Capnography is vital during sedation
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Capnography During Sedation
The line of demarcation between conscious sedation and general anesthesia is sometimes very thin. It is possible during conscious sedation, intravenous sedatives and narcotics administered to allay apprehension can result in the loss of consciousness and respiratory obstruction. If this is not recognized immediately, the patient can become hypoxic. In the majority of cases, the respiratory obstruction occurs well before the onset of hypoxia. Therefore monitoring of respiratory status is essential to enable corrective measures before the occurrence of hypoxia. Following illustration explains reinforces this concept .
Pulse oximetry is a monitor of oxygenation
Supplemental oxygen can mask apnea or hypoventilation
A Preponderance of evidence suggests that procedural sedation is associated with undetected apnea or hypoventilation that can result in oxygen desaturation.
Hence it is obvious that some type of ventilation monitoring is required to safeguard against hypoxia during sedation procedures outside of the operating room.
To detect apnea or hypoventilation during procedural sedation, a specific monitor of ventilation is required.
The value of capnography is well appreciated during anesthesia as an airway and ventilation monitor so much so that it has become a standard of practice in the operating room.
It is only a matter of time that capnography will find its way to becoming incorporated as a standard of practice for monitoring ventilation during sedation procedures.
Capnography has evolved into a standard of monitoring during anesthesia because it has proven itself to be a valuable tool in recognizing ventilatory and circulatory events that could potentially lead to deleterious effects. Hypoxia is our primary concern during anesthesia, and therefore, by all means, any situation that results in hypoxia is avoided. One of the greatest assets of capnography is that it can identify situations that can potentially result in hypoxia. Capnography serves as a warning device by instantly drawing the anesthesiologist's attention to the events that could potentially lead to hypoxia, if uncorrected. Because of this, care- providers have been encouraged to extend the benefit of capnography to areas beyond the domain of anesthesiologists. Examples include the use of capnography in the EMT / ambulance services for monitoring ventilation, and emergency medical rooms for procedures and sedation.
Presently, several procedures are being performed under sedation outside of the operating room. Although the aim of the conscious sedation nurse/personnel is to provide conscious sedation, the line between conscious sedation and sleep is very narrow and the patient drifts quite often into an unconscious state. During this state of sleep, airway obstruction or hypoventilation may occur that may not be detected until hypoxia occurs as is indicated by pulse oximetry. Occasionally endoscopies performed via the upper airway can also result in airway obstruction. The delayed identification of airway problems leads to a delayed intervention. It is not uncommon for anesthesiologists to be called in urgently to intervene under these circumstances. Capnography could provide early warning in identifying such respiratory or airway problems in advance so that corrective intervention can be undertaken before hypoxia ensues.
Policymakers who understand the potential benefits and strides made in the operating room by capnography, logically recommend and extend its use to areas beyond the operating room to enhance the safety of patients undergoing sedation procedures. Capnography is routinely used in patients undergoing cardiac electrophysiology studies and ablation, ICD placement and testing at our institution. Others look for evidence to determine if capnography has truly any beneficial role to play in sedation procedures outside of the operating room.
The value of capnography was recognized in the operating room settings prior to being adopted as standard of monitoring during anesthesia procedures. Similarly, several recent studies have shown the benefit of capnography in identifying events that can potentially lead to hypoxia during procedural sedation. This could be a precursor for capnography being accepted as standard of care during sedation procedures in the near future.
