title: "Shock: The Complete Guide"
Shock: The Complete Guide
Shock = Inadequate oxygen supply leading to anaerobic cellular metabolism, inefficient ATP production, and organ dysfunction.
The Unifying Definition
The unifying feature of shock, irrespective of the initiating disease or clinical features, is a failure to deliver and/or utilise adequate amounts of oxygen.
DO₂ = CO × CaO₂ where CO = HR × SV (determined by preload, afterload, and contractility).
Clinically, shock is expressed as impaired end-organ perfusion: drowsiness, delayed capillary refill, oliguria, and hyperlactatemia.
Cellular Consequences
If dysoxia persists:
- Oxygen limitation affects cell membrane ion channels
- Influx of sodium and water → cellular oedema
- Breaching of cell membrane integrity
- Cell injury → cell death
Organ vulnerability varies: The heart and brain have high metabolic requirements with high O₂ extraction—they're most vulnerable. Kidneys and skin have lower metabolic requirements and are more tolerant of decreased O₂.
Clinical Features of Shock
Hypotension develops late as systemic blood pressure is initially maintained by compensatory mechanisms (vasoconstriction, tachycardia, increased contractility).
| Feature | Significance |
|---|---|
| Hypotension | Late sign—sentinel feature of circulatory failure |
| Tachycardia | Early compensatory sign (but bradycardia causes shock in neurogenic) |
| Tachypnoea | Increases with worsening shock, falls in pre-terminal phase |
| Oliguria | Reduced GFR + increased reabsorption—useful perfusion guide |
| Altered mental state | Anxiety → agitation → confusion → delirium → drowsiness → coma |
| Peripheral perfusion | Cool/clammy = hypovolaemic/cardiogenic; Warm = distributive |
MAP < 60-65 mmHg is commonly associated with inadequate organ perfusion in adults. Targets vary, but most shock protocols aim for MAP ≥65 mmHg (often higher in chronic HTN/vascular disease).
Source: CC Bible; local ICU shock protocols.
Stages of Shock
Pre-shock → Shock → End-organ dysfunction
- Pre-shock (Compensated): Tachycardia, minimal signs
- Shock (Decompensated): Compensatory mechanisms overwhelmed, organ dysfunction begins
- End-organ dysfunction: Irreversible damage, multi-organ failure, death
During end-organ dysfunction: anuria develops, acidemia depresses CO, hypotension becomes refractory, lactate worsens, restlessness evolves to coma.
Classification of Shock
Four types of shock: Hypovolaemic, Cardiogenic, Obstructive, Distributive. Each has distinct pathophysiology and management.
Haemodynamic Profiles
| Type | Preload | CO | SVR | Clinical Clues |
|---|---|---|---|---|
| Hypovolaemic | ↓↓ | ↓ | ↑ | Cold, clammy, obvious fluid loss |
| Cardiogenic | ↑ or N | ↓↓ | ↑ | JVP elevated, pulmonary oedema |
| Obstructive | ↓ | ↓ | ↑ | JVP elevated, muffled hearts/unequal chest |
| Distributive | ↓ | ↑ or N | ↓↓ | Warm, vasodilated, bounding pulse |
Shock Types as Quadrants
Cardiac Output (CO) vs Systemic Vascular Resistance (SVR)
- • Cold peripheries
- • Tachycardia
- • Narrow pulse pressure
- • Look for subtle hypoperfusion
- • Check lactate, mentation, UO
- • Warm peripheries
- • Bounding pulses
- • Decompensation
- • Consider concurrent cardiogenic features
Hypovolaemic Shock
Hypovolaemic shock occurs when acute blood or fluid loss reduces circulating volume, decreasing preload and stroke volume.
