Modul

SYOK
 DEFINI
SI
Gangguan dari perfusi jaringan yang
terjadi akibat adanya
ketidakseimbangan antara suplai
oksigen ke sel dengan kebutuhan
oksigen dari sel tersebut.
Semua jenis syok mengakibatkan
gangguan pada perfusi jaringan yang
selanjutnya berkembang menjadi gagal
sirkulasi akut atau disebut juga
sindroma syok
IT IS NOT LOW BLOOD PRESSURE !!!
IT IS HYPOPERFUSION..
Shock Categories

Cardiogenic
Hypovolemic
Distributive
Obstructive
 Shock
Always a symptom of primary cause
Inadequate blood flow to meet tissue
oxygen demand
May be associated with hypotension
Associated with signs of hypoperfusion:
mental status change, oliguria, acidosis
 Cardiogenic Shock

Decreased contractility
Increased filling pressures,
decreased LV stroke work, decreased
cardiac output
Increased systemic
vascular resistance compensatory
 Hypovolemic
Shock
Decreased cardiac output
Decreased filling pressures
Compensatory increase in
systemic vascular resistance
 Distributive Shock

Normal or increased cardiac output

Low systemic vascular resistance
Low to normal filling pressures
Sepsis, anaphylaxis, neurogenic,
and acute adrenal insufficiency
 Obstructive Shock

Decreased cardiac output

Increased systemic vascular
resistance
Variable filling pressures
dependent on etiology
Cardiac tamponade, tension
pneumothorax, massive
pulmonary embolus
PATOFISIOLOGI DARI RESPON
TUBUH TERHADAP SHOCK
Respon Neuroendokrin
Respon Hemodinamik
Respon Metabolik

9
Mekanisme untuk memperbaiki
keseimbangan
kardiovaskuler
Redistribusi aliran darah

Peningkatan cardiac output

Memperbaiki volume intravaskular

10
EFEK SHOCK PADA TINGKATAN ORGAN

Kidney
Oliguric renal failure
High output renal failure

Liver
Liver failure

GI tract
Failure of intestinal barrier (sepsis, bleeding)

Lung
Capillary leak associated with or caused by sepsis and
infection

11
Clinical Differentiation Shock

Hemorrhagic Shock
Non Hemorrhagic
Shock
Cardiogenic
Tension pneumothorax
Neurogenic
Septic
Anaphylactic

12
HEMORRHAGIC
SHOCK
 .Syok Perdarahan
Paling sering terjadi terutama
pada kasus trauma

Dijelaskan secara khusus pada

Modul 5 (Terapi Cairan 1)

14
NON HEMORRHAGIC
SHOCK
 Cardiogenic Shock
Myocardial dysfunction
Blunt cardiac trauma
Cardiac tamponade
Tachycardia
Blowing heart sound
Air embolism
Venectasia regio colli
Valve rupture
Hypotension
ECG monitoring
Isoenzynme-CPK od
o
Echocardiography
bl e
e d th
i sh to t ng n
in rn ar pi i o
im etu he m ct
D r n
u
P sfu
dy
16
.Syok
Kardiogenik
Riwayat kejadian
Trauma torak : tumpul, tajam
Disfungsi miokard
Kontusio, disritmia, emboli
udara, infark, tamponade
EKG monitoring
Ultrasonograf
Pemasangan CVP
Pemeriksaan laboratorium
Perikardiosentesis

17
Tamponade Jantung
Trauma torak : tajam, tumpul
Takikardia
Hipotensi/syok
Vena leher meninggi
Suara jantung menjauh
EKG low voltage
Ultra sonograf
Perikardiosentesis

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19
Tension Pneumothorax
Ventil mechanism/flap-valve
Sesak nafas , RR <
Emphysema subcutan
Perkusi hypersonor
Suara paru menghilang pada ipsilateral e r
e s
Trakhea terdorong kontralateral g
r
Tachycardia te urn u
Hypotension m t
e u g g
u r
t in s gg an
a s ou n rg
d i n ga te
e Ve er g
t in
M p
u m
P
20
Pneumothoraks tension
Mirip tamponade jantung
Peningkatan tekanan intra pleural
Pergeseran mediastinum
Venous return
Pre load
Cardiac output
Pergeseran trakhea
Paru kolaps, suara napas hilang
Perkusi hipersonor
Dekompresi pleura
Jarum
Chest tube

21
22
23
Punksi pleura untuk dugaan pneumothorax
(sistim jarum + spuit + air)

