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Polysomnography

Polysomnography (also called a sleep study) simultaneously and continuously records multiple different biophysiological parameters across a sleep period to characterize sleep, identify, and sometimes treat sleep disorders. The resulting study is a polysomnogram (PSG). Recording multiple physiological signals in PSG concurrently allows us to correlate specific changes or abnormalities of one physiological variable with specific conditions defined by another variable (e.g., oxygen desaturation and sinus bradycardia occurring with an obstructive apnea; periodic limb movements [PLMs] causing arousal and sinus tachycardia during non-REM (NREM) 2 sleep; a confusional arousal from NREM 3 sleep). As a result, PSG is a far more powerful tool than individual independent measurements of each variable. This advantage is offset by difficulties related to optimal digital monitor display of disparate parameters and the challenges for reliably detecting multiple diagnostic patterns of clinical significance among all these variables.

INDICATIONS FOR POLYSOMNOGRAPHY

The American Academy of Sleep Medicine (AASM) has published comprehensive evidence- and consensus-based guidelines of indications for polysomnography in adults and children.^1–6 Table 12.1 summarizes these indications (Table 12.1 is available online only, see access url on the opening page of this chapter).

Comprehensive in-laboratory overnight (level 1) PSG is most often done to evaluate for sleep-disordered breathing (SDB). The confirmation of obstructive sleep apnea (OSA) in adults can be done (often demanded by their health insurance) performing home sleep apnea testing (HSAT). However, level 1 PSG evaluates for SDB in adults with chronic obstructive pulmonary disease, congestive heart failure, chronic kidney disease, morbid obesity, pulmonary hypertension, neuromuscular disorders, suspected central sleep apnea, sleep-related hypoventilation, and/or other comorbid primary sleep disorders.

When significant SDB is identified during the first half of a diagnostic level 1 PSG, positive airway pressure (PAP) and/or supplemental oxygen can be titrated in the second half of the study (so-called “split-night” PSG) to find the optimal treatment settings. Alternatively, if SDB was first identified on an HSAT, a full titration of PAP therapy (adding supplemental oxygen if needed) can be done (so-called “full night titration” PSG). We often perform level 1 PSG to confirm treatment efficacy (upper airway surgery, oral appliances, bariatric surgery). Level 1 PSG is also done to evaluate atypical parasomnias, sleep-related injurious behaviors, sleep-related hypoxemia and/or hypercapnia, and suspected nocturnal epilepsy. A level 1 PSG is done the night before multiple sleep latency testing (MSLT) to confirm a diagnosis of narcolepsy types 1 or 2, idiopathic hypersomnia, and/or to evaluate excessive daytime sleepiness (EDS).

280PSG is not the best first test for evaluating insomnia, restless legs syndrome (RLS), circadian rhythm sleep/wake disorders (CRSWDs), typical uncomplicated parasomnias, epilepsy, depression, chronic lung disease, sleep bruxism, and/or behaviorally based sleep problems.^1,3 However, if typical sleep terrors or sleepwalking events occur more than two to three times per week, a PSG is warranted to identify another sleep disorder triggering them (most often mild OSA, occasionally RLS or periodic limb movement disorder (PLMD).^7,8 Table 12.2 summarizes red flags for atypical parasomnia which warrant consideration of comprehensive in-laboratory video-PSG (Table 12.2 is available online only, see access url on the opening page of this chapter).

CLASSIFICATION OF SLEEP STUDIES (LEVELS 1–4)

The AASM and the Centers for Medicare and Medicaid Services (CMS) in the United States classify sleep studies into four categories (levels 1–4, Table 12.3) based upon how many different physiological signals are simultaneously recorded and whether a sleep technologist was present throughout the study.^9,10 A level 1 PSG (current procedural terminology [CPT] code 95810) is performed while attended in a sleep laboratory recording a minimum of 7 channels including EEG, bilateral electrooculogram (EOG), submental electromyogram (EMG), EKG, airflow, thoracic and abdominal respiratory effort, pulse oximetry (SpO₂), video, and sometimes carbon dioxide (CO₂) monitoring^1,11 (Table 12.4) (Table 12.4 is available online only, see access url on the opening page of this chapter). A type 1 sleep PSG is considered the reference standard against which other diagnostic methods are evaluated.¹² Figure 12.1 shows a representative example of a level 1 PSG from our laboratory.

