Professional Documents
Culture Documents
DEFINI
SI
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
10
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
11
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
SV
CO
Increased ventricular
ejection fraction
BP
SVR
12
Metabolic Respons
Release of :
Catecholamines
Cortisol
Glucagon
LIPOLYSIS
INCREASE IN PLASMA FREE
FATTY ACIDS
13
RESPON METABOLIK
Hyperglikemia
Mobilisasi lemak
Katabolisme/pemecahan Protein
Peningkatan sintesis urea
Peningkatan asam amino
aromatik
Penurunan sintesis reactan fase
akut
Peningkatan osmolalitas ekstrasel
14
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.
15
METABOLIC RESPONS
Decreased blood
volume
Decreased CO
Anaerobic glycolysis
Pyruvate converted to lactic acid
METABOLIC ACIDOSIS
16
17
REDISTRIBUSI
ALIRAN DARAH
HYPOTENSION
STIMULASI NEUROENDOKRIN
BLOOD FLOW
PROTECTED
Heart
Brain
Adrenal/pituitary gland
BLOOD FLOW
DECREASED
Skin
Muscle
Splanchnic circulation
18
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
MEMPERBAIKI VOLUME
DARAH
Transcapillary refill phase
Transcapillary refill phase
HYPOXIA
ACIDOSIS
ANAEROBIC
METABOLISM
DECREASED CELLULAR
ENERGY EFFICIENCY
21
22
L
CELTH
DEA
OSMOTIC
GRADIENT
Na+ entry
into cell
Water entry
into cell
CELLULAR
EDEMA
IMPAIRED
INTRACELLULAR
METABOLISM
23
Liver
Liver failure
GI tract
Lung
24
STAGES OF SHOCK
25
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
26
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
27
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
28
UNCOMPENSATED SHOCK
Easier to detect than compensated
shock
Prolonged capillary refill time
Marked increase in heart rate
Rapid thready pulse
Agitation, restlessness, confusion
29
Decompensation
30
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)
31
Clinical Differentiation
Shock
Hemorrhagic Shock
Non Hemorrhagic Shock
Cardiogenic
Tension pneumothorax
Neurogenic
Septic
Anaphylactic
Hemorrhagic Shock
.Syok Perdarahan
Paling sering terjadi terutama
pada kasus trauma
Dijelaskan secara khusus pada
Modul 5 (Terapi Cairan 1)
34
Non Hemorrhagic
Shock
Cardiogenic Shock
Myocardial dysfunction
Blunt cardiac trauma
Tachycardia
Cardiac tamponade
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
.Syok
Kardiogenik
Riwayat kejadian
Trauma torak : tumpul, tajam
Disfungsi miokard
Kontusio, disritmia, emboli
udara, infark, tamponade
EKG monitoring
Ultrasonografi
Pemasangan CVP
Pemeriksaan laboratorium
Perikardiosentesis
Tamponade Jantung
Trauma torak : tajam, tumpul
Takikardia
Hipotensi/syok
Vena leher meninggi
Suara jantung menjauh
EKG low voltage
Ultra sonografi
Perikardiosentesis
Tension
Pneumothorax
Ventil mechanism/flap-valve
Sesak nafas , RR >
Emphysema subcutan
Perkusi hypersonor
o a er
n
g t
e
r
V te ing
p
m
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
NEEDLE
THORACOSYNTHESIS
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
.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
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
.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)
Anaphylactic
Shock
SYOK ANAFILAKSIS
SYOK (HIPOVOLEMIK)
GAGAL NAFAS AKUT
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
Initial Assesment
Airway , Breathing ok?
Circulation
HR within normal limit
Pulse pressure WNL
Warm, Pink, Dry
NO SHOCK
Initial Assesment
Airway , Breathing ok?
Circulation
Tachycardia
Cutaneous vasoconstriction
Pulse pressure
Calmy
SHOCK
PRINSIP
RESUSITASI
Mempertahankan
ventilasi
Meningkatkan
perfusi
Terapi penyebab
57
MAINTAIN
VENTILATION
Increased oxygen
demand
Especially in:
Sepsis
Hypovolemia
Trauma
Hyperventilation
Respiratory fatigue
Respiratory failure
Respiratory acidosis, lethargy-coma, hypoxia
Organ injury
58
TREATMENT OF
Hypovolemia (blood
RESPIRATORY
FAILURE
loss)
Decreased CO
TREATMENT:
Primary resuscitation
Oxygenation
Mechanical ventilation if needed
59
TREATMENT CONCEPT
OF SHOCK
DO2 = CO x/ CaO
ENHANCING PERFUSION
OXYGEN
DELIVERY
2
Arterial O2
content
Cardiac
output
Inotropes
Fluids
Transfuse
Partially
dependent on
FIO2 and
pulmonary
status
60
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
Obstructive
Shock
Volume =
Blood
Fluids
Hypovolemic
Shock
62
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
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
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
Inotropic / Vasopressor
Agents
Dopamine
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
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
78
79
80
81