A capnometer is a device that measures carbon dioxide (CO2) concentrations in respired gases.
How does it Work?
How does it Work?
The end tidal Co2 can be measured by a mass spectrometer or an infrared analyser, which is attached to the ET tube. It measures the amount of infrared light absorbed by the Co2 in the sample of gas. This is displayed by a wave form called a capnogram or capnograph. 
Capnography comprises the continuous analysis and recording of carbon dioxide concentrations [CO2] in respiratory gases. Although the terms capnography and capnometry are sometimes considered synonymous, capnometry suggests measurement (ie, analysis alone) without a continuous written record or waveform.
Capnography comprises the continuous analysis and recording of carbon dioxide concentrations [CO2] in respiratory gases. Although the terms capnography and capnometry are sometimes considered synonymous, capnometry suggests measurement (ie, analysis alone) without a continuous written record or waveform. An infrared light beam with a narrow wavelength of light (4.3 µm) is projected through a gas sample and the intensity of the transmitted light measured, the light absorbed being dependent on the concentration of CO2 molecules in the sample.
Two types of capnometer are available that use different methods of gas sampling. Sidestream capnometers withdraw a continuous sample of gas through a capillary tube from the patient’s airway to the monitor. A water trap removes particles of water before measurement takes place. A disadvantage is that the narrow lumen of the sampling tube may become obstructed with pulmonary secretions or condensate. Mainstream capnometers employ a special breathing-circuit cuvette that is placed directly in the airway. The cuvette houses an infrared light source and photodetector and is heated to prevent condensation. Because there is no sampling system this capnometer has a fast response. The major disadvantage is the size and weight of the cuvette in the patient’s airway.
Capnography allows visual inspection of changes in CO2 concentration by means of a waveform display or paper recording. The CO2 waveform can be divided into segments that represent different phases of the respiratory cycle. At the start of normal expiration gas is expelled from the anatomic dead space and therefore contains very low CO2 concentrations. As more perfused alveoli empty, the increasing proportion of alveolar to dead space gas results in a greater concentration of exhaled CO2. Next, the synchronous emptying of areas with different ventilation-perfusion ratios and CO2 concentrations produces a nearly constant CO2 concentration, called the alveolar plateau. The end-tidal CO2 concentration (PETCO2) closely approximates the mean alveolar concentration when the alveolar plateau is achieved. At this point the difference between the PETCO2 and the arterial CO2 tension (PaCO2) is minimal, and the PETCO2 reflects the PaCO2. During healthy respiration the PETCO2 is an underestimate of the PaCO2 by less than 4 mm Hg, and a slightly positive PaCO2-PETCO2 gradient is therefore produced. Finally, with inspiration the CO2 concentration decreases rapidly to the baseline level, since there is no CO2 in the inspired gas.
In the case of pulmonary parenchymal disease the PETCO2 is the sum of the alveolar CO2 tensions from areas of widely differing ventilation-perfusion ratios and emptying times. Increased positivity of the PaCO2-PETCO2 gradient occurs because of the continued ventilation of alveoli that are no longer perfused (i.e., there is an enlargement of the regions of the lung with high ventilation-perfusion ratios). Other conditions that might lead to increased positivity of the gradient are hypovolemia with decreased pulmonary artery pressure, excessive positive end-expiratory pressure with increased alveolar pressure, pulmonary vascular occlusive disease and venous air embolism.
Changes in PETCO2 must be interpreted with extreme caution. A sudden decrease may indicate ventilator disconnection, a leakage in the system, an obstructed endotracheal tube, sudden hypotension, sudden hyperventilation or a massive pulmonary embolus. A gradual decline could be a sign of hyperventilation, reduced pulmonary perfusion or decreased CO2 production. A sudden increase in the PETCO2 may result from an injection of sodium bicarbonate, a sudden release of a tourniquet or a sudden increase in cardiac output. A gradual increase could indicate a greater production of CO2 or hypoventilation. Esophageal intubation would result in the total absence of a waveform. Therefore, although the analysis of respired gases is continuous it is greatly influenced by the differences in the ventilation-perfusion ratios in various regions of the lung, the total CO2 production and the total alveolar ventilation. Unfortunately, in the critically ill patient these variables may not be stable; hence, monitoring the PETCO2 may not provide a good warning of changes in the PaCO2 or be a substitute for ABG sampling during adjustments of or weaning from mechanical ventilation.
Clinical Capnometry
Clinical Capnometry
PETCO2 values may allow monitoring of changes in the PaCO2 of the healthy, hemodynamically stable patient but not in the critically ill patient, because the PETCO2 also reflects changes in pulmonary perfusion and dead space ventilation.A significant change in the PETCO2 may indicate that determination of the PaCO2 by means of ABG analysis is required; however, a constant PETCO2 does not ensure a constant PaCO2. Trends in the PETCO2 in the critically ill patient are often misleading because of the wide variability in the PaC02-PETCO2 gradient in the individual patient (with ventilator changes alone).
The routine use of capnometry as a substitute for PaCO2 measurement by means of ABG analysis or as a PaCO2 trend monitor in the intensive care unit should be discouraged.
The availability of a capnometer may be desirable to some physicians in intensive care units for other specific functions; for example, to confirm esophageal intubation, to document a changing ventilation-perfusion ratio through a changing PaCO2-PETCO2 gradient or to demonstrate restoration of the circulation after cardiopulmonary arrest and resuscitation.
Clinical Significance
Clinical Significance
Co2 is formed in the body cells as a product of metabolism, transported by the blood and excreted by the lungs. Therefore changes in exhaled Co2 may reflect changes in metabolism, circulation, respiration the airway or breathing system function.
Capnography is useful in the following Circumstances
Capnography is useful in the following Circumstances
To provide evidence of the correct placement of the ET. tube. This is especially important in a noisy A&E department.
To detect malignant hyperpyrexia. A massive increase in Co2 production is caused by increased muscle metabolism. This increase occurs early before the rise in temperature. Early detection of this is one of the most important reasons for routinely monitoring ETCo2 , post ingestion of ecstasy.
To detect air, fat or pulmonary emboli. A massive decrease in ETCo2 occurs as a result of increased dead space.
For routine monitoring of the adequacy of ventilation and the effects of IPPV. Hypoventilation and hyperventilation may be detected and can be confirmed by ABG analysis.
To assess the effectiveness of CPR. if no effective circulation is present Co2 may not be present in the lungs. The capnograph is not susceptible to the mechanical artefacts associated with chest compression like the ECG monitor and chest compressions do not have to be interrupted to assess circulation.
However if high dose adrenaline is used ETCo2 is not a good indicator of resuscitation methods.
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