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Shock
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Flashcards in this deck (40)

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  • What is the definition of shock?

    Systemic circulatory failure causing global tissue hypoperfusion that results in inadequate oxygen and nutrient delivery and leads to cellular dysfunction, organ failure, and death if untreated.

    shock definition

  • How does shock differ from hypotension?

    Shock is inadequate tissue perfusion; blood pressure may be normal early. Hypotension usually appears later; early shock can exist with 'normal' vital signs.

    shock hypotension clinical

  • What are the main types of shock?

    • Hypovolaemic
    • Cardiogenic
    • Distributive
    • Endocrine / metabolic
    classification shock

  • What are common causes of hypovolaemic shock?

    • External blood loss (trauma, surgery)
    • Internal bleeding (haemorrhage)
    • Severe burns (plasma loss)
    • Severe diarrhoea or vomiting
    • Fluid loss into body cavities (eg. peritonitis)
    hypovolaemic causes

  • What is the mechanism of hypovolaemic shock?

    Decreased circulating blood volume → reduced venous return → decreased cardiac output → reduced tissue perfusion → cellular hypoxia.

    hypovolaemic mechanism

  • What are common causes of cardiogenic shock?

    • Myocardial infarction
    • Severe arrhythmias
    • Cardiac tamponade
    • Massive pulmonary embolism
    cardiogenic causes

  • What is the mechanism of cardiogenic shock?

    Heart pump failure → cardiac output drops → blood backs up in lungs or systemic circulation → tissues receive inadequate oxygen → progressive organ dysfunction.

    cardiogenic mechanism

  • What defines distributive shock?

    Widespread vasodilation causing reduced systemic vascular resistance and venous pooling, producing relative hypovolaemia despite normal blood volume.

    distributive definition

  • What are the types of distributive shock?

    • Septic
    • Anaphylactic
    • Neurogenic
    • Heat-related
    distributive types

  • Outline the mechanism of septic shock.

    Infection releases endotoxins/exotoxins → macrophages release inflammatory cytokines → systemic vasodilation, capillary leak, possible microvascular thrombosis → worsened tissue hypoperfusion.

    septic mechanism

  • Outline the mechanism of anaphylactic shock.

    Allergen exposure → massive mast cell degranulation → release of vasoactive mediators → sudden vasodilation and increased vascular permeability → rapid drop in perfusion.

    anaphylactic mechanism

  • Outline the mechanism of neurogenic shock.

    Loss of sympathetic tone → widespread vasodilation → reduced vascular resistance → peripheral blood pooling → decreased venous return.

    neurogenic mechanism

  • Which endocrine abnormalities can cause shock?

    • Adrenal insufficiency
    • Pituitary infarction
    • Severe hypoglycaemia
    • Severe hyperglycaemia
    • Thyroid dysfunction
    endocrine causes

  • What is the general pathogenesis of shock?

    Initial insult → reduced perfusion → cellular hypoxia → switch to anaerobic metabolism → lactic acidosis → endothelial damage → inflammatory mediator release → microcirculatory dysfunction → organ damage.

    pathogenesis shock

  • How does shock become self-perpetuating?

    Organ damage reduces cardiac function; acidosis depresses myocardium; endothelial damage and microthrombi worsen perfusion → perfusion drops further and the cycle continues.

    progression shock

  • What physiological changes occur in compensated shock?

    Sympathetic activation → tachycardia increases cardiac output; peripheral vasoconstriction shunts blood to vital organs; renin-angiotensin system activated; blood pressure maintained.

    compensated physiology

  • What are the clinical features of compensated shock?

    • Tachycardia
    • Cold, clammy skin
    • Pale or cyanotic peripheries
    • Delayed capillary refill
    • Oliguria
    • Nausea
    • Restlessness
    • Blood pressure usually normal
    compensated clinical

  • What defines decompensated shock?

    Failure of compensatory mechanisms leading to falling blood pressure and evident organ dysfunction.

    decompensated definition

  • What are the clinical features of decompensated shock?

    • Hypotension
    • Weak, thready pulse
    • Tachypnoea
    • Confusion or decreased consciousness
    • Oliguria or anuria
    • Pulmonary oedema
    • Peripheral oedema
    decompensated clinical

  • Why does metabolic (lactic) acidosis occur in shock?

    Reduced perfusion causes cellular hypoxia, cells switch to anaerobic metabolism, and lactic acidosis develops.

    acidosis mechanism

  • What defines irreversible shock?

    • Extensive tissue necrosis
    • Multi-organ failure
    • Severe acidosis
    • Hypotension unresponsive to treatment
    • Death inevitable
    shock definitions

  • What sequence occurs when tissues receive inadequate oxygen delivery?

    • Cells switch to anaerobic metabolism
    • Lactic acid accumulates
    • Systemic acidosis develops
    pathogenesis shock

  • Why is the brain highly vulnerable in shock?

