Overview
Shock
Topic Overview
Summary
Shock is a life-threatening state of circulatory failure causing inadequate tissue perfusion and cellular hypoxia. It is classified by mechanism: hypovolaemic (blood/fluid loss), cardiogenic (pump failure), distributive (vasodilation — sepsis, anaphylaxis), and obstructive (PE, tamponade, tension pneumothorax). Recognition is based on hypotension, tachycardia, altered consciousness, elevated lactate, and oliguria. Treatment is urgent: IV fluids (except cardiogenic), vasopressors, and addressing the underlying cause.
Key Facts
- Definition: Inadequate tissue perfusion causing cellular hypoxia
- Types: Hypovolaemic, cardiogenic, distributive, obstructive
- Key markers: Low BP, elevated lactate, oliguria, confusion
- Treatment: Fluids (most types), vasopressors, treat cause
- Cardiogenic: Avoid excessive fluids — may worsen
Clinical Pearls
Lactate is rising = ongoing tissue hypoxia = shock is not corrected
Cold and clammy (low output) vs warm and vasodilated (distributive) — helps identify type
Septic shock is the most common type of shock in hospitalised patients
Why This Matters Clinically
Shock kills rapidly without treatment. Early recognition and goal-directed resuscitation improve survival. Identifying the type of shock guides treatment.
Visual Summary
Visual assets to be added:
- Types of shock comparison table
- Haemodynamic profiles diagram
- Shock assessment and management algorithm
- Lactate clearance targets
Epidemiology
Incidence
- Shock is common in critically ill patients
- Septic shock: Most common in ICU
- Cardiogenic shock: 5-10% of STEMI patients
Demographics
- All ages
- Higher mortality in elderly, comorbid patients
Types by Frequency (ICU)
| Type | Frequency |
|---|---|
| Distributive (septic) | 60-70% |
| Cardiogenic | 15-20% |
| Hypovolaemic | 10-15% |
| Obstructive | 2-5% |
Pathophysiology
Common Pathway
- Inadequate oxygen delivery to tissues
- Anaerobic metabolism
- Lactate production
- Cellular dysfunction and death
- Multi-organ failure
Types and Mechanisms
| Type | Mechanism | Examples |
|---|---|---|
| Hypovolaemic | ↓Preload (volume loss) | Haemorrhage, dehydration, burns |
| Cardiogenic | ↓Pump function | MI, arrhythmia, myocarditis |
| Distributive | ↓SVR (vasodilation) | Sepsis, anaphylaxis, neurogenic |
| Obstructive | Mechanical obstruction | PE, tamponade, tension pneumothorax |
Haemodynamic Profiles
| Type | CO | SVR | CVP |
|---|---|---|---|
| Hypovolaemic | ↓ | ↑ | ↓ |
| Cardiogenic | ↓ | ↑ | ↑ |
| Distributive | ↑/N | ↓ | ↓/N |
| Obstructive | ↓ | ↑ | ↑ |
Clinical Presentation
General Features of Shock
By Type
| Type | Features |
|---|---|
| Hypovolaemic | Bleeding, dehydration, collapsed veins, cool/clammy |
| Cardiogenic | Chest pain, JVD, pulmonary oedema, cool extremities |
| Septic | Fever, warm peripheries initially, then cold; source of infection |
| Anaphylactic | Rash, wheeze, angioedema, allergen exposure |
| Obstructive (PE) | Dyspnoea, chest pain, JVD, hypoxia |
| Obstructive (tamponade) | Beck's triad: hypotension, JVD, muffled heart sounds |
| Tension pneumothorax | Tracheal deviation, absent breath sounds, JVD |
Red Flags
| Finding | Significance |
|---|---|
| Lactate over 4 | Severe shock |
| MAP under 65 despite fluids | May need vasopressors |
| Altered consciousness | End-organ hypoperfusion |
| No urine output | AKI from hypoperfusion |
Hypotension (SBP under 90 or MAP under 65)
Common presentation.
Tachycardia
Common presentation.
Altered mental status (confusion, agitation)
Common presentation.
Oliguria (under 0.5 mL/kg/hr)
Common presentation.
Mottled skin
Common presentation.
Delayed capillary refill (over 3 seconds)
Common presentation.
Cool extremities (except distributive)
Common presentation.
