ICU · Resuscitation
Acute severe shock: classification, recognition, and management
Also known as Shock · Circulatory shock · Acute circulatory failure · Hypoperfusion
Shock = INADEQUATE TISSUE PERFUSION → cellular hypoxia → anaerobic metabolism → lactate → organ dysfunction → death if untreated. FOUR TYPES: (1) HYPOVOLAEMIC (blood/fluid loss — haemorrhage, dehydration, burns). (2) CARDIOGENIC (pump failure — MI, myocarditis, arrhythmia, valve failure). (3) DISTRIBUTIVE (vasodilation — septic, anaphylactic, neurogenic). (4) OBSTRUCTIVE (mechanical obstruction — tamponade, tension pneumothorax, massive PE). CLINICAL: COMPENSATED (tachycardia, narrowed pulse pressure, cool peripheries, anxious — BP normal [compensating]) → DECOMPENSATED (hypotension, oliguria, altered consciousness, mottled skin — BP falling [decompensating]) → IRREVERSIBLE (multi-organ failure — cell death — unresponsive to treatment). MONITORING: lactate (perfusion + prognosis), base excess (acidosis from hypoperfusion), SvO2/ScvO2 (tissue oxygen extraction — low = extracting more = worse perfusion), urine output (<0.5 mL/kg/hr = renal hypoperfusion). MANAGEMENT: ABC + TREAT CAUSE + FLUIDS (if responsive) + VASOPRESSORS (if vasodilated) + INOTROPES (if cardiac) + TRANSFUSION (if haemorrhagic) ± SURGERY (if mechanical/bleeding). GOAL: restore PERFUSION (lactate clearing, urine 0.5, MAP ≥65, conscious).
Checked against its sources on 11 Sept 2026
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CICMFFICMEDIC
Red flags
- Shock = inadequate tissue PERFUSION (not just low BP — BP is LATE sign)
- 4 types: hypovolaemic, cardiogenic, distributive, obstructive
- LACTATE is the best perfusion marker (clearing = improving; rising = worsening)
- Tachycardia + narrowed pulse pressure + cool peripheries = EARLY shock (BP still normal)
- TREAT THE CAUSE + restore PERFUSION (not just BP)
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Meet the patient
The patient. A 68-year-old man arrives in the resuscitation bay grey, clammy, and barely rousable. His blood pressure is 82/50 with a narrow pulse pressure, his heart rate is 128, and his capillary refill is 5 seconds. He is in shock; the question is which of the four haemodynamic patterns he carries, because the pattern decides the first drug: fluids for the empty tank, inotropes for the broken pump, vasopressors for the leaky pipes, and relief of obstruction for the blocked pipe.[1][2]
Perfusion, not pressure. Shock is the cell starving for oxygen, whatever the blood pressure number. By time pressure drops, a large fraction of circulating volume can already be lost. The early signs are tachycardia, narrowed pulse pressure and cool peripheries.[19][1]
Four types of shock
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| Feature | Hypovolaemic | Cardiogenic | Distributive (septic) | Obstructive |
|---|---|---|---|---|
| Problem | LOW VOLUME (empty tank) | PUMP FAILURE (broken pump) | VASODILATION (leaky pipes) | MECHANICAL OBSTRUCTION (blocked pipe) |
| Common causes | Haemorrhage, dehydration, burns, GI loss | MI, myocarditis, arrhythmia, valve failure | Sepsis, anaphylaxis, neurogenic (spinal cord) | Tamponade, tension PTX, massive PE |
| SVR | HIGH (compensatory vasoconstriction — cold) | HIGH (compensatory — cold) | LOW (vasodilation — warm) | HIGH (compensatory — cold) |
| Cardiac output | LOW (low preload) | LOW (pump failure) | HIGH early / LOW late (high HR + vasodilation → high output early; then cardiac dysfunction → low late) | LOW (obstructed flow) |
| PCWP (if measured) | LOW | HIGH (LV failure → backup) | LOW-NORMAL | LOW (tamponade/PTX) or normal-high (PE) |
