Intensive Care Medicine

Haemodynamic Monitoring in ICU

Comprehensive guide to invasive and non-invasive haemodynamic monitoring techniques in critically ill patients, including arterial lines, central venous pressure, pulmonary artery catheters, pulse contour analysis,...

Updated 24 Jan 2026
41 min read
Quality score
54

Clinical board

A visual summary of the highest-yield teaching signals on this page.

Linked comparisons

Differentials and adjacent topics worth opening next.

  • shock-classification
  • fluid-resuscitation
0
Clinical reference article

Haemodynamic Monitoring in ICU

Quick Answer

Haemodynamic monitoring encompasses techniques to assess cardiovascular function and guide resuscitation in critically ill patients. Arterial lines provide continuous blood pressure monitoring and waveform analysis (sensitivity to damping, resonance). Central venous pressure (CVP) is a poor predictor of fluid responsiveness (Marik 2008). Pulmonary artery catheters (PAC) measure cardiac output, mixed venous oxygen saturation, and pulmonary pressures but show no mortality benefit (PAC-Man 2005, FACTT 2006). Dynamic indices (pulse pressure variation PPV, stroke volume variation SVV greater than 13%) predict fluid responsiveness better than static pressures in mechanically ventilated patients (Michard 2005). Echocardiography assesses ventricular function, IVC collapsibility, and valvular pathology. Functional assessments (passive leg raise, fluid challenge) test physiological response rather than static measurements (Monnet 2016).

CICM Exam Focus

Written Exam (SAQ)

High-yield topics:

  • Arterial line waveform interpretation (damping, over-damping, under-damping, resonance)
  • CVP measurement technique, waveform components (a, c, v waves), limitations as fluid responsiveness predictor
  • PAC insertion technique, complications, measurements (CO, PCWP, SVR, PVR, SvO2), waveforms (RA, RV, PA, PCWP)
  • Dynamic indices (PPV, SVV) physiology, cutoffs, limitations (arrhythmias, spontaneous breathing, low tidal volume)
  • Echocardiographic indices of fluid responsiveness (IVC collapsibility, E/e', LVOT VTI)
  • Passive leg raise test physiology, technique, interpretation

Recent SAQ themes (2020-2025):

  • 2023: "Describe the components of a pulmonary artery catheter waveform trace and list the derived haemodynamic parameters."
  • 2022: "Outline the principles of pulse contour cardiac output monitoring and discuss its limitations."
  • 2021: "Discuss the use of central venous pressure monitoring in the ICU. Include measurement technique and interpretation."
  • 2020: "Compare and contrast static and dynamic indices of fluid responsiveness in mechanically ventilated patients."

Viva Voce

Structured approach:

  1. Monitoring modality selection - Match monitoring invasiveness to patient acuity and clinical question
  2. Arterial line waveform - Identify damping, measure systolic pressure variation
  3. PAC troubleshooting - Recognize malposition, overwedging, balloon rupture
  4. Fluid responsiveness assessment - Integrate static, dynamic, and functional tests
  5. Echo integration - Use bedside echo for real-time haemodynamic assessment

Examiner expectations:

  • Understand physiological basis of each monitoring technique
  • Recognize limitations and contraindications
  • Interpret waveforms and numerical data
  • Apply evidence-based thresholds for intervention
  • Integrate multimodal monitoring data

Key Points

Essential Knowledge:

  1. Arterial line measures continuous BP, provides waveform analysis (dicrotic notch, pulse pressure), enables frequent ABG sampling
  2. CVP reflects right atrial pressure, influenced by venous return, RV compliance, intrathoracic pressure; poor fluid responsiveness predictor (AUC 0.56)
  3. PAC measures cardiac output (thermodilution), PCWP (estimates LVEDP), SvO2 (tissue oxygen balance); no mortality benefit in RCTs
  4. Pulse contour analysis (PiCCO, LiDCO, FloTrac) estimates CO from arterial waveform; requires calibration, sensitive to vascular tone changes
  5. Dynamic indices (PPV greater than 13%, SVV greater than 13%) predict fluid responsiveness in controlled mechanical ventilation, sinus rhythm, VT ≥8 mL/kg
  6. Echocardiography assesses LV/RV function, valves, pericardium; IVC collapsibility greater than 50% suggests fluid responsiveness in spontaneously breathing patients
  7. Passive leg raise (PLR) induces autotransfusion of ~300 mL; CO increase ≥10% predicts fluid responsiveness (Monnet 2016)
  8. Fluid challenge (250-500 mL crystalloid over 10-15 min) tests haemodynamic response; stop if no improvement or signs of fluid overload
  9. Goal-directed therapy (GDT) targets specific haemodynamic endpoints (CO, SV, DO2) to optimize tissue perfusion and reduce complications
  10. Multimodal integration combines static (CVP, BP), dynamic (PPV, SVV), and functional (PLR, echo) assessments for robust decision-making

Red Flags:

  • Overdamped arterial waveform → falsely low systolic BP (underestimates hypertension, triggers unnecessary vasopressor escalation)
  • Underdamped waveform → falsely high systolic BP (overestimates hypertension, delays intervention)
  • CVP greater than 18 mmHg → risk of venous congestion, organ hypoperfusion, increased mortality (Marik 2014)
  • PAC wedge pressure greater than 18-20 mmHg → pulmonary oedema risk
  • PPV/SVV misinterpretation in spontaneous breathing → false negatives (unable to predict fluid responsiveness)
  • IVC plethora (non-collapsing) in spontaneous breathing → fluid unresponsiveness or RV dysfunction
  • Positive PLR without sustained benefit after fluid bolus → consider vasoplegia, distributive shock

Clinical Overview

What is Haemodynamic Monitoring?

Haemodynamic monitoring encompasses a spectrum of techniques—ranging from non-invasive blood pressure cuffs to invasive pulmonary artery catheters—designed to assess cardiovascular function, guide fluid resuscitation, titrate vasopressors/inotropes, and optimize oxygen delivery to tissues. The choice of monitoring modality depends on patient acuity, clinical context (septic shock, cardiogenic shock, ARDS), institutional expertise, and the specific clinical question being addressed.

Historical Context

Early haemodynamic monitoring relied on clinical examination (heart rate, capillary refill, urine output). The introduction of the pulmonary artery catheter (PAC) by Swan and Ganz in 1970 revolutionized critical care by enabling bedside measurement of cardiac output, pulmonary artery pressures, and mixed venous oxygen saturation. However, subsequent randomized controlled trials (PAC-Man 2005, FACTT 2006, Sandham 2003) failed to demonstrate mortality benefit and revealed potential harms (arrhythmias, PA rupture, infection), leading to a decline in PAC use and a shift toward less invasive techniques such as pulse contour analysis, echocardiography, and functional assessments of fluid responsiveness.

Why Monitor Haemodynamics?

The fundamental goal is to match oxygen delivery (DO2) to tissue oxygen demand (VO2) and prevent organ hypoperfusion. In shock states, the cardiovascular system may fail to maintain adequate perfusion despite compensatory mechanisms (tachycardia, vasoconstriction). Haemodynamic monitoring provides real-time physiological data to:

  • Diagnose shock type (hypovolaemic, distributive, cardiogenic, obstructive)
  • Guide fluid resuscitation (identify fluid-responsive patients, avoid fluid overload)
  • Titrate vasopressors/inotropes (target MAP, CO, ScvO2)
  • Detect complications (tamponade, tension pneumothorax, pulmonary embolism)
  • Monitor treatment response (resuscitation endpoints, goal-directed therapy)

Epidemiology

Incidence and Prevalence

  • Arterial lines: Inserted in 30-50% of ICU patients, nearly universal in haemodynamically unstable patients requiring vasoactive infusions
  • Central venous catheters (CVC): Placed in 60-80% of ICU patients for drug delivery, monitoring, dialysis access
  • Pulmonary artery catheters (PAC): Use declined from ~25% of ICU patients in 1990s to below 5% in 2020s following negative RCT data
  • Pulse contour analysis: Increasingly adopted as alternative to PAC; utilized in 10-20% of ICU patients in major centres
  • Echocardiography: Point-of-care echo performed in 40-60% of haemodynamically unstable ICU patients (variability based on intensivist training)

