Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4704_Библиотеки_им_академика_М_И_Перельмана
.pdf
recruited. On therapy, an AHI of <10/h was achieved in two out of seven using
oxygen (29%), six of seven using ASV (86%) and six of seven with (86%). Median
AHI on oxygen therapy: 13.4/h, ASV, 1.4/h. Over 8 weeks, ASV reduced CSA-CSR
more effectively than oxygen therapy, but it was not accepted for long-term use.
Neither treatment improved prognostic indices of heart failure or symptoms in the
short term. However, oxygen may be of value as an adjunct therapy (Campbell et al.
2012)
.
78 A. S. BaHammam et al.
Oxygen is effective in
patients with high-altitude periodic breathing by improving
the sleep architecture. The severity of the CSA can be reduced by descent, supple-
mental oxygen therapy and oral or intravenous acetazolamide. Bilevel noninvasive
ventilation can also be used in addition to oxygen. Sleep quality can also be
improved independently of the presence of CSA using benzodiazepines (Burgess
and Ainslie
2016).
5.11.4 Adaptive Servo-Ventilation (ASV)
ASV is used for treatment for CSA in selected patients. It is important to point out
that there are many controversies regarding the use of ASV in the treatment of
central sleep apnea. ASV provides both positive expiratory airway pressure (EPAP)
and inspiratory pressure support (IPAP), which is servo-controlled based on the
presence of CSA based on an algorithm. Adaptive servo-ventilation (ASV) provides
a varying amount of inspiratory pressure superimposed on a low level of CPAP, with
a backup respiratory rate based on the underlying algorithm. Phillippe et al. studied
patients regarding the compliance and effectiveness of ASV versus CPAP in treating
CSR in heart failure over 6 months (Philippe et al. 2006). Both ASV and CPAP
decreased the AHI, but noticeably, only ASV completely corrected CSA-CSR, with
AHI below 10/h (Philippe et al. 2006).
Cowie et al. reported the results of their trial on the use of ASV in patients with
CSA (Cowie et al.
2016). They randomly assigned 1325 patients with a left
ventricular ejection fraction of 45% or less, an apnea-hypopnea index (AHI) of
15 or more events (occurrences of apnea or hypopnea) per hour, and a predominance
of central events to receive guideline-based medical treatment with ASV or
guideline-based medical treatment alone (control) (Cowie et al. 2016
). In the ASV
group, the mean AHI at 12 months was 6.6 events per hour. The incidence of the
primary endpoint did not differ significantly between the adaptive servo-ventilation
group and the control group (54.1% and 50.8%, respectively; hazard ratio, 1.13; 95%
confidence interval [CI], 0.97 to 1.31; P = 0.10). All-cause mortality and cardio-
vascular mortality were significantly higher in the ASV group than in the control
group (hazard ratio for death from any cause, 1.28; 95% CI, 1.06 to 1.55; P = 0.01;
and hazard ratio for cardiovascular death, 1.34; 95% CI, 1.09 to 1.65; P = 0.006)
(Cowie et al.
2016). ASV had no significant effect on the primary endpoint in heart
failure patients with reduced ejection fraction and predominantly central sleep apnea,
https://t.me/medicina_free

but all-cause and cardiovascular mortality were both increased with this therapy
(Cowie et al. 2016).
5 Central Sleep Apnea: Advances in the Last Decade 79
Based on the SERVE-HF trial, AA
SM recommendations for the use of ASV in
central sleep apnea are as follows (Aurora et al.
2016):
Recommendation 1: ASV targeted to normalize the AHI should not be used for
the treatment of CSA syndrome (CSAS) related to CHF in adults with an ejection
fraction ≤45% and moderate or severe CSA predominant, sleep-disordered
breathing.
Recommendation 2: ASV targeted to normalize the AHI can be used to treat
CSAS related to CHF in adults with an ejection fraction >45% or mild
CHF-related CSAS.
The ADVENT-HF trial is designed to test whether ASV improves cardiovascular
outcomes in heart failure patients with sleep apnea and, so far, has better compliance
than previous trials, with no safety concerns to date. More than 600 patients have
been enrolled in ADVENT-HF to date, and the investigators hope to enroll more
than 800. On average, patients with obstructive sleep apnea (OSA) used the device
for 4.6 hours per night at 1 month and 4.1 hours at 12 months. In contrast, patients
with CSA consistently used the device for 5.2 hours per night at both 1 month and
12 months. The results of this study may help us in defining the future of CSA
Management (Burgess and Ainslie 2016; Philippe et al. 2006; Canadian Institutes of
Health Research 2021).
