Capnography In Sedation and Pain Management

Monitoring respiratory rate, effort and efficacy of ventilation during pain management and sedation can be difficult in the field. Capnography is an ideal monitor for use during the administration of narcotics and benzodiazepines. The addition of EtCO2 monitoring enables earlier identification of respiratory depression in this group of patients. Standard vital signs, oxygen saturation and EtCO2 must also be monitored continuously. End-tidal carbon dioxide monitoring, although not required on all patients, provides an earlier indication of respiratory depression than pulse oximetry and respiratory rate alone.

Capnography, the continuous and noninvasive measurement and graphical display of end-tidal carbon dioxide (EtCO2), has been used for decades within anesthesia and critical care in the hospital environment. Capnography was used originally in mechanically ventilated patients to continuously and noninvasively assess patient levels of carbon dioxide on a breath-by-breath basis. The patient’s inspired and expired CO2 is graphically displayed as a waveform on the monitor. Alternative uses of capnography include monitoring adequacy of ventilation during pain management and sedation in the nonintubated patient.1

Capnography in EMS

Capnography use in EMS enables EMS providers to immediately identify problems with endotracheal tube placement. It is also useful in monitoring patients who are not intubated to assess alveolar ventilation and perfusion of the pulmonary vessels.2 The EMS?provider can use capnography as a supplemental tool and an early warning system to identify trends in ventilation and perfusion.3

Capnography monitors measure the partial pressure of CO2 in inhaled and exhaled breath. Inspired concentrations are normally zero, as the atmosphere contains only trace amounts of carbon dioxide. Usually, CO2 concentration reaches its maximum level at the end of exhalation; this is referred to as end-tidal CO2 (EtCO2).

CO2 Production

Carbon dioxide is the waste product of cellular metabolism. As cells consume oxygen, CO2 is produced, transferred to the circulation and returned to the lungs via venous return.

A simple model of the physiology of CO2 production and transport is the cellular production of CO2 as a metabolic byproduct of the oxidative breakdown of metabolic fuels. The higher the metabolic rate, as during exercise or exertion, the higher the CO2 production rate. CO2 dissolves rapidly in the cell and easily diffuses out of cells and into the vascular system, which carries it through the heart and into the pulmonary arteries to reach the capillaries surrounding pulmonary alveoli, the small air sacs in the lungs responsible for exchanging CO2 and oxygen (O2) between blood and air.

As ambient, nearly CO2-free air is drawn into each tiny alveolus during inspiration, the CO2 in the blood diffuses through the capillary and alveolar walls into the alveolar air sacs. Under normal conditions, one pass of the blood through the alveolar capillary allows the partial pressure of CO2 in the alveolar air (PaCO2) to nearly match (usually within 5 mmHg) the partial pressure of CO2 in the arterial blood (PaCO2) as measured by arterial blood gas (ABG) assays. As expiration begins, CO2-containing air is forced from the alveoli to displace and mix with the CO2-free air in the bronchial tree.

As this CO2-air mixture reaches the mouth (or nose), the measured CO2 partial pressure rises sharply to a “plateau,” which then slowly increases to a peak as nearly pure alveolar air reaches the nose or mouth. This peak partial pressure of CO2 at the end of expiration (EtCO2) in healthy individuals is generally within 5 mmHg of the arterial PaCO2. These differences can be affected by many patient factors, increasing, for example, in patients undergoing aggressive clinical procedures and in patients with significant cardiorespiratory disease.

Once inspiration begins, CO2-free ambient air is drawn in, and the CO2 partial pressure measured at the mouth or nose drops rapidly to almost zero. The abrupt expiratory rise, slowly rising plateau and rapid fall at the beginning of inspiration is the characteristic waveform of the capnogram.

Excretion of CO2 is the final common pathway of metabolism and provides a useful global indication of patient status. Ventilation must be adequate to carry oxygen into the lungs and remove carbon dioxide from the alveoli. Oxygen is transferred into the erythrocyte and transported to the cell at the tissue level. Transport is a function of the cardiovascular system. The process of aerobic metabolism consumes oxygen and produces carbon dioxide. The carbon dioxide is transferred from tissues into red cells and is transported to the lungs for elimination. Hypoxemia and cerebral or coronary ischemia are possible even in the presence of normal capnography waveforms and numerical values. The critical importance of the EtCO2 waveform and numerical value resides in the ability to reflect the patient’s cardiopulmonary status during pain management and sedation.4 A capnographer provides this information to the prehospital clinician continuously.