| SvO2 | LOW (extracting more — low delivery) | LOW (can't deliver — pump failure) | HIGH early (can't extract — mitochondrial dysfunction/cytopathic dysoxia) / LOW late | LOW |
| Skin | COLD (vasoconstriction) | COLD (vasoconstriction) | WARM early (vasodilation) / COLD late (decompensated) | COLD (vasoconstriction) |
| Treatment | FLUIDS + BLOOD (restore volume) + stop bleeding | INOTROPES (improve pump) + treat cause (PCI for MI) | VASOPRESSORS (constrict) + FLUIDS (if depleted) + antibiotics (if septic) | RELIEVE OBSTRUCTION (decompress PTX, drain tamponade, thrombolyse PE) |
Management of acute shock
- Recognise early, before the BP drops. In compensated shock the BP is still normal because the body is compensating, and the early signs are: tachycardia (HR >100 — sympathetic drive maintaining cardiac output despite a low stroke volume); a narrowed pulse pressure (the systolic falls [low stroke volume] but the diastolic rises [vasoconstriction] — e.g., 100/80 [PP=20]; normally PP >40); cool peripheries (vasoconstriction shunting blood to the vital organs — capillary refill >3s); anxiety/agitation (adrenaline — early cerebral hypoperfusion); and tachypnoea (RR >20 — compensatory, blowing off CO2 from anaerobic metabolism, or metabolic acidosis compensation). In decompensated shock the BP is dropping because compensation is failing, and the late signs are: hypotension (SBP <90 or MAP <65 — the body can no longer maintain BP); oliguria (<0.5 mL/kg/hr — renal hypoperfusion, the kidney receiving inadequate blood); altered consciousness (confusion → coma — cerebral hypoperfusion); mottled skin (patchy cyanosis — severe vasoconstriction plus stagnation); and metabolic acidosis (lactate >2 → pH <7.25). Don't wait for hypotension — by the time the BP drops, significant volume has already been lost; recognise shock early (tachycardia, narrowed PP, cool peripheries, rising lactate) and intervene before decompensation.[19][1]
- Classify the shock type to guide treatment. The history points to the type: trauma/bleeding → hypovolaemic; chest pain/MI → cardiogenic; fever/infection → distributive (septic); allergy/exposure → anaphylactic; spinal cord injury → neurogenic; chest trauma → obstructive (tamponade/PTX). On examination, warm shock (distributive — vasodilation — warm peripheries, wide PP, bounding pulse) is distinguished from cold shock (hypovolaemic/cardiogenic/obstructive — vasoconstriction — cool peripheries, narrow PP, weak pulse); the JVP (internal jugular vein) is low (empty — hypovolaemic/distributive) or high (congested — cardiogenic/obstructive); the chest has bilateral crackles (cardiogenic — LV failure → pulmonary oedema) or is clear (hypovolaemic/distributive/obstructive); and the skin shows urticaria/angioedema (anaphylactic) or mottling (severe shock of any type). Bedside investigations: ECG (MI — ST changes; arrhythmia — AF/VT; PE — S1Q3T3/RV strain); lactate (elevated in all shock — from anaerobic metabolism — severity and prognosis); ABG (metabolic acidosis — from lactate plus renal failure); bedside echo (focused cardiac ultrasound — RUSH/BLUE protocol — identifying a hyperdynamic LV [empty — hypovolaemic/distributive], a depressed LV [cardiogenic], RV dilation [PE — obstructive] or a pericardial effusion [tamponade — obstructive]); CXR (pneumothorax [obstructive]; pulmonary oedema [cardiogenic]; pneumonia [septic source]); FBC (Hb — bleeding; WCC — infection); U&E (AKI — renal hypoperfusion); and group and crossmatch (if haemorrhagic — for transfusion). The classification guides treatment: hypovolaemic → fluids/blood; cardiogenic → inotrope; distributive → vasopressor plus fluids; obstructive → relieve the obstruction.