Vargo et al studied forty-nine patients undergoing therapeutic therapeutic upper endoscopy, who were monitored with standard methods including pulse oximetry, automated blood pressure measurement, and visual assessment. In addition, graphic assessment of respiratory activity with side-stream capnography was performed in all patients. Endoscopy personnel were blinded to capnography data. Episodes of apnea (cessation of respiration for 30 or more seconds) or disordered respiration (45 second interval that contained at least 30 seconds of cumulative apneic activity) detected by capnography were documented and compared with the occurrences of hypoxemia, hypercapnea, hypotension, and the recognition of abnormal respiratory activity by endoscopy personnel. Capnography identified 54 events of apnea or disordered respiratory events during the endoscopic procedure, whereas, pulse oximetry picked up only 27 events (50%) where the respiratory events that were detected by capnography progressed to result in hypoxia (as defined by oxygen saturation below 90%). Hypoxemia occurred approximately 45.6 seconds (15-120 seconds) after the capnographic detection of respiratory events. Visual inspection of the patient by the care providers detected none of the 54 events detected by capnography. Capnography also detected hypoventilation as shown by a 25% increase from baseline end expiratory carbon dioxide values.
Minor et al prospectively studied whether end-tidal carbon dioxide (ETCO2) monitors can detect respiratory depression (RD) and the level of sedation in emergency department (ED) patients undergoing procedural sedation. This was a prospective observational study conducted in an urban county hospital of adult patients undergoing procedural sedation. Patients were monitored for vital signs, depth of sedation per the physician by the Observer's Assessment of Alertness/Sedation scale (OAA/S), pulse oximetry, and nasal-sample ETCO2CO2 during procedural sedation. Respiratory depression was defined as an oxygen saturation <90%, an ETCO2 >50 mm Hg, or an absent ETCO2 waveform at any time during the procedure. The physician also determined whether protective airway reflexes were lost during the procedure and assisted ventilation was required, or whether there were any other complications. Seventy-four patients were enrolled in the study. Forty (54.1%) received methohexital, 21 (28.4%) received propofol, ten (13.5%) received fentanyl and midazolam, and three (4.1%) received etomidate. Respiratory depression was seen in 33 (44.6%) patients, including 47.5% of patients receiving methohexital, 19% receiving propofol (p = 0.008), 80% receiving fentanyl and midazolam, and 66.6% receiving etomidate. No correlation between OAA/S and ETCO2 was detected. Eleven (14.9%) patients required assisted ventilation at some point during the procedure, all of whom met the criteria for RD. Pulse oximetry detected 11 of the 33 patients with RD. Using the criteria of an ETCO2 >50 mm Hg, an absolute change >10 mm Hg, or an absent waveform may detect subclinical RD not detected by pulse oximetry alone. The authors concluded that the ETCO2 may add to the safety of procedural safety by quickly detecting hypoventilation during sedation in the Emergency department.
McQuillen and steele described ETCO2 changes associated with different sedation strategies. This was a prospective, observational patient series in an urban pediatric emergency department (PED). Participants included 106 children with a mean age of 6.8 years. (range 1.2-16.6 years). Sedation/analgesia was given for fracture reduction (55%), laceration repair (37%), abscess incision and drainage (4%), and lumbar puncture (LP) (4%). Medications included fentanyl, morphine, ketamine, and midazolam. Continuous ETCO2 waveforms were recorded via a Capnogard ETCO2 Monitor. Oxygen saturation was recorded using a Nelcor N-200 pulse oximeter. Recording began prior to sedation and continued until the patient was awake or when it was necessary to remove the patient from the monitor for further medical care. Each record was analyzed for peak ETCO2 and averaged over five consecutive breaths, before and after the administration of medications. The main outcome measure was the change in ETCO2 levels. The mean increase in ETCO2 was 6.7 mmHg (P is included in, 0.00001; range: +0.16 to +22.3). ETCO2 increased by 3.2 mmHg (95% CI = 2.2-4.2) for midazolam alone, 5.4 mmHg (95% CI = 4.5-6.4) for midazolam and ketamine, and 8.8 mmHg (95% CI = 7.4-10.2) for midazolam and opiate. Two patients had transient SpO2 desaturations below 93%, which corrected with stimulation. The authors concluded that commonly used agents for pediatric sedation result in significant increases in ETCO2. ETCO2 is a useful adjunct in assessing ventilation and may serve as an objective research tool for assessing different sedation strategies.
