SHOCK

Coass Anestesi Periode 12 Desember 2017 – 13 Januari

2018
 Inadequate celullar
oxygenation affecting
multiple organ
Concept of Shock systems.

Inadequate delivery of oxygen to the

tissues leads to “dysoxia”.
 Normal Cardiovascular System

Adequatly “filling
the tank”  first
step to resuscitation
shock state
Cardiac output determined by :
1. Preload
2. Heart Rate
3. Contractility
4. Afterload
 Classifications of Shock
Hypovolemia shock
(exemplified by hemorrhagic
shock)

Obstructive shock (pulmonary

Hypodinamic embolism, cardiac tamponade,
tension pneumothorax)

Cardiogenic shock (as in an

acute myocardial infarction)

Sepsis Shock
Shock

Anaphylaxis shock

Hyperdinamic/distri
butive or Neurogenic Shock

vasodilatory shock

Liver failure

Adrenal crisis
 Hb Hb Hb

O2 O2 O2
Saturation Saturation Saturation

CARDIAC OUTPUT
  Disturbances of oxygen supply to
demand  change the oxygen delivery.
(however, there is still redistribution of
cardiac output via catecolamin response
to shock)

HOW?? Change/decrease oxygen delivery 

decrease of oxygen consumption 
oxygen-supply dependent  the tissues
become dysoxic  produce lactic
acidosis.
  There is accumulate an oxygen debt

The greater the oxygen debt ,

the greater the risk of organ
system dysfunction or death

Disoxyia And also, oxidative anaerob

metabolism only produce 2 ATP
, meanwhile the aerob
metabolism can produce 28 ATP.
Thus , this can lead to rapidly
dead of celullar , followed by
organ dysfunction and death.
  Adequate oxygen delivery but are
unable to appropriately use oxygen
caused by impairment mitochondrial
oxygen use.
 Mediators of this state include :
- inflammatory cytokines
Cytopathic - nitric oxide
Hypoxia - peroxynitrite
- poly(ADP-ribose) polymerasi-1
- Inhibition of pyruvate
dehydrogenase
 Ischemia

Oxygen free
ATP
radicals are then
formed, lipid
mediators are
Reperfusion converted released.
Hypoxanthine
Injury and the
Reperfusion
Inflammatory TNF-alfa, NO

Response Endothelial cell

dysfunction, neutrophil
chemotaxis,
microvascular changes

Tissue injury
 Cardiac
complications

Intestinal Renal
ischemia dysfunction

Organ Failure Respiratory

failure
Shock Hepatic injury

brain Hematologic
Initial Management Of
Shock
 Airway

ABC Breathing
Circulation
 Ventilate (Pemberian O2)
VIP Infuse (Cairan Resusitasi)
rule Pump (Pemberian obat vasoaktif)

*definitive theraphy sould be sought.

 Fluid
resuscitation

General rule of Inotropic

management support

Vasopressor
support
 EARLY
Monitoring of
shock should be : AGGRESSIVE
POSSIBLE
 Physical
Hemodynamiics
examination

Monitoring
Acid-Base Regional
Status Measurements
Universal Algorithm