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Pulse Oximetry & Capnography: Complete Viva Reference
Sources: Miller's Anesthesia 10e, Barash/Stoelting Clinical Anesthesia 9e, Morgan & Mikhail 7e
PART A: PULSE OXIMETRY
1. DEFINITION & PRINCIPLE
Q: What is pulse oximetry?
Pulse oximetry is a continuous, non-invasive measurement of the functional arterial oxygen saturation (SpO2) of hemoglobin, using the differential light absorption of oxygenated (O2Hb) and deoxygenated (deO2Hb) hemoglobin.
- The value measured is called SpO2 (from pulse oximetry) to distinguish from SaO2 (directly measured arterial blood gas)
- Accuracy: SpO2 is within ±2-3% of SaO2 over the range of 70-100%
(Miller's Anesthesia 10e, p.5456)
2. PHYSICS & HOW IT WORKS
Q: Explain the Beer-Lambert Law as applied to pulse oximetry
Beer-Lambert Law: The intensity of light transmitted through a substance decreases exponentially with the concentration of the absorbing substance and the path length.
Two wavelengths used:
| Wavelength | Absorbed more by | Colour |
|---|
| 660 nm (red) | Deoxygenated Hb (deO2Hb) | Red light |
| 940 nm (infrared) | Oxygenated Hb (O2Hb) | Infrared light |
Why these two wavelengths? At 660 nm, deO2Hb absorbs ~10× more than O2Hb. At 940 nm, O2Hb absorbs more than deO2Hb. The difference is maximised - this gives the best discrimination between the two species.
AC/DC Separation - the key innovation:
Light absorption by tissue is divided into:
- DC component (non-pulsatile, "direct current"): Venous blood, capillary blood, tissue, bone, pigment - all constant
- AC component (pulsatile, "alternating current"): Arterial blood only - changes with each heartbeat
The ratio R is calculated:
R = (AC660/DC660) / (AC940/DC940)
This ratio R is then looked up on an empirically derived calibration curve (built by having volunteers breathe hypoxic mixtures across SpO2 70-100%) to yield SpO2.
(Miller's Anesthesia 10e, p.5456-5457)
Physical construction:
- Two LEDs (660 nm + 940 nm) that flash sequentially
- One photodetector on opposite side (transmission) or same side (reflectance)
- When both LEDs off: ambient light subtracted from signal automatically
3. FIVE SPECIES OF HAEMOGLOBIN (Critical Viva Point)
Q: Why is standard pulse oximetry a two-wavelength device a limitation?
Standard pulse oximetry measures functional saturation - only O2Hb and deO2Hb:
Functional SaO2 = O2Hb / (O2Hb + deO2Hb) × 100
But there are 5 species of Hb in blood:
| Species | Normal % | Notes |
|---|
| O2Hb (oxyhaemoglobin) | ~97% | Absorbs 940 nm more |
| deO2Hb (deoxyhaemoglobin) | ~2% | Absorbs 660 nm more |
| COHb (carboxyhaemoglobin) | <1% (smoker: up to 10%) | Absorbs 660 nm same as O2Hb → falsely HIGH SpO2 |
| MetHb (methaemoglobin) | <1% | Absorbs equally at both wavelengths → SpO2 drifts toward 85% regardless of true SaO2 |
| SHb (sulphaemoglobin) | <1% | Rare, causes SpO2 to read low |
Pulse co-oximetry (e.g., Masimo Rad-7) uses 8 wavelengths and can measure COHb and MetHb directly.
(Miller's Anesthesia 10e, p.5449-5462)
4. THE OXYHEMOGLOBIN DISSOCIATION CURVE (OHC)
Q: What is the clinical significance of the shape of the OHC for pulse oximetry?
