Parameters for hemodynamic

support of sepsis in adult patients:

2004 update
Erwin Pradian
Bagian Anestesiologi dan Reanimasi Fakultas Kedokteran Universitas
Padjadjaran/ Perjan RS. dr. Hasan Sadikin Bandung

Shock
occurs when circulatory
system fails to maintain
adequate cellular perfusion.
Syndrome that may arise
from any of several initiating causes: symptoms,
signs, and laboratory abnormalities hypoperfusion emerges.

Septic shock

Result when infectious agents or

infection-induced mediators in
the bloodstream produce
hemodynamic decompensation.
Primarily a form of distributive
shock.
A complex reaction between
pathologic vasodilation, relative
and absolute hypovolemia,
myocard dysfunction, and
altered blod flow distribution
occurs due to the inflammatory
response to infection.
Even after the restoration of
intravascular volume,
microcirculatory abnormalities
may persist and lead to
maldistribution of cardiac
output.

Septic shock
Cellular dysfunction final outcome with
multiple stimuli, eg:
- cellular ischemia.
- disruption of cellular metabolism
- free radical
caspases activation, HSP induction may
lead to apoptotic cell death.

Na
Ca

Neurotransmitter
gate channel

Na

Voltage sensitive channel

Na
v

Ca
v

Ca

Free radicals

Ca

Prostaglandins
Free Fatty Acids

Thromboxane

(Arachidonic acids)

Leukotrines

ATP

Ca
Ca
Ca

Membrane
lipids

Co-activated
phospholipase

Na

ATP

Na K

Free radicals

Ca

ATP

Therapy of Septic Shock

3 main components:
1. Maintain a reasonable MAP & CO.
2. Identified & eliminated nidus of
infection using antimicrobial drugs and
surgical drainage whenever indicated.
3. Interrupt the pathogenic sequence
leading to septic shock.