A level 2 study is level 1 PSG recorded unattended (i.e., without a sleep technologist present), in or out of the sleep laboratory. A level 3 study records a minimum of four cardiorespiratory channels including ventilation, oximetry, and EKG or heart rate. A level 4 study usually records only one to two cardiorespiratory signals (usually pulse oximetry, sometimes airflow). According to CMS, a level 3 or 4 study can be recorded in or out of the sleep laboratory, attended or unattended by a sleep technologist, but are usually recorded 281unattended at home. Most HSATs are level 3 studies. HSAT is considered the appropriate (and typically only sleep study covered by insurance) for adults who by history and exam have a moderate-to-high probability of having OSA. However, as of 2020, HSAT is not yet recommended to diagnose OSA in children, nor is it covered by medical insurance in the United States.¹³

ADVANTAGES, DISADVANTAGES, AND CONTRAINDICATIONS FOR LEVEL 1 POLYSOMNOGRAPHY

Level 1 PSGs are expensive and time- and labor-intensive to record, score, and read. Patients can wait weeks or months to get a study. Level 1 PSG, typically recorded for one night of sleep in the artificial environment of the sleep laboratory, provides a narrow view of how a patient naturally sleeps. This results in so-called First Night Effect: more time supine, less rapid eye movement (REM) and NREM 3 sleep, more Wake after Sleep Onset (WASO) and NREM 1 sleep on the first night.^14,15

There are no absolute contraindications to in-laboratory level 1 PSG if it is clinically indicated. However, a PSG is best recorded in those medically stable. Findings on a sleep study recorded in a sick patient (even near to hospital discharge) are unlikely to represent the baseline condition, and treatment strategies less likely to be implemented for concern the PSG findings were not representative (nor likely to be implemented because the patient often considers it was an acute episode). PSG is not recommended for patients with active respiratory infections or acute pain treated with high-dose opioids; chronic respiratory problems or chronic opioid doses do not preclude PSG.

An in-hospital bedside level 1 PSG can be an expensive endeavor, requiring a sleep technologist who could record two patients in one night to record only one, and reimbursement for the technical component of the procedure lost in the bundled hospital billing. If a sleep study is needed before discharge from the hospital, it usually should be the last test when the patient’s condition has been stabilized.

SLEEP STUDIES ARE RECORDED AND SCORED IN THE UNITED STATES USING THE AASM SCORING MANUAL

Accredited sleep centers in the United States record, score, and interpret level 1 PSGs in infants, children, and adolescents using The AASM Manual for the Scoring of Sleep and Associated Events: Rules, Terminology, and Technical Specifications.¹⁶ First published in 2007, the AASM Scoring Manual was designed to be revised and updated, available as a book or online (aasm.org/clinical-resources/scoring-manual). The AASM Scoring Manual was the first to provide standards for recording, scoring, and reporting of clinical PSG in the United States. We used the latest update (version 2.6, updated January 2020) to write this chapter.¹⁶

Overnight Level 1 Polysomnographic Recording Procedure

Once the PSG “hook-up” is complete, the sleep technologist escorts the patient to the study bedroom which has been made as inviting as it can be (save hospital grade beds, PAP machines, and oxygen delivery devices). Patients sometimes worry about “all the wires tying them down, preventing them from rolling in the bed, using the bathroom,” “being watched,” or fear they won’t sleep. We reassure the patient that they can easily be disconnected from the recording devices, and roll around or leave the bed without difficulty. We show them the bedroom is equipped with an infrared camera with audio system that 282allows the technologist to see, hear, and communicate with them without entering the bedroom. After connecting the patient, the technologist returns to the recording control room.

Before starting the PSG, the technologist performs a so-called biocalibration ensuring each of the signals are recording properly (Table 12.5) (Table 12.5 is available online only, see access url on the opening page of this chapter). Across the recording the technologist: (a) enters detailed observations onto the digital PSG recording; (b) recognizes and fixes malfunctioning sensors; (c) helps the patient out of bed to use the bathroom; (d) intervenes if potentially injurious behaviors occur; (e) intervenes if deemed a medical emergency; (f) decides if and when to titrate PAP or add supplemental oxygen; and (g) repositions the patient to obtain sleep in a particular body position (often supine). The study continues until the final awakening and “Lights On.” After the final awakening in the morning, the sensors are removed. The patient is offered a shower, but usually prefers to just go home.

