Monitoring and Nursing
October 2004 (Vol 26, No 10)

Capnography in Dogs

  • by
  • Melissa Marshall


Carbon dioxide (CO2) is linked to a patient's perfusion, ventilation, and metabolism. End-tidal carbon dioxide (ETCO2) is the measurement of CO2 in exhaled respiratory gases and serves as an estimate of arterial CO2. ETCO2 is measured by a capnograph in a mainstream or sidestream method. A normal capnogram has four phases: phase 0, the inspiratory downstroke; phase I, the expiratory baseline; phase II, the expiratory upstroke; and phase III, the expiratory plateau. Complete evaluation of a capnogram includes determining the shape and value of the four phases and measuring the alveolar to end-tidal CO2 gradient. Thorough evaluation gives a clinician information about a patient's state of perfusion, ventilation, and metabolism as well as equipment malfunction. Further veterinary studies are needed to determine the role of capnography in monitoring anesthetized patients, assessing response to treatment, diagnosing disease, and determining a prognosis.

Because of its many roles, carbon dioxide (CO2) is one of the most important molecules in the body. CO2 production and elimination is in­trinsically linked with the body's state of perfusion, ventilation, and metabolism. Arterial blood gas analysis is considered the gold standard for analyzing a patient's arterial CO2 and thus assessing its ventilatory status. Obtaining an arterial blood sample is not always possible in small animals. It is associated with a risk of thrombosis and infection and does not give continuous information. The ability to rapidly, noninvasively, and easily monitor CO2 levels of intubated patients can aid in evaluating and treating them.

Capnography involves continuous measurement and recording of CO2 in the respiratory gases. In 1943, Luft1 developed the principle of capnography based on the fact that CO2 absorbs infrared light. Capnography was first studied clinically by Smallhout and Kalenda2 in humans in the 1970s and has since been researched extensively. By 1985, capnography was considered the standard of care for basic anesthesia monitoring by the American Society of Anesthesiologists.3 In the mid-1990s, CO2 monitors (capnographs) became small and inexpensive enough to be used in veterinary medicine (TABLE 1). Capnography minimizes the need for repetitive arterial blood gas sampling, thus providing an excellent noninvasive monitoring and diagnostic tool. This article discusses CO2 physiology, the primary methods of measuring CO2 in the respiratory gases using capnography, factors affecting CO2 measurement, analysis of a capnogram, and the clinical applications of capnography.


Carbon Dioxide Physiology

CO2 is produced as an end product of cellular metabolism. CO2 diffuses from peripheral body cells into the venous system, where it is transported in three principal forms. Most (60% to 70%) CO2 is transported as bicarbonate ion after conversion in the red blood cells by carbonic anhydrase. Another 20% to 30% is transported bound to proteins, and the remaining 5% to 10% is transported in physical solution in plasma. This 5% to 10% is what is measured by blood gas analysis and reported as arterial partial pressure of carbon dioxide (Paco2).4 Once CO2 has been transported to the pulmonary circulation, the partial pressure difference between CO2 in the alveoli (PAco2) and pulmonary capillaries is the driving mechanism for CO2 diffusion from the blood into the alveoli. With normal perfusion, equilibration between the pulmonary capillaries and alveolar CO2 is reached in less than 0.5 seconds. Once the CO2 has diffused into the alveoli, it is exhaled from the mainstem bronchi and trachea. The amount of CO2 varies over the course of the breath because of several factors, including different parts of the lungs emptying at different rates and differing ventilation:perfusion ratios. Therefore, the portion of the breath that comes from and most closely resembles the composition of the air in the alveoli is the end-tidal portion. Capnography measures ETCO2, which is reported as a partial pressure.

Capnography is a noninvasive method of measuring systemic metabolism, cardiac output, pulmonary perfusion, and ventilation.5 Changes in the ETCO2 level reflect changes in one or more of these systems. If all but one of these systems stay relatively constant, the ETCO2 level will reflect changes in the system that have not been constant.6 When CO2 production remains relatively constant and cardiac output and pulmonary perfusion are normal, changes in ETCO2 reflect changes in ventilation.7

The normal arterial CO2 concentration in an awake healthy dog is 35 to 45 mm Hg.8,9 If ventilation and perfusion are well matched, the ETCO2 value should nearly equal that of the Paco2.10-13 The ETCO2 value is 2 to 5 mm Hg less than that of arterial CO2.7,10-15 This difference is the gradient between CO2 in the arterial blood and expired air [P(a-ET)co2] and can be accounted for by the fact that the Paco2 value represents all the perfused alveoli and the ETCO2 value represents all the ventilated alveoli. The ventilation:perfusion ratio (VA/Q) is usually 0.8 because of dead space ventilation.10,11,13 Alveolar dead space ventilation includes alveoli that are ventilated but not perfused. In cases of VA/Q mismatch due to increases in alveolar dead space ventilation (i.e., low cardiac output states, hypovolemia, air embolism, shock, arrest, pulmonary embolism), the ETCO2 level underestimates the PAco2 level and hence that of the Paco2. The ETCO2 level decreases because the nonperfused alveoli CO2 concentration is zero, whereas the perfused alveoli concentration is normal. Virtually any condition that increases dead space ventilation can abruptly lower the ETCO2 concentration, thereby increasing the difference between the Paco2 and ETCO2 levels. With severe decreases in cardiac output as in shock or cardiac arrest, ETCO2 values reflect changes in pulmonary blood flow and cardiac output, not ventilation.11-13