5.11.5 Overdrive Atrial Pacing
Garrigue et al. observed that patients who had received a pacemaker with atrial
overdrive pacing to reduce the incidence of atrial tachyarrhythmia had a reduction in
breathing disorders after the implantation of the pacemaker (Garrigue et al. 2002).
They studied 15 patients with central or obstructive sleep apnea who had recei ved
permanent atrial-synchronous ventricular pacemakers for symptomatic sinus brady-
cardia. All patients underwent three polysomnographic evaluations on consecutive
nights, the first night for baseline evaluation and then, in random order, one night in
spontaneous rhythm and one in dual chamber pacing mode with atrial overdrive. “In
patients with sleep apnea syndrome, atrial overdrive pacing significantly reduces the
number of episodes of central or obstructive sleep apnea without reducing the total
sleep time.” The number of patients who are eligible for this therapy may be small.
But this may help individual patients (Garrigue et al.
2002). However, others are not
able to reproduce the same result (Luthje et al.
2005).
https://t.me/medicina_free

80 A. S. BaHammam et al.
5.12 Phrenic Nerve Stimulation/Implantable Device
(Rremedē System)
Costanzo et al. studied patients with CSA associated with poor prognosis in CHF
patients. Their study aimed to evaluate if using phrenic nerve stimulation to treat
CSA in patients with CSA and HF was associated with changes in HF-specific
metrics. In patients with HF, 53% (41/77) had a ≥50% reduction in AHI from
baseline to 6 months and 57% (40/70) from baseline to 12 months. A reduction in
AHI occurred in 61 of 70 (87%) patients at 12 months. In October 2017, the US Food
and Drug Administration (FDA) approved an implantable device for the treatment of
central sleep apnea. The remedē system, as described by Costanzo et al. (
2016),
consists of a battery pack implanted under the skin on the upper chest. It delivers
electrical currents to the phrenic nerve to stimulate the diaphragm (Costanzo et al.
2016). The most common adverse effects in the trial were implant site infection,
concomitant device interaction, local tissue damage or pocket erosion, and swelling
(Sin et al.
2000; Costanzo et al. 2016). The follow-up study by Fox et al. showed that
at least 60% of patients in the treatment group achieved at least 50% reduction in
AHI through 24 months (Fox et al.
2019). There are no safety concerns over a period
of 36 months (Fox et al. 2019).
5.13 Theophylline
Theophylline is a phosphodiesterase-5 inhibitor has been used to manage CSR that is
associated with premature birth, the ascent to high altitudes, and heart failure
(AlDabal and BaHammam 2010). The mechanism by which theophylline treats
CSR is not yet clear. Patients with chronic heart failure have elevated levels of
adenosine, leading to a depression of respiration, and theophylline may stimulate
respiration by binding to adenosine receptors in the central nervous system (Funaya
et al.
1997). On the other hand, theophylline may cause hyperventila tion, thus
inhibiting an increase in PaCO
2
and stopping an essential step in the induction of
CSA. It may alter the central chemosensitivity reaction to PaCO
2
, or it may reverse
hypoxia-induced hypoventilation (Sanders et al.
1980). Irrespective of its mecha-
nism, many studies have shown that taking oral theophylline to patients with CHF
successfully treats CSR by droppi ng the number of episodes of central apnea and
hypopnea per hour (AlDabal and BaHammam
2010). Unfortunately, all these studies
were short-term and used small sample sizes. Nevertheless, there is insufficient data
on the long-term safety profile of this potentially hazardous medication and the
possibility of drug interactions. In particular, theophylline appears to be connected
with arrhythmia, which could negatively affect a poorly functioning left ventricle
(Huerta et al.
2005).
https://t.me/medicina_free

5 Central Sleep Apnea: Advances in the Last Decade 81
5.14 Acetazolamide (Diamox)
Acetazolamide is a weak diuretic that inhibits carbonic anhydrase in the brain,
kidneys, vascular endothelium, red blood cells, and peripheral and central chemo-
receptors with varying effects, depending on means and site of administration,
duration, and dose (Sharp et al.
