End-tidal CO2 Monitoring: Noninvasive Respiratory Monitoring for the Child in the ED

Author: Sharon E. Mace, MD, FACEP, FAAP, Associate Professor, Ohio State University School of Medicine; Faculty, MetroHealth Medical Center/Emergency Medicine Residency; Clinical Director, Observation Unit, Director, Pediatric Education/Quality Improvement, Cleveland Clinic Foundation, Cleveland, Ohio

Peer Reviewer: David Kramer, MD, FACEP, FAAEM, Program Director, Emergency Medicine Residency, and Vice-Chair, Department of Emergency Medicine, York Hospital, York, Pennsylvania

End-tidal CO2 monitoring has many clinical uses: confirmation of endotracheal tube placement, monitoring of intubated patients, or monitoring of children undergoing procedural sedation.

The ability to provide continuous confirmation of airway stability is critical in today's medical and legal environment. The inability of the physical examination to detect subtle changes in patient ventilation makes the use of this modality particularly critical during periods when the patient must be moved from the emergency department (ED) for diagnostic testing, such as computerized tomography, or sedated for procedures.

Familiarity with the uses, advantages, and limitations of this technology enables the ED physician to recognize clinical scenarios where end-tidal CO2 monitoring will provide a valuable adjunct to clinical care (e.g., endotracheal tube placement confirmation) and when the information provided must be interpreted cautiously (e.g., patients receiving cardiopulmonary resuscitation). The author provides a thorough review of the clinical indications, data interpretation, and limitations for end-tidal CO2 monitoring.

The Editor


End-tidal carbon dioxide (ETCO2) is the carbon dioxide (CO2) present in the airway at the end of expiration.1 ETCO2 monitoring is the noninvasive measurement of exhaled CO2.

Capnometry is the measurement and numerical display of the expired CO2 , and the capnometer is the machine that measures and displays the CO2 in a numeric form without a graphic waveform.2-3

Capnography is the measurement and graphic waveform display of the expired CO2 over time (e.g. throughout a given ventilatory cycle). The capnograph is the machine that measures and displays the CO2 level in both a numeric and graphic waveform.4 The graphic waveform displayed by a capnograph is called a capnogram.

There is a third type of CO2 monitoring device, probably more familiar to emergency physicians, used to confirm correct placement of an endotracheal tube.5 This is a colorimetric detector, which produces a color change in a chemically treated material in the presence of carbon dioxide.

Thus, there are three different techniques used to noninvasively monitor carbon dioxide during breathing or ventilation: 1) colorimetric qualitative devices (e.g., the Feneen or Nelcor disposable devices) and quantitative devices, 2) the capnometer, a device displaying a number, and 3) the capnograph, a machine that yields a waveform in addition to a numeric reading.

Clinical Uses of End-Tidal CO2 Monitoring

Verification of Endotracheal Tube Placement. One of the most widespread uses of ETCO2 monitoring is to determine endotracheal tube placement because undetected esophageal intubation can have disastrous results.6-8 Estimates of the incidence of misplaced or displaced oral endotracheal tubes range from 0-25% in prehospital intubations,11,14-23 to 10.6 % in the ED.11,12 Of anesthesia-related accidents resulting in brain injury or death, 15% were attributed to unrecognized esophageal intubation.15 Certain populations (e.g., pediatric patients/neonates) may have an even higher likelihood of misplaced endotracheal tubes.10,11,23-25 A 40-50% incidence of esophageal intubations has been documented in neonates in the neonatal intensive care unit.24,25 Also, practitioners with relatively less experience in intubation are reported to have higher rates of missed intubation.22,26-28

