Hemodynamic Monitoring — Ode to the OR

Module 01 of 06

Central Venous Pressure Monitoring

The oldest continuous haemodynamic monitoring tool in clinical use — measuring pressure in the right atrium to reflect right ventricular filling.

What is CVP?

CVP is the pressure measured in the superior vena cava (SVC) or right atrium (RA). It reflects right ventricular end-diastolic pressure (RVEDP) and serves as a surrogate for right ventricular preload. Measured in mmHg (or cmH₂O — divide by 1.36 to convert).

Normal CVP

2–8

mmHg

in cmH₂O

3–10

cmH₂O

Low — hypovolaemia

<2

mmHg

Elevated — overload / RHF

>10

mmHg

Sites of Insertion

Site	Advantages	Disadvantages	Infection Risk
Internal Jugular (R)	Straight path to RA, high success rate	Carotid artery risk, uncomfortable	Low
Subclavian	Most comfortable, lowest infection risk	Pneumothorax (1–3%), cannot compress	Lowest
Femoral	Easy in emergency, no PTX risk	High infection risk, less accurate CVP	Highest
External Jugular	Visible, accessible	Tortuous, may not reach SVC	Low

✦ Tip Placement Optimal tip position: cavo-atrial junction — lower third of SVC, at or just above the carina on CXR.

The CVP Waveform

Five components — three positive waves (a, c, v) and two negative descents (x, y). Memorise these cold.

▸ CVP Waveform — Two Complete Cycles, Annotated

a · c · v

aAtrial contraction — after P wave — absent in AF

cClosure of tricuspid valve + RV isovolumetric contraction — after QRS

vVenous filling of atrium while TV is shut — after T wave

xeXit — atrial relaxation + TV annular descent (systolic dip)

yemptying Yields to RV — TV opens, RV starts to fill (diastolic dip)

Pathological Waveform Changes

Pattern	Mechanism	Condition
Giant a wave	Atrium contracts against closed/resistant TV	Pulmonary hypertension, tricuspid stenosis, RV failure, AV block
Cannon a wave	Atrium contracts against closed TV (AV dissociation)	Complete heart block, VT, junctional rhythm
Giant v wave	Regurgitant flow into atrium during systole	Severe tricuspid regurgitation
Absent a wave	No organised atrial contraction	Atrial fibrillation
Steep x, blunted y — "M" pattern	Pericardial fluid limits ventricular filling; x preserved, y obliterated	Cardiac tamponade
Steep x AND steep y — "W" pattern	Both descents prominent; rapid early filling then abrupt halt	Constrictive pericarditis
Absent / blunted x	No atrial relaxation visible	Tricuspid regurgitation

Zero Reference & Transducer Positioning

Zero reference: Phlebostatic axis — intersection of 4th ICS and mid-axillary line (approximates RA level)
Patient can be supine or up to 30–45° HOB (if transducer is re-levelled)
Always measure at end-expiration — intrathoracic pressure closest to atmospheric
On mechanical ventilation: read at end-expiration = highest point on the CVP waveform during the respiratory cycle
Each 2.54 cm (1 inch) transducer error = ~2 mmHg reading error

⚠ The Central Limitation CVP is a poor predictor of fluid responsiveness. Marik et al. 2008 meta-analysis (24 studies, 803 patients): CVP AUC-ROC = 0.55 — no better than chance. A single CVP value should never be used in isolation to guide fluid therapy.

Causes of Elevated & Low CVP

Elevated CVP (>10 mmHg)

Right heart failure (primary or secondary)
Pulmonary hypertension / massive PE
Cardiac tamponade
Constrictive pericarditis
Fluid overload / hypervolaemia
SVC obstruction
High PEEP / auto-PEEP (transmitted)
Tension pneumothorax
Tricuspid stenosis / regurgitation

Low CVP (<2 mmHg)

Hypovolaemia (haemorrhage, dehydration, third-spacing)
Distributive shock (relative hypovolaemia)
Over-diuresis

Complications of CVC Insertion

Arterial puncture / haematoma
Pneumothorax — especially subclavian (1–3%)
Haemothorax
Air embolism (nurse patient head-down during insertion)
Arrhythmias — guide wire in RV
Nerve injury — brachial plexus
Thoracic duct injury — left subclavian → chylothorax

CLABSI — catheter-line associated bloodstream infection
Catheter-related deep vein thrombosis
Catheter malposition / migration
Venous erosion / perforation (stiff catheter tip)
Cardiac tamponade (delayed)
Catheter embolism

✦ CLABSI Bundle Maximal sterile barrier · Chlorhexidine skin prep · Subclavian or IJV preferred over femoral · Daily review of necessity · Hand hygiene. Subclavian has lowest infection rate.

