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Treatment withCPAP

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MarinaCarrasco-Llatas andJoanaVaz de Castro

Abbreviations

AASM American Academy of Sleep Medicine AHI Apnea-hypopnea index APAP Auto-adjusting positive airway pressure BMI Body mass index BPAP Bilevel positive airway pressure CPAP Continuous positive airway pressure CSA Central sleep apnea CSR Cheyne–Stokes respiration DISE Drug-induced sleep endoscopy EF Ejection fraction ENT Ear, nose, and throat EPAP Expiratory positive airway pressure ERS European Respiratory Society HF Heart failure

Supplementary Information The online version contains supplementary material available at

https://doi.org/10.1007/978-3-031-34992-8_15. The videos can be accessed individually by click-

ing the DOI link in the accompanying gure caption or by scanning this link with the SN More Media App.

M. Carrasco-Llatas (*) Department of Otorhinolaringology, Hospital Universitario Dr. Peset, Valencia, Spain

Department of Otorhinolaryngology, IMED Hospital, Valencia, Spain

J. Vaz de Castro ISAMB, Medicine of University of Lisbon, Lisbon, Portugal

Centro de Electroencefalograa e Neurosiologia Clínica (CENC), Lisbon, Portugal

Comprehensive Health Research Centre - CHRC, Lisbon, Portugal

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 M. Delakorda, N. de Vries (eds.), The Role of Epiglottis in Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-031-34992-8_15

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IPAP Inspiratory positive airway pressure MAD Mandibular advancement device MSA Multiple system atrophy OSA Obstructive sleep apnea PAP Positive airway pressure Pcrit Critical closing pressure PS Pressure support (related to Bilevel PAP) PSG Polysomnography SDB Sleep disordered breathing UA Upper airway

M. Carrasco-Llatas and J. Vaz de Castro

15.1 Introduction toPAP: AnOverview

Positive airway pressure (PAP) is the treatment modality in which air is delivered to the lungs through the nasal or oronasal route via a machine, a tube and an interface (mask) (Fig.15.1) [1]. The interface chosen may be a nasal mask, nasal pillows (nasal cushions) or oronasal (full face) mask (Figs.15.2, 15.3, 15.4 and 15.5). Air is delivered at a constant pressure (as is the case of continuous PAP- CPAP) or at different pressures, higher during inspiration and lower during expiration (known as bilevel PAP– BPAP) [1]. PAP therapy is the gold standard for treating moderate to severe obstructive sleep apnea (OSA) and other sleep disordered breathing disorders (SDB).

15.1.1 CPAP

Airow is maintained at a constant pressure throughout the respiratory cycle to splint the airways open, in the presence of spontaneous ventilation. Positive endexpiratory pressure (PEEP) maintains the airway pressure above atmospheric level by exerting pressure that opposes passive emptying of the lungs [2, 3]. This pressure is typically achieved by maintaining a positive pressure ow at the end of expiration [3]. CPAP maintains PEEP, during both inspiration and expiration [2]. Applying PEEP increases the upper airway (UA), alveolar pressure and volume. The latter increases the alveolar surface area by reopening and stabilizing collapsed or

Fig. 15.1 PAP machine and set up. Images courtesy of Philips Iberia

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Fig. 15.2 PAP therapy nasal masks. Images courtesy of Philips Iberia

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Fig. 15.3 PAP therapy nasal pillows. Images courtesy of Philips Iberia

unstable alveoli [3]. This splinting of the alveoli with positive pressure improves the ventilation–perfusion match, reducing the shunt effect [3].

The optimal pressure level (measured in cm H2O), may be determined during a night polysomnography (PSG) with CPAP titration or during a CPAP titration night study with standard manual titration. Fixed CPAP pressure derived from prediction formulas are not commonly adopted. With advances in hardware and software, auto-adjusting titrating PAP also known as AutoCPAP (APAP), a continuous pressure is delivered during the night, but at an adjusted pressure depending on events sensed using computer algorithms [4]. For APAP, an upper and lower limit of pressure is established, between the values of 4–20cm H2O, usually with intervals no larger than 10 cm H2O. Currently, the American Academy of Sleep Medicine (AASM) advocates initiating PAP therapy with APAP devices at home or inlaboratory PAP titration, depending on the comorbidities [1, 4].