More recent studies have reported on the intubation success rate (i.e., first-pass successful intubation versus multiple attempts).24 Estimates of failed intubation vary greatly, but higher incidences of failed intubations occur with less experienced personnel (e.g., residents) and in high-risk populations (e.g., pediatric patients/ neonates).22,24-28 The occurrence of failed oral intubations ranges from 47% for basic emergency medical technicians (first attempt only),29 13.2-16% for paramedics (includes multiple attempts),30-32 3-35% for air ambulance personnel (paramedics/nurses) (includes first attempt equals only 35%; other percentages are multiple attempts),34-38 to 20-50% for residents (pediatric and emergency medicine specialties).24-26, 28,39 The first-pass success rates for oral intubation has ranged from 43% to 90%.26 Several recent anesthesia studies using various intubation techniques have noted a first-attempt successful intubation rate of 92% for American Society of Anesthesiologists' (ASA) class III or IV patients and 95.5% for ASA I or II patients.41-42

In summary, endotracheal intubation can be difficult, may not be successful on the first attempt, and if unsuccessful, can have catastrophic results. Therefore, a reliable method or technique for early detection of displaced or misplaced endotracheal tubes is highly desirable.

Clinical tests to confirm tracheal intubation— including breath sound auscultation, chest rise visualization, auscultation over the stomach, and fogging of the endotracheal tube— have some limitations.40-44 Unfortunately, none of these primary confirmation techniques are 100% reliable. Each has false-positive and false-negative findings in some patients.40-44 For this reason, secondary confirmation of endotracheal tube placement with an exhaled CO2 (end-tidal carbon dioxide) detection device and/or an esophageal detector device is recommended by the American College of Emergency Physicians,45 the American Heart Association,46-48 and the National Association of EMS Physicians,49 while mandatory secondary confirmation of endotracheal tube placement is advocated by many clinicians.44 There have been some studies indicating that the colorimetric ETCO2 devices are better than the esophageal detector device for secondary confirmation of endotracheal tube placement.40,43,51

Anesthesia, Procedural Sedation. The Society of Critical Care Medicine has recommended end-tidal CO2 monitoring be available for ventilated patients in the intensive care unit, and during anesthesia, capnography is considered a standard of care.52-56 Capnography is used to monitor patients undergoing procedural sedation and analgesia.57-60 The result of hypoventilation/apnea with accompanying hypercarbia is hypoxia, detected by a decrease in pulse oximetry. Prior to the drop in pulse oximetry, there is generally a rise in the end-tidal CO2 level.61 Use of capnography along with pulse oximetry should increase the safety of procedural sedation.62,63 A prospective observational study in an ED found that capnography could detect subclinical respiratory depression not detected by pulse oximetry alone.63 The criteria used were 1) an ETCO2 measurement greater than 50 mmHg, 2) an absolute change greater than 10 mmHg, or 3) an absent waveform.63

Cardiopulmonary Resuscitation (CPR). End-tidal CO2 monitoring has been used to monitor the effectiveness of CPR, correlated with coronary perfusion pressure and cardiac output during CPR, used to detect the return of spontaneous circulation, and as a tool to predict the likelihood of successful CPR.64-73 During CPR, decreased cardiac output results in decreased systemic and pulmonary blood flow with decreased delivery of CO2 to the lungs and thus, decreased CO2 elimination by the lungs resulting in a low ETCO2 level.64,65 The adequacy of chest compressions during CPR can be assessed by capnography.65 Several studies have used capnography to predict the likelihood of return of spontaneous circulation (ROSC) during CPR, with a rise in ETCO2 levels heralding ROSC.67-70 In one study, no patients with an ETCO2 measurement less than 10 mmHg during CPR survived.70 The survivors had an average ETCO2 level of 15 mmHg compared with an average ETCO2 level of 7 mmHg in the nonsurvivors group.70

Mechanical Ventilation. ETCO2 monitoring has been used to monitor ventilated patients.74-77 The specific capnogram can indicate various problems that can occur during mechanical ventilation from a kinking of the endotracheal tube to disconnected equipment, airway leaks, rebreathing expired air, and a patient "fighting the tube" signifying a need for additional sedative/paralytic agents (Figure 1).78-80 Capnography also has been used in ventilator management and to wean selected patients without parenchymal lung disease from mechanical ventilation in the intensive care unit or post anesthesia.74-80