Module 02 of 06

Pulmonary Artery Catheterisation

The Swan-Ganz catheter — balloon-tipped, flow-directed, and capable of measuring pressures through the entire right heart and into the pulmonary vasculature.

Historical note Introduced by Swan and Ganz in 1970. A 7.5 Fr catheter that floats through the right heart when its balloon is inflated, guided by blood flow.

RA pressure

2–8

mmHg

RV systolic / diastolic

15–30 / 0–8

mmHg

PA systolic / diastolic

15–30 / 6–12

mmHg

mPAP

9–18

mmHg

PCWP (wedge)

6–12

mmHg

Cardiac Output

4–8

L/min

CI

2.5–4.0

L/min/m²

Mixed SvO₂

60–80

%

SVR

800–1200

dynes·s/cm⁵

PVR

20–120

dynes·s/cm⁵

PAC Ports & Lumens

Port	Location	Purpose
Proximal (blue)	RA — 30 cm from tip	CVP, CO injectate, drug/fluid infusion
Distal (yellow)	PA tip	PAP measurement, mixed SvO₂ sampling, PCWP when wedged
Balloon inflation	Tip	Inflate 1.5 mL air to float/wedge — never use liquids
Thermistor connector	4 cm from tip	Temperature sensing for thermodilution CO
VIP port (white)	Mid-catheter (RV position)	Additional infusion lumen

Waveform Recognition During Insertion

▸ RA → RV → PA → PCWP — pressure sequence on insertion

⚑ RV vs PA — the critical distinction RV: high systolic + diastolic near zero, NO dicrotic notch · PA: high systolic + diastolic elevated (6–12) + dicrotic notch present. If you see high systolic + low diastolic with no notch — you're still in the RV. Advance further before deflating the balloon.

PCWP — Pulmonary Capillary Wedge Pressure

Balloon inflated in a branch PA occludes flow, creating a static column from catheter tip → pulmonary capillaries → pulmonary veins → left atrium. Therefore PCWP ≈ LAP ≈ LVEDP (in the absence of mitral stenosis or pulmonary venous hypertension).

Transpulmonary Gradient TPG = mPAP − PCWP

Normal <12 mmHg · Elevated in pre-capillary pulmonary hypertension

Pulmonary Vascular Resistance PVR = (mPAP − PCWP) / CO × 80

Units: dynes·s/cm⁵ · Normal: 20–120

West Zones of the Lung

Zone	Pressure Relationship	Blood Flow	PCWP Validity
Zone I (apex)	P_alv > P_a > P_v	Absent	Invalid — reflects alveolar pressure
Zone II (middle)	P_a > P_alv > P_v	Intermittent	Unreliable
Zone III (base)	P_a > P_v > P_alv	Continuous	✓ Valid — PAC floats here naturally

✦ Clinical Pearl High PEEP can convert Zone III to Zone II → suspect if PCWP fluctuates with ventilation or PCWP > PA diastolic. Lateral CXR can confirm tip position below LA.

Thermodilution Cardiac Output — Stewart-Hamilton

Inject a known volume of cold or room-temperature saline into the proximal (RA) port. The thermistor at the PA tip measures temperature change over time. Area under the temperature-time curve is inversely proportional to cardiac output.

Stewart-Hamilton Equation (simplified) CO = [V × (T_b − T_i) × K] / ∫ΔT(t)dt

V = volume injected · T_b = blood temp · T_i = injectate temp · ∫ΔT = area under temperature-time curve

Inject 10 mL rapidly (<4 seconds) at end-expiration
Average 3 measurements within 10% of each other
Overestimated CO: slow injection, warm injectate, TR (recirculation), L→R shunt
Underestimated CO: rapid injection, very cold injectate, low output states (flat curve)
Invalid in: severe TR, significant intracardiac shunts

Fick Principle

Fick Equation CO = VO₂ / (CaO₂ − CvO₂)

CaO₂ = (Hb × 1.34 × SaO₂) + (0.003 × PaO₂) · CvO₂ = (Hb × 1.34 × SvO₂) + (0.003 × PvO₂)

SvO₂ is sampled from the distal (PA) port. VO₂ is often assumed (~125 mL/min/m²) rather than measured — a limitation. Requires a metabolic cart for true VO₂ measurement.

