II. Mechanism
- CO2 absorbs infrared light
- CO2 detector circuit
- Phototransmitter emits infrared light
- Carbon dioxide present in the airway absorbs infrared light in proportion to its airway concentration
- Photodetector receives the light not absorbed by carbon dioxide
III. Preparations
- Ventilator measurement of EtCO2
- Non-ventilated patients
- Commercial devices (e.g. Salter divided Nasal Cannula)
- Modified standard Nasal Cannula
- Block short tubing connecting the two nasal prongs on the cannula (e.g. with cotton or external clamp)
- Insert 14 gauge, 2 inch angiocatheter into one of the two tubes leading to the Nasal Cannula
- Attach the 14 gauge catheter to a sidestream CO2 detector
IV. Interpretation: Capnogram
- Periodic wave form with baseline low concentrations of airway CO2
- Increases to maximal CO2 concentrations during exhalation
- Normal gas exhange
- End-Tidal CO2 (pCO2 at end of expiration) is typically only 2-3 mmHg less than PaCO2 on the Arterial Blood Gas
- Abnormal gas exchange with increased dead space or increased CO2 production
- See causes below of abnormal PaCO2 - PetCO2
V. Precautions
- Test EtCO2 monitor by blowing on the device prior to use (should result in a monitor wave form)
- Loss of EtCO2 wave form may be loss of pulse (instead of esophageal intubation)
- Check a pulse first, prior to removing an Endotracheal Tube
- With Chest Compressions, CO2 will be flat between breaths, and will significantly increase with breaths
- Suspect esophageal intubation if with Chest Compressions, EtCO2 spikes are not seen with breaths
VI. Causes: Abnormal PetCO2 (and abnormal PaCO2 - PetCO2 gap)
- Decreased PetCO2 (Increased PaCO2 - PetCO2 gap)
- Open Ventilator circuit
- Shallow respirations
- Obstructive Lung Disease
- Lung hyperinflation
- Decreased Cardiac Output
- Pulmonary Embolism
- Increased PetCO2
- Very high O2 inhaled concentrations (displaces CO2 from Hemoglobin)
- Increased CO2 production AND low Tidal Volumes or high Cardiac Output
- Hypermetabolism
- Metabolic Acidosis
VII. Indications
-
Cardiac Arrest
- Monitoring for Return of Spontaneous Circulation (ROSC)
- Monitoring Chest Compressions for adequacy
- Prognosis in Resuscitation (PetCO2 <15-20 for >20 min of CPR is associated with poor chance of ROSC)
-
Cardiac Output monitoring
- PetCO2 correlates well with Cardiac Output
- Monitoring fluid Resuscitation response
-
Procedural Sedation
- Monitors ventilation during Procedural Sedation
- Detects apnea well before Oxygen Saturation falls
- Arterial PaCO2 monitoring surrogate
- Difference between PaCO2 to PetCO2 should remain constant until other parameters change (e.g. Ventilator settings)
- Recheck ABG when Ventilator settings change to re-calculate the PaCO2-PetCO2 gap
- End-Tidal CO2 is significantly lower than PaCO2 when alveolar dead space is high
- ICU complication monitoring (for sudden decrease in End-Tidal CO2)
- Alveolar hyperinflation (high Tidal Volume or excessive PEEP)
- Endotracheal Tube migration (e.g. right mainstem Bronchus)
- Acute Pulmonary Embolism
- Acute Pulmonary Edema
- Pneumonia
-
Ventilator Weaning
- Arterial PaCO2 monitoring surrogate (see above)
- PetCO2 increases with failed weaning and increased work of breathing (increasing exhaled CO2)
- PetCO2 decreases with Bellows Failure (respiratory Muscle Weakness) as patient exhausts in failed weaning attempt
VIII. References
- Marino (2014) ICU Book, 4th ed, Wolters-Kluwer, p. 334-5, 418-22
- Weingart and Orman in Herbert (2015) EM:Rap 15(8): 13-4