Patients with Cardiopulmonary Disease. Capnography has been used to diagnose and monitor the response to therapy in patients with various cardiopulmonary diseases.76,,80,81 Many respiratory diseases have characteristic capnogram waveforms (Figures 2,3).4,78-82 In a patient with respiratory distress/failure, the classic capnogram appearance may provide a clue to the underlying pulmonary disease (Figures 2,3). The capnogram also can indicate the severity of the disease as with asthma (Figure 3).83 Capnography also has been used to monitor the response to treatment. As a patient improves, the appearance of the capnogram returns to a normal appearance. The capnograms of asthmatic patients have been noted to correlate with spirometry measurements.83 Capnography may be especially helpful in pediatric patients; it is noninvasive, painless, effort independent, and may decrease the need for arterial blood gas measurements.6,9,75,84

Patients with Other Diseases. In pediatric patients with seizures, capnography correlates with the pCO2 level and has been used to detect hypercarbia and the need for ventilatory assistance (Figure 3).85 End-tidal CO2 monitoring has been suggested as a way to help monitor head injured patients with increased intracranial pressure.86,87 End-tidal CO2 levels have been utilized successfully in the evaluation of sleep apnea patients, as recommended by the American Thoracic Society.88 In patients who can not be monitored or visualized directly (e.g., during an MRI procedure), ETCO2 monitoring, in addition to pulse oximetry, may be a useful adjunct.89

During Transport. Because the patient's ventilatory state can change during transport, constant evaluation using end-tidal CO2 monitoring may be extremely useful and has been recommended by the American Heart Association.90,91

Evaluation of Alveolar Dead Space in the Evaluation for Pulmonary Emboli. Interruption of pulmonary blood flow, as occurs with pulmonary emboli, will increase the alveolar dead space. Because there is less pulmonary arterial blood flow available for participation in gas exchange, the ventilation/perfusion (V/Q) ratio increases and less CO2 is present in the exhaled breath as reflected in a decreased end-tidal CO2. The larger the pulmonary emboli, the greater the V/Q abnormality, the greater the drop in perfusion, the greater the dead space increase, and the larger the drop in ETCO2 with a greater widening of the (PaCO2 – ETCO2) gradient.

These principles have been used to diagnose pulmonary emboli. The dead space (VD) to tidal volume (VT) ratio or VD/VT is calculated using the Bohr equation:

VD/VT = (PaCO2 - ETCO2)/PaCO2

The physiological dead space is computed from the mixed expired CO2 tension or ETCO2. A dead space less than 0.4 in a patient with previously normal lungs (e.g., no pulmonary disease such as COPD) has a negative predictive value of 96.7% for pulmonary emboli.92

Feeding Tube Placement. Capnometry has been used to verify feeding tube placement.93 An end-tidal CO2 detector was attached to the proximal end of the feeding tube, left in place for one minute, and the color change observed. If the color of the qualitative end-tidal CO2 detector remained purple, the feeding tube was correctly placed in the gastrointestinal tract. If the color of the ETCO2 detector was yellow or tan, the feeding tube was incorrectly placed in the airway.

Mechanisms of End-tidal CO2 Detectors

To understand the advantages, disadvantages, and limitations of end-tidal CO2 monitoring, a discussion of how detectors work is warranted.

Colorimetric Devices: Mechanism. The colorimetric end-tidal CO2 detectors are qualitative or semiqualitative devices that change color in the presence of exhaled CO2 (Table 1).

