![]() ![]() ![]() Might be measured directly from the breathing circuit (mainstream) or sucked out of the circuit in a sampling tube (sidestream).Important to note that the waveform, and values for ETCO2 are very different in the spontaneously breathing patient, and we’ll come back to that later. Can be measured from a breathing circuit attached to an invasive airway device e.g supraglottic airway or endotracheal tube, or from a number of methods in the spontaneously breathing patient, such as a specific nasal cannula, or a sampling tube attached to an oxygen mask.Usually by infra-red absorption- CO2 absorbs infra-red light in a manner proportional to its concentration in the sampled gas.Global ventilation failure e.g airway obstruction, hypoventilation esp where tidal volume is very low- dead space is fixed, so as a proportion of each breath it gets higher as tidal volume reduces until there is minimal ALVEOLAR ventilation.atelectasis: collapse of alveoli from failure to expand, or absorption of the air out of the alveoli without replacing it.pneumonia and pulmonary edema, pulm haemorrhage (alveoli filled with fluid).Failure of alveolar gas to be transported out of the lungs because alveoli are perfused but not ventilated (shunt):.Failure of venous CO2 to cross to ventilated alveoliĪlveolar dead space- alveoli are ventilated but not perfusedĬlassically low cardiac output states, PE, etc.Loose connections, not having nasal prongs up nose, dilution with high oxygen flows (partic when using nasal prongs) What causes a discrepancy between arterial and ETCO2? What we are assuming when we ask ETCO2 to substitute for arterial CO2 is that there is normal matching of ventilation to perfusion occurring in the lungs, so that all the mixed venous CO2 returning to the lungs from respiring tissue can equilibrate with alveolar gas and be eliminated via ventilation.They ARE however filling with gas during breaths, and as such gas from this dead space DILUTES the gas containing CO2 that has come predominantly from the alveoli. So the trachea and first few generations of bronchi do not participate in gas exchange and are known as the dead space. Why is this? CO2 is only found in parts of the lung which participate in gas exchange, i.e are perfused with blood. In healthy people, ETCO2 is usually 0.5-1kPA LOWER than the arterial value.In non-brain injured patients, high arterial CO2 can lead to a respiratory acidosis, and low pH values are harmful to most body tissues, in particular the clotting cascade (because of its reliance on enzymes, which function best in a narrow range of pH), and cardiac contractility. What we’re REALLY interested in is arterial CO2 as this is the clinically significant value in a number of clinical scenarios for example in the brain-injured patient, we want to keep arterial CO2 values normal as we know that this determines the state of cerebral vasoconstriction or dilation, and thus affects ICP.Much better than pulse oximetry, because of the difference in lag time between clinical change occurring and being able to see it on the monitor- less than 3 seconds for sidestream capnography, compared to up to 90s for pulse oximetry. ![]() It is still extremely useful in prehospital care, but we just have to remember that an abnormal trace or value may be caused by problems with one or more of those systems i.e circulation, gas exchange, ventilation (rarely tissue metabolism).Brilliant monitor in anaesthesia in that in elective cases, we start off with healthy patients are looking for deviations from the norm- and a normal ETCO2 trace tells you that all those components are functioning.Gas in and out of the lung to excrete the CO2.Transfer of CO2 between the blood and the air in the lung.Circulation & cardiac output to carry that CO2 to the lungs in blood.Metabolically active tissue to produce CO2.To get a measurement the following systems need to be functioning:.% or partial pressure of carbon dioxide measured somewhere near the mouth at the end of a normal exhalation (hence end tidal, end of tidal volume breath).
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