    • High metabolic demand
    • Minimal energy reserves
    • Highly oxygen dependent
    • Sensitive neurons die quickly
    brain vulnerability

  • Name the types of brain injury that occur in shock.

    • Selective neuronal necrosis
    • Watershed infarcts
    • Laminar cortical necrosis
    • Global hypoxic-ischaemic encephalopathy
    brain injury

  • What are watershed infarcts?

    • Occur at boundary zones between arterial territories
    • Furthest areas from direct arterial supply
    • Most sensitive to drops in perfusion
    brain watershed

  • Why are the kidneys vulnerable in shock?

    • High metabolic activity
    • Tubules sensitive to hypoxia
    • Complex microvascular system
    kidney vulnerability

  • Outline acute tubular necrosis (ATN) in shock.

    • Ischaemic injury to renal tubules
    • Tubular cells swell and die
    • Oliguria develops
    • Potentially reversible if patient survives
    kidney atn

  • Outline acute cortical necrosis (ACN) in shock.

    • Severe prolonged shock
    • Thrombosis of afferent arterioles
    • Glomerular necrosis
    • Irreversible renal failure
    kidney acn

  • What cardiac pathologies may occur in shock?

    • Arrhythmias
    • Subendocardial infarction
    • Contraction band necrosis
    • Fatty change
    heart complications

  • Why is the subendocardium especially vulnerable in shock?

    • Furthest from coronary blood supply
    • High oxygen demand
    • Sensitive to reduced perfusion
    heart vulnerability

  • What lung injuries occur in shock?

    • Pulmonary oedema
    • Diffuse alveolar damage
    • Hyaline membrane formation
    • Progression to acute respiratory distress
    lung injury

  • What liver injuries occur in shock?

    • Centrilobular congestion
    • Hypoxia of central zones
    • Fatty change
    • Haemorrhagic necrosis
    liver injury

  • What gastrointestinal complications occur in shock?

    • Ischaemic colitis
    • Stress-related ulcers
    • Haemorrhagic gastroenteropathy
    • Barrier breakdown leading to bacterial translocation
    gi complications

  • What happens to the pancreas in shock?

    • Oedema initially
    • Enzyme leakage
    • Vascular damage
    • Haemorrhagic pancreatitis
    pancreas injury

  • What adrenal pathology can occur in shock?

    • Cortical cell necrosis
    • Medullary haemorrhage
    • Associated with severe sepsis and DIC
    adrenal injury

  • Define disseminated intravascular coagulation (DIC).

    • Widespread activation of coagulation
    • Formation of microthrombi in microcirculation
    • Consumption of clotting factors and platelets
    • Paradoxical bleeding
    dic definitions

  • Outline the mechanism of DIC.

    • Trigger (sepsis, trauma, malignancy, etc.)
    • Systemic coagulation activation
    • Fibrin deposition in small vessels
    • Platelets and clotting factors consumed
    • Fibrinolysis activated
    • Bleeding tendency develops
    dic mechanism

  • What are causes of DIC?

    • Severe sepsis
    • Obstetric complications
    • Major trauma
    • Malignancy
    • Severe shock
    • Endothelial injury
    • Liver disease
    dic causes

  • What laboratory findings are seen in DIC?

    • Decreased platelets & fibrinogen
    • Increased fibrin degradation products
    • Prolonged PT & PTT
    dic labs

  • Why does DIC cause organ failure?

    • Microthrombi block capillaries
    • Tissue perfusion decreases
    • Ischaemic injury develops
    • Multi-organ dysfunction follows
    dic organfailure
Appunti di studio

Shock — high-yield study notes

Definition

  • Shock: systemic circulatory failure causing global tissue hypoperfusion.
  • Results in inadequate oxygen and nutrient delivery → cellular dysfunction, organ failure, death if untreated.

Shock vs hypotension

  • Shock = inadequate tissue perfusion; blood pressure can be normal early on.
  • Hypotension = low blood pressure, often a late sign of shock.

Classification (main types)

  • Hypovolaemic: loss of circulating volume.
  • Cardiogenic: pump failure of the heart.
  • Distributive: widespread vasodilation and relative hypovolaemia.
  • Endocrine / metabolic: hormonal or metabolic failure impairing perfusion.

Hypovolaemic shock

  • Causes: external haemorrhage (trauma, surgery), internal bleeding, severe burns, diarrhoea/vomiting, third-space losses (peritonitis).
  • Mechanism: ↓ circulating volume → ↓ venous return → ↓ cardiac output → tissue hypoperfusion → cellular hypoxia.

Cardiogenic shock

  • Causes: large myocardial infarction, severe arrhythmias, cardiac tamponade, massive pulmonary embolism.
  • Mechanism: impaired myocardial pump → ↓ cardiac output → blood backup (lungs/systemic) → inadequate tissue oxygenation → organ dysfunction.