Sampling Methods

The two primary methods used for measuring CO2 in expired air are mass spectroscopy and infrared light absorption. The mass spectrograph separates gases and vapors of different molecular weights. These units are expensive and bulky and thus impractical for most veterinary practices. Infrared light absorption is the most common method for measuring CO2 in respiratory gases. Polyatomic gases (i.e., nonelementary gases such as nitrous oxide and CO2) and water vapor absorb infrared rays. CO2 selectively absorbs infrared light at 4.3 µm. The amount of light absorbed by the CO2 is directly proportional to the concentration of the absorbing molecules.

Capnometers and capnographs can be categorized based on the sensing device location. The two options for placement of the measuring device are mainstream or sidestream (FIGURE 1). In sidestream capnometers and capnographs, the measurement device is located away from the sampler, which is placed between the endotracheal tube and breathing circuit. A sampling tube transmits gases to the measurement chamber located away from the breathing circuit. The rate at which respiratory gases are aspirated from the gas column varies from 50 to greater than 400 ml/min. In humans, the optimal rate is considered to be 50 to 200 ml/min.6 In mainstream capnometers and capnographs, the measurement device is placed between the endotracheal tube and breathing circuit. Infrared light rays within the sensor traverse the respiratory gases and are detected by a photodetector within a cuvette. Mainstream sensors are heated to prevent condensation of water vapor, which can lead to falsely elevated CO2 readings.16

Advantages of sidestream analysis include a lightweight sampler, ease of manipulation near the patient, smaller sample chamber volume, and ability to sample other gases (i.e., inhaled anesthetics). Disadvantages include plugging of the sample line by secretions and condensation, a 2- to 3-second delay in determining the CO2 concentration, and aspiration of extraneous air from leaks in the breathing circuit that dilute the sample. Low-flow systems and high respiratory rates can lead to inadequate flushing of the sample cell or line and yield falsely elevated values, thus changing the slope of the capnogram and ETCO2 concentration.

The advantage of mainstream analysis is that it gives a real-time measurement (i.e., an immediate response rate of <100 milliseconds). However, there are several disadvantages to mainstream capnometry. The excessive dead space in the patient breathing circuit produced by the sensing chamber can lead to false readings. The weight of the device causes kinking of the endotracheal tube. The sensing chamber may be contaminated by secretions and condensation. In addition, patients may be burned by the heated cuvette.

The accuracy of infrared CO2 monitoring can be affected by several factors. Water vapor can yield falsely high ETCO2 values (a 1.5% to 2% increase in CO2) because of condensation on the window of the sensor and in the sample tubing.16 Methods of decreasing this interference include positioning the sampling tube vertically upward from the patient and using water filters at both ends of the sampling tube. The atmospheric pressure does not affect the ETCO2 reading because most capnometers have internal calibration devices that adjust for changes in atmospheric pressure. Halogenated anesthetics absorb infrared light at different wavelengths; however, their concentrations are so low that interference is not considered important. High fresh gas flow rates in small patients can dilute the sample, causing falsely low ETCO2 values and changes in the waveform. This occurs more often with sidestream than mainstream analysis. To decrease this inaccuracy, the fresh gas flow rate can be reduced to 10 to 30 ml/kg/min, which is currently considered a moderate flow rate for anesthesia maintenance. Higher respiratory rates cause underestimation of the ETCO2 value because of inadequate emptying of the alveoli. Two keys to obtaining predictable ETCO2 values and waveforms in animals with high respiratory rates are to program the response time of the analyzer to less than the respiratory cycle time of the patient and to ensure there is no leakage of respiratory gases.

A recent study compared sidestream and mainstream capnometers in mechanically ventilated dogs. This study found that mainstream analyzers were slightly more accurate than sidestream analyzers, but both analyzers satisfactorily reflected changes in the ventilatory status. In this study, Paco2 was compared with ETCO2. It was determined that the ETCO2 value may underestimate the degree of hypercarbia at Paco2 values greater than 60 mm Hg.17 A second study showed that ETCO2 values greater than 55 mm Hg may underestimate the degree of hypercarbia14 and the ETCO2 value (at 30 to 55 mm Hg) is the best estimate of the Paco2 value.14,17,18 In all situations, it is important to obtain a Paco2 reading from arterial blood gas analysis to verify the Paco2-ETCO2 gradient.