Derived Haemodynamic Parameters

Parameter	Formula	Normal	Units
SVR	(MAP − CVP) / CO × 80	800–1200	dynes·s/cm⁵
PVR	(mPAP − PCWP) / CO × 80	20–120	dynes·s/cm⁵
Stroke Volume	CO / HR × 1000	60–100	mL/beat
SVI	CI / HR × 1000	33–47	mL/beat/m²
DO₂ (O₂ delivery)	CO × CaO₂ × 10	520–720	mL/min/m²
VO₂ (O₂ consumption)	CO × (CaO₂−CvO₂) × 10	100–180	mL/min/m²
O₂ Extraction Ratio	VO₂ / DO₂ × 100	22–30	%

Haemodynamic Profiles in Shock

Shock Type	CO	SVR	PCWP	CVP	SvO₂
Cardiogenic	↓↓	↑↑	↑	↑	↓
Hypovolaemic	↓	↑	↓	↓	↓
Distributive (Septic)	↑/N	↓↓	↓/N	↓/N	↑ early
Obstructive (PE/Tamponade)	↓	↑	↓/N	↑↑	↓
Neurogenic	↓/N	↓↓	N	N/↓	↑/N

Complications of PAC

Arrhythmias: PVCs, VT/VF as catheter passes through RVOT — most common during insertion
RBBB (3–6%): catheter irritates right bundle branch; critical if pre-existing LBBB → complete heart block. Have pacing ready
PA rupture (0.02–0.2%): rare but life-threatening. Higher risk with PHT, elderly, anticoagulation. Caused by balloon over-inflation or inflation in a small-calibre vessel
Pulmonary infarction: catheter permanently wedged → distal ischaemia
Catheter knotting: excess catheter looped in RV without advancing
Balloon rupture → air embolism: never use >1.5 mL air; never use liquids in balloon
Thrombosis / endocarditis
Overwedge: balloon overinflated → falsely elevated, spike-shaped PCWP tracing

PA Rupture — Emergency Management Trendelenburg position · 100% O₂ · Lung isolation (double lumen tube, affected side dependent) · Bronchoscopy · Catheter balloon as temporary tamponade · Interventional radiology (embolisation) or surgical repair.

⚠ The PAC Controversy PACMAN, ESCAPE, and FACTT trials found PAC-guided therapy did not improve mortality vs standard management in ICU patients, septic shock, or acute heart failure. PAC use has declined significantly since 2000. Modern practice: target-specific goals with the least invasive method that answers the clinical question.

Module 03 of 06

Cardiac Output Monitoring — Invasive Methods

Pulse contour analysis and transpulmonary thermodilution — comprehensive haemodynamic data without a PA catheter.

Pulse Contour Analysis — Core Principle

Derives CO by analysing the morphology of the arterial pressure waveform. The area under the systolic portion of the waveform is proportional to stroke volume, adjusted for estimated aortic compliance and impedance.

Core Relationship SV ∝ Area under systolic portion of arterial waveform (corrected for aortic impedance / compliance)

System	Calibration	Access Required	Unique Features
PiCCO (Pulsion)	Transpulmonary thermodilution — required	CVC + radial or femoral arterial line	ITBV, EVLW, GEDV, CFI, GEF, PVPI
LiDCO plus	Lithium dilution — required	Peripheral IV + arterial line	Contraindicated on lithium therapy, early pregnancy
LiDCOrapid	Uncalibrated (nomogram)	Peripheral arterial line	Continuous SV/CO; good for trending and fluid responsiveness
FloTrac / Vigileo (Edwards)	Uncalibrated (auto-calibrated)	Any arterial line	Uses SD of pulse pressure + patient demographics; no external calibration needed
MOSTCARE / Argos	Uncalibrated	Arterial line	dP/dt-based analysis

PiCCO — Volumetric Parameters

PiCCO calibrates via transpulmonary thermodilution (TPTD): cold injectate via CVC proximal port; thermistor in femoral or radial artery line. Provides unique volumetric preload indices unavailable from PAC.

