TextbookAnaestheticsShock and Haemodynamic Monitoring

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.

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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

TypePreloadCOSVRTreatment
HypovolaemicIV fluids, blood products, stop bleeding
CardiogenicInotropes (dobutamine), diuretics, consider IABP/ECMO
Distributive (septic)↑ (early) ↓ (late)IV fluids, noradrenaline, antibiotics
ObstructiveTreat 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

DeviceMeasurementInvasiveness
Arterial lineContinuous BP, ABGMinimally invasive
CVP (CVC)Central venous pressure, ScvO2Moderately invasive
PiCCOCO (transpulmonary thermodilution + pulse contour)Arterial + CVC
LiDCOCO (lithium dilution + pulse power)Arterial
Oesophageal DopplerCO, SV, corrected flow timeMinimally invasive
PA catheterCO, PCWP, SVR, PVRHighly invasive (rarely used)
POCUS/EchoQualitative CO, fluid status, valvesNon-invasive

Classification of Haemorrhagic Shock (ATLS)

ClassBlood LossHRBPMental Status
I<750mL (<15%)<100NormalAlert
II750-1500mL (15-30%)100-120NormalAnxious
III1500-2000mL (30-40%)120-140DecreasedConfused
IV>2000mL (>40%)>140Very lowLethargic