13. Pathophysiology of Shock
Cells switch from aerobic to anaerobic metabolism
lactic acid production
Cell function ceases & swells
membrane becomes more permeable
electrolytes & fluids seep in & out of cell
Na+/K+ pump impaired
mitochondria damage
cell death
14. COMPENSATORY MECHANISMS:
Sympathetic Nervous System (SNS)-
Adrenal Response
Neurohormonal response
Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction
(Afterload)
Increased Preload
Hormonal: Renin-angiotension
system
Decrease renal perfusion
Releases renin--angiotension I
angiotension II ---potent
vasoconstriction & releases
aldosterone adrenal cortex
sodium & water retention (
intravascular volume )
15. SNS - Hormonal:
Antidiuretic Hormone
Osmoreceptors in
hypothalamus stimulated
ADH released by
Posterior pituitary gland
Vasopressor effect to
increase BP
Acts on renal tubules to
retain water
SNS - Hormonal: Adrenal
Cortex
Anterior pituitary releases
adrenocorticotropic hormone
(ACTH)
Stimulates adrenal Cortex to
release glucorticoids
Blood sugar increases to meet
increased metabolic needs
17. Stages of shock
• Initial : The cells become leaky and switch to
anaerobic metabolism.
• Non-progressive:(compensated stage)
Attempt to correct the metabolic upset of
shock.
• Progressive: (decompensated stage )
Eventually the compensation will begin to fail.
• Refractory : Organs fail and the shock can no
longer be reversed.
18. Clinical features
• Features of shock depend on the degree of loss of
volume & on duration of shock.
• Types
– Mild shock.
– Moderate shock.
– Severe shock.
23. Immediate Goals in Shock
Hemodynamic support MAP > 60mmHg
PAWP = 12 - 18 mmHg
Cardiac Index > 2.2 L/min/m2
Maintain oxygen delivery Hemoglobin > 9 g/dL
Arterial saturation > 92%
Supplemental oxygen and
mechanical ventilation
Reversal of oxygen dysfunction Decreasing lactate (< 2.2 mM/L)
Maintain urine output
` Reverse encephalopathy
Improving renal, liver function
tests
24. Principles of Resuscitation
• A: Airway
– patent upper airway
• B: Breathing
– adequate ventilation and oxygenation
• C: Circulation
– placement of adequate IV access
• cardiac function
• oxygenation
25. Fluid therapy
Crystalloids
• Lactated Ringer’s solution
• Normal saline
Colloids
• Hetastarch
• Albumin
Packed red blood cells
Infuse to physiologic endpoints
26. Hypovolemic Shock
Restore circulating volume with blood, colloid, or crystalloid
Control hemorrhage
Vasoconstrictor if BP still low after volume loading
Identify source of blood or fluid loss:
• Endoscopy/colonoscopy
• Angiography
• CT/MRI scan
27. Cardiogenic Shock
o Goal of Management :
o Treat Reversible Causes
o Protect ischemic myocardium
o Improve tissue perfusion
o Limiting/reducing myocardial damage during Myocardial
Infarction:
Increased pumping action & decrease workload of the heart
• Inotropic agents/Vasoactive drugs
• Intra-aortic balloon pump
• Cautious administration of fluids
• Transplantation
Consider thrombolytics, angioplasty in specific cases
29. Distributive Shock
Anaphylactic Shock
– Early recognition, treat aggressively
– Airway support
– IV epinephrine (open airways)
– Antihistamines
– Corticosteroids
– Immediate withdrawal of antigen if possible
– Judicious crystalloid administration
– Vasopressors to maintain organ perfusion
– Positive inotropes
30. Management of septic shock
A. Initial Resuscitation
• For sepsis induced hypoperfusion, at least
30ml/kg of IV crstalloid fluid should be given
within the first 3 hour.
• Additional fluids be guided by frequent
reassessment hemodynamic status.
B. Diagnosis
• Appropriate routine microbiological cultures.
31. C. Antimicrobial therapy
• IV antimicrobials as soon as possible after
recognition and within one hour for sepsis and
shock.
• Empiric broad spectrum therapy to cover all
pathogens.
• Antimicrobial treatment duration of 7 to 10 days
is adequate for most of infections.
32. D. Source control
• Recommend that a specific anatomic diagnosis be identified or
excluded as rapidly as possible in patients with sepsis or septic
shock, and that any required source control intervention be
implemented as soon as medically and logistically practical after
the diagnosis is made.
E. Fluid therapy
• recommend crystalloids as the fluid of choice for initial
resuscitation and subsequent intravascular volume replacement
• Use albumin in addition to crystalloids (if require substantial
amounts of crystalloids)
33. F. Vasoactive agents
• Recommend norepinephrine as the first choice
vasopressor.
• Suggest adding either vasopressin (up to 0.03 U/min)
or epinephrine to norepinephrine with the intent of
raising MAP to target, or adding vasopressin (up to
0.03 U/min) to decrease norepinephrine dosage.
• Use dobutamine in patient who show evidence of
persistent hypo perfusion despite adequate fliud and
vasopressors.
34. End Points of Resuscitation
Classic / Traditional
Restoration of blood pressure
Normalization of heart rate
and urine output
Appropriate mental status
Improved / Global
All of the above plus
Normalization of serum
lactate levels
Resolution of base deficit
Goal directed approach
Urine output > 0.5 mL/kg/hr
CVP 5 -10 cm H2o
MAP 65 to 90 mmHg
Central venous oxygen
concentration > 70%