1985). Acetazolamide interrelates with the central
and peripheral respiratory system in a compound way, and elements of its mecha-
nism of action are not yet clearly understood. Nevertheless, it is recognized that
acetazolamide inhibits carbonic anhydrase and hence produces mild metabolic
acidosis. This stimulates the central respiratory system, causing hyperventilation, a
reduction in PaCO
2
, and a rise in PaO
2
. Additionally, studies have demonstrated that
acetazolamide results in a condition of peripheral and central chemoreceptor depres-
sion (Teppema and Dahan
1999). Nevertheless, acetazolamide is likely to lose its
effects over time, and there are no long-term studies in patients with CSR and heart
failure.
References
AASM (2014) American Academy of Sleep Medicine (AASM). International classification of sleep
disorders (ICSD), 3rd edn. AASM, Darien
AlDabal L, BaHammam AS (2010) Cheyne-stokes respiration in patients with heart failure. Lung
188(1):5–14.
https://doi.org/10.1007/s00408-009-9200-4
Arzt M, Floras JS, Logan AG, Kimoff RJ, Series F, Morrison D, Ferguson K, Belenkie I, Pfeifer M,
Fleetham J, Hanly P, Smilovitch M, Ryan C, Tomlinson G, Bradley TD, CANPAP Investigators
(2007) Suppression of central sleep apnea by continuous positive airway pressure and
transplant-free survival in heart failure: a post hoc analysis of the Canadian Continuous Positive
Airway Pressure for Patients with Central Sleep Apnea and Heart Failure Trial (CANPAP).
Circulation 115(25):3173–3180.
https://doi.org/10.1161/circulationaha.106.683482
Aurora RN, Bista SR, Casey KR, Chowdhuri S, Kristo DA, Mallea JM, Ramar K, Rowley JA, Zak
RS, Heald JL (2016) Updated adaptive servo-ventilation recommendations for the 2012 AASM
guideline: “the treatment of central sleep apnea syndromes in adults: practice parameters with an
evidence-based literature review and meta-analyses”. J Clin Sleep Med 12(5):757–761. https://
doi.org/10.5664/jcsm.5812
Avidan AY, Guilleminault C, Robinson A (2006) The development of central sleep apnea with an
oral appliance. Sleep Med 7(2):187–191. https://doi.org/10.1016/j.sleep.2005.06.013
Badr MS, Dingell JD, Javaheri S (2019) Central sleep apnea: a brief review. Curr Pulmonol Rep
8(1):14–21. https://doi.org/10.1007/s13665-019-0221-z
BaHammam AS (2017) Treatment-emergent central sleep apnea (complex sleep apnea). Sleep
Vigilance 1:53–56. https://doi.org/10.1007/s41782-017-0015-8
Berry RB, Brooks R, Gamaldo C, Harding SM, Lloyd RM, Quan SF, Troester MT, Vaughn BV
(2020) AASM Scoring Manual updates for 2020 (Version 2.6). J Clin Sleep Med 13(5):
665–666. https://doi.org/10.5664/jcsm.6576
Bradley TD, Logan AG, Kimoff RJ, Series F, Morrison D, Ferguson K, Belenkie I, Pfeifer M,
Fleetham J, Hanly P, Smilovitch M, Tomlinson G, Floras JS, Investigators C (2005) Continuous
positive airway pressure for central sleep apnea and heart failure. N Engl J Med 353(19):
2025–2033. https://doi.org/10.1056/NEJMoa051001
https://t.me/medicina_free

82 A. S. BaHammam et al.
Burgess KR, Ainslie PN (2016) Central sleep apnea at high altitude. Adv Exp Med Biol 903:275–
283.
https://doi.org/10.1007/978-1-4899-7678-9_19
Campbell AJ, Ferrier K, Neill AM (2012) Effect of oxygen versus adaptive pressure support
servo-
ventilation in patients with central sleep apnoea-Cheyne Stokes respiration and congestive heart
failure. Intern Med J 42(10):1130–1136.
https://doi.org/10.1111/j.1445-5994.2011.02623.x
Canadian Institutes of Health Research (2021) Effect of adaptive servo ventilation (ASV) on
survival and hospital admissions in heart failure (ADVENT-HF) (trial registration).
