using the pathophysiology of obstructive sleep apnea osa to teach cardiopulmonary integration l.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Using the Pathophysiology of Obstructive Sleep Apnea (OSA) to Teach Cardiopulmonary Integration PowerPoint Presentation
Download Presentation
Using the Pathophysiology of Obstructive Sleep Apnea (OSA) to Teach Cardiopulmonary Integration

Loading in 2 Seconds...

play fullscreen
1 / 37

Using the Pathophysiology of Obstructive Sleep Apnea (OSA) to Teach Cardiopulmonary Integration - PowerPoint PPT Presentation


  • 868 Views
  • Uploaded on

Using the Pathophysiology of Obstructive Sleep Apnea (OSA) to Teach Cardiopulmonary Integration. Michael G. Levitzky, Ph.D. Department of Physiology Louisiana State University Health Sciences Center 1901 Perdido Street New Orleans, Louisiana 70112-1393 Phone:  504 568-6184

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Using the Pathophysiology of Obstructive Sleep Apnea (OSA) to Teach Cardiopulmonary Integration' - Melvin


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
using the pathophysiology of obstructive sleep apnea osa to teach cardiopulmonary integration
Using the Pathophysiology of Obstructive Sleep Apnea (OSA) to Teach Cardiopulmonary Integration

Michael G. Levitzky, Ph.D.

Department of Physiology

Louisiana State University Health Sciences Center

1901 Perdido Street

New Orleans, Louisiana 70112-1393

Phone:  504 568-6184

Fax:     504 568-6158

E-mail: mlevit@lsuhsc.edu

outline
Outline

I. Introduction: Clinical Aspects of OSA

A. Case scenario

B. Definition and epidemiology

C. Symptoms and signs

D. Description of sleep apnea event

E. Diagnosis: polysomnography

II. Pathophysiology of OSA

A. Mechanical/Anatomic

B. Pulmonary

1. Mechanics of breathing in OSA

2. Effects of obstruction/apnea on gas exchange

C. Cardiovascular effects of OSA

1. Effects on the pulmonary circulation

2. Effects on the systemic circulation

D. Disturbances in sleep architecture and hypersomnolence

III. Treatment of OSA: CPAP

IV. References

case scenario
Case Scenario

A 61 year old professor comes to the family physician because he feels tired all the time. He often falls asleep when he attends lectures, seminars, or boring meetings. Although he says he sleeps through the night (except to get up to urinate), his wife says he snores loudly and often seems to stop breathing and gasp for breath. He is restless and thrashes around in bed. He almost always wakes up with a headache and for the past year he has been having trouble remembering things. He is 5 feet 7 inches tall and weighs 250 pounds. His heart rate is 80/min, blood pressure is 135/95 mmHg and his respiratory rate is 15/min.His electrocardiogram, chest radiograph, and echocardiogram strongly suggest pulmonary hypertension.

Diagnosis: Obstructive Sleep Apnea

obstructive sleep apnea osa definition and epidemiology
Obstructive Sleep Apnea (OSA): Definition and Epidemiology
  • Definition: ≥ 15 apneas (> 10 sec) and/or hypopneas per hour of sleep because of sleep-related collapse of the upper airway (Note that as much as 40-70% of resistance to airflow is normally in upper airway)
  • Associated with snoring, but not everyone who snores has OSA
  • May occur in 9% of middle-aged men and 4% of middle-aged women in US; estimates in the literature have a very wide range—one source stated that 85% of people with OSA are undiagnosed
  • Prevalence increases with age, body weight, pregnancy
  • High prevalence in 3- to 5-year old children: may be as high as 5%
symptoms of obstructive sleep apnea
Symptoms of Obstructive Sleep Apnea

(In descending order of approximateincidence)

