Shock: classification and physiology

Surgical approach (if applicable)

• Not an operation. If shock is due to a surgical cause, the surgical priorities are:
  • Control haemorrhage: direct pressure, tourniquet, pelvic binder, damage control surgery, packing, vascular control, interventional radiology (embolisation).
  • Source control in sepsis: drain abscess, debride necrotic tissue, remove infected devices, laparotomy for perforation/ischemia when indicated.
  • Relieve obstruction: needle decompression/chest drain for tension pneumothorax; pericardiocentesis for tamponade; thrombolysis/thrombectomy for massive PE (selected).
  • Stabilise fractures/soft tissue injury to reduce ongoing blood loss and inflammatory burden (e.g., external fixation).

Anaesthetic management (contextual: management of a shocked patient)

• Type of anaesthesia: usually GA with controlled ventilation for unstable patients or urgent source control; regional may be inappropriate in severe shock due to sympathectomy and coagulopathy (case-dependent).
• Airway: ETT preferred (full stomach, need for high FiO2/PEEP, control of ventilation, ongoing resuscitation); SGA generally avoided in severe shock/aspiration risk.
• Duration: variable (minutes for damage control to hours for definitive surgery); aim for shortest effective procedure in profound shock (damage control).
• Analgesia/pain: often very painful pathology/trauma; use opioid-sparing where possible but avoid under-analgesia; ketamine useful (maintains sympathetic tone) but caution in catecholamine-depleted states.
• Induction: haemodynamically stable technique (titrated); consider ketamine/etomidate; reduce induction dose; early vasopressor bolus/infusion (e.g., metaraminol/noradrenaline).
• Monitoring/lines: arterial line early; large-bore IV/rapid infuser; consider central access for vasopressors; urinary catheter; temperature monitoring; point-of-care blood gas/lactate; coagulation (TEG/ROTEM).
• Resuscitation: balanced blood product strategy for haemorrhage; permissive hypotension until haemostasis (selected trauma without TBI); treat hypocalcaemia, hypothermia, acidosis; early antibiotics in sepsis; vasopressors/inotropes guided by physiology.

Definition and core concept

• Shock = acute circulatory failure causing inadequate cellular oxygen utilisation, leading to cellular dysfunction and organ failure.
• Mechanistic definition: mismatch between oxygen delivery (DO2) and oxygen consumption (VO2), or impaired extraction/utilisation (e.g., sepsis, cyanide).
• Clinical end-point: tissue hypoperfusion (often lactate rise, oliguria, altered mentation, cool peripheries—except distributive).

Classification (FRCA standard)

• Hypovolaemic: reduced preload (haemorrhage, dehydration, third-space losses, burns).
• Cardiogenic: pump failure (MI, myocarditis, severe cardiomyopathy, arrhythmia, acute valvular catastrophe).
• Obstructive: impaired filling or outflow (tension pneumothorax, cardiac tamponade, massive PE, severe dynamic hyperinflation/auto-PEEP).
• Distributive (vasodilatory): reduced SVR and maldistribution (sepsis, anaphylaxis, neurogenic shock, adrenal crisis, drug-induced vasodilation).
• Dissociative / cytopathic (sometimes included): impaired oxygen carriage or utilisation (severe anaemia, CO poisoning, methaemoglobinaemia, cyanide, mitochondrial dysfunction in sepsis).

Determinants of oxygen delivery and consumption (key physiology)

• Oxygen delivery: DO2 = CO × CaO2.
  • CO = HR × SV (SV depends on preload, afterload, contractility).
  • CaO2 ≈ (1.34 × Hb × SaO2) + (0.023 × PaO2) mL O2/dL.
• Oxygen consumption: VO2 = CO × (CaO2 − CvO2) (Fick principle).
• Oxygen extraction ratio (O2ER) = VO2/DO2; normally ~0.25 (SvO2 ~70%, ScvO2 ~70–75%).
• Critical DO2: below a threshold, VO2 becomes supply-dependent → anaerobic metabolism → lactate rise.
• Microcirculation matters: capillary flow heterogeneity, shunting, endothelial dysfunction (prominent in sepsis) can cause hypoxia despite normal/high CO.