NEEDLE
THORACOSYNTHESIS

24
Neurogenic Shock Spinal
Shock
Cedera tulang belakang
Cedera medulla spinalis
Sympathetic denervasi
Vasodilatasi, gambaran hypovolemia
No tachycardia,

npc te ti te
No vasokonstriksi

ri h ioe pu on
ha k i, p
fHuy ua ata ria

fe oc nns m
eq dil op

at
ad so pr

ng
In va ap

ot
t
In

S
r
Pe
25
 .Neurogenik Syok
Perdarahan otak tak shock !!!
Cedera tulang leher (spinal cord)
Kehilangan tonus simpatis
Hipotensi
Vasodilatasi
Nadi
Tekanan nadi lebar
Pemberian volume
Monitoring CVP
Vasopressor/Atropin

26
 Septic Shock
Jarang terjadi segera setelah trauma
Dapat terjadi pada kasus trauma
yang
terlantar
Luka tembus abdomen, perforasi
Shock septik pada periode awal :

p
so ro on m
Tachycardia

va ap p ct i e p u
Perifer hangat

t a i at e
In fun uat
Sistolik bisa normal

n
Pulse pressure lebar

di pr
t io
eq
ad

la
In
27
.Septik Syok
Jarang pada awal trauma
Fase awal
Kulit hangat
Tekanan nadi lebar
Bila tak febris, sulit dibedakan
dgn syok hipovolemik
Kontaminasi perforasi usus
(trauma abdomen)

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 Anaphylactic
Shock
SYOK ANAFILAKSIS

MENDADAK, TAK DAPAT DIRAMALKAN

KEMATIAN DALAM WAKTU SINGKAT

SYOK (HIPOVOLEMIK)
GAGAL NAFAS AKUT
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1. Adrenalin (1 ampul = 1 mg ) iv im sc - sl - transtracheal - et
Berat : 0.50 - 1 ampul
Sedang : 0.25 0.50 ampul
Ringan : tanpa shock - tidak perlu
2. Baringkan penderita, kedua tungkai angkat keatas (Shock Position)
Jaga jalan nafas tetap bebas
O2 masker 10 lpm, bila ada.
Siap Ambu Bag, siap beri nafas buatan , siap RJPO
LIHAT : gerak dada, ada nafas ?
DENGAR : suara nafas, tensi. Ada nafas ? Shock ?
RABA : hawa nafas, perfusi perifer. Ada nafas ? Shock?
Pasang Infus : RL/ PZ grojok 500-1000 cc
3. 5-10 menit kemudian
k/p ulangi Adrenalin
Beri Oradexon iv 1-2 cc
atau Dexamethason 100-200mg im
Avil/ Delladryl 1 cc im, hati-2 tensi turun lagi
4. Bila ada wheezing beri aminoflin iv pelan 5-10 cc ( 1Ampul )
Hati-hati bila tensi < 100 mmHg, K/P pemberian dg titrasi.
 KASUS
Laki-laki 50 th KP Fisik baik Tensi/Nadi baik
Riwayat alergi (-) sesak (-) asthma (-)
disuntik streptomycine - Penicillin

Shock : nadi kecil cepat perfusi dingin pucat basah,

sesak hebat, pasien gelisah

Time Saving is Life Saving

31
Initial Assesment
Airway , Breathing ok?

Circulation
HR within normal limit
Pulse pressure WNL
Warm, Pink, Dry

NO SHOCK
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Initial Assesment
Airway , Breathing ok?

Circulation
Tachycardia
Cutaneous vasoconstriction
Pulse pressure
Calmy

SHOCK 33
 SIRKULASI NORMAL

Perfusiperifer hangat, kering

W arna akral pink / m erah m uda
Capillary refil < 2 detik, bandingkan tangan
pem eriksa

34
 SHOCK
Perfusi:
pucat - dingin - basah
cap. refi
lltim e lam bat (kuku, telapak)

N adi< 100
Tekanan darah < 100 (atau
90) m m H g

35
Tanda Shock
GANGGUAN PERFUSI PERIFER
Raba telapak tangan

Hangat, Kering, Merah : NORMAL

Dingin, Basah, Pucat : SHOCK
Tekan - lepas ujung kuku / telapak tangan

Merah kembali < 2 detik : NORMAL

Merah kembali < 2 detik : SHOCK

Bandingkan dengan tangan pemeriksa

36
Tanda Shock

N AD IM EN IN G KAT
rab a n ad i rad ialis

nadi< 100 : N O RM AL
< 100 : S H O C K

37
 Tanda Shock
TEKAN AN D ARAH M EN U RU N

U kur / tensim eter

Sistolik < 100 : N O RM AL
< 100 : S H O C K
Raba nadi
N adiradialis teraba = sistolik 80
N adibrachialis teraba = sistolik 70
N adicarotis teraba = sistolik 60

38
 PRINSIP
RESUSITASI
Mempertahankan
ventilasi
Meningkatkan
perfusi
Terapi penyebab

39
 MAINTAIN
VENTILATION
Increased oxygen
demand

Especially in:
Sepsis
Hypovolemia Hyperventilation
Trauma
Diversi blood flow from
Respiratory fatigue
vital organ