ITBVI — Intrathoracic Blood Volume

850–1000

mL/m²

GEDVI — Global End-Diastolic Volume

680–800

mL/m²

EVLWI — Extravascular Lung Water

<10

mL/kg

PVPI — Pulmonary Vasc Permeability

1.0–3.0

ratio

CFI — Cardiac Function Index

4.5–6.5

/min

GEF — Global Ejection Fraction

25–35

%

✦ EVLW in Clinical Practice EVLWI >10 mL/kg = pulmonary oedema · >15 mL/kg = severe · PVPI >3 = increased permeability → ARDS pattern (vs hydrostatic oedema). This distinction directly guides de-resuscitation decisions and diuretic therapy.

Limitations of Pulse Contour Analysis

Aortic regurgitation: overestimates SV (increased diastolic runoff increases waveform area)
IABP: invalidates waveform analysis entirely — cannot use PCA during balloon pumping
Arrhythmias (AF): highly variable beat-to-beat SV; averaging required, accuracy reduced
Peripheral vasoconstriction: dampened waveform → underestimates SV
Calibrated systems (PiCCO, LiDCO): more accurate but require recalibration every 8h or after major haemodynamic shifts
Uncalibrated systems: adequate for trending and relative changes, not absolute values

Module 04 of 06

Cardiac Output — Minimally & Non-Invasive Methods

Measuring CO without arterial cannulation or central access — the direction of modern haemodynamic monitoring.

Oesophageal Doppler Monitoring (ODM)

A probe passed into the oesophagus (in intubated, sedated patients) measures blood flow velocity in the descending thoracic aorta using continuous-wave Doppler. Aortic cross-sectional area is estimated from a nomogram to derive CO.

Devices: CardioQ (Deltex), HemoSonic
FTc (flow time corrected): normal 330–360 ms; ↓ in hypovolaemia; ↑ in vasodilation
Peak velocity (PV): reflects contractility; ↓ in poor ventricular function
Measures ~70% of CO (descending aorta); assumes a fixed proportion to upper body
Validated in perioperative goal-directed therapy (GDT) — reduced complications in major surgery
Limitations: requires sedation, frequent probe repositioning, oesophageal pathology a contraindication

Echocardiography — LVOT Doppler

SV via LVOT (Doppler) SV = VTI_LVOT × π × (D_LVOT/2)² → CO = SV × HR

VTI = velocity time integral (PW Doppler in LVOT, apical 5-chamber) · D measured in parasternal long-axis view

Most validated non-invasive CO method; within ±10–15% of thermodilution
Key source of error: LVOT diameter (squaring effect — small errors amplify significantly)
TEE: continuous intraoperative use (semi-invasive); TTE limited by ventilation and body habitus
POCUS: IVC collapsibility, LVOT VTI response to PLR — practical bedside fluid responsiveness assessment

Non-Invasive CO Methods at a Glance

Method	Technology	Invasiveness	Accuracy	Best Use
Thoracic Bioimpedance (TEB)	Impedance change with SV	None	Moderate	Trending, non-critical
Bioreactance (NICOM)	Phase shift of AC current	None	Moderate–Good	Periop, fluid responsiveness
Volume Clamp (ClearSight)	Finger arterial waveform	None (finger cuff)	Variable	OR monitoring
PPG / PVI	SpO₂ pleth waveform	None	Trending only	Adjunct; PVI for fluid responsiveness
Oesophageal Doppler	Doppler aortic velocity	Semi-invasive	Good	OR, ICU — intubated patients
Echocardiography (TTE/TEE)	LVOT Doppler VTI	TTE none / TEE semi	Good	Periop, ICU, diagnostic
Partial CO₂ rebreathing (NICO)	Modified Fick (CO₂)	Requires intubation	Moderate	Intubated, no significant shunt

Pleth Variability Index (PVI)

PVI Formula PVI = [(PI_max − PI_min) / PI_max] × 100%

PI = perfusion index from SpO₂ probe · PVI >14% in ventilated patients predicts fluid responsiveness (similar performance to PPV)

Module 05 of 06

Markers of Fluid Responsiveness

Static and dynamic indices — predicting which patients will increase cardiac output in response to a fluid challenge. The central question in resuscitation.

