shock

agus setiyana,m.d.
cardiac anesthetist
acls provider
fccs provider
Atls provider
 Schock (ger), scoc (old ger.): push,
thrust, vibration, fright
Choc (1810): Prussian cavalry attack

Shock (medical) : 1st half 18th century,

english translation of Le Drans book and
french medical terms secousse, coup
saisissement, and commotion
The importance of fluids in non-bleeding persons was
not initially recognized!

Shock:
a state of general depression of
the nervous system induced by a
severe injury or by a powerful
disturbance of the emotional
centres.
Carr, JW. The Practitioners Guide.New York: Longmans, 1902;865-66.
Hypovolemic shock
Adams H.A. et al.: Intensivmed 38:541-553 (2001):

Hypovolemic shock
is a state of insufficient perfusion of vital
organs with consecutive imbalance of oxygen
supply and -demand
due to an intravascular volume deficiency
with critically impaired cardiac preload
Definitions of shock types:

Hypovolemic Neurogenic
shock shock

Cardiogenic Anaphylactic Septic

shock shock shock
 Konsekuensi shock
Impaired celluler Impaired capillary perf
O2 uptake/utilization

cell hypoxia ( anaerobic metabolism)

Lactic acidosis

decreased ATP production

Failure of the Na-K pump

cellular swelling

lysosomal rupture

CELL Death Organ Failure
 Shock pd System Organ
GI Tract
Ggn permeabilitas usus , berakibat ;
Translokasi bakteri enteric & toxin ke circulasi
motilitas usus, berakibat ileus paralitik
Ulcerasi pada gaster dan usus
Ggn absorpsi nutriens
Pelepasan mdf dr iskemik pankreas
 Muskulus skeletalis
Produksi asam laktat berlebih asidosis
metabolik
Katabolisme sel otot me sbg sumber energi
Kelelahan otot-otot pernafasan
Sistem Immune
Ggn sistem kekebalan
Rentan terhadap infeksi
Kulit
Ggn penyembuhan luka
Resiko perlukaan
 Liver
Awalnya ; pemecahan glycogen, me gluconeogenesis
me kadar glukosa darah
Lanjut ; me penyimpanan glukosa & ggn
gluconeogenesis
Selanjutnya hypoglikemia
Ggn metabolisme protein dan lemak
Ggn konversi asam laktat oleh hepar asidosis
metabolik
me pembentukan & ekskresi bile dr bilirubin me
serum bilirubin mild jaundice
Ggn netralisasi toxin bakterial & sisa metabolit spt
amonia
Ggn sel Kupffer utk membersihkan bakteri pd sirkulasi
 Ginjal
Awalnya ; me GFR. Aldosteron & ADH
mempertahankan kadar garam dan air
me urine output.
Lanjut ; ATN nekrosis kortek renalis
Gagal gnjal permanen
Hematologis
me platelet dan faktor pembekuan,oleh krn ;
1. Pemakaian akibat aktivasi cascade proses
pembekuan DIC
2. Hemodilusi o.k. penggantian cairan
3. me fungsi platelet o.k. sepsis & hipothermia
 Paru paru
V Q mismatch ggn oksigenasi
me ventilasi alveolar retensi CO2 &
hipoksia
Pembentukan mikrothrombi pd kapiler
pulmonal & keluarnya mediator2 ARDS
Jantung
Awalnya ; me stimulasi simphatis me rate
& kontraksi ventrikuler
Lanjut ; me CPP & keluarnya mdf ggn
kontraksi
Predisposisi terjadi arrhytmia
Infark transmural & subendocardial
 Otak
Awalnya ; release norepinephrine dan
adrenalin eksitasi CNS
Lanjut ; me CPP ggn fungsi serebral
Bila mempengaruhi brainstem ggn
vasomotor & ventilasi
Akhirnya ;
1. Penumpukan asam laktat di otak
2. Odema serebri o.k. masuknya Natrium & air
3. Destruksi sel membrane
4. Ggn neurotransmiter
5. Irreversible brain damage
 Tahapan shock

1. Fase I : Shock terkompensasi

me rate & kontraksi ventrikuler untuk
optimalisasi MAP & CO
Vasokonstriksi vena sistemik me venous
return & pengisian ventrikel
Vasokonstriksi arteri sistemik mengalihkan
aliran darah ke organ2 vital, hipoperfusi
perifer ditandai dengan kulit yg dingin dan
pucat, me urine output, kelemahan otot.
2. Fase II : Dekompensasi Shock
Hipotensi
Iskhemia serebral ; ggn kesadaran
Iskhemia myocard ; arrhytmia, perubahan
ST T iskhemia, me cardic output ditandai
hilangnya pulsasi perifer
me asam laktat, asidosis metabolik berat
Capillary leakage
 Fase III : Irreversible Shock
Systemic hypoperfusion
Leaky, porous capillaries
Resusitasi cairan tak banyak membantu
hanya mengisi sirkulasi perifer
Kerusakan & nekrosis organ2 vital
Translokasi toksin dan kuman hingga tampak
septic
Resusitasi jarang berhasil
Bila berhasil ,px akan meninggal o.k. MOF
 Pembagian shock;
1. Shock hipovolemik ;
1. Bleeding / haemorrhagic
2. GI losses ( vomit,diare,dehidrasi,3rd spaces
losses )
3. Reperfusion injury
4. Burn
5. Sepsis
Merupakan jenis shock terbanyak, ditandai dg deplesi
volume intravaskuler
 Hypovolemic Shock

Blood Pressure

Cardiac Output / Systemic

CO Vascular
Resistance (SVR)

