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Respiratory Physiology In Sleep

Respiratory Physiology In Sleep. Ritu Grewal, MD. States of Mammalian Being . Wake Non-REM sleep brain is regulating bodily functions in a movable body REM sleep : - highly activated brain in a paralyzed body. Wake NREM REM. EEG - Desynchronized EMG - Variable EEG - Synchronized

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Respiratory Physiology In Sleep

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  1. Respiratory Physiology In Sleep Ritu Grewal, MD

  2. States of Mammalian Being • Wake • Non-REM sleep • brain is regulating bodily functions in a movable body • REM sleep: - highly activated brain in a paralyzed body

  3. Wake NREM REM EEG - Desynchronized EMG - Variable EEG - Synchronized EMG - Attenuated but present EEG - Desynchronized EMG - Absent (active paralysis) Electrographic State Determination

  4. Normal Sleep Histogram

  5. Stage REM • Rapid eye movements • Mixed frequency EEG • Low tonic submental EMG

  6. Overview of Sleep and Respiratory Physiology I. CNS Ventilatory Control II. Respiratory Control of the Upper Airway III. Obstructive Sleep Apnea

  7. Ventilatory pump and its central neural control

  8. Main pontomedullary respiratory neurons • Dorsal view of the brainstem and upper spinal cord showing the medullary origin of the descending inspiratory and expiratory pathways that control major respiratory pump muscles, such as the diaphragm and intercostals. • Central respiratory neurons form a network that ensures reciprocal activation and inhibition among the cells to be active during different phases of the respiratory cycle. •  Respiratory-modulated cells in the pons • integrate many peripheral and central • respiratory and non-respiratory inputs • and modulate the cells of the medullary rhythm and pattern generator.

  9. Influences on Respiration in Wake State • Metabolic control /Automatic control • Maintain blood gases • Voluntary control/behavioral • Phonation, swallowing (wakefulness stimulus to breathing)

  10. Respiration during sleep • Metabolic control/automatic control • Controlled by the medulla • on the respiratory muscles • Maintain pCO2 and pO2

  11. Changes in Ventilation in sleep Decrease in Minute Ventilation (Ve)(0.5-1.5 l/min) Decrease in Tidal Volume) Respiratory Rate unchanged ↑ UA resistance (reduced activity of pharyngeal dilator muscle activity) Reduction of VCO2 and VO2 (reduced metabolism) Absence of the tonic influences of wakefulness Reduced chemosensitivity

  12. Changes in Blood Bases Decrease in CO2 production (less than decrease in Ve) Increase in pCO2 3-5 mm Hg Decrease in pO2 by 5-8 mm Hg O2 saturation decreases by less than 2%

  13. Chemosensitivity and Sleep

  14. Chemosensitivity and Sleep

  15. Metabolism Metabolism slows at sleep onset Increases during the early hours of the morning when REM sleep is at its maximum Ventilation is worse in REM sleep

  16. REM sleep Worse in REM sleep Hypotonia of Intercostal muscles and accessory muscles of respiration Increased upper airway resistance Diaphragm is preserved Breathing rate is erratic

  17. Arousal responses in sleep Reduced in REM compared to NonREM Hypercapnia is a stronger stimulus to arousal than hypoxemia Increase in pCO2 of 6-15 mmHg causes arousal SaO2 has to decrease to below 75% Cough reflex in response to laryngeal stimulation reduced (aspiration)

  18. Overview of Sleep and Respiratory Physiology I. CNS Ventilatory Control II. Respiratory Control of the Upper Airway III. Obstructive Sleep Apnea

  19. Anatomy of the Upper Airway The Upper Airway is a Continuation of the Respiratory System 20

  20. It transmits air, liquids and solids. It is a common pathway for respiratory, digestive and phonation functions. The Upper Airway is a Multipurpose Passage 21

  21. Collapsible Pharynx Challengesthe Respiratory System • Airflow requires a patent upper airway. • Nose vs. mouth breathing must be regulated. • State of consciousness is a major determinant of pharyngeal patency. 22

  22. Components of the Upper Airway • Nose • Nasopharynx • Oropharynx • Laryngopharynx • Larynx 23

  23. Anatomy of the Upper Airway • Alae nasi (widens nares) • Levator palatini (elevates palate) • Tensor palatini (stiffens palate) 24

  24. Anatomy of the Upper Airway • Genioglossus (protrudes tongue) • Geniohyoid (displaces hyoid arch anterior) • Sternohyoid (displaces hyoid arch anterior) • Pharyngeal constrictors(form lateral pharyngeal walls) 25

  25. Respiratory Control of the Upper Airway Pharyngeal Muscles are Activated during Breathing Mechanical Properties and Collapsibility of Upper Airway Reflexes Maintaining an Open Airway and Effects of Sleep

