Diagnosi & Therapie Shock Pusbankes 118 Compatibility Mode]

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



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



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.



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.



#. $anda $anda %hok



$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



7



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



$anda $anda %hok

1. Takikardia

2. Akral dingin

3. Kesadaran ↓

4. Takipnea

5. Tensi ↓



. Mengatasi enyebab%hok

1. Shock H$-ooleik :

. oc a+ oen :

#. Shock 0%s"+'k"if :

. Shock Dis"+i%'"if :



Syok ?????? :

• Hypovolumik Shock – Masalahnya : VOLUME Darah

• – Masalahnya : POMPA Jantung

• Distributif Shock [septic; anaphylactic; neurogenic]

– Masalahnya : Pembuluh darahnya



&. Penananan Shock

1. Penenalan ;an'an Pe+f'si2. Pen enalan De+a a" Shock

#. Penananan Shock



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



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



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



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



Klas I

750 mL BVL750 mL BVL



Klas II 750750 –– 1500 ml BVL1500 ml BVL



Klas III15001500 –– 2000 ml BVL2000 ml BVL



Klass IV Perdarahan≥ 2000 ml ≥ 2000 ML BVL≥ 2000 ML BVL



. 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+



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



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



Terapi shock : Stop bleeding



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



$ujuan akir terapi :

'espon asien :

"' ; bermakna dibanding (

!aluasi erfusi : @ 4O5

@ %irkulasi eriper5

@

Metaboli : @ Aidosis Metaboli

@6atate

$)% : reload. !aluasi : *O5*+56A5 AO56)%)B+



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)



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



'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



BLO

OD

RL

RA

NaCl 0.9 %

NaCl 3 %

Albumin

Plasma

Dextran

Gelatin

HES

COLLOIDCRYSTALLOID



Mau diganti seberapa ?

Crystalloid = 4.1 x hilangnya darah

• Colloid = 1.4 x hilangnya darah

Jika kehilangan darah ~1,400mLPikirkan Ganti Darah



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



Profil kompartment :

• Hypovolaemic shock :• Absolute dehydration

#C

.:

+ntra!a

• Septic shock

• Intra vascular <

• Interstitial >• Intracellular > :

C

7:

7C

/ormal

s&

+ntersti

siil

+ntrasel



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



Terapi shock : Akses vena

Vena periferVena perifer




Vena perifer (v. jugularis eksterna)Vena perifer (v. jugularis eksterna)




IntraIntra--oseusoseus




Vena SectieVena Sectie

VenoVeno--clysisclysis

Venous utVenous ut--downdown(VC)(VC)

Di depanDi depan

Mall.medialisMall.medialis




V.SubklaviaV.Subklavia




V.Jugularis internaV.Jugularis interna

6 MONITOR



6. MONITOR

RESPON PASIEN :

PENGARUH PENGGANTIAN CAIRAN PADA



PENGARUH PENGGANTIAN CAIRAN PADA

PERFUSI JARINGAN DAN FUNGSI ORGAN

cardiacoutput

tissueperfusion

bodycontrol

O2 supply

Summary

volume

replacement

metabolism

diuresisSHOCK PHASES

Respon thd resusitasi cairan



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



ResponRespon CepatCepat

Bila kehilangan darah <20 %

Respon terhadap resusitasi cairan

RESPON TERAPI

Konsultasi Bedah

Tetap dilanjukan monitor



RESPON TERAPI ResponRespon SementaraSementara

Bila kehilangan darah 20% -40%

Evaluasi, Konsultasi Bedah

Resusitasi Cairan lanjut, pikirkan darah

Perdarahan berlanjut : Operasi !!!!!!!!!



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



Reevaluasi Perfusi Organ :

MonitorMonitor Tanda Vital

Perfusi Kulit

UOP

Pulse oximetry



Evaluasi terhadap ResusitasiProduksiProduksi UrinUrin / jam : / jam :

Tidak adekwatnya UOP berarti

Tidak adekwatnya resusitasi



Asam Basa Abnormal

Monitor dengan ABGs ( Astruff )

Penyebab Umum

•

adekwatnya PerfusionPerfusion• Anak : Asidosis biasanya disebabkan tidak

adekwatnya VentilationVentilation



Abnormalitas Asam

Basa

Tx

• Oksigenasi dan ventilasi

•• Stop the bleeding !Stop the bleeding !• Biasanya inadekwat volume restorasi

Bikarbonat bukan indikasi



Thank youTerima kasih banyaksr_rahardjo @ yahoo.sg



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 :



KOMPONEN SELULER DARAH

leucocyte

Diagnosis :

Summary

eryt rocyte

thrombocyte



%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 :



"DO)O6M+K %"O*K :

• Medical • Cholera • Surgical

• Acute Adrenal Ins.

• Heat Stroke

• ayor trauma

• Mayor burns

• Massive surgery

• Crush Injury



E.

GAMBARAN KLINIK

GAMBARAN KLINIK



Faktor Penentu Curah Jantung

PREE LOAD HEART RATE

CVP

CARDIACOUT PUT

AFTER LOADCONTRACTILITY

PAOP

EF

LVSV SVR

F. REAKSI TUBUH TERHADAP



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




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




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



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%+%



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



%$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



CAPILLARY BED atau MICROCIRCULATION

Arterioles and arterial

Venules and venouspart of capillaries

par o cap ar es

MlCROCIRCULATION

PERPINDAHAN CAIRAN



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.

.



Sympatomimetik Endogen & Eksogen



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 :



%$+* %"O*K :

*a'ses : Infec"ion C Se-"ic

+ + '

o+ *ell'la+ Daae!

A$O-+%+O6OG+* :



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



PAT0/IS0L0;I SEPTI* SH0*K



(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/



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



– 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



– 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



• 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)



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.



$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



RESUSCITATION

• MACRO CIRCULATION.• Relief COMPENSATION State.

• Reverse NORMAL.

• MICRO CIRCULATION.• Decrease Lactate concentration



COLLABORATIVE MANAGEMENT

• Prevention !!!

• Find and kill thesource of the

• Maximize O2 deliverySupport

• Fluid Resuscitation• Vasoconstrictors

• Inotropic drugs

• Nutritional Support

• Comfort & Emotionalsupport

In summary,



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



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



*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



Cardiogenic Shock

• Decreased Contractility

• Increased Filling Pressure

• ecrease

• Decreased LV Stroke Work

• Increased SVR ( Compensatory )

3i i



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



$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



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



"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



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



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 :



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 :



+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 :



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 :



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



Key Point

Diagnosis Goals in Shock :



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



Therapeutic Goals in Shock.

• Increased O2 delivery

• Optimize O2 content of Blood

• mprove

• Match systemic O2 needs & O2 Delivery

• Reverse/Prevent organ hypo perfusion

Diagnosi & Therapie Shock Pusbankes 118 Compatibility Mode]

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