Stroke
Volume / SV Heart Rate

Contractility Afterload

Preload
 Klasifikasi shock hemorrhage
Cl I II III IV
BL(ml) >750 750- 1500- 2000
1500 2000
%BL/BV >15 15-30 30-40 40
Nadi <100 >100 >120 140
BP N N
PP N/
Ca Ref te N + + +
RR N 20-30 30-40 40
Ur out ml/hr 30 20-30 5-15
CNS Slight Mild Anx,con Conf,
fus
2. Shock kardiogenik
Infark myocard
Cardiomyopathy
Penyakit katub jantung
Burn & sepsis
Shock diakibatkan kegagalan sistem pompa
jantung ( cardiac output ) o.k. defek pd fungsi
jantung
 Cardiogenic Shock
Blood Pressure

Cardiac Output / Systemic

CO Vascular
Resistance (SVR)

Stroke
Volume / SV Heart Rate

Preload Afterload
 Faktor2 pd Cardiac Output
Variabel assessment
Heart rate perabaan pulsasi
& rhythm pulse oximetry
ECG
Preload
Right heart CVP, JVP, liver
Left heart DOE, orthopnea, Arterial
BP, PAOP
Afterload Mean Arterial BP,SVR
Contractility Ejection Fraction,
Echocardiography
3. Shock distributif
Shock anaphylactic
Shock neurogenic
Reperfusion injury
Burn & sepsis
Terjadi hipovolemia relatif o.k. adanya pooling
cairan tubuh di venous parifer dan rongga
non vaskuler ( kebocoran )
Pada anafilaksis terjadi vasodilatasi hebat sbg
konsekuensi reaksi anafilaksis
 Circulatory Shock
Blood Pressure

Cardiac Output / Systemic

CO Vascular
Resistance (SVR)

Stroke
Volume / SV Heart Rate

Preload Afterload
Shock neurogenik
Terjadi vasodilatasi sebagai akibat hilangnya tonus
otot pembuluh darah.
Regulasi tonus hilang setelah cedera CNS dan cedera
spinal letak tinggi.
Shock sepsis
Merupakan sebab terbanyak shock distributif
antigen dan toxin bakterial dlm aliran darah
memicu cascade reaksi inflamasi release
inflammatory mediators;
Vasodilatasi sistemik
Capillary leakage
Abnormal koagulasi ; DIC , spontaneus systemic
hemorrhagic, etc.
4. Shock obstruktif
Tension pneumothorak
Tamponade cardiac
Embolus pulmonair
Lebih sering diakibatkan trauma
Resusitasi cairan dan penggunaan inotropik
hanya membantu sementara waktu
Tindakan pembedahan untuk pengurangi
tekanan merupakan pilihan
 Tata laksana
penyebabab primer
Oksigenasi
Resusitasi cairan
Stabilisasi
Spesifik ;
Pembedahan
Antibiotika
Inotropik, vasokonstriktor, antiarrhytmia
IABP
 Fluid Therapy

RESUSCITATION MAINTANANCE

Crystalloid Coloid Electrolite Nutrition

Repair
Replacement of an acute 1. Normal Requirement
loss (hemoragic, GI loss, 2. Nutrition support
3rd space)
 CO = SV x HR

Preload Contractility Afterload

Vasoconstriction

Tissue Perfusion
 Treatment Concept of Shock
Enhancing perfusion / Oxygen Delivery

DO2 = CO x CaO2
Cardiac
Output Arterial O2 content

O2 delivery/ DO2 = HR x SV x Hb x SaO2 x 1.34 + Hb x PaO2

Inotropik Fluids Transfuse Partially

dependent on
Contractility Preload
FIO2 &
Vasoactive pulmonary
status
Afterload
Volume Replacement Therapy

Crystalloids Colloids

Lactated Ringers
Normal Saline
Hypertonic
Sodium Lactate

Albumi Dextra
Gelatin HES
n n
 Dextrose (free water)
water added to intravascular space

Vascul
ar
space

ECF

Expansions of total body water no volume effect

Isotonic crystalloids
Crystalloids added to intravascular space

Vascul
ar Kt
space

Kt = 250 ml.min-1
Svensen et.al, Br.J.Anaesth,
ECF 1998
ECF

Proportional expansion of intra- and

extravascular spaces
 Hypertonic Solutions
Hypertonic fluid added to intravascular space

Vascul
ar
space

ECF
ECF

Expansion of intravascular space

Contraction of ECF
 Crystalloids solutions are
distributed over the intire
Extracellular space.
And therefore crystalloids are indicated and
most effective when this space is depleted.
 Colloids

Advantages:
Good IVVP
Prolonged plasma volume support
Moderate volume needed
Minimal risk of tissue edema
Enhances micovascular flow
 Colloids

Disadvantages:
Risk of volume overload
Adverse effect on hemostasis
Adverse effect on renal function
Anaphylactic reaction
Expensive
 Characteristics of colloids

Product Name Conc.% Oncotic Initial Stays Max. Hemost.

Pressure Expansion (days) dose
%

Albumin 4,5 20 80-100 200-400 0

Dext70 Macrod 6 60-70 120 30-40 1.5g/kg +++

Dext40 Rheom 10 170-190 200 6 1.5g/kg +++

Gelatin Gelfusin 3-4 42 70-90 7 0-+

HES450/0 Plasmas6 6 24-30 100 120-182 20ml/kg +++

.7

HES200/0 Hesteril 6 30-37 100 3-4 33ml/kg +

.5

HES130/0 Voluven 6 36 100-110 50ml/kg 0-+

.4
 Changes in volume of body
compartments during fluid infusion

Compartment Glucose 5% NaCl 0.9% Colloids

Intravascular

Interstitial -

Intracellular -