ClinicalTrials.gov Identifi er: NCT01128816. https://clinicaltrials.gov/ct2/show/results/
NCT01128816?view=results
Carmona-Bernal C, Ruiz-Garcia A, Villa-Gil M, Sanchez-Armengol A, Quintana-Gallego E,
Ortega-Ruiz F, Baron-Esquivias G, Capote F (2008) Quality of life in patients with congestive
heart failure and central sleep apnea. Sleep Med 9(6):646–651. https://doi.org/10.1016/j.sleep.
2007.11.008
Correa D, Farney RJ, Chung F, Prasad A, Lam D, Wong J (2015) Chronic opioid use and central
sleep apnea: a review of the prevalence, mechanisms, and perioperative considerations. Anesth
Analg 120(6):1273–1285. https://doi.org/10.1213/ANE.0000000000000672
Costanzo MR, Ponikowski P, Javaheri S, Augostini R, Goldberg L, Holcomb R, Kao A, Khayat
RN, Oldenburg O, Stellbrink C, Abraham WT, Remede System Pivotal Trial Study Group
(2016) Transvenous neurostimulation for central sleep apnoea: a randomised controlled trial.
Lancet 388(10048):974–982.
https://doi.org/10.1016/S0140-6736(16)30961-8
Cowie MR, Wegscheider K, Teschler H (2016) Adaptive servo-ventilation for central sleep apnea
in heart failure. N Engl J Med 374(7):690–691.
https://doi.org/10.1056/NEJMc1515007
Dohi T, Kasai T, Narui K, Ishiwata S, Ohno M, Yamaguchi T, Momomura S (2008) Bi-level
positive airway pressure ventilation for treating heart failure with central sleep apnea that is
unresponsive to continuous positive airway pressure. Circ J 72(7):1100–1105.
https://doi.org/
10.1253/circj.72.1100
Douglas NJ, White DP, Weil JV, Pickett CK, Zwillich CW (1982) Hypercapnic ventilatory
response in sleeping adults. Am Rev Respir Dis 126(5):758–762.
https://doi.org/10.1164/arrd.
1982.126.5.758
Dowell AR, Buckley CE 3rd, Cohen R, Whalen RE, Sieker HO (1971) Cheyne-Stokes respiration.
A review of clinical manifestations and critique of physiological mechanisms. Arch Intern Med
127(4):712–726. https://doi.org/10.1001/archinte.127.4.712
Fox H, Oldenburg O, Javaheri S, Ponikowski P, Augostini R, Goldberg LR, Stellbrink C,
McKane S, Meyer TE, Abraham WT, Costanzo MR (2019) Long-term efficacy and safety of
phrenic nerve stimulation for the treatment of central sleep apnea. Sleep 42(11):zsz158. https://
doi.org/10.1093/sleep/zsz158
Funaya H, Kitakaze M, Node K, Minamino T, Komamura K, Hori M (1997) Plasma adenosine
levels increase in patients with chronic heart failure. Circulation 95(6):1363–1365. https://doi.
org/10.1161/01.cir.95.6.1363
Garrigue S, Bordier P, Jais P, Shah DC, Hocini M, Raherison C, Tunon De Lara M,
Haissaguerre M, Clementy J (2002) Benefit of atrial pacing in sleep apnea syndrome. N Engl
J Med 346(6):404–412. https://doi.org/10.1056/NEJMoa011919
Goldstein C, Kuzniar TJ (2012) The emergence of central sleep apnea after surgical relief of nasal
obstruction in obstructive sleep apnea. J Clin Sleep Med 8(3):321–322. https://doi.org/10.5664/
jcsm.1926
Gould GA, Gugger M, Molloy J, Tsara V, Shapiro CM, Douglas NJ (1988) Breathing pattern and
eye movement density during REM sleep in humans. Am Rev Respir Dis 138(4):874–877.
https://doi.org/10.1164/ajrccm/138.4.874
Hackett PH, Roach RC (2001) High-altitude illness. N Engl J Med 345(2):107–114. https://doi.org/
10.1056/NEJM200107123450206
Huerta C, Lanes SF, Garcia Rodriguez LA (2005) Respiratory medications and the risk of cardiac
arrhythmias. Epid emiology 16(3):360
–3
66.
https://doi.org/10.1097/01.ede.0000158743.
