End-tidal carbon dioxide (ETco₂) monitoring provides valuable information about CO₂ production and clearance (ventilation). Also called capnometry or capnography, this noninvasive technique provides a breath-by-breath analysis and a continuous recording of ventilatory status. In fact, it’s commonly called the “ventilation vital sign.”

By providing instantaneous feedback on the patient’s ventilation effectiveness, ETco₂ monitoring gives early warning of respiratory compromise. It also may reflect cardiac perfusion changes and has been used to indicate the effectiveness of chest compressions in cardiac arrest. What’s more, it confirms endotracheal tube placement and helps monitor ventilator circuit integrity.

A standard of care in the operating room for more than 25 years, ETco₂ monitoring is becoming a common adjunct in the intensive-care and procedural-care settings. In the prehospital arena, it provides immediate feedback on the patient’s ventilatory status.

Wherever ETco₂ monitoring is used, it can enhance patient safety—as long as bedside clinicians understand the interplay among ventilation, perfusion, and CO₂ production. Although the principles underlying ETco₂ monitoring have been known for many years, recent technological advances have made the technique feasible for routine clinical application. To fully optimize its use, clinicians must understand certain basic principles. This article explains these concepts, discusses ETco₂ waveforms, and describes the assessment capabilities of this monitoring meth­od. Although ETco₂ is used in non-intubated patients, here we focus on its use in patients with endotracheal intubation. Keep in mind that ETco₂ findings are interpreted within the context of physical and other traditional assessment methods.

The science behind the technique

CO₂ is a byproduct of cellular metabolism. Cells take in oxygen and glucose and release water, carbon dioxide, and energy. CO₂ plays an important role in acid–base buffering. Depending on blood pH at any given time, CO₂ converts either to carbonic acid (H₂CO₃, an acid) or to bicarbonate (HCO₃-, a base).

CO₂ exists in three primary states in the blood: as HCO₃– (70%), bound to hemoglobin (20%), and dissolved in the plasma (10%). As HCO₃-, CO₂ influences blood pH; direct CO₂ measurement indicates ventilatory effectiveness. Both pH and CO₂ are measured from arterial blood gas (ABG) samples. While ETco₂ monitoring doesn’t directly indicate acid-base balance, it can shed light on ventilation efficacy.

CO₂ combines with water to create H₂CO₃, which can degrade to bicarbonate, water, and CO₂. This process occurs in red blood cells, where HCO₃– is released back into the plasma ready to accept another hydrogen ion (H+), while CO₂ and H₂O are carried to the arterial-alveolar junction for release into the atmosphere. The lungs serve as a pump to promote the activity of ventilation.

Gas diffusion

Gases diffuse from areas of higher concentrations to areas of lower concentration. In the pulmonary artery, deoxygenated blood has a partial pressure of carbon dioxide (Pco₂) of approximately 46 mm Hg and a partial pressure of oxygen (Po₂) of roughly 40 mm Hg. As a result, oxygen from the alveolus (where Po₂ is about 100 mm Hg) diffuses into the blood, and CO₂ diffuses from the blood into the alveolus (where Pco₂ measures about 40 mm Hg). Because inspired air has negligible CO₂ amounts (less than 0.04%), exhaled CO₂ can be monitored and used as a correlate to assess CO₂ gas exchange and effective ventilation.

Ventilation/perfusion matching

ETco₂ reflects metabolism, circulation, and ventilation. In patients with normal pulmonary function, CO₂ (normally 35 to 45 mm Hg) and ETco₂ should correlate closely, with a deviation of about 2 to 5 mm Hg. Circulating blood CO₂ is slightly greater than exhaled CO₂ due to a ventilation-perfusion (.V/Q) mismatch. (Not all alveoli participate in gas exchange at a given time, resulting in some shunting.) In acutely ill patients, especially those on mechanical ventilators, pronounced changes in ventilation and/or perfusion may occur, causing a much greater disparity between arterial and end-tidal values. That’s why it’s important to know the patient’s arterial CO₂ baseline, track trends, and correlate ETco₂ values with ABG values in the event of sudden or dramatic deviations.

