Respiratory abnormalities during sleep

2. Respiratory abnormalities during sleep Prof. Dr. J. Verbraecken Dept of Pulmonary Medicine and Sleep Disorders Center Antwerp University Hospital, Belgium

3. outlines Snoring Obstructive sleep apnea (OSA) Central sleep apnea (CSAS) Cheyne-Stokes respiration (CSR) UARS Hypoventilation Nocturnal dyspnea DD COPD, asthma, pulmonary oedema Sleep related laryngospasm Sleep choking, �

4. Snoring Turbulence of inspired air Vibrations of the mucosa Mostly during inspiration Partial occlusion/flow limitation of the pharynx during sleep

7. Anamnesis Snoring Intermittent and discrete snoring only when lying in the supine position Constant and loud snoring Supine/all positions Socially unacceptable snoring sleeping with partner impossible, disturbing environment Bothers relationship Maximal limit for noise in the house at night: 45 decibel

8. Snoring according to body position

9. Snoring

11. outlines Snoring Obstructive sleep apnea (OSA) Central sleep apnea (CSAS) Cheyne-Stokes respiration (CSR) UARS Hypoventilation Nocturnal dyspnea DD COPD, asthma, pulmonary oedema Sleep related laryngospasm Sleep choking, �

12. SLEEP APNEADEFINITIONS Apnea= interruption of flow at nose and mouth during at least 10 seconds. Central apnea Obstructive apnea Mixed apnea Hypopnea

15. OSAS: CURRENT DEFINITION Sleep apnea-syndrome: > 5 apneas-hypopneas/hour sleep AND Excessive daytime sleepiness unexplained by any other factors OR 2 or more of the following symptoms: choking or gasping during sleep Awakening regularly during sleep Unrefreshed in the morning Fatigue Disturbed concentration Obstructive sleep apnea syndrome (OSAS) Central sleep apnea syndrome (CSAS)

16. Severity criteria

18. Repetitive Oxygen desaturations

20. OSA and cardiovascular consequences: negative thoracic pressure (1) Obstructive apneas will lower intrathoracic pressures and therefore increase transmural systolic left ventricular pressure. This will increase left ventricular afterload and compromise left ventricular functionObstructive apneas will lower intrathoracic pressures and therefore increase transmural systolic left ventricular pressure. This will increase left ventricular afterload and compromise left ventricular function

22. OSA and cardiovascular consequences: arousal reaction (2) During the apnea the reflex from pulmonary stretch receptors, that normally suppresses SNA, is interrupted leading to an increase in SNA. Hypoxia and hypercapnia also increases SNA by stimulation of the peripheral chemoreceptors and by provoking arousals. Increased sympathetic nervous system activity, a cardinal feature of obstructive apnea, results from the interaction of several excitatory mechanisms normally dormant during sleep. During apnea, the reflex arising from pulmonary stretch receptors that suppresses central sympathetic discharge during normal breathing ceases, disinhibiting central sympathetic outflow. The ensuing hypoxia and hypercapnia further augment sympathetic activity by stimulating peripheral and central chemoreceptors.39,40 Although arousal from sleep at the termination of obstructive apnea facilitates the resumption airflow by stimulating pharyngeal dilator muscles,37,42 the resulting excitatory input from cortical centers will cause a further burst of sympathetic outflow accompanied by a loss of vagal tone.11,43 During the apnea the reflex from pulmonary stretch receptors, that normally suppresses SNA, is interrupted leading to an increase in SNA. Hypoxia and hypercapnia also increases SNA by stimulation of the peripheral chemoreceptors and by provoking arousals. Increased sympathetic nervous system activity, a cardinal feature of obstructive apnea, results from the interaction of several excitatory mechanisms normally dormant during sleep. During apnea, the reflex arising from pulmonary stretch receptors that suppresses central sympathetic discharge during normal breathing ceases, disinhibiting central sympathetic outflow. The ensuing hypoxia and hypercapnia further augment sympathetic activity by stimulating peripheral and central chemoreceptors.39,40 Although arousal from sleep at the termination of obstructive apnea facilitates the resumption airflow by stimulating pharyngeal dilator muscles,37,42 the resulting excitatory input from cortical centers will cause a further burst of sympathetic outflow accompanied by a loss of vagal tone.11,43