Normal Capnogram

The capnogram is the graphic representation of the amount of CO2 in the respiratory gases versus time. There are two different types of time capnograms: a slow speed to show CO2 trends, and a fast speed that shows changes in each breath. The fast speed capnogram waveform is useful in determining causes of changes in ETCO2. The shape of the waveform is altered in various situations, such as breathing circuit leaks, delayed alveolar emptying, and rebreathing expired CO2. There is considerable variation in terminology describing the normal capnogram. Terminology representing various phases of the time capnogram based on logic, convention, and tradition was introduced by Bhavani-Shankar et al in 1992.19 The capnogram waveform has three phases of expiration and one of inspiration (FIGURE 2):

  • Phase I (expiratory baseline) is the beginning of exhalation and corresponds to exhalation of CO2­-free dead space gas from the larger conducting airways. The CO2 value during this phase should be zero.
  • Phase II (expiratory upstroke) involves exhalation of mixed alveolar and decreasing dead space gas, which rapidly increases the CO2 concentration.
  • Phase III (expiratory plateau) occurs when all the dead space gas has been exhaled, resulting in exhalation of completely alveolar air. The highest point of phase III corresponds with the actual ETCO2 value. The plateau has a slight positive slope because of the continuous diffusion of CO2 from the capillaries into the alveolar space.
  • Phase 0 (inspiratory downstroke)—Because of inhalation of CO2-free gas, the CO2 concentration rapidly declines­ to zero.

The alpha angle is between phases II and III. In humans, the average angle is 100° to 110°. The alpha angle increases as the slope of phase III increases. Thus the alpha angle is an indirect indication of the VA/Q status of the lungs. The beta angle is between phases III and 0 and is usually 90°. The beta angle is used to assess the degree of rebreathing. During rebreathing, the beta angle increases as well as the response time of the capnometer compared with the respiratory cycle time of the patient. Normal values for these angles have not been published for dogs or cats.


Analysis Of Capnogram

Thorough examination and interpretation of the capnogram yields information about a patient's ventilation, perfusion, and metabolism. A suggested systematic approach to capnogram interpretation follows:

  • Positively identify a waveform (absence of a waveform indicates cardiac or respiratory arrest, disconnection, improper intubation, apnea, or equipment malfunction).
  • Determine the actual ETCO2 and inspiratory CO2 values
  • Evaluate the waveform.
  • Phase I (expiratory baseline): Is the absolute value zero?
  • Phase II (expiratory upstroke): Is it too steep, sloping, or prolonged?
  • Phase III (expiratory plateau): Is it flat (compared with a slight positive upstroke), prolonged, or notched?
  • Phase 0 (inspiratory downstroke): Is it prolonged?
  • Measure the (a-ET)CO2 gradient: Is it increased, decreased, or stable?

Analysis of ETCO2 and Inspiratory CO2 Values

When there are abnormalities in ETCO2 values or the waveform, it is helpful to consider the factors that affect them (i.e., metabolism, cardiac output/perfusion, ventilation, and mechanical problems). A sudden decrease in the capnogram reading to zero or an abnormally low value should alert clinicians to a potentially catastrophic event, including failure to ventilate, complete circulatory collapse, cardiac or respiratory arrest, disconnection of the patient from the circuit or machine, or capnograph malfunction. Failure to ventilate could be caused by esophageal intubation, inadvertent extubation, obstruction of the endotracheal tube or breathing circuit, disconnection, or apnea. Circulatory collapse results in absence of a waveform; possible causes include massive pulmonary embolism, cardiac arrest, or exsanguination. Mechanical failures must also be ruled out. The anesthetic machine, ventilator, patient breathing circuit, sensor, and sampling lines should be routinely checked. An easy way to test for mechanical failure of a capnograph is to exhale into the sampling portion of the device. However, this requires that the patient be disconnected and is recommended only after ruling out cardiac or respiratory problems in the patient.

Another way to determine the most likely cause of a low or absent ETCO2 value is to evaluate the rate of decline using the trend information versus the capnogram waveform. This allows observation of changes that occur in multiple waveforms over time. An abrupt decrease in the ETCO2 concentration is more likely with inadvertent extubation, circuit disconnection, total obstruction of the endotracheal tube or breathing circuit, or ventilator malfunction. A rapid decrease in the ETCO2 value occurs with loss of pulmonary blood flow or cardiac output, as in sudden hypotension, cardiac arrest, and pulmonary embolism. A gradual decrease in the ETCO2 value may indicate decreased CO2 production, as in hypothermia, or increased elimination, as in hyperventilation. Table 2 lists the causes of decreased ETCO2 concentrations.

