End Tidal CO2

 

Note:  I’d love to take credit for this lovely article on End Tidal CO2 - but I can’t.  I copied it off of some manufacturers website in the mid 90’s for my own use and, a while later when I went to look for it again, it was gone.  I don’t know who produced it, but it’s a great article.  So, I decided I’d risk the horrible lawsuit and post it anyway.  If anyone knows who the original authors are I would love to give them credit.  It just seemed such a shame to not have these great graphics on the internet anymore.  Please don’t write to me and ask me if you can use this information.  I stole it.  If you want to steal it too, go ahead, but don’t tell anyone I gave you permission to. [Marc]





Introduction


    ETCO2 is the partial pressure or maximal concentration of carbon dioxide (CO2) at the end of an exhaled breath, which is expressed as a percentage of CO2 or mmHg. The normal values are 5% to 6% CO2, which is equivalent to 35-45 mmHg. CO2 reflects cardiac output (CO) and pulmonary blood flow as the gas is transported by the venous system to the right side of the heart and then pumped to the lungs by the right ventricles. When CO2 diffuses out of the lungs into the exhaled air, a device called capnometer measures the partial pressure or maximal concentration of CO2 at the end of exhalation. During CPR, the amount of CO2 excreted by the lungs is proportional to the amount of pulmonary blood flow.



Discussion of Theory/Pathophysiology


    To understand the significant value of ETCO2, one needs to be familiar with the following:


(1) normal physiology of CO2,

(2) principle determinants of ETCO2,

(3) CO2 gradient with normal VQ relationship,

(4) ETCO2 analyzer (capnometer), and

(5 limitations of ETCO2 measurements.


    ETCO2 represents the partial pressure or maximal concentration of CO2 at the end of exhalation. CO2 reflects cellular metabolism. There are four main stages of normal physiology of CO2:


(1) production,

(2) transport,

(3) buffering and

(4) elimination.


Production:   

    CO2 is a metabolic byproduct of aerobic cell metabolism. As the intracellular CO2 increases, CO2 diffuses out into the tissue capillaries and is carried by the venous circulation to the lungs, where it diffuses from pulmonary capillaries into the alveoli. The partial pressure of CO2 (PaCO2) of venous blood entering pulmonary capillaries is normally 45 mmHg; the partial alveolar pressure of CO2 (PACO2) is normally 40 mmHg. The pressure difference of 5 mmHg will cause all the required CO2 to diffuse out of pulmonary capillaries into the alveoli.



Transport:

    The second stage is CO2 transport, which is a way of maintaining the CO2 tension of arterial blood at approximately 35-45 mmHg despite high CO2 production.


Buffering:

    The third stage is where the buffer action of hemoglobin and pulmonary blood flow maintain the normal level of CO2 tension by eliminating the excess CO2. CO2 can either be carried, dissolved or combined with water (H20) to form carbonic acid (H2CO3), which can dissipate to hydrogen ions (H+) and bicarbonate ions (HCO3-): (CO2 + H20 <=> H2CO3 <=> H+ + HCO3-). The hydrogen ions are buffered by hemoglobin, and the bicarbonate ions are transported into the blood. This mechanism accounts for 90% of CO2 transport.


Elimination:

    The fourth stage involves CO2 elimination by alveolar ventilation under the control of the respiratory center. This process allows the diffusion of CO2 from blood to the alveoli where the partial alveolar pressure of CO2 is lower than the tissue pressure.


    During normal circulatory condition with equal VQ relationship, PACO2 is closely comparable to PaCO2 and ETCO2; therefore, PaCO2 is equivalent to ETCO2. The difference between PaCO2 and ETCO2 is known as the CO2 gradient. The normal ETCO2 is about 38 mmHg at 760 mmHg of atmosphere with less then 6 mmHg gradient between PaCO2 and ETCO2.


The principle determinants of ETCO2 are:

(1) alveolar ventilation,

(2) pulmonary perfusion (cardiac output) and

(3) CO2 production.


During acutely low cardiac output state as in cardiac arrest, decreased pulmonary blood flow becomes the primary determinant resulting in abrupt decrease of ETCO2. Changes in alveolar ventilation can also influence ETCO2 as PACO2 closely approximates PaCO2 and ETCO2. If ventilation and chest compressions are constant with the assumption that CO2 production is uniform, then the change in ETCO2 reflects the changes in systemic and pulmonary blood flow. Ultimately, ETCO2 can be used as a quantitative index of evaluating adequacy of ventilation and pulmonary blood flow during CPR.



ETCO2 Monitoring Technologies


    One way of measuring ETCO2 is with the infrared capnometer, which contains a source of infrared radiation, a chamber containing the gas sample, and a photodetector. When the expired CO2 passes between the beam of infrared light and photodetector, the absorbence is proportional to the concentration of CO2 in the gas sample. The gas samples can be analyzed by the mainstream (in-line) or sidestream (diverting) techniques.



EtCO2 Production Stages




Capnography Depicts Respiration




Physiologic Factors Affecting EtCO2 Levels




Normal Values




Arterial to End Tidal CO2 Gradient




Deadspace




Ventilation - Perfusion Relationship: 1




Ventilation - Perfusion Relationship: 2




Capnogrpahy vs. Capnometry




The Capnogram



The Normal Capnogram Waveform










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2009