The Capnogram

Capnography is the measurement of carbon dioxide in respiratory gas. Capnometry involves the measurement and numerical display of CO2 values. A capnograph displays a waveform of CO2 (measured in millimeters of mercury or volume percent). The capnograph also displays the value of CO2 at the end of exhalation (EtCO2), the minimum value of CO2 during inspiration (FiCO2) and respiration rate (RR). The capnographic waveform has clinical value, as the waveform allows for interpretation just as ECGs are interpreted, diagnosed and treated.-

The capnogram (capnograph waveform) displays concentration across time. The horizontal axis reflects time; the vertical axis displays the concentration of EtCO2. Most devices manufactured today allow the display of ETCO2 in either a percentage (normal range of 5%–6%) or in millimeters of mercury (normal range of 35–45 mmHg). Displaying the EtCO2 value in percent correlates with measurement of oxygen delivery; display of the EtCO2 value in mmHg correlates with measurement of PaCO2.

Each waveform represents a single respiratory cycle, including both inspiration and expiration. The first segment of the waveform is the flat area near the beginning of exhalation. This flat area is gas in the dead space. The rapid rise in the waveform matches the mixture of air with gas from the alveoli. The waveform reaches the plateau as alveolar gas is exhaled. The EtCO2 level is measured at the peak of this plateau. As the patient inspires, the waveform rapidly drops to the baseline, which should remain at or near 0 mmHg, as inspired gas should not contain carbon dioxide.

In addition to displaying a single breathing cycle, capnography can display a trend, compressing many breaths together so that changes over time can be easily seen.

Monitoring During Pain Management and Sedation

Respiratory depression is a consistent effect of opioid and narcotic analgesics and may occur with therapeutic doses. Rate, minute volume and tidal exchange are all affected, diminishing alveolar gas exchange. The decreased responsiveness of brain stem respiratory neurons to CO2 is dose-related. With sufficient suppression of CO2 responsiveness, hypoxia may be the only stimulus for respiration through chemoreceptors in aortic arch and carotid body; administration of supplemental oxygen and the subsequent maintenance of oxygenation may completely suppress breathing.

Duration of the respiratory depressant effect of narcotic analgesics may be longer than the analgesic effect, resulting in the re-emergence of pain while the patient’s respiratory drive remains suppressed. The patient’s diminished sensitivity to an increase in CO2 may persist longer than the depression of their respiratory rate. The duration and degree of respiratory depression are dose-related. Profound analgesia is accompanied by marked respiratory depression, which can persist or recur. Hyperventilation due to pain or other stimulation may alter the patient’s responses to CO2, thus affecting respiration following administration of appropriate pain medications. Patients must remain under appropriate monitoring and assessment throughout prehospital treatment and transport.

Analgesics with the potential for respiratory depression should be used with caution in patients with severe impairment of pulmonary function because of the possibility of rapid and profound respiratory depression. This would include patients with chronic obstructive pulmonary disease, decreased respiratory reserve, or any patient with potentially compromised respiration. In such patients, narcotics may additionally decrease respiratory drive and increase airway resistance. This can be managed by assisted or controlled ventilation, not just administration of supplemental oxygen.

Benzodiazepines and other sedatives

These medications certainly can depress respiration following intravenous administration, although respiratory depression is more typically associated with barbiturates and opioids. Nevertheless, midazolam (Versed), for example, can cause an increase in PaCO2 and rapid respiratory depression.

In terms of respiratory depression, sedative-hypnotics are synergistic with opioids, alcohol and other respiratory depressants. Therefore, increased respiratory depression would be expected upon the concomitant administration of opioids with benzodiazepines.

Patients receiving narcotic pain medications or sedatives such as benzodiazepines should be continually monitored and evaluated for adequacy of ventilation. Clinical signs such as chest excursion, observation of the patient’s efforts and auscultation of breath sounds are valuable in EMS as well, but are of limited effectiveness in determining the quality of alveolar ventilation. Using medications that may impair protective airway reflexes or alveolar ventilation necessitates the use of capnography. Further, capnography facilitates better detection of potentially life-threatening problems than clinical judgment alone. Capnography can be used to monitor the adequacy of spontaneous ventilation not only during pain management and sedation, but also in the awake and unintubated patient with respiratory problems in the field.

Capnography has been shown to rapidly detect hypoventilation and early signs of respiratory distress before visual assessment of pulse oximetry. This advance in technology may reduce the incidence of respiratory emergencies.5 Capnography, using sidestream analysis, can be used to monitor the nonintubated patient for any reason.6

Respiratory Depression and Medications

Patients receiving medications that may impair ventilation are frequently monitored solely with a pulse oximeter—a monitoring device focused solely on oxygenation. In theory, a pulse oximeter measures the peak of arterial pressure and calculates oxygen saturation on the arterial pulse wave, yielding an accurate picture of arterial oxygenation. Oxygen saturation may or may not provide a good picture of the patient’s clinical condition. If the patient is receiving supplemental oxygen, the pulse oximeter may continue to display an elevated and correct SpO2 for several minutes following apnea. Patients can become apneic and maintain a relatively good SpO2 value due to the supplemental oxygen during this period. The process of carbon dioxide elimination through ventilation is best measured with EtCO2 monitoring.

