Shock and Haemodynamic Monitoring
Shock is a state of circulatory failure resulting in inadequate tissue oxygen delivery. Classification into hypovolaemic, cardiogenic, distributive, and obstructive guides targeted resuscitation.
Key Facts
- Shock is defined as inadequate tissue perfusion and oxygen delivery - lactate >2 mmol/L is an early marker
- Four types: Hypovolaemic, cardiogenic, distributive (septic, anaphylactic, neurogenic), obstructive (PE, tamponade, tension pneumothorax)
- MAP ≥65 mmHg is the minimum target for adequate organ perfusion in shock (Surviving Sepsis Campaign)
- Noradrenaline is the first-line vasopressor for septic shock - 0.05-1 mcg/kg/min
- Invasive arterial monitoring provides continuous beat-to-beat BP and allows frequent ABG sampling
- Pulse pressure variation (PPV) >13% and stroke volume variation (SVV) >13% predict fluid responsiveness in mechanically ventilated patients
- Passive leg raise (PLR) test predicts fluid responsiveness in spontaneously breathing patients - increase in CO >10% is positive
- Point-of-care echocardiography (POCUS) is invaluable for rapid assessment of cardiac function, fluid status, and cause of shock
Overview
Key Facts
Shock is a life-threatening condition requiring rapid identification and targeted treatment. Haemodynamic monitoring guides resuscitation to achieve adequate tissue perfusion while avoiding fluid overload.
Epidemiology
Shock affects approximately 30-40% of ICU patients. Septic shock is the most common form in ICU (62%), followed by cardiogenic (16%), hypovolaemic (16%), and obstructive (2%). In-hospital mortality for septic shock is approximately 30-40%.
Aetiology
- Hypovolaemic: Haemorrhage, burns, dehydration, third-space losses
- Cardiogenic: MI, arrhythmia, valvular disease, cardiomyopathy
- Distributive: Sepsis (most common), anaphylaxis, neurogenic
- Obstructive: PE, cardiac tamponade, tension pneumothorax
Pathophysiology
Tissue hypoxia is the final common pathway in all forms of shock. Compensatory mechanisms (tachycardia, vasoconstriction, ADH/aldosterone release) initially maintain vital organ perfusion. Decompensation leads to lactic acidosis, cellular dysfunction, and multi-organ failure. The type of shock determines the primary circulatory abnormality: reduced preload (hypovolaemic), reduced contractility (cardiogenic), reduced SVR (distributive), or mechanical obstruction to flow (obstructive).
Clinical Presentation
General Features of Shock
- Tachycardia, hypotension (MAP <65 mmHg)
- Tachypnoea, altered mental status
- Oliguria (<0.5 mL/kg/hr)
- Cool, clammy peripheries (except distributive - warm peripheries early)
- Raised lactate (>2 mmol/L)
Differentiating Features
- Hypovolaemic: Dry mucous membranes, flat neck veins, clear lungs
- Cardiogenic: Raised JVP, pulmonary crackles, S3 gallop
- Septic: Fever/hypothermia, warm peripheries, suspected source of infection
- Obstructive: Distended neck veins, muffled heart sounds (tamponade), absent breath sounds (tension pneumothorax)
Red Flags
- MAP <65 mmHg despite fluid resuscitation - start vasopressors
- Lactate >4 mmol/L - high mortality, aggressive resuscitation needed
- Rising lactate despite treatment - reassess diagnosis and adequacy of resuscitation
- New onset AF with hypotension - consider cardioversion if haemodynamically unstable
Differential Diagnosis
| Type | Preload | CO | SVR | Treatment |
|---|---|---|---|---|
| Hypovolaemic | ↓ | ↓ | ↑ | IV fluids, blood products, stop bleeding |
| Cardiogenic | ↑ | ↓ | ↑ | Inotropes (dobutamine), diuretics, consider IABP/ECMO |
| Distributive (septic) | ↓ | ↑ (early) ↓ (late) | ↓ | IV fluids, noradrenaline, antibiotics |
| Obstructive | ↑ | ↓ | ↑ | Treat cause (chest drain, pericardiocentesis, thrombolysis) |
Diagnosis / Investigation
Bedside
- ABG with lactate: Immediate - assess oxygenation, ventilation, acid-base, tissue perfusion
- ECG: Arrhythmia, MI, PE (right heart strain)
- POCUS/echocardiography: Cardiac function, fluid status, pericardial effusion, RV dilatation