283WHICH BIOPHYSIOLOGIC SIGNALS ARE RECORDED IN LEVEL 1 POLYSOMNOGRAPHY AND WHY

The recommended signals when recording a diagnostic level 1 PSG include: EEG (frontal, central, occipital referenced to the contralateral mastoid), bilateral EOG, chin EMG, EKG, bilateral anterior tibialis leg EMG, SpO2, snore microphone, nasal pressure (NP), and oronasal thermal sensors measuring airflow, thoracic and abdominal respiratory effort, end-tidal and/or transcutaneous CO₂, body position, and digital video recording (Figure 12.1).

Electroencephalography

EEG is the best indicator of sleep and wakefulness (except in infants 0–2 months of age, where regularity of respiration is a better biomarker of sleep/wake states). The AASM Scoring Manual recommends preferentially recording EEG from the right frontal, central, and occipital scalp regions referenced to the left mastoid (F4-M1, C4-M1, O2-M1). The left frontal, central, or occipital electrodes referenced to the right mastoid (F3-M2, C3-M2, O1-M2) are also placed to be used as backup if the F4, C4, or O2 malfunction.

Recording frontal, central, and occipital EEG permits recognition of the distinctive EEG markers of sleep/wake states: (a) W is best identified by the presence of a reactive dominant posterior rhythm (DPR) in the occipital EEG derivations; (b) sleep spindles, vertex waves, and sawtooth waves are usually best seen in central EEG derivations. K-complexes and slow wave activity (SWA) of N3 in the frontal EEG channels. We score sleep/wake states displaying PSG epochs lasting 30 seconds (10 mm/sec).

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EEG in PSG is recorded with the low-frequency filter set at 0.3 Hz and the high-frequency filter at 35 Hz. We begin the recording with the sensitivity set at 7 μV/mm but often have to decrease the sensitivity to 10 to 15 μV/mm in children, especially in N3 sleep where SWA often measures 100 to 400 μV peak-to-peak, and increase the sensitivity to 5 μV/mm in older adults.

When interictal epileptiform or ictal EEG activity is observed, we increase the high-frequency filter to 70 Hz. We sometimes record so-called expanded EEG montages when we want to correlate sleep events, arousals, and awakening with interictal epileptiform discharges (IEDs), nocturnal events, and seizure occurrence.¹⁷ Figure 12.2 shows an expanded EEG montage recorded on an adult from our laboratory.

Electrooculography

Eye movements help us to identify sleep onset and REM sleep: slow eye movements (SEMs) are a reliable biomarker of drowsiness and N1 sleep, and REMs of R sleep. EOG detects changes in electrical fields generated by the movement of the eyeballs because the eye has a horizontal dipole with a strong positive charge in the cornea and a minor negative charge at the retina.

SEMs are: (a) sinusoidal conjugate eye movements with an initial deflection that usually lasts >500 msec; (b) typically first seen before dropout of the dominant posterior rhythm (so-called DPR); (c) continue to occur during NREM 1 and usually disappear before sleep spindles and K-complexes of N2 sleep appear; (d) prevalence of them progressively decreases across NREM-REM sleep cycles of a night of sleep.¹⁶ Figure 12.3 shows SEMs in N1.

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REMs are: (a) sharply peaked eye movements with an initial deflection lasting <500 msec (usually <200 msec), frequency >1 Hz, amplitude ≥20 μV, and duration 50–200 msec; (b) more often conjugate, but can be asymmetric or dysconjugate; and (c) they occur preferentially in REM sleep, but are observed during wakefulness.^18,19 Figure 12.4 shows REMs in REM sleep.

The AASM manual recommends EOG (and EEG) recordings be displayed using a low frequency filter (LLF) filter setting of 0.3 Hz, high frequency filter (HFF) 35 Hz, and initial sensitivity 7 µV/mm.¹⁶ Using the same sensitivity for the EEG and EOG derivations allows us to view frontal EEG activity in the EOG derivations. Setting the HFF to 35 Hz is necessary to identify the rapid upslope of REMs.

The AASM permits use of two different EOG montages. The recommended EOG montage places the left EOG (E1) 1 cm below and 1 cm lateral to the left outer canthus and the right EOG (E2) 1 cm above and 1 cm lateral to the right outer canthus and referencing both to the right mastoid electrode (M2). The recommended EOG montage is: E1-M2, E2-M2. The left mastoid electrode (M1) is placed as a backup reference should M2 malfunction.

Using the recommended EOG derivation: (a) conjugate eye movements produce out-of-phase movements, EEG activity in-phase voltage deflections; (b) it is easy to distinguish EEG and artifacts, but the direction of eye movements cannot be determined and some low-amplitude eye movements (including eye blinks) missed.