ETCO2 levels greater than 45 mm Hg indicate hypercarbia. Elevated ETCO2 values are seen primarily with increased CO2 production or decreased CO2 elimination. Increased production occurs with hypermetabolic states. Decreased elimination is caused by hypoventilation. Trend information can be used to determine the cause of hypercarbia. An abrupt transient increase in the ETCO2 value can be seen with bicarbonate administration, release of a limb tourniquet, and transient increases in central nervous system activity. Gradual increases are seen with rising body temperature and hypoventilation. A high ETCO2 value can also be due to an elevated baseline, as seen with malfunctioning rebreathing circuits and exhausted soda lime absorber.

Elevated inspiratory CO2 values distinguished by an elevated phase I can be seen with rebreathing circuits in which fresh gas flow rates are inadequate and soda lime absorber has been exhausted. Table 2 lists the causes of increased ETCO2 concentrations. Acceptable inspiratory CO2 values are 0.1% to 1% (up to 7 mm Hg).

Analysis of the Waveform

The normal baseline (phase I) is zero. An increase in the baseline represents rebreathing of expired CO2. A rise in the baseline is seen with exhausted soda lime absorber, faulty one-way valves, or a nonrebreathing circuit when inadequate fresh gas flow rates are used. If both the baseline and ETCO2 values rise precipitously, the sensor may be contaminated with secretions16 (FIGURE 3).


In a normal capnogram, the expiratory upstroke (phase II) is steep. If the upstroke slope is lessened, CO2 delivery to the sampling site may be delayed. This delay could be physiologic or mechanical. Mechanical factors include obstruction of the breathing circuit with secretions, condensation, or kinking as well as a delay in the sampling rate with sidestream analyzers. Physiologic factors of a slow upstroke include uneven alveoli emptying typical of that found in asthma or bronchitis.

The expiratory plateau (phase III) should be nearly horizontal, with the highest point of the plateau representing the actual ETCO2 value. The positive slope is due to the contribution of CO2 from slow-emptying alveoli with a low VA/Q , allowing accumulation of higher levels of CO2.18 When evaluating the plateau, the slope, height, and shape should be considered. An increasing slope (increased alpha angle) is frequently seen in patients with obstructive lung disease (FIGURE 4). The rate at which the alveolus empties depends on airway resistance in the alveolus, compliance of the alveolus, and inflation pressure.19 A dip in phase III can occur in mechanically ventilated patients with spontaneous breathing (FIGURE 4). This dip results from spontaneous breath initiation after a ventilator-delivered breath. During this time, a small amount of fresh gas is drawn over the detector. This is known as a curare cleft because it occurs commonly when patients are emerging from neuromuscular blockade. This may also be a sign of hypoxemia, hypercarbia, or insufficient anesthesia. Plateau height should be evaluated. If the shape is normal but the plateau height is low, there may be a situation in which well-perfused and underperfused alveoli empty simultaneously (FIGURE 5). Decreases in pulmonary and systemic perfusion, hypothermia, hyperventilation, and increased dead space ventilation can cause low plateau height.



The inspiratory downstroke (phase 0) is a nearly vertical drop to baseline. Numerous cyclical irregularities in the downstroke that blend with the expiratory plateau are called cardiogenic oscillations (FIGURE 6). This is due to a small amount of gas flow produced after the lungs passively empty as the heart beats against the nearly gas-depleted lungs. If the slope is prolonged and blends with the expiratory phase, there may be a leak in the expiratory circuit (i.e., a loose-fitting endotracheal tube) or a cuff (FIGURE 6). A prolonged slope can also result from dispersion of gases in the sampling tube or a prolonged response time by the analyzer.


Comparing the Arterial to ETCO2 Gradient

There is normally a 2 to 3 mm Hg difference between arterial and alveolar CO2 values [P(a-Aco2) gradient]. The Paco2 value is obtained via arterial blood gas analysis. The difference between Paco2 and ETCO2 values is known as the P(a-ET)co2 gradient. The arterial to ETCO2 gradient is usually less than or equal to 5 mm Hg in both humans and anesthetized dogs.7,10-15 The gradient results from the alveolar dead space, which results from temporal, spatial, and alveolar mixing defects in normal lungs. Changes in alveolar dead space correlate well with changes in the P(a-ET)co2 value only when phase III has a flat or minimal slope.18 To evaluate changes in the gradient, a P(a-ET)co2 baseline must first be calculated early in the course of events.

Causes of Increased (a-ET)CO2

There are three main causes for increase of the (a-A)CO2 gradient and hence increase of the (a-ET)CO2 gradient, including VA/Q abnormalities, respiratory patterns that cause incomplete alveolar emptying, and poor sampling techniques.

