Use of ETCO2 Monitors

[Ace844]

Here's a great review article on this for all who are interetsed.

HTH,

ACE844

(Noninvasive Pco2 Monitoring for Respiratory Depression in the Nonintubated Patient

By Nancy G. Murphy @ MD, and Neal L. Benowitz, MD)

Arterial blood gas measurement of CO2 remains the gold standard for measuring the adequacy of ventilation, most commonly in the context of general anesthesia or critical illness in intubated (mechanically ventilated) patients. However, in these patients, as well as in nonintubated patients undergoing sedation, noninvasive measurements of CO2 have gained considerable importance in the last several years. The increasing frequency of procedural sedation, outpatient surgical and other painful procedures, and advanced pre hospital care, as well as the recognition that invasive monitoring has limitations, all have made noninvasive monitoring an important potential consideration in medical care. This is particularly true in the pediatric population, in which noninvasive monitoring is much less traumatic than more invasive monitoring procedures, such as arterial blood gas measurement.

This paper will describe the physiology of CO2, the available techniques for monitoring CO2, the interpretation of CO2 values, and the clinical settings in which this type of monitoring is currently being used. The main focus of this review will be on monitoring of nonintubated patients with therapeutic or iatrogenic drug-induced respiratory depression. Procedural sedation and analgesia is the prime example of this clinical scenario. Potent, rapidly acting IV medications are administered to patients requiring brief, painful procedures, such as fracture reductions, electrical cardioversion, incision and drainage of abscesses, or reduction of joint dislocations. These medications are given in successive boluses to achieve both analgesia and sedation, with the goal of maintaining protective airway reflexes and respiratory drive. Titrating these pharmacologic agents can be challenging. Noninvasive monitoring can provide continuous, dynamic information to alert the clinician to subclinical respiratory depression. Although respiratory depression from self-administered pharmacologic agents, including drugs of abuse, is beyond the scope of this review, many of the same general principles covered should also apply to CO2 monitoring in that context.

Physiology

The CO2 levels as measured clinically are a reflection of the balance between metabolism, circulation, and ventilation.

Cellular metabolism results in CO2 production, which can be substantially increased during marked motor activity (seizures, shivering) or with fever. CO2 production diminishes during general anesthesia or hypothermia.1

Changes in circulation can affect the partial pressure of CO2, or Pco2. The alveolar CO2 may markedly diminish in the context of decreased systemic blood flow, such as in cardiac arrest, even when alveolar ventilation is maintained. This is the result of concomitantly reduced pulmonary blood flow, thus leading to a lower amount of CO2 that is delivered to the lungs and exhaled air. Pulmonary embolism is another cause of reduced pulmonary blood flow that may also lead to a lower alveolar Pco2, or Paco2. The poorly perfused but ventilated areas of the lung result in an increase in the arterial-to-alveolar (Paco2 -Paco2 ) gradient, which is normally about 5 mm Hg.2

With respect to ventilation, alveolar gas exchange can usually compensate for changes in CO2 production. In most clinical settings, CO2 production remains relatively constant, such that Paco2 is mainly a function of alveolar ventilation.1 In the context of drug-induced respiratory depression, as may be encountered in procedural sedation, alveolar ventilation is reduced by either a reduced respiratory rate, reduced tidal volume, or both. Thus, the Pco2 measurements will increase, indicating inadequate alveolar gas exchange.

Noninvasive Monitoring Techniques

Noninvasive CO2 monitoring provides continuous, dynamic information about the adequacy of ventilation in patients. Arterial blood gas measurements are invasive and, although very accurate, provide only intermittent information about alveolar gas exchange, even if an indwelling arterial line allows relatively frequent assessment. There are currently two main techniques for noninvasive Pco2 monitoring in the clinical setting: end-tidal and transcutaneous methods.

