Shock — Types, Recognition, Emergency Treatment & Management Guide — Symptoms, Causes & Treatment | MyMedicPlus

Shock is a life-threatening syndrome of acute circulatory failure in which the cardiovascular system cannot deliver sufficient oxygen and nutrients to meet tissue metabolic demands. This results in cellular hypoxia, anaerobic metabolism, lactate accumulation, organ dysfunction, and — if untreated — irreversible organ failure and death. Shock is classified by its primary mechanism: hypovolaemic (reduced circulating volume), cardiogenic (pump failure), distributive (abnormal vasodilation — septic, anaphylactic, neurogenic), and obstructive (mechanical obstruction to blood flow — pulmonary embolism, tension pneumothorax, cardiac tamponade). Septic shock is the most common form in the ICU, carrying in-hospital mortality of 40-50%. Haemorrhagic shock (from major trauma or gastrointestinal bleeding) is the most common preventable cause of death in trauma globally. Prompt recognition and aggressive resuscitation within the first hour are critical determinants of survival.

Hypovolaemic shock: blood loss (haemorrhage from trauma, gastrointestinal bleeding, ruptured aortic aneurysm, ectopic pregnancy); fluid loss (severe vomiting/diarrhoea, burns, diabetic ketoacidosis). Cardiogenic shock: myocardial infarction (most common — loss of more than 40% of left ventricular myocardium), severe heart failure, acute valvular failure (mitral regurgitation, aortic stenosis), cardiac arrhythmias, myocarditis. Distributive shock: septic shock (most common — from overwhelming infection releasing inflammatory mediators causing profound vasodilatation); anaphylactic shock (IgE-mediated systemic hypersensitivity reaction to allergen — bee sting, food, medication); neurogenic shock (loss of sympathetic tone after high spinal cord injury). Obstructive shock: massive pulmonary embolism (thrombus blocking more than 50% of pulmonary vascular bed); tension pneumothorax (air trapped under pressure in pleural space compressing mediastinum); pericardial tamponade (blood/fluid in pericardium compressing cardiac chambers).

Clinical features of shock arise from compensatory mechanisms and tissue hypoperfusion. Early (compensated) shock: tachycardia (heart rate above 100 bpm — earliest sign), mild hypotension or normal blood pressure (compensation maintains BP initially), cool and clammy skin with peripheral vasoconstriction (except distributive shock — which may have warm, flushed peripheries), anxiety, restlessness, and subtle confusion. Late (decompensated) shock: hypotension (systolic BP below 90 mmHg), profound tachycardia, confusion and reduced consciousness, oliguria (urine output below 0.5 mL/kg/hr), mottled cyanotic skin, and respiratory distress. Distributive shock (septic): fever or hypothermia, rigors, wide pulse pressure, warm vasodilated peripheries early. Cardiogenic: pulmonary oedema (crackles), elevated JVP, third heart sound. Obstructive: distended neck veins, muffled heart sounds (tamponade), absent breath sounds (tension pneumothorax — immediate needle decompression required). Shock index (HR/SBP) above 1.0 indicates haemodynamic compromise.

Shock is a clinical diagnosis — do not delay treatment for investigation results. Rapid bedside assessment: ABC (Airway, Breathing, Circulation), heart rate, blood pressure, SpO2, capillary refill time, urine output, mental status. Point-of-care investigations: arterial blood gas (pH, lactate — above 2 mmol/L indicates tissue hypoperfusion; above 4 mmol/L severe shock), blood glucose. Venous access and bloods: FBC (haemoglobin, white cell count), renal function and electrolytes, LFTs, coagulation (DIC screen), serum lactate, blood cultures (two sets before antibiotics), troponin, BNP/NT-proBNP. ECG: myocardial infarction (STEMI — immediate PCI), arrhythmia. Chest X-ray: cardiomegaly, pulmonary oedema, pneumothorax. Bedside ultrasound (RUSH protocol): heart (tamponade, LV function, RV strain), IVC (volume status), aorta (AAA), lungs (pneumothorax). CT imaging for stable patients: CT pulmonary angiography (PE), CT aorta (dissection, AAA).

