Published online August 1, 2008
PEDIATRICS Vol. 122 No. 2 August 2008, pp. 293-298 (doi:10.1542/peds.2007-2385)

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ARTICLE

Supplemental Oxygen Compromises the Use of Pulse Oximetry for Detection of Apnea and Hypoventilation During Sedation in Simulated Pediatric Patients

Ilan Keidan, MD^a,b, Dietrich Gravenstein, MD^b, Haim Berkenstadt, MD^a,c, Amitai Ziv, MD^c, Itay Shavit, MD^d and Avner Sidi, MD^a,b

^a Department of Anesthesia and Intensive Care
^c Israel Center for Medical Simulation, Sheba Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
^b Department of Anesthesiology, University of Florida College of Medicine, Gainesville, Florida
^d Department of Pediatric Emergency Medicine, Rambam Medical Center, Haifa, Israel

	ABSTRACT

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 
OBJECTIVE. The goal was to assess the time to recognition of apnea in a simulated pediatric sedation scenario, with and without supplemental oxygen.

METHODS. A pediatric human patient simulator mannequin was used to simulate apnea in a 6-year-old patient who received sedation for resetting of a fractured leg. Thirty pediatricians participating in a credentialing course for sedation were randomly assigned to 2 groups. Those in group 1 (N = 15) used supplemental oxygen, and those in group 2 (N = 15) did not use supplemental oxygen. A third group (N = 10), consisting of anesthesiology residents (postgraduate years 2 and 3 equivalent), performed the scenario with oxygen supplementation, to ensure validity and reliability of the simulation. The time interval from simulated apnea to bag-mask ventilation was recorded. Oxygen saturation and PaCO₂ values were recorded. All recorded variables and measurements were compared between the groups.

RESULTS. The time interval for bag-mask ventilation to occur in group 1 (oxygen supplementation) was significantly longer than that in group 2 (without oxygen supplementation) (173 ± 130 and 83 ± 42 seconds, respectively). The time interval for bag-mask ventilation to occur was shorter in group 3 (anesthesiology residents) (24 ± 6 seconds). PaCO₂ reached a higher level in group 1 (75 ± 26 mmHg), compared with groups 2 and 3 (48 ± 10 and 42 ± 3 mmHg, respectively). There was no significant difference between the groups in oxygen saturation values at the time of clinical detection of apnea (93 ± 5%, 88 ± 5%, and 94 ± 7%, respectively).

CONCLUSIONS. Hypoventilation and apnea are detected more quickly when patients undergoing sedation breathe only air. Supplemental oxygen not only does not prevent oxygen desaturation but also delays the recognition of apnea.

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Key Words: supplemental oxygen • simulation • sedation • pulse oximetry

Abbreviations: SpO₂—pulse oxygen saturation • SaO₂—arterial oxygen saturation • FIO₂—fraction of inspired oxygen • PETCO₂—end-tidal carbon dioxide pressure • PAO₂—partial pressure of oxygen in the alveolae • PIO₂—inspired partial pressure of oxygen

Pediatric patients undergoing sedation should be continuously monitored with continuous heart rate and pulse oxygen saturation (SpO₂) monitoring, electrocardiography, and noninvasive blood pressure monitoring.¹ Although no formal study has demonstrated the benefit of providing supplemental oxygen during sedation, it is commonly used to prevent desaturation.² When supplemental oxygen is administered, hemoglobin saturation measurements do not provide sufficient feedback to gauge the adequacy of ventilation.^3,4 Despite this recognized monitoring weakness, no routine monitoring of ventilation, other than clinical observation, is recommended for sedated pediatric patients who are not intubated.¹

Children are at high risk for ventilatory compromise. Their resting oxygen consumption of 5 to 8 mL of oxygen per kg per minute corresponds to a basal metabolic rate approximately twice that of adults.^5,6 Carbon dioxide production is increased similarly, which puts children at increased risk for becoming hypercarbic during hypoventilation or apnea. This underscores the importance of accurate monitoring of ventilation when sedative and other respiratory depressant drugs are administered. Unfortunately, detecting hypoventilation in patients undergoing sedation is difficult.^7–9 Children tend to move, to tolerate sampling of nasal cannulae poorly, and to have low-tidal volume breathing, compared with adults, all of which may complicate monitoring and may partly explain why capnometry has not become a standard of care.

Can ventilation be safely and reliably monitored without capnometry? We think that it can, by using SpO₂ as an indirect but more-accurate indicator of hypoventilation.^4,10 To test this theory, clinical responses to hypoventilation and apnea were measured when pediatric sedation was performed by using only room air, and results were compared with responses observed when supplemental oxygen was administered.