Tobias in his study used both end-tidal carbon dioxide (ETCO2) monitoring and pulse oximetry to evaluate the respiratory effects of revised midazolam and ketamine protocol. Fifty children who required sedation during invasive procedures formed the cohort for the study. During sedation, ETCO2 was sampled from nasal cannulae of spontaneously breathing patients and measured by a side-stream aspirating infrared device. During the procedure, O2 saturation decreased by 3% or more in three patients. Supplemental oxygen at 2 liters per minute was administered to these patients. The lowest oxygen saturation was 84%. During the total of 767 minutes of monitoring, there were 3068 ETCO2 values recorded. The high ETCO2 values ranged from 37 to 53 mmHg (40.5 +/- 3.3 mmHg). Ninety percent, or 2760, of the values were 40 mmHg or less, 7% or 214 were between 41 and 45 mmHg, 3% or 92 were between 46 and 49 mmHg, and 2 isolated values were greater than 50 mmHg. One episode of airway obstruction was identified by noting cessation of the ETCO2 waveform. This was relieved by repositioning the patient's airway. The three episodes of O2 desaturation, two ETCO2 values greater than 50 mmHg, and the episode of upper airway obstruction all occurred in three patients. Two of these patients had trisomy 21 with macroglossia, and the third had had a recent upper respiratory infection and a history of tonsillar hypertrophy. The incidence of adverse cardiorespiratory events associated with the current sedation regimen of midazolam-ketamine is lower than that reported with other commonly used regimens. The addition of ETCO2 monitoring provides an additional monitor to allow for early detection of airway obstruction or subclinical degrees of respiratory depression.
Hart et al state that many studies have evaluated conscious sedation regimens commonly used in pediatric patients and recent advances in capnography equipment now enable physicians to assess respiratory parameters, specifically end-tidal CO2 (et-CO2), more accurately in spontaneously breathing sedated children than was possible in the earlier studies. They designed the study to: 1) compare the safety and efficacy of intravenous fentanyl, intravenous fentanyl combined with midazolam, and intramuscular meperidine-promethazine-chlorpromazine (MPC) compound when used for painful emergency department (ED) procedures: and 2) to determine whether the addition of et-CO2 monitoring enabled earlier identification of respiratory depression in this population. Forty-two children requiring analgesia and sedation for painful ED procedures were randomly assigned to receive either fentanyl, fentanyl-midazolam, or MPC compound. Vital signs, oxygen saturation, and et-CO2 were monitored continuously. Pain, anxiety, and sedation scores were recorded every five minutes. Respiratory depression (O2 saturation < or = 90% for over the minute or any et-CO2 > or = 50) occurred in 20% of fentanyl, 23% of fentanyl-midazolam, and 11% of MPC patients (P = NS). Of those patients manifesting respiratory depression, 6/8 were detected by increased et-CO2 only. MPC patients required significantly longer periods of time to meet discharge criteria than fentanyl and fentanyl-midazolam patients (P < 0.05). No differences were noted in peak pain, anxiety, or sedation scores. The authors concluded that Fentanyl, fentanyl-midazolam, and MPC produced a high incidence of subclinical respiratory depression. End-tidal CO2 monitoring provided an earlier indication of respiratory depression than pulse oximetry and respiratory rate alone. MPC administration resulted in a significantly delayed discharge from the ED.
All the above studies are unanimous in that airway compromise and hypoventilation events do occur during procedural sedation and capnography identifies these events earlier than pulse oximetry. Thus, capnography serves as an early warning device of an impending hypoxia.