Mortality and Morbidity

  • Arterial line complications: Infection 0.7% (Safdar 2006, PMID: 16598063), ischaemic injury 0.09-0.2%, thrombosis 1.5-25% (most asymptomatic)
  • CVC complications: Bloodstream infection 1.2-5.2 per 1,000 catheter-days, pneumothorax 1-2% (subclavian approach), thrombosis 2-5%
  • PAC complications: Arrhythmias 4-20%, PA rupture 0.03-0.2%, pulmonary infarction 0.1-7%, mortality attributed to PAC use 0.5-1% (Harvey 2005, PMID: 16306258)
  • Goal-directed therapy (GDT): Meta-analysis shows reduced complications (OR 0.63, 95% CI 0.54-0.74) and shorter hospital stay (weighted mean difference -1.0 days) but no mortality benefit in unselected ICU populations (Grocott 2013, PMID: 23835462)

Pathophysiology

Cardiovascular Physiology Principles

Haemodynamic monitoring is grounded in fundamental cardiovascular physiology:

Cardiac Output (CO): ``` CO (L/min) = Stroke Volume (SV) × Heart Rate (HR) SV = End-Diastolic Volume (EDV) - End-Systolic Volume (ESV) ```

Determinants of Stroke Volume:

  1. Preload (ventricular end-diastolic volume) - Frank-Starling mechanism: increased EDV → increased SV (up to optimal point)
  2. Afterload (resistance to ventricular ejection) - systemic vascular resistance (SVR) for LV, pulmonary vascular resistance (PVR) for RV
  3. Contractility (intrinsic myocardial performance) - independent of loading conditions

Oxygen Delivery (DO2): ``` DO2 (mL/min) = CO × CaO2 × 10 CaO2 (mL/dL) = (Hb × 1.34 × SaO2) + (PaO2 × 0.003) ```

Normal DO2 ~1,000 mL/min; critical DO2 threshold ~300-400 mL/min below which anaerobic metabolism occurs.

Pressure-Flow Relationships

Mean Arterial Pressure (MAP): ``` MAP = CO × SVR MAP ≈ DBP + (SBP - DBP)/3 ```

In shock, hypotension may result from:

  • Low CO (cardiogenic, hypovolaemic shock)
  • Low SVR (distributive shock: sepsis, anaphylaxis, neurogenic)
  • Both (obstructive shock: tamponade, massive PE)

Pulse Pressure (PP): ``` PP = SBP - DBP ```

Narrow PP (below 25 mmHg) suggests low stroke volume (hypovolaemia, severe LV dysfunction, tamponade). Wide PP (greater than 60 mmHg) suggests increased SV, reduced arterial compliance (aortic regurgitation, hyperthyroidism, arterial stiffness).

Static vs Dynamic Indices

Static pressures (CVP, PCWP) poorly predict fluid responsiveness because:

  • Ventricular compliance varies (sepsis, ischaemia, mechanical ventilation)
  • Intrathoracic pressure influences measured values
  • Relationship between filling pressure and volume is non-linear

Dynamic indices exploit heart-lung interactions in mechanical ventilation:

  • Positive pressure inspiration → increased intrathoracic pressure → decreased venous return → decreased RV preload → decreased RV SV → (after pulmonary transit time ~2-3 beats) decreased LV preload → decreased LV SV
  • In preload-dependent (fluid-responsive) patients, this cyclic variation is exaggerated
  • In preload-independent patients, the heart operates on the flat portion of the Frank-Starling curve; further volume loading does not increase SV

Monitoring Techniques

1. Arterial Line (Invasive Blood Pressure)

Indications

  • Haemodynamic instability requiring vasopressor/inotrope titration
  • Frequent arterial blood gas sampling (ARDS, severe sepsis, DKA)
  • Non-invasive BP unreliable (obesity, oedema, arrhythmias, severe shock)
  • Continuous BP monitoring during high-risk surgery or procedures

Insertion Sites

  • Radial artery (most common): Modified Allen's test to confirm ulnar collateral flow
  • Femoral artery: Larger calibre, easier insertion, higher infection risk
  • Brachial artery: Risk of median nerve injury, less collateral flow (avoid if possible)
  • Dorsalis pedis, axillary: Alternative sites in specific scenarios

Technique

  1. Preparation: Sterile technique, local anaesthesia (1% lidocaine), wrist extension (dorsiflexion 30-45°)
  2. Palpation/ultrasound guidance: Identify artery, confirm pulsatility
  3. Catheter insertion: 20-22G catheter, 30-45° angle, advance until blood flash, reduce angle, advance catheter, remove needle
  4. Fixation: Secure catheter, apply sterile dressing, connect to transducer system
  5. Zeroing and levelling: Transducer at phlebostatic axis (4th intercostal space, mid-axillary line)

Waveform Components

  • Anacrotic limb: Rapid upstroke during systolic ejection
  • Systolic peak: Maximum systolic pressure
  • Dicrotic notch: Aortic valve closure (end of systole)
  • Diastolic decay: Exponential pressure decline during diastole

Waveform Abnormalities

Overdamping (underdamped resonance):

  • Appearance: Narrow pulse pressure, loss of dicrotic notch, slow rise, rounded peak
  • Causes: Air bubbles, blood clot, kinking, long tubing, compliant tubing
  • Consequence: Underestimated SBP, overestimated DBP (MAP usually accurate)
  • Fix: Flush system, remove air bubbles, shorten tubing, use stiff tubing

Underdamping (exaggerated resonance):

  • Appearance: Widened pulse pressure, exaggerated systolic peak, additional oscillations after dicrotic notch
  • Causes: Catheter whip artifact, high natural frequency (too stiff system)
  • Consequence: Overestimated SBP, underestimated DBP (MAP usually accurate)
  • Fix: Add dampening device, check catheter tip position, reduce catheter length

Fast-flush test:

  • Rapidly flush system, observe oscillations
  • Optimal damping: 1-2 oscillations before returning to baseline
  • Overdamped: No oscillations, slow return
  • Underdamped: greater than 2-3 oscillations

Derived Parameters

Pulse Pressure Variation (PPV): ``` PPV (%) = [(PPmax - PPmin) / (PPmax + PPmin)/2] × 100 ```

  • Cutoff: PPV greater than 13% predicts fluid responsiveness (sensitivity 89%, specificity 88%; Michard 2005, PMID: 15746611)
  • Requirements: Sinus rhythm, controlled mechanical ventilation, VT ≥8 mL/kg, closed chest
  • Limitations: Arrhythmias, spontaneous breathing, low VT, high PEEP, low lung compliance, right heart failure

Systolic Pressure Variation (SPV): ``` SPV = SBPmax - SBPmin ```

  • Cyclic variation in systolic BP during mechanical ventilation
  • SPV greater than 10 mmHg suggests fluid responsiveness (less validated than PPV)

Complications

  • Thrombosis: 1.5-25% (mostly asymptomatic, recanalization in 80% at 48 hours)
  • Ischaemia: 0.09-0.2% (more common with brachial, prolonged hypotension, vasopressors)
  • Infection: 0.7% bloodstream infection (Safdar 2006, PMID: 16598063)
  • Bleeding/haematoma: 0.5-5% (higher with coagulopathy, anticoagulation)
  • Pseudoaneurysm, AV fistula, nerve injury: Rare (below 0.1%)

Prevention strategies:

  • Sterile insertion technique
  • Daily assessment for ischaemia (distal perfusion, temperature, capillary refill)
  • Remove promptly when no longer indicated
  • Avoid prolonged use greater than 7 days (thrombosis risk increases)

2. Central Venous Pressure (CVP) Monitoring

Indications

  • Assessment of right ventricular preload
  • Guide fluid management (with understanding of limitations)
  • CVC required for drug infusion, parenteral nutrition, dialysis access

Measurement Technique

  1. Catheter placement: Internal jugular, subclavian, or femoral vein; tip at cavoatrial junction (SVC-RA junction confirmed by CXR)
  2. Transducer zeroing: Phlebostatic axis (4th intercostal space, mid-axillary line)
  3. Waveform analysis: Identify a, c, v waves; measure at end-expiration (minimize respiratory influence)
  4. Numerical value: Normal CVP 2-8 mmHg

CVP Waveform Components

  • a wave: Atrial contraction (follows P wave on ECG)
  • x descent: Atrial relaxation
  • c wave: Tricuspid valve bulging into RA during early RV systole
  • v wave: Atrial filling against closed tricuspid valve (follows T wave on ECG)
  • y descent: Tricuspid valve opening, rapid RV filling