	METHODS

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 
The Israeli Ministry of Health published guidelines on the sedation of children by nonanesthesiologists in May 2003.¹¹ The Ministry of Health position statement became a first step toward implementation of procedural sedation and analgesia treatment protocols in Israeli pediatric emergency departments^12,13 and led to the development of guidelines for pediatric sedation by nonanesthesiologists.

Consequently, a 1-day course in pediatric procedural sedation and analgesia was established by a group of experts, consisting of senior pediatric anesthesiologists and pediatric emergency department directors. The guidelines mandated that every provider of sedation to children complete and successfully pass a 1-day course on safe sedation practices, hosted by the National Medical Simulation Center. The contents of the course hosted by the National Medical Simulation Center blended theoretical discussions with practice on advanced simulators. The course program included 2 sections, that is, (1) a structured lecture component on the topics of assessment and treatment of pain and anxiety in the emergency department, the continuum of sedation, presedation evaluation, monitoring and recording during the procedure, pharmacokinetic and pharmacodynamic characteristics of analgesics, sedatives, and reversal agents, postsedation monitoring, and discharge criteria and (2) a simulation-based component that included practice in case scenarios using human patient simulators and actors.

Before the beginning of the course, 30 pediatricians were enrolled to participate in the study. They were presented with a simulated 6-year-old patient (pediatric human patient simulator; METI, Sarasota, FL) with a leg fracture who required sedation for positioning, fracture reduction, and casting and then became apneic. The participants were randomly assigned to 2 groups. Participants in group 1 (N = 15) provided supplemental oxygen to the patient throughout the scenario, and those in group 2 (N = 15) provided no supplemental oxygen. Group 3 (N = 10) was composed of anesthesiology residents (postgraduate years 2 and 3 equivalent) trained in airway management, who performed the scenario with oxygen supplementation to ensure the validity and reliability of the simulation. Ensuring validity means allowing us to demonstrate construct-related validity (ie, simulator scores improve with additional training), in a way that more-qualified clinicians would detect and act better when challenged in the simulated scenario, and ensuring reliability (ie, a measure of the reproducibility or consistency of a test, taking into account the effect of the simulator) means ensuring that a delayed or absent response is clinician related, rather than a fault within the simulated study model.

The simulated patient was monitored with continuous SpO₂ monitoring, electrocardiography, and noninvasive blood pressure monitoring. The child was breathing regularly, talking, and complaining of pain and anxiety before the administration of any sedative medication by the participating physician. Once any medication was administered, the child shut his eyes and became apneic, through implementation of an apnea protocol by the simulator operator.

The time course data with the rate of increase of PaCO₂ without clinician intervention, according to the apnea protocol used by the simulator, is described in the Appendix. The rate at which PaCO₂ increases is logarithmic and multifactorial, related to lung volume, obstruction level, and anesthesia effect.^14–16 The Appendix presents the PaCO₂ increase in each of the different possible situations and in our scenario. Our model assumes an open airway and apneic oxygenation, but it also has an element of conscious rather than anesthetized apnea, which increases PaCO₂ faster than in anesthetized patients. This is the condition that could be expected from a sedated (rather than anesthetized) simulated patient with nonobstructive apnea.

The time interval from the point of apnea to the initiation of bag-mask ventilation, SpO₂, and PaCO₂, calculated with the human patient simulator software, were recorded. All recorded measurements were compared between the groups. Differences among groups were analyzed with 1-way analysis of variance followed by posthoc Bonferroni multiple comparisons. Significance was accepted at P < .05. All analyses were performed by using statistical software (SPSS 14.0; SPSS, Chicago, IL). Values are presented as mean ± SD.

	RESULTS

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 
The results for the time interval from the point of simulated apnea to the initiation of bag-mask ventilation, the PaCO₂ level, and the SpO₂ reached at that time point are presented in Table 1. The time intervals from apnea to bag-mask ventilation were different among the 3 groups (F_2,35 = 8.6, P = .001). The time interval to bag-mask ventilation was significantly longer in group 1 (oxygen supplementation) than in group 2 (no oxygen supplementation) (P = .01). The time interval to bag-mask ventilation was shorter in group 3 (anesthesiology residents) (P > .01, compared with group 1). The time interval to bag-mask ventilation in group 2 was not different from that in group 3 (P = .13). The PaCO₂ values were different among the 3 groups (F_2,35 = 11.84, P = .001). The PaCO₂ reached a higher level in group 1, compared with groups 2 and 3 (P < .01 for both). The difference between the groups in SpO₂ values at the time of clinical detection of apnea was not significant (P = .06).