Call for emergency help immediately. ABCDE approach — treat each problem as identified. Airway and breathing: high-flow oxygen 15L/min via non-rebreather mask; intubation and mechanical ventilation if GCS below 8 or respiratory failure. Circulation: establish two large-bore IV cannulae (14-16G); fluid resuscitation — 500 mL crystalloid boluses (Hartmann's or 0.9% saline) titrated to response; target MAP above 65 mmHg, SpO2 above 95%, urine output above 0.5 mL/kg/hr, improving lactate. Specific shock management: haemorrhagic — transfuse packed red cells (target Hb above 70-80 g/L), haemostatic resuscitation (1:1:1 RBC:FFP:platelets), control bleeding (tourniquet, pressure, surgery, IR). Septic shock — Surviving Sepsis Campaign: IV antibiotics within 1 hour of recognition, vasopressors (noradrenaline) if MAP below 65 despite fluid resuscitation, hydrocortisone 200 mg/day for vasopressor-refractory shock. Cardiogenic — urgent revascularisation (PCI) for STEMI; inotropes (dobutamine), mechanical support (IABP, Impella). Anaphylactic — IM adrenaline (epinephrine) 0.5 mg immediately, IV antihistamines, IV corticosteroids. Tension pneumothorax — immediate needle decompression. Tamponade — urgent pericardiocentesis.

Irreversible multi-organ failure is the most catastrophic complication of untreated or refractory shock — progressive hypoperfusion causes ischaemic damage to the kidneys (acute tubular necrosis requiring renal replacement therapy), liver (ischaemic hepatitis — 'shock liver' with massive transaminase elevation), gut (mesenteric ischaemia, bacterial translocation perpetuating the inflammatory cascade), and brain (hypoxic-ischaemic encephalopathy). Acute respiratory distress syndrome (ARDS) develops in up to 40% of patients with septic and haemorrhagic shock — diffuse alveolar damage from inflammatory mediators causes refractory hypoxaemia requiring protective lung ventilation (tidal volume 6 mL/kg ideal body weight, PEEP titration, prone positioning for PaO2/FiO2 below 150 mmHg). Disseminated intravascular coagulation (DIC) from massive tissue factor release (trauma, sepsis) causes simultaneous microvascular thrombosis and haemorrhage — particularly severe in amniotic fluid embolism and abruption placentae. Reperfusion injury — paradoxical oxidative stress and inflammatory cell influx upon restoration of flow to ischaemic tissue — worsens organ function after fluid resuscitation. Abdominal compartment syndrome from massive fluid resuscitation causes intra-abdominal hypertension (IAP above 20 mmHg) — compressing the IVC, reducing venous return, and causing bowel ischaemia; decompressive laparotomy may be required. Obstructive shock from massive PE can cause cardiac arrest (PEA — pulseless electrical activity); survivors may develop chronic thromboembolic pulmonary hypertension (CTEPH). Mortality ranges from 10–20% in early reversible shock to above 80% in refractory multi-organ failure despite maximal support.

Many cases of shock are preventable or can be identified early before full decompensation. Sepsis prevention: hand hygiene, early appropriate antibiotic use, infection source control, vaccination. Track vital signs with early warning scores (NEWS2 in UK) in hospitalised patients to detect early deterioration. Anaphylaxis prevention: avoidance of known allergens, prescription of adrenaline auto-injectors (EpiPen) for high-risk individuals, and written emergency action plans. Haemorrhagic shock prevention: use of direct pressure and tourniquet in trauma, early haemostatic resuscitation, pre-hospital blood products in major trauma systems. Cardiogenic shock prevention: timely revascularisation for myocardial infarction — every hour of delay in STEMI treatment increases mortality. Inpatient deterioration: Intensive care outreach teams and rapid response systems enable early intervention before shock fully develops.

Shock is a life-threatening emergency. Call emergency services (999/911) immediately for: sudden collapse, loss of consciousness, severe chest pain, large-volume blood loss (from any source), high fever with confusion and rapid breathing (sepsis), allergic reaction with difficulty breathing or swelling of the throat (anaphylaxis), or any sudden deterioration in a person's level of consciousness. Do not wait or drive to hospital — these conditions require immediate paramedic assessment and resuscitation. For hospitalised patients showing signs of deterioration (falling blood pressure, rising heart rate, reduced consciousness), activate the medical emergency team or rapid response system without delay. Early recognition and treatment within the first hour dramatically improves survival outcomes.