Shock — Types, Vasopressors, Fluid Resuscitation & Critical Care Guide — Symptoms, Causes & Treatment | MyMedicPlus

Shock is a life-threatening medical emergency defined as acute circulatory failure causing inadequate tissue oxygen delivery relative to demand — leading to cellular hypoxia, anaerobic metabolism, lactic acidosis, and ultimately multi-organ failure and death if untreated. Shock is not simply hypotension: it is a state of inadequate perfusion, and some patients in early distributive shock may have a normal blood pressure. The clinical definition used in resuscitation is a systolic blood pressure below 90 mmHg (or a fall over 40 mmHg from baseline) with evidence of end-organ hypoperfusion. Shock is classified into four pathophysiological categories: distributive shock (maldistribution of blood flow — septic, anaphylactic, neurogenic — the most common, accounting for 60-70% of cases); hypovolaemic shock (inadequate circulating volume — haemorrhage, dehydration); cardiogenic shock (pump failure — MI, arrhythmia, myocarditis — 5-8% of STEMI cases; 50% in-hospital mortality); and obstructive shock (mechanical obstruction to cardiac output — tension pneumothorax, massive PE, cardiac tamponade). Prompt identification of the shock type is critical because treatment differs fundamentally between categories.

Distributive shock — septic shock (most common type): caused by dysregulated host immune response to infection producing vasodilation, endothelial leak, and myocardial depression; Gram-negative bacteria (LPS/endotoxin), Gram-positive bacteria (exotoxins), and fungi are the commonest organisms in ICU settings. Anaphylactic shock: IgE-mediated type I hypersensitivity reaction releasing massive histamine and other mediators causing profound vasodilation, increased vascular permeability, and bronchospasm; common triggers: drugs (penicillin, NSAIDs, contrast media, neuromuscular blocking agents), insect stings (Hymenoptera venom), and food allergens (peanuts, tree nuts, shellfish). Neurogenic shock: spinal cord injury above T6 causing loss of sympathetic vasoconstrictor tone. Hypovolaemic shock causes: haemorrhage (trauma — most common cause globally; GI bleeding — peptic ulcer, variceal haemorrhage; obstetric haemorrhage; aortic aneurysm rupture); severe dehydration (diarrhoea and vomiting — particularly cholera causing massive fluid loss; diabetic ketoacidosis). Cardiogenic shock causes: acute myocardial infarction (most common — typically anterior STEMI with >40% LV mass loss); acute valve failure (mitral regurgitation from papillary muscle rupture, aortic stenosis); arrhythmia (VT/VF, complete heart block); myocarditis; takotsubo cardiomyopathy. Obstructive shock causes: tension pneumothorax (needle decompression is emergency treatment); massive PE; cardiac tamponade (Beck's triad: hypotension, raised JVP, muffled heart sounds).

Common clinical features of all shock types reflecting cellular hypoperfusion: altered consciousness or agitation (early — from cerebral hypoperfusion); confusion, drowsiness, coma (late, severe shock); tachycardia (heart rate above 100 bpm — compensatory; often the first sign, may precede hypotension); hypotension (systolic below 90 mmHg, or MAP below 65 mmHg — the target of resuscitation); cold, mottled, cyanotic skin with prolonged capillary refill over 2 seconds (except in distributive shock — where skin is warm and flushed); oliguria (urine output below 0.5 mL/kg/hour) or anuria; tachypnoea and metabolic acidosis (Kussmaul breathing from lactic acidosis and bicarbonate buffering). Serum lactate over 2 mmol/L indicates inadequate tissue perfusion; above 4 mmol/L with hypotension defines septic shock by Sepsis-3 criteria and carries approximately 40% mortality. Distinguishing features by type: distributive/septic shock — warm peripheries, wide pulse pressure, fever/hypothermia, rigors, signs of infection focus; anaphylaxis — urticaria, angioedema, stridor, wheeze; hypovolaemic — cold/clammy, evidence of blood loss, history of vomiting/diarrhoea; cardiogenic — raised JVP, S3 gallop, pulmonary oedema (bilateral crackles), low oxygen saturations; obstructive (tension pneumothorax) — deviated trachea, absent breath sounds unilaterally, raised JVP.

Shock is a clinical diagnosis — the priority is immediate recognition and resuscitation; investigations run concurrently with treatment. Urgent bedside assessment: blood pressure (both arms), heart rate, oxygen saturation, temperature, respiratory rate, mental state (GCS), capillary refill time, and urine output (catheterise for accurate monitoring). Monitoring: continuous ECG monitoring (arrhythmia, STEMI), continuous oxygen saturation (SpO2). Point-of-care blood tests (immediate): arterial blood gas (pH, PaO2, PaCO2, HCO3, BE, lactate); serum lactate (above 2 mmol/L indicates shock; above 4 mmol/L with hypotension = septic shock per Sepsis-3); blood glucose; full blood count (haemoglobin for haemorrhagic shock); U&E, creatinine; coagulation screen (DIC in septic shock); troponin (myocardial injury); blood cultures (2 sets before antibiotics — in septic shock). Bedside echocardiography (POCUS — point-of-care ultrasound): critical for differentiating shock types — assesses LV/RV function (cardiogenic), inferior vena cava collapsibility (hypovolaemic), pericardial effusion (tamponade), right heart strain (PE). Chest X-ray: pulmonary oedema (cardiogenic), pneumothorax, ARDS pattern (septic/inflammatory). Specific investigations: CTPA for massive PE; CT aorta for aortic dissection; coronary angiography for cardiogenic shock from acute MI — immediate PCI for STEMI.