View this table: [in this window] [in a new window]   TABLE 1 Time Interval From Apnea to Bag-Mask Ventilation, PaCO2, and SpO2 Reached at That Time Point

 

	DISCUSSION

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 
Respiratory depression and airway obstruction have been cited as the primary causes of adverse events associated with pediatric sedation.¹ Current assessment of these conditions is through clinical observation and continuous SpO₂ monitoring. Clinical observation of the patient is known to be limited in its ability to detect respiratory depression and obstruction.^1,17 Continuous SpO₂ monitoring also is limited for detection of respiratory depression and obstruction, given the physiologic differences between oxygenation and ventilation. The practice of routine supplementation of inspired oxygen during pediatric sedation may further delay the detection of hypoventilation or apnea. Administration of supplemental oxygen during sedation in children initially prevents hypoxemia, as shown by the simplified alveolar gas equation, PAO₂ = PIO₂ – (PaCO₂/R), relating the partial pressure of oxygen in the alveolae (PAO₂), the inspired partial pressure of oxygen (PIO₂) in the central airways (humidified), PaCO₂ measured during inhalation, and the respiratory quotient R (carbon dioxide production/oxygen consumption ratio = 0.8); PIO₂ equals FIO₂ in the central airways, humidified = FIO₂* (barometric pressure – water vapor pressure), the fraction of inspired oxygen (FIO₂) is 0.21 in room air, the barometric pressure is 760 mmHg at sea level, and the water vapor pressure is 47 mmHg at 37°C.

This equation describes how increased FIO₂ (through the administration of supplemental oxygen) increases PAO₂. Although PAO₂ may be higher, increases above 100 mmHg do not increase arterial oxygen saturation (SaO₂) substantially, because of the plateau reached in the oxygen-hemoglobin dissociation curve. In fact, the alveolar gas equation predicts that, with only modest oxygen supplementation, PIO₂ would increase dramatically. When the PIO₂ is high, only prolonged hypoventilation/apnea is capable of increasing PaCO₂,^14,18 and consequently decreasing PAO₂, enough to cause hemoglobin desaturation. This relationship between FIO_2, PaCO₂, and SaO₂ is described 3-dimensionally in Fig 1. In the absence of supplemental oxygen, PIO₂ remains 150 mmHg and desaturation to 95% reliably occurs once PaCO₂ increases above 60 mmHg.

View larger version (45K): [in this window] [in a new window]   FIGURE 1 Relationships between FIO2, PaCO2, and SaO2 described 3-dimensionally, according to the alveolar gas equation. This equation describes how increased FIO2 (through administration of supplemental oxygen) increases PAO2. When PIO2 is high, hypoventilation/apnea is capable of increasing PaCO2 high enough and yielding PAO2 low enough to cause a SaO2 decrease. In the absence of supplemental oxygen, PIO2 remains 150 mmHg and desaturation to 95% reliably occurs once PaCO2 increases above 60 mmHg.

 
Even the last statement does not show the full picture, however. In the absence of supplemental oxygen, desaturation may occur well before PaCO₂ increases above 60 mmHg. As demonstrated in a previous study,⁴ SpO₂ decreases far more rapidly than predicted by the alveolar gas equation because the respiratory quotient R is disturbed and is no longer 0.8. As sudden hypoventilation occurs, oxygen consumption is unchanged but carbon dioxide production in the exhaled air is dramatically decreased. Therefore, the carbon dioxide production/oxygen consumption ratio decreases until PaCO₂ reaches the new equilibrium. Only when equilibrium occurs does the ratio R value return to 0.8. Until then, PIO₂ and PAO₂ continue to decrease, much as would occur with reduced FIO₂.

With apnea, PaCO₂ equals venous PCO₂ within minutes, whereupon no excretion of carbon dioxide is possible and R approaches infinity. The ultimate effects are profound rapid decreases in PAO₂, PaO₂, and SaO₂, as would be seen during breathing of a hypoxic gas mixture. Calculated SaO₂ and PaO₂ are dependent on FIO₂ (which was 0.6 in our experiment) and R (which was decreased during hypoventilation until PaCO₂ reached the new equilibrium; only then did the R value return to 0.8). The calculated "monitored" SaO₂ in our experiment in groups 1 and 3 (with oxygen) likely was higher than it would have been if it had been calculated accurately by using a dynamically changing R. Lower calculated SaO₂ values in these 2 groups would leave them nonsignificantly different from the group 2 low SaO₂ value (Table 1). In addition, this might have demonstrated that group 1 detected apnea as rapidly as did the anesthesiology residents in group 3. However, the purpose of the study was not to show the benefit of training but rather to demonstrate the advantage of avoiding supplemental oxygen. The quicker recognition of apnea in this experiment by anesthesiology residents may reflect the problem of using a constant R of 0.8 (rather than a changing R value) when calculating SaO₂ during apnea in a simulated scenario.