If anesthesiologists are involved in laying out guidelines for non-operating-room locations, they are more likely to include capnography to monitor ventilation. This is probably because, by nature, anesthesiologists are trained to think about airway and ventilation at all times. This is also the reason why our cardiac electrophysiology/ablation rooms and minor Obstetric procedure rooms are provided with capnography as we oversee the sedation and anesthesia care here. The American Society of Anesthesiology in their document on "Practice Guidelines for Sedation and Analegesia by Non-Anesthesiologists" under the section 'Pulmonary ventilation' (http://www.asahq.org/publicationsAndServices/practiceparam.htm) states as follows:
"It is the opinion of the Task Force that the primary causes of morbidity associated with sedation/analgesia are drug-induced respiratory depression and airway obstruction. For both moderate and deep sedation, the literature is insufficient to evaluate the benefit of monitoring ventilatory function by observation or auscultation. However, the consultants strongly agree that monitoring of ventilatory function by observation or auscultation reduces the risk of adverse outcomes associated with sedation/analgesia. The consultants were equivocal regarding the ability of capnography to decrease risks during moderate sedation, while agreeing that it may decrease risks during deep sedation. In circumstances where patients are physically separated from the caregiver, the Task Force believes that automated apnea monitoring (by detection of exhaled CO2 or other means) may decrease risks during both moderate and deep sedation, while cautioning practitioners that impedance plethysmography may fail to detect airway obstruction. The Task Force emphasizes that because ventilation and oxygenation are separate though related physiological processes, monitoring oxygenation by pulse oximetry is not a substitute for monitoring ventilation."
Therefore, there are recommendations to monitor ventilation during procedural sedation 'particularly' if deep, but not a standard. Yet, it is up to the care-providers to decide how and what method is best for their practicing environment. Certainly capnography provides an early warning device to draw attention to abnormal ventilation.
No doubt, capnography has limitations, particularly in nasal sampling. This limitation should be understood. However, there are devices to improve sampling of carbon dioxide in expired air and thus decrease artifacts. I generally get a baseline waveform and ETCO2 values, and focus attention to any changes from the baseline values. Thinking, always in my mind that any changes in ETCO2 from the baseline are due to depression of ventilation or airway obstruction until otherwise proven by close examination. In my opinion, a decrease in pulse oximetry is a late finding, and I would use other methods to identify events before they have had a chance to produce hypoxia.
In conclusion, capnography seems to be a logical device to monitor ventilation during procedural sedation. This is because (a) The general consensus among anesthesiologists is that airway problems are primary causes of morbidity associated with sedation/analgesia are drug-induced respiratory depression and airway obstruction; (b) Available studies on procedural sedation confirm that respiratory events precede hypoxia, and capnography is a valuable monitoring device to detect respiratory events that could culminate in hypoxia; (c) Sedation procedures are being performed more often by non-anesthesiologists at remote locations from the 'OR' (operating room). They may not be as well experienced and adept as anesthesiologists in recognizing airway obstruction, apnea and hypoventilation; (d) Endoscopic physicians are preferring to use hypnotic agents such as propofol for quick recovery and discharge to reduce health care cost. These agents can result in respiratory depression and apnea. Just like the evolution of capnography in the operating room from a guideline status to the status of standard of practice, it is only a question of time that capnography will be accepted as a standard of care to enhance patient safety during procedural sedation.
1. Vargo JJ, Zuccaro G, Dumont JA, Conwell DL, Morrow JB, Shay SS. Automated graphic assessment of respiratory activity is superior to pulse oximetry and visual assessment of the detection of early respiratory depression during therapeutic upper endoscopy. Gastrointestinal Endoscopy 2002;55:826-31.
2. Miner JR, Heegaard W, Plummer D. End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med 2002;9:275-80.
3. McQuillen KK, Steele DW. Capnography during sedation/analgesia in the pediatric emergency department. Pediatr Emerg Care 2000;16:401-4.
4. 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;15:173-5.
5. Hart LS, Berns SD, Houck CS, Boenning DA. The value of end-tidal CO2 monitoring when comparing three methods of conscious sedation for children undergoing painful procedures in the emergency department. Pediatr Emeg Care 1997;13:189-93.
6. Practice Guidelines For Sedation And Analgesia By Non-Anesthesiologists (Approved by the House of Delegates on October 25, 1995, and last amended on October 17, 2001).