Pathology and Physiology of Shock

Pathology of Shock

• Shock is defined as systemic tissue hypoperfusion due to reduced cardiac output and/or reduced effective circulating blood volume.
• Hypoperfusion of cells and tissues leads to insufficient oxygen (cellular hypoxia) and nutrient supply. Waste product clearance is inadequate and metabolism shifts from aerobic to anaerobic.
• Widespread cellular metabolism impairment/dysfunction occurs.
• Prolonged shock state causes irreversible tissue injury resulting in multi-organ damage and potential patient death.

Pathophysiology of Shock

• Cells switch from aerobic to anaerobic metabolism, producing lactic acid.
• Cell function ceases and the cell swells.
• Cell membranes become more permeable, leading to electrolyte and fluid leakage in and out of the cells.
• The Na+/K+ pump, essential for maintaining cell function, is impaired.
• Mitochondria are damaged, leading to cell death.

Aetiology and Classification of Shock

• Types of shock:
  • Cardiogenic shock
  • Hypovolaemic shock
  • Distributive shock
    • Shock associated with systemic inflammation (e.g., septic shock)
    • Neurogenic shock
    • Anaphylactic shock

Cardiogenic Shock

• Acute circulatory failure with a sudden fall in cardiac output without a reduction in blood volume.
• Caused by myocardial pump failure.
• Causes include:
  • Deficient emptying (e.g., myocardial infarction, papillary muscle rupture, ventricular rupture, acute myocarditis, cardiac arrhythmias, cardiomyopathies)
  • Deficient filling (e.g., cardiac tamponade from haemopericardium)
  • Obstruction to outflow (e.g., pulmonary embolism, tension pneumothorax, dissecting aortic aneurysm)

Hypovolaemic Shock

• Results from loss of blood or plasma volume.
• Causes include:
  • Severe haemorrhage
  • Fluid loss (severe burns, diarrhoea, vomiting, extensive injury, uncontrolled diabetes mellitus, diabetes insipidus, diuretic overdose)

Shock Associated with Systemic Inflammation (e.g., Septic Shock)

• Caused by various insults such as microbial infections, burns, trauma, or pancreatitis.
• Characterized by a massive outpouring of inflammatory mediators causing arterial vasodilation, vascular leakage, and venous blood pooling.
• Widespread endothelial cell activation and injury often leading to a hypercoagulable state (DIC - Disseminated Intravascular Coagulation).
• Several microbial constituents initiate the process of septic shock.

Neurogenic Shock

• Less common, caused by loss of vascular tone and peripheral pooling of blood.
• Common causes include spinal cord injury and anaesthesia.

Anaphylactic Shock

• Initiated by generalized IgE-mediated hypersensitivity reaction.
• Characterized by widespread systemic peripheral vasodilation and increased vascular permeability.
• Leads to tissue hypoperfusion and hypoxia.

Two Basic Features of Shock Pathogenesis

• Reduced effective circulating blood volume
• Reduced oxygen supply to cells and tissues (resultant anoxia)

Stages of Shock

• Initial non-progressive phase
• Progressive stage
• Irreversible/intractable stage

Initial Non-Progressive Stage

• The body attempts to maintain adequate cerebral and coronary blood supply by redistribution.
• This involves mechanisms like baroreceptor reflexes, chemoreceptor reflexes, and the renin-angiotensin-aldosterone system (RAAS).
• These mechanisms lead to tachycardia, peripheral vasoconstriction, and fluid conservation.

Progressive Stage

• Widespread tissue hypoxia occurs, with anaerobic glycolysis and lactic acidosis.
• Tissue pH lowers, reducing effectiveness of vasomotor response and leading to pooling in microcirculation.
• Decreased cardiac output, anoxic injury, and progression to DIC are common.

Irreversible/Intractable Stage

• Widespread cell damage (with lysosomal enzyme leakages).
• Decreased myocardial contractility
• Renal shutdown (acute tubular necrosis)
• Ischemia of the bowel might introduce intestinal bacteria into the blood, causing or worsening septic shock.

Morphology of Shock

• Characterised by multisystem failure due to hypoxia causing extensive degeneration and necrosis in numerous organs.
• Major affected organs: heart, brain, kidneys, lungs, GIT, and adrenals.
• Specific organ-level structural changes are described in detail.

Clinical Manifestation of Shock

• Clinical findings like hypotension, weak rapid pulse, tachypnea, cool clammy/warm flushed skin, and oliguria (a decreased amount of urine output) are presented
• The presence of any of the aforementioned symptoms could indicate shock.

Diagnosis of Shock

• A detailed history coupled with a physical examination (including vital signs assessment) is critical
• Various laboratory investigations (e.g., blood culture, blood count, biochemistry panel, C-reactive protein, ECG, blood lactate, arterial blood gases, and clotting profile) are essential to confirm shock.

Management of Septic Shock

• Treat infection with broad-spectrum antibiotics.
• Establish an intravenous line for fluid resuscitation, monitoring blood pressure.
• Administer oxygen.
• Provide nutritional support when needed.
• Use vasoconstrictors and inotropes when needed.
• Manage hyperglycemia with insulin therapy as required.

Toxic Shock Syndrome

• Similar to septic shock, caused by toxins produced by Staphylococcus aureus.
• Associated with the use of absorbent tampons during menstruation, which facilitates staph aureus growth in the menstrual blood.

Neurogenic Shock

• Due to loss of vascular tone leading to peripheral pooling of blood.
• Common causes are spinal cord injury and anaesthesia.

Anaphylactic Shock

• Initiated by IgE-mediated hypersensitivity reaction.
• Characterized by widespread vasodilation and increased vascular permeability resulting in tissue hypoperfusion and hypoxia.