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Definition of Shock

Shock is a major critical illness that


involves almost every organ system. It is
not simply a problem of decreased blood
pressure. Rather, it is a problem of
inadequate tissue perfusion and
oxygenation (Rice,1991)
.syok merupakan keadaan sakit kritis berat yang
mengakibatkan perburukan pada hampir setiap
sistem organ, masalahnya tidak sesederhana berupa
penurunan tekanan darah. Melainkan problem tidak
kuatnya perfusi dan oksigenasi jaringan..

Inadequate oxygenation or
perfusion causes:

Inadequate cellular oxygenation


Shift from aerobic to anaerobic
metabolism

Definisi
Hipotensi
Tekanan Darah Sistolik < 90 mmHg
Tekanan Darah Sistolik berkurang > 40 mmHg

Hipoperfusi
Perubahan status mental
Oliguria
Asidosis
defisit basa > 2
laktat > 2.5 mmol/L

Syok Hipovolemik
Syok yg disebabkan krn tubuh
kehilangan darah, plasma atau cairan
tubuh yg lain
Misalkan : pembedahan, trauma, luka
bakar atau muntah & diare
.... Syok akibat perdarahan syok
yang paling umum pada pasien
trauma/cidera
(..terutama pada pasien dengan multiple trauma, fraktur tulang2 panjang/pelvis,
trauma dengan ruptur/perdarahan organ di rongga abdomen, >> kadar hematokrit
& hemoglobin tidak dapat menjadi parameter berat ringanya perdarahan pada
perdarahan akut/mendadak)

Kehilangan bentuk lain spt peritonitis,


pancreatitis, obstruksi ileus (third space)

Blood Flow ????


Keadekuatan aliran darah
dipengaruhi oleh :
Pompa jantung yg adekuat
vaskulator/sistem sirkulasi yg
efektif
Volume darah yg adekuat
Bila salah satu komponen
terganggu/rusak
syok>>kematian

..CO = SV x SVR

Blood pressure

Cardiac output

Tissue perfusion

Vascular resistance

Faktor yg Mempengaruhi Stroke


Volume
1. Pre-Load : volume pengembalian darah
ke jantung ** ... Dipengaruhi oleh pengisian vena,
keadaan volume darah & perbedaan antara tekanan
sistemik vena serta tekanan atrium kanan

2. Kontraktilitas jantung : kemampuan


jantung dlm memompa Hk. Starling
3. After load : tahanan pembuluh darah
perifer/sistemik

SIRKULASI PEMBULUH DARAH ARTERI & VENA

Four Respiration Processes

Breathing (ventilation): air in to and


out of lungs
External respiration: gas exchange
between air and blood
Internal respiration: gas exchange
between blood and tissues
Cellular respiration: oxygen use to
produce ATP, carbon dioxide as
waste

DO2 = CO x CaO2
Cardiac
output

Arterial O2
content

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.39 + 0.03 X PaO2

Hypoperfusi

Pathogenesis

Met. Anaerob

ATP

Na+ pump #

Apoptosis

Shock Cascade in Haemorrhage


Hypovolaemia and Shock
decreased blood volume

septic shock

decreased cardiac output


decreased oxygen delivery

impaired macrocirculation
vasoconstriction

Inadequate perfusion
Erythrocyte aggregation

impaired micro circulation


tissue ischemia

organ failure

endotoxin
release
bowel
kidney

Impaired Oxidative
Metabolism

Hypoperfusion
Free radical
Inflammatory Mediators
Impair mitochondria function

Fink , P. M 2005

.....respon selular terhadap syok

Respon seluler : akibat oksigenasi yang rendah


metabolisme anaerob >> asam laktat asidosis
metabolik....
Bila semakin parah (..prolong syok) maka membran
sel rusak dan kehilangan fungsi
....retikulum endoplasma membengkak, lisosom
pecah dan mengeluarkan enzim yang dapat merusak
sel... terjadi edema dan kematian sel

Organ Dysfunctions
Ischemic injury related to tissue
hypoperfusion ;
MAP < 60 mmHg result ischemic injury,
anaerobic metabolism productions highenergy phosphate bellow level for cellular
function and membrane integrity