90664.a7
https://t.me/medicina_free

5 Central Sleep Apnea: Advances in the Last Decade 83
Liu D, Armitstead J, Benjafield A, Shao S, Malhotra A, Cistulli PA, Pepin JL, Woehrle H (2017)
Trajectories of emergent
central sleep apnea during CPAP therapy. Chest 152(4):751–760.
https://doi.org/10.1016/j.chest.2017.06.010
Luthje L, Unterberg-Buchwald C, Dajani D, Vollmann D, Hasenfuss G, Andreas S (2005) Atrial
overdrive pacing in patients with sleep apnea with implanted pacemaker. Am J Respir Crit Care
Med 172(1):118–122. https://doi.org/10.1164/rccm.200409-1258OC
Mohan A, Henderson J, Mador MJ (2016) Mandibular advancement device-emergent central sleep
apnea can resolve spontaneously: a case report. J Clin Sleep Med 12(1):137–138.
https://doi.
org/10.5664/jcsm.5414
Muza RT (2015) Central sleep apnoea-a clinical review. J Thorac Dis 7(5):930–937. https://doi.org/
10.3978/j.issn.2072-1439.2015.04.45
Nigam G, Pathak C, Riaz M (2016) A systematic review on prevalence and risk factors associated
with treatment—emergent central sleep apnea. Ann Thorac Med 11(3):202–210.
https://doi.org/
10.4103/1817-1737.185761
Philippe C, Stoica-Herman M, Drouot X, Raffestin B, Escourrou P, Hittinger L, Michel PL,
Rouault S, d’Ortho MP (2006) Compliance with and effectiveness of adaptive servoventilation
versus continuous positive airway pressure in the treatment of Cheyne-Stokes respiration in
heart failure over a six month period. Heart 92(3):337–342.
https://doi.org/10.1136/hrt.2005.
060038
Randerath W, Javaheri S (2016) Sleep-disordered breathing in patients with heart failure. Curr
Sleep Medicine Rep 2:99–106.
https://doi.org/10.1007/s40675-40016-40047-y
Sanders JS, Berman TM, Bartlett MM, Kronenberg RS (1980) Increased hypoxic ventilatory drive
due to administration of aminophylline in normal men. Chest 78(2):279–282.
https://doi.org/10.
1378/chest.78.2.279
Sasayama S, Izumi T, Matsuzaki M, Matsumori A, Asanoi H, Momomura S, Seino Y, Ueshima K,
CHF-HOT Study Group (2009) Improvement of quality of life with nocturnal oxygen therapy in
heart failure patients with central sleep apnea. Circ J 73(7):1255–1262. https://doi.org/10.1253/
circj.cj-08-1210
Schafer T, Schlafke ME (1998) Respiratory changes associated with rapid eye movements in
normo- and hypercapnia during sleep. J Appl Physiol (1985) 85(6):2213–2219.
https://doi.
org/10.1152/jappl.1998.85.6.2213
Sharp JT, Druz WS, D’Souza V, Diamond E (1985) Effect of metabolic acidosis upon sleep apnea.
Chest 87(5):619–624.
https://doi.org/10.1378/chest.87.5.619
Sin DD, Fitzgerald F, Parker JD, Newton G, Floras JS, Bradley TD (1999) Risk factors for central
and obstructive sleep apnea in 450 men and women with congestive heart failure. Am J Respir
Crit Care Med 160(4):1101–1106. https://doi.org/10.1164/ajrccm.160.4.9903020
Sin DD, Logan AG, Fitzgerald FS, Liu PP, Bradley TD (2000) Effects of continuous positive
airway pressure on cardiovascular outcomes in heart failure patients with and without Cheyne-
Stokes respiration. Circulation 102(1):61–66. https://doi.org/10.1161/01.cir.102.1.61
Skatrud JB, Dempsey JA (1983) Interaction of sleep state and chemical stimuli in sustaining
rhythmic ventilation. J Appl Physiol Respir Environ Exerc Physiol 55(3):813–822. https://doi.
org/10.1152/jappl.1983.55.3.813
Teppema LJ, Dahan A (1999) Acetazolamide and breathing. Does a clinical dose alter peripheral
and central CO(2) sensitivity? Am J Respir Crit Care Med 160(5 Pt 1):1592–1597. https://doi.
org/10.1164/ajrccm.160.5.9903088
Wedewardt J, Bitter T, Prinz C, Faber L, Horstkotte D, Oldenburg O (2010) Cheyne-Stokes
respiration in heart failure: cycle length is dependent on left ventricular ejection fraction.