23. OSA and cardiovascular consequences: myocardial ischemia (3) During the apnea the reflex from pulmonary stretch receptors, that normally suppresses SNA, is interrupted leading to an increase in SNA. Hypoxia and hypercapnia also increases SNA by stimulation of the peripheral chemoreceptors and by provoking arousals. Increased sympathetic nervous system activity, a cardinal feature of obstructive apnea, results from the interaction of several excitatory mechanisms normally dormant during sleep. During apnea, the reflex arising from pulmonary stretch receptors that suppresses central sympathetic discharge during normal breathing ceases, disinhibiting central sympathetic outflow. The ensuing hypoxia and hypercapnia further augment sympathetic activity by stimulating peripheral and central chemoreceptors.39,40 Although arousal from sleep at the termination of obstructive apnea facilitates the resumption airflow by stimulating pharyngeal dilator muscles,37,42 the resulting excitatory input from cortical centers will cause a further burst of sympathetic outflow accompanied by a loss of vagal tone.11,43 During the apnea the reflex from pulmonary stretch receptors, that normally suppresses SNA, is interrupted leading to an increase in SNA. Hypoxia and hypercapnia also increases SNA by stimulation of the peripheral chemoreceptors and by provoking arousals. Increased sympathetic nervous system activity, a cardinal feature of obstructive apnea, results from the interaction of several excitatory mechanisms normally dormant during sleep. During apnea, the reflex arising from pulmonary stretch receptors that suppresses central sympathetic discharge during normal breathing ceases, disinhibiting central sympathetic outflow. The ensuing hypoxia and hypercapnia further augment sympathetic activity by stimulating peripheral and central chemoreceptors.39,40 Although arousal from sleep at the termination of obstructive apnea facilitates the resumption airflow by stimulating pharyngeal dilator muscles,37,42 the resulting excitatory input from cortical centers will cause a further burst of sympathetic outflow accompanied by a loss of vagal tone.11,43

24. OSA: inhibition lung stretch receptors (4) During the apnea the reflex from pulmonary stretch receptors, that normally suppresses SNA, is interrupted leading to an increase in SNA. Hypoxia and hypercapnia also increases SNA by stimulation of the peripheral chemoreceptors and by provoking arousals. Increased sympathetic nervous system activity, a cardinal feature of obstructive apnea, results from the interaction of several excitatory mechanisms normally dormant during sleep. During apnea, the reflex arising from pulmonary stretch receptors that suppresses central sympathetic discharge during normal breathing ceases, disinhibiting central sympathetic outflow. The ensuing hypoxia and hypercapnia further augment sympathetic activity by stimulating peripheral and central chemoreceptors.39,40 Although arousal from sleep at the termination of obstructive apnea facilitates the resumption airflow by stimulating pharyngeal dilator muscles,37,42 the resulting excitatory input from cortical centers will cause a further burst of sympathetic outflow accompanied by a loss of vagal tone.11,43 During the apnea the reflex from pulmonary stretch receptors, that normally suppresses SNA, is interrupted leading to an increase in SNA. Hypoxia and hypercapnia also increases SNA by stimulation of the peripheral chemoreceptors and by provoking arousals. Increased sympathetic nervous system activity, a cardinal feature of obstructive apnea, results from the interaction of several excitatory mechanisms normally dormant during sleep. During apnea, the reflex arising from pulmonary stretch receptors that suppresses central sympathetic discharge during normal breathing ceases, disinhibiting central sympathetic outflow. The ensuing hypoxia and hypercapnia further augment sympathetic activity by stimulating peripheral and central chemoreceptors.39,40 Although arousal from sleep at the termination of obstructive apnea facilitates the resumption airflow by stimulating pharyngeal dilator muscles,37,42 the resulting excitatory input from cortical centers will cause a further burst of sympathetic outflow accompanied by a loss of vagal tone.11,43