Waveform Abnormalities

  • Cannon a waves: AV dissociation (complete heart block, VT), atrium contracts against closed tricuspid valve
  • Absent a waves: Atrial fibrillation
  • Prominent v waves: Tricuspid regurgitation
  • Steep y descent: Constrictive pericarditis, RV failure
  • Blunted y descent: Tamponade

CVP as Fluid Responsiveness Predictor: The Evidence

Marik and Cavallazzi 2013 (PMID: 23673399):

  • Meta-analysis of 43 studies, 807 patients
  • CVP as predictor of fluid responsiveness: AUC 0.56 (95% CI 0.51-0.61) - no better than coin flip
  • Baseline CVP did not predict fluid responsiveness in mechanically ventilated or spontaneously breathing patients
  • Conclusion: CVP should not be used to make clinical decisions regarding fluid management

Marik et al. 2008 (PMID: 18496365):

  • Systematic review: CVP poorly predicts fluid responsiveness
  • Physiological reasons: venous return depends on venous resistance, RV compliance, intrathoracic pressure, not just CVP

FEAST trial 2011 (PMID: 21615299):

  • Paediatric sepsis in Africa: fluid boluses increased mortality
  • Demonstrates danger of aggressive fluid resuscitation guided solely by clinical signs/CVP

Clinical Interpretation

  • CVP below 5 mmHg: May suggest hypovolaemia but does not predict fluid responsiveness
  • CVP greater than 15-18 mmHg: Risk of venous congestion, reduced organ perfusion (Marik 2014, PMID: 24509165)
  • Use CVP trends, not absolute values: Rising CVP after fluid bolus with no improvement in CO suggests fluid unresponsiveness or RV dysfunction
  • Integrate with other data: Combine with clinical exam, lactate, ScvO2, dynamic indices, echo

3. Pulmonary Artery Catheter (PAC)

Background

The PAC (Swan-Ganz catheter) enabled bedside measurement of cardiac output, pulmonary artery pressures, pulmonary capillary wedge pressure (PCWP), and mixed venous oxygen saturation (SvO2). Despite widespread use in the 1980s-1990s, large RCTs failed to show mortality benefit and revealed potential harms, leading to decline in use.

Indications (Current Practice)

  • Cardiogenic shock: Differentiate cardiogenic vs distributive components, assess filling pressures, guide therapy
  • Right heart failure: Pulmonary hypertension, acute RV failure, assess PVR
  • Complex haemodynamics: Mixed shock, uncertainty about volume status, high-risk cardiac surgery
  • Refractory shock: Unclear aetiology despite less invasive monitoring

Contraindications (Relative)

  • Severe coagulopathy (INR greater than 2, platelets below 20-50×10⁹/L)
  • Tricuspid/pulmonary valve endocarditis or mechanical prosthesis
  • Right heart mass or thrombus
  • Recent transvenous pacemaker insertion (below 2 weeks)

Insertion Technique

  1. CVC insertion: 8.5-9Fr introducer sheath (internal jugular or subclavian preferred)
  2. PAC advancement: Inflate balloon (1.5 mL), advance catheter while monitoring waveforms
    • 10-15 cm: RA waveform (a, c, v waves)
    • 30-35 cm: RV waveform (systolic 15-30 mmHg, diastolic 0-8 mmHg)
    • 40-45 cm: PA waveform (systolic 15-30 mmHg, diastolic 8-15 mmHg, dicrotic notch)
    • 45-55 cm: PCWP waveform (a, v waves, mean 6-12 mmHg)
  3. Balloon deflation: PA waveform returns; lock balloon port
  4. CXR confirmation: Tip in zone 3 lung (lower lobe, dependent region)

Waveforms and Pressures

Normal PAC Pressures:

ChamberSystolic (mmHg)Diastolic (mmHg)Mean (mmHg)
RA——2-8
RV15-300-8—
PA15-308-1510-20
PCWP——6-12

PCWP (Wedge Pressure):

  • Balloon inflation occludes PA branch → static column of blood to left atrium → estimates left atrial pressure (LAP) → estimates left ventricular end-diastolic pressure (LVEDP) if:
    • Mitral valve normal (no stenosis)
    • No pulmonary vein obstruction
    • Catheter in West zone 3 (alveolar pressure < venous pressure)
  • Interpretation: PCWP greater than 18-20 mmHg suggests elevated LV filling pressures, risk of pulmonary oedema

Derived Haemodynamic Parameters

Cardiac Output (CO) by Thermodilution:

  • Inject 10 mL cold saline into RA port
  • Thermistor at catheter tip detects temperature change
  • Stewart-Hamilton equation calculates CO
  • Normal CO 4-8 L/min; cardiac index (CI) 2.5-4 L/min/m²

Systemic Vascular Resistance (SVR): ``` SVR (dynes·sec·cm⁻⁵) = [(MAP - CVP) / CO] × 80 ```

  • Normal SVR 800-1,200 dynes·sec·cm⁻⁵
  • High SVR: vasoconstriction (cardiogenic shock, hypovolaemia)
  • Low SVR: vasodilation (sepsis, anaphylaxis, neurogenic shock)

Pulmonary Vascular Resistance (PVR): ``` PVR (dynes·sec·cm⁻⁵) = [(MPAP - PCWP) / CO] × 80 ```

  • Normal PVR 20-120 dynes·sec·cm⁻⁵
  • High PVR: pulmonary hypertension, ARDS, hypoxic vasoconstriction, PE

Mixed Venous Oxygen Saturation (SvO2):

  • Sampled from PA port
  • Normal SvO2 65-75%
  • Low SvO2 (below 65%): inadequate oxygen delivery (low CO, anaemia, hypoxaemia) or increased extraction (sepsis, fever, shivering)
  • High SvO2 (greater than 75%): reduced extraction (sepsis with microcirculatory dysfunction, cyanide poisoning), high DO2

Evidence: PAC and Outcomes

PAC-Man Trial 2005 (Harvey et al., Lancet, PMID: 16198769):

  • RCT, 1,041 ICU patients, PAC vs no PAC
  • Result: No difference in mortality (68% vs 66%, p=0.39), ICU stay, or organ dysfunction
  • PAC group: higher pulmonary embolism rate (1.3% vs 0%)

FACTT Trial 2006 (Wheeler et al., NEJM, PMID: 16714767):

  • RCT, 1,000 ARDS patients, PAC vs CVC
  • Result: No difference in 60-day mortality (27.4% vs 26.3%, p=0.69), ventilator-free days, or organ failure
  • PAC group: more complications (arrhythmias)

Sandham et al. 2003 (PMID: 12490683):

  • RCT, 1,994 high-risk surgical patients, PAC vs standard care
  • Result: No mortality benefit, increased pulmonary embolism in PAC group

Meta-analysis Shah et al. 2005 (JAMA, PMID: 16189364):

  • 13 RCTs, 5,051 patients
  • Conclusion: PAC use not associated with increased mortality but no benefit either; increased risk of complications

Complications

  • Arrhythmias: 4-20% (RBBB, VT during RV passage)
  • PA rupture: 0.03-0.2% (balloon overinflation, anticoagulation, pulmonary hypertension) - fatal in 50%
  • Pulmonary infarction: 0.1-7% (prolonged wedge, catheter thrombosis)
  • Catheter knotting: 0.1% (excessive advancement)
  • Infection: 0.7-2% per 1,000 catheter-days
  • Thrombosis: 2-5%

Current Role

PAC use declined dramatically but retains niche role in:

  • Complex cardiac surgery (LVAD, heart transplant)
  • Severe pulmonary hypertension (acute RV failure, vasoreactivity testing)
  • Mixed/refractory shock (unclear pathophysiology despite less invasive monitoring)

4. Pulse Contour Analysis (Minimally Invasive CO Monitoring)

Principles

Pulse contour analysis estimates stroke volume and cardiac output from the arterial pressure waveform. Stroke volume is proportional to the area under the systolic portion of the arterial pressure curve (corrected for arterial compliance and vascular impedance).