Mediator related 0rgandysfunctions


Reperfusion Injury

MENGENAL SYOK
Tanda syok yg didapatkan mrpk reaksi
kompensasi tubuh terhadap syok
Respon dini : tachicardia & vasoconstricti
kulit
Mrpk kompensasi utk menjamin
aliran/perfusi darah ke otak, jantung & ginjal
Kompensasi ini dpt mencegah penurunan
darah sistolik meskipun penderita telah
kehilangan 30 % vol darah
hrs diperhatikan jg tanda & gejala klinis syok
yg lain

Syok Phase
1. Compensatory phase
2. Progresive phase
3. Irreversible phase

Temuan Klinis Berdasarkan Fase


Syok
Kompen
sasi
HR > 100
x/mnt
TD Normal

RR >20

Progresif

Irreversibel

> 150x/mnt

Eratik/sistol

TDS < 80-90 Mbthkan dukungan


mmHg
mekanik &
farmakologis
Cepat,
Membutuhkan
dangkal,
intubasi
Krekels

Kulit

Dingin,
kusam

Bercak,
ptekie

Urin
output

Menurun

Fgs
mental

Kelam
pikir

<20 ml/jam Anuria,


membutuh
kan
dialisis
Lethargi
Tdk sadar

Keseimba Respirator Metabolik


ngan
i alkalosis asidosis
asam-basa

Ikterik

Asidosis
berat

Tanda & Gejala Syok


Respiratory system
nafas cepat & dangkal
Circulation system

Ekstremitas pucat, dingin & berkeringat dingin


Nadi cepat & lemah
CRT > 2 detik
TD turun bila kehilangan darah mencapai 30 %
Vena tampak kolaps

Sistem saraf pusat


Keadaan mental/kesadaran tergantung
derajat syok
Dimulai gelisah/bingung sampai tdk sadar

Sistem ginjal produksi urin menurun


Sistem pencernaan mual & muntah
Sistem kulit & otot
Turgor menurun
Mata cekung
Mukosa & lidah kering

Kelas I

Kelas II

Kelas III

Kelas IV

Kehilangan darah
(ml)

Sampai 750

750-1500

1500-2000

>2000

Kehilangan
darah(%
vol.darah)

Sampai 15 %

15 % - 30 %

30 % - 40 %

> 40 %

Denyut nadi

< 100

>100

>120

>140

Tek. Darah

Normal

Normal

Menurun

Menurun

Tek. Nadi

Normal/naik

Menurun

Menurun

Menurun

Frek. Nafas

14-20

20-30

30-40

>35

Prod. Urin
(ml/jam)

>30

20-30

5-15

Tdk berarti

Status CNS/
status mental

Sedikit cemas

Agak cemas

Cemas, bingung

Bingung, lesu
(lethargic)

Penggantian
cairan (hk. 3 : 1)

Kristaloid

Kristaloid

Kristaloid &
darah

Kristaloid &
darah

Hubungan antara derajat perdarahan dengan


kematian sel

Critical Oxygen Delivery

Course of hypovolemic shock in


absence of therapy
Blood pressure mmHg
150

Heart rate
min

Bleeding

100
Blood
pressure

50

Compensation

Decompensation

Three Shock phases

Irreversibility

Jika terjadi perdarahan yang sangat banyak, dan jantung


tidak mampu memperbaiki aliran darah ke jaringan
produksi asam laktat menurunkan pHa menurunnya
afinitas Hb-O2 meningkatkan transport oksigen ke
jaringan hipoksik (pergeseran kurva disosiasi ke kanan)

Tabel Respon Thd Pemberian Cairan Awal


Respon cepat

Respon
sementara

Tanpa respon

Tanda vital

Kembali ke normal

Perbaikan sementara
Tensi & nadi kembali
turun

Tetap abnormal

Dugaan kehil.
Darah

Minimal (10 % - 20
%)

Sedang, msh ada (20


% - 40 %)

Berat (>40%)

