End-tidal CO2 Monitoring

By: Anne Bile RN

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 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. 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) (2) (3) (4)

production, transport, buffering and 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.

ETCO2 Monitoring Technologies

Colorimetry

Colorimetry is a chemical device that provides continuous, semiquantitative EtCO2 monitoring. This device has 3 color ranges A- Purple-EtCO2 < 0.5% B- Tan -EtCO2 0.5-2%

C- YellowEtCO2 >2% Normal EtCO2 is >4% hence the device should turn yellow when endotracheal tube is inserted in patients with intact circulation. Limitations of this device 1. It is a useful device to confirm endotracheal tube placement in patients not in cardiac arrest. In patients with cardiac arrest, a value of <0.5% EtCO2, the device is virtually of no use in confirming the endotracheal tube, because the tube could be in the esophagus or that the circulation is not bringing enough CO2 to the lungs. In non-arrest patients the device is 100% sensitive, while it is 69% in patients with cardiac arrest. 2. 2. The membrane can turn yellow (implies EtCO2 > 2%) when the device is contaminated with acidic substances like gastric acid, Lidocaine-HCl, epinephrine HCl or if the person had a carbonated beverage immediately prior to intubation. 3. 3.The device is unable to give a reading if it is clogged with secretions, or the device broken.

INFRARED CAPNOMETER with Zoll M-Series

Our preferred method 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 absorbance is proportional to the concentration of CO2 in the gas sample. The gas samples can be analyzed by the mainstream (in-line) or side stream (diverting) techniques.

Capnography versus Pulse Oximetry Capnography provides an immediate picture of patient condition. Pulse oximetry is delayed. Hold your breath. Capnography will show immediate

apnea, while pulse oximetry will show a high saturation for several minutes.

Circulation and Metabolism

While capnography is a direct measurement of ventilation in the lungs, it also indirectly measures metabolism and circulation. For example, an increased metabolism will increase the production of carbon dioxide increasing the ETCO2. A decrease in cardiac output will lower the delivery of carbon dioxide to the lungs decreasing the ETCO2. The capnogram wave form begins before exhalation and ends with inspiration. Breathing out comes before breathing in.

A to B is post inspiration/dead space exhalation, B is the start of alveolar exhalation, B-C is the exhalation upstroke where dead space gas mixes with lung gas, C-D is the continuation of exhalation, or the plateau(all the gas is alveolar now, rich in C02). D is the end-tidal value the peak concentration, DE is the inspiration washout. In a resuscitated patient, if you see the stabilized ETCO2 number significantly drop in a person with ROSC, immediately check pulses. You may have to restart CPR.

The graph below demonstrates three episodes of ROSC, followed by loss of circulation during a cardiac arrest:

ETCO2 in Asthma, COPD, and CHF

End-tidal CO2 monitoring on non-intubated patients is an excellent way to assess the severity of Asthma/COPD, and the effectiveness of treatment. Bronchospasm will produce a characteristic shark fin wave form, as the patient has to struggle to exhale, creating a sloping B-C upstroke. The shape is caused by uneven alveolar emptying.

End-Tidal Carbon Dioxide and Outcome of Out-ofHospital Cardiac Arrest

Robert L. Levine, M.D., Marvin A. Wayne, M.D., and Charles C. Miller, Ph.D N Engl J Med 1997; 337:301-306July 31, 1997

Abstract Article References Citing Articles (51) Letters

BACKGROUND
Survival after cardiac arrest occurring outside the hospital averages less than 3 percent. Unfortunately, the outcome of prolonged resuscitative attempts cannot be predicted. End-tidal carbon dioxide levels reflect cardiac output during cardiopulmonary resuscitation. We prospectively determined whether death could be predicted by monitoring end-tidal carbon dioxide during resuscitation after cardiac arrest.

Full Text of Background...

METHODS
We performed a prospective observational study in 150 consecutive victims of cardiac arrest outside the hospital who had electrical activity but no pulse. The patients were intubated and evaluated by mainstream end-tidal carbon dioxide monitoring. Our hypothesis was that an end-tidal carbon dioxide level of 10 mm Hg or less after 20 minutes of standard advanced cardiac life support would predict death.

Full Text of Methods...

RESULTS

There was no difference in the mean age or initial end-tidal carbon dioxide level between patients who survived to hospital admission (survivors) and those who did not (nonsurvivors). After 20 minutes of advanced cardiac life support, endtidal carbon dioxide (SD) averaged 4.42.9 mm Hg in nonsurvivors and 32.87.4 mm Hg in survivors (P< 0.001). A 20-minute end-tidal carbon dioxide value of 10 mm Hg or less successfully discriminated between the 35 patients who survived to hospital admission and the 115 nonsurvivors. When a 20-minute end-tidal carbon dioxide value of 10 mm Hg or less was used as a screening test to predict death, the sensitivity, specificity, positive predictive value, and negative predictive value were all 100 percent.
CONCLUSIONS

An end-tidal carbon dioxide level of 10 mm Hg or less measured 20 minutes after the initiation of advanced cardiac life support accurately predicts death in patients with cardiac arrest associated with electrical activity but no pulse. Cardiopulmonary resuscitation may reasonably be terminated in such patients.

Test Yourself
A.

B.

C.

D.

E.

F.

Answers
A. Tube in esophagus, Missed intubation B. Inadequate seal of ET tube, leak or tube is too small for patient

C. Hypoventilation-decreased respiratory rate, tidal volume or increase in metabolic rate or rapid rise in body temperature

D. Hyperventilation-increase respiratory rate, tidal volume or decrease in metabolic rate or decrease in body temperature E. Rebreathing- fault in exhalation valve, inadequate inspiratory flow, insufficient expiratory time

F. Obstruction in airway or breathing circuit, kinked tubing, increased secretions/mucus plug, bronchial spasm.