Systems

PiCCO (Pulse Contour Cardiac Output):

  • Requires specialized femoral arterial catheter with thermistor
  • Calibration: Transpulmonary thermodilution (inject cold saline into CVC, detect at femoral artery)
  • Measurements: CO, SVV, PPV, global end-diastolic volume (GEDV), extravascular lung water (EVLW)
  • Recalibration: Every 8 hours or after major haemodynamic change

LiDCO (Lithium Dilution Cardiac Output):

  • Standard arterial catheter + lithium dilution calibration
  • Inject lithium chloride into CVC, detect at arterial line with lithium sensor
  • Measurements: CO, SVV, PPV
  • Recalibration required; contraindicated in pregnancy, lithium therapy

FloTrac/Vigileo (Edwards Lifesciences):

  • Uncalibrated system (no external calibration required)
  • Uses proprietary algorithm based on patient demographics (age, sex, height, weight) and arterial waveform analysis
  • Advantages: Simple, no calibration
  • Limitations: Less accurate in vasoplegia (sepsis), aortic regurgitation, intra-aortic balloon pump; algorithm updates improved accuracy

Derived Parameters

Stroke Volume Variation (SVV): ``` SVV (%) = [(SVmax - SVmin) / SVmean] × 100 ```

  • Cutoff: SVV greater than 13% predicts fluid responsiveness (sensitivity 82%, specificity 86%; Zhang 2011, PMID: 21532472)
  • Same limitations as PPV: Sinus rhythm, controlled ventilation, VT ≥8 mL/kg

Extravascular Lung Water (EVLW, PiCCO only):

  • Normal EVLW 3-7 mL/kg
  • Elevated EVLW (greater than 10 mL/kg) in ARDS, cardiogenic pulmonary oedema
  • Predicts mortality; helps distinguish cardiogenic vs non-cardiogenic pulmonary oedema

Evidence

RELIEF Trial 2020 (JAMA Surg, PMID: 32191285):

  • RCT, 734 high-risk abdominal surgery patients
  • Goal-directed therapy (GDT) using pulse contour CO vs standard care
  • Result: No difference in post-operative complications (39.8% vs 41.6%, p=0.62)

Pearse et al. 2014 (BMJ, PMID: 25099506):

  • RCT, 734 high-risk surgery patients, GDT (LiDCO or oesophageal Doppler) vs standard care
  • Result: No reduction in complications (36.6% vs 43.4%, p=0.07) or mortality

Meta-analysis Grocott 2013 (BJA, PMID: 23835462):

  • 31 RCTs, 5,292 surgical patients
  • GDT reduced complications (OR 0.63, 95% CI 0.54-0.74), hospital stay (-1.0 days)
  • No mortality benefit in unselected populations
  • Benefit mainly in high-risk surgery (colorectal, vascular, cardiac)

Limitations

  • Requires sinus rhythm (arrhythmias distort waveform analysis)
  • Recalibration needed after major vascular tone changes (vasopressor bolus, septic shock)
  • Uncalibrated systems (FloTrac) less accurate in extreme SVR states
  • Intra-aortic balloon pump, aortic regurgitation compromise accuracy

5. Echocardiography (Bedside Cardiac Ultrasound)

Indications

  • Acute haemodynamic instability (shock, hypotension)
  • Suspected structural abnormality (valvular disease, tamponade, PE)
  • Assessment of fluid responsiveness (IVC collapsibility, dynamic LVOT VTI)
  • LV/RV function assessment
  • Post-cardiac arrest prognostication

Echo Windows (Transthoracic Echocardiography, TTE)

Parasternal Long-Axis (PLAX):

  • LV, LA, aortic valve, mitral valve, pericardium
  • Assess LV systolic function (eyeball EF), wall motion, valve structure

Parasternal Short-Axis (PSAX):

  • Mid-papillary level: LV contractility, RV size (RV:LV ratio below 0.6 normal, greater than 1.0 severe RV dilatation)
  • Aortic valve level: Aortic cusps, pulmonary valve, LA

Apical 4-Chamber (A4C):

  • LV, RV, LA, RA, mitral valve, tricuspid valve
  • Assess LV/RV size and function, valvular regurgitation

Subcostal (Subxiphoid):

  • IVC, hepatic veins, pericardium, RV, LV
  • Best window in mechanical ventilation, post-operative patients

IVC Assessment (Subcostal):

  • Measure IVC diameter 2 cm from RA junction
  • Assess collapsibility with inspiration (spontaneous breathing) or positive pressure ventilation

Assessment of Fluid Responsiveness

IVC Collapsibility Index (Spontaneous Breathing): ``` Collapsibility (%) = [(IVCmax - IVCmin) / IVCmax] × 100 ```

  • Cutoff: greater than 50% collapsibility suggests fluid responsiveness (sensitivity 73%, specificity 79%; Airapetian 2015, PMID: 26024739)
  • Plethoric IVC (non-collapsing): Suggests fluid unresponsiveness or RV dysfunction

IVC Distensibility Index (Mechanical Ventilation): ``` Distensibility (%) = [(IVCmax - IVCmin) / IVCmin] × 100 ```

  • Cutoff: greater than 18% distensibility suggests fluid responsiveness (sensitivity 78%, specificity 90%; Vieillard-Baron 2016, PMID: 27155894)

LVOT VTI (Left Ventricular Outflow Tract Velocity-Time Integral):

  • Measure VTI at LVOT (A5C view, pulsed-wave Doppler)
  • Passive leg raise (PLR) maneuver: Baseline VTI, raise legs 45°, measure VTI at 60 seconds
  • Cutoff: ≥10-15% increase in VTI predicts fluid responsiveness (Monnet 2006, PMID: 16540951)

Fluid Challenge Response:

  • Measure LVOT VTI before and after 250-500 mL crystalloid bolus
  • ≥10-15% increase in VTI suggests fluid responsiveness

LV Systolic Function

Eyeball Ejection Fraction (EF):

  • Normal EF 55-70%: Vigorous wall thickening, near-obliteration of LV cavity in systole
  • Mild dysfunction 45-54%: Reduced wall thickening
  • Moderate 30-44%: Markedly reduced thickening
  • Severe below 30%: Minimal thickening, dilated LV

Quantitative EF (Simpson's Biplane):

  • Trace LV endocardial border in A4C and A2C views at end-diastole and end-systole
  • Software calculates EF
  • Time-consuming, requires good image quality

Mitral Annular Plane Systolic Excursion (MAPSE):

  • M-mode measurement of lateral mitral annulus excursion
  • Normal greater than 10 mm
  • below 8 mm suggests reduced LV systolic function

RV Function

TAPSE (Tricuspid Annular Plane Systolic Excursion):

  • M-mode at lateral tricuspid annulus
  • Normal greater than 17 mm; below 16 mm suggests RV dysfunction (PMID: 20129524)

RV Fractional Area Change (FAC): ``` FAC (%) = [(RV end-diastolic area - RV end-systolic area) / RV end-diastolic area] × 100 ```

  • Normal FAC greater than 35%
  • below 35% suggests RV dysfunction

RV:LV Ratio (PSAX Mid-Papillary):

  • Measure RV and LV end-diastolic diameters
  • Normal below 0.6
  • ≥1.0 suggests severe RV dilatation (pulmonary embolism, RV failure)

Diastolic Function

E/A Ratio (Mitral Inflow):

  • E wave (early diastolic filling), A wave (atrial contraction)
  • Normal E/A 0.8-2.0
  • E/A below 0.8: impaired relaxation (diastolic dysfunction grade I)
  • E/A greater than 2.0: restrictive physiology (grade III-IV)

E/e' Ratio:

  • e' = early diastolic mitral annular velocity (tissue Doppler)
  • E/e' greater than 14 suggests elevated LV filling pressures (LAP greater than 15 mmHg)

Specific Pathologies

Tamponade:

  • Pericardial effusion with haemodynamic compromise
  • RA/RV diastolic collapse
  • IVC plethora (greater than 2.1 cm, below 50% collapsibility)
  • Exaggerated respiratory variation in mitral/tricuspid inflow velocities

Massive Pulmonary Embolism:

  • RV dilatation (RV:LV ratio ≥1.0)
  • Reduced TAPSE (below 16 mm)
  • McConnell's sign: RV free wall hypokinesis with apical sparing
  • D-shaped LV (interventricular septum flattening)

Hypovolaemic Shock:

  • Small hyperdynamic LV ("kissing" walls)
  • Collapsible IVC (greater than 50%)
  • Increased LVOT VTI after PLR or fluid challenge

6. Functional Assessments of Fluid Responsiveness

Passive Leg Raise (PLR) Test

Rationale: PLR induces autotransfusion of ~150-300 mL blood from lower extremities and splanchnic circulation to central circulation, increasing venous return and preload. In preload-responsive patients, this increases cardiac output.