Kebutuhan
kristaloid

Sedikit

Banyak

Banyak

Kebutuhan darah

Sedikit

Sedang-banyak

Segera

Persiapan darah

Tipe spesifik &


crossmatch

Tipe spesifik

Emergensi

Operasi

Mungkin

Sangat mungkin

Hampir pasti

Perlu

perlu

Kehadiran dini ahli Perlu


bedah

Ringer Laktat 2000 cc pd dewasa, 20 CC/Kg BB pd anak-anak

TREATMENT CONCEPT OF SHOCK


ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2
Cardiac
output

Arterial O2
content

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.39 + 0.03 X PaO2

Inotropes :
Dopamin
Dobutamin
Norepinephrin
Epinephrin

Fluids

Transfuse

Partially
dependent on
FIO2 and
pulmonary
status

Therapeutic Goals in Shock


Control of bleeding

establish adequate ventilation and oxygenation


Restoration blood volume
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

Goals for fluid resuscitation


Maintenance or achievement of normovolemia
and hemodynamic stability
Restitution of fluid balance between the different

fluid compartments
Maintenance of an adequate colloid oncotic
pressure

Enhancement of microvascular bloodflow

End points of resuscitation


Basic clinical signs
Heart rate
Blood pressure

Urine output

Capillary refill
Monitor for deterioration of oxygenation

B
L
O
O
D

CRYSTALLOID

COLLOID

RL
RA

Albumin
Plasma

NaCl 0.9 %
NaCl 3 %

Dextran
Gelatin
HES

What do you replace with?


Crystalloid

4.1 x blood loss


Colloid*
1.4 x blood loss

Body Fluid Compartments


Total body water = 60 % of body weight (BW)
2/3

Intracellular water
= 40 % of BW

1/3

Extracellular
water
= 20 % of BW

Plasma (5 % of BW)

KRISTALOID
Keuntungan
Komposisi elektrolit seimbang

Tidak ada resiko alergi


Tidak mempengaruhi hemostasis
Mengakibatkan terjadinya diuresis

Murah

KRISTALOID
Kerugian
Perlu 3-4 x jumlah perdarahan
Bisa mengakibatkan edema
Mengakibatkan TOP berkurang.
Hypothermia

Lama kerja + 90 menit


NaCl 0.9% : asidosis hiperchloremia

KOLOID
KEUNTUNGAN
Tetap berada dalam volume
intravaskular
Kebutuhan sama dengan
jumlah darah yang hilang
Meningkatkan TOP
Resiko edema minimal

Meningkatkan aliran darah


microvaskular

KOLOID
KERUGIAN
Kelebihan beban cairan
Mengganggu hemostasis

Mempengaruhi fungsi ginjal


Reaksi anafilaktoid
Mahal

CHARACTERISTICS OF INTRAVENOUS
COLLOID FLUIDS
AVERAGE
MOLECULAR
WEIGHT * (DALTONS)

ONCOTIC
PRESSURE**

PLASMA
VOLUME
EXPANSION***

SERUM
HALF-LIFE

5 % ALBUMIN

69.000

20 mm Hg

0.7 1.3

16 hr

25 % ALBUMIN

69.000

70 Mm Hg

4.0 5.0

16 hr

6 % HETASTARCH

69.000

30 Mm Hg

1.0 1.3

17 day

10 % PENTASTARCH

120.000

40 Mm Hg

1.5

10 hr

10 % DEXTRAN-40

26.000

40 Mm Hg

1.0 1.5

6 hr

6 % DEXTRAN-70

41.000

40 Mm Hg

0.8

12 hr

FLUID

The History of Transfusion


Triggers
1980 the 10/30 rule
The American Society of Anesthesiology. 6-10,
g/dl

The American College of Physician. 8, g/dl


The National Institute of Health. 7, g/dl
The Transfusion Requirements in Critical Care.
7-9, g/dl

ASA Practice Guidelines for Blood


transfusion
Rarely indicated if Hb > 10 gr%, always
indicated Hb < 6 gr% esp in acute anemia
If Hb between 6 - 10 gr%, indication of RBC
transfusion should be based on the patients risk for
complication of inadequate oxygenation
Not recommended to use a single Hb trigger
for all patients, without considering all
important physiologic & surgical factors
affecting oxygenation

Postoperative Outcomes of
Anemic Jehovahs Witnesses
Preoperative Hemoglobin
Level

Mortality

<6 g/dl

61.5 %

6.1 to 8 g/dl

33 %

8.1 to 10 g/dl

0%

>10 g/dl

7.1 %

Addison K M et al. Rational use of blood production in : Lanten PN ed the intensive care unit manual
2001. P181-92