End-tidal CO2 (ETCO2) is a reflection of mixed alveolar CO2 and can be assessed by either chemical reactions (colorimetry) or measurement of CO2 molecules. This latter technique provides both a waveform and an actual Pco2 value, whereas colorimetry provides a single indication of the presence or absence of CO2 in exhaled air through a change in pH, and thus a change in the color of the test paper.2 The test paper turns blue or purple if the exhaled air contains <0.5% CO2 , and yellow if there is >2 to 4% CO2 in the exhaled air. For values between 0.5% and 2 to 4%, the colors are dependent on the manufacturer and should be verified prior to interpretation. Colorimetric indicators are small devices that attach to the endotracheal tube and are removed and discarded after use. Colorimetry is most useful in the confirmation of endotracheal tube placement in the prehospital setting, and for intermittent verifications of the proper positioning of the endotracheal tube.3

Measurement of CO2 molecules can be done by infrared spectroscopy, mass spectrometry, Raman gas analysis, or photoacoustic spectrography. Infrared spectroscopy is the most commonly used method. The Paco2 should be measured within the endotracheal tube in intubated patients, either by mainstream (directly in the endotracheal tube) or sidestream (air drawn through tubing to an analyzer) analysis. In nonintubated patients, the measurement should take place near the nares or mouth. This is accomplished via an oral/nasal cannula, with or without a port for oxygen administration.1

The waveform generated by this method can provide important information on ventilatory patterns. The most common display mode on the monitor is Pco2 vs time. The respiratory cycle is defined in four phases, as shown in Figure 1. Phase I is exhaled CO2 from the large airways, when Pco2 is zero. Phase II is the transition between large airway and alveolar gas. Phase III, the alveolar plateau, is normally flat and the end of this phase corresponds to ETCO2. Phase IV is inspiration, when once again the Pco2 decreases to baseline. If the waveform is absent (flat line), this could indicate apnea, airway obstruction, or a problem with the monitor or ventilator connections.

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Figure 1. Top, the respiratory cycle as displayed on a capnogram. The ETCO2 is measured at the end of phase III. Bottom, apnea as displayed on a capnogram, in which case CO2 is equal to zero.

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Good correlation between ETCO2 values and arterial values has been documented in several studies in the context of pediatric seizures, general anesthesia, and ICU monitoring.4-9 Other studies involving patient populations with pulmonary disease or other significant medical conditions, however, have found a lack of correlation between these two methods.10,11 If there is a significant ventilation/ perfusion mismatch, or a decrease in pulmonary blood flow, ETCO2 measurements will be much lower than arterial Pco2 (underestimated the extent of hypercapnia) because of a lower amount of CO2 reaching the alveoli. In general, patients undergoing procedural sedation do not tend to have significant pulmonary disease, and thus ETCO2 measurements should be reliable for monitoring purposes.

Transcutaneous CO2 (TcCO2) monitors measure tissue CO2 through a skin electrode by means of the electrochemical Stow-Severinghaus method of analysis. The electrode is heated to about 42 to 44 °C to cause local vasodilation and arterialization of the tissue. The electrode may be attached to the abdomen or, as in newer models, to the earlobe. Once the electrode is applied, the monitor requires approximately 10 to 15 min for calibration. To avoid thermal injury, the site of the electrode must be changed every 4 to 12 hours, depending on the model. Because the CO2 measurements are taken through the skin, they may be affected by edema, scarring, hypoperfusion, and use of vasopressors,5 although using an earlobe sensor may minimize these issues.

TcCO2 monitoring has been studied in adult and pediatric patients under general anesthesia, in nonintubated adults, and in pediatric and newborn patients in the ICU.12-14 The studies on this method of noninvasive monitoring have demonstrated excellent correlation between TcCO2 and arterial Pco2, with a higher accuracy than ETCO2.

Direct comparison of end-tidal vs transcutaneous CO2 monitoring reveals advantages and disadvantages for both methods, depending on the clinical situation (Table 1). As previously mentioned, ETCO2 is a reflection of mixed alveolar gas and can become inaccurate if there is a ventilation/perfusion mismatch caused by abnormal pulmonary function. In addition, dramatically reduced systemic blood flow, as seen in cardiac arrest or systemic shock, can cause a significant decrease in ETCO2 and a widening of the ETCO2 -Paco2 gradient.15,16 In contrast, TcCO2 maintains its accuracy in the presence of pulmonary pathology, but can also be affected by hypoperfusion, abnormal skin conditions, and use of vasopressor agents. In addition, there is a lag time between changes in ventilation and reflection of these changes by TcCO2 of 1 min to several minutes,13 making ETCO2 more useful if sudden changes in ventilation are expected. Thus, there is no suitable substitute for ETCO2 monitoring in the setting of apnea, confirmation of endotracheal tube placement, or a disconnection of the ventilator to the patient, as the change in ETCO2 is reflected rapidly and is represented visually by a major change in the waveform.2 Another potential disadvantage of TcCO2 is the time needed to calibrate and equilibrate the monitor, the more regular maintenance required (changing the electrode membrane, replacing the calibration gas canister), and the potential for cutaneous thermal injury. However, when ETCO2 monitoring is not feasible, TcCO2 can play a crucial role. For example, measuring ETCO2 during bronchoscopy, thoracoscopy, or noninvasive positive pressure ventilation is difficult.12,13 In addition, TcCO2 monitoring in newborns is more convenient, more accurate, and better tolerated than ETCO2. When the accuracy of Pco2 measurements is of critical importance —such as in monitoring diabetic ketoacidosis or in head-injured patients with increased intracranial pressure—TcCO2 may also prove to be advantageous.7,17,18 In the setting of procedural sedation, only ETCO2 has been studied and therefore a direct comparison of the two methods cannot be made.

