2.2 Capnography, Waveforms & Dead-Space Evaluation

Key Takeaways

  • Arterial CO2 is often modestly higher than end-tidal CO2 in healthy lungs, but the gradient varies with age, dead space, ventilation-perfusion matching, sampling, and disease. A widening positive gradient can support increased alveolar dead space from pulmonary hypoperfusion, overdistension, or vascular obstruction.
  • A classic 'shark fin' capnogram with a prolonged, upward-sloping Phase III indicates expiratory airflow obstruction, whereas an abrupt drop of PetCO2 to zero signals accidental extubation, complete airway obstruction, or cardiac arrest.
  • Mainstream capnometry responds instantly but adds 1 to 5 mL of mechanical dead space and airway weight, while sidestream adds no dead space and is preferred in extremely low-birth-weight and non-intubated patients despite a 1 to 3 second transit delay.
  • The alpha angle between Phase II and Phase III is normally 100 to 110 degrees and widens with bronchospasm, mucous plugging, or uneven ventilation distribution.
Last updated: September 2026

2.2 Capnography, Waveforms & Dead-Space Evaluation

End-Tidal CO2 (PetCO2) Capnography

Capnography provides continuous, real-time graphical display of exhaled carbon dioxide tension throughout the respiratory cycle. It reflects the triad of metabolism (CO2 production), systemic perfusion (cardiac output and pulmonary blood flow), and alveolar ventilation.

Mainstream vs. Sidestream Analyzers

Technical ParameterMainstream AnalyzerSidestream Analyzer
Sensor LocationDirectly in-line at airway adapterRemote; gas aspirated via capillary tube
Response TimeFast (instantaneous, no transit delay)Delayed by 1 to 3 seconds (transit time)
Added Mechanical DeadspaceModerate to High (adds 1–5 mL deadspace)Zero added mechanical deadspace
Airway Weight & DragBulky, heavy; increases extubation riskLightweight; minimal traction on ETT
Neonatal SuitabilityAvoid in ELBW infants (< 1 kg)Preferred in ELBW and non-intubated patients
Moisture ManagementHeated sensor prevents condensationWater traps required; prone to bore occlusion
Gas ScavengingNone requiredSample gas (50–150 mL/min) evacuated

Capnogram Waveform Anatomy

   PCO2 (mmHg)
    40 ┼                      ┌──────────────────────┐ PetCO2
       │                     /      Phase III         ▲
    20 ┼                    /                         │ Phase IV
       │       Phase I     / Phase II                 │
     0 ┼──────────────────┘                           └────────
       0                 Exhalation                  Inspiration
  • Phase I (Baseline): Anatomic deadspace exhalation. Gas is free of CO2; baseline must sit at 0 mmHg.
  • Phase II (Early Exhalation / Ascending Limb): Rapid upward curve representing mixed anatomic deadspace gas and alveolar gas.
  • Phase III (Alveolar Plateau): Exhalation of pure alveolar gas. The slope reflects the distribution of ventilation/perfusion (V/Q) ratios. The peak value at the very end of Phase III immediately before inspiration is the PetCO2.
  • Alpha (α) Angle: The angle between Phase II and Phase III (normally 100° to 110°). Widens significantly with bronchospasm, mucous plugging, or uneven ventilation.
  • Beta (β) Angle: The angle between Phase III and Phase IV (normally ~90°). Widens when rebreathing occurs.
  • Phase IV (Inspiratory Downstroke): Rapid decrease to baseline zero as fresh gas enters the airway.

Arterial-to-End-Tidal CO2 Gradient (P(a-et)CO2)

Under normal physiological conditions, arterial PaCO2 is slightly higher than end-tidal PetCO2 by 2 to 5 mmHg due to normal, baseline alveolar deadspace:

P(a-et)CO2 = PaCO2 - PetCO2 = 2 to 5 mmHg

A widening of the P(a-et)CO2 gradient (> 5 mmHg) reflects an increase in alveolar deadspace ventilation (V/Q units with ventilation in excess of perfusion):

  • Pulmonary hypoperfusion (hypovolemic shock, cardiac arrest, low cardiac output)
  • Pulmonary embolism / vascular thrombosis
  • High Mean Airway Pressure or excessive PEEP causing pulmonary capillary microvascular compression