25. Severe (O)SAS

26. Extremely severe OSAS

27. Hypoxia/reoxygenation Alterations in energy (ATP) metabolism and oxidative stress In response to hypoxia the aerobic production of ATP is impaired and degradation products as ADP, AMP, hypoxanthine and uric acid accumulate, indicating energy crisis. As a consequence, glycolysis is upregulated. Concomitantly, due to hypoxia, circulating xanthine oxidase and endothelial xanthine oxidase are activated by action of proteases (xanthine dehydrogenase is converted to xanthine oxidase). During the period of reoxygenation, the newly activated xanthine oxidases utilize the hypoxanthine and molecular oxygen to produce free radicals and oxidants as superoxide. ROS production is amplified, namely due to the potent oxidant OH-. Several independent studies that demonstrate increased accumulation of ATP degradation products in OSA patients are consistent with this mechanism: - Findley: increase in plasma adenosine levels in OSA (3 fold increase).In response to hypoxia the aerobic production of ATP is impaired and degradation products as ADP, AMP, hypoxanthine and uric acid accumulate, indicating energy crisis. As a consequence, glycolysis is upregulated. Concomitantly, due to hypoxia, circulating xanthine oxidase and endothelial xanthine oxidase are activated by action of proteases (xanthine dehydrogenase is converted to xanthine oxidase). During the period of reoxygenation, the newly activated xanthine oxidases utilize the hypoxanthine and molecular oxygen to produce free radicals and oxidants as superoxide. ROS production is amplified, namely due to the potent oxidant OH-. Several independent studies that demonstrate increased accumulation of ATP degradation products in OSA patients are consistent with this mechanism: - Findley: increase in plasma adenosine levels in OSA (3 fold increase).

28. As you know three models have been proposed to explain the pathophysiology of UAC: As you know different mechanisms are possible to explain the pathophysiology of UAC and each mechanism has its place, but no one is able to fully explain UAC. Therefore it is important to keep in mind a potential influence of all these mechanisms. The mechanisms leading to upper airway collapse can be put in 3 different models: 1) The oldest model explains UAC by the occurrence of an anatomic abnormality which causes structural narrowing, (but there are more than enough arguments against an important role for this model: Cephalometric variables and BMI only explain 33% of the variance of AHI and the UAC can occur at different sites.) 2) In the balance of forces theory UAC occurs due to an imbalance between activation of diaphragm and upper airway muscle activity Impaired reflex activation of upper airway dilator muscle activity 3) In the third model the upper airway is considered as a rigid tube with a flexible segment which behaves like a Starling resistor. When we want to evaluate the upper airway, we have to keep in mind a potential influence of all these measurements. As you know three models have been proposed to explain the pathophysiology of UAC: As you know different mechanisms are possible to explain the pathophysiology of UAC and each mechanism has its place, but no one is able to fully explain UAC. Therefore it is important to keep in mind a potential influence of all these mechanisms. The mechanisms leading to upper airway collapse can be put in 3 different models: 1) The oldest model explains UAC by the occurrence of an anatomic abnormality which causes structural narrowing, (but there are more than enough arguments against an important role for this model: Cephalometric variables and BMI only explain 33% of the variance of AHI and the UAC can occur at different sites.) 2) In the balance of forces theory UAC occurs due to an imbalance between activation of diaphragm and upper airway muscle activity Impaired reflex activation of upper airway dilator muscle activity 3) In the third model the upper airway is considered as a rigid tube with a flexible segment which behaves like a Starling resistor. When we want to evaluate the upper airway, we have to keep in mind a potential influence of all these measurements.


30. Spectrum of sleep-disordered breathing

31. Pathogenesis of SDB Mechanisms of unstable breathing ? drive occurs as part of the breathing instability that can be caused by several mechanisms: ? �wakefulness drive�, breathing becomes dependent of feedback control mechanisms Depressed central drive & defective effector organs (respiratory muscles/thoracic wall) � So inspiratory drive is linked by this mechanism to upper airway collapse Drive may decrease due to lower central drive or defective effector organs So inspiratory drive is linked by this mechanism to upper airway collapse Drive may decrease due to lower central drive or defective effector organs

32. Mechanisms of unstable breathing ? drive occurs as part of the breathing instability that can be caused by several mechanisms: � ? O2 (HVR) and CO2 drive (HCVR) Unmasking of CO2 threshold Stage effects and arousals Upper airway reflexes So inspiratory drive is linked by this mechanism to upper airway collapse Drive may decrease due to lower central drive or defective effector organs So inspiratory drive is linked by this mechanism to upper airway collapse Drive may decrease due to lower central drive or defective effector organs