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Procedural Sedation and Noninvasive Pco2 Monitoring

Brief, painful procedures in the emergency department and ICU are commonly performed and require rapidly acting, potent sedatives and analgesics. Most of the medications used have the potential to cause respiratory depression. In particular, IV administration of propofol, opioids, methohexital, benzodiazepines (in combination with other medications), ketamine, and etomidate may result in subclinical or overt respiratory depression, as detected by hypercapnia, absent waveform, or hypoxia.19-24 Respiratory depression in this setting is defined as a change from baseline CO2 of >10 mm Hg, ETCO2 >50 mm Hg, or oxygen desaturation of <90% for at least 1 min. Capnography is superior to pulse oximetry in detecting subclinical respiratory depression, especially if supplemental oxygen is administered. As a result, capnography might alert the physician to hold off on further doses of sedatives, or to provide airway interventions as needed.25

The methods for performing procedural sedation have evolved considerably in the last decade, with development of specific protocols to ensure patient safety. The rate of adverse events during procedural sedation is relatively low in the hands of skilled, experienced health-care providers following an established protocol. Nonetheless, such complications do occur, including respiratory depression, hypotension, vomiting, laryngospasm, and rarely, pulmonary aspiration.26 Moroever, an ever-expanding variety of sedative agents also introduces opportunities for medical misadventure. Capnography provides additional information beyond that provided by standard cardiorespiratory monitoring that could further decrease the rate of adverse events.

Interpretation of Pco2 Measurements

Arterial Pco2 values are normally in the range of 35 to 45 mm Hg. ETCO2 tends to underestimate the Paco2 by 3 to 5 mm Hg, whereas TcCO2 tends to overestimate Paco2 by 2 to 4 mm Hg. There is no known interference between carbon monoxide and infrared spectroscopic measurement of ETCO2 , as is the case with pulse oximetry.27 An important concept is the arterial-to-alveolar gradient, which can change in certain disease states. This gradient has been well described and is normally about 5 mm Hg. The gradient has been used not only to describe the accuracy of ETCO2 compared with arterial blood gas measurements under normal conditions, but also to diagnose and monitor the treatment of pulmonary embolism.28

Hypercapnia is the major concern during procedural sedation in the nonintubated patient for all of the reasons stated previously. ETCO2 is inversely proportional to minute ventilation. When medications that depress respiratory drive are administered, respiratory rate and tidal volume may decrease, resulting in alveolar hypoventilation and an increase in the ETCO2. According to standard procedural sedation monitoring protocols, respiratory depression is defined as a change in ETCO2 from baseline of >10 mm Hg, any reading of >50 mm Hg, or apnea, as reflected by the absence of a waveform. As was noted previously, hypocapnia can occur during hypothermic states, under general anesthesia, in states of decreased pulmonary blood flow (pulmonary embolism), and in shock states (ie, cardiac arrest). In this context, ETCO2 has been used as a predictor of outcome in cardiac arrest and response to cardiopulmonary resuscitation (CPR). It has been shown that patients undergoing CPR for cardiac arrest have a poorer prognosis when the ETCO2 does not increase from <10 mm Hg compared with patients whose ETCO2 values increase closer to normal during CPR.15,16 In addition, ETCO2 has been shown to reflect the response to thrombolytic therapy in severe pulmonary embolism by increasing closer to normal values as pulmonary blood flow improves.27 Noninvasive CO2 monitoring of diabetic ketoacidosis has recently been investigated as well. Hypocapnia exists in this setting as a result of hyperventilation in response to a primary metabolic acidosis, and capnography has been shown to correlate well with serum bicarbonate values. Noninvasive CO2 monitoring in this setting may limit the need for frequent measurement of acid-base status and can also provide continuous, rather than intermittent, monitoring of the acid-base status.17,18

Conclusion

Noninvasive CO2 measurement is evolving and is likely to become an integral technique for respiratory monitoring in the nonintubated patient undergoing procedural sedation. Understanding the limitations as well as the advantages of this technique will ensure appropriate interpretation of the CO2 values clinically. In addition, both end-tidal and transcutaneous CO2 monitoring can provide noninvasive and continuous clinical information for patients with metabolic, pulmonary, and circulatory disease.