The acceptable EOG montage places the E1 1 cm below and 1 cm lateral to the left outer canthus and E2 1 cm below and 1 cm lateral to the right outer canthus both referenced to the midline frontopolar electrode (FPZ). The acceptable EOG montage is EP1-FPZ, EP2-FPZ and which we prefer because it better detects subtle eye blinks and the specific direction of eye movements.

Mentalis Electromyography (Chin EMG)

Chin EMG is recorded during a PSG to assess axial skeletal muscle tone and activity. The chin EMG is particularly useful for identifying the loss of EMG activity during REM sleep (called REM sleep without atonia). It is also useful in identifying arousals, awakenings, swallowing, chewing, and bruxism during PSG. The chin EMG tends to decrease at sleep onset, further diminishes with increasing depth of NREM sleep, and reaches its 286lowest level of activity in REM sleep. The onset, presence, and offset of REM sleep is identified when the chin EMG is absent or at its lowest amplitude in the recording. The AASM Scoring Manual requires a transient increase in chin EMG lasting ≥1 second to score an EEG arousal during REM sleep (but not in NREM).¹⁶

The AASM Scoring Manual recommends placing three electrodes to record chin EMG: chin Z (midline 1 cm above inferior edge of mandible); chin 1 (2 cm below inferior edge of mandible and 2 cm to left of midline); chin 2 (2 cm below inferior edge of mandible and 2 cm to right of midline). The chin EMG montage is Chin Z-Chin 1 or Chin Z-Chin 2. If the midline chin electrode malfunctions, the AASM manual recommends replacing it because the inferior mandibular electrodes cannot be linked to each other. The frequency range of submentalis muscle activity is typically 20- to 200-Hz so the LLF is set at 10 Hz, the HFF at 100 Hz, and the initial sensitivity 2 to 3 µV adjusted to provide an adequate baseline EMG level during wakefulness.

Multiple Biological Signals Recorded to Assess Breathing During Sleep

Multiple different respiratory sensors are used to record respiration during a level 1 PSG because most provide only qualitative data (and frequently malfunction). The AASM Scoring Manual specifies which sensor is preferentially recommended to identify a particular respiratory event and alternative sensors if the recommended sensor becomes unreliable or unreadable. The recommended sensor to identify apneas in a diagnostic study is the oronasal thermal sensor, the PAP device flow signal during PAP titration. If one recommended sensor becomes unreliable or unreadable, alternative sensors are recommended by the AASM Scoring Manual. Table 12.6 summarizes AASM Manual recommended and acceptable sensors for different respiratory events in level 1 PSG (Table 12.6 is available online only, see access url on the opening page of this chapter).

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Thermal and NP Sensors Monitor Airflow

The AASM Scoring Manual recommends simultaneously recording airflow during a level 1 PSG using both an NP and oronasal thermal sensors because they provide complementary information and can serve as a backup sensor when the other malfunctions or becomes unreliable.¹⁶ The NP sensor measures airflow through the nose and is a nasal cannula connected to a pressure transducer which provides a signal proportional to the square of the airflow.²⁰ It is sensitive to even very small changes in airflow and preferentially used to identify hypopneas and respiratory effort-related arousals (RERAs) in infants, children, and adults.

The NP signal can be recorded with or without square root transformation of the signal. Square wave transformation of the NP signal improves detection of hypopneas that are ≤50% of baseline, and uncommonly done in routine PSG. The inspiratory portion of the NP waveform can display flattening which is surrogate of flow limitation. Flow limitation is regarded as a manifestation of upper airway resistance in obstructive SDB. Figure 12.5 shows flow limitation. The NP sensor is more sensitive than the thermal sensor for detecting hypopneas.^21–23

Oronasal thermal airflow sensors are recommended as the preferred sensor to detect apneas. Thermal sensors detect changes in airflow signal through the mouth and nares because expired air is warmed to body temperature. The signal from oronasal thermal sensors is not proportional to flow and overestimates flow as flow rates decrease. The thermal sensor LFF is set at 0.01 Hz and HFF at 15 Hz.

Respiratory Effort Monitored Using Respiratory Inductance Plethysmography

Thoracic and abdominal respiratory effort in a level 1 PSG is preferentially recorded using dual belt (thoracic and abdominal) respiratory inductance plethysmography (RIP). A RIP belt consists of a sinusoid wire coil insulated in elastic.²⁴ Changes in the magnetic field and cross section of the wire (one around the chest at the level of the nipple and the other around the abdomen near the umbilicus) are converted into a small electrical signal which is then amplified for display on the PSG trace.