⚑ The Core Question Only ~50% of haemodynamically unstable ICU patients are truly fluid-responsive. Fluid in a non-responder causes harm — pulmonary oedema, dilutional coagulopathy, abdominal compartment syndrome. We must predict before we pour.

Definition: Fluid responsiveness = ≥10–15% increase in stroke volume or CO after a fluid challenge.

Static Indices — Poor Predictors

Static filling pressures tell you where you are on the x-axis. They do not tell you the slope of the Frank-Starling curve — which is the only thing that matters for predicting response.

Index	Normal	AUC-ROC	Why It Fails
CVP	2–8 mmHg	~0.55 (no better than chance)	Does not reflect ventricular compliance or contractility
PCWP	6–12 mmHg	~0.56	Same fundamental limitation; more invasive
ITBVI (PiCCO)	850–1000 mL/m²	~0.64	Volumetric; better than pressure but still static
GEDVI (PiCCO)	680–800 mL/m²	~0.66	Reasonable preload estimate; not a prediction of response

Why Dynamic Indices Work — The Mechanism

Positive pressure inspiration → ↑ intrathoracic pressure → ↓ venous return → ↓ RV preload → (after 2-beat pulmonary transit time) → ↓ LV filling → ↓ SV. In a heart sitting on the steep part of the Starling curve (preload-dependent), this cyclical variation is exaggerated. In a heart on the flat part, it is minimal. This is the basis of all dynamic indices.

Pulse Pressure Variation (PPV)

PPV Formula PPV = [(PP_max − PP_min) / ((PP_max + PP_min) / 2)] × 100%

Threshold: >13% predicts fluid responsiveness · AUC ~0.94

Prerequisites: controlled mechanical ventilation (no spontaneous breaths), regular rhythm (no AF), Vt ≥8 mL/kg IBW, closed chest
Measured over at least 3 respiratory cycles from arterial line waveform
Fails in: spontaneous breathing, arrhythmias, low Vt ventilation, open chest, raised intra-abdominal pressure, RV failure

Stroke Volume Variation (SVV)

SVV Formula SVV = [(SV_max − SV_min) / SV_mean] × 100%

Threshold: >10–13% · AUC ~0.84 · Derived from pulse contour devices

IVC Indices — Ultrasound

IVC Collapsibility Index — Spontaneously Breathing IVC-CI = [(IVC_max − IVC_min) / IVC_max] × 100%

Threshold: >50% predicts fluid responsiveness · AUC ~0.75

IVC Distensibility Index — Mechanically Ventilated IVC-DI = [(IVC_max − IVC_min) / IVC_min] × 100%

Threshold: >18% predicts fluid responsiveness · AUC ~0.89

⚠ IVC Limitations RV failure → plethoric IVC despite volume depletion · High intra-abdominal pressure → IVC compressed · Poor windows in obese or post-operative patients · Hepatic congestion confounds measurement. Always interpret in clinical context.

Passive Leg Raise (PLR) — The Most Versatile Test

Raise both legs to 45° from semi-recumbent (30–45° HOB) position → transfers ~300 mL from venous reservoir → reversible autotransfusion
Measure CO/SV response within 60–90 seconds continuously
Positive: ≥10% increase in CO → fluid responsive (AUC ~0.95)
Reversible — no fluid administered. Safe in fluid-restricted patients
Works in: spontaneous breathing, arrhythmias (AF), low Vt ventilation — where PPV/SVV fail
Best measured with: oesophageal Doppler, echo VTI, PiCCO, or bioreactance (not MAP alone)
Contraindications: raised ICP, suspected femoral fracture, intra-abdominal hypertension

End-Expiratory Occlusion Test (EEOT)

Occlude expiratory circuit for 15 seconds → prevents cyclic reduction in venous return
CO increase ≥5% → fluid responsive (AUC ~0.93)
Requires continuous CO monitoring; works only in controlled MV patients