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References

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Ahrens T, Sona C. Capnography application in acute and critical care. AACN Clin Issues 2003; 14:123–132

Bhende MS, LaCovey DC. End-tidal carbon dioxide monitoring in the prehospital setting. Prehosp Emerg Care 2001; 5:208–213

Reid CW, Martineau RJ, Miller DR, et al. A comparison of transcutaneous, end-tidal and arterial measurements of carbon dioxide during general anesthesia. Can J Anesth 1992; 39:31–36

Berkenbosch JW, Lam J, Burd RS, et al. Noninvasive monitoring of carbon dioxide during mechanical ventilation in older children: end-tidal versus transcutaneous techniques. Anesth Analg 2001; 92:1427–1431

Phan CQ, Tremper KK, Lee SE, et al. Noninvasive monitoring of carbon dioxide: a comparison of the partial pressure of transcutaneous and end-tidal carbon dioxide with the partial pressure of arterial carbon dioxide. J Clin Monit 1987; 3:149–154

McBride DS Jr, Johnson JO, Tobias JD. Noninvasive carbon dioxide monitoring during neurosurgical procedures in adults: end-tidal versus transcutaneous techniques. South Med J 2002; 95:870–874

Nosovitch MA, Johnson JO, Tobias JD. Noninvasive intraoperative monitoring of carbon dioxide in children: endtidal versus transcutaneous techniques. Paediatr Anaesth 2002; 12:48–52

Abramo TJ, Wiebe RA, Scott S, et al. Noninvasive capnometry monitoring for respiratory status during pediatric seizures. Crit Care Med 1997; 25:1242–1246

Prause G, Hetz H, Lauda P, et al. A comparison of the end-tidal CO2 documented by capnometry and the arterial Pco2 in emergency patients. Resuscitation 1997; 35:145–148

Sanders MH, Kern NB, Costantino JP, et al. Accuracy of end-tidal and transcutaneous Pco2 monitoring during sleep. Chest 1994; 106:472–483

Chhajed PN, Kaegi B, Rajasekaran R, et al. Detection of hypoventilation during thoracoscopy. Chest 2005; 127:585–588

Janssens JP, Howarth-Frey C, Chevrolet JC, et al. Transcutaneous Pco2 to monitor noninvasive mechanical ventilation in adults. Chest 1998; 113:768–773

Bernet-Buettiker V, Frey B, Hug MI, et al. Evaluation of a new combined transcutaneous measurement of Pco2/pulse oximetry oxygen saturation ear sensor in newborn patients. Pediatrics 2005; 115:e64–e68

Grmec S, Lah K, Tusek-Bunc K. Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting. Crit Care 2003; 7:R139–R144

Grmec S, Klemen P. Does the end-tidal carbon dioxide (ETCO2) concentration have prognostic value during out-of-hospital cardiac arrest? J Emerg Med 2001; 8:263–269

Garcia E, Abramo TJ, Okada P, et al. Capnometry for noninvasive continuous monitoring of metabolic status in pediatric diabetic ketoacidosis. Crit Care Med 2003; 31:2539–2543

McBride ME, Berkenbosch JW, Tobias JD. Transcutaneous carbon dioxide monitoring during diabetic ketoacidosis in children and adolescents. Paediatr Anaesth 2004; 14:167–171

Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med 2002; 9:275–280

Tobias JD. End-tidal carbon dioxide monitoring during sedation with a combination of midazolam and ketamine for children undergoing painful, invasive procedures. Pediatr Emerg Care 1999; 15:173–175

Hart LS, Berns SD, Houck CS, et al. The value of end-tidal CO2 monitoring when comparing three methods of conscious sedation for children undergoing painful procedures in the emergency department. Pediatr Emerg Care 1997; 13:189–193

Vinson DR, Bradbury DR. Etomidate for procedural sedation in emergency medicine. Ann Emerg Med 2002; 39:592–598

