Shock — Classification & Approach (4 Types, RUSH, Targets)

📘 1 · Washington Manual of Critical Care, 4th Ed

Overview — Shock Is Inadequate Tissue Oxygenation

"Shock is not a blood pressure — it is a state of inadequate cellular oxygen utilisation. A patient may be in shock with a normal blood pressure (compensated), and conversely a chronically low pressure may not represent shock at all. The clinician's task is to recognise tissue hypoperfusion early — through lactate, mentation, urine output, and skin — determine which of the four mechanisms is responsible, and reverse it before irreversible organ injury occurs."

Washington Manual of Critical Care, 4th Ed. Wolters Kluwer 2023. Chapter: Approach to Shock.

The Three Windows of Perfusion (clinical, fast, free)

Brain — altered mentation (agitation → confusion → obtundation)
Kidney — urine output <0.5 mL/kg/h
Skin — cold, mottled, prolonged capillary refill (>3 s) — though warm in early distributive shock

Add a lactate (>2 mmol/L suggests hypoperfusion; >4 is severe) and you have a rapid bedside assessment of shock severity before any monitor is attached.

📗 2 · Marino's The ICU Book, 5th Edition (2025)

Marino Physiology — Oxygen Delivery & the Determinants of Pressure

🔬 How shock reaches organ failure — whatever the cause

TriggerCirculatory insult — ↓ preload · pump failure · obstruction · vasodilatation

Failure of a determinant of MAP = CO × SVRCO = HR × SV (preload · contractility · afterload)

↓ Oxygen delivery (DO₂ = CO × CaO₂) relative to tissue demand

Tissue hypoperfusion → anaerobic metabolismlactate accumulation, ATP depletion, membrane pump failure

Pathological stateCellular injury → multi-organ dysfunction & death if uncorrected

"All forms of shock converge on a single end-point: a mismatch between oxygen delivery and oxygen demand. Blood pressure is the product of cardiac output and systemic vascular resistance, and cardiac output is itself the product of heart rate and stroke volume — which depends on preload, contractility, and afterload. Localising a shock state is the discipline of asking which of these variables has failed."

Marino PL. The ICU Book, 5th Ed. Circulatory Shock. Wolters Kluwer; 2025.

📗 Marino — The Equations That Localise Shock

MAP = CO × SVR and CO = HR × SV (SV depends on preload, contractility, afterload)

Hypovolaemic / haemorrhagic → ↓preload → ↓SV → ↓CO (SVR rises to compensate)
Cardiogenic → ↓contractility (pump failure) → ↓SV → ↓CO (SVR rises)
Obstructive → mechanical block to filling/output (tamponade, tension PTX, massive PE) → ↓CO
Distributive → ↓SVR (vasodilatation, capillary leak) → CO usually high/normal

This is why the three "low CO / high SVR" shocks feel cold and the distributive shock feels warm early — the body's compensation (or its failure) is written on the skin.

📗 Marino — Oxygen Delivery (DO₂) & the Goal of Resuscitation

DO₂ = CO × [(1.34 × Hb × SaO₂) + (0.003 × PaO₂)]

Resuscitation works on the modifiable levers of DO₂: cardiac output (fluids, inotropes), haemoglobin (transfusion when truly needed), and arterial saturation (oxygen, ventilation). A normal blood pressure achieved by vasoconstriction alone can mask a dangerously low cardiac output — treat flow and perfusion, not just the pressure number.

📋 3 · The Four Types & Their Haemodynamic Profiles

Pattern Recognition at a Glance

Parameter	Hypovolaemic	Cardiogenic	Obstructive	Distributive
Preload (CVP/PCWP)	↓	↑	↑ / variable*	↓ / normal
Cardiac output	↓	↓	↓	↑ / normal
SVR (afterload)	↑	↑	↑	↓↓
SvO₂ (mixed venous)	↓	↓	↓	↑ / normal
Skin	Cold	Cold	Cold	Warm (early)
Examples	Haemorrhage, GI loss, burns, DKA	MI, arrhythmia, severe HF, myocarditis	Tamponade, tension PTX, massive PE	Sepsis, anaphylaxis, neurogenic, adrenal

*Obstructive: tamponade gives equalised high filling pressures; tension pneumothorax/PE give a high CVP with a small, underfilled left heart.