- Urine output: Catheterise - target >0.5 mL/kg/hr
- CVP monitoring: Useful trend; absolute value less informative
Bloods
- FBC, U&Es, LFTs: Organ function
- Lactate (serial): Guide resuscitation; clearance rate is prognostic
- Troponin: If cardiogenic shock suspected
- Blood cultures (×2): Before antibiotics in sepsis
- Coagulation, fibrinogen: DIC screening
- Procalcitonin: Differentiate septic from non-septic causes
Imaging
- CXR: Pulmonary oedema, pneumothorax, mediastinal widening
- CTPA: If PE suspected
- CT abdomen: If intra-abdominal source of sepsis suspected
- Focused echocardiography: Rapid assessment (FATE/FICE protocol)
Special Tests
- Cardiac output monitoring: PiCCO (transpulmonary thermodilution), LiDCO, oesophageal Doppler, PA catheter (now rarely used)
- Fluid responsiveness assessment: PLR test, SVV/PPV on arterial waveform, IVC variability on USS
- Mixed/central venous oxygen saturation (ScvO2): <70% suggests inadequate oxygen delivery
Management
Non-pharmacological
- ABCDE assessment: Simultaneous assessment and resuscitation
- IV access: Two large-bore cannulae; central venous access for vasopressors
- Position: Supine with legs raised (if hypovolaemic); sit up (if cardiogenic pulmonary oedema)
Pharmacological
Fluid resuscitation:
- Crystalloid (Hartmann's or 0.9% NaCl) 250-500mL boluses, reassess after each
- Blood products for haemorrhagic shock (O-neg → crossmatched; 1:1:1 ratio in massive haemorrhage)
Vasopressors and inotropes:
- Noradrenaline: First-line vasopressor for septic/distributive shock - 0.05-1mcg/kg/min
- Vasopressin: 0.03 units/min - adjunct to noradrenaline in septic shock
- Dobutamine: 2.5-20mcg/kg/min - inotrope for cardiogenic shock with low CO
- Adrenaline: 0.05-0.5mcg/kg/min - combined inotrope/vasopressor; anaphylactic shock first-line (500mcg IM)
- Milrinone: PDE3 inhibitor - inodilator for acute heart failure (not first-line)
Sepsis-specific:
- IV antibiotics within 1 hour (Surviving Sepsis Campaign hour-1 bundle)
- Hydrocortisone 200mg/day if vasopressor-dependent >4 hours despite adequate fluid resuscitation
Surgical/Interventional
- Chest drain: Tension pneumothorax
- Pericardiocentesis: Cardiac tamponade
- Thrombolysis/embolectomy: Massive PE
- Source control: Drainage of abscess, debridement, laparotomy for peritonitis
- IABP/Impella/ECMO: Cardiogenic shock refractory to medical therapy
Referral Criteria
- Any shock not responding to initial resuscitation - ICU referral
- Cardiogenic shock - cardiology/cardiac surgery
- Massive PE - interventional radiology or cardiothoracic surgery
- Septic shock - ICU admission
Prognosis
- Septic shock: 30-40% mortality despite best care; early antibiotics and fluids improve outcomes
- Cardiogenic shock (MI-related): ~50% mortality; PCI/CABG improve outcomes
- Haemorrhagic shock: Outcome depends on rapidity of haemorrhage control and transfusion
- Lactate clearance: >10% decrease in lactate at 6 hours is associated with improved survival
- Obstructive shock: Rapidly fatal if cause not identified and treated; excellent recovery if treated promptly
Other Relevant Information
Haemodynamic Monitoring Devices
| Device | Measurement | Invasiveness |
|---|---|---|
| Arterial line | Continuous BP, ABG | Minimally invasive |
| CVP (CVC) | Central venous pressure, ScvO2 | Moderately invasive |
| PiCCO | CO (transpulmonary thermodilution + pulse contour) | Arterial + CVC |
| LiDCO | CO (lithium dilution + pulse power) | Arterial |
| Oesophageal Doppler | CO, SV, corrected flow time | Minimally invasive |
| PA catheter | CO, PCWP, SVR, PVR | Highly invasive (rarely used) |
| POCUS/Echo | Qualitative CO, fluid status, valves | Non-invasive |
Classification of Haemorrhagic Shock (ATLS)
| Class | Blood Loss | HR | BP | Mental Status |
|---|---|---|---|---|
| I | <750mL (<15%) | <100 | Normal | Alert |
| II | 750-1500mL (15-30%) | 100-120 | Normal | Anxious |
| III | 1500-2000mL (30-40%) | 120-140 | Decreased | Confused |
| IV | >2000mL (>40%) | >140 | Very low | Lethargic |