloa!
P*RP 1 H *oon Sin *a+!ioenic Shock
Dec+ease! P*RP
D+'s = Mechanical *i+c'la"o+$ Assis"ance
M it i
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Monitoring :
A line :
*en"+al 7eno's *a"he"e+ 4 *7P 5
3 3 3 3 e+ 's on3
EK;3 Hea+" En$e 3 A;D3 Lac"a"e
S8an ;an.
Echoca+!io+a-h$
3
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3rugs :
*ate&holamine : Inc+ease! A+"e+$ P+ess'+e & *o+ona+$ Pe+f'sion3*on"+ac"ili" Hea+" )a"e S7)
Inc+ease! A+"e+$ P+ess'+e sho'l! %e inc+ease! D2
Inc+ease! A+"e+$ P+ess'+e : Po"en"ial A++h$"hia
3opamine :
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3opamine : 1 ( cCk >RCQ : )enal & esen"e+ic
( 1 cCk >RCQ : Ino"+o-ic
1 : α a!+ene+ic 4cons"+ic"s5
β a!+ene+ic Lo8 !ose inial effec" H) & S7)
Dec+ease! P ena3 S7) H$-o"ension3 H)
)ane !ose 2 cCk >RCQ
3igo,in :
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+nrease $oca+!ial con"+ac"ili"$.
0nse" .
Less effec"ieness as ino"+o-ic *S
Dec+ease M$oca+!ial con"+ac"ili"$Dec+ease *o+ona+$ 02 cons'-"ionInc+ease *o+ona+$ Pe+f'sion P+ess'+e
Dec+ease L'n E!ea
Me&hani&al *ir&ulatory Assistan&e :
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Me&hani&al *ir&ulatory Assistan&e : Mechanic ci+c'la"ion assis"ance.
H$-o"ension & Shock 4!+'s +esis"ance 5 :
1. IA>P 4 In"+a A+"e+$ >allon P'- 52. 7AD 7en"+icle Assis" Deice
%pe&ifi& : S'+ical +e asc'la+.
7ale *o++ec"ion 4 MI3MS53*los'+e C Lia"ion 4 7SDCASD3 PDA 5
rognosis :
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rognosis :
Un!e+l$in !isease
Ino"+o-ic
ec an c +c' a on ss s ance.
)e asc'la+ O F
IA>P ( F
Key Point
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Key Point
Diagnosis Goals in Shock :
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Diagnosis Goals in Shock : • Abnormally Low Organ Perfusion
• Usually associated with decrease ( BP )• Sign Organ Hypo perfusion:
• .
• Acidosis.
• Oligurie. ( Discuss the differential diagnosis of oligurie )
• Define Mayor Type of Shock & Principle of Management.
• Review : Fluid Resuscitation, Inotropes, Vasopressors
• Address the balances of O2 Supply-O2 Demand.
Therapeutic Goals in Shock
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Therapeutic Goals in Shock.
• Increased O2 delivery
• Optimize O2 content of Blood
• mprove
• Match systemic O2 needs & O2 Delivery
• Reverse/Prevent organ hypo perfusion
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