Syok Hipovolemia

Dr.Irfan Hamdani,Sp.An
Dept.Anestesiologi dan Terapi Intensif
Fak.Kedokteran UMSU
Medan

Syok
suatu kondisi dimana sistem
kardiovaskular gagal dalam
menghasilkan perfusi jaringan
yang adekuat
2

Perfusi jaringan yang tidak adekuat akan

menghasilkan :

hipoksia celluler generalisata

gangguan berat metabolisme seluler

Kerusakan jaringan
gagal organ
kematian

Diagnosis Syok

MAP < 60
Klinis :
terdapat gejala
dan tanda
hipoperfusi
jaringan

IT IS NOT LOW BLOOD PRESSURE !!!

IT IS HYPOPERFUSION..

Gangguan
Pompa
jantung

Sistem sirkulasi

Volume

Gangguan aliran ke
Jaringan
5

PATHOPHYSIOLOGY OF
SHOCK SYNDROME
CELLULAR
OXYGEN
SUPPLY
CELLULAR
OXYGEN
DEMAND

Impaired tissue perfusion occurs when an

imbalance develops between cellular oxygen

supply and cellular oxygen demand.

PATHOPHYSIOLOGY OF
SHOCK SYNDROME
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell

Na+/K+ pump impaired

mitochondria damage
cell death

COMPENSATORY MECHANISMS:

Sympathetic Nervous System (SNS)Adrenal Response

SNS - Neurohormonal response
Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (SVR-Afterload)
Increased Preload
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COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)Adrenal Response

SNS

- Hormonal: Renin-angiotension

system

Decrease renal perfusion

Releases renin

angiotension I
Angiotension II
potent vasoconstriction &
Releases aldosterone adrenal cortex
Sodium & water retention
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COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-Adrenal
Response
SNS

- Hormonal: Antidiuretic Hormone

Osmoreceptors

in hypothalamus stimulated
ADH released by Posterior pituitary gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water
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COMPENSATORY MECHANISMS
Sympathetic Nervous System (SNS)
Adrenal Response

SNS

- Hormonal: Adrenal Cortex

Anterior

pituitary releases
adrenocorticotropic hormone (ACTH)
Stimulates adrenal Cx to release
glucorticoids
Blood sugar increases to meet increased
metabolic needs
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Failure of Compensatory Response

Decreased

blood flow to the tissues causes

cellular hypoxia
Anaerobic metabolism begins
Cell swelling, mitochondrial disruption,
and eventual cell death
If Low Perfusion States persists:

IRREVERSIBLE

DEATH IMMINENT!!
12

Stages of Shock

Initial stage - tissues are under perfused, decreased CO,

increased anaerobic metabolism, lactic acid is building
Compensatory stage - Reversible. SNS activated by low
CO, attempting to compensate for the decrease tissue
perfusion.
Progressive stage - Failing compensatory mechanisms:
profound vasoconstriction from the SNS
ISCHEMIA Lactic acid production is high
metabolic acidosis
Irreversible or refractory stage - Cellular necrosis and
Multiple Organ Dysfunction Syndrome may occur

DEATH IS IMMINENT!!!!

13

14

Pathophysiology Systemic Level

Net results of cellular shock:

systemic lactic acidosis

decreased myocardial contractility
decreased vascular tone
decrease blood pressure, preload, and
cardiac output

15

Clinical Presentation:
Generalized Shock

Vital signs

Hypotensive:(may be WNL or due to

compensatory mechanism) < 90
mmHg

MAP < 60 mmHg

Tachycardia: Weak and Thready pulse

Tachypneic-blow off CO2

Respiratory alkalosis

16

Clinical Presentation:
Generalized Shock

Mental status:
restless, irritable, apprehensive

unresponsive, painful stimuli only

Decreased Urine output

17

Shock Syndromes
Hypovolemic

blood VOLUME problem

Cardiogenic

Shock

Shock

blood PUMP problem

Distributive

Shock

[septic;anaphylactic;neurogenic]

blood VESSEL problem

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Hypovolemic Shock
Loss of circulating volume Empty tank
decrease tissue perfusion general shock
response
ETIOLOGY:

Internal or External fluid loss

Intracellular and extracellular
compartments
Most common causes:
Hemmorhage
Dehydration

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Hypovolemic Shock
External loss of fluid
Fluid

loss: Dehydration

Nausea & vomiting, diarrhea, massive diuresis,

extensive burns

Blood

loss:

trauma: blunt and penetrating

BLOOD YOU SEE
BLOOD YOU DONT SEE
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Hypovolemic Shock:
Internal fluid loss
Loss

of Intravascular integrity

Increased

capillary membrane
permeability

Decreased

Colloidal Osmotic Pressure

(third spacing)

21

Pathophysiology of
Hypovolemic Shock
Decreased intravascular volume leads to.
Decreased venous return (Preload, RAP) leads
to...
Decreased ventricular filling (Preload, PAWP)
leads to.
Decreased stroke volume (HR, Preload, &
Afterload) leads to ..
Decreased CO leads to...(Compensatory
mechanisms)
Inadequate tissue perfusion!!!!
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Assessment & Management