Diagnostic Waveform Interpretation

Waveform DescriptionCharacteristic MorphologyClinical EtiologiesCorrective Action
Airflow Obstruction / Bronchospasm'Shark fin' appearance; prolonged, upward-sloping Phase III; widened α-angle.Status asthmaticus, bronchiolitis, kinked ETT, bronchial secretions.Administer bronchodilator; clear airway secretions; check ETT patency.
RebreathingElevation of Phase I baseline above 0 mmHg (> 2–3 mmHg); elevated PetCO2.Incompetent expiratory valve, depleted CO2 absorber, inadequate bias flow.Increase ventilator bias flow; inspect and replace exhalation valve/absorber.
Curare CleftSharp downward dip or notch in the middle-to-late Phase III plateau.Neuromuscular blockade wearing off; spontaneous diaphragmatic effort against vent.Re-sedate, adjust ventilator synchrony, or administer muscle relaxant if indicated.
HypoventilationNormal waveform morphology; progressive stair-step rise in PetCO2 (> 45 mmHg).Central hypoventilation, respiratory depression, insufficient tidal volume.Increase minute ventilation (increase tidal volume, rate, or PIP).
HyperventilationNormal waveform morphology; progressive decrease in PetCO2 (< 35 mmHg).Metabolic acidosis compensation, pain, excessive ventilator rate/volume.Adjust ventilator settings to lower minute ventilation; treat underlying cause.
Esophageal IntubationImmediate low-amplitude decaying waveforms that rapidly drop to 0 within 2–5 breaths.ETT misplaced into esophagus; detecting swallowed gastric CO2.Remove ETT immediately; hand-bag ventilate and re-intubate trachea.
Sudden Loss of PetCO2 to ZeroAbrupt, complete disappearance of capnographic tracing to flatline.Accidental extubation, total ETT obstruction, ventilator disconnect, cardiac arrest.Immediately check chest rise, pulse, and circuit connections; begin CPR/bag-valve ventilation.

Worked Clinical Calculation: Deadspace Fraction & Gradient

Clinical Scenario

An intubated 6-year-old child with pneumonia is mechanically ventilated. An arterial blood gas shows PaCO2 = 52 mmHg. Simultaneous capnography demonstrates a regular waveform with an end-tidal PetCO2 of 32 mmHg.

Step-by-Step Calculation

  1. Calculate the P(a-et)CO2 gradient: P(a-et)CO2 = PaCO2 - PetCO2 = 52 - 32 = 20 mmHg Interpretation: The gradient is markedly widened (normal is 2–5 mmHg), indicating elevated alveolar deadspace.

  2. Calculate the modified Enghoff-Bohr physiological deadspace fraction (VD / VT): VD / VT = (PaCO2 - PetCO2) / PaCO2 Substituting PetCO2 as a clinical approximation for mixed expired CO2: VD / VT = (52 - 32) / 52 = 20 / 52 ≈ 0.385 (38.5%) Clinical Decision: The therapist must investigate causes of pulmonary capillary hypoperfusion, excessive alveolar overdistension from PEEP, or localized microvascular occlusion.


NPS Exam Traps

NPS Exam Trap 1: Pre-Ductal Site Selection

On the NBRC-NPS exam, candidates often incorrectly select the left hand or earlobe as a pre-ductal monitoring site. The right hand or right wrist is the ONLY reliable pre-ductal site because the innominate artery originates upstream of the ductus arteriosus. The left subclavian artery arises adjacent to or downstream from the ductus in many infants.

NPS Exam Trap 2: Widened P(a-et)CO2 vs. Hypoventilation

When PaCO2 rises to 60 mmHg while PetCO2 drops from 38 to 22 mmHg, do NOT conclude the patient is hyperventilating. A falling PetCO2 in the presence of a rising PaCO2 indicates a catastrophic increase in deadspace ventilation (e.g., massive pulmonary embolism, air leak, or hypovolemic shock), NOT alveolar hyperventilation.

NPS Exam Trap 3: Transcutaneous Burns in ELBW Preterms

ELBW skin is especially vulnerable to heated-sensor injury. Select temperature and dwell time from the device and neonatal-unit protocol, use the lowest setting that gives useful trending, inspect the skin, and rotate promptly. Do not convert one device's 42°C–43°C/two-hour protocol into a universal limit.

Test Your Knowledge

While monitoring a mechanically ventilated 4-year-old child with severe status asthmaticus, the respiratory therapist observes that the capnogram waveform shows an elevation of the Phase I baseline to 8 mmHg and the end-tidal CO2 reads 48 mmHg. What is the most likely cause of this capnographic abnormality, and what is the immediate corrective action?

A
B
C
D