Table 1. Colorimetric End-tidal CO2 Detectors

A chemically treated pH sensitive foam indicator is placed in the device under a transparent cover that is embedded in a casing that serves as an endotracheal tube adapter. The device is placed between the endotracheal tube and the bag and changes from a purple color (CO2 absent) to a yellow color in the presence of CO2, confirming endotracheal tube placement. Various pneumonics have been devised for these colorimetric ETCO2 detectors:

Purple = Problem (no or little CO2 detected),
Tan = Think about a problem,
Yellow = Yes (CO2 detected)37 or
Yellow = Good as gold (CO2 detected).94

With the colorimetric devices, when the pH sensitive paper is exposed to CO2, hydrogen ions are formed, resulting in a color change in the paper according to the CO2 concentration. The color change is reversible and varies from breath to breath. A color scale is associated with the ETCO2 concentration:

"A" purple < 4 torr (< 0.5% CO2),
"B" tan 4-15 torr (0.5 – 2% CO2),
"C" yellow > 15 torr (> 2% CO2).

Capnometers and Capnographs: Mechanism. Quantitative measurement of CO2 concentration is performed by either mass spectrometry or infrared absorption spectrophotometry (Table 2).95.96 The advantage of mass spectrophotometry is that it can measure many gases from carbon dioxide to oxygen or nitrogen, and even anesthetic gases. The disadvantage is its high cost, therefore, its use usually is restricted to the operating suite and for research.

Table 2. Types of Carbon Dioxide Monitoring Devices

For clinical use, CO2 analysis generally is measured by infrared absorption spectrophotometry. With this method, a beam of infrared light is passed through the gas being sampled. Carbon dioxide molecules present in the path of light absorb some of the infrared light. The CO2 concentration of the sample is calculated by comparing the amount of infrared energy absorbed as the light is beamed through the sample with the amount of light absorbed by a CO2 reference cell.

The sampling techniques employed in infrared absorption spectrophotometry are either mainsteam or sidestream (Table 3 and Figure 4).78,95,96 With mainstream sampling, the sample measurement chamber is located in line with the patient's airway. The advantage of mainstream sampling is an almost instantaneous response time for readings. Unfortunately, mainstream sample chambers can add mechanical dead space to the airway adapter and tend to be fragile, easily damaged, bulky/clumsy, and add weight on the airway, which may cause a pull on the airway circuit. However, recent technological improvements have made mainstream sensors lighter, with less dead space, and more durable.

With sidestream sensors, a gas sample is withdrawn from the patient's airway and diverted by a sampling adapter and narrow-bore tubing to the capnograph (Figure 4B). Technical problems related to transport of the sample gas to a distant site for analysis creates the potential for partial obstruction or even occlusion of the tubing by secretions or water vapor as well as creating a delay in response time. Response time is primarily a function of the flow rate by which the sample gas is diverted to the capnograph. Very slow gas-sampling flow rates also may cause artifacts in the capnogram waveform.


End-tidal CO2 detectors are reliable in patients who have enough circulation to pump CO2-containing blood to the lungs for excretion. Patients in cardiopulmonary arrest have negligible systemic and pulmonary blood flow. Without sufficient blood flow, CO2 is not delivered to the lungs; therefore, CO2 in exhaled air is nonexistent. Thus, during CPR, there is the danger of a false-negative reading or a type I error.47 The endotracheal tube is in the correct position in the trachea, but no CO2 is exhaled (i.e., the colorimetric detectors remain a purple color) because no CO2 is transported to the alveoli to be excreted.

Conversely, if ETCO2 is detected (e.g., colorimetric device turns yellow), it is very likely that the endotracheal tube is in the airway. Detection of CO2 indicates that the endotracheal tube is in the airway but does not indicate the specific location or depth in the airway.

A dangerous false-positive result or type II error (e.g., colorimetric device turns yellow when the endotracheal tube is actually in the esophagus) may occur if the patient has recently ingested a carbonated beverage, resulting in the presence of CO2 in the esophagus.97-99 To avoid this possibility, ventilate six or more times following intubation, then check for ETCO2.100-101 Ventilating six or more times will permit the "cleansing" ventilations to eliminate CO2 by washing out any extraneous CO2 in the esophagus secondary to the ingestion of carbonated beverages.100-101

