End-Tidal CO₂ Monitoring for Respiratory Therapists
Waveform capnography, airway confirmation, ventilation trending, CPR monitoring, and common clinical patterns — a practical reference for RT practice.
For educational and informational reference only. This content does not constitute medical advice, does not establish a standard of care, and should not replace physician orders, licensed clinical judgment, or institutional policy. Clinical decisions must be made by qualified healthcare professionals using patient-specific assessment.
See also: RTB2 Medical Disclaimer · Editorial Policy
What Is End-Tidal CO₂?
End-tidal CO₂ (ETCO₂) is the partial pressure of carbon dioxide measured at the end of a normal exhalation — representing the peak CO₂ concentration in exhaled gas before the next inhalation dilutes it. Capnography is the continuous, waveform-based measurement of CO₂ throughout the respiratory cycle; capnometry refers to the numeric value alone.
Normal ETCO₂ in a spontaneously breathing adult is approximately 35–45 mmHg, closely tracking (though slightly lower than) arterial PaCO₂ due to dilution by dead space gas. The difference between PaCO₂ and ETCO₂ (the PaCO₂–ETCO₂ gradient) reflects dead space ventilation and is normally 2–5 mmHg. A widened gradient indicates increased dead space (PE, decreased cardiac output, ARDS) or sampling issues.
For respiratory therapists, ETCO₂ monitoring serves several distinct clinical purposes: confirming airway placement, continuously monitoring ventilation trends, guiding CPR quality assessment, and detecting physiologic changes in ventilation-perfusion matching.
The Capnography Waveform (Capnogram)
A normal capnogram has a characteristic four-phase waveform:
Airway Placement Confirmation
Continuous waveform capnography is the most reliable real-time method for confirming endotracheal tube placement in the trachea. Current advanced life support guidelines and airway management standards recommend capnography as a primary confirmation method following intubation.
Tracheal placement: Consistent CO₂ waveforms with each ventilation cycle confirm that gas exchange is occurring in the lungs. A sustained waveform across multiple breaths — typically 6 consecutive breaths — provides high confidence of tracheal placement.
Esophageal intubation: May initially produce a brief CO₂ waveform from gastric CO₂, but this rapidly extinguishes within 4–6 breaths. Persistent absence of CO₂ or rapidly diminishing waveforms should prompt immediate reassessment of tube position by laryngoscopy.
Important limitation: In patients with very low cardiac output (cardiac arrest, severe circulatory shock), CO₂ delivery to the lungs may be insufficient to produce detectable ETCO₂ even with correct tracheal placement. In cardiac arrest, a low or absent ETCO₂ value does not reliably exclude correct tube placement.
Continuous Ventilation Monitoring
In mechanically ventilated patients, ETCO₂ provides continuous, breath-by-breath feedback on alveolar ventilation — supplementing periodic ABG results with real-time trending.
Rising ETCO₂ indicates increasing CO₂ accumulation — hypoventilation, increasing CO₂ production (fever, sepsis, increased metabolic rate), or increasing dead space. In a patient on controlled ventilation, rising ETCO₂ without a change in ventilator settings should prompt clinical reassessment and may indicate a need for ABG analysis.
Falling ETCO₂ may reflect hyperventilation, decreasing CO₂ production (sedation, hypothermia), improving cardiac output (after resuscitation), or increasing dead space (PE, decreased perfusion).
A sudden drop to near-zero in a mechanically ventilated patient is a critical alarm: possible circuit disconnect, endotracheal tube displacement, cardiac arrest, or massive PE with near-absent pulmonary perfusion.
ETCO₂ During CPR
Capnography has become a standard monitoring tool during cardiac arrest resuscitation. ETCO₂ during CPR reflects pulmonary blood flow — which depends entirely on the quality of chest compressions. Higher ETCO₂ values during CPR (generally >10–15 mmHg) correlate with better quality compressions and improved survival probability.
Uses of ETCO₂ during cardiac arrest:
- CPR quality feedback: A sudden rise in ETCO₂ during CPR (to >40 mmHg) is a sensitive early indicator of return of spontaneous circulation (ROSC).
- Prognostication: Persistent ETCO₂ values below 10 mmHg after 20 minutes of resuscitation are associated with very low survival probability — though this must be integrated with clinical context.
- Tube confirmation: Continuous waveform confirms the airway remains in the trachea throughout the resuscitation effort.
Common Waveform Abnormalities
Shark fin / slanted upstroke (obstructive pattern)
Slow, slanted rise in Phase II with a prolonged, upward-sloping Phase III plateau — characteristic of obstructive airway disease (asthma, COPD, bronchospasm). The upsloping plateau reflects delayed and uneven alveolar emptying across lung units with different time constants.
Curare cleft (notch in plateau)
A notch in the Phase III plateau that occurs when the patient attempts a spontaneous breath against controlled ventilation — commonly seen with inadequate sedation or neuromuscular blockade reversal. The patient's diaphragmatic effort transiently drops ETCO₂ mid-exhalation.
Prolonged plateau with gradual rise
Progressive upsloping Phase III plateau suggests worsening V/Q mismatch or auto-PEEP. Can be seen in evolving bronchospasm, secretion accumulation, or dynamic hyperinflation.
Sudden loss of waveform (flatline)
Complete loss of CO₂ signal: circuit disconnect, cuff failure with massive leak, tube displacement, cardiac arrest, or capnograph sampling failure. Treat as a critical event — immediately assess the patient and circuit.
Elevated baseline
CO₂ not returning to zero between breaths: rebreathing of exhaled gas. Causes include exhausted CO₂ absorber (circle system), inadequate fresh gas flow, or malfunctioning HME.
Low Perfusion States and ETCO₂ Limitations
ETCO₂ depends on CO₂ delivery from the tissues to the lungs via the pulmonary circulation. In states of severe low perfusion — cardiac arrest, profound shock, massive PE, or severe hemorrhage — CO₂ transport to the alveoli is dramatically reduced, causing ETCO₂ to fall independently of ventilation status.
Clinical implications:
- A low ETCO₂ in a hypotensive patient may reflect circulatory failure rather than hypoventilation.
- The PaCO₂–ETCO₂ gradient increases significantly in low perfusion states — ETCO₂ underestimates true PaCO₂.
- In massive PE, ETCO₂ may fall precipitously while PaCO₂ rises — producing an extreme gradient and falsely low ETCO₂.
- Never titrate ventilator settings based on ETCO₂ alone without correlating with ABG in hemodynamically unstable patients.
Reviewed by RTB2 Editorial Team
Last updated April 2026