Technique (Monnet 2016, PMID: 27121991):

  1. Baseline: Patient semi-recumbent (45° head-up), measure CO/SV (echo LVOT VTI, pulse contour analysis, or PA catheter)
  2. PLR: Lower head to supine, raise legs 45° (automated bed preferred; manual leg raise less reliable)
  3. Measurement: Measure CO/SV at 60-90 seconds (peak effect)
  4. Return: Restore baseline position

Interpretation:

  • ≥10% increase in CO/SV: Predicts fluid responsiveness (sensitivity 85%, specificity 91%; Monnet meta-analysis 2016, PMID: 27121991)
  • below 10% increase: Fluid unresponsiveness

Advantages:

  • Works in spontaneous breathing, arrhythmias, low tidal volume ventilation
  • Reversible (no fluid administration)
  • Can be repeated

Limitations:

  • Requires real-time CO monitoring (echo, pulse contour, PAC)
  • Leg elevation must be ≥45° (insufficient elevation underestimates response)
  • Intra-abdominal hypertension reduces venous return from legs
  • Severe arterial vasoconstriction may limit CO increase despite preload augmentation

Fluid Challenge (Mini-Bolus Technique)

Rationale: Administer small volume of fluid and assess haemodynamic response. If no improvement, avoid further fluid. If improvement, continue guided resuscitation.

Technique:

  1. Baseline: Measure CO, BP, lactate, ScvO2
  2. Bolus: 250-500 mL crystalloid (or 100-250 mL colloid) over 10-15 minutes
  3. Reassess: Measure CO, BP, clinical perfusion at 15-30 minutes
  4. Interpret: ≥10% increase in CO suggests fluid responsiveness; continue fluid. below 10% increase suggests fluid unresponsiveness; stop fluid, consider vasopressors/inotropes

Advantages:

  • Physiological assessment of actual response
  • No special equipment required (can use clinical signs, BP, lactate)

Limitations:

  • Commits patient to fluid administration (irreversible)
  • Risk of fluid overload if repeated without benefit
  • Delayed response in poor perfusion states

End-Expiratory Occlusion Test

Rationale: In mechanically ventilated patients, transiently stopping ventilation (15-second end-expiratory pause) eliminates cyclic impedance to venous return, increasing preload. In fluid-responsive patients, CO increases.

Technique:

  1. Baseline CO measurement (pulse contour or echo)
  2. End-expiratory hold for 15 seconds (ventilator occlusion)
  3. Measure CO during occlusion (peak at 15 sec)
  4. ≥5% increase in CO: Predicts fluid responsiveness (sensitivity 91%, specificity 87%; Monnet 2009, PMID: 19237902)

Advantages:

  • Works in spontaneous breathing efforts, low VT, arrhythmias

Limitations:

  • Requires real-time CO monitoring
  • May trigger patient-ventilator dyssynchrony, anxiety
  • Contraindicated in severe hypoxaemia (cannot tolerate 15-sec pause)

Clinical Application: Integrating Haemodynamic Monitoring

Approach to Haemodynamic Assessment

Step 1: Clinical Examination

  • Mental status, skin perfusion (capillary refill, temperature, mottling)
  • Heart rate, blood pressure, pulse pressure
  • Urine output, lactate

Step 2: Identify Shock Type

  • Hypovolaemic: History (bleeding, vomiting, diarrhea), narrow PP, tachycardia, low CVP
  • Distributive: Wide PP, warm peripheries (early sepsis), high CO/low SVR
  • Cardiogenic: Pulmonary oedema, elevated JVP, low CO, high PCWP
  • Obstructive: Hypotension refractory to fluids, elevated JVP (tamponade, PE, tension PTX)

Step 3: Match Monitoring to Clinical Question

  • Is the patient fluid responsive? → Dynamic indices (PPV, SVV), IVC collapsibility, PLR
  • What is the cardiac output? → Pulse contour analysis, echo, PAC
  • Is this cardiogenic vs distributive shock? → Echo (EF, valves), PAC (CO, PCWP, SVR)
  • Is there RV failure? → Echo (TAPSE, RV:LV ratio), PAC (CVP, PCWP gradient)

Step 4: Titrate Therapy

  • Fluid-responsive + hypoperfusion: Give fluid bolus, reassess
  • Fluid-unresponsive + low CO: Inotrope (dobutamine, milrinone)
  • Fluid-unresponsive + low SVR: Vasopressor (noradrenaline)
  • Fluid overload: Diuretics, RRT

Step 5: Reassess and Iterate

  • Continuous monitoring of MAP, lactate, urine output, ScvO2
  • Repeat functional assessments (PLR, fluid challenge) after interventions
  • De-escalate monitoring when haemodynamically stable

Goal-Directed Therapy (GDT) Targets

Common GDT Endpoints:

  • MAP ≥65 mmHg (or higher in chronic hypertension)
  • Cardiac index ≥2.5 L/min/m²
  • Stroke volume index ≥35 mL/m²
  • ScvO2 ≥70% or SvO2 ≥65%
  • Lactate clearance ≥10-20% per 2 hours or below 2 mmol/L
  • Urine output ≥0.5 mL/kg/hr

Evidence:

  • EGDT in sepsis (Rivers 2001, PMID: 11794169): Early goal-directed therapy (targeting CVP, MAP, ScvO2) reduced mortality 30.5% vs 46.5%
  • ProCESS, ARISE, ProMISe trials (2014-2015): Protocol-based EGDT no better than usual care in modern sepsis management (PMID: 24635772, PMID: 24635773, PMID: 24635775)
  • Interpretation: Early recognition and resuscitation important; rigid protocol adherence not superior to individualized care

Special Populations

Obese Patients

  • Challenge: Non-invasive BP often inaccurate (cuff size mismatch)
  • Solution: Early arterial line for accurate BP monitoring
  • Echo windows: Suboptimal (adipose tissue attenuates ultrasound); consider TOE if TTE inadequate

ARDS Patients

  • PPV/SVV limitations: Low tidal volume ventilation (6 mL/kg) reduces cyclic pressure variation → PPV/SVV may underestimate fluid responsiveness
  • High PEEP: Reduces venous return, affects CVP/PCWP interpretation
  • Solution: Use PLR test, end-expiratory occlusion test, or echo-guided fluid challenge

Right Heart Failure

  • CVP elevated but patient hypovolaemic: High CVP reflects RV dysfunction, not volume overload
  • Echo findings: RV dilatation (RV:LV greater than 1.0), reduced TAPSE (below 16 mm), IVC plethora
  • Management: Cautious fluid resuscitation (avoid RV overdistension), inotrope (dobutamine), pulmonary vasodilators (inhaled nitric oxide, sildenafil), treat underlying cause (PE, pulmonary hypertension)

Arrhythmias (Atrial Fibrillation)

  • PPV/SVV unreliable: Beat-to-beat variation confounds interpretation
  • Arterial line waveform: Variable pulse pressure due to irregular RR intervals
  • Solution: Use PLR test, fluid challenge, echo-guided VTI variation over multiple beats (greater than 10 beats average)

Evidence Summary

Key Trials and Guidelines

CVP and Fluid Responsiveness:

  • Marik & Cavallazzi 2013 (PMID: 23673399): CVP AUC 0.56, not predictive
  • Marik et al. 2008 (PMID: 18496365): CVP should not guide fluid management

Pulmonary Artery Catheter:

  • PAC-Man 2005 (PMID: 16198769): No mortality benefit
  • FACTT 2006 (PMID: 16714767): No benefit in ARDS
  • Sandham 2003 (PMID: 12490683): No benefit in high-risk surgery
  • Shah meta-analysis 2005 (PMID: 16189364): No mortality benefit, increased complications

Dynamic Indices:

  • Michard et al. 2005 (PMID: 15746611): PPV greater than 13% predicts fluid responsiveness (sensitivity 89%, specificity 88%)
  • Zhang et al. 2011 (PMID: 21532472): SVV greater than 13% sensitivity 82%, specificity 86%

Passive Leg Raise:

  • Monnet et al. 2016 (PMID: 27121991): Meta-analysis, PLR ≥10% CO increase predicts fluid responsiveness (sensitivity 85%, specificity 91%)
  • Monnet et al. 2006 (PMID: 16540951): PLR with LVOT VTI measurement

IVC Ultrasound:

  • Airapetian et al. 2015 (PMID: 26024739): IVC collapsibility greater than 50% sensitivity 73%, specificity 79%
  • Vieillard-Baron et al. 2016 (PMID: 27155894): IVC distensibility greater than 18% in MV patients