The OHC is sigmoid (S-shaped):
SpO2 (%)
100 |----___
98 | \
90 | \ ← STEEP PART: small ΔPO2 = big ΔSpO2
75 | \
50 | | P50 = 27 mmHg
|__________|___
PaO2 (mmHg)
Clinical implications:
- Flat upper portion (PaO2 >70 mmHg): SpO2 cannot detect hyperoxia - dangerous in premature neonates (retinopathy of prematurity risk)
- Steep lower portion: Once SpO2 starts falling rapidly, PaO2 is already critically low - pulse oximetry gives late warning
- SpO2 of 90% corresponds to PaO2 ~60 mmHg (onset of respiratory failure)
- SpO2 of 75% corresponds to PaO2 ~40 mmHg (mixed venous level)
Shifts of the curve:
| Shift LEFT (↑ affinity, ↓ O2 release) | Shift RIGHT (↓ affinity, ↑ O2 release) |
|---|
| ↓ Temperature | ↑ Temperature |
| ↓ CO2 / alkalosis | ↑ CO2 / acidosis |
| ↓ 2,3-DPG | ↑ 2,3-DPG |
| Fetal Hb (HbF) | Sickle cell disease |
| COHb, MetHb | Exercise, anaemia |
5. PHOTOPLETHYSMOGRAPHY - BONUS VIVA POINT
The pulse oximeter trace is also a photoplethysmograph (PPG):
- Shows arterial blood volume changes with each heartbeat
- Respiratory variation in PPG amplitude (ΔPOP / PVI) predicts fluid responsiveness in mechanically ventilated patients
- PVI (Pleth Variability Index) - commercially available on Masimo devices
- More reliable in mechanically ventilated than spontaneously breathing patients
(Miller's Anesthesia 10e, p.5461)
6. PROBE SITES
| Site | Notes |
|---|
| Finger (standard) | Most common; affected by vasoconstriction, nail polish |
| Ear lobe | Faster response time (~6 sec); good during vasoconstriction |
| Forehead (reflectance) | Best during hypotension/vasoconstriction/hypothermia - least responsive to catecholamines |
| Nose | Alternative site |
| Toe/foot | Post-ductal in neonates (different from right hand pre-ductal) |
| Palm/wrist | Neonates |
In vasopressor-dependent patients: use ear or forehead probe - less vasoconstriction at these sites compared to fingers
(Miller's Anesthesia 10e, p.5469-5470)
7. LIMITATIONS & SOURCES OF ERROR
This is the most popular viva topic:
A. Causes of FALSELY HIGH SpO2 (reads higher than true SaO2)
| Cause | Mechanism |
|---|
| Carbon monoxide poisoning (COHb) | COHb absorbs 660 nm same as O2Hb; SpO2 reads near 100% even in severe CO poisoning |
| Methaemoglobinaemia (early) | MetHb initially drives SpO2 up before plateau |
B. Causes of FALSELY LOW SpO2 (reads lower than true SaO2)
| Cause | Mechanism |
|---|
| Methaemoglobinaemia (established) | Regardless of true SaO2, SpO2 drifts toward 85% |
| Dyes (methylene blue, indocyanine green, indigo carmine) | Absorb at 660 nm - cause transient drop in SpO2 |
| Nail polish (blue/black/green) | Absorbs 660 nm; dark colours more problematic |
| Severe jaundice (bilirubin >20 mg/dL) | Absorbs at 460 nm - minimal clinical effect in adults |
C. Causes of INACCURATE or NO READING
| Cause | Mechanism |
|---|
| Vasoconstriction / poor perfusion | Reduced pulsatile component (AC signal too small) |
| Hypothermia | Peripheral vasoconstriction |
| Hypotension / shock | Weak peripheral pulse |
| Movement artefact | Most common cause of false alarms; next-generation signal processing (e.g., Masimo SETS) mitigates this |
| Ambient light interference | Bright theatre lights; resolved by shielding probe |
| Venous pulsation | Tricuspid regurgitation, high venous pressure → venous "pulsation" misread as arterial |
| Anaemia (severe) | At very low Hb, insufficient absorbing molecules; generally accurate unless Hb <5 g/dL |
| Melanin (dark skin) | May cause slight overestimation of SpO2 - subject of recent concern and regulatory review |
KEY VIVA POINT - Racial bias: Studies (including Sjoding et al., NEJM 2020) showed pulse oximeters overestimate SpO2 in patients with dark skin by ~3.5%, potentially masking hypoxemia. This is an active area of regulatory review by FDA.