With the colorimetric devices, whenever an indeterminate reading occurs (e.g., a tan color) or if there is a fixed yellow discoloration, don't use the device. The pH sensitive paper in the colorimetric device may have been contaminated with acidic gastric contents, respiratory secretions, drugs (e.g., epinephrine), or humidity,102-106 Do not use any colorimetric device that produces a tan or yellow reading throughout the respiratory cycle, and replace it with another colorimetric device.102,106

Colorimetric devices have a limited life span. They are accurate for two hours of continuous use, for 24 hours of intermittent use, and only 15 minutes if humidified oxygen or nebulized aerosols are used; the colorimetric devices are affected by humidity.1,106,107

Another limitation is the failure of the colorimetric devices to detect hypercarbia or hypocarbia. A false-negative result (e.g., remains purple when in the trachea) could occur when severe hypocarbia exists. Colorimetric devices detect a minimum level of ETCO2. Clinical states that result in extremely low exhaled CO2 levels below the threshold detected by the colorimetric devices may yield a false-negative result. In addition to cardiac arrest, other conditions that may result in a false-negative result include severe airway obstruction, pulmonary edema, and severe hypocarbia.99,108 False-negative results occur in approximately 25% of all intubated cardiac arrest patients.109

The device should not be used continuously in small infants since the dead space from the end-tidal CO2 detector may result in the rebreathing of expired air.110 The recommendation has been to avoid using the adult size end-tidal CO2 detectors in children weighing less than 15 kg or younger than 2 years because the detector's large dead space (38 mL) may cause dilution of the infant's small tidal volume with the inability to detect CO2 (yielding a false-negative reading). However, now there are colorimetric end-tidal CO2 devices with a dead space of 3 mL for use in infants weighing less than 1 kg.111 A recent study indicated that pediatric devices can be used successfully in neonates/ infants weighing less than 15 kg or younger than 2 years.93,95

Numeric capnometry is less popular then either the colorimetric or the waveform capnography devices for several reasons.90,112 It costs more than the disposable colorimetric devices, can be contaminated by secretions/fluids, which may affect the accuracy, and most people find it easier to remember a color (e.g., "gold is good") rather than the normal range of ETCO2 numbers.93,109 Furthermore, the capnography waveform may yield more clinically relevant information than the colorimetric or numeric capnometer.78,87,114

There is also a Capno-Flo resuscitation bag in which the colorimetric device is built into the resuscitation bag. The disadvantage of the Capno-Flo resuscitation bag is that it does not provide a true breath-to-breath color change. However, there is a new INdGOÔ resuscitation bag that has built-in replaceable CO2 detectors and gives breath-to-breath color changes.94

When nasal cannulas are used, supplemental oxygen, inhaled gases, and/or "mouth breathing" may dilute the ETCO2 concentration and yield falsely low CO2 readings.2,113,114 When nasal cannulas are used with sidestream analyzers, ambient air may be entrained causing dilution of the ETCO2 concentration with falsely low estimates of the CO2 level. Similarly, with sidestream analyzers, the locations of the sampling tube in the patient's nasopharyngeal airway or nares may affect the accuracy of the ETCO2 reading. Sidestream analyzers with a slow sampling flow rate in a tachynpeic pediatric patient with a low tidal volume will give a falsely low ETCO2 reading.1,2,77 Water vapor and secretions also can obstruct the nasal cannula.113,115

Cost has been cited as a limitation to the use of end-tidal CO2 monitoring.103,116 The initial purchase price of a capnography unit is greater than for a capnometer device, with the disposable qualitative devices having the least initial cost. However, even the more expensive units have been justified on a cost-benefit ratio based upon several factors. These benefits include reduced ordering of V/Q or spiral computerized tomography scanning of the chest to rule out pulmonary emboli, decreased frequency of arterial blood gases measurements, limiting or discontinuing futile CPR, and avoiding missed intubations with their potential for malpractice litigation.116,117

As with pulse oximetry, there are no absolute contraindications to capnography. Most of the limitations of capnography are related to its design and technical aspects and the interpretation of the results, therefore, a review of pathophysiology is warranted.


