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Modul

SYOK
Dept. Anestesiologi & Terapi Intensif
FK USU/RSUP H.Adam Malik Medan

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

CARDIOGENIC
OBSTRUCTIVE
O2
O2

HYPOVOLEMIC

O2

SEPTIC

PATOFISIOLOGI DARI RESPON


TUBUH TERHADAP SHOCK
Respon Neuroendokrin
Respon Hemodinamik
Respon Metabolik

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FEAR

Stimulation of limbic
area of brain
Increased:
hypothalamic,
adrenomedullary
adrenocortical activity

Neuroendocrine
Respons
Adrenal cortex

R atrium

low-pressure stretch
receptors

LOSS OF TONIC
INHIBITION OF
CENTRAL AND
HYPOVOLEMIA
SYMPATHETIC
Aorta/carotids NERVOUS SYSTEMS
High-pressure
baroreceptors

Decreased renal
perfusion

Cortisol release

Renal
Renin release
Pituitary gland
ACTH, ADH and GH release
Adrenal gland (medulla)
Epinephrine/norepinephrine
release

Angiotensin II

Adrenal cortex

Aldosterone release
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Haemodynamic Respons
Venoconstriction
Sympathetic n. system (SNS)
Catecholamines (CA)
Angiotensin II (ATII)
ADH

Reduced venous
capacitance

Arteriolar constriction
SNS, CA, ATII, ADH

Increased
ventricular filling
P

Decreased capillary P
Fluid shift from interstitium into
vascular compartment

Restoration of
blood volume

Increased distal tubular


reabsorption
Aldosterone, ADH
Increased proximal tubular
reabsorption
SNS, CA, ATII
Increased myocardial
contractility
SNS, CA

SV
CO

Increased ventricular
ejection fraction

BP
SVR

Increased SVR due to arteriolar


construction
SNS, CA, ATII, ADH

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Metabolic Respons
Release of :
Catecholamines
Cortisol
Glucagon

LIPOLYSIS
INCREASE IN PLASMA FREE
FATTY ACIDS
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RESPON METABOLIK
Hyperglikemia
Mobilisasi lemak
Katabolisme/pemecahan Protein
Peningkatan sintesis urea
Peningkatan asam amino
aromatik
Penurunan sintesis reactan fase
akut
Peningkatan osmolalitas ekstrasel
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RESPON METABOLIK
Release of:
Catecholamines
Cortisol
Glucagon
Growth hormone

HYPERGLYCEMIA

Impaired
peripheral
glucose
uptake

Glycogen
breakdow
n
Conversio
n of a.a.
to glucose

Breakdown of
skeletal
muscle into
a.a.

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METABOLIC RESPONS
Decreased blood
volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysis
Pyruvate converted to lactic acid

METABOLIC ACIDOSIS
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Mekanisme untuk memperbaiki


keseimbangan
kardiovaskuler
Redistribusi aliran darah
Peningkatan cardiac output
Memperbaiki volume intravaskular

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REDISTRIBUSI
ALIRAN DARAH
HYPOTENSION
STIMULASI NEUROENDOKRIN

BLOOD FLOW
PROTECTED
Heart
Brain
Adrenal/pituitary gland

BLOOD FLOW
DECREASED
Skin
Muscle
Splanchnic circulation
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PENINGKATAN
CARDIAC OUTPUT

Limited to 180
beats/min before
decreased CO due to
decreased diastolic
filling time

CARDIAC OUTPUT = HR X
SV
Increased
contractility
Sympathetic
n. system
Catecholamine
release

Increase EDV via:


Venoconstriction
Arteriolar constriction
Renal reabsorption
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MEMPERBAIKI VOLUME
DARAH
Transcapillary refill phase
Transcapillary refill phase

1. Decreased capillary pressure caused by hypotension


2. Sympathetic increase in precapillary arteriolar constriction

Decrease capillary hydrostatic pressure promotes passage of fluid


from interstitium to intravascular space

Plasma protein restitution phase

Increased plasma osmolarity due to mainly hepatic release of


glucose, pyruvate, amino acids, etc.
Increased interstitial osmolarity
Increased interstitial volume and pressure
Transcapillary movement of albumin into intravascular space
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EFEK SHOCK PADA TINGKATAN


SEL
LOW-FLOW,
POOR PERFUSION

HYPOXIA
ACIDOSIS

ANAEROBIC
METABOLISM

DECREASED CELLULAR
ENERGY EFFICIENCY
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Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does


not require oxygen). It yields pyruvic acid, with toxic byproducts such as lactic acid, and very little energy. (B) Stage two
is aerobic (requires oxygen). In a process called the Krebs or
citric acid cycle, pyruvic acid is degraded into carbon dioxide and
water, which produces a much higher yield of energy.

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EFEK SHOCK PADA TINGKATAN


SEL
CELL MEMBRANE FAILURE:
DIRECT
Endotoxin
Complement
INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient
Decreased oxidative phosphorylation

L
CELTH
DEA

OSMOTIC
GRADIENT

Na+ entry
into cell

Water entry
into cell

CELLULAR
EDEMA

IMPAIRED
INTRACELLULAR
METABOLISM
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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

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STAGES OF SHOCK

COMPENSATED SHOCK
Body defense mechanisms attempt
to preserve major organs
Precapillary sphincters close,
blood is shunted
Increased heart rate and strength
of contractions
Increased respiratory function,
bronchodilation
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COMPENSATED SHOCK
Will continue until problem solved or
shock progresses to next stage
Can be difficult to detect with subtle
indicators
Tachycardia
Decreased skin perfusion
Alterations in mental status
Some medications such as propranolol
can hide signs and symptoms
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UNCOMPENSATED
SHOCK
Physiological response
Precapillary sphincters open,
blood pressure falls
Cardiac output falls
Blood surges into tissue beds,
blood flow stagnates
Red cells stack up in rouleaux