D. Calibration limit
- Calibration curves only validated down to SpO2 70% - accuracy below 70% is unknown
8. CLINICAL APPLICATIONS
- Intraoperative monitoring (mandatory standard ASA/AAGBI)
- Sedation monitoring (procedural sedation, endoscopy, ICU)
- PACU / ward monitoring
- Transport monitoring
- Newborn screening for critical congenital heart disease (detects pre-ductal vs post-ductal difference)
- Pulse oximetry during COVID-19: enabled remote monitoring
- Fluid responsiveness assessment (via PPG waveform variation)
PART B: CAPNOGRAPHY
1. DEFINITIONS
| Term | Definition |
|---|
| Capnometry | Numerical measurement of CO2 concentration in a gas sample |
| Capnography | Continuous graphical display of CO2 concentration over time (waveform = capnogram) |
| End-tidal CO2 (EtCO2 / PETCO2) | CO2 concentration at the end of tidal exhalation (approximates alveolar CO2) |
| Volumetric capnography | CO2 plotted against exhaled volume (rather than time) |
Normal EtCO2 = 35-45 mmHg (or 4.7-6.0 kPa)
2. PHYSICAL PRINCIPLE
Infrared (IR) spectroscopy:
- CO2 absorbs infrared radiation at 4.28 μm wavelength
- The amount of IR absorbed is proportional to CO2 concentration (Beer-Lambert Law)
- A light source emits IR; the detector measures transmission; CO2 concentration calculated from absorption
Two system types:
| Type | Description | Pros/Cons |
|---|
| Sidestream (aspirating) | Gas sample drawn from circuit via fine tubing to analyser outside the airway | Pro: lightweight probe, works with LMA/mask; Con: 5-10 sec delay, sampling tube can block with water/secretions |
| Mainstream (non-aspirating) | Sensor sits directly in the breathing circuit | Pro: no delay, no sampling tube blockage; Con: heavy sensor on circuit, adds dead space, sensor can get hot |
(Miller's Anesthesia 10e, p.11316)
3. THE CAPNOGRAM WAVEFORM - FOUR PHASES
This is the most tested viva topic on capnography:
CO2
(mmHg)
45 | __________D
| / \
| /C \
| / \
0 |____/A B \E___
|←expiration→|←inspiration→|
I II III IV
| Phase | Name | What it represents |
|---|
| Phase I (A-B) | Inspiratory baseline | Dead space gas - no CO2; should be at zero |
| Phase II (B-C) | Expiratory upstroke | Mixture of dead space + alveolar gas; rapid CO2 rise |
| Phase III (C-D) | Alveolar plateau | Mostly alveolar gas; slight upslope due to ongoing CO2 diffusion from different lung units |
| Point D | End-tidal CO2 | The peak CO2 at end of exhalation = EtCO2 |
| Phase IV (D-E) | Inspiratory downstroke | Fresh gas displaces CO2; rapid return to zero |
Normal angle (alpha angle): Junction of Phase II and Phase III; normally ~100°. Widened in obstructive disease.
Beta angle: Junction of Phase III and Phase IV (downstroke); normally ~90°. Increased in rebreathing.
4. PaCO2 - EtCO2 GRADIENT
Q: What is the normal PaCO2 - EtCO2 gradient? What does it mean?
- Normal gradient = 2-5 mmHg (PaCO2 slightly higher than EtCO2)
- EtCO2 is always ≤ PaCO2 in healthy lungs
- Why? Because EtCO2 represents a mixture of gas from different alveoli including those with V/Q mismatch and dead space
The gradient INCREASES when dead space increases:
- Pulmonary embolism (major cause - reduced perfusion, high V/Q)
- Pulmonary hypotension
- Overdistended alveoli (high PEEP)
- Low cardiac output
- Haemorrhage / hypovolaemia
Alveolar Dead Space Fraction:
AVDSf = (PaCO2 - EtCO2) / PaCO2
(Miller's Anesthesia 10e, p.11316)
5. CAUSES OF CHANGES IN EtCO2 - COMPLETE TABLE
A. INCREASED EtCO2
| Cause | Mechanism |
|---|
| Hypoventilation | ↓ minute volume → CO2 accumulates |
| Rebreathing | Exhausted soda lime, incompetent inspiratory valve |
| Malignant hyperthermia | Massive ↑ CO2 production - often first/most sensitive sign |
| Fever / sepsis / shivering | ↑ metabolic rate → ↑ CO2 production |