Sleep Med 11(2):137–142. https://doi.org/10.1016/j.sleep.2009.09.004
White DP, Gleeson K, Pickett CK, Rannels AM, Cymerman A, Weil JV (1987) Altitude acclima-
tization: influence
on periodic breathing and chemoresponsiveness during sleep. J Appl Physiol
(1985) 63(1):401–412.
https://doi.org/10.1152/jappl.1987.63.1.401
https://t.me/medicina_free

84 A. S. BaHammam et al.
Xie A
, Wong B, Phillipson EA, Slutsky AS, Bradley TD (1994) Interaction of hyperventilation and
arousal in the pathogenesis of idiopathic central sleep apnea. Am J Respir Crit Care Med 150(2):
489–495.
https://doi.org/10.1164/ajrccm.150.2.8049835
Xie A, Skatrud JB, Puleo DS, Rahko PS, Dempsey JA (2002) Apnea-hypopnea threshold for CO
2
in patients with congestive heart failure. Am J Respir Crit Care Med 165(9):1245–1250. https://
doi.org/10.1164/rccm.200110-022OC
https://t.me/medicina_free

Chapter 6
Current Clinical Perspective of Adult
Obstructive Sleep Apnea: Symptomatology,
Clinical Features, and Different Phenotypes
Ahmed S. BaHammam, Mahadevappa Hunasikatti,
and Seithikurippu R. Pandi-Perumal
Abstract The incidence and prevalence of obstructive sleep apnea (OSA) continue
to rise in the United States and the world. The prevalence of OSA is conservatively
estimated to be 3% among women and 10% among men 30 to 49 years of age and
9% among women and 17% among men 50 to 70 years of age, including an
estimated 24 million persons in the United States who have not received a diagnosis.
Symptoms of OSA generally begin gradually and insidiously, and are often present
for years before the patient is referred for treatment. Also, in general, OSA patients
use healthcare resources at approximately twice the rate of controls as far back as
10 years before their diagnosis.
OSA is a complex and heterogeneous disorder, and the used severity criteria for
OSA based on the apnea-hypopnea index (AHI) do not capture the diverse spectrum
of the condition. Therefore, we may need to subcategorize the OSA into well-
recognized phenotypes, which help us in the management and outcome of clinical
studies. A “phenotype” is defined as an observable expression of an individual’s
characteristics that result from the interaction between the individual’s genes (geno-
type) and the environment, without any implication of a mechanism. A phenot ype is
distinct from an “endotype,” which is the subtype of a disease defined by a unique or
distinctive functional or pathophysiologic mechanism.
A. S. BaHammam
The University Sleep Disorders Center, Department of Medicine, College of Medicine, King
Saud University, Riyadh, Saudi Arabia
King Saud University Medical City, King Saud University, Riyadh, Saudi Arabia
M. Hunasikatti (
✉)
Division of Respiratory, Sleep and Anesthesiology (DSRA), OHT1, Food and Drug
Administration (FDA), Silver Spring, MD, USA
S. R. Pandi-Perumal
Somnogen Canada Inc., College Street, Toronto, ON, Canada
Saveetha Medical College and Hospitals, Saveetha Institute of Medical and Technical Sciences,
Saveetha University, Chennai, Tamil Nadu, India
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
A. S. BaHammam, M. Hunasikatti (eds.), Sleep Apnea Frontiers, Progress in Sleep
Research,
https://doi.org/10.1007/978-981-99-7901-1_6
85
https://t.me/medicina_free

86 A. S. BaHammam et al.
Some of the specific OSA phenotype s may have an impact on the management of
OSA. REM-related SDB was more prevalent in women, younger individuals, and
African Americans. Compared to non-stage-specific OSA, patients with
REM-related OSA were less symptomatic with less sleepiness. REM sleep is
associated with greater sympathetic activity and cardiovascular instability in healthy
individuals than NREM sleep. REM-related OSA has been found to be associated
with an increased risk of hypertension, metabolic complications such as insulin
resistance, and metabolic syndrome. Patients with OSA have high sympathetic
activity when awake, with further increases in blood pressure and sympathetic
activity during sleep. These increases are attenuated by treatment with CPAP. This
may have an impact on the treatment of these specific populations.
