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 cause1: 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 sign2.
- The general approach is the same whatever the cause2.
- What shock does to cells: oxygen delivery falls below need, cells switch to anaerobic metabolism and lactate accumulates. Injured cells release danger signals and inflammatory mediators that further damage the microcirculation, a vicious cycle that ends in multi-organ failure3.
- Three stages4:
- Compensated: baroreceptor reflexes, catecholamines, renin-angiotensin, ADH and the sympathetic system raise heart rate, constrict skin, gut and kidney vessels and retain fluid. Brain and heart flow is protected.
- Progressive: tissue hypoxia and lactic acidosis relax arterioles, blood pools in the microcirculation, endothelium is injured and DIC can start.
- Irreversible: cell injury is so severe that correcting the haemodynamics no longer saves the patient; acute tubular necrosis and gut barrier failure (with bacteria entering the blood) are typical.
- Built-in compensation: arteriolar constriction lowers capillary pressure, so fluid moves from the tissues back into the vessels. Veins hold about two-thirds of the blood volume, and venoconstriction pushes it back to the heart3.
- Brain and heart autoregulate their flow until mean arterial pressure falls to about 60 mmHg, after which their perfusion drops3.
- Septic and other inflammatory shock: cytokines and nitric oxide dilate arterioles, leaky endothelium causes protein-rich oedema, the blood becomes procoagulant (DIC in up to half), and the myocardium is depressed. Hyperglycaemia, lactic acidosis and relative adrenal insufficiency follow, and a hyperinflammatory phase can swing to immune suppression3,4. The same picture can follow burns, major trauma or pancreatitis4.
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 dehydration2.
- Warm versus cold: most shock gives pale, cool skin from vasoconstriction, but early septic shock can cause warm, flushed skin from vasodilation4.
- Organ clues: the kidneys conserve salt and water (small volumes of concentrated urine) before acute tubular necrosis sets in. Rapid breathing causes respiratory alkalosis early; shock and resuscitation can trigger ARDS3.
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/bicarbonate2, plus ECG, bloods, lactate and bedside ultrasound.
- Consider early invasive monitoring: urinary catheter (target urine above 0.5 mL/kg/hour) and central line2.
- Mixed venous (or central venous) oxygen saturation reflects whole-body oxygen balance: low when output is low, and can be normal or high in early sepsis when tissues fail to extract oxygen3.
Typical haemodynamic patterns3.
| Type | Filling pressure (JVP/CVP) | Cardiac output | Vascular resistance |
|---|---|---|---|
| Hypovolaemic | Low | Low | High (cold, clamped down) |
| Cardiogenic | High | Low | High |
| Septic, early (hyperdynamic) | Low to normal | High | Low (warm) |
| Septic, late | Variable | Low | High |
| Neurogenic | Low | Low | Low (loss of sympathetic tone) |
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 hypoxaemia2.
- 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 oedema2. 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 shock2.
- Treat the cause: stop haemorrhage and give blood; antibiotics and source control in sepsis; adrenaline in anaphylaxis; reperfusion or valve surgery in cardiogenic shock2.
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 surgery2.
- Obstructive causes (tension pneumothorax, tamponade, PE) need decompression, drainage or reperfusion, not just fluid1.
- Outlook depends on cause: more than 90% of young, otherwise healthy people with hypovolaemic shock survive with good care; septic shock and cardiogenic shock from large MI do much worse4.
- Adrenal insufficiency can cause or worsen shock; consider it when hypotension does not respond to fluids3.
References
- ANZCOR Guideline 9.2.3: Recognition and first aid management of the seriously ill person, including shock and sepsis (Appendix A classification)
- EMSA ED Handbook: Shock
- Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors. Harrison's Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Chapter 270, Approach to the patient with shock.
- Kumar V, Abbas AK, Aster JC, editors. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Philadelphia: Elsevier Saunders; 2015. Chapter 4, Hemodynamic disorders, thromboembolic disease, and shock.
Last updated from Sen’s notes on 22 October 2026.