| Tourniquet release | Sudden flush of accumulated CO2 |
| NaHCO3 administration | CO2 released from buffering |
| Thyrotoxicosis | ↑ metabolic rate |
| Laparoscopy (CO2 insufflation) | Absorption of CO2 from peritoneum |
| Light anaesthesia (pain/response) | ↑ sympathetic activity, ↑ metabolism |
B. DECREASED EtCO2
| Cause | Mechanism |
|---|
| Hyperventilation | ↑ CO2 elimination |
| Pulmonary embolism | ↑ dead space → less alveolar CO2 |
| Cardiac arrest / circulatory collapse | No pulmonary perfusion → near-zero EtCO2 |
| Hypothermia | ↓ metabolic rate, ↓ CO2 production |
| Severe haemorrhage / hypovolaemia | ↓ pulmonary perfusion |
| Air embolism | ↑ dead space |
| Pulmonary hypoperfusion (any cause) | ↑ V/Q mismatch |
C. ABSENT EtCO2
| Cause | Mechanism |
|---|
| Oesophageal intubation | Most critical - no CO2 from stomach (though transient CO2 from carbonated drinks) |
| Complete circuit disconnect | No gas sampling |
| Complete circuit obstruction | No gas flow |
| Cardiac arrest | No pulmonary blood flow |
| Blocked sidestream sampling tube | Water/secretions |
6. ABNORMAL WAVEFORM PATTERNS - VIVA FAVOURITES
Pattern 1: Slanted / shark-fin upstroke (Phase II-III slope increased)
/\
/ \
/ \
/ \___
- Obstructive airway disease (asthma, COPD, bronchospasm)
- Different lung units empty at different rates → prolonged, sloping plateau
- Increased alpha angle
Pattern 2: Elevated baseline (Phase I not returning to zero)
_____
/ \
___/ \_____ ← does not return to 0
- Rebreathing of exhaled CO2
- Exhausted soda lime
- Stuck/incompetent inspiratory valve
- Insufficient fresh gas flow (esp. Mapleson circuits)
Pattern 3: Sudden drop to zero
___|||||||||_____ (suddenly flat at 0)
- Oesophageal intubation (most critical diagnosis)
- Extubation / disconnection
- Complete circuit obstruction
- Cardiac arrest
Pattern 4: Exponential decrease toward zero
↓↓↓
...becoming smaller
- Pulmonary embolism (sudden) or decreasing cardiac output
- Cardiac arrest (gradual decline)
Pattern 5: Suddenly elevated then decreasing
↑↑
...then slowly falling
- Malignant hyperthermia onset
- CO2 insufflation starting (laparoscopy)
- Tourniquet release
- NaHCO3 bolus
Pattern 6: Cardiogenic oscillations (notches on plateau)
___/^\__/^\_____
- Heart motion transmitted to lungs during cardiac surgery
- Normal variant with slow RR and strong cardiac output
Pattern 7: Cleft/notch during Phase III
- Patient taking spontaneous breath during IPPV (curare cleft)
- Indicates neuromuscular block wearing off or patient fighting ventilator
7. CLINICAL USES OF CAPNOGRAPHY
| Use | Details |
|---|
| Confirm ETT in trachea | Standard of care - 6 consecutive waveforms confirm tracheal placement; zero waveform = oesophageal |
| Monitor ventilation adequacy | EtCO2 guides ventilator settings |
| Detect disconnection / circuit failure | Sudden drop to zero |
| Detect malignant hyperthermia | Unexplained sudden rise in EtCO2 |
| Pulmonary embolism detection | Sudden decrease in EtCO2 with clinical deterioration |
| CPR quality assessment | EtCO2 during CPR correlates with cardiac output; EtCO2 >10 mmHg suggests adequate CPR |
| ROSC during CPR | Sudden rise in EtCO2 during CPR = return of spontaneous circulation (ROSC) |
| Assess NMB reversal | Curare cleft = spontaneous breathing returning |
| Dead space estimation | AVDSf calculation |
| Fluid responsiveness (volumetric) | Changes in Bohr dead space with PEEP titration |
| Sedation monitoring | Non-intubated patients (via nasal/oral sampling cannula) |
| Rebreathing detection | Baseline elevation |
8. EtCO2 IN SPECIAL SITUATIONS
Cardiac Arrest
- Before ROSC: EtCO2 <10 mmHg = inadequate CPR / very poor prognosis
- Sudden rise to >40 mmHg during CPR = ROSC (most reliable non-invasive sign)