Carbon Dioxide Metabolism. CO2 is produced as a byproduct of aerobic metabolism in the cells of the body and transported to the lungs.118 It is transported in the blood from the cells via the systemic veins to the superior and inferior vena cava to the right side of the heart to the pulmonary artery, and then to the pulmonary capillary bed. There, CO2 diffuses from the pulmonary capillaries across the pulmonary capillary–alveolar membrane into the alveoli. With ventilation, CO2 is exhaled to the outside air and eliminated. The now-oxygenated blood in the pulmonary capillary bed then returns to the heart (e.g. left atrium) via the pulmonary veins. Summarizing, CO2 metabolism/excretion involves three processes: 1) metabolism or production by the cells, 2) circulation that transports CO2 to the lungs, and 3) ventilation whereby CO2 is eliminated via expiration.119 Any factor or disease that affects any one or combination of these three processes will, in turn, affect the exhaled CO2 level (Table 4). This exhaled CO2 is then detected with the result displayed by the various devices.

Respiration. Ventilation is the delivery of fresh air (and thus, oxygen) to the lung and removal of CO2 from the blood. Perfusion is the circulation of blood through the vasculature. Gas exchange (i.e., carbon dioxide removal and oxygen delivery) occurs in the pulmonary capillaries. Diffusion is the movement of air between the alveoli and the pulmonary capillaries. Ventilation-perfusion matching is the contact between the alveolar gas and the pulmonary capillary bed. Thus, for normal respiration to occur, all components (i.e., ventilation [V], perfusion [Q], with matching of ventilation-perfusion [V-Q] and diffusion) need to be functioning appropriately.118

Ventilation-Perfusion (V/Q). In the ideal situation where all alveolar capillary units have equal matching of ventilation and perfusion, the V/Q ratio = 1. The V/Q ratio, the net PO2 and net PCO2 levels of the blood coming from all areas of the lung (e.g., in the pulmonary veins returning to the left atrium) is an average of what is occurring in all the individual alveolar capillary units.

Because of gravity, in the normal upright individual, there is an increasing gradient of blood flow from the apices of the lungs to the lung bases. A similar gradient (but less marked) in the opposite direction occurs for ventilation. In the healthy individual, ventilation is greatest in the apices and perfusion is greatest in the bases. Thus, under normal conditions, the V/Q ratio = 0.8.

Theoretically, the V/Q ratio could range from 0, where ventilation is totally absent (V = O, V/Q ratio = 0), to infinity (∞), when perfusion is completely absent (Q = 0, V/Q ratio = V/0 = ∞). When ventilation is totally absent, the alveolar capillary unit acts like a "shunt" (V = 0, V/Q = 0, shunt). When perfusion is totally absent, the alveolar capillary unit functions as "dead space" (Q = 0, V/Q = ∞, dead space).

Dead Space. The anatomic dead space is the part of each breath that does not reach the alveoli and does not participate in gas exchange. With each breath, part of the fresh air inspired (about 30%) does not reach the alveoli but stays in the conducting airways (i.e., nasopharynx, oropharynx, larynx, trachea, mainstem bronchus, right/left bronchi, and terminal bronchioles).120

The other 70% of the air inspired with each breath does reach the alveoli and does participate in gas exchange.120 This is the alveolar ventilation. In a normal adult at rest with a respiratory rate (RR) of 12-16 breaths per minute and a tidal volume (TV) of 500 mL, the total ventilation (VT) per minute is seven liters (VT = RR X TV = 14/min x 500 mL/min = 7000 mL/min = 7 l/min). The dead space ventilation (VD) is about 2 liters and the alveolar ventilation (VA) (the ventilation available for gas exchange) is approximately 5 liters, where VT = VD + VA or 7 liters = 5 liters + 2 liters. In certain diseases, some alveoli will be ventilated but not perfused. Thus, the ventilation in these nonperfused alveoli is wasted, resulting in an increase in dead space. When dead space increases with total minute ventilation staying the same, alveolar ventilation decreases and PACO2 increases. An example of increased dead space occurs with pulmonary emboli.


