Shahid Sulaiman
INTRODUCTION
Definition:
Shock is a pathological process characterized by intense
failure of the circulatory system to maintain an appropriate
blood supply to the microcirculation. This results in life-
threatening inadequate perfusion (hypoperfusion) of vital
organs.
TYPES OF SHOCK
TYPES CAUSES
Cardiogenic • Myocardial infarction
•Ventricular rupture
•Arrhythmia
•Cardiac tamponade (pathologic compression
of heart)
•Pulmonary embolism
Hypovolemic Fluid loss (eg,hemorrhage, vomoting, diarrhea,
burns)
Septic Severe microbial infections (bacterial and
fungal)
Less common types During anesthetic accident or a spinal cord
Neurogenic shock injury IgE-mediated (type1) hypersensitivity
Anaphylactic shock reaction.
PATHOGENESIS OF CARDIOGENIC SHOCK
Cardiogenic shock is due to failure of myocardial pump.
The various causes lead to decrease in the cardiac output and
perfusion of tissue.
The left-sided failure also obstructs the entry of blood from
pulmonary vein into the left atrium.
This causes movement of fluid from pulmonary vessels into the
pulmonary interstitial space and later into the alveoli
(pulmonary edema).
PATHOGENESIS OF HYPOVOLEMIC SHOCK
Inadequate blood or plasma volume due to various causes leads
to hypovolemia(abnormal decrease in the volume of circulating
blood) and hypotension. The result is inadequate perfusion of
tissues.
PATHOGENESIS OF SEPTIC SHOCK
Causative organism,
Septic shock is most commonly due to infections by
Gram-positive bacteria, followed by Gram-negative bacteria
and fungi
Major pathogenic pathways in septic shock
The major contribution to pathophysiology of septic shock are:
- Inflammatory mediators
- Endothelial cell activation and injury
- metabolic abnormalities
- immune suppression
- organ dysfunction
Inflammatory mediators
Microbial components can activate the following:
- Activation of neutrophils and macrophages
- Activation of the complement cascade.
Endothelial cell activation and injury
Microbial constituents, inflammatory mediators produced by
leukocytes, hypoperfusion,and activation of complement
cascade cause endothelial activation or injury.
This lead to thrombi in small vessels, increased vascular
permeability and vasodialation.
The net result is decreased oxygen and nutrient supply to the
tissues due to hypoperfusion and dysfunction of many organs.
Metabolic abnormalities
Septic patients show hyperglycemia due to the action of
cytokines.
The hyperglycemia decreases neutrophil function and
suppresses bactericidal activity.
Immune suppression
The hyperinflammatory state initiated by sepsis can suppress
the immune system.
Organ dysfunction
High levels of cytokines and secondary
mediators may diminish myocardial
contractility and cardiac output.
Ultimately, there may be failure of multiple
organs, such as the kidneys, liver, lungs and
heart, terminating in death
STAGES OF SHOCK
Shock is a progressive disorder.
If not corrected, it can lead to death.
The exact mechanism(s) of death from sepsis is not
clear.
Shock evolves through three general phases
1) Non progressive (compensated/ reversible)
phase
2) Progressive phase
3) Irreversible phase
1) Nonprogressive (compensated/Reversible)
phase:
During the initial phase, various
compensatory mechanisms develop and
redistribute the blood in such a way that the
perfusion of vital organs is maintained.
2) Progressive phase:
If the underlying causes are not corrected, shock
passes to the progressive phase.
During this phase there is widespread tissue
hypoperfusion, tissue hypoxia and blood begins to
pool in the microcirculation.
This worsens the cardiac output and there will be
widespread hypoxic damage to the vital organs and
they begin to fail.
3) Irreversible phase:
Without intervention, the shock enters an
irreversible stage widespread cell injury further
aggravates the shock state.
Acute renal failure may develop and cause
death.
PROGNOSIS
Patients with hypovolemic shock
survive with appropriate
management.
Septic shock, or cardiogenic shock
associated with massive myocardial
infarction, prognosis is worse,