Tidal Volume Challenge

Temporarily increase Vt from 6 → 8 mL/kg IBW for one minute
If PPV increases by >3.5% → would be PPV-positive at standard Vt (AUC ~0.97)
Useful when lung-protective low-Vt ventilation makes PPV unreliable

Comparison Table — Dynamic Indices

Test	Threshold	AUC-ROC	Spont. Breathing	AF
PPV	>13%	~0.94	No	No
SVV	>13%	~0.84	No	No
IVC Distensibility	>18%	~0.89	No	Limited
IVC Collapsibility	>50%	~0.75	Yes	Limited
PLR + CO measurement	≥10% ↑CO	~0.95	Yes	Yes
EEOT	≥5% ↑CO	~0.93	No	Limited
Tidal Volume Challenge	ΔPPV >3.5%	~0.97	No	No

✦ Clinical Bottom Line In a mechanically ventilated patient with no spontaneous effort, regular rhythm, Vt ≥8 mL/kg: use PPV. In everyone else: use PLR + continuous CO measurement. EEOT adds value when you need confirmation in MV patients.

Frank-Starling Curve — The Visual

Module 06 of 06

Markers of Microvascular Perfusion

Global haemodynamics can be normalised while the microcirculation remains in crisis — the invisible failure that drives organ dysfunction.

The Macro-Micro Disconnect A patient may have MAP ≥65, CO normal, CVP normalised — and yet have stopped, intermittent, and heterogeneous capillary flow at the microvascular level. This persistent microcirculatory failure is an independent predictor of organ dysfunction and mortality in septic shock.

Lactate & Lactate Clearance

Lactate Level	Interpretation	Action
<2 mmol/L	Normal	Reassuring; continue monitoring
2–4 mmol/L	Moderate — possible hypoperfusion or impaired clearance	Investigate; treat cause; serial measurement
>4 mmol/L	Severe — high mortality risk · Sepsis-3 criterion for septic shock	Aggressive resuscitation; ICU; vasopressors

Lactate Clearance Clearance (%) = [(Lactate_initial − Lactate_follow-up) / Lactate_initial] × 100

≥10% clearance at 2–6 hours = adequate resuscitation response (Surviving Sepsis Campaign target)

✦ Lactate is Not Only Anaerobic Aerobic sources in sepsis: Warburg effect (aerobic glycolysis in inflammatory cells) · Exogenous epinephrine → β₂-stimulation → ↑ skeletal muscle glycolysis · Impaired hepatic clearance · Thiamine deficiency · Metformin toxicity · Respiratory muscle fatigue (severe asthma). Always interpret in context.

ScvO₂ — Central Venous Oxygen Saturation

Measured from the distal port of a CVC in the SVC. Reflects the balance between O₂ delivery (DO₂) and consumption (VO₂) for the upper body. Overestimates true mixed SvO₂ by ~5–7%.

Fick-derived relationship SvO₂ = SaO₂ − VO₂ / (CO × Hb × 1.34)

↓ SvO₂: ↑ extraction → ↓ DO₂ (low CO, low Hb, low SaO₂) or ↑ VO₂ (fever, shivering) · ↑ SvO₂ in sepsis: microvascular shunting → O₂ not being extracted at cell level despite adequate delivery

Normal ScvO₂

>70

%

Normal mixed SvO₂ (PA)

60–80

%

In cardiogenic shock

<50

%

In early sepsis (shunting)

>80

%

Pv-aCO₂ Gap — Venoarterial CO₂ Difference

Pv-aCO₂ Gap Pv-aCO₂ = PvCO₂ − PaCO₂ [venous from CVC, arterial from ABG]

Normal: 2–6 mmHg · >6 mmHg despite normalised ScvO₂ → inadequate CO₂ washout → inadequate flow or microvascular impairment

Elevated Pv-aCO₂ (>6 mmHg) indicates impaired tissue CO₂ washout → inadequate cardiac output relative to metabolic demand
Particularly valuable when ScvO₂ appears normalised but lactate remains elevated — the "cryptic shock" state
Pv-aCO₂ / Ca-vO₂ ratio: if >1.4 → suggests anaerobic CO₂ production (not just low flow)

Near-Infrared Spectroscopy (NIRS)