The capnogram is a graph of the CO2 concentration (in mm) on the X-axis versus time on the Y-axis (Figure 5).4,61 The capnogram is a waveform or graphic representation of the CO2 levels during a breath or ventilatory cycle. The capnogram yields more data than a single ETCO2 reading.

Figure 5. Normal Capnogram: 4 Phases

There are four distinct components of a single-breath capnogram (Figure 5).4 The baseline with a "zero" ETCO2 (Phase 1) represents inspiration with air taken into the alveoli and early expiration. The ETCO2 level is zero because inspired air is essentially free of CO2. Phase 1 or the baseline of zero (A to B on Figure 5) also includes initial expiration because the initial gases expelled are from the anatomic dead space (e.g., the conducting airways that do not participate in gas exchange).

There is a sudden increase in ETCO2 level from baseline (Phase 2) as exhalation of alveolar gas occurs (from B to C on Figure 5). During the alveolar or expiratory plateau phase, expiration continues with alveolar air being exhaled (from C to D on Figure 5). There is a mild upward slope to the plateau phase as air is first exhaled from parts of the lung with lower resistance, higher V/Q ratio, and lower CO2 levels than from areas of the lung with higher resistance, lower V/Q ratio, and higher CO2 levels. The end of expiration is at point D. This is the highest point on the graph, and represents ETCO2 levels, the number displayed by the capnometer. The inspiratory phase (phase 4) (point D to E on Figure 5) is a sharp downslope to return to baseline caused by the influx of essentially CO2-free inspired air into the alveoli.

Diseases/Conditions Affecting the Capnograms. The appearance of the capnogram can be diagnostic of various disorders (Figures 1, 2, 3).1,4,121 For example, a capnogram with an increased baseline (phase 1), but normal overall waveform appearance indicates rebreathing of CO2. This can occur with a malfunctioning ventilator circuit in intubated patients, with insufficient inspiratory flow, or an inadequate expiratory time (Figure 1).

A prolonged upstroke of phase 2 is caused by conditions that lengthen or impede expiration: reactive airway diseases (e.g., acute bronchospasm as with asthma, chronic obstructive pulmonary disease, or bronchiolitis) or in ventilated patients with a kinked endotracheal tube (Figures 1, 2, 3).4

The slope of the expiratory plateau phase (phase 3) is affected by both the expiratory resistance and pulmonary dead space. Evaluating changes in the expiratory phase (phase 3) and phase 2 has been suggested as a way to monitor the response of asthmatic patients to therapy (Figure 3). In ventilated patients, a spontaneous inspiratory effort is denoted by a dip or cleft in phase 3. This curare cleft is a result of some CO2-free inspired air (from the patient's spontaneous inspiration) passing over the capnograph's sampling port (Figure 1).

Lengthening of inspiration results in a prolonged phase 4 downstroke. For example, this condition could occur with airway obstruction. In a ventilated patient, there may be a leak, either in the endotracheal tube cuff or in the ventilation circuit (Figure 1).

A loss of the waveform with a decrease in ETCO2 level to near zero in a ventilated patient indicates extubation or an acute equipment malfunction, while a decrease in ETCO2 levels to low (but not zero) values with an abnormal waveform may occur with partial airway obstruction or a kinked endotracheal tube (Figure 1).

Use of ETCO2 During Mechanical Ventilation. The ETCO2 measurement can be used to estimate the PaCO2 level only in patients with stable hemodynamics without underlying lung disease (e.g., chronic obstructive pulmonary disease) and at a constant temperature.4,74,77,121,122

Relationship of End-Tidal CO2 to Alveolar CO2 and Arterial CO2. Under normal conditions, the alveolar CO2 measurement correlates with the mixed venous CO2 (PVCO2) measurement, which in turn equilibrates with the arterial blood carbon dioxide (PaCO2) measurement. Assuming normal circumstances, there is a small gradient of 2-5 mmHg between the PaCO2 measurement and the ETCO2 (or PETCO2) measurement. Thus, the P (a-ET)CO2 gradient should be less than 6 mmHg.