  • Loud snoring
  • Hypersomnolence (Excessive Daytime Sleepiness)
  • Depressed mentation
  • Altered personality
  • Impotence
  • Headaches upon waking
  • Nocturia
signs of obstructive sleep apnea
Signs of Obstructive Sleep Apnea
  • Systemic hypertension
  • Pulmonary hypertension (right axis deviation on ECG)
  • Polycythemia
  • Cor pulmonale
  • Bradycardia during apneic event
  • Tachycardia after airflow restored
  • Typically no respiratory abnormality while awake
  • Arterial blood gasses while awake may show metabolic alkalosis
description of sleep apnea event
Description of Sleep Apnea Event
  • Upper airway obstruction

Intermittent obstruction: snoring

Complete obstruction

  • Decreased alveolar ventilation
  • Decreased alveolar PO2 ; increased alveolar PCO2
  • Decreased arterial PO2 ; increased arterial PCO2
  • Stimulation of arterial chemoreceptors; central chemoreceptors
  • Arousal
  • Secondary hyperventilation?
slide8

Effects of Breathhold on Arterial PO2 and PCO2

O2

100

80

Arterial Partial Pressure

(mmHg)

60

40

CO2

20

10

20

30

Time (sec)

All figures created by Betsy Giaimo

slide9

Effects of Arterial PO2 and PCO2 on Carotid Body Activity

Pa

, torr

O

2

20

40

60

80

100

120

140

Carotid Body Activity

10

20

30

40

50

60

, torr

Pa

CO

2

diagnosis polysomnography
Diagnosis: Polysomnography

Variables that may be determined include:

  • EEG and electrooculogram (for sleep state); EMG
  • Airflow at nose or mouth (thermistor, pneumotachograph)
  • End-tidal CO2
  • Chest and abdominal motion (impedance plethysmography)
  • ECG
  • Blood pressure
  • Pulse oximetry
  • Esophageal pressure (intrapleural pressure)
  • Autonomic nervous system activity (finger tonometer)
slide11

Normal Polysomnograph

EEG

EMG

ECG

BP

Abd

Chest

Vt (air flow)

100

75

Pulse Oxygen Saturation

Time (minutes)

20 sec

slide12

Obstructive Sleep Apnea

EEG

ECG

BP

Abd

Chest

Vt (air flow)

100

75

Pulse Oxygen Saturation

Time (minutes)

20 sec

pathophysiology of obstructive sleep apnea

Pathophysiology of Obstructive Sleep Apnea

Mechanical

Short, thick neck

Neck flexion, supine position

Nasal obstruction, congestion, polyps

Surface tension of upper airway lining fluid

pathophysiology of obstructive sleep apnea continued
Pathophysiology of Obstructive Sleep Apnea (continued)

Anatomic

  • Enlarged tonsils and adenoids (esp. ages 3-5), enlarged uvula
  • Macroglossia
  • Retrognathia, craniofacial abnormalities
  • Compliant (floppy) pharynx, especially soft palate
  • Fat deposition in lateral walls of pharynx, pharyngeal dilator muscles (obesity)
  • Submucosal edema in lateral walls of pharynx
pathophysiology of obstructive sleep apnea continued15
Pathophysiology of Obstructive Sleep Apnea (continued)

Physiologic

  • Decreased function of upper airway dilator muscles (more than 20 skeletal muscles normally involved)
  • Decreased pharyngeal dilator reflex response
  • Decreased chemoreceptor drive/central drive (mixed with central sleep apnea)
  • Impaired arousal response
  • Alcohol, depressant drugs
slide16

Eupneic Inspiration

(Revised from Fig. 2-1 in Levitzky’s Pulmonary Physiology)

Atmospheric Pressure : 0 cm H2O

Atmospheric Pressure : 0 cm H2O

Flow in

No flow

Inspiratory force

Outward recoil

of chest wall

Alveolar

pressure:

0 cm H2O

Alveolar

pressure:

0 cm H2O

Alveolar

pressure:

-1 cm H2O

Inward recoil of alveoli

Intrapleural pressure:

-5 cmH2O

Intrapleural pressure:

-8 cmH2O

Transmural pressure=

0 cmH2O - (-5cmH2O)= +5 cmH2O

Transmural pressure=

-1 cmH2O - (-8cmH2O)= +7 cmH2O

DURING INSPIRATION

END EXPIRATION

slide17

Forced Inspiration

(Revised from Fig. 4-10C in Levitzky’s Pulmonary Physiology)