PAP treatment should provide a low residual apnea-hypopnea index (AHI) and patient tolerance, albeit with an acceptable leakage level (<24 L/min) [1] (Fig.15.6).

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Fig. 15.4 PAP therapy oronasal mask. Images courtesy of Philips Iberia

M. Carrasco-Llatas and J. Vaz de Castro

Fig. 15.5 PAP therapy full-face mask. Images courtesy of Philips Iberia

Fig. 15.6 Air pressure delivered with CPAP and with APAP. (Modied from Ref. [5])

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15.1.2 Effects ofCPAP intheUpper Airway

Increased intraluminal pressure in the upper airway (UA) acts as pneumatic splint. When intraluminal UA pressure exceeds critical closing pressure (Pcrit), passive collapse is prevented [6]. Schwab etal. as well as Torre etal. demonstrated with UA imaging and drug-induced sleep endoscopy (DISE), respectively, that the effect of enlarging the UA is more pronounced in the latero-lateral diameter, compared to the anteroposterior diameter [7, 8]. In 2006, a study by Crawford etal. found that in nine infants (5–12 months old) submitted to an elective brain MRI under anesthesia, with increasing depth of anesthesia cross-sectional area at the tip of the epiglottis decreased by 51% [9]. This resulted from important reductions in antero-posterior diameter but also in the transverse dimensions (38% and 21%, respectively) [9]. Application of CPAP completely reversed the reduction in cross-sectional area primarily by increasing the transverse dimension, by 58% [9]. Therefore, with CPAP, the increase in UA patency is not mediated by its effects on the velopharynx, tongue base, or epiglottis, but on the reduction of thickness of the lateral pharyngeal walls and redistribution of the pharyngeal fat pads [7, 8]. Considering that the anteroposterior diameter is harder to surpass, generally pressures >10cm H2O are needed to maintain epiglottic patency in epiglottic obstruction [8]. This pressure may increase further when considering oronasal interfaces, that usually need increased pressures to match the nasal interface. In another study, pressures of >18cm H2O were needed to maintain epiglottic patency, meanwhile lesser pressures pushed the epiglottis downwards [10].

Considering the physiological route for breathing begins with the nose, where air can be conditioned, humidied, and ltered, nasal interfaces are preferred. Additionally, promoting nasal breathing stabilizes the velopharynx, promotes correct positioning of the tongue against the hard palate which further increases retropalatal and retroglossal space. Hsu etal. compared oral/oronasal breathers with nasal breathers and found a higher degree and prevalence of lateral pharyngeal wall and tongue base collapse in the former [11]. Therefore, nasal masks should be initially adopted, and only in case of failure, oronasal masks should be provided [1]. Nasal pillows are recommended for those who are claustrophobic, need low- pressure ow, sleep in lateral position, or have a history of skin allergy to silicone [12].

Bear in mind, although in OSA, CPAP therapy is used mainly to increase UA patency, it has benets elsewhere: (1) increases intrapulmonary pressure and maintains larger end expiratory lung volume, thereby increasing functional residual capacity, (2) decreases breathing effort, (3) improves stability of central respiratory drive, and (4) reduces cardiac preload and afterload with improved cardiac function [1].

15.1.3 Clinical Impact ofCPAP

PAP therapy is generally considered the gold-standard for moderate to severe adult OSA (AHI > 15/h). In compliant and tolerant patients, it may be considered superior to other treatment modalities in lowering AHI.CPAP therapy has been shown to be

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efcacious and indicated in the treatment of excessive sleepiness, impaired quality of life, and comorbid (especially resistant) hypertension [4, 13]. Reecting how quickly an AHI can be reduced and the UA splinted, CPAP treatment can be used as proof of the causal role of OSA in symptom etiology.

Patients prescribed CPAP should be examined within approximately 2 weeks of starting the treatment and then again between 1 and 2 months later with compliance and efcacy monitored at every visit. Interfaces are replaced every 3–6 months. Patients are followed for as long as they are on CPAP, generally at 6–12 month intervals, depending on treatment success. Repeating polysomnography (PSG) is advocated in case of signicant weight change (>10 kg), surgery, or symptom reappearance [14].

