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A 6-Month-Old Infant With Different Capnography Values in Polysomnography FREE TO VIEW

Lourdes M. DelRosso, MD; Pacifico Palacay, RPSGT; Ngoc P. Ly, MD, MPH
Author and Funding Information

Department of Pediatrics, University of California, San Francisco, San Francisco, CA

CORRESPONDENCE TO: Lourdes M. DelRosso, MD, Department of Pediatrics, University of California, 744 52nd St, San Francisco, San Francisco, CA 94609


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2017;151(2):e45-e48. doi:10.1016/j.chest.2016.08.1463
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A 6-month-old infant with a past medical history of hypoxic ischemic encephalopathy was referred for evaluation of snoring. She was born at 41 weeks’ gestational age to a 25-year-old gravida 1, para 1 mother via vacuum-assisted delivery due to cardiac decelerations. The infant’s Apgar scores were 1, 4, and 6 with nuchal cord and meconium at delivery. She was started on positive-pressure ventilation but eventually required intubation at approximately 40 minutes of life. Brain MRI showed abnormal areas of restricted diffusion, involving the corpus callosum, bilateral posterior limb of the internal capsules, and possible scattered areas of frontal and occipital lobe cortices.

Figures in this Article

At the time of presentation the infant was being fed thickened formula every 2 hours with minimal spitting up. During wakefulness she did not have any breathing problems, choking, or gagging, and no noisy breathing was reported. During sleep she snored every night. The family had not noticed any abnormal posturing, stiffening, spasms, or abnormal movement activity.

The infant lived with both parents and slept in a crib in her parents’ room. There was no exposure to smoking.

A review of systems indicated hypotonia. Her physical examination showed vital signs within normal ranges. An airway examination showed tonsils 1+ in size, the cardiovascular examination yielded normal results, and the neurologic examination indicated hypotonia.

An overnight polysomnogram (PSG) showed an apnea-hypopnea index of 0.2 and saturation nadir of 94%. Both end-tidal Pco2 and transcutaneous Pco2 were determined during the PSG. A 30-second epoch is shown in Figure 1.

Figure 1
Figure Jump LinkFigure 1 Thirty-second epoch. Electroencephalogram leads (F4-M1, F3-M2, C3-M2, C4-M1, O1-M2, O2-M1), electromyogram leads (chin, Leg-L, Leg-R), ocular leads (E1-M2, E2-M1), respiratory sensors (thermistor, nasal pressure), transcutaneous Pco2 (Pco2), end-tidal Pco2 (ETco2 value), EKG leads, oxyhemoglobin saturation (Spo2), pulse waveform (PWF).Grahic Jump Location

What is the diagnosis?

Figure 1shows transcutaneous Pco2signal and end-tidal Pco2signal; which one is accurate? And why do the end-tidal Pco2values change while the transcutaneous Pco2remains constant?

Answer: The transcutaneous Pco2 values are accurate. The end-tidal Pco2 signal is not accurate, as can be deduced from the “peak” shape of the end-tidal Pco2 waveform. To be accurate the end-tidal Pco2 wave must have a plateau as depicted in Figures 2 and 3.

Figure 2
Figure Jump LinkFigure 2 Thirty-second epoch, showing end-tidal Pco2 values correlating with transcutaneous Pco2 values. Notice normal plateau expected in accurate end-tidal Pco2 waveform. Electroencephalogram leads (F4-M1, F3-M2, C3-M2, C4-M1, O1-M2, O2-M1), electromyogram leads (chin, Leg-L, Leg-R), ocular leads (E1-M2, E2-M1), respiratory sensors (thermistor, nasal pressure), Pco2, ETco2, EKG leads, Spo2, PWF. See Figure 1 legend for expansion of abbreviations.Grahic Jump Location
Figure 3
Figure Jump LinkFigure 3 The four phases of the capnogram: A, Baseline; B, ascending phase of early exhalation; C, alveolar plateau; end-tidal; and D, descending phase of inhalation. ∗End-tidal value.Grahic Jump Location

The American Academy of Sleep Medicine recommends the use of arterial Pco2, transcutaneous Pco2, or end-tidal Pco2 for detection of hypoventilation during a diagnostic polysomnogram. During a positive airway pressure titration PSG, the American Academy of Sleep Medicine recommends the use of either arterial Pco2 or transcutaneous Pco2 for detection of hypoventilation. These recommendations are for both adult and pediatric sleep studies. The sleep physician and polysomnography technician must be familiarized with the interpretation and use of these tests.

Determination of arterial blood gases is the “gold standard” for evaluation of oxygenation and ventilation. However, the test is not practical in the outpatient sleep laboratory setting as it is invasive, provides a spot result only, requires trained personnel, and has potential side effects (pain, bleeding, infection). In contrast, end-tidal Pco2 and transcutaneous Pco2 assessments are noninvasive procedures that provide continuous monitoring during the PSG.

End-tidal Pco2 monitoring is performed via a nasal cannula. The signal must have a plateau to be accurate. Signals without a plateau as seen in Figure 1 occur when patients mouth-breathe, breathe too fast, have secretions collecting in the sensor, or are receiving supplemental oxygen or positive-pressure ventilation. The value is measured with each breath. In contrast, transcutaneous Pco2 determination measures arterial Pco2 by warming the skin via heated electrochemical sensors to estimate the Pco2 from capillary blood flow. Transcutaneous Pco2 is more useful in detecting trends than breath-to-breath changes. This method had limited use in patients with skin lesions and obese patients.

  • 1.

    Measurement of Pco2is an important part of the PSG for detection of hypoventilation.

  • 2.

    Arterial Pco2, end-tidal Pco2, and transcutaneous Pco2are recommended in diagnostic PSG.

  • 3.

    End-tidal Pco2is not accurate during titration studies, and therefore it is recommended that either arterial Pco2or transcutaneous Pco2be used.

  • 4.

    The presence of a plateau on the end-tidal Pco2waveform indicates a valid signal.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.


Figures

Figure Jump LinkFigure 1 Thirty-second epoch. Electroencephalogram leads (F4-M1, F3-M2, C3-M2, C4-M1, O1-M2, O2-M1), electromyogram leads (chin, Leg-L, Leg-R), ocular leads (E1-M2, E2-M1), respiratory sensors (thermistor, nasal pressure), transcutaneous Pco2 (Pco2), end-tidal Pco2 (ETco2 value), EKG leads, oxyhemoglobin saturation (Spo2), pulse waveform (PWF).Grahic Jump Location
Figure Jump LinkFigure 2 Thirty-second epoch, showing end-tidal Pco2 values correlating with transcutaneous Pco2 values. Notice normal plateau expected in accurate end-tidal Pco2 waveform. Electroencephalogram leads (F4-M1, F3-M2, C3-M2, C4-M1, O1-M2, O2-M1), electromyogram leads (chin, Leg-L, Leg-R), ocular leads (E1-M2, E2-M1), respiratory sensors (thermistor, nasal pressure), Pco2, ETco2, EKG leads, Spo2, PWF. See Figure 1 legend for expansion of abbreviations.Grahic Jump Location
Figure Jump LinkFigure 3 The four phases of the capnogram: A, Baseline; B, ascending phase of early exhalation; C, alveolar plateau; end-tidal; and D, descending phase of inhalation. ∗End-tidal value.Grahic Jump Location

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