Anemia is tolerated better than


Hypovolemia
Allows the initial fluid resuscitation
to be non Blood

Oxygen Delivery = CO x CaO2


CO (SVxHR) x CaO2 (Hb x SpO2 x 1,39 + 0,003xPaO2)
CO= cardiac output

CaO2= Oxygen content

Important determinant to tissue


oxygenation
Component : Cardiac Output, Hb,
SpO2 arterial & venous blood

PENTING !
VOLUME INTRA-VASKULAR
O2 TRANSPORT ( ERITROSIT )
JUMLAH OKSIGEN YANG TERSEDIA UNTUK JARINGAN :

CO X (SAT.O2 X Hb X 1.39 + PO2 X 0.03)


= 5 l/m X 20 l/m O2/100 ml

= 1 liter O2/m

KEBUTUHAN = 25 % = 250 ml O2/m

Transfusion Guidelines for Unstable Patients Who Are


Acutely Bleeding
Clinical situation

Recommended response

Evidence of rapid acute


hemorrhage without immediate
control

Tranfuse PRBC

Estimated blood loss > 30-40%,


Tranfuse PRBC
presence of symptoms of severe
blood loss
Estimated blood loss < 25-30%
without uncontrolled
hemorrhage

Crystalloid-colloid resuscitation,
proceed to blood transfusion if
recurrent signs of hypovolemia

Presence of comorbid factors

Consider transfusion with lesser


degrees of blood loss

Evidence of rapid acute


Requires emergent control of
hemorrhage or > 30-40% blood
bleeding source
loss K M et al. Rational use of blood product in : Lanken PN ed the intensive care unit manual
Addison
2001. P181-92

Guidelines for Blood Transfusions and management of


Blood Loss During the Perioperative period
Hb > 10 g/dL transfusions rarely indicated
Hb < 6 g/dL transfusions almost always indicated, especially when
the anemia is acute
Hb 6 -10 g/dL decision to transfuse is determined by patients risk
for complications of decreased tissue oxygenation (patients with
ischemic heart disease)
Transfusion trigger : not recommended for application to all patients as it
ignores phsiologic and surgical factors to individual patients
Preoperatif autologous donation in selected patients
Intraoperatif blood salvage when appropiate
Acute normovolemic hemodilution when appropiate

(Stoelting,RK, 2002)

PENUTUP
SHOCK MERUPAKAN KONDISI KRITIS (MENGANCAM
JIWA),
PRIORITAS PERTAMA YANG HARUS DILAKUKAN
ADALAH RESUSITASI
RUMUS RESUSITASI :
A B C D dst.
D : DRUGS & FLUIDS (resusitasi cairan)

Lanjutan penutup

BODY FLUID, ELECTROLYTES AND ACID-BASE HAVE A


CLOSED RELATION ONE TO ANOTHER

DISTURBANCE OF THE FLUIDS BALANCE HAS IMPACT


TO ELECTROLYTES AND ACID-BASE REGULATION
DALAM RESUSITASI CAIRAN PD SHOCK, JUGA MELIPUTI
MENORMALKAN KADAR ELEKTROLIT DAN
KESEIMBANGAN ASAM-BASA (HOMEOSTASIS MILLIEU
INTERNA)

Lanjutan Penutup . . .

Terapi diberikan atas dasar diagnosis


ditambah kesimpulan data2 monitoring.
(bukan menerapi jumlah/volume defisit
cairan dan angka-angka hasil
laboratorium).

Etiology of circulatory shock

intravascular fluid volume loss


hemorrhage, fluid depletion or
sequestration

1. Hypovolemic -

2. Cardiogenic

impairment of heart pump


myopathic lesions: myocardial
infarction, cardiomyopathies
dysrhythmias

obstructive and regurgitant lesions of


intracardial blood flow mechanics

factors extrinsic to cardiac valves and


myocardium
v. cava obstruction, pericardial
tamponade,
pulmonary embolism,
coarctation of aorta

3. Obstructive

4. Distributive

pathologic redistribution of intravascular


fluid volume
septicaemia: endotoxic, secondary to
specific infection
anaphylactic

NORMAL
2. CARDIOGENIC

1. HYPOVOLEMIC

3. DISTRIBUTIVE
Low Resistance

High Resistance

4. OBSTRUCTIVE

Pathogenesis of circulatory shock


Usually results from inadequate cardiac output (CO)
Any factor reducing CO will likely lead to shock