End-tidal clearance must be evaluated in the context of the patient’s perfusion status. Dead-space ventilation results in ventilated alveoli with insufficient perfusion, which leads to low ETco₂. This may result from such ventilatory problems as high mean airway pressure or inadequate exhalation time (resulting in overdistention), or from such circulatory problems as shock, massive fluid loss, or pump failure (resulting in hypotension). To visualize ventilation and perfusion, see Lung zones.

CO₂ production

Measured CO₂ also is influenced by CO₂ production. In critically ill patients, CO₂ production may increase from such conditions as sepsis, fever, seizures, agitation, and carbohydrate overloading. Because variances may occur over hours, ETco₂ values must be trended for clinical application.

Types of ETco₂ monitors

Three primary types of ETco₂ monitors are available: sidestream, main­stream, and Microstream^®. All have evolved to be lighter, more accurate, and easier to calibrate. Each type has certain advantages and limitations.

Sidestream monitors

Sidestream monitors rely on a separate monitor or analyzer connected to the patient’s airway by tubing. Gas samples are aspirated from exhaled gas flow via the ventilator circuit through a T-adapter and are read at the monitor. Sampling rates usually range from 150 to 200 mL/minute, making these monitors unsuitable for neonates. A slight delay in data retrieval may occur due to the lag time between airway and monitor. Sidestream monitors can be used with noninvasive ventilation and are relatively inexpensive when part of a monitoring package.

Mainstream monitors

With these monitors, a sampling window is inserted directly in-line with the ventilator circuit for CO₂ measurement. This allows a more rapid response time and requires a smaller amount of sample gas than sidestream monitoring. But mainstream monitors increase mechanical dead space, depending on size of the chamber used to collect a gas sample, while adding weight on the airway. Also, they can’t be used for noninvasive ventilation.

Microstream monitors

While sidestream and mainstream monitors rely on infrared absorption, the newest type of ETco₂ monitor uses molecular correlation spectrography for greater precision. The Microstream monitor has a rapid response time and may be used with both invasive and noninvasive ventilation. It’s commonly used in procedural areas, such as gastroenterology labs, where moderate sedation is administered. Its main limitations are cost and the need for a monitor separate from the bedside monitor or ventilator.

Interpreting ETco₂ monitoring data

Data obtained from ETco₂ monitoring depends on proper equipment function and is only as useful as the clinician’s ability to interpret and apply it. This section discusses ETco₂ waveforms and the assessment capabilities of ETco₂ monitoring.

ETco₂ values may be displayed solely as a numeric value (capnometry) or with a waveform (capnography). Waveforms may be time-based (CO₂ over time) or volume-based (CO₂ plotted over exhaled tidal volume). A time-based capnogram can provide useful information based on its morphology and phases; it’s commonly used in the clinical arena. (See Basic time-based capnogram)

Volume-based (expiratory) capnography yields a waveform with characteristic phases plotted over a known exhaled volume. (See Volume-based capnogram.) The CO₂ waveform relative to exhaled tidal volume allows calculation of physiologic dead-space components (alveolar plus anatomic), adding more depth to ETco₂ monitoring. To maximize its application, a Paco₂ reading should be obtained.

Clinical indices for increased arterial-to-ETco₂ gradients

In a state of perfect equilibrium, arterial and end-tidal CO₂ levels correlate on a 1:1 basis. But even in an ideal physiologic state, a difference of 2 to 5 mm Hg usually exists. Known as the arterial-to-etco2 gradient, this differential results from small amounts of dead-space ventilation (ventilation without perfusion) and a slight venous admixture.

The arterial-to-ETco₂ gradient widens in two basic conditions—increased physiologic dead space (anatomic dead space plus alveolar dead space) and low perfusion states.

• Anatomic dead space measures approximately 150 mL in an adult male and doesn’t change. Alveolar dead space may increase with chronic obstructive pulmonary disease, pulmonary embolism, and positive-pressure ventilation. Simply stated, alveolar pressures exceed perfusion pressure in some areas (such as lung zone I), contributing to decreased CO₂ ventilation.
• In low perfusion states, decreased blood passing by the alveoli and lower diffusion across the alveolar-arterial junction lead to exhaled gas with less CO₂. Common reasons for decreased perfusion include blood or fluid loss, cardiac pump failure, and profound systemic vasodilation.

