End-Tidal CO2

Aka: End-Tidal CO2, End-Tidal pCO2, EtCO2, End Tidal Carbon Dioxide, End-Tidal CO2 Concentration, Expired Carbon Dioxide Concentration, Capnography, End Tidal Carbon Dioxide Tension, Capnometry, Infrared Capnography

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II. Indications

  1. Cardiac Arrest
    1. Monitoring for Return of Spontaneous Circulation (ROSC)
    2. Monitoring Chest Compressions for adequacy
    3. Prognosis in Resuscitation (PetCO2 <15-20 for >20 min of CPR is associated with poor chance of ROSC)
  2. Cardiac Output monitoring
    1. PetCO2 correlates well with Cardiac Output
    2. Monitoring fluid Resuscitation response
  3. Procedural Sedation
    1. Monitors ventilation during Procedural Sedation
    2. Detects apnea well before Oxygen Saturation falls
  4. Arterial PaCO2 monitoring surrogate
    1. Difference between PaCO2 to PetCO2 should remain constant until other parameters change (e.g. Ventilator settings)
    2. Recheck ABG when Ventilator settings change to re-calculate the PaCO2-PetCO2 gap
    3. End-Tidal CO2 is significantly lower than PaCO2 when alveolar dead space is high
  5. ICU complication monitoring (for sudden decrease in End-Tidal CO2)
    1. Alveolar hyperinflation (high Tidal Volume or excessive PEEP)
    2. Endotracheal Tube migration (e.g. right mainstem Bronchus)
    3. Acute Pulmonary Embolism
    4. Acute Pulmonary Edema
    5. Pneumonia
  6. Ventilator Weaning
    1. Arterial PaCO2 monitoring surrogate (see above)
    2. PetCO2 increases with failed weaning and increased work of breathing (increasing exhaled CO2)
    3. PetCO2 decreases with Bellows Failure (respiratory Muscle Weakness) as patient exhausts in failed weaning attempt

III. Mechanism

  1. CO2 absorbs infrared light
  2. CO2 detector circuit
    1. Phototransmitter emits infrared light
    2. Carbon dioxide present in the airway absorbs infrared light in proportion to its airway concentration
    3. Photodetector receives the light not absorbed by carbon dioxide

IV. Preparations

  1. Ventilator measurement of EtCO2
  2. Non-ventilated patients
    1. Commercial devices (e.g. Salter divided Nasal Cannula)
    2. Modified standard Nasal Cannula
      1. Block short tubing connecting the two nasal prongs on the cannula (e.g. with cotton or external clamp)
      2. Insert 14 gauge, 2 inch angiocatheter into one of the two tubes leading to the Nasal Cannula
      3. Attach the 14 gauge catheter to a sidestream CO2 detector

V. Interpretation: Capnogram

  1. Periodic wave form with baseline low concentrations of airway CO2
    1. Increases to maximal CO2 concentrations during exhalation
  2. Normal gas exhange
    1. End-Tidal CO2 (pCO2 at end of expiration) is typically only 2-3 mmHg less than PaCO2 on the Arterial Blood Gas
    2. Regular wave pattern corresponding to exhalation, increasing etCO2 to 35 mmHg, then inhalation with etCO2 drop to 0 mmHg
  3. Abnormal gas exchange with increased dead space or increased CO2 production
    1. See causes below of abnormal PaCO2 - PetCO2
    2. Bradypneic hypoventilation (decreased Respiratory Rate)
      1. Increased etCO2 wave amplitude with decreased frequency of respiration waves
    3. Hypopneic hypoventilation (shallow respirations)
      1. Decreased etCO2 wave amplitudes with Respiratory Rate that may be decreased or normal
    4. Complete airway obstruction
      1. Flat etCO2 at 0 mmHg with loss of respiration waves

VI. Precautions

  1. Test EtCO2 monitor by blowing on the device prior to use (should result in a monitor wave form)
  2. Loss of EtCO2 wave form may be loss of pulse (instead of esophageal intubation)
    1. Check a pulse first, prior to removing an Endotracheal Tube
    2. With Chest Compressions, CO2 will be flat between breaths, and will significantly increase with breaths
      1. Suspect esophageal intubation if with Chest Compressions, EtCO2 spikes are not seen with breaths

VII. Causes: Abnormal PetCO2 (and abnormal PaCO2 - PetCO2 gap)

  1. Decreased PetCO2 (Increased PaCO2 - PetCO2 gap)
    1. Open Ventilator circuit
    2. Shallow respirations
    3. Obstructive Lung Disease
    4. Lung hyperinflation
    5. Decreased Cardiac Output
    6. Pulmonary Embolism
  2. Increased PetCO2
    1. Very high O2 inhaled concentrations (displaces CO2 from Hemoglobin)
    2. Increased CO2 production AND low Tidal Volumes or high Cardiac Output
      1. Hypermetabolism
      2. Metabolic Acidosis

VIII. References

  1. Marino (2014) ICU Book, 4th ed, Wolters-Kluwer, p. 334-5, 418-22
  2. Weingart and Orman in Herbert (2015) EM:Rap 15(8): 13-4

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