Ventilation:Perfusion Abnormalities

The overall VA/Q in a normal lung is 0.8. Dead space ventilation is characterized as a high VA/Q, resulting in less involvement of tidal volume in gas exchange. The portion of the tidal volume reaching the nonperfused or poorly perfused alveoli creates physiologic dead space. Any condition that increases the physiologic dead space ventilation effectively lowers exhaled CO2 and increases the gradient. Examples include low forward flow states, hypotension, hypothermia, bradycardia, cardiogenic shock, and pulmonary embolism. In addition, patients undergoing a thoracotomy have altered gradients due to an altered VA/Q. In dorsal or sternal recumbency, the lungs receive approximately equal ventilation. With lateral recumbency, however, ventilation of the upper lungs increases and perfusion of the lower lungs increases. In addition to positional effects, opening the pleurae increases CO2 elimination of the upper lung and thereby decreases the P(a-et)co2 gradient. Retraction of the lung produces the exact opposite effects. The lower lung gradient is not affected by these maneuvers, but the combined ETCO2 reading and hence the gradient can be altered.20

Respiratory Patterns

Respiratory patterns that increase the gradient by incomplete lung emptying include hyperventilation with incomplete exhalation as well as ventilation with inadequate tidal volumes. Patients with asthma or obstructive pulmonary disease may develop an increased gradient because of constricted airways and decreased chest wall elasticity, making complete lung emptying more difficult.10 To obtain a more accurate ETCO2 in humans with restrictive diseases, a chest wall squeeze may be performed.21 This can be applied manually at the end of a patient's expiration, but the value of this has not been evaluated in veterinary patients.

Technical Errors

Sampling errors by capnography, such as sampling tube leaks and calibration errors, or blood gas analysis may also increase the gradient.

Causes of Low P(a-ET)CO2 Gradients or Reverse Gradients

Shunt perfusion (normal to increased perfusion in less than normally ventilated alveoli) results in a low VA/Q and, consequently, a low to normal P(a-ET)CO2 gradient. This is a rare finding in dogs, cats, and humans. Situations that induce shunt perfusion are mucous plugging, atelectasis, and alveolar secretions. There are few reports of ETCO2 values being greater than those of Paco2 (reverse gradients)22,23; these are reported in humans, with a greater incidence during pregnancy24 and exercise,25 and in patients with large tidal volumes. A hypothesis for this occurrence involves patients with large tidal volumes and low respiratory rates, as seen in barrel- or deep-chested dogs. In this situation, highly perfused slow-emptying alveoli add additional accumulated CO2 to the end of each breath, increasing the ETCO2.25 The existence of such negative gradients further complicates the assumption of Paco2 from ETCO2 values.

Clinical Uses

Although some studies have shown that the ETCO2 concentration does not always accurately reflect the Paco2 concentration in critically ill patients, it is valuable in detecting trends and sudden changes. A high or rising ETCO2 concentration likely reflects high or rising arterial CO2, whereas a decreasing ETCO2 value may indicate a decrease or rise or no change in the Paco2 value, depending on a patient's temperature, perfusion, and ventilation. Nevertheless, changes in the ETCO2 should prompt the clinician to evaluate the patient's ventilatory and hemodynamic status.

ETCO2 has been shown to be superior to pulse oximetry in early detection of airway mishaps, both technical and pathophysiologic (FIGURE 7). It takes a longer time for oxygen saturation to drop and hence the percentage of oxygenation of hemoglobin (SpO2) to change compared with changes in ETCO2, where the absence of CO2 is detected instantaneously when the next breath fails to occur.26-29 In this manner, capnography is superior to pulse oximetry in detecting apnea. In addition to monitoring patients during anesthesia, capnography can be used to confirm correct endotracheal tube and nasal esophageal feeding tube placement, guide cardiopulmonary cerebral resuscitation (CPCR), and assist treatment planning for patients receiving mechanical ventilatory support.


Endotracheal Tube Position and Feeding Tube Placement Confirmation

ETCO2 monitoring for the verification of correct endotracheal tube placement has been studied extensively in humans30 and animals31,32 in both arrest and nonarrest settings. The theory behind this involves the fact that CO2 is normally exhaled through the trachea and not through the esophagus or gastrointestinal tract; hence CO2 should be detected only from a correctly placed endotracheal tube. Mask ventilation and aerophagia cause the stomach to insufflate with air and may initially result in a false-positive ETCO2 reading when used with esophageal intubation. In humans, recent ingestion of an antacid may also cause false-positive ETCO2 readings when using esophageal intubation (). To avoid a false-positive ETCO2 value after suspected inappropriate intubation, the ETCO2 reading should be interpreted after six breaths.33,34

Capnography can be used as an adjunct to radiography to determine correct placement of nasal"esophageal feeding tubes. The same principles used to determine correct endotracheal tube position are applied. The partial pressure of CO2 in the stomach and esophagus is considered to be negligible. The ETCO2 value should be zero in correctly placed feeding tubes.35

