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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Shock = inadequate tissue perfusion → cellular hypoxia → organ dysfunction. Medical emergency
- Four types: hypovolaemic (bleeding/dehydration), cardiogenic (pump failure), distributive (vasodilation — septic, anaphylactic, neurogenic), obstructive (mechanical obstruction — PE, tamponade, tension pneumothorax)
- Recognition: tachycardia, hypotension (systolic <90 or MAP <65), prolonged CRT, altered consciousness, oliguria, raised lactate
- ABCDE approach. Aggressive IV fluid resuscitation (250–500 mL crystalloid bolus) for hypovolaemic/distributive. AVOID excess fluid in cardiogenic
- Vasopressors (noradrenaline first-line) if hypotension persists despite fluids — requires ICU/HDU
- Identify and treat cause: stop bleeding (hypovolaemic), treat infection (septic), treat PE/tamponade/pneumothorax (obstructive), support pump (cardiogenic)
Overview
Shock is a state of circulatory failure resulting in inadequate tissue perfusion and cellular oxygen delivery, leading to cellular dysfunction and organ damage. It is classified by mechanism: hypovolaemic (loss of circulating volume — haemorrhage, burns, dehydration), cardiogenic (cardiac pump failure — MI, arrhythmia, valvular emergency), distributive (inappropriate peripheral vasodilation — sepsis, anaphylaxis, neurogenic), and obstructive (mechanical obstruction to cardiac output — massive PE, cardiac tamponade, tension pneumothorax). Sepsis is the most common cause of distributive shock. Haemorrhagic shock is the most common cause in trauma. Early recognition and cause-directed treatment are critical — untreated shock progresses to multi-organ failure and death.
Epidemiology
Shock accounts for approximately one-third of ICU admissions. Septic shock (distributive) is the most common type in ICU, accounting for ~60% of shock cases. Cardiogenic shock complicates approximately 5–8% of STEMI cases and carries a mortality of 40–50%. Hypovolaemic shock from trauma is the leading preventable cause of death in major trauma. Obstructive shock from PE is responsible for approximately 5–10% of in-hospital sudden deaths. The overall mortality of undifferentiated shock in ED is approximately 20–30%, but varies widely by type and cause.
Clinical Features
Symptoms
Altered consciousness: confusion, agitation, drowsiness, unresponsiveness
Thirst (hypovolaemic)
Chest pain (cardiogenic — MI; obstructive — PE)
Breathlessness
Fever or rigors (septic shock)
Symptoms of underlying cause: haematemesis, melaena, trauma, cough, dysuria
Signs
Tachycardia (usually >100 bpm — may be absent in beta-blocked patients or neurogenic shock)
Hypotension: systolic <90 mmHg or MAP <65 mmHg or >40 mmHg drop from baseline
Prolonged capillary refill time (>2 seconds)
Cool, clammy, mottled peripheries (hypovolaemic/cardiogenic). Warm peripheries in early distributive shock
Oliguria (<0.5 mL/kg/h) — sign of renal hypoperfusion
Raised JVP (cardiogenic, obstructive). Flat JVP (hypovolaemic)
Distended neck veins + hypotension + muffled heart sounds = Beck triad (tamponade)
Tracheal deviation + absent breath sounds + distended neck veins = tension pneumothorax
Investigations
First-line
Venous blood gas (VBG)Lactate (>2 mmol/L indicates tissue hypoperfusion; >4 = severe), pH, base excess
FBC, U&Es, LFTs, clotting, group and save/crossmatchBaseline. Hb for haemorrhage, renal function, coagulopathy
Blood glucoseExclude hypoglycaemia
ECGMI (cardiogenic), PE (right heart strain — S1Q3T3, RBBB), arrhythmia
Blood cultures (if sepsis suspected)BEFORE antibiotics if possible without delaying treatment
Second-line
CXRPneumothorax, pulmonary oedema, widened mediastinum, pneumonia
