Chapter 152 - Pathophysiology of Shock

Question 1

Perfusion-related shock

Answer 1

• hypovolemic
• obstructive,
• maldistributive
• cardiogenic

Question 2

Definition of shock

Answer 2

Shock is the result of any condition in which the metabolic demand for oxygen exceeds uptake and utilization

Question 3

Main mediators of mitochondrial dysfunction ?

Answer 3

TNF-alpha, reactive oxygen and nitrogen species

Question 4

What is the formula for the arterial content in O2 CaO2 ?

Answer 4

CaO2 = 1.34 × Hb × SO2 + 0.003 PaO2

Question 5

What are the 3 phases of shock?

What are 3 mechanisms intervening in the first phase?

Answer 5

1. Compensated:
   - activation of the SNS => catecholamine release: peripheral vasoconstriction, tachycardia, increased contractility
   - Activation of RAAS: further vasocontriction, decrease urinary water loss
   - Starling’s law: decrease in hydrostatic pressure, causing fluid shift from interstitial to vascular space
2. Decompensated: systemic hypotension, herperlacatemia, progressively resulting in metabolic acidosis
3. Terminal: Irreversible. Acidemia leads to catecholamine insensitivity and exhaustion of compensatory mediators => loss of vasomotor tone, decrease in venous return, decrease in cardiac output => CV collapse and death

Question 6

Draw the tree of life.

Answer 6

Page 981.

Question 7

What are the 4 mechanisms by which the ischemia due to shock causes SIRS?

Answer 7

1. Activation of neutrophils
   - Cellular damage => release of IL-6 and G-CSF (granulocyte colony stimulating factor)
   => enhanced filtration of neutrophils into affected tissues
   => after diapedesis, neutrophils release ROS, RNS, proteolytic enzymes: =» vasodilation, increased capillary permeability, destruction of ECM
   => tissue edema
2. Activation of the complement system:
   - Tissue injury => release of anaphylatoxin: increase vasc permeability, histamine, arachidonic acid, cytokine release, increase activ of granulocytes
3. Increased activity of phospholipase A2 and C: stimulate prod of PG and leukotrienes
4. Reperfusion injury: liberation of toxic metabolites and ROS after reperfusion

Question 8

What does the “shock gut” refer to?

Answer 8

Reduced intestinal perfusion => increased intestinal permeability => translocation bacteria + inflammatory mediators

Question 9

In cellular hypoxia - Can the damage to the mitochondria be persistent after resuscitation?

Answer 9

Yes. The membrane-bound nature of mitochondria is particularly susceptible to lipid peroxidation and free radical injury, as are the various proteins associated with electron transport.

Question 10

What are 5 causes of micocirculatory dysfunction in shock?

Answer 10

• Endothelial edema
• Inflammation induced endothelial activation
• Increased leukocyte adhesion
• Less deformable RBC
• Arterial microthrombi
  => capillary plugging