When ventilation is effective, ETco₂ numbers are higher. When perfusion is poor, ETco₂ numbers are lower.

Obtaining and trending the arterial-to-ETco₂ gradient can provide valuable assessment data that help identify pulmonary and perfusion disorders. Periodically checking the arterial-to-ETco₂ gradient should be a routine part of ETco₂ monitoring. It ensures that the monitor is accurately indicating what’s happening in the blood and can provide useful information about changes in compliance, resistance, and ventilatory status. Be aware that equipment malfunction and contamination caused by wetness or leaks in the monitoring system may lead to inaccurate exhaled CO₂ measurement.

Waveform analysis

Clinicians’ ability to assess ETco₂ waveforms helps distinguish equipment malfunction from changes in the patient’s condition. The waveform should have distinct phases corresponding to exhaled CO₂. A change in or loss of these phases may indicate alterations in the monitoring system or the patient’s perfusion status. Of course, waveform monitoring can’t replace the use of sound clinical judgment in assessing a patient’s condition. (See Capnographic states)

Special indications for ETco₂ monitoring

In the field, monitoring ETco₂ during endotracheal-tube placement can verify correct tube placement and indicate tube dislodgement during transport. During cardiopulmonary resuscitation (CPR), adequate chest compressions generate a cardiac output of 17% to 27%, allowing CO₂ circulation for exhalation. ETco₂ and coronary artery perfusion pressures have a linear correlation. Thus, ETco₂ monitoring is a noninvasive way to measure coronary artery blood flow and return of spontaneous circulation during CPR; evidence suggests a persistently low ETco₂ value and a widened Paco₂-to-ETco₂ gradient during CPR are associated with poor outcomes.

Another use of ETco₂ monitoring is during procedural sedation and analgesia (PSA). Respiratory depression and airway obstruction are the primary causes of PSA-related adverse events; ETco₂ changes are the earliest indicators of airway compromise.

Researchers continue to explore the use of ETco₂ monitoring in such areas as metabolism and perfusion related to ketoacidosis and gastroenteritis, as well as for blind nasal intubation and optimizing endotracheal-cuff filling.

Many settings, many uses

ETco₂ monitoring yields significant information about a patient’s ventilation status when combined with thorough physical assessment. It can be used in a wide range of settings, from prehospital settings to emergency departments and procedural areas.

The authors work at the R Adams Cowley Shock Trauma Center at the University of Maryland Medical Center in Baltimore. Mark Bauman is nurse manager of the Trauma Acute Care Unit. Cindy Cosgrove is a senior Clinical Nurse I in the Neurotrauma Critical Care Unit.

References

Brochard L, Martin GS, Blanch L, et al. Clinical review: Respiratory monitoring in the ICU—a consensus of 16. Crit Care. 2012 Apr 36; 16(2):219.

Lah K, Križmari´c M, Grmec S. The dynamic pattern of end-tidal carbon dioxide during cardiopulmonary resuscitation: difference between asphyxial cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest. Crit Care. 2011;15(1):R13.

McSwain SD, Hamel DSS, Smith PB, et al. End-tidal and arterial carbon dioxide measurements correlate across all levels of physiologic dead space. Respir Care. 2010 Mar;55(3):288-93.

Porth CM, Matfin G. Pathophysiology: Concepts of Altered Health States. 8th ed. Phila­delphia: Lippincott Williams & Wilkins; 2010.

Walsh BL, Crotwell DN, Restrepo RD, (2011) Capnography/Capnometry during mechanical ventilation: 2011. Resp Care. 2011 Apr;56(4):503-9.

West JB, Dollery CT, Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures. J Appl Physiol. 1964 Jul;19:713-24.

Whitaker DK. Time for capnography—everywhere. Anaesthesia. 2011 Jul;66(7):544-9.