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Changes in thoracic and/or abdominal diameter, cross-sectional area, and circumference are all directly proportional to changes in lung volume such that with normal tidal breathing the amplitude of the RIP waveform correlates with lung volume.²⁵ Dual effort belts are recommended because: (a) some patients have larger excursions in either the thorax or abdominal belts during the night, and this can vary with body position; (b) if one belt fails, we still have the other to read; and (c) dual belts are particularly useful for detecting paradoxical motion of the thorax and abdomen to identify obstructive breathing.²⁰ Figure 12.6 shows paradoxical breathing in a patient with OSA.

Although RIP has been regarded as the “gold standard” for recording respiratory effort in a level 1 PSG, sensors made of polyvinylidene fluoride (PVDF) are increasingly used in PSG. PVDF is a plastic material that is lightweight, flexible, and does not require an external power source to generate electrical signals. Piezoelectric sensors made of PVDF are increasingly used to record snoring, airflow, and respiratory effort in children and adults. PVDF sensors generate a recordable electrical signal when exposed to changes in pressure, force, temperature, or sound; hence its use in monitoring airflow, snoring, and respiratory effort during PSG.

We additionally record and display the sum of the thoracic and abdominal respiratory effort signal using either RIP or PVDF (called RIPsum or PVDFsum). The excursions of the sum of the signals from the thoracic and abdominal respiratory belts using RIP or PVDF are an estimate of tidal volume. During normal breathing, thoracic and abdominal respiratory belts move in phase and when their signals are summed, additive. However, paradoxical motion of chest and abdomen zeros out the sum channel and confirms a respiratory effort is obstructive in type (Figure 12.6).

Pulse Oximetry

We use pulse oximetry to continuously record arterial oxyhemoglobin saturation (SpO₂) in PSG. The wavelength of blood changes depending upon the amount of oxygen in the blood. The pulse oximeter consists of a light-emitting diode which emits alternating pulses of red and infrared light. A photodiode placed on the other side of the probe measures the intensity of the transmitted light comparing red and infrared light absorbance of oxyhemoglobin as blood pulses through arterioles in the skin beneath the probe. SpO₂ can 289be recorded from a finger or toe nail bed, earlobe, and nasal bridge (the side of the foot in neonates). The more peripheral the sensor, the greater the delay between a respiratory event and the detected desaturation. This delay is often even more pronounced in patients with prolonged circulation time due to systolic heart failure.

The AASM manual recommends pulse oximetry be recorded with short sampling times (≤3 seconds at heart rates ≤80 beats per minute). Using a 3-second moving window, the oximeter updates its average every 1 second, and the displayed value reflects 90 values collected in the past 3 seconds averaged. Oximeters with longer sampling rates (6 or 12 seconds) are used in the critically ill because artifact is more likely to be cancelled out by longer averaging times (but small desaturations are then missed).

We confirm the reliability of the pulse oximetry tracing by recording and displaying the pulse amplitude waveform which helps identify desaturations to poor probe function.²⁶ Figure 12.7 shows a falsely low oxygen saturation because of a malfunctioning oximeter probe confirmed by loss of the pulse waveform.

Causes of pulse oximeter artifact or malfunction include: (a) movement; (b) poor perfusion in patient who is hypovolemic, hypotensive, or cold; (c) inadequate light transmission detected by device because of tissue edema, nail polish, dark or thick skin, or improper probe placement; (d) excessive ambient room light; and (e) venous pulsations misinterpreted as arterial. SpO₂ can be with dark skin pigmentation, presence of carboxyhemoglobin, or nail polish (especially black or blue tints). The SpO₂ can be falsely low if methemoglobin is >85%; falsely high if it is <85%.

CO₂ Monitoring (Capnometry)

We sometimes record CO₂ in level 1 PSG; all children and patients with respiratory failure, hypoventilation, morbid obesity, and neuromuscular disease, and when adjusting mechanical ventilation settings during sleep. Recording techniques include end-tidal (etCO₂) and/or transcutaneous CO₂ (tcCO₂); rarely arterial pCO₂.

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etCO₂ Monitoring

The etCO₂ sensor measures the partial pressure or maximum concentration of CO₂ at the end of an exhaled breath. etCO₂ is not a flow signal but measures molecules of expired CO₂. Measured via a nasal cannula, it provides breath-to-breath variability with respect to the partial pressure of carbon dioxide (PaCO_2).