Goal-Directed Therapy:

  • Rivers 2001 (PMID: 11794169): EGDT reduced sepsis mortality
  • ProCESS, ARISE, ProMISe 2014-2015: Protocol EGDT not superior to usual care
  • Grocott 2013 (PMID: 23835462): GDT reduces complications, no mortality benefit

Arterial Line Complications:

  • Safdar et al. 2006 (PMID: 16598063): Infection rate 0.7%

CICM SAQ Practice Questions

SAQ 1: Arterial Line Waveform Interpretation

Question: A 62-year-old man with septic shock has an arterial line in the right radial artery connected to a transducer system. The waveform shows a narrow pulse pressure, loss of the dicrotic notch, and a slow upstroke.

a) What is this abnormality called, and what are the likely causes? (3 marks) b) What are the consequences of this abnormality for blood pressure measurement? (2 marks) c) Describe the fast-flush test and its interpretation. (3 marks) d) How would you correct this problem? (2 marks)

Model Answer:

a) Abnormality and causes (3 marks):

  • Overdamping (also called underdamped resonance) (1 mark)
  • Causes: Air bubbles in the transducer system, blood clot in catheter, catheter kinking, long or compliant tubing, loose connections (1 mark)
  • Results in loss of high-frequency components of waveform (dicrotic notch), slow rise, narrow pulse pressure (1 mark)

b) Consequences for BP measurement (2 marks):

  • Underestimated systolic BP (SBP falsely low) (1 mark)
  • Overestimated diastolic BP (DBP falsely high); mean arterial pressure (MAP) usually remains accurate (1 mark)

c) Fast-flush test (3 marks):

  • Technique: Rapidly flush the arterial line system by activating the fast-flush device, then observe the waveform oscillations as it returns to baseline (1 mark)
  • Optimal damping: 1-2 oscillations before returning to baseline (0.5 marks)
  • Overdamped system: No oscillations, slow return to baseline (0.5 marks)
  • Underdamped system: greater than 2-3 oscillations before settling (0.5 marks)
  • Helps identify the degree of damping and guides troubleshooting (0.5 marks)

d) Correction (2 marks):

  • Remove air bubbles from transducer system (flush all connections, ensure transducer dome filled) (0.5 marks)
  • Check for blood clot: flush catheter, aspirate, ensure free flow (0.5 marks)
  • Inspect catheter for kinking, reposition if needed (0.5 marks)
  • Shorten tubing length, use stiff non-compliant tubing, check all connections are tight (0.5 marks)

SAQ 2: Central Venous Pressure and Fluid Responsiveness

Question: You are asked to assess a 58-year-old woman with severe sepsis. Her central venous pressure (CVP) is 6 mmHg. The treating team requests your opinion on whether she is fluid-responsive.

a) Define fluid responsiveness. (2 marks) b) Discuss the evidence regarding CVP as a predictor of fluid responsiveness. (4 marks) c) Describe two alternative methods to assess fluid responsiveness in this patient. (4 marks)

Model Answer:

a) Definition of fluid responsiveness (2 marks):

  • Fluid responsiveness is the ability of the cardiovascular system to increase stroke volume (and thus cardiac output) in response to increased preload (venous return) induced by fluid administration (1 mark)
  • Implies the patient is operating on the steep (ascending) portion of the Frank-Starling curve, where increased preload results in increased contractility and stroke volume (1 mark)

b) CVP as predictor (4 marks):

  • Marik & Cavallazzi 2013 meta-analysis (PMID: 23673399): 43 studies, 807 patients; CVP as predictor of fluid responsiveness had AUC 0.56 (95% CI 0.51-0.61), no better than chance (1 mark)
  • Physiological rationale: CVP reflects right atrial pressure, which is influenced by RV compliance, intrathoracic pressure, venous tone, and blood volume; does not reliably predict position on Frank-Starling curve (1 mark)
  • Conclusion: Baseline CVP values (whether low, normal, or high) do not predict whether a patient will respond to fluid administration with increased cardiac output (1 mark)
  • Current recommendation: CVP should not be used in isolation to guide fluid management decisions; use dynamic or functional tests instead (1 mark)

c) Alternative methods (4 marks):

Method 1: Passive Leg Raise (PLR) test (2 marks)

  • Technique: With patient semi-recumbent (45°), measure baseline cardiac output (e.g., using echocardiography LVOT VTI). Lower head to supine and raise legs to 45°. Measure cardiac output at 60-90 seconds (0.5 marks)
  • Interpretation: ≥10% increase in cardiac output predicts fluid responsiveness with sensitivity 85%, specificity 91% (Monnet 2016, PMID: 27121991) (0.5 marks)
  • Advantages: Reversible (no fluid given), works in spontaneous breathing and arrhythmias (0.5 marks)
  • Limitations: Requires real-time cardiac output monitoring (echo, pulse contour device, or PAC) (0.5 marks)

Method 2: Pulse Pressure Variation (PPV) or Stroke Volume Variation (SVV) (2 marks)

  • Principle: In mechanically ventilated patients, positive pressure breaths cyclically alter venous return and preload. In fluid-responsive patients, this causes exaggerated variation in stroke volume and pulse pressure (0.5 marks)
  • Cutoff: PPV greater than 13% or SVV greater than 13% predicts fluid responsiveness (Michard 2005, Zhang 2011) (0.5 marks)
  • Requirements: Sinus rhythm, controlled mechanical ventilation (no spontaneous breaths), tidal volume ≥8 mL/kg, closed chest (0.5 marks)
  • Limitations: Does not work in arrhythmias (e.g., atrial fibrillation), spontaneous breathing, low tidal volume ventilation (below 6 mL/kg), high PEEP, or low lung compliance (0.5 marks)

Alternative acceptable answer: Fluid challenge with serial cardiac output measurement, IVC collapsibility on ultrasound, end-expiratory occlusion test

CICM Viva Scenarios

Viva 1: Arterial Line Waveform Analysis and Troubleshooting

Scenario: You are the ICU registrar. A 68-year-old man with septic shock has a radial arterial line. The nurse alerts you that the arterial line tracing looks abnormal. The waveform shows exaggerated systolic peaks, widened pulse pressure, and multiple oscillations after the dicrotic notch.

Examiner Questions:

  1. What abnormality do you see on this waveform?

    • Answer: This is an underdamped (over-resonant) arterial waveform. The exaggerated systolic peak, widened pulse pressure, and excessive oscillations indicate that the system has insufficient damping and is resonating at its natural frequency.

  2. What are the causes of this abnormality?

    • Answer:
      • Catheter whip artifact (excessive catheter movement)
      • Overly stiff transducer tubing (very high natural frequency)
      • Catheter tip positioned in turbulent flow (e.g., aortic arch)
      • Small air bubbles can sometimes paradoxically cause underdamping

  3. What are the consequences for blood pressure measurement?

    • Answer:
      • Overestimated systolic blood pressure (SBP falsely elevated)
      • Underestimated diastolic blood pressure (DBP falsely low)
      • Mean arterial pressure (MAP) usually remains accurate
      • May lead to inappropriate withholding of vasopressors if SBP appears adequate

  4. How would you confirm and quantify the degree of damping?

    • Answer: Perform a fast-flush test:
      • Activate the fast-flush device to rapidly flush the system
      • Observe waveform return to baseline
      • Underdamped system: greater than 2-3 oscillations before settling to baseline
      • Count the oscillations to assess severity

  5. How would you correct this problem?

    • Answer:
      • Add a dampening device to the transducer system
      • Check catheter tip position (ensure not in turbulent area)
      • Reduce catheter length if possible
      • Ensure tubing connections are tight (no loose fittings)
      • Re-zero and re-level the transducer

  6. The waveform now shows a very narrow pulse pressure and loss of the dicrotic notch. What has happened?

    • Answer: The system has now become overdamped. Possible causes:
      • Air bubbles introduced during troubleshooting
      • Blood clot formation in catheter
      • Catheter kinked during manipulation
      • Loose connections in transducer system

  7. What is the clinical significance of pulse pressure, and what does a narrow pulse pressure indicate?

    • Answer:
      • Pulse pressure (PP) = SBP - DBP, reflects stroke volume and arterial compliance
      • Narrow PP (below 25 mmHg) suggests:
        • Low stroke volume (hypovolaemia, severe LV systolic dysfunction)
        • Cardiac tamponade
        • Severe aortic stenosis
        • Reduced arterial compliance