The ABCDE approach applies universally: secure airway (intubation if GCS below 8 or respiratory failure), provide high-flow oxygen, obtain large-bore IV access (bilateral antecubital fossa or central venous catheter), monitor continuously. Septic shock: Surviving Sepsis Campaign (SSC) 1-hour bundle — IV crystalloid 30 mL/kg (0.9% NaCl or Hartmann's solution) within 3 hours; broad-spectrum IV antibiotics within 1 hour (meropenem or piperacillin-tazobactam ± vancomycin — do not delay for culture results); blood cultures before antibiotics if possible; source control (drain abscess, remove infected lines, surgery); noradrenaline vasopressor (target MAP above 65 mmHg) via central line; vasopressin (0.03-0.04 units/minute) as second-line vasopressor; serum lactate reassessment to confirm resuscitation adequacy; hydrocortisone 200 mg/day IV in vasopressor-refractory shock. Anaphylactic shock: IM adrenaline 0.5 mg (1:1000, 0.5 mL) into the lateral thigh immediately — first-line, life-saving; repeat every 5 minutes if no response; IV normal saline; IM chlorphenamine 10 mg; IV hydrocortisone 200 mg (treats prolonged and biphasic reactions); salbutamol nebuliser for wheeze. Hypovolaemic shock: IV crystalloid and blood products (massive haemorrhage protocol: packed red cells, FFP, and platelets in 1:1:1 ratio); surgical haemorrhage control; tranexamic acid (1 g IV over 10 minutes for traumatic haemorrhage — within 3 hours of injury). Cardiogenic shock: dobutamine (inotrope — 2.5-20 mcg/kg/min); noradrenaline if severe hypotension; immediate PCI for AMI-related cardiogenic shock; intra-aortic balloon pump (IABP) for mechanical support. Obstructive shock: tension pneumothorax — immediate needle decompression (2nd intercostal space, midclavicular line), followed by chest drain; cardiac tamponade — pericardiocentesis; massive PE — systemic thrombolysis (alteplase 100 mg IV) or surgical embolectomy.

Multi-organ dysfunction syndrome (MODS): the principal complication of prolonged shock from any cause — sequential organ failure following inadequate perfusion and reperfusion injury. Acute kidney injury (AKI): oliguric AKI from renal hypoperfusion — requiring renal replacement therapy (haemofiltration) in severe cases; kidney recovery depends on duration and severity of hypoperfusion. Acute respiratory distress syndrome (ARDS): inflammatory lung injury causing bilateral consolidation, hypoxaemia, and stiff lungs — requiring mechanical ventilation with lung-protective strategy (low tidal volume 6 mL/kg, PEEP). Disseminated intravascular coagulation (DIC): widespread microvascular thrombosis consuming clotting factors and platelets, causing simultaneous bleeding and organ ischaemia; common in septic shock and obstetric haemorrhage. Myocardial dysfunction: even non-cardiogenic shock causes cytokine-mediated myocardial depression — contributing to a vicious cycle of worsening perfusion. Ischaemic gut (non-occlusive mesenteric ischaemia): from splanchnic vasoconstriction — may require surgical resection. Death: septic shock carries 25-30% 28-day mortality; cardiogenic shock 50% in-hospital mortality without mechanical support.

Prevention of septic shock: early recognition and treatment of infection before it progresses to sepsis and septic shock — the Sepsis 6 bundle within 1 hour (oxygen, blood cultures, IV antibiotics, IV fluids, lactate measurement, urinary catheter); hospital infection prevention (hand hygiene, appropriate antibiotic stewardship, line care, urinary catheter care bundles). Prevention of anaphylactic shock: carry a personalised AAI (adrenaline auto-injector — EpiPen or Emerade) at all times; wear medical alert identification; give written emergency action plan; inform school, family, and workmates; allergy specialist referral for allergen identification and immunotherapy. For severe food and venom allergy, allergen immunotherapy (AIT) modifies the immune response and provides long-term protection. Prevention of haemorrhagic shock: trauma prevention; management of known GI bleeding risk factors (peptic ulcers — H. pylori eradication, PPI therapy; oesophageal varices — beta-blocker, banding prophylaxis). Prevention of cardiogenic shock: primary PCI for STEMI within 90 minutes — reduces infarct size and cardiogenic shock incidence by over 60%. All ICU patients with vasopressor requirements require invasive arterial blood pressure monitoring (radial arterial line) for continuous MAP assessment.

Call 999 immediately for any suspected shock — this is a life-threatening emergency. Call 999 or ask someone to do so while you act for: sudden collapse with altered consciousness or unresponsiveness (start CPR if no pulse); anaphylaxis — administer adrenaline auto-injector (EpiPen) immediately into the lateral thigh and call 999, even if symptoms appear to improve (biphasic anaphylaxis can occur 1-8 hours later); and signs of severe sepsis — fever or hypothermia with confusion, rapid heart rate, low blood pressure, or mottled skin. Warning signs preceding shock that require urgent 999 or A&E attendance (within minutes): rapid heart rate with low blood pressure; dizziness and near-collapse with sweating; severe allergic reaction (throat swelling, difficulty breathing, generalised rash); known allergy history with sudden onset of any systemic symptoms after exposure to an allergen; and any trauma patient with persistent hypotension. Do not wait or drive yourself to hospital — call 999.