Capnography: physiology and waveform interpretation

10 min read Last updated April 8, 2026

How to read a capnogram (structured approach)

  • Confirm the basics: is this ETCO₂ (end-tidal) or FICO₂ (inspired), and is it mainstream or sidestream sampling?
    • Mainstream: fast response, adds dead space/weight at airway; can be affected by secretions/condensation on windows.
    • Sidestream: aspirates gas (e.g. 50–250 mL/min); delay and waveform distortion possible; sampling line leaks/obstruction common.
  • Check presence of a waveform: absent/near-flat trace is an emergency until proven otherwise.
    • Think: oesophageal intubation, circuit disconnection, apnea, complete obstruction, cardiac arrest/very low pulmonary blood flow, sampling failure.
  • Assess baseline (inspired CO₂): should return to ~0 kPa/mmHg in normal systems.
    • Raised baseline suggests rebreathing (e.g. exhausted soda lime, incompetent unidirectional valve, inadequate fresh gas flow, prolonged expiratory time constant) or contamination of sampling line.
  • Assess shape: phases I–III, alveolar plateau slope, and inspiratory downstroke.
    • Look for obstructive pattern (slow upstroke, slanted plateau), curare cleft, cardiogenic oscillations, oscillations from ventilation mode.
  • Assess ETCO₂ value and trend: interpret with ventilation, metabolism, and pulmonary perfusion in mind.
    • Sudden change = equipment/disconnection/embolism/circulatory event; gradual change = ventilation/metabolism trend.

Immediate actions when ETCO₂ changes (practical algorithm)

  • Sudden loss of trace: call for help, check patient first, then equipment.
    • Patient: chest movement, auscultation, airway patency, tube position, pulse/ECG, consider arrest.
    • Equipment: circuit connections, APL/ventilator, sampling line connection/kink/water, capnograph power/zeroing.
  • Sudden drop in ETCO₂ with trace present: think reduced pulmonary blood flow or hyperventilation/disconnection leak.
    • Consider: pulmonary embolism/air embolism, severe hypotension, arrest, massive haemorrhage, venous return reduction, anaphylaxis/bronchospasm with poor ventilation.
  • Sudden rise in ETCO₂: consider increased CO₂ delivery or rebreathing.
    • Consider: hypoventilation, tourniquet release, bicarbonate administration, malignant hyperthermia, sepsis/pyrexia, CO₂ insufflation (laparoscopy), exhausted soda lime/incompetent valves.

What capnography measures (physics/technology essentials)

  • Clinical capnographs use infrared absorption spectroscopy: CO₂ absorbs IR at ~4.3 μm; absorption proportional to CO₂ concentration (Beer–Lambert law).
  • Mainstream: sensor at airway; minimal delay; more accurate for rapid changes; adds dead space and weight; prone to contamination/secretions.
  • Sidestream: aspirates sample to analyser; delay (transport + analyser response); waveform can be damped; sampling line blockage/leak common; may entrain room air if leak → falsely low ETCO₂.
  • Units: kPa (UK) or mmHg. Normal ETCO₂ ~4.5–5.5 kPa (35–45 mmHg) in healthy adult with controlled ventilation.

Physiology: determinants of ETCO₂

  • ETCO₂ reflects the balance of CO₂ production (V̇CO₂), alveolar ventilation (V̇A), and pulmonary perfusion.
  • Alveolar ventilation equation (concept): PaCO₂ ∝ V̇CO₂ / V̇A. If V̇A falls → PaCO₂ rises; ETCO₂ usually rises too (unless perfusion fails).
  • ETCO₂ is usually slightly lower than PaCO₂ due to alveolar dead space and V/Q mismatch: PaCO₂ − ETCO₂ gradient normally ~0.3–0.7 kPa (2–5 mmHg) but can be larger.
    • Gradient increases with increased physiological dead space: PE, low cardiac output, emphysema, high PEEP/overdistension, ARDS, hypovolaemia.
    • Gradient may decrease/ETCO₂ may approach PaCO₂ with very high CO₂ production and good perfusion, or in pregnancy (increased ventilation lowers PaCO₂).
  • CO₂ production increases with: fever, shivering, seizures, malignant hyperthermia, sepsis, thyrotoxicosis, catecholamines; decreases with hypothermia, reduced metabolism.
  • Pulmonary perfusion effects: ETCO₂ falls with reduced cardiac output/PE/arrest; during CPR ETCO₂ correlates with pulmonary blood flow and quality of compressions.

Normal time capnogram: phases and angles

  • Phase I (A–B): dead space gas (conducting airways) → near zero CO₂.
  • Phase II (B–C): rapid upstroke as mixed dead space + alveolar gas reaches sensor.
  • Phase III (C–D): alveolar plateau; slight positive slope due to sequential emptying and V/Q heterogeneity. Point D = ETCO₂.
  • Phase 0 (D–E): inspiratory downstroke to baseline as fresh gas enters.
  • α angle (between phase II and III): increases with expiratory outflow obstruction (asthma/COPD, kinked tube, bronchospasm).
  • β angle (between phase III and inspiratory downstroke): increases with rebreathing or incompetent inspiratory valve.