- Resuscitate: ABC, fluids, vasopressors. Airway and breathing: oxygen (100% initially to maximise O2 delivery; reduce if SpO2 >96%), and intubate if GCS <8 or respiratory failure (shock → respiratory muscle fatigue → respiratory failure). Circulation: 2 large-bore IV cannulae (14-16G) for rapid fluid/blood administration. Fluid challenge: 250-500 mL crystalloid (balanced — Hartmann's/Ringer's — preferred over saline for less hyperchloraemic acidosis — SMART/SALT-ED) over 15-30 min, then reassess (MAP, HR, urine output, lactate, capillary refill, skin temperature). If the patient responds (MAP rises, HR falls, urine increases, lactate falls), more may be given (titrated); if not, stop fluids (the patient is not volume-responsive, and more fluid → overload → pulmonary oedema) and start a vasopressor. Vasopressors (if hypotensive despite fluids): noradrenaline first-line (alpha-1 — vasoconstriction — raises SVR → raises BP), target MAP ≥65 mmHg, peripheral initially if urgent (large vein, forearm — SSC 2021 — then central), dose 0.05-0.5 mcg/kg/min (titrate); add vasopressin (0.03 U/min — if NA >0.25-0.5) and hydrocortisone (200 mg/day — if vasopressor-dependent). Inotropes (if cardiogenic): dobutamine (beta-1 — positive inotropy and chronotropy — improves cardiac output — 2.5-10 mcg/kg/min) or milrinone (phosphodiesterase inhibitor — inodilator — 0.125-0.75 mcg/kg/min). Blood (if haemorrhagic): massive transfusion protocol (RBC:plasma:platelet 1:1:1 — PROPPR — ratio of products), TXA within 3h (CRASH-2 — reduces mortality), targets Hb >70-80 (restrictive — TRICC), INR <1.5, platelets >50, fibrinogen >1.5. Monitor continuous BP (arterial line if on vasopressors), HR, SpO2, urine output (catheter) and lactate (trend); consider advanced monitoring — ScvO2 (central venous O2 saturation — target >70%; if low, the tissues are extracting more and delivery is inadequate — give more fluids/blood/inotrope) and cardiac output monitoring (PiCCO/LiDCO/thermodilution — if complex/unresponsive shock).[1][20]
- Treat the cause — the #1 priority. Shock is secondary, driven by its underlying cause: unless the cause is treated, shock persists, organs fail and the patient dies, so treat the cause and support perfusion simultaneously. Haemorrhagic hypovolaemic shock: stop the bleeding (surgery, interventional radiology, endoscopy — GI bleed → endoscopy; trauma → surgery; aortic → surgery) plus transfusion (massive transfusion protocol plus TXA). Non-haemorrhagic hypovolaemic shock: replace fluid (crystalloid — for dehydration/GI loss) and electrolytes (K+, Mg2+). Cardiogenic: ACS → PCI (primary PCI for STEMI) or thrombolysis; arrhythmia → cardiovert (if unstable AF/VT) or pace (if bradycardia/heart block); valve failure → surgery (AVR/MVR); myocarditis → supportive ± MCS (VA-ECMO — bridge to recovery); MCS if refractory (IABP/Impella/VA-ECMO — bridge to recovery/decision). Septic: antibiotics within 1h (broad-spectrum) plus source control (drain abscess, remove infected line, surgery for perforation). Anaphylactic: adrenaline IM 0.5 mg (lateral thigh — repeat every 5-15 min) plus fluids, O2, antihistamine and steroid. Neurogenic (spinal cord injury): noradrenaline (for vasodilation — loss of sympathetic tone) plus atropine (for bradycardia — unopposed vagal). Tamponade: pericardiocentesis (drain fluid — relieve compression) or surgery (if surgical cause — aortic dissection into pericardium). Tension pneumothorax: needle decompression (2nd ICS mid-clavicular or 5th ICS mid-axillary — BATLS) then chest tube (definitive). PE: thrombolysis (systemic — if massive/high-risk) or embolectomy (if lysis contraindicated).[12][13][14][15][17][18]