1. Cardiac abnormalities

decreased ability of the heart to pump blood


-

myocardial infarction
toxic states of heart
severe heart valve dysfunction
arrhythmias

2. Decreased venous return


- diminished blood volume
- decreased vasomotor tone
- obstruction to blood flow at some
points in the circulation

Stages of shock
1. Nonprogressive stage (compensated)
Compensatory mechanisms (negative feedback) of the circulation can
return CO and BP to normal levels

- baroreceptor reflexes sympathetic stimulation constrict arteriols in


most parts of the body and
venous reservoirs protection of
coronary and
cerebral blood flow

angiotensin-aldosteron, ADH vasoconstriction,


water and salt retention by the kidneys

- absorption of fluid from ISF and GIT, increased thirst

2. Progressive shock
- circulatory system themselves begin to deteriorate,
without therapy shock becomes steadily worse until death
- positive feedback mechanisms are developed and can
cause vicious circle of progressively decreasing CO
Cardiac depression - coronary blood flow, contractility
Vasomotor failure - cerebral blood flow
Release of toxins by ischemic tissues: histamine,
serotonin, tissue enzymes
Intestines hypoperfusion mucosal barrier disturbance
endotoxin formation and absorption
vasodilatation, cardiac depression

Vasodilation

in precapillary bed

Generalised cellular deterioration: K+ , ATP, release of hydrolases first signs


of multiorgan failure

3. Irreversible shock
- despite therapy circulatory system continues to
deteriorate and death ensues
- marked hypoxic tissue damage
- endothelial dysfunction adhesive molecules,
neutrophils, macrophages inflammation
- progressive acidosis
- microcirculation failure plasma proteins leak
to interstitium
- advanced disseminated intravascular coagulation

Cardiogenic shock
- infarction process (45% loss of functional mass of
left ventricle)

ventricle fails as a pump

- BP 90 torr for at least 30 min,


pulmonary capillary pressure lung edema

self-perpetuing cycle then ensues (vicious circle): metabolic acidosis and


reduced coronary perfusion further impairing ventricular function and
predisposing to the development of dysrhythmias

Progression of myocardial dysfunction:

hypotension, tachycardia, fluid retention, hypoxemia

Septic shock
Typical causes: peritonitis, gangrenous infection, pyelonephritis

Special features:
1. high fever
2. marked vasodilatation (inflammation)
3. or normal CO: vazodilatation, metabolic rate
4. disseminated intravascular coagulation clotting factors to
be used up hemorrhages occur into many tissue (GIT)

IL-1 and TNF: PGE2, leukotrienes and NO


- vascular relaxation
- endothelial permeability (deficit of intravascular volume)
- myocardial contractility

Early stage: no signs of circulatory insufficiency


Progression of infection: circulatory disorders becomes

Bacterial toxins deterioration of circulation


end-stage is not greatly different from the end-stage
of hemorrhagic shock (hypodynamic stage)

Death:

- hypotension
- multiorgan failure

Cell dysfunction

prolong tissue hypoperfusion cell membrane


lesion, lysosomal enzymes cell death

mechanisms: hypoxia, inflammatory mediators,


free radicals

Multiorgan failure

Kidney
- blood flow (to 10%) GF oliguria
- ischemia acute tubular necrosis
- countercurrent mechanism failure izostenuria
- marked lesions acute renal failure

Lungs
- disturbances of pneumocytes and
endothelium
- accumulation of Tr, Neu in pulmonary
circulation release of proteases
- leukotriens and free radicals
- permeability - surfactant, edema
and hemorrhagies
respiratory insufficiency (ARDS)

100

% SURVIVAL
( 142 Pts)

75

50

25

0-1

1-2

2-3

3-4

4-6

LACTATE mM/l

6-11 11-16 > 16

EXTRACARDIAC
HYPOVOLEMIC

Fluid loss,
hemorrhage

Obstruction

e.g., Pericardial
tamponade

Reduced
filling
Reduced
preload

Low cardiac
output

Decreased arterial
pressure

CARDIOGENIC

DISTRIBUTIVE

Decreased
systemic
vascular
resistance

Myocardial
injury or
necrosis

Reduced
systolic performance
Myocardiac
dysfunction

High or normal
cardiac output

Shock

Multiple organ
system failure

Maldistribution
of blood flow in
microcirculation