Clinical Examination
Vital Signs
- Hypotension
- Tachycardia (or bradycardia in late shock)
- Tachypnoea
Skin
- Cold, clammy (hypovolaemic, cardiogenic)
- Warm, flushed (early septic)
- Mottled (all types — late)
Cardiovascular
- JVP (low in hypovolaemic; high in cardiogenic, obstructive)
- Heart sounds (muffled in tamponade)
- Pulmonary oedema (cardiogenic)
Capillary Refill
- Over 3 seconds = poor perfusion
Investigations
Blood Tests
| Test | Purpose |
|---|---|
| Lactate | Tissue hypoxia marker; trend |
| ABG | pH, lactate, oxygenation |
| FBC | Anaemia, infection |
| U&E | AKI |
| Troponin | Cardiogenic shock |
| Blood cultures | If septic |
| Coagulation | DIC |
Imaging
| Modality | Purpose |
|---|---|
| CXR | Pulmonary oedema, pneumothorax |
| Echo (bedside) | Cardiac function, tamponade, RV strain |
| CTPA | If PE suspected |
Other
- ECG (arrhythmia, STEMI)
- Urine output monitoring
Classification & Staging
By Mechanism
| Type | Mechanism |
|---|---|
| Hypovolaemic | Volume loss |
| Cardiogenic | Pump failure |
| Distributive | Vasodilation |
| Obstructive | Mechanical obstruction |
By Severity
- Compensated shock (normal BP with signs of hypoperfusion)
- Decompensated shock (hypotension + organ dysfunction)
- Refractory shock (not responding to treatment)
Management
Immediate — ABCDE Approach
| Action | Details |
|---|---|
| Airway | Secure if compromised |
| Breathing | High-flow oxygen |
| Circulation | Large bore IV access x2; IV fluids |
| Disability | GCS, glucose |
| Exposure | Identify cause |
Fluid Resuscitation
| Type of Shock | Fluid Approach |
|---|---|
| Hypovolaemic | Aggressive fluids (crystalloid 20-30 mL/kg) |
| Septic | 30 mL/kg crystalloid within 3 hours (Sepsis-3) |
| Cardiogenic | Cautious — may worsen; small boluses if needed |
| Obstructive | Treat cause (decompress tamponade, chest drain, thrombolysis) |
Vasopressors
| Agent | Notes |
|---|---|
| Noradrenaline | First-line for most shock (central line preferred) |
| Adrenaline | Anaphylaxis; cardiogenic with low CO |
| Dobutamine | Add if low CO despite pressors (cardiogenic) |
| Vasopressin | Second-line in septic shock |
Treat Underlying Cause
| Type | Treatment |
|---|---|
| Hypovolaemic | Stop bleeding; transfuse; replace fluids |
| Cardiogenic | Revascularisation (PCI for STEMI); inotropes; mechanical support |
| Septic | Source control; antibiotics within 1 hour |
| Anaphylaxis | IM adrenaline 0.5mg; repeat |
| Tension pneumothorax | Needle decompression then chest drain |
| Tamponade | Pericardiocentesis |
| PE | Thrombolysis or embolectomy |
Monitoring
- Continuous ECG, SpO2, BP
- Hourly urine output
- Serial lactate (target clearance)
- Consider arterial line, central line
Complications
Organ Failure
- Acute kidney injury
- Liver failure
- ARDS
- DIC
- Encephalopathy
Multi-Organ Dysfunction Syndrome (MODS)
- Failure of 2 or more organ systems
- High mortality
Prognosis & Outcomes
Mortality
- Depends on type and cause
- Septic shock: 30-50%
- Cardiogenic shock: 40-60%
- Higher with multi-organ failure
Lactate as Prognostic Marker
- Decreasing lactate = good sign
- Persistent/rising lactate = poor prognosis
Evidence & Guidelines
Key Guidelines
- Surviving Sepsis Campaign Guidelines
- Resuscitation Council UK Guidelines
- ESC Guidelines on Cardiogenic Shock
Key Evidence
- Early goal-directed therapy improves sepsis outcomes
- Noradrenaline is first-line vasopressor for most shock
Patient & Family Information
What is Shock?
Shock is when your body is not getting enough blood and oxygen to your vital organs. It is a medical emergency.
Causes
- Severe bleeding
- Heart attack
- Serious infection (sepsis)
- Severe allergic reaction
Symptoms
- Feeling faint or confused
- Cold, clammy skin
- Rapid heartbeat
- Low blood pressure
Treatment
- Fluids through a drip
- Medication to support blood pressure
- Treatment for the underlying cause
Resources
References
Primary Guidelines
- Evans L, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063-e1143. PMID: 34605781
Key Reviews
- Vincent JL, De Backer D. Circulatory shock. N Engl J Med. 2013;369(18):1726-1734. PMID: 24171518
- Thiele H, et al. Management of cardiogenic shock. Eur Heart J. 2015;36(20):1223-1230. PMID: 25732762