Atmospheric Pressure : 0 cm H2O

Atmospheric Pressure : 0 cm H2O

Flow in

No flow

Inspiratory force

Outward recoil

of chest wall

Alveolar

pressure:

0 cm H2O

Alveolar

pressure:

0 cm H2O

Alveolar

pressure:

-23 cm H2O

Inward recoil of alveoli

Intrapleural pressure:

-5 cmH2O

Intrapleural pressure:

-30 cmH2O

Transmural pressure=

0 cmH2O - (-5cmH2O)= +5 cmH2O

Transmural pressure=

-23 cmH2O - (-30 cmH2O)= +7 cmH2O

END EXPIRATION

DURING INSPIRATION

mechanics of breathing in obstructive sleep apnea
Mechanics of Breathing in Obstructive Sleep Apnea

Does negative pressure in the upper airway cause obstruction or does obstruction cause negative pressure in the upper airway?

  • Forced inhalation through the nose causes increased nasal resistance to airflow
  • Mueller maneuver causes intrapleural pressure to fall to approximately -30 cm H2O; as low as -80 cm H2O during episodes of obstructive sleep apnea?
slide19

Sites of obstruction during sleep apnea

Obstructive Sleep Apnea

Upper airway anatomy

Hard Palate

Tongue

Tongue

Hyoid bone

Larynx

Soft Palate

Nasopharynx

Oropharynx

Epiglottis

Laryngopharynx

slide20

Obstructive Sleep Apnea

Upper airway anatomy

Sites of obstruction during sleep apnea

Hard Palate

Tongue

Tongue

Hyoid bone

Larynx

Soft Palate

Nasopharynx

Oropharynx

Laryngopharynx

Epiglottis

why obstruction occurs during sleep
Why Obstruction Occurs During Sleep
  • Supine position
  • Control of breathing during normal non-rapid eye movement sleep

Lack of “wakefulness” drive

Minute volume decreases about 16%

PaCO2 increases 4-6 mmHg

SaO2 decreases as much as 2%

Decreased tone of pharyngeal muscles

Depressed reflexes, including pharyngeal dilator

Depressed response to hypoxia in men

  • REM sleep decreases tone of intercostal and accessory muscles, less effect on diaphragm; depression of minute volume, increase in CO2 not as great, depression of response to hypoxia greater
possible explanation for metabolic alkalosis when patient is awake
Possible Explanation for Metabolic Alkalosis When Patient is Awake
  • Chronic repeated obstructions cause carbon dioxide retention and therefore respiratory acidosis
  • Compensatory renal retention of bicarbonate and excretion of hydrogen ions leads to metabolic alkalosis when PaCO2 is normal during awake state
effects of obstruction on pulmonary circulation and right ventricle
Effects of Obstruction on Pulmonary Circulation and Right Ventricle
  • Hypoxic and hypercapnic pulmonary vasoconstriction cause pulmonary hypertension
  • Chronic nighttime hypoxia may cause erythropoiesis and polycythemia
  • Increased hematocrit increases blood viscosity
  • Hypoxic pulmonary vasoconstriction (HPV), increased blood viscosity, pulmonary hypertension increase right ventricular afterload
  • Increased right ventricular afterload may lead to right ventricular hypertrophy and eventually cor pulmonale
slide24

Hypoventilation with HPV

O2 = 150 torr

CO2 = 0 torr

Decreased O2

Increased CO2

O2 = 40 torr

CO2 = 45 torr

Decreased O2

Increased CO2

slide25

Effects of Hematocrit on Human Blood Viscosity

8

6

Relative Viscosity

4

2

0.2

0.4

0.6

0.8

Hematocrit

possible explanation for systemic hypertension
Possible Explanation for Systemic Hypertension
  • Repeated increases in sympathetic tone and systemic blood pressure during arousals may cause vascular remodeling and changes in endothelial function
explanation for morning headaches
Explanation for Morning Headaches
  • Hypoxia and hypercapnia during obstruction cause dilatation of cerebral blood vessels
slide28

