Shock | Shock- clinical features | Classification | Cardiogenic shock – |Hypovolemic shock – | Septic shock – | Neurogenic shock-| Anaphylactic shock-  | Pathogenesis of septic shock | Stages of shock | Non-progressive phase- | Progressive stage-  | Irreversible stage- | Morphology | Clinical features of shock |

 Shock 

Definition- Systemic hypoperfusion owing to reduction in either cardiac output or in the effective circulating blood volume.


Shock- clinical features


  • Hypotension
  • Tachycardia
  • Cold clammy skin
  • Rapid shallow respiration.
  • Drowsiness. 
  • confusion, irritability
  • Multi organ failure.


Classification 

Cardiogenic shock – 


  • myocardial pump failure –
  • Intrinsic myocardial damage (infarction), vent. Arrhythmias, 
  • extrinsic comopression (cardiac tamponade) or outflow obstruction (pulmonary embolism).


Hypovolemic shock – 


  • loss of blood or plasma volume- 
  • by h’hage, fluid loss from severe burns or trauma.

Septic shock –

  •  systemic microbial infection most commonly in gram negative infectns(endotoxic shock) ,can occur with gram +ve & fungal infectns


Neurogenic shock-


  • anaesthetic accident or spinal cord injury.

Anaphylactic shock- 


  • due to loss of vascular tone & peripheral pooling of blood-
  • IgE mediated response
  • -sys vasodilatation & increased vascular permeability.

Pathogenesis of septic shock


  • Results from spread & expansion of initially localised infection (eg. Abscess, peritonitis , pneumonia) into the blood stream.
  • Most cases are caused by endotoxin (ET) producing gram –ve bacilli . 
  • ET’s are bacterial wall lipopolysaccharides
  • Systemic vasodilatation(hypotension)
  • Decreased myocardial contractility
  • Widespread endothelial injury &activation  (ARDS)
  • Activation of coagulation sys (DIC).

   All this induces multiorgan system failure  affecting liver, kidneys & CNS .

Stages of shock


Non-progressive phase-


  •  reflex compensatory mech are activated & perfusion of vital organs is maintained. These include- 
  • Baroreceptors, 
  • Catecholamine release,
  • Activatn of renin-angiotensin axis,ADH release 
  • generalised Sympathetic stimulation.


Progressive stage- 


  • tissue hypoperfusion 
  • onset of worsening circulatory & metabolic imbalances including acidosis.
  • Clinically patient may become confused & urine output decreases.


Irreversible stage-


  • after the body has suffered cellular & tissue injury so severe that even if hemodynamic defects are corrected, survival is not possible. 
  • Here pt has complete renal shutdown due to acute tubular necrosis.


Morphology


  • Brain- ischemic encephelopathy
  • Heart- focal or widespread coagulation necrosis or subendocardial h’hage or contraction band necrosis.
  • Kidneys- tubular ischemic injury (ATN)-causes oliguria, anuria & electrolyte disturbances.
  • Lungs – less commonly affected ,resistant to hypoxic injury in hypovolemic shock. But in bacterial sepsis or trauma, changes of diffuse alveolar damage- shock lung.
  • Adrenals- cortical cell lipid depletion 

Clinical features of shock


  • Hypotension
  • Tachycardia
  • Cold clammy skin
  • Rapid shallow respiration.
  • Drowsiness, confusion, irritability
  • Multi organ failure.











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