Volumetric capnography is the graphical representation of the partial pressure of carbon dioxide (CO2) versus exhaled volume. This measurement is made noninvasively at every breath by a combination of flow and CO2 sensors, which are positioned together at the Y-piece of the ventilator circuit and well synchronized. Volumetric capnography provides much more information than time capnography, primarily about the metabolism, cardiovascular function, ventilation, and ventilation/perfusion (V̇/Q̇) ratio.
- Volumetric capnography is the graphical representation of the partial pressure of carbon dioxide (CO2) versus exhaled volume, and provides more information than time capnography.
- A volumetric capnogram is divided into three phases that correspond with the changing dynamics of gas as the lung empties.
- A number of physiological variables can be measured and calculated from volumetric capnography, including anatomical or airway dead space, alveolar dead space, end-tidal CO2, the volume of CO2 exhaled at each breath, and the slope of Phase III.
- These variables provide information about the metabolism, cardiovascular function, ventilation, and the ventilation/perfusion (V̇/Q̇) ratio.
The volumetric capnogram is divided into several phases that correspond with the changing dynamics of gas as the lung empties (1, 2):
- Phase I is the first gas exhaled that comes from the conducting airways and contains no CO2.
- Phase II is shaped like an S with a rapid increase in CO2. This phase represents gas exhaled from conducting airways mixed with gas from fast-emptying alveoli.
- Phase III is plateau-shaped with a positive slope. This phase represents gas exhaled from the alveoli, and the slope represents the changing time constant of the emptying alveoli; i.e., alveoli with a low V̇/Q̇ ratio empty last and contain the highest amount of CO2 (3).
From volumetric capnography, a number of physiological variables can be measured and calculated:
- The anatomical or airway dead space (VDaw in ml) is measured as the volume from the beginning of exhalation through to a vertical line that bisects Phase II (4). Based on VDaw, the ratio VDaw/VT (%), the alveolar ventilation (V’alv in ml= VT VDaw), and the alveolar minute ventilation (V’alv in ml/min= VDaw x respiratory rate) can be calculated. The physiological dead space is the sum of VDaw and alveolar dead space (VDalv in ml). VDalv can be calculated using the measurement of PaCO2 and the Bohr-Enghoff equation, and corresponds with the area between the volumetric capnogram and the horizontal line of PaCO2 (5, 6).
- End-tidal CO2 (PetCO2 in mmHg) is measured at the end of Phase III and represents the CO2 content of the alveoli with the lowest V̇/Q̇ ratio. PetCO2 is usually several mmHg lower than PaCO2; the CO2 gradient (PaCO2-PetCO2) reflects the V̇/Q̇ inequalities (7).
- The volume of CO2 exhaled at each breath is calculated as the area underneath the curve of the volumetric capnogram (VeCO2 in ml). VeCO2 multiplied by the respiratory rate equals the total CO2 exhaled per minute, which is assumed to be equal to CO2 production (V’CO2 in ml/min) in a steady, stable condition of circulation and ventilation.
- The slope of Phase III represents V̇/Q̇ mismatching (SlopeCO2 in %CO2/l). Airflow obstruction and lung inhomogeneity increase the slope of Phase III (1, 3, 8).
Metabolism: If the cardiovascular function and ventilation remain stable, a change in V’CO2 represents a change in CO2 production, i.e., a metabolic change. V’CO2 increases in the case of fever, sepsis, shivering, seizures, bicarbonate infusion, hyperthyroidism, or insulin therapy. The first symptom of sepsis is generally an increase in V’CO2 that occurs before the onset of fever. Conversely, V’CO2 decreases in the case of hypothermia, sedation, paralysis, or brain death. When the patient’s condition evolves to brain death, the cessation of brain perfusion may be demonstrated by a sudden decrease in V’CO2.