Waveform patterns: common clinical interpretations

  • Obstructive pattern (“shark fin”): slow upstroke, slanted plateau, increased α angle.
    • Causes: bronchospasm, COPD/asthma, partial tube obstruction (secretions/bite), kinked circuit, low expiratory flow settings, small ETT.
  • Rebreathing / raised baseline: inspired CO₂ > 0; β angle increased; baseline fails to return to zero.
    • Causes: exhausted soda lime, inadequate fresh gas flow (esp. Mapleson systems), incompetent unidirectional valve, excessive apparatus dead space, insufficient expiratory time (air trapping), ventilator malfunction.
  • Curare cleft: notch in plateau during spontaneous effort in a mechanically ventilated patient → inadequate neuromuscular blockade or return of respiratory effort.
  • Cardiogenic oscillations: small rhythmic oscillations on plateau/downstroke; more obvious with low tidal volumes, paediatrics, or hyperdynamic heart.
  • Sudden loss of ETCO₂: consider disconnection/oesophageal intubation/apnoea/arrest; sampling line failure can mimic.
  • Sudden sustained fall in ETCO₂: pulmonary embolism/air embolism, severe hypotension, arrest, major haemorrhage; also large circuit leak.
  • Gradual rise in ETCO₂: hypoventilation, increased V̇CO₂ (fever, MH), CO₂ absorption (laparoscopy), rebreathing developing (soda lime exhaustion).
  • Sudden rise in ETCO₂: tourniquet release, bicarbonate administration, sudden increase in CO₂ delivery, ventilator setting error (reduced minute ventilation).
  • Low ETCO₂ with normal waveform shape: hyperventilation or increased dead space (PE/low CO) with preserved ventilation.

Capnography in key scenarios (high-yield)

  • Confirmation of tracheal intubation: persistent CO₂ waveform over several breaths indicates tracheal placement (in presence of pulmonary blood flow).
    • False reassurance: CO₂ in stomach after bag-mask ventilation or carbonated drinks can produce transient CO₂; should rapidly wash out.
    • False negative: cardiac arrest/very low pulmonary blood flow can give minimal/absent ETCO₂ despite correct placement—use direct laryngoscopy, fibreoptic, ultrasound, clinical signs.
  • CPR: ETCO₂ reflects pulmonary blood flow; rising ETCO₂ suggests improved compressions or ROSC; sudden increase often indicates ROSC.
    • Persistently very low ETCO₂ despite good technique suggests poor prognosis, but interpret in context (ventilation rate, airway leak, metabolic state).
  • Laparoscopy: CO₂ insufflation increases V̇CO₂ and PaCO₂/ETCO₂; sudden fall may indicate gas embolism or major haemodynamic compromise.
  • Malignant hyperthermia: early sign can be unexplained rising ETCO₂ despite increased minute ventilation; accompanied by tachycardia, hyperthermia (later), acidosis, rigidity.
Explain the physiology that determines ETCO₂ and why it differs from PaCO₂.

Aim: link ETCO₂ to ventilation, metabolism, and perfusion; then explain the PaCO₂–ETCO₂ gradient via dead space/VQ mismatch.

  • ETCO₂ approximates alveolar CO₂ at end-expiration and depends on V̇CO₂, alveolar ventilation (V̇A), and pulmonary perfusion.
  • Relationship: PaCO₂ ∝ V̇CO₂ / V̇A; if V̇A falls, PaCO₂ rises and ETCO₂ usually rises (if perfusion maintained).
  • ETCO₂ is usually lower than PaCO₂ because exhaled gas is a mixture of alveolar gas and dead space gas (no CO₂).
  • The PaCO₂–ETCO₂ gradient increases with increased physiological dead space/VQ mismatch: PE, low CO, emphysema, high PEEP/overdistension, ARDS, hypovolaemia.
Describe the normal time capnogram and label phases I–III and the alpha and beta angles.

Examiners want a clear description of phases and what each represents physiologically.

  • Phase I: dead space gas, CO₂ ~0.
  • Phase II: rapid upstroke as alveolar gas mixes with dead space gas.
  • Phase III: alveolar plateau; slight positive slope due to non-uniform alveolar emptying; end of this phase is ETCO₂.
  • Alpha angle (phase II–III): increases with expiratory obstruction (bronchospasm/COPD, kinked tube).
  • Beta angle (phase III–inspiratory downstroke): increases with rebreathing/inspiratory valve incompetence.
You see a 'shark fin' capnogram. What does it indicate and what are your immediate checks and actions?

Treat as expiratory flow limitation/obstruction until proven otherwise.

