Shock: Types, Mechanisms, and Causes by Dr. Sanjiv Kumar

 
SHOCK
 
 
 
Dr. SANJIV KUMAR
ASSTT.  PROFESSOR,
DEPTT.  OF PATHOLOGY, BVC, PATNA
 
Definition
Failure of the circulatory system to adequately perfuse
vital organs.
 
An emergency condition.
 
 
Types
 
Cardiogenic shock
Hypovolemic shock
Septic/Endotoxic shock
Neurogenic shock
Anaphylactic shock
 
Results from cardiac pump failure
 
Cardiac output= heart rate x stroke volume
Cause:
Myocarditis
-Septicaemia or viral infection
Myocardial degeneration
-Vita E/Se def, infarcts
Cardiac temponade
-Haemopericardium
Electrolyte imbalance
-Hyperkalemia in uremic animals
 
CARDIOGENIC SHOCK
 
Mechanism
 
Inadequate cardiac output
 
Hypotension
 
Impaired tissue perfusion
Cellular hypoxia
 
Sudden severe loss of blood volume
Acute haemorrhage->1/4
th
 to 1/3rd
Loss of fluid: vomiting, diarrhoea etc.
Increased vascular permeability
Loss of intravascular fluid & proteins
 
Hypovolemic Shock
 
Hypovolemic Shock
 
Cardiogenic shock
 
Internal
fluid loss
 
External
fluid loss
 
Increased
vascular
permeability
Endotoxaemia
Burns
Haemorrhage
Diarrhoea
 
Decreased
blood
volume
 
Decreased
venous return
Myocarditis
Cardiac
temponade
 
Decreased
cardiac output
 
Decreased tissue
perfusion
 
Anoxic cell injury
 
Endothelial damage
 
Heart failure
 
Anaerobic
glycolysis in
muscles
 
Metabolic
acidosis
 
Renal failure
 
Results from bacterial infection in which large quantities of
endotoxins are released into circulation.
Endotoxins are complex components of cell wall of gram -ve
bacteria (LPS)
Endotoxins bind to serum proteins
Resulting complex bind to Macrophage/monocyte
TNF alpha, IL-1 secreted into circulation
Marked capillary dilation
Severe pooling of venocapillary blood
Decreased cardiac venous return
Cardiovascular collapse
 
SEPTIC/ENDOTOXIC SHOCK
 
Systemic manifestation of an acute allergic response
Exposure to allergens
Activation of mast cells or other effector cells
Release of histamine and other chemical mediators
Marked venocapillary dilation
Increased vascular permeability
Loss of intravascular fluid
Decreased cardiac venous return
Cardiovascular collapse
 
Anaphylactic shock
 
Severe trauma, anaesthetic accident, spinal cord injury.
There is disruption of vasomotor control, loss of vascular tone,
vasodilation and peripheral pooling of blood.
 
NEUROGENIC SHOCK
 
Decreased tissue perfusion causes anoxic injury
Anoxic injury to endothelial cells     Insufficient renal & muscular
 
perfusion
 
Increased vascular permeability                       metabolic acidosis
 
      Loss of intravascular fluid                           Suppress cardiac output
 
 
Insufficient myocardial perfusion         Anoxic injury to myocytes
 
                                                                        Decreased cardiac output
 
CLINICAL CONSEQUENCES OF SHOCK
 
Increase in heart rate and contractibility
Increased blood pressure through vasoconstriction
Conserve body water
 
BODY RESPONSE TO SHOCK
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Shock, a critical medical emergency, results from the failure of the circulatory system to adequately perfuse vital organs. This comprehensive overview delves into the different types of shock such as cardiogenic, hypovolemic, septic/endotoxic, neurogenic, and anaphylactic shock. Each type is explored in detail, covering their mechanisms, causes, and manifestations. Dr. Sanjiv Kumar, Assistant Professor at the Department of Pathology, BVC Patna, provides valuable insights into the diagnosis and management of shock conditions.

  • Shock
  • Circulatory System
  • Cardiogenic Shock
  • Hypovolemic Shock
  • Septic Shock

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  1. SHOCK Dr. SANJIV KUMAR ASSTT. PROFESSOR, DEPTT. OF PATHOLOGY, BVC, PATNA

  2. Definition Failure of the circulatory system to adequately perfuse vital organs. An emergency condition.

  3. Types Cardiogenic shock Hypovolemic shock Septic/Endotoxic shock Neurogenic shock Anaphylactic shock

  4. CARDIOGENIC SHOCK Results from cardiac pump failure Cardiac output= heart rate x stroke volume Cause: Myocarditis-Septicaemia or viral infection Myocardial degeneration-Vita E/Se def, infarcts Cardiac temponade-Haemopericardium Electrolyte imbalance-Hyperkalemia in uremic animals

  5. Mechanism Inadequate cardiac output Hypotension Impaired tissue perfusion Cellular hypoxia

  6. Hypovolemic Shock Sudden severe loss of blood volume Acute haemorrhage->1/4thto 1/3rd Loss of fluid: vomiting, diarrhoea etc. Increased vascular permeability Loss of intravascular fluid & proteins

  7. Hypovolemic Shock Cardiogenic shock Myocarditis Cardiac temponade Internal fluid loss External fluid loss Endotoxaemia Burns Haemorrhage Diarrhoea Metabolic acidosis Increased vascular permeability Decreased blood volume Decreased venous return Decreased cardiac output Heart failure Decreased tissue perfusion Anaerobic glycolysis in muscles Endothelial damage Anoxic cell injury Renal failure

  8. SEPTIC/ENDOTOXIC SHOCK Results from bacterial infection in which large quantities of endotoxins are released into circulation. Endotoxins are complex components of cell wall of gram -ve bacteria (LPS) Endotoxins bind to serum proteins Resulting complex bind to Macrophage/monocyte TNF alpha, IL-1 secreted into circulation Marked capillary dilation Severe pooling of venocapillary blood Decreased cardiac venous return Cardiovascular collapse

  9. Anaphylactic shock Systemic manifestation of an acute allergic response Exposure to allergens Activation of mast cells or other effector cells Release of histamine and other chemical mediators Marked venocapillary dilation Increased vascular permeability Loss of intravascular fluid Decreased cardiac venous return Cardiovascular collapse

  10. NEUROGENIC SHOCK Severe trauma, anaesthetic accident, spinal cord injury. There is disruption of vasomotor control, loss of vascular tone, vasodilation and peripheral pooling of blood.

  11. CLINICAL CONSEQUENCES OF SHOCK Decreased tissue perfusion causes anoxic injury Anoxic injury to endothelial cells Insufficient renal & muscularperfusion Increased vascular permeability metabolic acidosis Loss of intravascular fluid Suppress cardiac output Insufficient myocardial perfusion Anoxic injury to myocytes Decreased cardiac output

  12. BODY RESPONSE TO SHOCK Increase in heart rate and contractibility Increased blood pressure through vasoconstriction Conserve body water

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