Skip to content

Shock: Types, Pathogenesis, Symptoms, Morphology-NotesMed

Spread the love

What is shock?

Shock is defined as characterized by systemic hypoperfusion of tissues, caused by diminished cardiac output or by reduced effective circulating blood volume.


It is a pathological process that results from inadequate tissue perfusion, leading to cellular dysfunction and body organ failure. It is resulting in hypotension, impaired tissue perfusion, and cellular hypoxia.

Characteristic features

Types of shock

  1. Cardiogenic
  2. Hypovolemic
  3. Septic
  4. Anaphylactic
  5. Neurogenic

Cardiogenic Shocks

In this condition, there is low cardiac output due to the fact that myocardial pump failure. It is caused by the following conditions such as intrinsic myocardial damage (e.g. acute myocardial infarction), Ventricular arrhythmias, Extrinsic compression e.g. cardiac tamponade, and Outflow obstruction e.g., pulmonary embolism.

Hypovolemic shocks

It is due to inadequate blood or plasma volume and caused by the following conditions such as internal or external hemorrhage, vomiting, diarrhea, burns, and severe gastroenteritis.

Anaphylactic shocks

It is a systemic form of Ig E mediated hypersensitivity reaction. In these conditions, there is systemic vasodilation and increased vascular permeability occur.

Neurogenic shocks

The principal mechanism is a result of loss of vascular tone and peripheral pooling of blood, For clinical example is an anesthetic accident or spinal cord injury.

Septic shocks

It is defined as a shock due to severe sepsis with hypotension, which cannot be corrected by infusing fluids.

It results from vasodilation and peripheral pooling of blood and is associated with the dysfunction of multiple organs distant from the site of infection.

Etiopathogenesis of septic

  • Causes:
    • Gram-positive bacterial infections lipoteichoic acid/cell wall muramyl peptides
    • Gram-negative bacteria- lipopolysaccharide
    • Fungi
    • Superantigens (Staphylococcal toxic shock syndrome toxin)-toxic shock syndrome.

Stages of shock

  • Non-progressive phase
  • Progressive stage
  • Irreversible stage

These stages are mainly seen in hypovolemic and cardiogenic shocks.

Non-progressive stage

  • Reflex compensatory mechanisms activated and maintain perfusion of vital organs by maintaining cardiac output
  • Neurohumoral mechanism:
    • Baroreceptor reflexes
    • Release of Catecholamines
    • Activation of the renin-angiotensin-aldosterone axis
    • Release of ADH
    • Sympathetic stimulation
  • Tachycardia, peripheral vasoconstriction, and renal conservation of fluid.

Progressive phase

  • If the underlying causes are not treated, shock passes to the progressive phase
  • Tissue hypoperfusion occur
  • Metabolic acidosis due to anaerobic glycolysis
  • Vasodilation  and peripheral pooling of blood
  • Further endothelial  cell injury
  • Disseminated intravascular coagulation (DIC)
  • Tissue hypoxia of vital organs  

Irreversible stage

  • Without intervention, the shock finally enters an irreversible stage.
  • Severe tissue injury
  • No survival even with vigorous correction of circulatory imbalances
  • Heart- myocardial contractility fails
  • Kidney- acute tubular necrosis– acute renal failure
  • Bowel- intestinal flora may enter circulation and superimposed septic shock
  • Inevitable death


Coagulation necrosis in vital organs:

  • Heart- petechial hemorrhages in the epicardium and endocardium.
  • Kidneys – patchy tubular necrosis
  • Lungs- diffuse alveolar damage
  • Adrenal glands- cortical cell lipid depletion
  • Gastrointestinal tract- mucosal hemorrhage and ischemic necrosis
  • Liver- fatty change
  • Septic shock- widespread microthrombi formation and petechial hemorrhages on the serosal surface and the skin.
Organ Changes
Adrenal Lipid depletion in the cortical cells
Kidney Acute tubular necrosis
Lungs Relatively resistant to hypoxic injury. However, septic shock shows diffuse alveolar damaged (called shock lung) with hyaline membrane
Heart Coagulative necrosis & contraction band necrosis
Liver Congestion & necrosis of the centrilobular region of your liver
Brain Encephalopathy (ischemic or septic) and cortical necrosis
Gastrointestinal tract Diffuse gastrointestinal hemorrhage. Erosions of the gastric mucosa and superficial ischemic necrosis in the intestine

Clinical features

The clinical features are different in the depends upon the initiating cause such as,

  • Hypovolemic and cardiogenic shock
    • Weak rapid pulse, tachypnea; cool clammy cyanotic skin
  • Septic shock@
    • Warm and flushed skin
  • Initial threat to life depends upon the precipitating cause of shock- MI, sepsis
  • Soon- multiorgan failure– heart, brain, lungs  aggravate the condition
  • Worsening renal function – progressive oliguria, acidosis, electrolyte imbalance
  • Death

Treatment of shock

  • Replacement Therapy
    • The shock caused by hemorrhage: best therapy is transfusion of whole blood.
    • The shock caused by plasma loss: best therapy is the administration of plasma. In dehydration administration of electrolyte solution can correct the shock.
    • Dextran Solution as a Plasma Substitute
      • Dextran is a large polysaccharide polymer of glucose
      • Does not filter through the capillary pores
      • Nontoxic & contain appropriate electrolytes
      • Can replace plasma proteins as colloid osmotic agents
  • Sympathomimetic drugs:
    • Norepinepinephrine & epinephrine
    • Useful especially in neurogenic and anaphylactic shock@ have not proved to be very valuable in hemorrhagic shock
  • Other therapy
    • Treatment by head-down position.
    • Oxygen therapy
    • Treatment with glucocorticoids in severe @shock: increase the strength of heart, stabilizes lysosomes in tissue cells.

Leave a Reply

Your email address will not be published. Required fields are marked *