basics and pathogenesis in various types of shock

1. Shock
Suman Raj Baral

2. • A clinical condition that is commonly seen in practise but not
commonly understood
• The most difficult part: Defining Shock
• O2 Delivery ≠ O2 consumption (Do2≠ Vo2)
• Most cases of shock due to decreased delivery of blood to tissues

3. Less blood- less oxygen- cessation of cellular aerobic
metabolism- decreased ATP- increased cellular dysfunction-
Death
Sustained anaerobic metabolism- increased cytokines, lactate,
NO leading to complicated shock.

4. Multiple factors determine delivery of
oxygen to tissues, however simplest way
to envision oxygen delivery is to consider
cardiac output being roughly equivalent
to blood delivered to tissues.
However, is CO always decreased ??

5. NO !!!!
• Increased oxygen demand due to increased cellular metabolism –
Overwhelming Infections: CO can be normal.
• Similarly:
Abnormal perfusion of tissues- large number of cells are bypassed by
oxygenated blood, an imbalance in oxygen demand and delivery develops
that leads to shock. ( in cases of SIRS/ reperfusion injury)

6. Mainly described
on 4 categories-
however clinical
cases neatly do
not fall on each
single category
and multiple
coexists.

7. Compensatory
Mechanisms
Neural/Hormonal
ACUTE VS MODERATE VS CHRONIC
Acute( within minutes)-
Catecholamines : (SNS / Hypoxemia)
Cortisol : ( effect not understood- stimulates glycogenolysis, mobilizes
fat and protein store from gluconeogenesis: endothelial cells of blood
vessels are powered by energy to contract, feed myocardial cells to continue
contration and allow brain cells to function in short term)
Trans-capillary Shifts: interstitium to blood vessel ( starling force),
protein shift from liver to vascular space that maintains oncotic pressure)
Moderate( 10 mins -1hr) - Angiotensin II ,Vasopressin
Chronic( 1- 48 hours): Aldosterone, Antidiuretic Hormone

8. Compensatory
Mechanisms
Neural/Hormonal
ACUTE VS MODERATE VS CHRONIC
Moderate( 10 mins -1hr)
Angiotensin II- Decreased barorecepetor activity in JG apparatus
Renin release- converts angiotensinogen to angiotensin I in blood stream-
Angiotensin I- Angiotensin II (Lungs- with ACE ): Vasoconstrictor
- improves circulation from splanchnic to brain/heart/kidney
- Retains water and sodium in kidneys to help maintain blood
volume through renal artery vasoconstriction that reduces filtration
of blood through direct effects on the tubules
Vasopressin: released from posterior pituitary owing to increased osmolarity due to
increased sodium and decreased water in blood that passes by the osmoreceptors in
hypothalamus or decreased effective circulating volume sensed by baroreceptors and
Stretch receptors ( atrial receptors: usually inhibit vasopressin when atria are full)
VASOPRESSIN binds V1 receptors on arterioles causing vasoconstriction

9. Compensatory
Mechanisms
Neural/Hormonal
ACUTE VS MODERATE VS CHRONIC
Chronic( 1- 48 hours):
Aldosterone : stimulated by angiotensin II on adrenal cortex to
release aldosterone- increases sodium reabsorption in DCT
along with water
Antidiuretic Hormone : binds to V2 receptors in collecting
ducts- induces insertion of aquaporin channels into the
Collecting ductto allow absorption of water/ stimulates
thirst to increase consumption of water

10. Physical Findings, Diagnosis and Management
Next Class