  26. Respiratory pump muscles generate airflow Upper airway muscles modulate airflow • Primary Respiratory Muscles (e.g., Diaphragm, Intercostals) • Contraction generates airflow into lungs • Secondary Respiratory Muscles (e.g., Genioglossus of tongue) • Contraction does not generate airflow but modulates resistance Upper Airway (collapsible tube) Respiratory Pump

  27. Sleep and respiratory muscle activity Non-REM REM Awake Genioglossus +++ ++ + Intercostals +++ + ++ ++ ++ Diaphragm +++ Consequences: Lung ventilation in sleep caused by both  Upper airway resistance (major contributor) and  pump muscle activity Clinical Relevance: Airway narrowing in sleep (potential for hypopneas and obstructions) Sleep reduces upper airway muscle activity more than diaphragm activity

  28. Tendency for upper airway collapse in sleep Sleep Awake Genioglossus Genioglossus + +++ Diaphragm Diaphragm ++ +++ Tongue movement Tendency for Airway Collapse: Reduced muscle activation in sleep Weight of tongue Weight of neck - worse with obesity Worse when supine Clinical Relevance: Snoring Airflow limitation (hypopneas) Obstructive Sleep Apnea (OSA) The pharynx is a collapsible tube vulnerable to closure in sleep – especially when supine

  29. Determinants of pharyngeal muscle activity Genioglossus muscle: Respiratory-related activity superimposed upon background tonic activity Tensor veli palatini (palatal muscle): Mainly tonic activity Enhances stiffness in the airspace behind the palate Tonic and respiratory inputs summate to determine pharyngeal muscle activity

  30. Overview of Sleep and Respiratory Physiology Pharyngeal Muscles are Activated during Breathing Mechanical Properties and Collapsibility of Upper Airway Reflexes Maintaining an Open Airway and Effects of Sleep

  31. Airway anatomy and vulnerability to closure Retropalatal Airspace Glossopharyngeal Airspace The airway is narrowest in the region posterior to the soft palate Redrawn from Horner et al., Eur Resp J, 1989

  32. Upper airway size varies with the breathing cycle Normal Normal OSA OSA Expiration Inspiration Retropalatal Airspace Glossopharyngeal Airspace The upper airway is: (1) Narrowest in the retropalatal airspace (2) Narrower in obstructive sleep apnea (OSA) patients vs. controls (3) Varies during the breathing cycle (narrowest at end-expiration) Redrawn from Schwab, Am Rev Respir Dis, 1993

  33. Upper airway size varies with the breathing cycle Normal Normal OSA OSA The upper airway is narrowest at end-expiration and so vulnerable to collapse on inspiration Glossopharyngeal Airspace Retropalatal Airspace Upper airway at end-expiration is most vulnerable to collapse on inspiration Tonic muscle activity sets baseline airway size and stiffness ( in sleep) Any factor that  airway size makes the airway more vulnerable to collapse Redrawn from Schwab et al., Am Rev Respir Dis, 1993

  34. Fat deposits around the upper airspace OSA patients have larger retropalatal fat deposits and narrower airways Fat deposit Retropalatal airspace Magnetic resonance image showing large fat deposits lateral to the airspace These fat deposits are larger in OSA patients compared to weight matched controls Weight loss decreases size of fat deposits and increases airway size From Horner, Personal data archive

  35. Determinants of upper airway collapsibility PN RN 500 RN = 1/slope PCRIT 400 ● VMAX 300 VMAX (ml/sec) 200 PCRIT 100 ● 0 Lungs 0 -8 4 -4 8 PN (cmH2O) The upper airway has been modeled as a collapsible tube with maximum flow (VMAX) determined by upstream nasal pressure (PN) and resistance (RN). Airflow ceases in the collapsible segment of the upper airway at a value of critical pressure (PCRIT). VMAX is determined by: VMAX = (PN - PCRIT) / RN ● ● ● Mechanics of the upper airway and influences on collapsibility Redrawn from Smith and Schwartz, Sleep Apnea: Pathogenesis, Diagnosis and Treatment, 2002

  36. Influences on upper airway collapsibility ● ● 500 VMAX (ml/sec)  VMAX Normal 500 Active Upper Airway  PCRIT 400 Snorer Hypopnea 300 VMAX (ml/sec) OSA Passive Upper Airway 200 ● 100 0 0 -15 -5 10 -10 0 5 15 0 -8 4 -4 8 PN (cmH2O) PN (cmH2O) PCRIT is more positive (more collapsible airway) from groups of normal subjects, to snorers, and patients with hypopneas and obstructive sleep apnea (OSA). Increases in pharyngeal muscle activity (passive to active upper airway) increase VMAX and decrease PCRIT, i.e., make the airway less collapsible. ● Mechanics of the upper airway influences airway collapsibility Redrawn from Smith and Schwartz, Sleep Apnea: Pathogenesis, Diagnosis and Treatment, 2002