Keywords Obstructive sleep apnea (OSA) · Apnea-hypopnea index (AHI) · REM-
related sleep-disordered breathing (SDB) · Phenotypes and endotypes · Continuous
positive airway pressure (CPAP)
6.1 Introduction
The incidence and prevalence of obstructive sleep apnea (OSA) continue to rise in
the United States as well as in the world. The prevalence of OSA is conservatively
estimated to be 3% among women and 10% among men 30 to 49 years of age and
9% among women and 17% among men 50 to 70 years of age, including an
estimated 24 million persons in the US who have not recei ved a diagnosis (Peppard
et al. 2013). This has resulted in major economic, social, and health consequences.
Approximately one billion of the world’s population of 7.3 billion people, between
the ages of 30 and 69 years, are estimated to have the most common type of sleep-
disordered breathing, OSA. OSA prevalence is rising and affects all countries. The
increase in prevalence is driven by the global increase in obesity, the major risk
factor for OSA, and improved diagnostic methods.
Obstructive sleep apnea is characterized by episodic sleep state-dependent col-
lapse of the upper airway, resulting in periodic reductions or cessations in ventila-
tion, with consequent hypoxia, hypercapnia, or arousals from sleep (Dempsey et al.
2010).
6.2 Epidemiology
6.2.1 Global Burden Versus United States Burden
Benjafield et al. estimated that nearly one billion adults aged 30–69 years worldwide
could have OSA, and the number of people with moderate to severe obstructive sleep
apnea, for which treatment is generally recommended, is estimated to be almost
425 million. This analysis represents the first set of global estimates of OSA
https://t.me/medicina_free

prevalence (Benjafield et al. 2019). The estimated number of individuals with OSA
was highest in China, followed by the United States, Brazil, and India. The world-
wide obesity epidemic and the aging population demographic are likely to contribute
to the rising global prevalence of obstructive sleep apnea. Additionally, the high
prevalence in countries such as China is likely to be due to racial and genetic
differences in common anatomical features that increase the likelihood of obstructive
sleep apn
ea, such as a narrower airway (Lam et al.
2005).
The high estimated global
prevalence suggests that the development of cheaper alternative devices to diagnose
and treat OSA is required. The new wearable devices with adequate sensitivity and
specificity in diagnosing OSA may fill this need. Some fear that this large prevalence
of this may overburden the healthcare system. However, the timely management of
obstructive sleep apnea is not just cost-effective but potentially cost-saving because
of the prevention of ma
jor complications like cardiovascular disease, stroke, and
reduction in motor vehicle accidents with associated improved quality of health
(Ayas et al.
2006). The cost of treatment devices might be an important barrier to
treatment not only in low-income and middle-income countries, but also in indus-
trialized countries like the United States wher e disparity of health care results in
inaccessibility to the treatment of OSA (Frost, and Sullivan, American Academy of
Sleep Medicine 2016).
6 Current Clinical Perspective of Adult Obstructive Sleep Apnea:... 87
Definition: Symptoms of OSA generally begin gradually
and insidiously, and are
often present for years before the patient is referred for treatment. Also, in general,
OSA patients use healthcare resources at approximately twice the rate of controls as
far back as 10 years before their diagnosis. Analysis of the two main components of
medical costs, physician claims and hospital stay, demonstrates greater utilization of
both in the patient group (BaHammam et al. 1999; Ronald et al. 1999). Even though
most patients are referred to sleep clinics because of snoring, excessive daytime
sleepiness, and witnessed apneas, a comprehensive list of presenting symptoms are
as follows:
6.2.2 Major Nocturnal Symptoms
• Snorin g, usually loud, habitual, and bothersome to others.
• Witnessed apneas, which often interrupt the snoring and end with a snort.
• Gasping and choking sensations: Gasping and choking sensations that arouse the
patient from sleep, though in an extremely low proportion relative to the number
of apneas they experience. Choking or gasping during sleep or awakening with a
dry mouth are commonly reported, often in association with snoring. Myers et al.
found that nocturnal choking or gasping was the most predictive symptom for
identifying patients with OSA, with a summary likelihood ratio of 3.3, when the
diagnosis was established by an AHI of 10 or more events per hour. Snoring is
common in sleep apnea patients but is not useful for establishing the diagnosis
(summary LR, 1.1). Patients with mild snoring and a body mass index lower than
26 are unlikely to have moderate or severe obstructive sleep apnea (LR, 0.07 at
https://t.me/medicina_free
Соседние файлы в папке Библиотека им академика М.И. Перельмана