Shock Can Be Mixed — and Often Is

The critically ill frequently have more than one mechanism at once: septic shock (distributive) with septic cardiomyopathy (cardiogenic) and hypovolaemia (capillary leak + poor intake); or trauma with haemorrhage (hypovolaemic) plus tension pneumothorax (obstructive). Re-assess continuously — the dominant mechanism can shift during resuscitation.

🔍 4 · The RUSH Exam & Bedside Workup

RUSH — Rapid Ultrasound in SHock

"Pump · Tank · Pipes"

Pump (heart): contractility (good vs poor → cardiogenic), pericardial effusion/tamponade (obstructive), RV strain/D-sign (massive PE → obstructive).
Tank (volume): IVC size & collapsibility (small/collapsing → hypovolaemic/distributive; full/fixed → cardiogenic/obstructive), lung B-lines (pulmonary oedema), pleural/peritoneal free fluid (haemorrhage), pneumothorax (absent lung sliding).
Pipes (vessels): aorta (AAA/dissection), femoral/popliteal veins (DVT → supports PE).

Core Workup for Undifferentiated Shock

ABG + lactate, FBC, U&E, LFT, coagulation, glucose, cultures (if sepsis), troponin + ECG (cardiogenic/PE), CXR (pneumothorax, oedema, mediastinum), bedside echo/RUSH, point-of-care Hb. Establish invasive arterial line early in established shock; central access for vasopressors. SvO₂/ScvO₂ and dynamic indices guide ongoing resuscitation.

🇮🇳 Indian ED/ICU Context

Distributive (septic) shock dominates — tropical infections, late presentations. Always look for an occult source (urinary, abdominal, soft-tissue, tropical fever — see the Febrile Illness topic).

Haemorrhagic shock from trauma (RTAs) and obstetric causes is common; whole blood and early TXA are pragmatic where component MTP is limited.

Point-of-care ultrasound (RUSH) is increasingly available and invaluable where advanced monitoring is scarce — it localises the shock type in minutes at the bedside.

💊 5 · Resuscitation Targets & Drugs

Targets & the Right Vasoactive for Each Shock

Resuscitation Targets

MAP ≥65 mmHg (individualise — higher if chronic hypertension; SSC 2026 notes a lower target may be acceptable in selected older patients). Lactate clearance ≥10%/2h, goal <2 mmol/L. Urine output ≥0.5 mL/kg/h. Normalising mentation and skin perfusion (capillary refill) are validated bedside endpoints (ANDROMEDA-SHOCK: capillary-refill-guided resuscitation non-inferior/possibly better than lactate).

Shock type	First steps	Vasoactive / definitive
Hypovolaemic / haemorrhagic	Stop the loss; fluids; blood products (1:1:1) for haemorrhage; TXA	Vasopressors only as a bridge; definitive = volume/haemostasis
Distributive (septic)	30 mL/kg crystalloid (individualised), source control, antibiotics <1h	Noradrenaline first-line; add vasopressin 0.03 U/min; steroids if refractory
Distributive (anaphylactic)	IM adrenaline, fluids, remove trigger	Adrenaline (IM → infusion); see Anaphylaxis topic
Cardiogenic	Treat cause (PCI for MI), cautious fluids, optimise rhythm	Noradrenaline for pressure + dobutamine for output; MCS (IABP/Impella/VA-ECMO)
Obstructive	Relieve the obstruction	Tamponade → pericardiocentesis; tension PTX → decompress; massive PE → thrombolysis

⚠️ Match the Treatment to the Mechanism

Fluids help hypovolaemic and (initially) distributive shock but harm cardiogenic and obstructive shock (worsen pulmonary oedema / RV distension). Vasopressors raise pressure but do not fix obstruction or haemorrhage. The first job is always to identify the mechanism — then the treatment follows logically. See the dedicated Vasopressors and Sepsis topics.