- If EtCO2 persistently <10 mmHg after 20 min of good CPR = consider stopping resuscitation (prognostic marker)
Paediatric patients
- Same principles apply
- EtCO2-PaCO2 gradient may be slightly larger due to V/Q immaturity in neonates
- Sidestream capnography preferred in small children (lightweight)
- Accuracy reduces with very high respiratory rates and small tidal volumes (gas mixing in sidestream tubing)
- Time-based capnography less accurate at very high RRs (>40/min) - gaps between breaths too short to develop clear plateau
Laparoscopy
- CO2 absorbs from peritoneum → EtCO2 rises by 5-10 mmHg
- Increase minute ventilation by 10-15% at start
- Subcutaneous emphysema → very high EtCO2 even with hyperventilation
- Steep Trendelenburg → ↑ airway pressure + atelectasis → ↑ EtCO2
Malignant Hyperthermia
- EtCO2 rise is the earliest and most sensitive indicator - precedes temperature rise
- Often >80-100 mmHg despite maximal ventilation
- Treat with dantrolene + cooling + hyperventilation
9. VOLUMETRIC CAPNOGRAPHY
Plots CO2 against exhaled volume (rather than time):
- Provides direct Bohr dead space measurement
- Helpful for PEEP optimisation (titrate PEEP to minimise dead space without overdistension)
- Can demonstrate response to bronchodilator therapy
- Available on modern ICU ventilators
(Miller's Anesthesia 10e, p.11317)
10. TRANSCUTANEOUS CO2 (TcCO2)
- Probe heats skin → dilates capillaries → CO2 diffuses through skin → measured by IR sensor
- Continuous non-invasive PaCO2 estimate
- Useful in high-frequency ventilation where capnography inadequate
- Requires calibration against blood gas; drift over time
- Less accurate in: low cardiac output, thick skin/obesity, cyanotic heart disease
(Miller's Anesthesia 10e, p.11317)
11. COMPARISON TABLE: PULSE OXIMETRY vs CAPNOGRAPHY
| Feature | Pulse Oximetry | Capnography |
|---|
| What it measures | O2 saturation (SpO2) | CO2 concentration (EtCO2) |
| What it monitors | Oxygenation | Ventilation |
| Normal values | SpO2 >95% (>92% in COPD) | EtCO2 35-45 mmHg |
| Response time | ~6 seconds (ear fastest) | Sidestream: 5-10 sec; mainstream: near-instant |
| First sign of hypoventilation | Late (SpO2 falls only after significant O2 reserve depleted) | Early (EtCO2 rises immediately) |
| Confirms ETT placement | No | Yes (6 waveforms) |
| Detects oesophageal intubation | No (SpO2 takes time to fall) | Yes (immediate - no waveform) |
| Detects MH | No | Yes (early EtCO2 rise) |
| Detects PE | Indirect (SpO2 fall) | Yes (EtCO2 falls) |
| Detects ROSC | Indirect | Yes (sudden EtCO2 rise) |
| Circuit disconnect | No | Yes (EtCO2 → 0) |
| Main limitation | Does NOT detect ventilation failure until SpO2 falls | EtCO2 ≠ PaCO2 when dead space increased |
QUICK-RECALL VIVA CARD
PULSE OXIMETRY
- Wavelengths: 660 nm (red) + 940 nm (infrared)
- AC (pulsatile) = arterial; DC (steady) = everything else
- COHb: falsely HIGH SpO2 (660 nm same as O2Hb)
- MetHb: SpO2 drifts to 85% regardless
- Methylene blue: falsely LOW SpO2
- Vasoconstriction → no signal
- OHC flat top: cannot detect hyperoxia
- SpO2 90% ≈ PaO2 60 mmHg
CAPNOGRAPHY
- Phases: I=dead space, II=upstroke, III=plateau, IV=downstroke
- Normal EtCO2: 35-45 mmHg; gradient PaCO2-EtCO2 = 2-5 mmHg
- Gradient INCREASES with: PE, ↓ cardiac output, overdistension
- Sudden EtCO2 to ZERO: oesophageal intubation / disconnection / cardiac arrest
- Sudden EtCO2 RISE: MH / hypoventilation / laparoscopy / NaHCO3
- Sudden EtCO2 DROP: PE / haemorrhage / ↓ cardiac output
- CPR: EtCO2 >10 = adequate; sudden rise = ROSC
- Shark-fin: obstructive disease
- Elevated baseline: rebreathing (exhausted soda lime / bad valve)
Sources: Miller's Anesthesia 10e (Ch.37, p.5449-5470; Ch.31, p.11316-11317); Barash Clinical Anesthesia 9e; Morgan & Mikhail Clinical Anesthesiology 7e