Cardiopulmonary Cerebral Resuscitation

Capnography is a valuable tool during CPCR. At the onset of cardiac arrest, the ETCO2 values fall abruptly because of decreased cardiac output and subsequent pulmonary perfusion. The levels increase slightly with effective CPCR and transiently overshoot prearrest values with return of spontaneous circulation (ROSC)36,37 (). During effective CPCR, ETCO2 values have been shown to correlate with cardiac output,38,39 coronary perfusion pressure,40 efficacy of cardiac compression, ROSC, and even survival.41,42 A clinical human pediatric and an experimental canine pediatric model of asphyxial arrest showed that the higher the initial ETCO2 value following arrest, the greater was the short-term survival.43,44 Ventricular fibrillation is the most commonly researched mode of arrest in animal and human studies of CPCR. Ventricular fibrillation has a characteristic ETCO2 pattern of a sudden drop followed by an increase with effective CPCR. Respiratory arrests followed by cardiac arrest have an initial markedly elevated CO2 level, which decreases to low levels with CPCR and finally increases with ROSC.43 This increase is due to accumulation of CO2 in the lungs after respiratory arrest and before cardiac arrest.45 Multiple studies have shown that ETCO2 values of 10 mm Hg or less after 20 minutes of CPCR predicted death in humans.46,47

One of the most important factors that determines successful resuscitation of a patient in cardiac arrest is coronary perfusion pressure; in a porcine ventricular fibrillation model, coronary perfusion pressure was shown to be highly correlated with ETCO2 concentration.48 In human and animal studies, an ETCO2 value greater than 10 mm Hg is highly predictive of successful resuscitation; this value is achieved when coronary perfusion pressure exceeds 30 mm Hg.49 To date, the ETCO2 value is the only noninvasive monitor of the effectiveness of CPCR.

Several investigators50-52 have noted a transient decrease in expired ETCO2 tension after administering epinephrine in patients with nontraumatic prehospital cardiac arrest and in an experimental setting of canine ventricular fibrillation. This finding was marked with high-dose (0.2 mg/kg) epinephrine administration in a porcine model of cardiac arrest.52 In human clinical trials, 82% of patients with ROSC had a decreased ETCO2 value after receiving epinephrine compared with 25% of patients who did not regain a pulse.53 It has also been reported that the greatest accuracy in predicting prognosis is achieved by evaluating an ETCO2 reading taken after several minutes of initial resuscitation but before epinephrine administration. However, in one clinical human study, epinephrine administration did not significantly affect the ability to predict ROSC based on the ETCO2 value.53,54

Mechanical Ventilation

The ETCO2 value can be used to estimate the Paco2 value in critically ill, mechanically ventilated, hemodynamically stable patients and in patients without rapidly progressive lung pathology. It is most useful to have initial paired Paco2 and ETCO2 values. The P(a-ET)CO2 gradient can be used to determine optimal levels of positive end-expiratory pressure.18 The gradient should be smallest when there is maximal recruitment of perfused or functional gas exchange units without overdistention of alveolar areas contributing to dead space. To ensure the smallest P(a-ET)CO2 gradient, patients should be breathing synchronously with the ventilator. The P(a-ET)CO2 gradient is also useful in detecting and delineating mechanical failure, including breaks in the breathing circuit, and CO2 rebreathing; in monitoring patient progress during weaning from the ventilator; and in noting the clinical consequences of changes in mechanical support.3,53"57

Future of ETCO2 Monitoring

Capnography is being used and studied in diagnosing pulmonary embolism and measuring cardiac output using volume capnograms. Future study of ETCO2 will include assessing the degree of physiologic dead space in patients with lung pathology. As this monitoring methodology is increasingly used in veterinary medicine, further research will be needed to evaluate its multiple uses, reliability, and cost effectiveness.


ETCO2 monitoring provides clinicians with a valuable tool to assess and monitor patients. Because the physiology of CO2 production, metabolism, and excretion is so intricately linked to proper cardiopulmonary function, ETCO2 monitoring can provide information concerning the status of patient ventilation, circulation, and metabolism. ETCO2 is best analyzed in a systematic fashion, in which the actual value, waveform, and trend of waveforms over time are evaluated. Capnography can be used to identify potentially life-threatening situations such as esophageal intubation, circuit disconnection, a defective anesthetic system, hypoventilation, hypotension, and airway obstruction. Most of the data presented in this review are from the human literature. The ease and practicality of this monitoring tool make it useful in veterinary medicine. Additional research and clinical studies are needed to correlate its multiple uses in humans to animals as well as identify species and breed differences unique to veterinary medicine. As additional studies are conducted, the diagnostic and monitoring capabilities of capnography will be further defined.

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1. Luft K: Uber eine neue methode der registrierenden gasanalyse mit hilfe der absorption ultraroter strahlen ohne spektrale zerlegung. Zeitschrift Fur Technische Physik 24:97-104, 1943.

2. Smallhout B, Kalenda Z: An Atlas of Capnography, vol 1. Amsterdam, Kerkebosh/Zeist, 1975.

3. Saidman LJ, Smith NT: Monitoring in Anesthesia, ed 3. Woburn, UK, Butterworth-Heinmann, 1993.

4. Guyton AC: Transport of oxygen and carbon dioxide in the blood and body fluids, in Guyton AC, Hall JE (eds): Textbook of Medical Physiology. Philadelphia, WB Saunders, 2000, pp 463-473.