33. Central sleep apnea occurs in 2 categories Normocapnia or hypocapnia: normal CO2 drive Idiopathic or Cheyne-Stokes breathing PB at high altitude Acromegaly Intracranial hypertension Congestive heart failure Chronic renal failure Use of opioids Hypercapnia: reduced CO2 drive Sleep hypoventilation syndrome Idiopathic or secondary alveolar hypoventilation Neuromuscular disorders Brainstem dysfunction Musculoskeletal disorders

35. CSR-CSA

37. Clinical picture Normocapnic central sleep apnea symptoms similar to OSA frequent nocturnal awakenings and insomnia Hypercapnic central sleep apnea polycythemia, cor pulmonale, peripheral edema, muscle weakness, morning headache, snoring, equal M/F ratio

38. Hypoxia and hypercapnia related with the apnea can lead to arousal, stimulation of CR and thus increased SNA. The increased SNA can give a higher heart rate and rise in blood pressureHypoxia and hypercapnia related with the apnea can lead to arousal, stimulation of CR and thus increased SNA. The increased SNA can give a higher heart rate and rise in blood pressure

39. Hypoxia and hypercapnia related with the apnea can lead to arousal, stimulation of CR and thus increased SNA. The increased SNA can give a higher heart rate and rise in blood pressureHypoxia and hypercapnia related with the apnea can lead to arousal, stimulation of CR and thus increased SNA. The increased SNA can give a higher heart rate and rise in blood pressure

40. Cheyne-Stokes breathing

41. CSR Cycle length and circulation time

42. Central Sleep Apnea

43. CSR and deterioration of heart function Changes in cycle length and apnea length


46. A � Excessive Daytime Sleepiness or B � At least two of the following items Nocturnal gasping or breathing arrests Frequent awakenings Non restorative sleep Chronic fatigue Loss of concentration and C - > 5 obstructive events / hour (A, H, RERA�s) As you know, SDB is characterized by the presence of: �.. The minimal criteria to define OSAS are based on the Chicago criteria. There are however patients who demonstrate an AHI<5 and have the same complaints. In these patients UARS can be considerd. As you know, SDB is characterized by the presence of: �.. The minimal criteria to define OSAS are based on the Chicago criteria. There are however patients who demonstrate an AHI<5 and have the same complaints. In these patients UARS can be considerd.

47. UARS A disease which is characterized by chronic sleepiness and daytime somnolence in the absence of frank apneas/hypopneas. EDS unexplained by another cause and associated with more than 50% of respiratory events that are non apneic and non hypopneic ? more subtle changes in breathing pattern

50. A � Pattern of progressively negative oesophageal pressure terminated by a sudden return to normal, associated with a micro-arousal and B � Duration of >10 seconds Requires the use of an oesophageal catheter Alternatives : nasal canula (IFL detection) and PTT In the new definitions of UARS RERA�s are implemented, which are characterized by �In the new definitions of UARS RERA�s are implemented, which are characterized by �

51. UARS: most typical features

53. Flow limitation Flattening index: mean of flow-limitation of the 5 previous breaths: 0.30: patent airway 0.20-0.30: normal breath 0.10-0.15: flow limitation 0.05-0.10: severe flow limitation 0.00: closed airway


56. HYPOVENTILATION

57. HYPOVENTILATION

58. HYPOVENTILATION MANY DEFINITIONS Nocturnal oxygen desaturation: SaO2 ? 4% 10% Nocturnal hypoxemia: (ICSD-2) - SaO2 <90% >30% TIB - SaO2 <90% > 5 min ; nadir <85% AASM Task Force: One or more of the following: cor pulmonale, PHT, EDS, polycythemia, PaCO2>45 mmHg Overnight monitoring: one or both of the following An increase in PaCO2 during sleep >10 mmHg from awake supine values Oxygen desaturation during sleep not explained by apnea or hypopnea events.

60. Hypoventilation(Chronic) Respiratory Failure COPD Restrictive disorders: Musculoskeletal Disorders Neuromuscular disorders Obesity Central Alveolar Hypoventilation Syndrome

62. Changes in FRC during sleep in normals (? V/Q mismatch)

63. Ventilatory changes during sleep in COPDChadwick (MD thesis)1989

64. Ventilatory patterns in chronic lung disease COPD and asthma: significant ?TV during sleep with little change in breath frequency Overall, MV falls during sleep. Interstitial lung disease: Significant ? freq ?TV MV is not significantly lower during sleep. The change in breathing pattern during sleep in ILD: suggests that the rapid shallow breathing pattern that is characteristic of these patients may in part be a conscious behaviour.