Total blood volume: ~70 mL/kg (blood cells + plasma)
Compensatory Mechanisms
VACH:
- V - Venoconstriction (venous system holds 80% of blood, early response)
- A - Arteriolar constriction (increases perfusion pressure)
- C - Contractility increase (heart contracts more vigorously)
- H - Heart rate increase (compensates for reduced SV)
Causes
Blood Loss:
- Vascular injury, GI bleeding, obstetric bleeding
- Intra-abdominal/retroperitoneal haemorrhage
- Long-bone fracture, haemothorax
Fluid Loss:
- Vomiting, diarrhoea, ileostomy losses
- Polyuria, sweating, burns
- Pancreatitis, ascites
Classes of Haemorrhagic Shock
Class I: Less than 15% loss, minimal changes, compensated by interstitial fluid shift. Class II: 15-30% loss, orthostatic hypotension, tachycardia. Class III: 30-40% loss, hypotension, tachypnoea, altered mental state. Class IV: Greater than 40% loss, life-threatening, requires immediate intervention.
Source: ATLS.
Cardiogenic Shock
Cardiogenic shock = intracardiac pump failure causing reduced cardiac output. Has very high in-hospital mortality.
Most common cause: Myocardial ischaemia
Causes
- Myocardial ischaemia/infarction
- Acute valve dysfunction
- Myocarditis, contusion
- Septal/ventricular rupture
- Drug toxicity (calcium channel blockers)
- Bradyarrhythmias (complete heart block)
- Tachyarrhythmias (VT, SVT with rapid ventricular response)
Treatment priorities: urgent correction of underlying cardiac disease + consideration of afterload reduction while ensuring adequate perfusion.
Obstructive Shock
Obstructive shock = extracardiac mechanical obstruction to blood flow, often associated with poor RV output.
Causes
Pulmonary Vascular:
- Massive pulmonary embolism
- Severe pulmonary hypertension
Mechanical:
- Tension pneumothorax
- Pericardial tamponade
- Constrictive pericarditis
- Restrictive cardiomyopathy
Treatment is urgent removal of the obstruction (e.g., pericardiocentesis, needle decompression).
Distributive Shock
Distributive shock = failure of vascular regulation leading to inappropriate blood distribution (vasodilatory shock). CO may be initially increased.
Most common cause in ICU: Sepsis
Causes
STANK:
- S - Septic shock
- T - Toxic shock / Toxins (drugs, venom)
- A - Anaphylactic shock
- N - Neurogenic shock
- endocrine (adrenal/thyroid) insufficiency (K for Kortext - adrenal)
Key Features by Type
Septic shock:
- Decreased preload, decreased contractility, decreased SVR
- Warm peripheries, bounding pulse, hyperdynamic circulation early
Neurogenic shock:
- Disruption of autonomic pathways → decreased SVR + altered vagal tone
- Common in severe TBI and spinal cord injury
Anaphylactic shock:
- IgE-mediated (insect stings, food, drugs)
- Haemodynamic collapse + bronchospasm + increased airway resistance
Management of Shock
Resuscitation of shock is a medical emergency. Aim: rapidly restore systemic O₂ delivery and improve tissue perfusion.
SOAR-VV-MM:
- S - Supply oxygen
- O - Obtain vascular access
- A - Administer fluids (volume resuscitation)
- R - Review for vasoactive agents
- V - Verify—manage precipitating illness/injury
- M - Monitor response
1. Supply Oxygen
- Correct hypoxia urgently
- Ensure adequate FiO₂
- Ensure adequate ventilation
- Correct reversible causes of shunt (pleural collection, bronchus obstruction)
2. Vascular Access
- Essential for fluids and medications
- Peripheral IV initially, central line for vasoactives
3. Fluid Resuscitation
Fluid resuscitation is usually the first therapeutic strategy in shock management, particularly in hypovolaemic and distributive shock.
4-6. Vasoactives, Source Control, Monitoring
- See Fluid Resuscitation and Vasopressors & Inotropes for details
- Monitor: lactate trending, urine output, mental status, MAP
Exam-Relevant MCQs
Summary: Approach to Undifferentiated Shock
- Recognise shock: Hypoperfusion (lactate, altered mental state, oliguria, mottling)
- Identify pattern: Pump/pipes/volume—use clinical signs + bedside echo
- Treat immediately: O₂, access, fluids, vasoactives as needed
- Find and fix cause: Source control, definitive management
- Monitor response: Lactate clearance, urine output, mental state
Blood pressure is a late marker of shock. Don't wait for hypotension—look for early signs: tachycardia, altered mental state, rising lactate, poor urine output.