  37. Overview of Sleep and Respiratory Physiology Pharyngeal Muscles are Activated during Breathing Mechanical Properties and Collapsibility of Upper Airway Reflexes Maintaining an Open Airway and Effects of Sleep

  38. Reflex responses to sub-atmospheric pressure Sub-atmospheric airway pressures cause reflex pharyngeal muscle activation 0 Suction Pressure (cmH2O) -25 Genioglossus Electromyogram 100 msec Sub-atmospheric airway pressures cause short latency (reflex) genioglossus muscle activation in humans Reflex thought to protect the upper airway from suction collapse during inspiration Reflex is reduced in non-REM sleep and inhibited in REM sleep From Horner, Personal data archive

  39. Afferents mediating reflex response 0 Suction Pressure (cmH2O) -25 Genioglossus Electromyogram Normal response 100 msec Major contribution of nasal and laryngeal afferents to negative pressure reflex in humans Anesthesia of nasal afferents Anesthesia of laryngeal afferents From Horner, Personal data archive

  40. Upper airway reflex and clinical relevance Sleeping normal subject Structural (e.g., obesity, position) Narrower than normal airway  muscle activity (e.g., alcohol) Exaggerated negative airway pressure Reflex pharyngeal dilator muscle activation (e.g., genioglossus) Big responder Small responder Any decrement in reflex e.g., age, alcohol No change in reflex Snoring, hypopneas and occasional OSA Remain normal Decrement in upper airway mucosal sensation to pressure Worsening snoring and OSA Decrement in upper airway reflex Upper airway trauma may impair responses to negative pressure and predispose to OSA Redrawn from Horner, Sleep, 1996

  41. Responses to hypercapnia in sleep Wakefulness Respiratory-Related Genioglossus Activity (mV) Non-REM sleep REM sleep Inspired CO2 (%) Chemoreceptor stimulation cause reflex pharyngeal muscle activation Chemoreceptor stimulation increases genioglossus muscle activity Reflex is reduced in sleep, especially REM sleep Modified from Horner, J Appl Physiol, 2002

  42. Overview of Sleep and Respiratory Physiology I. CNS Ventilatory Control II. Respiratory Control of the Upper Airway III. Obstructive Sleep Apnea

  43. State-dependent respiratory disorders - OSA Obstructive Sleep Apnea (OSA) Syndrome • Very common; affects 2-5% of middle-aged persons, both men and women. • The initial cause is a narrow and collapsible upper airway (due to fat deposits, predisposing cranial bony structure and/or hypertrophy of soft tissues surrounding the upper airway).

  44. State-dependent respiratory disorders - OSA • OSA patients have adequate ventilation during wakefulness because they develop a compensatory increase in the activity of their upper airway dilating muscles (e.g., contraction of the genioglossus, the main muscle of the tongue, effectively protects against upper airway collapse). However, the compensation is only partially preserved during SWS and absent during REMS. This causes repeated nocturnal upper airway obstructions which in most cases require awakening to resolve.

  45. Polysomnographic tracings in OSA OSA is characterized by cessation of oro-nasal airflow in the presence of attempted (but ineffective) respiratory efforts and is caused by upper airway closure in sleep Hypopneas are caused by reductions in inspiratory airflow due to elevated upper airway resistance Redrawn from Thompson et al., Adv Physiol Educ, 2001

  46. Site of obstruction in OSA REM: Obstruction extends caudally All patients obstruct at level of soft palate ~50% of patients: obstruction behind tongue in non-REM The site of obstruction varies within and between patients with obstructive sleep apnea

  47. State-dependent respiratory disorders - OSA • In severe OSA, 40-60 episodes of airway obstruction and subsequent awaking occur per hour; due to overwhelming sleepiness, the patient is often unaware of the nature of the problem. • In light OSA, loud snoring is associated with periods of hypoventilation due to excessive airway narrowing.

  48. State-dependent respiratory disorders - OSA • Sleep loss, sleep fragmentation and recurring decrements of blood oxygen levels (intermittent hypoxia) have multiple adverse consequences for cognitive and affective functions, regulation of arterial blood pressure (hypertension), and metabolic regulation (insulin resistance, hyperlipidemia).

  49. Summary Increased upper airway resistance-OSAS Circadian changes in airway muscle tone Reduced ventilation COPD Neuromuscular diseases Interstitial lung disease

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