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Hypovolaemic shock !

Hypovolaemic shock is a life-threatening state in which the body loses so much blood or fluid that organs no longer get enough blood flow.

Updated 2026-10-29

Structures involved

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In biochemistry

In the clinical exam

In physiology

Why it happens

What it is

A life-threatening state of poor tissue perfusion caused by loss of intravascular volume, from bleeding (haemorrhagic shock) or from fluid losses such as vomiting, diarrhoea, burns or diuresis.

Who gets it

Haemorrhage is a leading preventable cause of death after trauma, which in Colombia includes road traffic injuries and violence. Diarrhoeal dehydration remains an important cause of hypovolaemia in young children.

Causes

  • Haemorrhage: trauma (chest, abdomen, pelvis, long bones, external), gastrointestinal bleeding, ruptured aortic aneurysm, ectopic pregnancy, postpartum haemorrhage
  • Gastrointestinal losses: vomiting and diarrhoea
  • Kidney losses: osmotic diuresis (diabetic ketoacidosis), diuretics, adrenal insufficiency
  • Skin losses: burns, heat illness
  • Third-space losses: pancreatitis, bowel obstruction, sepsis capillary leak

Risk factors

  • Major trauma
  • Anticoagulant or antiplatelet use
  • Extremes of age
  • Severe gastroenteritis in infants
  • Limited access to early care

Pathophysiology

Reduced venous return lowers preload, stroke volume and cardiac output. Sympathetic activation causes tachycardia and vasoconstriction, keeping blood pressure normal at first. As losses grow, compensation fails: hypotension, anaerobic metabolism and lactic acidosis follow. In trauma, hypothermia, acidosis and coagulopathy reinforce each other (the lethal triad).

Classification

  • Haemorrhagic shock classes (ATLS) by estimated blood loss: class I (up to about 15%), II (15 to 30%), III (30 to 40%) and IV (over 40%)
  • Non-haemorrhagic hypovolaemia (fluid losses)
  • Compensated or decompensated shock

Symptoms and signs

  • Early: tachycardia, anxiety, cool pale skin, delayed capillary refill, narrowed pulse pressure
  • Thirst, dry mucous membranes (dehydration)
  • Reduced urine output
  • Late: hypotension, confusion or drowsiness, rapid breathing
  • Visible bleeding or signs of internal bleeding (distended abdomen, pelvic or femoral deformity)

Diagnosis

Clinical
A clinical diagnosis: a source of loss plus signs of hypoperfusion. In trauma the primary survey (ABCDE) looks for bleeding in the chest, abdomen, pelvis, long bones and externally; the shock index (heart rate divided by systolic pressure) helps.
Tests
Lactate and base deficit (perfusion), haemoglobin (may be normal early in acute bleeding), blood type and cross-match, coagulation tests or viscoelastic testing, electrolytes, kidney function and blood gas.
Imaging
Bedside ultrasound (FAST/eFAST) for blood in the abdomen, pericardium or chest; chest and pelvic X-rays in trauma; CT once the patient is stable; ultrasound of the inferior vena cava to estimate volume status.

Differential diagnosis

  • Cardiogenic shock (myocardial infarction)
  • Obstructive shock (tension pneumothorax, cardiac tamponade, pulmonary embolism)
  • Septic shock
  • Anaphylactic shock
  • Neurogenic shock (spinal cord injury)

Goal of treatment

Stop the loss, restore circulating volume and oxygen delivery quickly, and prevent organ failure and the lethal triad of hypothermia, acidosis and coagulopathy.

Treatment

Acute
Haemorrhage control first: direct pressure, tourniquets, pelvic binder; urgent surgery or interventional radiology for internal bleeding.
Acute
Haemorrhagic shock: early balanced blood products (massive transfusion protocol), little crystalloid, permissive hypotension until bleeding is controlled (not in head injury), early antifibrinolytic in trauma.
Acute
Non-haemorrhagic losses: warmed isotonic crystalloids given in boluses with reassessment, and correction of electrolytes.
Follow-up
Heart rate, blood pressure, urine output, mental status, lactate and temperature to guide resuscitation.
Medical
Treating the cause: for example antiemetics, insulin and fluids in ketoacidosis, or hormone replacement in adrenal crisis.

Drugs for this condition

Complications

  • Acute kidney injury
  • Multiple organ dysfunction
  • Coagulopathy and dilution from large volumes of crystalloid
  • Hypothermia and metabolic acidosis
  • Abdominal compartment syndrome
  • Cardiac arrest and death

Prognosis

Depends on the cause, the amount lost and how quickly the source is controlled. Early haemorrhage control and blood product resuscitation improve survival; prolonged shock leads to irreversible organ failure.

Prevention

  • Road safety and injury prevention
  • Oral rehydration for diarrhoea in children
  • Early recognition and treatment of bleeding in hospital and before arrival

Test yourself

Think of the answer, then tap the question to see it.

Which is an early sign of hypovolaemic shock, and which is late?

Tachycardia (with cool skin and narrowed pulse pressure) is early; hypotension is late, as compensation has failed after a large loss.

From which ATLS class of haemorrhagic shock does systolic blood pressure usually fall?

Class III (about 30 to 40% of blood volume lost); classes I and II usually keep a normal blood pressure.

What is the lethal triad of trauma?

Hypothermia, acidosis and coagulopathy, which worsen each other and increase bleeding and death.

Why is large-volume crystalloid avoided in haemorrhagic shock?

It dilutes clotting factors and red cells, cools the patient and can worsen bleeding; early balanced blood products are preferred.

Why may haemoglobin be normal right after acute bleeding?

Whole blood is lost in proportion, so the concentration falls only after fluid shifts in or is given; normal haemoglobin does not exclude major blood loss.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Hypovolemia and Hypovolemic Shock (StatPearls (NCBI Bookshelf), 2025).

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Representative model, for educational purposes only.

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