Miner JR, Martel ML, Meyer M, et al. Procedural sedation of critically ill patients in the emergency department. Acad Emerg Med 2005; 12:124–128

Bassett KE, Anderson JL, Pribble CG, et al. Propofol for procedural sedation in children in the emergency department. Ann Emerg Med 2003; 42:773–782

Yildizdas D, Yapicioglu H, Yilmaz HL. The value of capnography during procedural sedation or sedation/analgesia in pediatric minor procedures. Pediatr Emerg Care 2004; 20:162–165

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[AZCEP]

To tie into Ace's last post, great information by the way, we've made it semi-policy that any patient receiving medications, or with complaints above the waist, have EtCO2 documented on them. The waveform makes it that much easier to justify what needs/doesn't need to be done.

The receiving faciltiies look rather puzzled when I explain to them the capnography is to monitor ventilation, not oxygenation.

[Ridryder 911]

As the infamous Dr. Krauss ( Jems several articles on EtC02) calls it the....."the tail, wagging the dog syndrome"...... In one of his lectures, he describes EMS is more educated on the use of EtC02, than possibly 95% of ER physicians.

This is very true even in my area. Even though I spec. every ER cardiac rooms (21 beds) with EtC02 (side stream even) they have used 10 times .... 9 of those times I was the one. We have had a problem of the ER physician "pulling the tube" announcing it was not in place, even though we had a nice wave form and lung sounds... I politely discussed with our new Medical Director, which so happens to be the new ER director as well. I informed him of the accuracy of EtC02 and how foolish, and problematic this could be as well as potential litigation ( the former physician pulled an ETT and was unable to re-intubate). Ironically, this "problem physician, now asks if we have lung sounds and wave form..no longer an argument. We need to educate the Doc's slowly an professionally, they will come around.

R/r 911

[chbare]

Thank you Ridryder 911 everybody else. This a worthy topic in and out of the hospital.

Take care,

chbare.

[redwolfef6]

To tie into Ace's last post, great information by the way, we've made it semi-policy that any patient receiving medications, or with complaints above the waist, have EtCO2 documented on them. The waveform makes it that much easier to justify what needs/doesn't need to be done.

The receiving faciltiies look rather puzzled when I explain to them the capnography is to monitor ventilation, not oxygenation.

That sounds like a great idea. In my agency we routinely use Capnography on all respiratory complaints & confirming Ett placement. I haven't heard of it being used for CPR effectiveness or pacemaker.

Could you explain the use of capnography in the pacemaker setting? Sounds very interesting.

[AZCEP]

It is a bit of an extrapolation of what you are already using it for, but not too tough to figure.

If the patient has a pacemaker, and for some reason you think it is not being effective. Be it rate, contraction of the heart, reduced cardiac output, will all show as changes to the size of the waveform. If you see a EtCO2 value that is less than what you know should be normal, you need to start looking for a cause.

Cardiac arrest is the easiest to see this happen in. Initial values should be close to normal, because the CO2 gets trapped in the hypopharynx. Then, in short order, the value drops as you ventilate and blood doesn't return to the lungs as well. When your CPR is effective, you will get a steep increase in the amount of CO2 that is picked up. More blood returning from the periphery, wouldn't you know. As your compressor gets tired, the CO2 value drops. Change rescuers, CO2 increases. On the ROSC, the CO2 should increase as well, and has been shown to indicate better long term survival.

Very good stuff, and so easy to use I commonly tell my BLS colleagues to use it.

[redwolfef6]

8) Very cool thanks for the response. Where might I find more info?

[Ace844]

8) Very cool thanks for the response. Where might I find more info?

doing a search here might help...Just a thought... :roll:

[itku2er]

We use them to see CO2 detection and tube placement.........but me i prefer the old and proven way.......I WANT TO LISTEN but that is just me.......... 8) 8) 8)

There is a room for error here ........what if you get a defective unit? If you use it for placement checks then you are gonna screw up somewhere........ :wink:

[Ace844]

We use them to see CO2 detection and tube placement.........but me i prefer the old and proven way.......I WANT TO LISTEN but that is just me.......... 8) 8) 8)

There is a room for error here ........what if you get a defective unit? If you use it for placement checks then you are gonna screw up somewhere........ :wink:

Not if you follow the GOLD STANDARD OF ETI CONFIRMATION and thats TO WATCH IT PASS THROUGH THE CORDS UNDER DIRECT VISUALIZATION!!! Everything else is 2nd best :wink: