Capnography

1

What is capnometry?

Capnometry is a monitor which detects and measures expired carbon dioxide (CO ₂ ). Capnometry can be qualitative where the device changes color when CO ₂ is detected, or quantitative where the device measures the expired CO ₂ concentration. The capnogram is a waveform tracing of the quantified CO ₂ concentration over time. Interpreting the capnography waveform can be helpful with troubleshooting equipment problems and assessing the patient’s physiology.

2

Describe the most common method of gas sampling/analysis and the associated problems.

Sidestream capnography devices aspirate gas (typically 50–250 mL/min), usually from the Y-piece of the circuit, and transport the gas via a small-bore tubing to the analyzer by suction. Sampling can also be performed from a nasal cannula; however, because of room air entrainment causing dilution of the CO ₂ concentration, sampling directly from the circuit in an intubated patient provides qualitatively and quantitatively a better sample than nasal cannula. Problems with CO ₂ measurement include a finite delay, until the results of the gas sample are displayed and possible clogging of the tubing with condensed water vapor or mucus. Infrared spectrography is the most common method of CO ₂ analysis. Because CO ₂ absorbs infrared radiation at a specific wavelength (4.25 μm), Beer’s law can be used to calculate the CO ₂ concentration by measuring the amount of radiation absorbed at this specific wavelength.

3

Why is measuring end-tidal carbon dioxide important?

Measuring end-tidal carbon dioxide (ETCO ₂ ) is an important standard of American Society of Anesthesists monitoring. Short of bronchoscopy, CO ₂ monitoring is considered the best method to verify correct endotracheal tube (ETT) placement. ETCO ₂ is dependent upon many important physiological processes, such as metabolic activity, cardiac output, and ventilation. It is often used to assess the following:

• ETT placement

• Respiratory ventilation

• Cardiac output

• Hypermetabolism (e.g., malignant hyperthermia)

4

How well does ETCO ₂ correlate with PaCO ₂ ?

Because CO ₂ can easily diffuse between blood and alveoli approximately 20 times faster than oxygen (O ₂ ), alveolar CO ₂ (partial pressure of carbon dioxide [PACO ₂ ]) readily reaches equilibrium with blood CO ₂ at the level of the alveoli. Recall, O ₂ gas exchange at the alveoli is primarily diffusion dependent, whereas CO ₂ is perfusion dependent. Therefore the PACO ₂ in a poorly or nonperfused alveolus (i.e., alveolar dead space) will not reach equilibrium with blood CO ₂ in the pulmonary vascular bed. In healthy lungs, this alveolar dead space will dilute expired CO ₂ , causing a small 3 to 5 mm Hg drop in ETCO ₂ , compared with arterial blood CO ₂ (PaCO ₂ ). It is important to emphasize that any process which increases alveolar dead space (i.e., asthma, chronic obstructive pulmonary disease [COPD], pulmonary embolism, cardiac arrest) will cause a “drop in ETCO ₂ ” and a wider gradient between PaCO ₂ and ETCO ₂ .

5

How can ETCO ₂ be used to assess cardiac output?

Because CO ₂ is perfusion dependent, anything that decreases perfusion will decrease ETCO ₂ . Stated another way, well-perfused and well-ventilated alveoli have a ventilation/perfusion ( $\dot{V}$ / $\dot{Q}$ = 1) and alveolar dead space occurs when ventilation exceeds perfusion ( $\dot{V}$ / $\dot{Q}$ > 1), such as in zone 1 of the lung or in diseases processes, such as COPD or asthma. However, decreased perfusion ( $\dot{Q}$ ) can also cause $\dot{V}$ / $\dot{Q}$ greater than 1, assuming no change in ventilation ( $\dot{V}$ ). Therefore any condition associated with decreased cardiac output, such as pulmonary embolism or cardiac arrest, will also cause an increase in alveolar dead space ( $\dot{V}$ / $\dot{Q}$ > 1) and a “drop in ETCO ₂ .”