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UNCOMPENSATED SHOCK
Easier to detect than compensated
shock
Prolonged capillary refill time
Marked increase in heart rate
Rapid thready pulse
Agitation, restlessness, confusion

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Decompensation

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IRREVERSIBLE
SHOCK
Compensatory mechanisms fail,
cell death begins, vital organs
falter
Patient may be resusitated but
will die later of (ARDS, renal and
liver failure, sepsis)

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Clinical Differentiation
Shock
Hemorrhagic Shock
Non Hemorrhagic Shock
Cardiogenic
Tension pneumothorax
Neurogenic
Septic
Anaphylactic
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Hemorrhagic Shock

.Syok Perdarahan
Paling sering terjadi terutama
pada kasus trauma
Dijelaskan secara khusus pada
Modul 5 (Terapi Cairan 1)
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Non Hemorrhagic
Shock

Cardiogenic Shock
Myocardial dysfunction
Blunt cardiac trauma

Tachycardia

Cardiac tamponade

Blowing heart sound


Venectasia regio colli
Hypotension

Air embolism
Valve rupture
ECG monitoring
Isoenzynme-CPK
Echocardiography

d
o
o
l
b e
d th
e
sh to t ng n
i
o
in urn ar pi
i
t
im et he m
c
D r
n
u

P sfu
y
d

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.Syok
Kardiogenik
Riwayat kejadian
Trauma torak : tumpul, tajam
Disfungsi miokard
Kontusio, disritmia, emboli
udara, infark, tamponade
EKG monitoring
Ultrasonografi
Pemasangan CVP
Pemeriksaan laboratorium
Perikardiosentesis
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Tamponade Jantung
Trauma torak : tajam, tumpul
Takikardia
Hipotensi/syok
Vena leher meninggi
Suara jantung menjauh
EKG low voltage
Ultra sonografi
Perikardiosentesis
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Tension
Pneumothorax

Ventil mechanism/flap-valve
Sesak nafas , RR >
Emphysema subcutan
Perkusi hypersonor

Suara paru menghilang pada ipsilateral


m
u
Trakhea terdorong kontralateral
in
t
n
r
s
r
a se t u
u
i
Tachycardia
g
ed rge re gu ng
Hypotension
M te us ng ga

o a er
n
g t
e
r
V te ing
p
m
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u
P

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
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Punksi pleura untuk dugaan pneumothorax


(sistim jarum + spuit + air)

NEEDLE
THORACOSYNTHESIS
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Neurogenic Shock

Spinal

Shock
Cedera tulang belakang

In
In va app
ad s o r
eq dil op
fHuy ua ata ria
Pe S npco te tio te
ri h titoen pu n
fe oc n s m
r
ha k i, p
ng
at

Cedera medulla spinalis


Sympathetic denervasi
Vasodilatasi, gambaran hypovolemia
No tachycardia,
No vasokonstriksi

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.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
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Septic Shock

In
a

Tachycardia
Perifer hangat
Sistolik bisa normal
Pulse pressure lebar

de
qu
I n fu n a t
va app cti e pu
so ro on m
di pr
p
la
ta iate
ti o
n

Jarang terjadi segera setelah trauma


Dapat terjadi pada kasus trauma yang
terlantar
Luka tembus abdomen, perforasi
Shock septik pada periode awal :

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.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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Reaksi Anafilaktik
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 aminofilin 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

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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

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PRINSIP
RESUSITASI
Mempertahankan
ventilasi
Meningkatkan
perfusi
Terapi penyebab

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MAINTAIN
VENTILATION
Increased oxygen
demand

Especially in:
Sepsis
Hypovolemia
Trauma

Hyperventilation

Respiratory fatigue

Respiratory failure
Respiratory acidosis, lethargy-coma, hypoxia

Diversi blood flow from


vital organ

Organ injury

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TREATMENT OF
Hypovolemia (blood
RESPIRATORY
FAILURE
loss)
Decreased CO

Decreased oxygen delivery,


increased oxygen requirement

Metabolic acidosis, hypoxemia


,tachypnea

TREATMENT:

Primary resuscitation
Oxygenation
Mechanical ventilation if needed
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TREATMENT CONCEPT
OF SHOCK
DO2 = CO x/ CaO
ENHANCING PERFUSION
OXYGEN
DELIVERY
2
Arterial O2
content

Cardiac
output

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

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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
Shock

Distributive
Shock

Inotropes
(Dob,Dop,Adr,Amr)
Release
tamponade,etc

Vasopressor ( NE,PE,Adr,Dop)

Pump =
Heart

Pipe = Vascular

Blood Pressure

Cardiac Output x SVR

Obstructive
Shock
Volume =
Blood

Fluids

Hypovolemic
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 filling


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

Pediatric Considerations
BP not good indication of hypoperfusion
Capillary refill, extremity temperature better
signs of poor systemic perfusion
Epinephrine preferable to norepinephrine due to
more chronotropic benefit
Fluid boluses of 20 mL/kg titrated to BP or total
60 mL/kg, before inotropes or vasopressors

Pediatric Considerations
Neonates consider congenital
obstructive left heart syndrome as
cause of obstructive shock
Oliguria
<2 yrs old, urine volume <2 mL/kg/hr
Older children, urine volume
<1 mL/kg/hr

What Do You Need to Know


When You Resuscitate a
Patient in Shock?

Arterial blood 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
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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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