The graphical display of the etCO₂ signal is called the capnograph. etCO₂ values sample exhaled CO₂ at the point of end exhalation of the breathing cycle. It is crucial to obtain a plateau in etCO₂ capnograph waveform for the signal to be considered valid (as shown in Figure 12.8).

Normal etCO₂ values are 30 to 45 mmHg and correspond with a 5% to 6% total concentration of CO₂ and a PaCO₂ of 35 to 45 mmHg. The PaCO₂ normally rises in sleep 2 to 8 mm Hg during NREM sleep and 5 to 10 mm Hg in REM sleep in healthy adults without respiratory disease or SDB. etCO₂ tends to underestimate CO₂ values obtained from arterial blood. The etCO₂ is typically 4 to 6 mm Hg lower than the PaCO₂ during normal tidal breathing. The etCO₂ is often even lower in patients with congestive heart failure or chronic lung diseases. The relationship between etCO₂ and PaCO₂ values is roughly linear in the absence of concomitant respiratory diseases. The etCO₂ is often falsely low compared with the PaCO₂ in patients with acute respiratory illnesses, small lung volumes, obesity and/or chronic lung disease.

A sustained low etCO₂ with a good alveolar plateau warrants consideration of hyperventilation; a high etCO₂ with a good plateau suspicious for hypoventilation. A low etCO₂ without a good plateau can be seen with tachypnea. The etCO₂ signal can be inaccurate or unreliable in the presence of: (a) mouth breathing; (b) profuse nasal secretions; (c) cannula resting against posterior aspect of nares; (d) only one cannula prong in nostril; (e) nasal obstruction; (f) kink or excessive moisture in etCO₂ tubing; (g) PAP or O₂ therapy also being delivered via the nasal cannula; (h) tachypnea; and/or (i) small lung volumes.

Transcutaneous CO₂ Monitoring

Transcutaneous CO₂ monitoring approximates PaCO₂ and PaO₂ values by dilating the capillary bed with heat to measure capillary blood O₂ and CO₂ levels through skin. The tcCO₂ sensor is usually placed on the trunk (right second intercostal space and midclavicular space) but if the patient is obese, the right forearm, or ear lobe. The sensor applied to 291the skin induces a local hypermetabolic state (hyperemia increases arterial blood supply to superficial vessels) which leads to increased CO₂ production detected in the pH of the sensor’s electrolyte solution.

Because of this, the tcCO₂ does not provide breath-to-breath changes in CO₂, rather trends in PaCO₂ over 2 minutes. The tcCO₂ membrane requires 10 minutes for stabilization when first applied so values within the first minutes are unreliable. As opposed to the etCO₂, the tcCO₂ measurements correspond well with ABG even in the medically ill and are typically 4 to 5 mm Hg higher than the ABG. TcCO₂ is not affected by therapeutic interventions such as supplemental oxygen or PAP therapy. Most tcCO₂ device manufacturers recommend moving the skin electrode every 4 hours to prevent thermal injury, poor signal, or signal drift.

The tcCO₂ can be unreliable when: (a) there are abnormally high values due to calibration problems of device; (b) values are abnormally low due to poor fixation of electrode; (c) there is insufficient electrode temperature; (d) there are wide fluctuations of values caused by motion artifacts; or (e) perfusion problems such as skin diseases, edema, and/or hypovolemia are present. Use of the heated tcCO₂ electrode may cause the skin underlying it to blister (rare).

Electrocardiography

EKG is recorded in level 1 PSG using a modified lead II placement with a positive electrode on the left torso just beneath the last rib in the midclavicular line (and parallel to the left hip) and the negative electrode right just below the right clavicle (and parallel to the right shoulder). The ground electrode is placed below the left clavicle or on the left arm. Waveforms are surface positive. Using a single EKG channel, we can identify the heart rate, sinus bradycardia and tachycardia, wide and narrow complex tachycardia, sinus pause, atrial fibrillation/flutter. A single channel cannot be used to identify cardiac ischemia or PQRST complex abnormalities. The EKG LLF is 0.3 Hz and HFF 70 Hz. Table 12.7 summarizes AASM rules for scoring cardiac events in level 1 PSG (Table 12.7 is available online only, see access url on the opening page of this chapter).

TABLE 12.7. AASM cardiac event definitions

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