CTPAIf PE suspected as cause of obstructive shock
Echocardiography (bedside/POCUS)Pericardial effusion (tamponade), RV dilatation (PE), LV dysfunction (cardiogenic), IVC assessment (volume status)
eFAST (in trauma)Free fluid (haemorrhage), pneumothorax, pericardial effusion
Specialist
Invasive haemodynamic monitoringArterial line, central venous catheter, cardiac output monitoring — ICU
CT abdomen/pelvisIf intra-abdominal source suspected (trauma, AAA, surgical pathology)
1
Immediate — ABCDE approach
- Airway: secure if compromised (intubation if GCS ≤8)
- Breathing: high-flow oxygen 15 L/min. Decompress tension pneumothorax immediately (needle then chest drain)
- Circulation: two large-bore IV cannulae (14–16G). Rapid fluid bolus 250–500 mL crystalloid (reassess after each)
- Bloods: FBC, U&Es, lactate, clotting, crossmatch, blood cultures. ABG/VBG
- Monitor: continuous ECG, SpO₂, BP, urine output (catheterise)
2
Type-specific management
- HYPOVOLAEMIC: stop bleeding (direct pressure, tourniquet, surgical intervention). Transfuse (major haemorrhage protocol: 1:1:1 ratio RBC:FFP:platelets). Tranexamic acid 1 g IV within 3 h of injury
- CARDIOGENIC: avoid excessive IV fluids. Vasopressors/inotropes (noradrenaline ± dobutamine). Treat cause: PCI for MI, antiarrhythmics, valve intervention. Consider mechanical support (IABP, Impella)
- DISTRIBUTIVE (septic): IV antibiotics within 1 hour. Fluid bolus 30 mL/kg crystalloid within 3 h (Sepsis 6). Noradrenaline if MAP <65 despite fluids. Hydrocortisone 200 mg/day if vasopressor-refractory
- DISTRIBUTIVE (anaphylactic): IM adrenaline 0.5 mg (see Anaphylaxis entry)
- OBSTRUCTIVE (PE): systemic thrombolysis (alteplase 50 mg IV bolus if peri-arrest). Surgical embolectomy if thrombolysis fails
- OBSTRUCTIVE (tamponade): pericardiocentesis (percutaneous or surgical)
- OBSTRUCTIVE (tension pneumothorax): immediate needle decompression (2nd ICS MCL or 4th/5th ICS MAL) then chest drain
3
Escalation
- Early ICU/HDU involvement for any patient requiring vasopressors or inotropes
- Senior surgical review if surgical source suspected (haemorrhage, peritonitis)
- Monitor: serial lactate (should fall with adequate resuscitation — failure to clear = poor prognosis)
- Reassess response to fluids — if not responding consider alternative diagnosis or escalate
Complications
- Multi-organ failure: Prolonged hypoperfusion → renal, hepatic, respiratory, cardiac, and neurological dysfunction
- ARDS: Acute respiratory distress syndrome — common in septic and haemorrhagic shock
- DIC: Disseminated intravascular coagulation — consumptive coagulopathy, particularly in sepsis and massive transfusion
- AKI: From renal hypoperfusion — may require renal replacement therapy
- Death: Mortality varies by type: septic ~30–40%, cardiogenic ~40–50%, haemorrhagic (if uncontrolled) >50%
UKMLA Exam Tips
- 1Classify the shock type based on clinical picture: cold/clammy + flat JVP = hypovolaemic. Cold/clammy + raised JVP = cardiogenic/obstructive. Warm + bounding pulse = early distributive
- 2Lactate >4 mmol/L = severe tissue hypoperfusion. Serial lactate clearance is a marker of adequate resuscitation
- 3Tension pneumothorax: clinical diagnosis → immediate needle decompression. Do NOT wait for CXR confirmation
- 4Beck triad (tamponade): hypotension + distended neck veins + muffled heart sounds. Treat with pericardiocentesis
- 5Sepsis 6 (within 1 hour): give oxygen, IV fluids, IV antibiotics; take blood cultures, lactate, urine output
- 6Massive transfusion protocol: 1:1:1 ratio RBC:FFP:platelets. TXA 1 g within 3 h for trauma haemorrhage
- 7Noradrenaline is first-line vasopressor for septic, cardiogenic, and other shock types requiring vasopressor support
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