🗂 6 · Clinical Flowchart

Undifferentiated Shock — Step by Step

Recognise shock

Hypotension OR signs of hypoperfusion (lactate, mentation, urine, skin) — even with normal BP.
ABC, high-flow O₂, two large IVs/IO, monitor, arterial line; send lactate + bloods.

Localise with RUSH + ECG

Pump/Tank/Pipes scan; ECG + troponin; CXR.
Assign the dominant mechanism (often mixed).

Treat the mechanism

Fluids/blood (hypovolaemic), antibiotics + noradrenaline (septic), inotrope + revascularise (cardiogenic), decompress/lyse (obstructive).
Assess fluid responsiveness dynamically before each bolus (see Haemodynamic Monitoring topic).

Reassess to targets

MAP ≥65, lactate clearance, urine output, capillary refill, mentation.
Re-scan if not improving — the mechanism may have shifted or be mixed.

❌ 7 · Common Mistakes

Common Mistakes in Shock

❌ Mistake 1 — Waiting for Hypotension to Diagnose Shock

Compensated shock maintains BP through vasoconstriction until sudden collapse. Use lactate, mentation, urine output and skin perfusion to recognise hypoperfusion early — a "normal" BP is not reassurance.

❌ Mistake 2 — One-Size-Fits-All Fluids

Large fluid boluses help hypovolaemic/early distributive shock but worsen cardiogenic and obstructive shock. Identify the mechanism (RUSH) before reflexively loading fluid.

❌ Mistake 3 — Chasing Blood Pressure With Vasopressors Alone

A normal MAP from vasoconstriction can hide a low cardiac output and ongoing tissue hypoxia. Treat flow and perfusion (lactate, ScvO₂, capillary refill), not just the pressure.

❌ Mistake 4 — Missing Obstructive Shock

Tension pneumothorax, tamponade and massive PE kill quickly and need a mechanical fix, not fluids/pressors. A focused echo/lung scan in any unexplained shock prevents this lethal miss.

❌ Mistake 5 — Forgetting Shock Is Often Mixed

Septic patients develop cardiomyopathy; trauma patients develop tension pneumothorax; treating only the first-identified mechanism leaves the patient in shock. Reassess continuously.

❌ Mistake 6 — Delaying Source Control / Definitive Therapy

Vasopressors and fluids buy time but rarely cure — haemorrhage needs haemostasis, sepsis needs source control + antibiotics, cardiogenic MI needs revascularisation, obstruction needs decompression. Don't let stabilisation delay the definitive intervention.

📑 8 · References

References

Marino PL. The ICU Book, 5th Ed. Circulatory Shock; Haemodynamic Monitoring. Wolters Kluwer; 2025.
Washington Manual of Critical Care, 4th Ed. Chapter: Approach to Shock. Wolters Kluwer 2023.
Vincent JL, De Backer D. Circulatory Shock. N Engl J Med 2013;369:1726–1734.
Hernández G, Ospina-Tascón GA, Damiani LP et al. (ANDROMEDA-SHOCK). Effect of a resuscitation strategy targeting peripheral perfusion status vs serum lactate on mortality in septic shock. JAMA 2019;321:654–664.
Perera P, Mailhot T, Riley D, Mandavia D. The RUSH exam: Rapid Ultrasound in SHock. Emerg Med Clin North Am 2010;28:29–56.
Evans L, Rhodes A, Alhazzani W et al. Surviving Sepsis Campaign Guidelines (and 2026 update). Crit Care Med.