5. Clark JS, Votteri B, Ariagno RL, et al: Noninvasive assessment of blood gases. Am Rev Respir Dis 145:220-232, 1992.

6. Sanders AB: Capnometry in emergency medicine. Ann Emerg Med 18:1287-1290, 1989.

7. Raffe M: Oximetry and capnography, in Wingfield W, Raffe M (eds): The Veterinary ICU Book. Jackson Hole, WY, Teton New Media, 2000, pp 85-95.

8. Davis H: Arterial and venous blood gases, in Wingfield W, Raffe M (eds): The Veterinary ICU Book. Jackson Hole, WY, Teton New Media, 2000, pp 258-265.

9. Hackett T: Pulse oximetry and end-tidal carbon dioxide monitoring. Vet Clin North Am Small Anim Pract 32:1021-1029, 2002.

10. Gravenstein JHS, Paulus DA, Hayes TJ: Capnography in Clinical Practice. Stoneham, UK, Butterworth, 1989.

11. Bhende MS: Capnography in the pediatric emergency department. Pediatr Emerg Care 15:64-69, 1999.

12. Falk JL: ETCO2 monitoring during cardiopulmonary resuscitation. Ad Anesth 39:617-632, 1992.

13. Ward KR, Yealy DM: End-tidal CO2 monitoring in emergency medicine, Part I: Basic principles. Acad Emerg Med 5:628-636, 1998.

14. Grosenbaugh DA, Muir III W: Accuracy of noninvasive oxyhemoglobin saturation, ETCO2 concentration, and blood pressure monitoring during experimentally induced hypoxemia, hypotension or hypertension in anesthetized dogs. Am J Vet Res 159(2):205-212, 1998.

15. Hightower CE, Kiorpes AL, Butler HC, Fedde MR: End-tidal partial pressure of CO2 as an estimate of arterial partial pressure of CO2 during various ventilatory regimens in halothane-anesthetized dogs. Am J Vet Res 41(4):610-612, 1980.

16. Raemer DB, Calalang I: Accuracy of end-tidal CO2 tension analyzers. J Clin Monit 7:195-208, 1991.

17. Teixeira Neto FJ, Carregaro AB, Mannarino R, et al: Comparison of sidestream capnograph and mainstream capnograph in mechanically ventilated dogs. JAVMA 221(2):1582-1585, 2002.

18. Bhavani-Shankar K, Kumar AY, Moseley HS, et al: Terminology and current limitations of time capnography: A brief review. J Clinical Monit 11:175-182, 1995.

19. Bhavani-Shankar K, Moseley H, Kumar AY: Capnometry and anaesthesia. Can J Anaesth 39(6):617-632, 1992.

20. Fletcher R: The Arterio-end-tidal CO2 difference during cardiothoracic surgery. J Cardiothorac Anesth 5:105-117, 1990.

21. Chopin C, Fresard P, Mangaloboy J, et al: Use of capnography in diagnosis of pulmonary embolism during acute respiratory failure of COPD. Crit Care Med 18:353-356, 1990.

22. Russel G, Graybeal J: End tidal carbon dioxide as an indicator of arterial carbon dioxide in neurointensive care patients. J Neurosurg Anesthesiol 4:245-249, 1992.

23. Wagner AE, Gaynor JS, Dunlop CI, et al: Monitoring adequacy of ventilation by capnometry during thoracotomy in dogs. JAVMA 212(3):377-379, 1998.

24. Shankar K, Mosely Y, Kumar AY, Vemula V: Arterial to end tidal carbon dioxide tension difference during caesarean section anesthesia. Anesthesia 41:698-702, 1986.

25. Jones N, Robertson D, Kane J: Differences between end tidal and arterial Pco2 in exercise. J Appl Physiol 47:954-960, 1979.

26. Vaghadia H, Jenkins LC, Ford RW: Comparison of end-tidal carbon dioxide, oxygen saturation and clinical signs for the detection of oesophageal intubation. Can J Anaesth 36:560-564, 1989.

27. Guggenberger H, Lenz G, Gederte R: Early detection of inadvertent oesophageal intubation, pulse oximetry vs capnography. Acta Anaesth Scand 33:112-115, 1989.

28. Poirier MP, Gonzalez Del Rey JA, McAneney CM, et al: Utility of monitoring capnography, pulse oximetry and vital signs in detection of airway mishaps: A hyperoxemic animal model. Am J Emerg Med 16:350-352, 1998.

29. Eichorn JH: Effects of monitoring standards on anesthesia outcome. Int Anesth Clin 31(3):181-193, 1993.

30. Linko K, Paloheimo M, Tammisto T: Capnography for detection of accidental esophageal intubation. Acta Anaesthesiol Scand 27:199-202, 1983.