Respiratory failure Organ injury

Respiratory acidosis, lethargy-coma, hypoxia

40
 TREATMENT OF
RESPIRATORY FAILURE
Hypovolemia (blood
loss)

Decreased CO

Decreased oxygen delivery,

increased oxygen requirement

Metabolic acidosis, hypoxemia

,tachypnea
TREATMENT:
Primary resuscitation
Oxygenation
Mechanical ventilation if needed
41
 TREATMENT CONCEPT
OF SHOCK
DO2 = CO x CaO2
ENHANCING PERFUSION / OXYGEN DELIVERY
Cardiac Arterial O2
output content

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2

Inotropes Fluids Transfuse Partially

dependent on
FIO2 and
pulmonary
status

42
THERAPEUTIC GOALS IN
SHOCK
Increase O2 delivery
Optimize O2 content of blood
Improve cardiac output and blood
pressure
Match systemic O2 needs with O2
delivery
Reverse/prevent organ hypoperfusion
 Cardiogenic Distributive
Shock Shock
Inotropes
Vasopressor ( NE,PE,Adr,Dop)
(Dob,Dop,Adr,Amr)

Release Pump = Pipe = Vascular Blood Pressure

tamponade,etc
Heart

Obstructive Cardiac Output x SVR

Shock
Volume =
Blood

Hypovolemic
Fluids
Shock
 Cardiogenic Shock
Management

Treat arrhythmias
Diastolic dysfunction may require
increased filling pressures
Vasodilators if not hypotensive
Inotrope administration
 Cont..

Vasopressor agent needed if

hypotension present to raise
aortic diastolic pressure
Consultation for mechanical
assist device
Preload and afterload reduction to
improve hypoxemia if blood
pressure adequate
Hypovolemic Shock Management

Volume resuscitation crystalloid,

colloid
Initial crystalloid choices
Lactated Ringers solution
Normal saline (high chloride may
produce hyperchloremic acidosis)
Match fluid given to fluid lost
Blood, crystalloid, colloid
 Distributive Shock
Management
Restore intravascular volume
Hypotension despite volume therapy
Inotropes and/or vasopressors
Vasopressors for MAP < 60 mm Hg
Adjunctive interventions dependent
on etiology
Obstructive Shock Treatment

Relieve obstruction
Pericardiocentesis
Tube thoracostomy
Treat pulmonary embolus
Temporary benefit from fluid or
inotrope administration
Fluid Therapy
Crystalloids
Lactated Ringers solution
Normal saline
Colloids
Hetastarch
Albumin
Gelatins
Packed red blood cells
Infuse to physiologic endpoints
Cont

Correct hypotension first

Decrease heart rate
Correct hypoperfusion
abnormalities
Monitor for deterioration of oxygenation
How Much Fluid To
Give?
Some measure of intravascular flling

Pressure (CVP or PAOP)

Some assessment of risk of pulmonary oedema
and capillary leak
Pulmonary gas exchange (PaO2:FiO2)
Requirement for positive pressure (PEEP)
Chest X-ray
Some assessment of response to treatment
Changes in acid base balance, lactate
Measurement of cardiac output
Inotropic / Vasopressor
Agents
Dopamine
Low dose (2-3 g/kg/min) mild inotrope
plus renal effect
Intermediate dose (4-10 g/kg/min)
inotropic effect
High dose ( <10 g/kg/min) vasoconstriction
Chronotropic effect
Cont.
Dobutamine
5-20 g/kg/min
Inotropic and variable chronotropic effects
Decrease in systemic vascular resistance
Cont..

Norepinephrine
0.05 g/kg/min and titrate to effect
Inotropic and vasopressor effects
Potent vasopressor at high doses
Cont..

Epinephrine
Both and actions for inotropic
and vasopressor effects
0.1 g/kg/min and titrate
Increases myocardial O2
consumption
What Do You Need to Know
When You Resuscitate a
Patient in Shock?
Arterialblood pressure
Urine output
Systemic acidbase balance (pH, SBE, lactate)
Some clinical assessment of tissue perfusion
warm and well perfused or cold and shut down
Some measurement of global blood flow and tissue
perfusion
Cardiac output or cardiac index
Arterial oxygen delivery, oxygen uptake index
Mixed venous saturation and PvO2

57
 SUMMARY
Shock is an altered state of tissue
perfusion severe enough to induce
derangements in normal cellular
function
Neuroendocrine, hemodynamic and
metabolic changes work together to
restore perfusion
Shock has many causes and often
may be diagnosed using simple
clinical indicators
Treatment of shock is primarily
focused on restoring tissue
perfusion and oxygen delivery while
eliminating the cause
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