There are many conditions that can affect the P (a-ET) CO2 gradient. This gradient is increased with age, under anesthesia as well as in disease states such as with pulmonary emboli and low cardiac output. The pitfalls in using ETCO2 to estimate PaCO2 levels in all patients is obvious when the variables that affect ETCO2 levels are reviewed. Variables that affect the ETCO2 level can be categorized into several groups:

  1. CO2 production,
  2. pulmonary perfusion, and
  3. alveolar ventilation.

A fourth category may be technical factors.

Assuming perfusion and ventilation are constant, then variables that increase CO2 production will lead to an increased delivery of CO2 to the alveoli causing an increase in ETCO2 levels. Factors that result in an increased metabolic rate causing an increased CO2 production include sepsis, the administration of sodium bicarbonate, seizures, fever, thyrotoxicosis, hypertension, the addition of CO2 (e.g., during laparoscopy), physical activity (e.g., exercise and shivering), high cardiac output states, and malignant hyperthermia.

Conversely, factors with decreased ETCO2 levels from decreased CO2 production (with decreased delivery of CO2 to the lungs) are conditions with a decreased metabolic rate including hypothyroidism, hypothermia, sedation, and paralysis.

The ETCO2 level is decreased in conditions where the pulmonary perfusion is decreased including cardiopulmonary arrest, hypovolemia, low cardiac output states, and hypotension.

The ETCO2 level is increased in states where the cardiac output—and thus pulmonary blood flow—is increased due to increased delivery of CO2 to the alveoli.

Under conditions of hypoventilation such as apnea, respiratory insufficiency or central nervous system depression of respiration, or during rebreathing of expired air, the ETCO2 level is increased (Figures 2, 3). Conversely, when hyperventilation occurs, the ETCO2 level is decreased (Figure 3).

Any situation that causes V/Q mismatch can affect the P (a-ET) CO2 gradient. When dead space is increased, the P (a-ET)CO2 gradient is increased because more lung units are ventilated than perfused with less blood flow containing CO2 going to the lung. Therefore, less CO2 is presented to the alveoli for excretion, therefore, the ETCO2 level is decreased.

The capnogram will demonstrate a rounded, more slowly rising expiratory upstroke when there is V/Q mismatch from increased dead space. The normal capnogram has a flat alveolar plateau (C to D on Figure 5) because the expired gas from the lung units have comparable V/Q relationships. With significant V/Q abnormalities, the ETCO2 level differs because some lung units have low ETCO2 concentrations; they are underventilated (due to dead space), while other lung units that are normal will have a high ETCO2 concentration.

Pulmonary emboli is a condition associated with increased dead space and a low ETCO2 concentration with an increased PaCO2 – ETCO2 gradient.


There are numerous uses of end-tidal CO2 monitoring that should be beneficial to clinicians (Table 5). The first and most important application is as an aid for intubation where typically an absence of CO2 indicates esophageal intubation and the presence of CO2 indicates placement in the airway. It can be an additional—but not exclusive—monitoring tool in ED patients yielding a clue to inadvertent dislodgement of an endotracheal tube or a sudden change in clinical condition. It has a negative predictive value for diagnosing pulmonary emboli. It can be used during CPR to predict the efficacy of CPR and the outcome of resuscitation. In patients with stable cardiopulmonary hemodynamics, the ETCO2 concentration correlates with the PaCO2 level, and the trend can be used to follow a given patient (e.g., a head injured patient), which may decrease the number of arterial blood gases measurements needed. End-tidal CO2 monitoring can be a valuable tool for the emergency physician in many clinical situations (Table 6).

Table 5. Clinical Uses of End-tidal CO2 Monitoring

Table 6. Pearls and Pitfalls


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