5. Arterial hypotension associated with signs of
altered tissue perfusion, visualized through
three windows of body :
Peripheral window: skin that is cold, clammy
and blue ,pale or discolored.
Renal window: decreased urine output
:<0.5ml/kg/h.
Neurological window : Altered mental state
characterized by obtundation ,disorientation
and confusion.
6. Usually not clinically apparent
Metabolism changes from aerobic to
anaerobic.
◦ Lactic acid accumulates -must be removed by blood
and broken down by liver. usual cut-off value is
2mEq/L. but lactate level of >1.5mmol/L in patients
with septic shock are associated with increased
mortality.
7. Clinically apparent –Neural, Hormonal
&Biochemical compensatory mechanisms
Attempts aimed to overcome consequences
of anaerobic metabolism and maintaining
homeostasis.
8. 8
•Baroreceptors in carotid and aortic bodies activate SNS in
response to ↓ BP.
•Vasoconstriction, while blood to vital organs maintained.
•↓ blood to kidneys > activates renin– angiotensin system ↑
venous return to heart, CO, BP.
•Impaired GI motility- Risk for paralytic ileus.
•Cool, clammy skin .
Except septic patient who is warm and flushed
9. Shunting of blood from lungs increases
physiologic dead space.
↓ arterial O2 levels
Increase in rate/depth of respirations
V/Q mismatch
SNS stimulation increases myocardial O2
demands.
If perfusion deficit corrected, patient recovers
with no residual sequelae .
If deficit not corrected, patient enters
progressive stage
10. Begins when compensatory mechanisms
fail
Aggressive interventions to prevent
multiple organ dysfunction syndrome
(MODS)
Hallmarks -↓ cellular perfusion & altered
capillary permeability
Leakage of protein into interstitial
space
↑ systemic interstitial edema
11. Fluid leakage affects solid organs and
peripheral tissues.
• Anasarca
Movement of fluid from pulmonary vasculature
to interstitium(decreased blood flow to
pulm.Cap.)
Pulmonary edema
Bronchoconstriction
↓ residual capacity
Fluid moves into alveoli
Edema-Red. surfactant
Worsening V/Q mismatch
Tachypnea, Crackles
Incr.work of breathing
12. CO begins to fall
Red. peripheral perfusion
Hypotension
Weak peripheral pulses
Ischemia of distal extremities
Myocardial dysfunction results in
Dysrhythmias
Ischemia; Myocardial infarction
End result: complete deterioration of cardiovascular
system
13. Liver fails to metabolize drugs and waste.
Jaundice; Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
Mucosal barrier of GI system becomes ischemic
Ulcers
Bleeding
Risk of translocation of bacteria
Reduced ability to absorb nutrients
14. Exacerbation of anaerobic
metabolism
Accumulation of lactic acid
↑ capillary permeability
Profound hypotension and hypoxia
Tachycardia worsens.
Failure of one organ system
affects others.
Recovery unlikely
15. Myocardial Injury or Obstruction to Flow
◦ Arrythymias
◦ valvular lesions
◦ AMI
◦ Severe CHF
◦ VSD
◦ Hypertrophic Cardiomyopathy
20. Peripheral Vasodilation secondary to disruption
of cellular metabolism by the effects of
inflammatory mediators.
Gram negative or other overwhelming
infection.
Results in decreased Peripheral Vascular
Resistance.
24. Correct underlying disorder if possible and
then direct efforts at increasing the blood
pressure to increase oxygen delivery to the
tissues.
Maintain a mean arterial pressure of 65mmHg
(1/3 systolic + 2/3 diastolic)
Keep O2 sats >92%, intubate if neccesary
25. Normal Saline should be administered
anytime a patient is hypotensive.
If possible give colloid.
Vasopressors specially for septic shock .
Inotropic agents for cardiogenic shock
Intra-aortic Balloon Pump for cardiogenic
27. Attempt to correct problem and increase
cardiac output by diuresing and providing
inotropic support.
IABP is utilized if medical therapy is
ineffective. Cardiac Catheterization if
ongoing ischemia despite maximum medical
therapy.
Cardiogenic shock is the exception to the rule
that NS is always given for hypotension NS
will exacerbate cardiac shock.
28. Early goal directed therapy
Identification of source of infection
Broad Spectrum Antibiotics
IV fluids
Vasopressors
Steroids ??
Recombinant human activated protein C (
Xygris)
Bicarbonate if pH < 7.1
29. Correct bleeding abnormality
If PT or PTT elevated then FFP
Aggressive Fluid replacement with 2 large
bore IV’s or central line.
Pressors are last line, but commonly required.
30. HARRISON 18TH EDITION. Page no. 1689-
1695.
Consensus on circulatory shock and
hemodynamic monitoring. Task force of
European society of Intensive care
Medicine(Intensive care Med(2014)40:1795-
1815 DOI 10.1007/s00134-014-3525-z.
The swan –Ganz catheter: past ,present and
future(circulation .2009:119:147-152.)