65. HYPOVENTILATION IN SLEEP IN COPD MECHANISMS NON-REM ? ? ? Wakefulness drive Position on O2-Hb-dissociation curve Chemoreceptor responses ? Respiratory muscle function ? Hyperinflation REM Gamma paralysis intercostals and upper airways Diaphragm in bad position on length tension curve Chemoreceptor responses further ? Arousability ?


69. Nocturnal dyspnea attacks: quit ? (Apnea) COPD, asthma, pulmonary oedema Sleep related laryngospasm Sleep choking Nocturnal stridor (inspiratory) Mostly in MSA, NMD

70. In COPD: ? vagal activity ? levels of bronchoconstrictive cholinergic tone at night NL: FEV1: -7% at 4 AM COPD: FEV1: -27% at 4 AM Postma. Clin Sci 1985;251.

71. COPD and sleep apnea: overlap syndrome

72. COPD and sleep apnea: overlap syndrome OSAS occurs no more frequently in COPD than a similarly aged normal population. Inadequate ventilatory drive in some patients with COPD may favour the development of OSA Awake hypoxaemia, hypercapnia and pulmonary hypertension are more common than in either condition alone. Patients develop more marked oxygen desaturation during apnoea because of the lower starting SaO2.

73. NOCTURNAL ASTHMA Clinical picture: Asthma symptoms at night or early morning: wheezing/awakening with decreases in PEFR Is not a different condition, but is severe asthma Prevalence: > 50% asthmatics sometimes > 80% asthmatics if unstable ? normal circadian variation in airway calibre (max 4 PM, min 4 AM): In asthmatics: 15-50% (morning dip) Relevant dip > 20% In normals: variability PEF 8% Mechanisms: Airway resistance progressively ? in asthmatics during sleep Raw norm < 2x, NA 4x Bellia V et al Chest 1988 Diurnal variation in bronchomotor tone Hetzel, Thorax 1980 in circulating hormones (cortisol, cholinergic tone, histamine, epinephrine�) Related to PC20

74. Mechanisms of Nocturnal Asthma

76. Nocturnal asthma and OSAS: �overlap syndrome� ? Yigla et al. J Asthma 2003 22 consecutive patients with severe unstable asthma 14 on continuous oral CS (for a mean of 9?3 y) 8 on intermittent use of oral CS Polysomnography regardless of sleep symptoms All but one patient had OSA (mean AHI 18?3) Prevalence OSA 95.5% AHI significantly higher in the continuous CS group (21?3 vs. 11?2, p < 0.05]. The study group had above normal NC and BMI

77. NOCTURNAL DYSPNEA Pulmonary oedema Usually associated with a history of heart disease, chest pain, cardiomegaly and typical radiographic features

78. NOCTURNAL DYSPNEA Sleep related laryngospasm Related to acid reflux in the distal part of the oesophagus Reflex mechanism leading to spasm of the vocal cords Occurs in the middle of the night Severe dyspnea, suffocation, palpitations, anxiety; suffer agony Duration: 30 to 60 seconds ?? quicker relief after apnea R/ PPI Sleep choking Related to stress Always in the beginning of sleep (within a few minutes after falling asleep) R/ relaxation, information, reassurance DD apnea

79. Varia: Expiratory vocalization Sharp, intense noise during expiration Episodic bradypneas CA Prolonged expiration (narrowed glottis) Mostly during REM (93% of all events) No underlying NMD

80. Varia: Expiratory vocalizationTreatment disappointing BE= bradypneic episodesBE= bradypneic episodes

81. Conclusions Sleep disordered breathing has a broad spectrum from simple snoring over UARS and sleep apnea to hypoventilation syndrome. Different clinical features in each entity Nocturnal symptoms in asthma and COPD are characteristic for severe disease. Coexistence of astma/COPD and sleep apnea. Be aware of less common causes of nocturnal dyspnea.

Respiratory abnormalities during sleep

Respiratory abnormalities during sleep

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