Haemodynamic relationships (MAP, SVR, venous return)

• MAP ≈ CO × SVR (more precisely: MAP = CO × SVR + CVP; CVP usually small).
• Venous return depends on the gradient between mean systemic filling pressure (MSFP) and right atrial pressure (RAP): VR ∝ (MSFP − RAP)/venous resistance.
  • Stressed vs unstressed volume: venoconstriction converts unstressed to stressed volume → increases MSFP → increases venous return.
  • Positive pressure ventilation increases RAP and can reduce venous return (especially in hypovolaemia).
• Shock often involves reduced effective circulating volume (true loss or relative via venodilation/capillary leak).

Compensatory responses to shock

• Immediate neural: baroreceptor-mediated sympathetic activation → tachycardia, increased contractility, arteriolar vasoconstriction (↑SVR), venoconstriction (↑MSFP), redistribution to heart/brain.
• Hormonal: RAAS (angiotensin II vasoconstriction; aldosterone Na+/water retention), ADH (water retention + vasoconstriction), catecholamines, cortisol.
• Microcirculatory/metabolic: increased O2 extraction (↓SvO2), increased 2,3-DPG (right shift), anaerobic glycolysis → lactate.
• Failure/decompensation: myocardial ischaemia, acidosis, hypothermia, coagulopathy, inflammatory mediator release → spiral to multi-organ dysfunction.

Physiological patterns by shock type (typical, not absolute)

• Hypovolaemic: ↓preload → ↓SV/CO; ↑SVR; narrow pulse pressure; cool peripheries; low JVP/CVP; dynamic indices (SVV/PPV) often high if ventilated and sinus rhythm.
• Cardiogenic: ↓CO with ↑filling pressures; ↑SVR (compensatory); pulmonary oedema; raised JVP; cool peripheries; may have arrhythmia/ischaemia.
• Obstructive: ↓CO due to impaired filling/outflow; ↑SVR; raised JVP; specific signs (tamponade: pulsus paradoxus; tension PTX: tracheal deviation/absent breath sounds; PE: RV strain).
• Distributive (early sepsis/anaphylaxis): ↓SVR with normal/high CO (warm shock), wide pulse pressure, bounding pulses; later sepsis may become low CO (cold shock).
• Dissociative/cytopathic: CO and SVR may be normal; low CaO2 (anaemia/CO/metHb) or impaired utilisation (cyanide) → high lactate; SvO2 may be high in impaired extraction.

Cellular physiology of shock (why organs fail)

• Hypoxia → reduced oxidative phosphorylation → ↓ATP → failure of Na+/K+ ATPase → cell swelling, membrane dysfunction.
• Anaerobic metabolism → lactate and H+ accumulation → acidaemia (reduces contractility, blunts catecholamine response).
• Reperfusion injury: ROS generation, mitochondrial dysfunction, calcium influx, endothelial activation.
• Endothelial glycocalyx damage (especially sepsis/trauma) → capillary leak, oedema, impaired microvascular flow; contributes to relative hypovolaemia.
• Coagulopathy: dilutional + consumptive + hypothermia + acidosis; trauma-associated coagulopathy includes fibrinolysis and protein C pathway activation.

Markers of tissue perfusion (limitations matter)

• Lactate: marker of anaerobic metabolism and stress; elevated in hypoperfusion but also in beta-agonism, seizures, liver failure; trend is more useful than single value.
• Urine output: target often ≥0.5 mL/kg/h (adult), but affected by CKD, obstruction, diuretics, neurohormonal responses.
• SvO2/ScvO2: low suggests low DO2 or high VO2; high can indicate impaired extraction/shunting (sepsis, cyanide) or high FiO2.
• Base deficit: reflects metabolic acidosis; useful in trauma resuscitation as a severity marker.
• Capillary refill time/skin mottling: quick bedside microcirculation surrogates; can guide resuscitation in sepsis (context-dependent).

Effects of anaesthesia and ventilation on shock physiology

• Induction agents reduce sympathetic tone and SVR; in hypovolaemia this can cause precipitous hypotension (unmasking low preload).
• Positive pressure ventilation: reduces venous return; increases RV afterload if high airway pressures/PEEP; can worsen obstructive shock (tension PTX, tamponade) and hypovolaemia.
• Hyperventilation: decreases PaCO2 → cerebral vasoconstriction; left shift of oxyhaemoglobin curve; may reduce oxygen unloading.
• Hypothermia: worsens coagulopathy, increases SVR, shifts ODC left, reduces drug metabolism; active warming is resuscitation.