SHOCK

(circulatory collapse)

Dr Bushra Al-Ayadhy
Department of Pathology, Faculty of Medicine,
Kuwait University.
 Definition
• A condition of profound hemodynamic and
metabolic disturbance characterized by failure of
the circulatory system to maintain adequate
perfusion of vital organs

• It results from reduction in either cardiac output

or the effective circulating blood volume

• This reduction results in hypotension followed by

impaired tissue perfusion and cellular hypoxia
It is the final common pathway for many fatal
events:

Severe hemorrhage
Extensive trauma
Extensive myocardial infarction
Massive pulmonary embolism and
Widespread sepsis
1. Cardiogeneic shock

• This is due to failure of myocardial pump

owing to intrinsic myocardial damage,
extrinsic pressure or obstruction to outflow

• For example, myocardial infarction,

arrhythmias, ventricular rupture,
pulmonary embolism, cardiac tamponade
2. Hypovolemic shock
• This is due to inadequate blood or plasma volume
– hemorrhage
– fluid loss (vomiting, diarrhea, burns or trauma)
3. Neurogenic
• loss of vascular tone and peripheral pooling. e.g
anesthetic accident or spinal cord injury
4. Anaphylactic
• IgE-mediated with systemic vasodilatation and
increased vascular permeability
5. Septic (endotoxic) shock

• Overwhelming microbial infectious process

• Most cases (70%) of septic shock are caused by
gram -ve bacilli expressing endotoxins
• Endotoxins 
•    These are bacterial lipopolysaccharides
(LPS) released when cell walls are
degraded. It consists of toxic fatty acid
(lipid A) core and a complex polysaccharide
coat
• Analogous molecules in the walls of gram
+ve bacteria and fungi can also elicit
septic shock
•    LPS binds CD14 molecules on leukocytes
(monocytes and macrophages)
At low doses LPS activates complement and
monocyte, leading to enhanced bacterial
eradication
•Mononuclear phagocytes produce TNF that
induces interlukin-1 synthesis
•TNF & IL-1 act on endothelial cells to produce
further cytokines (IL– 6&8)
•Cytokine cascade augments local acute
inflammation and microbe clearance
At moderate doses and higher LPS
levels
•Cytokines induces secondary
effectors (Nitric oxide, platelets
activating factor)
•Systemic effects of TNF & IL-I are
seen (fever & synthesis of acute -
phase reactants)
At higher doses LPS directly injures endothelial cells --->
coagulation cascade ↑ (and higher LPS levels). Septic shock
supervene; high dose cytokines & secondary mediators cause
- Systemic vasodilation (hypotension)
- Diminished myocardial contractility
- Widespread endothelial injury (Adult respiratory distress
syndrome)
- Activation of the coagulation system ---> DIC
- Hypoperfusion ---> multi-organ system failure
 Morphology of Renal damage in shock

Impaired renal blood flow ---> acute tubular necrosis.

Gross: Kidney is large, swollen, congested.
Pale cortex adjacent to hyperaemic outer medullar due to
blood pooling.
Micro: Foci of tubular epithelial loss. Epithelial
Casts (dead epithelial cells present in tubular lumens)
 
Renal clinical presentation in
shock
• Oliguria (urine output of 40-400
ml/day )
• normal (1500 ml/day)
•Salt & water overload
• ↑ K + ↑ Urea
• Metabolic acidosis
• ---> acute renal failure that can
be corrected by dialysis.
  Brain damage in shock
•Varies from mild to severe

•It affect large purkinje cells of the cerebellum

and pyramidal cells in the Hippocampus

•Prolonged ischemia will result in infarction at

“water shed” areas (junctional zones between the
main arterial territories).

•Severe permanent damage ---> coma ---> death.

      
 Cardiac damage in shock

Due to hypoperfusion

Petechial haemorrhage and

infarcts
  

Adult Respiratory Distress

Syndrome (ARDS)

A life threatening situation

occuring due to difficulty in
maintaining adequate perfusion/
ventilation even with mechanical
ventilator
 Adult Respiratory Distress
Syndrome (ARDS)
Pathogenesis
•Shock cause release of mediatros such as activated
complement (C5a) leukotriene B4 and platelets activating
factor, which promote larcocytes aggregation and
activation in the lung
•The neutrophils produce an achidonic acid metabolites,
such as thromboxane (cause pulmonary vascoconstriction,
oxygen- derived free radicals which injure the endothelial
and epithelial cells
•Lyzosomal enzymes digest structural proteins
The damaged endothelial cells are leaky
interstitial alveolar edema and fibrin exudation

The damaged epithelial cells (type 1

pneumocyte) desquamate to form the
characteristic hyaline membrane in
combination with surfactant and protein-rich
edema fluid (severe epithelial injury with lack of
surfactant ---> collapsed alveolar air spaces
(atelectasis) --> reduce compliance and gas
transfer
 Other causes of ARDS
1.Diffuse pulmonary infection
esp, viral
2.Oxygen toxicity
3.Inhalation of toxins or organic
solvents
4.Aspiration pneumonia
5.Cardiac surgery involving extra
- corporal pumps.