Distributive shock and subtypes

  • Definition: widespread vasodilation → ↓ systemic vascular resistance → venous pooling → relative hypovolaemia despite normal volume.
  • Septic shock (mechanism): infection → endotoxins/exotoxins → macrophage cytokine release → systemic vasodilation + capillary leak → possible microvascular thrombosis → worsened tissue hypoperfusion.
  • Anaphylactic shock (mechanism): allergen → mast cell degranulation → vasoactive mediators → sudden vasodilation and increased permeability → rapid perfusion drop.
  • Neurogenic shock (mechanism): loss of sympathetic tone → widespread vasodilation → decreased venous return.

Endocrine / metabolic causes

  • Examples: adrenal insufficiency, pituitary infarction, severe hypo- or hyperglycaemia, thyroid dysfunction.

General pathogenesis of shock (high-level steps)

  • Initial insult (bleeding, infection, pump failure).
  • Reduced tissue perfusion → cellular hypoxia.
  • Cells switch to anaerobic metabolism → lactic acidosis.
  • Endothelial injury and inflammatory mediator release → microcirculatory dysfunction.
  • Microthrombi, capillary leak and ongoing hypoperfusion → organ damage.

How shock becomes self-perpetuating

  • Organ injury (especially myocardial) reduces pump function.
  • Acidosis depresses cardiac contractility.
  • Endothelial damage and microthrombi worsen perfusion → a vicious cycle of declining perfusion.

Clinical stages and features

  • Compensated shock (early): sympathetic activation → tachycardia, peripheral vasoconstriction, renin-angiotensin activation; blood pressure often maintained.
  • Clinical signs: tachycardia, cold clammy skin, delayed capillary refill, oliguria, restlessness; BP usually normal.
  • Decompensated shock (progressive): compensatory mechanisms fail → hypotension, organ dysfunction.
  • Clinical signs: hypotension, weak thready pulse, tachypnoea, confusion/reduced consciousness, oliguria/anuria, pulmonary oedema.
  • Irreversible shock (late): extensive tissue necrosis, multi-organ failure, severe acidosis, refractory hypotension, death inevitable.

Why metabolic acidosis occurs

  • Inadequate oxygen delivery → anaerobic metabolism → lactic acid accumulation → systemic metabolic acidosis.

Organ-specific injuries (key points)

  • Brain: very high metabolic demand and low reserves → selective neuronal necrosis, watershed infarcts (border zones), laminar cortical necrosis, global hypoxic-ischaemic encephalopathy.
  • Watershed infarcts occur in regions farthest from arterial supply and are most vulnerable to perfusion drops.
  • Kidney: highly susceptible due to active tubular transport and delicate microvasculature.
  • Acute tubular necrosis (ATN): ischaemic injury to tubules, reversible if patient survives.
  • Acute cortical necrosis (ACN): severe prolonged shock causing arteriolar thrombosis and irreversible glomerular necrosis.
  • Heart: subendocardium is vulnerable (furthest from coronary perfusion); may develop arrhythmias, subendocardial infarction, contraction band necrosis, fatty change.
  • Lungs: pulmonary oedema, diffuse alveolar damage, hyaline membrane formation → can progress to acute respiratory distress.
  • Liver: centrilobular congestion and hypoxic injury of central zones → fatty change and haemorrhagic necrosis in severe cases.
  • Gastrointestinal tract: ischaemic colitis, stress ulcers, haemorrhagic gastroenteropathy; barrier breakdown may allow bacterial translocation.
  • Pancreas: initial oedema, enzyme leakage, vascular damage → possible haemorrhagic pancreatitis.
  • Adrenals: cortical necrosis and medullary haemorrhage can occur, especially with severe sepsis and DIC.

Disseminated intravascular coagulation (DIC)

  • Definition: systemic activation of coagulation causing widespread microthrombi and consumption of clotting factors/platelets, with paradoxical bleeding.
  • Mechanism (sequence): trigger (sepsis, trauma, malignancy) → systemic coagulation activation → fibrin deposition in small vessels → consumption of platelets/clotting factors → secondary fibrinolysis → bleeding tendency.
  • Common triggers: severe sepsis, obstetric complications, major trauma, malignancy, severe shock, endothelial injury, liver disease.
  • Laboratory features: thrombocytopenia, low fibrinogen, elevated fibrin degradation products (e.g., D-dimer), prolonged PT and PTT.
  • Why DIC causes organ failure: microthrombi obstruct capillaries → tissue ischaemia and multi-organ dysfunction.

Key clinical recognition points (quick checklist)

  • Early signs often sympathetic: tachycardia, cool clammy skin, delayed capillary refill, oliguria, restlessness.
  • Hypotension is a late sign; do not wait for low BP to suspect shock.
  • Watch for organ-specific clues: confusion (brain), low urine output (kidney), respiratory distress (lungs), bleeding/coagulopathy (DIC).

High-yield summary

  • Shock is defined by inadequate tissue perfusion, not just low blood pressure; prompt recognition of type and stage is vital because mechanisms and organ injuries differ and the process can rapidly become self-perpetuating.