Cardiovascular emergencies

Shock — mechanisms and classification

Overview and approach

Shock is inadequate tissue perfusion; classify hypovolaemic, distributive, cardiogenic and obstructive mechanisms, often mixed.

  • ANZCOR classes shock by cause (1): hypovolaemic (bleeding, trauma, burns, severe vomiting and diarrhoea, dehydration); cardiogenic (MI, arrhythmia, cardiomyopathy); distributive (sepsis, anaphylaxis, neurogenic, brief faints); obstructive (tension pneumothorax, tamponade, PE, aortocaval compression in pregnancy).
  • Unrecognised circulatory failure is the commonest cause of preventable death in the ED and hospital wards; hypotension is a late sign (2).
  • The general approach is the same whatever the cause (2).
Assessment and clinical features

ABCDE, mentation, skin/peripheral perfusion, urine output, pulse/BP trends and context; normal BP does not exclude shock.

  • Early signs: tachycardia, cool peripheries or sweating, poor capillary refill or mottling, altered mental state, reduced urine output, low venous bicarbonate and metabolic acidosis. "If you see a low bicarbonate, think shock" (2).
  • Hypotension occurs only after compensation fails (decompensated shock) (2).
  • Commonly missed: sepsis, occult GI bleeding, internal bleeding in thoraco-abdomino-pelvic trauma, severe dehydration (2).
Differentials and investigations

ECG, selected blood gas/lactate, blood counts/chemistry and focused ultrasound or other imaging; reassess response rather than relying on one number.

  • Venous gas/bicarbonate (2), plus ECG, bloods, lactate and bedside ultrasound.
  • Consider early invasive monitoring: urinary catheter (target urine above 0.5 mL/kg/hour) and central line (2).
Management and follow-up

Call senior/resuscitation support, treat the cause and individualise fluid, blood, vasopressors or mechanical intervention under monitored care.

  • Airway: protect if comatose. Breathing: high-flow oxygen, ventilate if inadequate effort or refractory hypoxaemia (2).
  • The ED Handbook (SA, older text) gives: two large-bore IV lines, crystalloid or blood replacement, 500-1000 mL boluses over 5 minutes (250 mL if heart failure, ESRF, AMI or cardiogenic shock), repeat until clinical improvement or pulmonary oedema (2). The handbook also names colloids (Gelofusin/Haemacell), which are no longer standard; follow current local fluid policy.
  • Pressors (noradrenaline; metaraminol boluses) when pulmonary oedema coexists, septic shock does not respond to fluids, or spinal shock. Inotropes (adrenaline) for anaphylaxis, cardiogenic or refractory septic shock (2).
  • Treat the cause: stop haemorrhage and give blood; antibiotics and source control in sepsis; adrenaline in anaphylaxis; reperfusion or valve surgery in cardiogenic shock (2).
Red flags and clinical pearls

Avoid automatic large fluid loads in every shock state. Tamponade, tension pneumothorax, PE, haemorrhage and sepsis need prompt cause-specific treatment.

  • Relative fluid caution in ruptured aortic aneurysm and penetrating truncal trauma, which need urgent surgery (2).
  • Obstructive causes (tension pneumothorax, tamponade, PE) need decompression, drainage or reperfusion, not just fluid (1).
References
  1. ANZCOR Guideline 9.2.3: Recognition and first aid management of the seriously ill person, including shock and sepsis (Appendix A classification)
  2. EMSA ED Handbook: Shock

Last updated from Sen’s notes on 9 October 2026.