31. Savah AJ, Peacock WF, Overton DT: End-tidal CO2 measurement in detection of esophageal intubation during cardiac arrest. Ann Emerg Med 19:857-860, 1990.

32. Murray IP, Modell JH: Early detection of endotracheal tube accidents by monitoring CO2 concentration in respiratory gases. Anesthesiology 59:344-346, 1983.

33. Garnett AR, Gervin CA, Gervin AS: Capnographic waveforms in esophageal intubation: Effect of carbonated beverages. Ann Emerg Med 18:387-390, 1989.

34. Bhende MS, Thompson AE, Howland DF: Validity of a disposable ETCO2 detector in verifying ETT position in piglets. Crit Care Med 19:566-568, 1991.

35. Johnson P, Mann F, Dodam J, et al: Capnographic documentation of nasoesophageal and nasogastric feeding tube placement in dogs. J Vet Emerg Crit Care 12(4):227"233, 2002.

36. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB: End-tidal CO2 monitoring during CPR. JAMA 7(257):512-515, 1998.

37. Falk JL, Rackow Ed, Weil MH: End-tidal CO2 concentration during CPR. NEJM 318:607-611, 1998.

38. Weil MH, Bisera J, Trevino RP, Rackow EC: Cardiac output and ETCO2. Crit Care Med 13:907-909, 1985.

39. Gazmuri R, von Planta M, Wil MH, et al: Arterial PCO2 as an indicator of systemic perfusion during cardiopulmonary resuscitation. Crit Care Med 18:358, 1990.

40. Sanders AB, Atlas M, Ewy GA, et al: Expired CO2 as an index of coronary perfusion pressure. Am J Emerg Med 3:147-149, 1985.

41. Sanders AB, Ewy GA, Bragg S, et al: Expired Pco2 as a prognostic indicator of successful resuscitation from cardiac arrest. Ann Emerg Med 14(10):948-952, 1985.

42. Kern KB, Sanders AB, Voorhees WD, et al: Changes in expired ETCO2 during cardiopulmonary resuscitation in dogs: A prognostic guide for resuscitation efforts. J Am Coll Cardiol 13:1184-1189, 1989.

43. Bhende MA, Bafula DP, Menegazzi JJ: Evaluation of an ETCO2 detector during CPR in paediatric canine asphyxial arrest model. Pediatr Emerg Med 11:365-369, 1995.

44. Bhende MS, Thompson AE: Evaluation of an ETCO2 detector during paediatric CPR. Paedriatrics 95:395-399, 1995.

45. Bhende MS, Karasic DG, Karasic RB: End-tidal CO2 changes during cardiopulmonary resuscitation after experimental asphyxial cardiac arrest. Am J Emerg Med 14:349-350, 1996.

46. Cantineau JP, Lambert Y, Merckx P, et al: End-tidal CO2 during CPR in humans presenting for asystole: A predictor of outcome. Crit Care Med 24:791-796, 1996.

47. Levine RL, Wayne MA, Miller CC: ETCO2 and outcome of out of hospital cardiac arrest. N Engl J Med 337:301-306, 1997.

48. Weil MH, Bisera J, Trevino RP, et al: Cardiac output and end-tidal CO2. Crit Care Med 13:907, 1985.

49. Gudipati CV, Weil MH, Biser J, et al: Expired CO2: A noninvasive monitor of cardiopulmonary resuscitation. Circulation 77:234, 1988.

50. Ahrens T, Schallom L, Bettorf K, et al: End tidal CO2 measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care 10(6):391-398, 2001.

51. Callaham M, Barton C: Prediction of outcome of cardiopulmonary resuscitation from end-tidal CO2 concentration. Crit Care Med 18:358-362, 1990.

52. Martin GB, Gentile NT, Paradis NA, et al: Effect of epinephrine on end-tidal CO2 monitoring during CPR. Ann Emerg Med 19:396-398, 1990.

53. Tang W, Weil M, Gazumuri RJ, et al: Pulmonary perfusion defects induced by epinephrine during cardiopulmonary resuscitation. Circulation 84:2101- 2107, 1991.

54. Callaham M, Barton C, Matthay M: Effect of epinephrine on the ability of end-tidal CO2 readings to predict initial resuscitation from cardiac arrest. Crit Care Med 20(3):337-343, 1992.

55. Schena J, Thompson J, Crowe RK: Mechanical influence on the capnogram. Crit Care Med 12:672-674, 1984.

56. Szaflarski NL, Cohen NH: Use of capnography in critically ill adults. Heart Lung 20:363-374, 1991.

57. Carlon GC, Ray Jr C, Miodownik S, et al: Capnography in mechanically ventilated patients. Crit Care Med 16:50-56, 1988.

Tags: Monitoring and Nursing Compendium Compendium Canine