These facts led one authority to conclude that "probably the best way for the nonanesthesia provider to stay out of trouble during intravenous sedation is to titrate drugs slowly for a patient breathing room air."¹⁹ Anesthesiologists have long been admonished to follow this practice.^4,10,20 One of the 6 primary causes of arterial hypoxemia is hypoventilation.²¹ With only a modest increase in FIO₂, however, substantial hypoventilation can occur without causing arterial hypoxemia. In the past, this well-known phenomenon was the basis for recommending oxygen supplementation during procedures requiring intravenous sedation and for patients recovering from anesthesia, when hypoventilation can occur. However, these recommendations occurred before the advent of pulse oximeters in such environments.²¹ A profound degree of hypoventilation may be present before arterial hypoxemia occurs when FIO₂ is supplemented, which renders pulse oximetry unreliable as a means to monitor ventilation. In contrast, patients breathing room air can have only moderate decreases in ventilation before the pulse oximeter warns the clinician of hypoventilation.^4,22 Therefore, oxygen supplementation during intravenous sedation and recovery from general anesthesia may prevent the early diagnosis of hypoventilation and thus prevent appropriate timely intervention. With this in mind, the data strongly suggest that "patients in postanesthesia care units should not receive supplemental oxygen unless SaO₂ consistently falls below 90% and stimulation is ineffective in reversing the arterial hypoxemia."^4,21 At this stage when a problem is identified, diagnosis and treatment of the problem causing the hypoxemia should be carried out with oxygen administration, because oxygen administration by itself is only a temporary "cover" and not a solution for the problem. Until the problem is resolved, additional monitoring, invasive (blood gas analyses) or noninvasive (capnometry), may be warranted. When the problem is resolved and SpO₂ is consistently >90%, even during short trial periods without oxygen, oxygen supplementation and additional monitoring can be withdrawn.

The value of capnometry for monitoring ventilation is well described.²³ An emergency department study on procedural sedation was unblinded after an interim analysis showed a 60% incidence of abnormal end-tidal carbon dioxide pressure (PETCO₂), 4 times the expected 15% occurrence.²³ Unexpectedly, abnormal PETCO₂ findings were observed before changes in SpO₂ or respiratory rate in 70% of the patients with acute respiratory events. Similarly, Lightdale et al²⁴ concluded that addition of capnometry to routine monitoring during pediatric endoscopy cases with 2 L/minute nasal cannula oxygen treatment allowed detection of hypoventilation (56% of procedures) and apnea (24% of procedures), whereas routine monitoring without capnography identified only 3% of the cases as having compromised ventilation and found no cases of apnea.

A noteworthy similarity in both of those recent studies is that the capnometric change observed was not elevation in PETCO₂, which might be expected to follow periods of hypoventilation and apnea. Instead, the capnometry showed a heavy preponderance of decreased PETCO₂ (not to be confused with PaCO₂), with only a few cases of increased PETCO₂. In fact, the capnographic pattern was a stronger indicator of ventilatory compromise than was the reported PETCO₂ value. Multiple factors might have prevented unmixed alveolar gas from reaching the analyzer, including rapid shallow breathing induced by sedative medications, significantly obstructed ventilation, and/or dilution of exhaled gas by the supplemental oxygen.

The improved performance by anesthesiology residents in recognizing ventilatory compromise with supplemental oxygen well before the pediatricians likely reflects the core emphases of their training program on airway management and apnea recognition. However, the quicker recognition of apnea by anesthesiology residents also may reflect previous exposure to simulation training or the simulator environment and the issue of calculating SaO₂ accurately during apnea in a simulated scenario.

This simulation of hypoventilation and apnea can be criticized for not realistically representing the chest wall movements, retractions, nostril flaring, and audible cues of a child's obstructed breathing pattern. Simulators do not display pallor or sweat or become cyanotic. Simply participating in a simulated scenario requires some suspension of reality and a genuine effort by those being tested, because participants are aware that no real patient is at risk. All 3 groups faced identical simulation limitations, however, and we think that the conclusions remain valid.