According to a statement by the European Respiratory Society (ERS), CPAP is indicated in moderate to severe OSA (AHI > 5/h) for children 1–23 months old, if they are not candidates for, or do not improve after adenotonsillectomy, or other surgical procedures (e.g., supraglottoplasty for severe laryngomalacia) [15]. It may also be applied as a temporary intervention while waiting for the craniofacial surgery, or in cases of hypoventilation with OSA (e.g., spinal muscular atrophy type 1) [15]. In children 1–23 months, CPAP is initiated at 4–6cm H2O and titrated up to 10cm H2O [15]. After CPAP initiation, PSG is advocated every 2–4 months during the rst year of life and every 6 months thereafter to conrm the continued need for treatment and potential need for increased pressure [15].

Children between 2 and 18 years of age with AHI > 5 episodes/hour are at increased risk of sleepiness if they are older but in preschoolers the most common symptom is aggressiveness, attention and cognitive decits, behavior disorders, elevated blood pressure, primary nocturnal enuresis, decreased quality of life, and respiratory complications post operatively, all conditions which can be reversed with PAP therapy [16]. Usual indications for CPAP for children between 2 and 18 years are: residual OSA after adenotonsillectomy (AHI > 5 episodes/hour), OSA related to obesity, craniofacial abnormalities, or neuromuscular disorders [16]. If nocturnal hypoventilation occurs (e.g., end-tidal carbon dioxide PCO2 > 50mmHg for 25% of total sleep time or peak end-tidal PCO2 > 55mmHg), BPAP is preferred [16]. Treatment priority should be given to SDB children with major craniofacial abnormalities, neuromuscular disorders, achondroplasia, Chiari malformation, Down syndrome, mucopolysaccharidoses, and Prader–Willi syndrome [16].

PSG is used to titrate CPAP or BPAP, and is then repeated at least annually (or more often depending on UA growth, changes in percentile, or surgery). There is limited evidence about optimal respiratory supervision for pediatric PAP treatment, but follow-up based on adult CPAP management, with regular and closely scheduled appointments may be warranted [16].

M. Carrasco-Llatas and J. Vaz de Castro

15.1.4 Side Effects, Adherence, andCompliance

Undesired side effects of PAP therapy include: nasal congestion, rhinorrhea, xerostomia, xerophthalmia, epistaxis, skin erythema/eczema, pressure sores, abdominal

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211

distention, aerophagia, chest discomfort, difculty exhaling, and claustrophobia [17, 18]. Other complaints that decrease adherence and compliance related to the device are device loudness, interface leakage, and water condensation in the interface or circuit. In children, a special concern is facial growth, especially in very young children with craniofacial abnormalities. Patient history, physical examination including awake laryngoscopy and DISE may also provide insight to UA obstruction or collapse that once alleviated may also increase CPAP tolerance. The CPAP device can additionally be adjusted to increase compliance with the addition of adequate humidication, temperature setting, interface comfort, and optimized sensor algorithms with modied pressure proles (e.g., initial pressure relief at expiration) [4, 13].

It is an AASM recommendation that patients should be offered educational interventions prior to PAP therapy initiation, and once treatment is initiated, behavioral, troubleshooting, and telemonitoring-guided interventions [13] (Table15.1).

Patients most likely to be adherent are either more symptomatic, have higher AHI, or are accompanied with comorbid conditions, such as refractory hypertension. Compliance can be optimized with adequate support systems, be it with family, friends, health practitioners, telemonitoring, educational and psychological support [13]. Adequate CPAP compliance is dened as at least 4h of use per night during at least 70% of nights, and optimal when used at least 6h per night [4, 17]. There is a continuous dose–response relationship between hours of use and therapeutic response [4, 13]. Taking into the account that many events occur at the end of the night, which is when patients sometimes take off their interface, this could be an important period of use for CPAP.Ceasing PAP use at the end of the night may be relevant in attenuating PAP therapy benets.