Cardiovascular function: If CO2 production and ventilation remain stable, V’CO2 changes according to cardiac output and lung perfusion. Therefore, V’CO2 increases in the case of peripheral vasodilatation and cardiac output increase. An increase in V’CO2 during passive leg rising can probably be used as a predictor of fluid responsiveness (9). In addition, a PEEP-induced decrease in V’CO2 by more than 10% predicts volume responsiveness (10). Conversely, V’CO2 decreases in the case of low cardiac output, shock, and pulmonary embolism. In the case of pulmonary embolism, the CO2 gradient increases.
Ventilation: If CO2 production and cardiovascular function remain stable, a change in V’CO2 occurs as a change in alveolar ventilation. V’CO2 increases transiently in the case of hyperventilation and decreases transiently in the case of pulmonary edema, pneumothorax, V̇/Q̇ inequalities and ARDS. However, the time required for V’CO2 to return to baseline is shorter in the case of hyperventilation than in that of hypoventilation (7).
Ventilation/perfusion mismatching: If CO2 production, cardiovascular function, and ventilation remain stable, a change in ventilator settings that potentially modify the V̇/Q̇ ratio can be monitored using V’CO2. For example, an increase of PEEP in an ARDS patient may recruit and homogenize the lung on the one hand, but may impair lung perfusion on the other. The net effect on ventilation/perfusion can be assessed by the rapid change in VeCO2 and SlopeCO2 (11). In morbidly obese patients, the highest dynamic compliance during decremental PEEP titration after a recruitment maneuver occurs at the PEEP level producing the lowest SlopeCO2 (12).
Volumetric capnography is available as an optional feature on almost all Hamilton Medical ventilators*. The volumetric capnogram can be displayed on the screen and the ventilator automatically calculates VDaw, VDaw/VTe, V’alv, PetCO2, SlopeCO2, VeCO2, and V’CO2 at every breath.
* Not available on HAMILTON-MR1
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- Fletcher R. Deadspace, invasive and non-invasive. Br J Anaesth 1985; 57:245-249.
- Fowler WS. Lung function studies III: Uneven pulmonary ventilation in normal subjects and in patients with pulmonary disease. J Appl Physiol 1949; 2:283-299.
- Fowler WS. Lung function studies II: The respiratory dead space. Am J Physiol 1948; 154:405-416.
- Bohr C. Ueber die Lungenathmung. Skand Arch Physiol 1891; 2:236-268.
- Enghoff H. Volumen inefficax. Upsala Lakaref Forh 1938; 44:191-218.
- Kreit JW. Volume Capnography in the Intensive Care Unit: Physiological Principles, Measurements, and Calculations. Ann Am Thorac Soc. 2019 Mar;16(3):291-300.
- DuBois AB, Fowler RC, Soffer A, Fenn WO. Alveolar CO2 measured by expiration into the rapid infrared gas analyzer. J Appl Physiol 1952; 4:526-534.
- Monnet X, Bataille A, Magalhaes E, Barrois J, Le Corre M, Gosset C, Guerin L, Richard C, Teboul JL. End-tidal carbon dioxide is better than arterial pressure for predicting volume responsiveness by the passive leg raising test. Intensive Care Med 2013; 39:93-100.
- Tusman G, Groisman I, Maidana GA, Scandurra A, Martinez Arca J, Bohm SH, Suarez-Sipmann F. The sensitivity and specificity of pulmonary carbon dioxide elimination for noninvasive assessment of fluid responsiveness. Anesth Analg 2016; 122:1404-1411.
- Tusman G, Suarez Sipmann F, Bohm SH, Borges JB, Hedenstierna G. Capnography reflects ventilation/perfusion distribution in a model of acute lung injury. Acta Anaesthesiol Scand 2011; 55:597-606.
- Bohm SH, Maisch S, von Sandersleben A, Thamm O, Passoni I, Martinez Arca J, Tusman G. The effects of lung recruitment on phase III slope of volumetric capnography in morbidly obese patients. Anesth Analg 2009; 109:151-159.
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