Effects of Arterial PO2 and PCO2 on Cerebral Blood Flow

Arterial PCO2 (mm Hg)

20

40

60

80

100

100

75

Cerebral Blood Flow (ml/100mg/min)

50

25

20

40

60

80

100

Arterial PO2 (mm Hg)

possible explanations for bradycardia during obstruction tachycardia after airflow restored
Possible Explanations for Bradycardia During Obstruction, Tachycardia after Airflow Restored
  • Stimulation of arterial chemoreceptors usually increases heart rate because it increases tidal volume (lung inflation reflex)
  • Stimulation of arterial chemoreceptors without stretching the lungs causes bradycardia
  • After arousal leads to restoration of airflow, large tidal volumes stretch lungs and cause tachycardia
  • May hyperventilate immediately after arousal, then hypoventilate until CO2 is restored
possible explanation for nocturia
Possible Explanation for Nocturia
  • HPV, increased blood viscosity, pulmonary hypertension increase right ventricular afterload
  • Increased afterload leads to increased right ventricular end diastolic pressure and volume
  • Increased right ventricular end diastolic pressure and volume lead to increased right atrial volume
  • Increased right atrial volume increases secretion of atrial natriuretic peptide from atrial myocytes, which increases sodium excretion, and stretches receptors that suppress ADH secretion from the posterior pituitary gland
explanation for hypersomnolence or excessive daytime sleepiness
Explanation for Hypersomnolence or Excessive Daytime Sleepiness
  • Repeated arousals (may be hundreds per night) interfere with sleep architecture, especially rapid eye movement sleep
  • Abnormal sleep architecture leads to daytime somnolence, decreased attentiveness, blunted mentation, depression, personality changes
  • Hypersomnolence increases risk of motor vehicle accidents
ethanol exacerbates obstructive sleep apnea
Ethanol Exacerbates Obstructive Sleep Apnea
  • Ethanol depresses the responses to hypoxia and hypercapnia
  • Ethanol depresses the activity and tone of the genioglossal and pharyngeal dilator muscles
  • Ethanol depresses protective respiratory reflexes
treatment of osa
Treatment of OSA
  • Lifestyle:

Body position during sleep

Weight loss

Decreased ethanol consumption

  • Oral appliances
  • Continuous Positive Airway Pressure (CPAP)
  • Surgical:

Uvulopalatopharyngoplasty

Tracheostomy

cpap mask
CPAP Mask

Photo of CPAP Mask

slide35

Obstructive Sleep Apnea

Sites of obstruction during sleep apnea

With CPAP

Tongue

Tongue

Laryngopharynx

obstructive sleep apnea web sites
Obstructive Sleep Apnea Web Sites
  • http://www.aafp.org/afp/991115ap/2279.html
  • http://www.sleepdisorderchannel.com/osa/
references
References
  • Caples SM, Gami AS, Somers, VK. Obstructive sleep apnea. Ann. Intern. Med. 142: 187-197, 2005
  • Guilleminault C, Tilkian A, Dement WC. The sleep apnea syndromes. Annu. Rev. Med. 27: 465-484, 1976
  • Kirkness JP, Krishnan V, Patil SP, Schneider H. Upper airway obstruction in snoring and upper airway resistance syndrome. In: Randerath WJ, Sanner BM, Somers VK (eds): Sleep Apnea. Prog. Respir. Res. Basel, Karger, 35: 79-89, 2006
  • Levitzky, Michael G. Pulmonary Physiology (7th ed.). 2007. New York: McGraw Hill
  • Ryan CM, Bradley TD. Pathogenesis of obstructive sleep apnea. J. Appl. Physiol. 99: 2440-2450, 2005
  • Schaefer T. Physiology of breathing during sleep. In: Randerath WJ, Sanner BM, Somers VK (eds): Sleep Apnea. Prog. Respir. Res. Basel, Karger, 35: 21-28, 2006