	CONCLUSIONS

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 
The presented data suggest that procedural sedation is associated with episodes of hypoventilation and undetected apnea. The ability to recognize clinical signs of hypoventilation and apnea improves with experience. The adoption of practice habits that improve patient safety during sedation has led to the incorporation of routine monitoring methods that include pulse oximetry. Addition of supplemental oxygen is common but has the unintended consequence of delaying desaturation and recognition of hypoventilation and apnea. Monitoring capnometry is feasible even for very small children and can expose abnormal ventilation.^22,24 However, the inconsistent direction of PETCO₂ changes and the pattern recognition required to interpret the capnographic data correctly, given the reported variability, may add undesired complexity.

The most important element of monitoring during sedation is close continuous observation of the sedated child. We think that the safest economical method for reliably monitoring children's ventilatory status during procedures performed under sedation is pulse oximetry, without supplemental oxygen treatment, unless severe arterial hypoxemia is present. There is no basis in the data collected to support or to reject recommendations for capnometry. The utility of capnometry as a monitoring tool depends on reliable capnographic pattern recognition by the clinicians using it.

	APPENDIX

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 
Appendix 1 describes the time course data with the rate of increase of PaCO₂ without clinician intervention. Without oxygen supplementation, the SpO₂ decreased from 97% to 96% 10 seconds after the induction of apnea to 95% 20 seconds after the induction of apnea and reached 90% 45 seconds after the induction of apnea. During this time, the PaCO₂ increased from 41 ± 1 mmHg to 47 ± 2 mmHg. After oxygen administration with a mask with a reservoir, SpO₂ decreased from 100% to 99% 70 seconds after the induction of apnea to 98% 180 seconds after the induction of apnea and reached 90% 300 seconds after the induction of apnea. During this time, the PaCO₂ increased from 41 ± 1 mmHg to 67 ± 3 mmHg. The rate at which PaCO₂ increases is probably logarithmic and multifactorial, related to lung volume, obstruction level, and anesthesia effect. The metabolic rate and carbon dioxide levels during anesthesia are significantly lower than levels during conscious apnea, which probably accounts for the different rates of increase in PaCO₂.

The rates of PaCO₂ increases in conscious volunteers with apnea,¹⁴ anesthetized patients with apnea,¹⁵ anesthetized patients with airway obstruction,¹⁶ and our simulated apnea scenario are presented in Appendix 2. It is clearly demonstrated that our model basically assumes an open airway and apneic oxygenation but also has an element of conscious rather than anesthetized apnea, which increases PaCO₂ faster than in anesthetized patients. This is the condition that could be expected from a sedated (rather than anesthetized) simulated patient with nonobstructive apnea.

View this table: [in this window] [in a new window]   APPENDIX 1 PaCO2 Increases in Different Scenarios

 

View this table: [in this window] [in a new window]   APPENDIX 2 PaCO2 Increases in Different Situations and Our Scenario

 

	FOOTNOTES

 
Accepted Nov 27, 2007.

Address correspondence to Avner Sidi, MD, Department of Anesthesiology, University of Florida College of Medicine, Box 100254, Gainesville, FL 32610-0254. E-mail: asidi{at}anest.ufl.edu

The authors have indicated they have no financial relationships relevant to this article to disclose.

What's Known on This Subject The literature is scant on evidence of oxygen use delaying the recognition of apnea, especially in children.

 

What This Study Adds This study shows that hypoventilation and apnea are detected more quickly when patients undergoing sedation breathe only air. Supplemental oxygen not only does not prevent oxygen desaturation but also delays the recognition of apnea.

 

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TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSIONS APPENDIX REFERENCES

 

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PEDIATRICS (ISSN 1098-4275). ©2008 by the American Academy of Pediatrics

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This article has been cited by other articles:

				A. E. A. Hemelaar and J. Lemson Patients Under Sedation Should Always Be Monitored by Well-Trained Personnel and Should Be Given Supplemental Oxygen Pediatrics, December 1, 2008; 122(6): 1415 - 1416. [Full Text] [PDF]

				D. Gravenstein, I. Keidan, and A. Sidi Patients Under Sedation Should Always Be Monitored by Well-Trained Personnel and Should Be Given Supplemental Oxygen: In Reply Pediatrics, December 1, 2008; 122(6): 1416 - 1416. [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services E-mail this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My File Cabinet Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Keidan, I. Articles by Sidi, A. Search for Related Content PubMed PubMed Citation Articles by Keidan, I. Articles by Sidi, A. Related Collections Premature & Newborn Social Bookmarking                         What's this?