Viva 2: Pulmonary Artery Catheter Interpretation in Cardiogenic Shock

Scenario: A 72-year-old woman is admitted to ICU with acute decompensated heart failure and cardiogenic shock. A pulmonary artery catheter is inserted. The following data are obtained:

  • Heart rate 110 bpm
  • Blood pressure 85/60 mmHg (MAP 68 mmHg)
  • CVP 18 mmHg
  • PA pressure 55/28 mmHg (mean 38 mmHg)
  • PCWP 26 mmHg
  • Cardiac output 3.2 L/min
  • Cardiac index 1.7 L/min/m² (BSA 1.85 m²)
  • SvO2 52%

Examiner Questions:

  1. Interpret these haemodynamic data. What is the primary problem?

    • Answer:
      • Cardiogenic shock with:
        • Low cardiac output (normal 4-8 L/min) and cardiac index (normal 2.5-4 L/min/m²)
        • Elevated filling pressures: CVP 18 mmHg (normal 2-8), PCWP 26 mmHg (normal 6-12)
        • Elevated pulmonary artery pressures (PA systolic 55, normal 15-30)
        • Low SvO2 52% (normal 65-75%), indicating inadequate oxygen delivery relative to demand
      • This pattern indicates severe LV systolic dysfunction with secondary pulmonary hypertension and biventricular failure

  2. Calculate the systemic vascular resistance (SVR). Interpret this value.

    • Answer:
      • SVR = [(MAP - CVP) / CO] × 80
      • SVR = [(68 - 18) / 3.2] × 80 = 1,250 dynes·sec·cm⁻⁵
      • Interpretation: Normal to mildly elevated SVR (normal 800-1,200). The SVR is appropriate compensatory vasoconstriction in response to low cardiac output. This is typical of cardiogenic shock (contrast with distributive shock where SVR is low).

  3. Calculate the pulmonary vascular resistance (PVR). What does this indicate?

    • Answer:
      • PVR = [(MPAP - PCWP) / CO] × 80
      • PVR = [(38 - 26) / 3.2] × 80 = 300 dynes·sec·cm⁻⁵
      • Interpretation: Elevated PVR (normal 20-120). This indicates secondary pulmonary hypertension due to elevated left atrial pressure (PCWP 26 mmHg) causing passive pulmonary venous congestion and reactive pulmonary arterial vasoconstriction.

  4. The SvO2 is 52%. What does this indicate, and what are the possible causes?

    • Answer:
      • SvO2 52% is low (normal 65-75%), indicating inadequate oxygen delivery (DO2) relative to tissue oxygen consumption (VO2)
      • Causes of low SvO2:
        • Low cardiac output (as in this case) → reduced oxygen delivery
        • Anaemia → reduced oxygen content
        • Hypoxaemia → reduced SaO2
        • Increased oxygen consumption (fever, shivering, agitation)
      • In this patient, the primary cause is low cardiac output (3.2 L/min) resulting in inadequate oxygen delivery to tissues

  5. What are the management priorities for this patient?

    • Answer:
      • Optimize preload: PCWP 26 mmHg is elevated (pulmonary oedema range); diuretics (furosemide) to reduce preload and improve oxygenation
      • Inotropic support: Dobutamine (β1-agonist) to increase contractility and cardiac output; consider milrinone (phosphodiesterase inhibitor) if beta-blocked or as adjunct
      • Vasopressor if needed: If MAP remains below 65 mmHg despite inotropes, add noradrenaline (low-dose to avoid excessive afterload increase)
      • Mechanical circulatory support: Consider if refractory to medical therapy (intra-aortic balloon pump, Impella, VA-ECMO, LVAD)
      • Treat underlying cause: Acute coronary syndrome (revascularization), acute valvular pathology (surgical repair), myocarditis (immunosuppression)
      • Monitoring: Serial PAC measurements, echocardiography, lactate, urine output

  6. What are the major complications of pulmonary artery catheters?

    • Answer:
      • Arrhythmias: 4-20% (RBBB, ventricular ectopy, VT during RV passage)
      • Pulmonary artery rupture: 0.03-0.2% (balloon overinflation, pulmonary hypertension, anticoagulation); 50% mortality
      • Pulmonary infarction: 0.1-7% (prolonged wedge position, catheter thrombosis)
      • Catheter knotting: 0.1% (excessive advancement without waveform guidance)
      • Infection: 0.7-2% per 1,000 catheter-days
      • Thrombosis, valve damage, balloon rupture

  7. Discuss the evidence for PAC use in critically ill patients.

    • Answer:
      • PAC-Man trial 2005 (PMID: 16198769): RCT, 1,041 ICU patients; no mortality difference (68% vs 66%), increased PE rate in PAC group
      • FACTT trial 2006 (PMID: 16714767): RCT, 1,000 ARDS patients; no mortality difference (27.4% vs 26.3%), more complications with PAC
      • Sandham 2003 (PMID: 12490683): High-risk surgery patients; no benefit, increased PE
      • Meta-analysis Shah 2005 (PMID: 16189364): No mortality benefit, increased complications
      • Conclusion: PAC provides detailed haemodynamic data but does not improve outcomes in unselected ICU populations. Current use limited to complex cases where precise haemodynamic phenotyping is required (e.g., cardiogenic shock with uncertain aetiology, pulmonary hypertension, high-risk cardiac surgery).

Key References

  1. Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. Crit Care Med. 2013;41(7):1774-1781. PMID: 23673399

    • Meta-analysis: CVP AUC 0.56 for predicting fluid responsiveness; CVP should not guide fluid management

  2. Harvey S, Harrison DA, Singer M, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet. 2005;366(9484):472-477. PMID: 16198769

    • RCT: PAC vs no PAC in 1,041 ICU patients; no mortality benefit (68% vs 66%)

  3. National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wheeler AP, Bernard GR, et al. Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. N Engl J Med. 2006;354(21):2213-2224. PMID: 16714767

    • FACTT trial: PAC vs CVC in 1,000 ARDS patients; no mortality difference, more complications with PAC

  4. Sandham JD, Hull RD, Brant RF, et al. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med. 2003;348(5):5-14. PMID: 12490683

    • RCT: PAC in 1,994 high-risk surgical patients; no mortality benefit, increased PE

  5. Michard F, Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. Am J Respir Crit Care Med. 2000;162(1):134-138. PMID: 10903232

    • PPV greater than 13% predicts fluid responsiveness in septic shock patients on mechanical ventilation

  6. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology. 2005;103(2):419-428. PMID: 16052125

    • Review of dynamic indices (PPV, SVV) physiology and clinical application

  7. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1):172-178. PMID: 18496365

    • Systematic review: CVP poorly predicts fluid responsiveness; physiological explanation

  8. Monnet X, Marik PE, Teboul JL. Passive leg raising for predicting fluid responsiveness: a systematic review and meta-analysis. Intensive Care Med. 2016;42(12):1935-1947. PMID: 27121991

    • Meta-analysis: PLR ≥10% CO increase predicts fluid responsiveness (sensitivity 85%, specificity 91%)

  9. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. 2006;34(5):1402-1407. PMID: 16540951

    • PLR with echo LVOT VTI measurement to assess fluid responsiveness

  10. Zhang Z, Lu B, Sheng X, Jin N. Accuracy of stroke volume variation in predicting fluid responsiveness: a systematic review and meta-analysis. J Anesth. 2011;25(6):904-916. PMID: 21892779

    • Meta-analysis: SVV greater than 13% sensitivity 82%, specificity 86% for fluid responsiveness

  11. Grocott MP, Dushianthan A, Hamilton MA, et al. Perioperative increase in global blood flow to explicit defined goals and outcomes after surgery: a Cochrane Systematic Review. Br J Anaesth. 2013;111(4):535-548. PMID: 23835462

    • Meta-analysis: GDT reduces complications (OR 0.63), hospital stay (-1.0 days), no mortality benefit

  12. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368-1377. PMID: 11794169

    • EGDT reduced sepsis mortality 30.5% vs 46.5%; landmark trial (later trials showed no benefit of protocol)

  13. ProCESS Investigators, Yealy DM, Kellum JA, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med. 2014;370(18):1683-1693. PMID: 24635773

    • Protocol EGDT vs usual care in septic shock; no mortality difference

  14. ARISE Investigators, ANZICS Clinical Trials Group, Peake SL, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med. 2014;371(16):1496-1506. PMID: 25272316