S/S vary depending on severity of fluid loss:
15%[750ml]- compensatory mechanism
maintains CO
15-30% [750-1500ml- Hypoxemia, decreased
BP & UOP
30-40% [1500-2000ml] -Impaired
compensation & profound shock along with
severe acidosis
40-50% - refactory stage:
loss of volume= death
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Clinical Presentation
Hypovolemic Shock
Tachycardia

and tachypnea
Weak, thready pulses
Hypotension
Skin cool & clammy
Mental status changes
Decreased urine output: dark &
concentrated
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Hypovolemic Shock:

Hemodynamic Changes
Correlate with volume loss
Low

CO
Decreased RAP ( Preload)
Decreased PAD, PAWP
Increased SVR (Afterload)
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Hypovolemic Shock

Initial Management
Management goal:
Restore circulating volume, tissue perfusion,
& correct cause:

Early Recognition- Do not relay on BP! (30%

fluid loss)
Control hemorrhage
Restore circulating volume
Optimize oxygen delivery
Vasoconstrictor if BP still low after volume
loading
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Restore circulating volume

Hemorrhage
Dehydration
27

Physiologic principles
of fluid management

Perdarahan

ISF

IVF

ICF

28

PRE-LOAD

CONTRACTILITY

STROKE VOLUME

CARDIAC OUTPUT

AFTER-LOAD

HEART-RATE

SYSTEMIC
VASCULAR
RESISTANCE

BLOOD
PRESSURE
29

Oxygen Transport

CaO2 = (SaO2 x Hb x 1.34) + (PaO2 x 0.003)

DO2 = CO x CaO2

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PERDARAHAN

HILANG VOLUME
HILANG ERITROSIT

THE FLUIDS
CRYSTALLOID
HYPERTONIC FLUID
NATURAL COLLOID
ARTIFICIAL COLLOID
BLOOD, COMPONENT
32

Physiologic principles
of fluid management
TOTAL BODY WATER : 60% TOTAL BODY WEIGHT

60 kg
9L

3L

ISF
ISF

IVF

36 L
24 L
ICF

33

Physiologic principles
of fluid management

3L

D5W

EDEMA

9L
2750ml
ISF
ISF

3L

24 L

250 ml
IVF

ICF
34

Physiologic principles
of fluid management
Require large volume
Cheaper
Fewer adverse side effects
But

CRYSTALLOID

3L

RL, RA,
NaCl 0.9%

EDEMA

9L
2250ml
ISF
ISF

3L

24 L

750 ml
IVF

ICF
35

Physiologic principles
of fluid management

Albumin-5%
1L

expensive

9L

3L

24 L

1L
ISF
ISF

IVF

ICF
36

Physiologic principles
of fluid management
More rapidly correct
hypovolemia
Maintain intravascular
oncotic pressure
More expensive than
crystalloid

9L

3L

HES-6%, 200/0.5
1L

24 L

1L
ISF
ISF

IVF

ICF
37

Physiologic principles
of fluid management
Subjected to recent
intensive investigation
Resuscitate rapidly,
reduced volume of fluid

7.5%-Hypertonic Saline
+ Dextran
500 ml

Reduce cerebral edema

9L

3L

EDEMA

24 L

625 ml
ISF
ISF

IVF

ICF
38

Estimated Fluid and Blood Losses

Based on Patients Initial Presentation
Class I

Class II

Class III

Class IV

Blood-Loss[ml]

->750

750-1500

1500-2000

>2000

Blood-loss [%BV]

->15%

15-30%

30-40%

>40%

Pulse-Rate [x/min.]

<100

>100

>120

>140

Blood-Pressure

Normal

Normal

Decreased

Decreased

Pulse-Pressure

N or
increased

Decreased

Decreased

Decreased

Respiratory Rate

14-20

20-30

30-35

>35

Urine out-put [ml/hour]

>30

20-30

5-15

Negligible

Mental status/CNS

Slightly
anxious

Midly anxious

Anxious and
confused

Confused and
lethargic

BV = 70 ml/kg
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Oxygen Transport

CaO2 = (SaO2 x Hb x 1.34) + (PaO2 x 0.003)

DO2 = CO x CaO2

40

PRE-LOAD

CONTRACTILITY

STROKE VOLUME

CARDIAC OUTPUT

AFTER-LOAD

HEART-RATE

SYSTEMIC
VASCULAR
RESISTANCE

BLOOD
PRESSURE
41

Pola kerja penanganan

shock perdarahan
Penderita datang
dengan perdarahan
Pasang infus jarum
kaliber besar (16G, 18G),
ambil sample darah

Rahardjo.E, 1990
Hasanul, 2003

Ukur tekanan darah, hitung

nadi, nilai perfusi, produksi
urine

Tentukan estimasi jumlah

perdarahan, minta darah
Guyur cepat Ringer Laktat atau
NaCl 0.9% [hangat, 390C] 3x
prakiraan lost-volume [1-2 liter]

evaluasi
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FLUID REPLACEMENT
3 : 1 Rule

Class I
Crystalloid
Class II
Crystalloid
+ Colloid ?
Class III Crystalloid
+Colloid, Blood
Class IV Crystalloid
+Colloid, Blood
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1000 ml berdarah

3000 ml kristalloid
(RL, RA, NaCl 0.9%)
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Management
selanjutnya
Rapid response,

perdarahan <20%
Transient response,
perdarahan 20-40% BV
ongoing loss
resusitasi tdk adekwat
RL, NaCl 0.9%, Kolloid, Darah ?
Minimal, no response
Tindakan bedah segera
Transfusi darah
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