Table 15.1 PAP therapy side effects and possible solutions. According to Ref. [1, 18]

Focus Side effects

Patient Nose Dryness, obstruction

Rhinorrhea

Epistaxis Mouth Xerostomia Humidier Eye Xerophtalmia Interface adaptation, eye drops Skin Rash, abrasion, erythema,

pruritis UA Feeling suffocation ENT consultation (possible anatomical

CPAP High

pressure

Mask Claustrophobia Change to nasal pillows Tube Condensation in tube Use heated PAP, increase ambient

Noise Airow leakage Interface adaptation (change mask or

Chest discomfort, abdominal

distention, aerophagia, or

other ectopic insufation

Possible solutions Humidier, nasal gels or vaseline, nasal

steroid, anti-histamine, ear, nose and throat (ENT) consultation

Interface adaptation (check mask material, type and untighten)

obstruction) Pressure adaptation. Exclusion of acid reux

Pressure adaptation (reduce pressure), change to APAP from CPAP

temperature, reduce humidication

tighten)

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Fig. 15.7 Air pressure delivered with BPAP and AutoBPAP. IPAP inspiratory PAP, EPAP expira- tory PAP, PS pressure support, ↑initiation of inspiratory phase, ↓ initiation of expiratory phase. (Modied from Ref. [5])

M. Carrasco-Llatas and J. Vaz de Castro

15.1.5 BiLevel PAP

Bilevel positive airway pressure delivers a higher inspiratory PAP (IPAP) and a lower expiratory PAP (EPAP). There are three different possibilities how BPAP devices interact with the patient’s breathing. Respiratory circles can be triggered exclusively by the patients (S modus), be dependent on a minimum breathing frequency or otherwise the device will initiate an inspiration (S/T modus) or are exclusively dependent on the BPAP device (T-modus). Usually, these devices are used in the S/T modus in respiratory failure; however, in SDB patients, they may be used: (1) in concomitant hypoventilation-OSA disorders if hypercapnia does not normalize with CPAP, (2) in patients intolerant to high pressure levels, by encompassing an IPAP, the EPAP may be reduced, (3) in patients needing pressure levels above 20cm H2O, (4) to control central sleep apnea (CSA) and Cheyne Stokes respiration (CSR)- there exists very little evidence to justify this indication. Since BPAP might enhance hyperventilation, this therapy, especially in the S modus, is at present not recommended for CSA and CSR [4, 19] (Fig.15.7).

15.1.6 Adaptive Servo-Ventilation (ASV)

In ASV, positive airway pressure is delivered in an anticyclical manner to the periodic hypo/hyperventilation typical for CSA/CSR [1]. EPAP is either titrated similarly to CPAP or applied by automatic regulation, while pressure support and thus IPAP is adaptive in order to stabilize tidal volume over a device specic time frame [1]. ASV revealed a better control of AHI, excessive daytime sleepiness and biomarkers associated with cardiac heart failure (HF) when compared to oxygen, CPAP, and Bilevel [20]. ASV however is controversial in reducing overall and cardiovascular mortality in CSA with HF and reduced ejection fraction (<45%). In the study on ASV for HF, this therapy reduced the AHI, nevertheless, it was associated with a higher cardiovascular mortality [21]. This applied specially for patients with a severe reduction in the ejection fraction (EF < 30%) and more than 50% central respiratory events [21]. At present, both AASM and ERS do not recommend ASV therapy in heart failure patients with an ejection fraction <45% [21, 22]. While

15 Treatment withCPAP

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initially developed for CSA with CSR in CHF patients, ASV has been successfully used in patients with idiopathic CSA-CSR, treatment emergent CSA, opioidassociated CSA, and CSA after stroke [1].