- Monitor and assess the response. The goal is restored perfusion, not just BP: the markers are lactate clearing, urine >0.5, MAP ≥65, a conscious patient, warm skin and normal capillary refill. Clinically, MAP ≥65 is the BP target; a falling HR, warming skin (capillary refill <3s), urine output >0.5 mL/kg/hr (renal perfusion restored) and an improving conscious level (cerebral perfusion restored) all mean improvement. On the labs, lactate clearing by ≥20% per 2h means improvement (Jansen 2010 — LACTATE trial — lactate-guided therapy improved outcomes), while a rising lactate means ongoing hypoperfusion and a reassessment (more fluids? higher vasopressor? treat cause? alternative diagnosis?); base excess normalising (a marker of acid-base correction), pH normalising and creatinine improving (AKI recovering) also mean improvement; ScvO2 (central venous O2 saturation) >70% means adequate delivery, and <70% means the tissues are extracting more because delivery is inadequate — give more fluids/blood/inotrope. If the patient is not improving: reassess the shock type (was it distributive but actually cardiogenic too? mixed shock is common — e.g., septic plus cardiogenic [septic cardiomyopathy]); repeat the echo (has LV/RV function changed? a new cardiogenic component?); reassess fluid responsiveness (passive leg raise, fluid challenge, IVC ultrasound — the patient may be fluid-responsive again after initial non-response, or may now be overloaded); escalate vasopressors (NA → vasopressin → hydrocortisone → methylene blue → angiotensin II — see the vasoplegic shock topic); consider advanced monitoring (ScvO2, cardiac output monitoring, PA catheter in complex/unresponsive shock); and search for an undiagnosed cause (missed source of sepsis? ongoing bleeding? new MI? new tamponade? mesenteric ischaemia? adrenal insufficiency?).[6]
- Complications and prognosis. Shock is life-threatening; early recognition (before the BP drops), treating the cause and restoring perfusion (lactate clearing, urine, MAP, consciousness) give the best outcomes, and MODS and PICS are the legacy of shock even when it is survived. The complications are: multi-organ dysfunction syndrome (MODS — shock → hypoperfusion → organs fail: AKI, ARDS, liver, brain, gut, coagulation — DIC); metabolic acidosis (from lactate plus renal failure — worsens cardiac function and vasopressor response — treat the cause and consider bicarbonate if pH <7.1 [BICAR-ICU]); coagulopathy (from dilution [massive transfusion], consumption [DIC], hypothermia and acidosis — the 'lethal triad' — worsens bleeding); hypothermia (from exposure, transfusion [cold blood] and reduced metabolism — worsens coagulopathy and arrhythmia); ICU-acquired weakness (CIP/CIM — from prolonged immobility and critical illness — delayed recovery); and post-intensive care syndrome (PICS — cognitive impairment, depression/PTSD, physical weakness — 30-50% of survivors). Mortality by type: haemorrhagic hypovolaemic 20-40% (depends on the speed of bleeding control and transfusion); cardiogenic 40-50% (high even with MCS — IABP-SHOCK II — IABP no benefit); distributive (septic) 30-50% (septic shock — SSC 2021); obstructive 30-70% (depends on the cause — tamponade drained early → good; massive PE not thrombolysed → poor) — 20-70% overall depending on type and timeliness. Predictors of poor outcome: higher lactate (lactate >4 = severe; not clearing = worse), older age, more comorbidity, longer duration of shock before treatment (delay = worse), more organs failing (SOFA score — higher = worse) and no response to treatment (refractory shock = worst).
References20ShowHide
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