Capnography can identify apnea or airway compromise much earlier than pulse oximetry. Neither pulse oximetry nor direct clinical observation of respiratory effort produce an immediate alarm for apnea. Capnography produces an alarm within seconds of an airway compromise.-

Capnography is an important tool in EMS monitoring simply because it allows rapid differential diagnosis of respiratory problems. When ventilation stops and oxygenation is impacted, time has already begun to work against the patient. A falling value on a pulse oximeter means that oxygen deprivation to the brain and vital tissues has already begun to affect the patient. A rise in EtCO2, however, measured on a capnograph, indicates that ventilation is impaired or impeded. No associated fall in oxygenation has yet occurred. Correcting the problem at this point means no loss of oxygen to the critical organs and an added margin of safety.

Capnography as Standard of Care

Although the use of capnography has not yet become a standard of care for monitoring patients during pain management and sedation, the clinical value is considerable. Capnography is the only way to assess adequacy of ventilation (not oxygenation) for patients on controlled mechanical ventilation, such as a bag-valve mask (BVM). If patients on a ventilator become hypoxic for any reason, and the PaCO2 remains constant, they do not necessarily become agitated (hypercarbia-induced catecholamine release and agitation). The pulse oximeter, while a valuable monitor of oxygenation, will not alarm in hypercarbic or hypocarbic states in the face of normal oxygenation.

Therefore, capnography is necessary to assess whether ventilation is proceeding normally in real time. It also assesses possible bronchospasm, thumbnail guesses of dead space and, of course, whether air is entering the patient’s trachea after intubation. Capnography gives a tremendous amount of useful information at a glance and allows troubleshooting in real time.

Capnography as a Respiratory Monitor

Respiration is defined as the process of molecular exchange of oxygen and carbon dioxide within the body’s tissues. EMS providers have widely embraced the importance of monitoring oxygenation via pulse oximetry, but have not yet adopted ventilation monitoring (capnography) to complete the view of the respiratory process. Although pulse oximetry has become a standard of care and is called the fifth vital sign, it cannot warn clinicians of ventilatory problems.

Ventilation monitoring, the other half of noninvasive respiratory monitoring, is best accomplished by capnography. During pain management and sedation, supplemental oxygen is usually delivered to maintain normal oxygenation status of the patient. The increase in the fraction of inspired oxygen (FiO2) may help to provide a normal pulse oximetry reading while hiding a dangerous case of hypoventilation-induced hypercapnia.

Historical Perspective on Capnography in EMS

EMS providers have not embraced capnography as they have pulse oximetry for several reasons. Historically, the equipment used to monitor EtCO2 was bulky and cumbersome to use; mainstream airway adapters were heavy and could easily displace a neonatal endotracheal tube; mainstream cables were costly to replace; and sensors could become clouded by condensation. Some equipment could be used only for intubated patients (or required further calibration and manipulation before use on nonintubated patients).

Sidestream sampling has had problems as well. Secretions and condensation caused constant occlusion alarms. High sample flow rates in sidestream monitors also competed for tidal volume in low-weight patients. EMS clinicians had to be cognizant of proper sample techniques or mixing would occur, rendering the resulting number and waveform useless.

New Technology

With availability of new capnographs, many of the old problems have been resolved. Several manufacturers make small monitors that are ideal for use in prehospital or intrahospital transport situations. Defibrillator/monitors also integrate the latest technologies in capnography. The technology does not require cumbersome calibration in the presence of other gases, and a spontaneously breathing patient can easily be monitored via nasal cannula or mask interface. If the same patient deteriorates and requires intubation, continued monitoring is accomplished by simply changing the interface connection at the monitor.

Sample tubes and filters have also been updated to allow significantly improved moisture handling, as well as to complement low sample flow rate aspiration. These advances in capnography technology and its ease of use will result in increased use.

Conclusion

The clinical applications of capnography in EMS are numerous and span several areas of prehospital care.7 Information related to ventilation, metabolism and perfusion can be obtained by monitoring EtCO2. Patients must have blood flow or cardiac output in order to return carbon dioxide to the lungs and then expel gas from them. Increased metabolism (as seen in fever) will increase carbon dioxide produced at the cellular level; therefore, when observing the EtCO2 value and waveform for abnormalities, clinicians should consider the most likely cause of abnormalities based on the clinical picture. A gradual change in the EtCO2 value can be due to a physiological problem, such as hypoventilation or hypovolemia. The pre-hospital clinician’s involvement in monitoring ventilation is vital. Noninvasive respiratory monitoring should provide an assessment of both oxygenation via pulse oximetry and ventilation via capnography. The capability and functionality of the newest equipment make capnography easier to perform in the field and more valuable for its clinical applications.

References

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