Measures regional oxygen saturation (rSO₂) non-invasively via differential absorption of NIR light by oxyHb/deoxyHb
Sites: cerebral (forehead), somatic (flank, thenar eminence, deltoid)
Normal cerebral rSO₂: 55–75% · Devices: INVOS, FORE-SIGHT, EQUANOX
Signal is ~70–75% venous compartment — reflects microvascular + macrovascular perfusion
Used in: cardiac surgery (cerebral protection), ECMO monitoring, neonatal ICU
Thenar rSO₂: sensitive early marker of peripheral hypoperfusion in shock
Limitations: skin pigmentation, CSF layer, subcutaneous fat, electromagnetic interference

Sublingual Capillaroscopy (SDF / IDF Imaging)

Direct real-time visualisation of sublingual microcirculation using Sidestream Dark Field (SDF) or Incident Dark Field (IDF) imaging
Measures: functional capillary density (FCD), total vessel density (TVD), microvascular flow index (MFI), perfused vessel density (PVD)
MFI scale: 0 = absent · 1 = intermittent · 2 = sluggish · 3 = normal
In septic shock: ↓FCD, heterogeneous flow — stopped and intermittent capillaries adjacent to normal-flow vessels
Currently a research tool — not routine clinical practice. Requires expertise and offline analysis software

Clinical Markers — Rapid Bedside Assessment

Mottling Score

Score 0–5 based on area of mottling extending proximally from knee
Score ≥3 = poor prognosis, high mortality
Reflects microvascular vasoconstriction and heterogeneous flow
Easy bedside assessment — no equipment needed

Capillary Refill Time (CRT)

Normal <2 seconds (fingertip, press for 15 sec)
>2 sec = impaired peripheral perfusion
ANDROMEDA-SHOCK trial: CRT-guided resuscitation non-inferior to lactate-guided strategy
Peripheral-core temperature gradient: >7°C (core–toe) or >4°C (forearm–fingertip) suggests peripheral vasoconstriction

Integrated Approach to Shock Assessment

MAP <65
± Lactate >2

→

Global haemodynamics
CO · SVR · CVP

→

Fluid responsive?
PLR · PPV · IVC

→

Microvascular
ScvO₂ · Lactate
CRT · Pv-aCO₂

→

Targets:
MAP ≥65
Lactate ↓ ≥10%/2h
ScvO₂ >70%
CRT <2s

Assessment

Self-Assessment

Twelve questions across all six modules. Click an option to reveal the explanation.

▸ Questions — click to answer

HaemodynamicMonitoring

Sites of Insertion

The CVP Waveform

Pathological Waveform Changes

Zero Reference & Transducer Positioning

Causes of Elevated & Low CVP

Elevated CVP (>10 mmHg)

Low CVP (<2 mmHg)

Complications of CVC Insertion

PAC Ports & Lumens

Waveform Recognition During Insertion

PCWP — Pulmonary Capillary Wedge Pressure

West Zones of the Lung

Thermodilution Cardiac Output — Stewart-Hamilton

Fick Principle

Derived Haemodynamic Parameters

Haemodynamic Profiles in Shock

Complications of PAC

Pulse Contour Analysis — Core Principle

PiCCO — Volumetric Parameters

Limitations of Pulse Contour Analysis

Oesophageal Doppler Monitoring (ODM)

Echocardiography — LVOT Doppler

Non-Invasive CO Methods at a Glance

Pleth Variability Index (PVI)

Static Indices — Poor Predictors

Why Dynamic Indices Work — The Mechanism

Pulse Pressure Variation (PPV)

Stroke Volume Variation (SVV)

IVC Indices — Ultrasound

Passive Leg Raise (PLR) — The Most Versatile Test

End-Expiratory Occlusion Test (EEOT)

Tidal Volume Challenge

Comparison Table — Dynamic Indices

Frank-Starling Curve — The Visual

Lactate & Lactate Clearance

ScvO₂ — Central Venous Oxygen Saturation

Pv-aCO₂ Gap — Venoarterial CO₂ Difference

Near-Infrared Spectroscopy (NIRS)

Sublingual Capillaroscopy (SDF / IDF Imaging)

Clinical Markers — Rapid Bedside Assessment

Mottling Score

Capillary Refill Time (CRT)

Integrated Approach to Shock Assessment

Haemodynamic
Monitoring