    • EGDT vs usual care in septic shock (Australia/NZ); no mortality difference

  15. Mouncey PR, Osborn TM, Power GS, et al. Trial of early, goal-directed resuscitation for septic shock. N Engl J Med. 2015;372(14):1301-1311. PMID: 25776532

    • ProMISe trial (UK): EGDT vs usual care; no mortality difference

  16. Safdar N, Maki DG. Risk of catheter-related bloodstream infection with peripherally inserted central venous catheters used in hospitalized patients. Chest. 2005;128(2):489-495. PMID: 16100134

    • Arterial catheter infection rate 0.7 per 1,000 catheter-days

  17. O'Grady NP, Alexander M, Burns LA, et al. Guidelines for the prevention of intravascular catheter-related infections. Clin Infect Dis. 2011;52(9):e162-e193. PMID: 21460264

    • CDC guidelines for prevention of catheter infections (arterial, central venous)

  18. Marik PE, Lemson J. Fluid responsiveness: an evolution of our understanding. Br J Anaesth. 2014;112(4):617-620. PMID: 24535604

    • Review of fluid responsiveness concepts, static vs dynamic indices

  19. Marik PE. Iatrogenic salt water drowning and the hazards of a high central venous pressure. Ann Intensive Care. 2014;4:21. PMID: 25114829

    • CVP greater than 12-15 mmHg associated with increased mortality, organ dysfunction (venous congestion)

  20. Vieillard-Baron A, Evrard B, Repessé X, et al. Limited value of end-expiratory inferior vena cava diameter to predict fluid responsiveness impact of intra-abdominal pressure. Intensive Care Med. 2018;44(2):197-203. PMID: 29340737

    • IVC diameter alone insufficient; collapsibility/distensibility better predictor

  21. Airapetian N, Maizel J, Alyamani O, et al. Does inferior vena cava respiratory variability predict fluid responsiveness in spontaneously breathing patients? Crit Care. 2015;19:400. PMID: 26542305

    • IVC collapsibility greater than 50% predicts fluid responsiveness (sensitivity 73%, specificity 79%)

  22. Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena cava collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med. 2004;30(9):1734-1739. PMID: 15375649

    • SVC collapsibility in mechanically ventilated patients

  23. Kuriyama A, Jackson JL, Kamei J. Performance of the 2016 Sepsis-3 criteria in patients with suspected infection presenting to the emergency department. J Infect Chemother. 2020;26(3):284-289. PMID: 31744777

    • Sepsis-3 qSOFA validation

  24. Monnet X, Teboul JL. Transpulmonary thermodilution: advantages and limits. Crit Care. 2017;21(1):147. PMID: 28625169

    • Review of PiCCO technology, EVLW, GEDV measurements

  25. Sakka SG, Reuter DA, Perel A. The transpulmonary thermodilution technique. J Clin Monit Comput. 2012;26(5):347-353. PMID: 22833180

    • Transpulmonary thermodilution principles and clinical use

  26. Pearse RM, Harrison DA, MacDonald N, et al. Effect of a perioperative, cardiac output-guided hemodynamic therapy algorithm on outcomes following major gastrointestinal surgery: a randomized clinical trial and systematic review. JAMA. 2014;311(21):2181-2190. PMID: 24842135

    • GDT in major surgery: no mortality benefit, trend toward reduced complications

  27. Jhanji S, Vivian-Smith A, Lucena-Amaro S, Watson D, Hinds CJ, Pearse RM. Haemodynamic optimisation improves tissue microvascular flow and oxygenation after major surgery: a randomised controlled trial. Crit Care. 2010;14(4):R151. PMID: 20712865

    • GDT improves microvascular perfusion

  28. Reuter DA, Felbinger TW, Kilger E, et al. Optimizing fluid therapy in mechanically ventilated patients after cardiac surgery by on-line monitoring of left ventricular stroke volume variations. Br J Anaesth. 2002;88(1):124-126. PMID: 11881866

    • SVV-guided fluid therapy after cardiac surgery

  29. Bellomo R, Kellum JA, Ronco C, et al. Acute kidney injury in sepsis. Intensive Care Med. 2017;43(6):816-828. PMID: 28364303

    • Haemodynamic monitoring to prevent AKI in sepsis

  30. Cecconi M, De Backer D, Antonelli M, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014;40(12):1795-1815. PMID: 25392034

    • European consensus on haemodynamic monitoring and shock management

  31. Vincent JL, Rhodes A, Perel A, et al. Clinical review: Update on hemodynamic monitoring--a consensus of 16. Crit Care. 2011;15(4):229. PMID: 21884645

    • Consensus recommendations on haemodynamic monitoring techniques and application

  32. Perner A, Gordon AC, De Backer D, et al. Sepsis: frontiers in diagnosis, resuscitation and antibiotic therapy. Intensive Care Med. 2016;42(12):1958-1969. PMID: 27695884

    • Review of sepsis management including haemodynamic monitoring

  33. Magder S. Right atrial pressure in the critically ill: how to measure, what is the value, what are the limitations? Chest. 2017;151(4):908-916. PMID: 27916618

    • Review of CVP physiology, measurement, and interpretation

  34. Magder S. Volume and its relationship to cardiac output and venous return. Crit Care. 2016;20(1):271. PMID: 27613370

    • Physiology of venous return and cardiac output

  35. Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA. Fluid resuscitation in septic shock: a positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med. 2011;39(2):259-265. PMID: 20975548

    • Positive fluid balance and high CVP associated with mortality

  36. Alhazzani W, Møller MH, Arabi YM, et al. Surviving Sepsis Campaign: guidelines on the management of critically ill adults with Coronavirus Disease 2019 (COVID-19). Crit Care Med. 2020;48(6):e440-e469. PMID: 32224769

    • Haemodynamic monitoring and fluid management in COVID-19

  37. De Backer D, Bakker J, Cecconi M, et al. Alternatives to the Swan-Ganz catheter. Intensive Care Med. 2018;44(6):730-741. PMID: 29572598

    • Review of minimally invasive CO monitoring alternatives to PAC

Summary

Haemodynamic monitoring in the ICU is an essential tool for diagnosing shock, guiding resuscitation, and titrating therapies. However, no monitoring device has been shown to improve mortality in randomized trials; the value lies in how clinicians integrate data and respond with appropriate interventions. The shift away from invasive monitoring (PAC) toward less invasive techniques (pulse contour, echo) and functional assessments (PLR, fluid challenge) reflects an evidence-based understanding that static pressures (CVP, PCWP) poorly predict fluid responsiveness, and that dynamic indices and real-time physiological testing provide more actionable information.

Key Takeaways:

  1. Arterial lines are indispensable for continuous BP monitoring and waveform analysis; recognize and correct damping artifacts
  2. CVP does not predict fluid responsiveness (AUC 0.56); use for trending and detection of venous congestion (CVP greater than 15-18 mmHg)
  3. PAC provides comprehensive haemodynamic data but no mortality benefit; reserve for complex cases (cardiogenic shock, pulmonary hypertension)
  4. Dynamic indices (PPV, SVV greater than 13%) are the best bedside predictors of fluid responsiveness in mechanically ventilated patients with sinus rhythm
  5. Echocardiography is the cornerstone of modern haemodynamic assessment (IVC collapsibility, LVOT VTI, LV/RV function)
  6. Passive leg raise is the gold standard functional test for fluid responsiveness; works in all patient populations
  7. Integrate multimodal data (clinical exam, lactate, ScvO2, dynamic indices, echo) rather than relying on single parameters
  8. Avoid fluid overload: Positive fluid balance and high CVP are associated with increased mortality; use functional assessments to stop fluid when not beneficial

The future of haemodynamic monitoring lies in non-invasive, continuous, automated systems that integrate multiple physiological signals (wearable sensors, AI-driven algorithms) to provide real-time decision support. However, clinical acumen, understanding of cardiovascular physiology, and individualized patient assessment remain the foundation of effective haemodynamic management.

Document Statistics:

  • Line count: 1,603 lines
  • Citation count: 37 PubMed citations
  • Target audience: CICM Second Part candidates, intensivists, advanced trainees
  • Last updated: 2026-01-24

MedVellum Intensive Care Medicine Series Evidence-Based Medical Education

Learning map

Use these linked topics to study the concept in sequence and compare related presentations.

Related Topics

Adjacent pages worth reading next.