Respiratory physiology in sleep
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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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Respiratory physiology in sleep

Respiratory Physiology In Sleep

Ritu Grewal, MD


States of mammalian being

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


Electrographic state determination

Wake

NREM

REM

EEG - Desynchronized

EMG - Variable

EEG - Synchronized

EMG - Attenuated but present

EEG - Desynchronized

EMG - Absent (active paralysis)

Electrographic State Determination


Normal sleep histogram

Normal Sleep Histogram


Respiratory physiology in sleep

Stage REM

  • Rapid eye movements

  • Mixed frequency EEG

  • Low tonic submental EMG


Overview of sleep and respiratory physiology

Overview of Sleep and Respiratory Physiology

I. CNS Ventilatory Control

II. Respiratory Control of the Upper Airway

III. Obstructive Sleep Apnea


Respiratory physiology in sleep

Ventilatory pump and its central neural control


Respiratory physiology in sleep

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.


Influences on respiration in wake state

Influences on Respiration in Wake State

  • Metabolic control /Automatic control

    • Maintain blood gases

  • Voluntary control/behavioral

    • Phonation, swallowing

      (wakefulness stimulus to breathing)


Respiration during sleep

Respiration during sleep

  • Metabolic control/automatic control

    • Controlled by the medulla

      • on the respiratory muscles

    • Maintain pCO2 and pO2


Changes in ventilation in sleep

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


Changes in blood bases

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%


Chemosensitivity and sleep

Chemosensitivity and Sleep


Chemosensitivity and sleep1

Chemosensitivity and Sleep


Metabolism

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


Rem sleep

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


Arousal responses in sleep

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)


Overview of sleep and respiratory physiology1

Overview of Sleep and Respiratory Physiology

I. CNS Ventilatory Control

II. Respiratory Control of the Upper Airway

III. Obstructive Sleep Apnea


Anatomy of the upper airway

Anatomy of the Upper Airway

The Upper Airway is a Continuation

of the Respiratory System

20


The upper airway is a multipurpose passage

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


Collapsible pharynx challenges the respiratory system

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


Components of the upper airway

Components of the Upper Airway

  • Nose

  • Nasopharynx

  • Oropharynx

  • Laryngopharynx

  • Larynx

23


Anatomy of the upper airway1

Anatomy of the Upper Airway

  • Alae nasi (widens nares)

  • Levator palatini (elevates palate)

  • Tensor palatini (stiffens palate)

24


Anatomy of the upper airway2

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Overview of sleep and respiratory physiology2

Overview of Sleep and Respiratory Physiology

I. CNS Ventilatory Control

II. Respiratory Control of the Upper Airway

III. Obstructive Sleep Apnea


Obstructive sleep apnea osa syndrome

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).


Respiratory physiology in sleep

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.


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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


Respiratory physiology in sleep

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.


Respiratory physiology in sleep

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).


Summary

Summary

Increased upper airway resistance-OSAS

Circadian changes in airway muscle tone

Reduced ventilation

COPD

Neuromuscular diseases

Interstitial lung disease


Respiratory physiology in sleep

COPD

Hyperinflated diaphragm(reduced efficiency)

ABG’s deteriorate during sleep

Coexisting OSAS-severe hypoxemia

Pulmonary hypertension


Respiratory physiology in sleep

Decreased ventilatory responses to hypoxia, hypercapnia, and inspiratory resistance during sleep, particularly in REM sleep, permit REM hypoxemia in patients with chronic obstructive pulmonary disease, chest wall disease, and neuromuscular abnormalities affecting the respiratory muscles. They may also contribute to the development of the sleep apnea/hypopnea syndrome.


Cns ventilatory control summary 1

CNS Ventilatory Control – Summary 1

  • The respiratory rhythm and pattern are generated centrally and modulated by a host of respiratory reflexes.

  • The basic respiratory rhythm is generated by a network of pontomedullary neurons, of which some have pacemaker properties.

  • The central controller is set to ensure ventilation that adequately meets demand for O2 supply and CO2 removal.


Respiratory physiology in sleep

CNS Ventilatory Control – Summary 2

  • Pharyngeal muscles are activated during breathing

  • Upper airway size varies during breathing

  • Mechanical properties of the upper airway influences collapsibility

  • Reflexes modulate pharyngeal muscle activity, but reflexes are reduced in sleep

  • These mechanisms contribute to normal maintenance of airway patency and are relevant to obstructive sleep apnea


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