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15.2 CPAP Diagnostic Possibilities

CPAP might have a role as a tool in patient selection for non-CPAP treatments. It has been shown that the critical closing pressure (Pcrit) has a strong correlation with CPAP pressure. According to Landry etal., lower therapeutic CPAP levels are associated with more negative Pcrit values (less collapsible airway) [23]. Specically, patients with a CPAP requirement below 6–8cm H2O are highly likely to have a mildly collapsible UA (dened by a Pcrit ≤ −2cm H2O). Patients who need higher CPAP pressure have more collapsible upper airways and should be more difcult to cure with surgery or mandibular advancement devices (MADs) [23]. The CPAP pressure needed to open the airway may offer a hint on the structure responsible for the collapse. Torres etal. demonstrated with nasal CPAP and DISE that a pressure of 15cm H2O was enough to splint collapses in all their patients (n = 15), while values at 5cm H2O did not make much of a difference. Nasal CPAP pressures of 10cm H2O were sufcient to surpass velopharyngeal and oropharyngeal obstructions, but 15cm H2O was necessary for tongue base and epiglottic obstruction [8]. Similarly, Sung et al., using simultaneous PAP-DISE, demonstrated that most patients with isolated epiglottic collapse needed pressures >12 cm H2O [24]. Likewise, Kim etal. showed that patients with epiglottic collapse had relatively low body mass index (BMI) and less severe OSA [25]. Additionally, they were unlikely to respond to CPAP therapy; therefore, it is possible that patients with mild OSA that are intolerant to CPAP at low pressures (due to a sense of suffocation), may have predominantly epiglottic collapse, and this could be solved with higher pressures. Nevertheless, this idea needs to be proven in prospective studies and with larger populations.

Although it is not directly the focus of this chapter, the authors found it pertinent to report that CPAP may also be used to diagnose laryngeal clefts using exible endoscopy. Laryngeal clefts are uncommon but important causes of stridor in infants, for which direct laryngoscopy is the recommended method, as exible endoscopy is not sensitive enough [26]. CPAP-exible laryngoscopy applied via an endoscopy mask can be titrated to open the upper esophageal sphincter and spread the inter-arytenoid folds at 10–15cm H2O unmasking obscured laryngeal clefts [26].

On the other hand, CPAP can be used during DISE to demonstrate the etiology of patient intolerance [27]. Ideally, the same mask that the patient is using at home should be employed; however, testing other types of masks during DISE could reveal the impact of UA collapse with different masks maintaining the same pressure levels [28]. Fig.15.8 (Video 15.1) shows DISE-CPAP performed to evaluate the best mask to be attached to CPAP. The exam was performed with the same

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Fig. 15.8 (Video 15.1) DISE-CPAP performed to evaluate the best mask to be attached to CPAP (► https://doi.org/10.1007/000-bfc)

M. Carrasco-Llatas and J. Vaz de Castro

pressure and three different masks (nasal, oronasal, and prong), showing a better airway area with nasal mask when compared to the other two. As epiglottis continued to eventually collapse even with nasal mask, chin strap was added. This maneuver juxtaposed to nasal mask prevented the epiglottic collapse.

15.3 CPAP Treatment inCertain Epiglottic Pathologies

Epiglottic obstruction is associated with certain states, such as, multiple system atrophy (MSA) and laryngomalacia, both of which are frequently associated with OSA.In MSA, UA obstruction occurs not only at the level of vocal cords, but also at the tongue base, velopharynx, and laryngeal inlet. Obstruction of the laryngeal inlet is provoked by a oppy epiglottis that is sucked in during inspiration, by an unknown mechanism [29]. Although awake laryngoscopy did not reveal oppy epiglottis in any of the patients included in the study conducted by Shimohata etal. (n = 17), DISE revealed a oppy epiglottis in 71% (12/17) with 5 patients worsening with CPAP >8cm H2O.Of these 5 cases, 3 had severe oppy epiglottis (downward displacement of the epiglottis with covering of the laryngeal inlet during inspiration), but two had mild laryngomalacia (no covering of the laryngeal inlet). Oneyear follow-up revealed another mild patient developing severe oppy epiglottis over the time. In patients with MSA, a laryngeal motor tone abnormality associated with neurodegeneration and Bernoulli effect may inuence the development of oppy epiglottis [29]. This suggests that in MSA there might be a disease progression of epiglottic obstruction with CPAP.

As many as 77–93% of children with laryngomalacia may have OSA [30, 31]. Infants with laryngomalacia can achieve improved ventilatory pattern and unloaded respiratory muscle effort (decreased respiratory rate and esophageal pressure swings) with CPAP (pressures between 8 and 10cm H2O) which is preferred compared to BPAP [15, 32].

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