  • Interpretation: expiratory obstruction → slow phase II upstroke, slanted phase III plateau, increased α angle.
  • Immediate checks: listen for wheeze; check ETT patency (kink, bite, secretions), circuit obstruction, HME filter blockage, ventilator settings (I:E, expiratory time).
  • Actions: deepen anaesthesia, give bronchodilator, suction ETT, consider manual ventilation to assess compliance/resistance, treat anaphylaxis if suspected.
The capnogram baseline does not return to zero. Give causes and how you would differentiate them.

Key concept: inspired CO₂ indicates rebreathing or contamination.

  • Causes: rebreathing from exhausted soda lime, incompetent unidirectional valve, inadequate fresh gas flow (Mapleson), excessive dead space, insufficient expiratory time/air trapping.
  • Also consider: sampling line contamination (water/secretions), analyser zeroing error.
  • Differentiate: check absorber temperature/colour change and canister, check valve movement, increase fresh gas flow and see if baseline returns to zero, inspect sampling line and water trap.
During controlled ventilation the ETCO₂ trace suddenly disappears. Give a differential diagnosis and an immediate management plan.

This is a high-stakes scenario: prioritise patient oxygenation/ventilation and confirm airway/circulation.

  • Differential: circuit disconnection, ventilator failure, extubation/ETT displacement, complete airway obstruction, oesophageal intubation (if just intubated), apnea, cardiac arrest/very low CO, capnograph/sampling line failure.
  • Immediate plan: switch to manual ventilation with 100% O₂, check chest rise and reservoir bag, auscultate, check ETT depth/cuff, suction if obstructed.
  • Check circulation: pulse/ECG/BP; if arrest suspected start ALS; ETCO₂ during CPR helps assess compression quality and ROSC.
  • Equipment: check all circuit connections, APL/ventilator, sampling line connection/kink/water trap, analyser function.
Explain the 'curare cleft': what causes it and what should you do?

A classic waveform interpretation question.

  • Cause: spontaneous inspiratory effort during the alveolar plateau in a mechanically ventilated patient → transient dilution of exhaled CO₂.
  • Implication: inadequate neuromuscular blockade, light anaesthesia, or ventilator–patient dyssynchrony.
  • Actions: assess depth of anaesthesia/analgesia, check neuromuscular monitoring and top up relaxant if indicated, adjust ventilator trigger/synchrony settings.
How does pulmonary embolism affect ETCO₂ and the capnogram? Include the PaCO₂–ETCO₂ gradient.

Link reduced pulmonary perfusion to increased dead space and reduced CO₂ delivery to alveoli.

  • ETCO₂ typically falls (often abruptly) due to reduced pulmonary blood flow and increased alveolar dead space.
  • PaCO₂ may be normal or high depending on ventilation and severity; the PaCO₂–ETCO₂ gradient increases because ETCO₂ underestimates arterial CO₂ more when dead space rises.
  • Waveform shape may remain relatively normal early; interpret with haemodynamics and oxygenation.
Discuss capnography in CPR: what does ETCO₂ tell you and what changes suggest ROSC?

ETCO₂ is a surrogate for pulmonary blood flow during CPR (assuming consistent ventilation).

  • Higher ETCO₂ generally indicates better cardiac output from compressions; falling ETCO₂ suggests fatigue/poor compressions or worsening physiology.
  • A sudden sustained rise in ETCO₂ (often to near-normal values) can indicate ROSC.
  • Interpret with ventilation rate/tidal volume and airway leaks; avoid hyperventilation which can lower ETCO₂ despite adequate perfusion.
A patient undergoing laparoscopy shows a gradual rise in ETCO₂. Give causes and management.

Most commonly increased CO₂ absorption plus relative hypoventilation; always consider serious causes if abrupt or with instability.

  • Causes: increased CO₂ absorption from pneumoperitoneum, reduced minute ventilation, increased dead space from positioning/PEEP, increased V̇CO₂ (fever/sepsis).
  • Management: increase minute ventilation, check circuit for rebreathing, liaise with surgeon about insufflation pressure and duration; assess haemodynamics and temperature.
  • If sudden fall with instability: consider CO₂ embolism/air embolism and treat accordingly (stop insufflation, 100% O₂, Durant/left lateral head down if appropriate, aspirate via central line if present, supportive measures).
Compare mainstream and sidestream capnography: advantages, disadvantages, and common artefacts.

Common equipment viva: focus on response time, dead space, sampling issues, and practical pitfalls.

  • Mainstream: fast response, good for rapid changes; disadvantages include added dead space/weight at airway and contamination of optical windows.
  • Sidestream: lightweight at airway; disadvantages include sampling delay, waveform damping, line blockage/kink/water, leaks causing dilution with room air → falsely low ETCO₂.
  • Artefacts: water/secretions causing erratic readings; high O₂/N₂O generally minimal effect with modern compensation but older devices may be affected; calibration/zeroing errors can shift baseline.

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