Transcript Document
PowerPoint® Lecture Slides
prepared by
Barbara Heard,
Atlantic Cape Community
College
CHAPTER
22
The Respiratory
System
© Annie Leibovitz/Contact Press Images
© 2013 Pearson Education, Inc.
The Respiratory System
• Major function-respiration
– Supply body with O2 for cellular respiration;
dispose of CO2, a waste product of cellular
respiration
– Its four processes involve both respiratory and
circulatory systems
• Also functions in olfaction and speech
© 2013 Pearson Education, Inc.
Processes of Respiration
• Pulmonary ventilation (breathing)movement of air into and out
of lungs
• External respiration-O2 and CO2
exchange between lungs and blood
• Transport-O2 and CO2 in blood
• Internal respiration-O2 and CO2
exchange between systemic blood
vessels and tissues
© 2013 Pearson Education, Inc.
Respiratory
system
Circulatory
system
Respiratory System: Functional Anatomy
• Major organs
– Nose, nasal cavity, and paranasal sinuses
– Pharynx
– Larynx
– Trachea
– Bronchi and their branches
– Lungs and alveoli
© 2013 Pearson Education, Inc.
Figure 22.1 The major respiratory organs in relation to surrounding structures.
Nasal cavity
Oral cavity
Nostril
Pharynx
Larynx
Trachea
Carina of
trachea
Right main
(primary)
bronchus
Right
lung
Left main
(primary)
bronchus
Left lung
Diaphragm
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Functional Anatomy
• Respiratory zone-site of gas exchange
– Microscopic structures-respiratory
bronchioles, alveolar ducts, and alveoli
• Conducting zone-conduits to gas
exchange sites
– Includes all other respiratory structures;
cleanses, warms, humidifies air
• Diaphragm and other respiratory muscles
promote ventilation
PLAY
Animation: Rotating face
© 2013 Pearson Education, Inc.
The Nose
• Functions
– Provides an airway for respiration
– Moistens and warms entering air
– Filters and cleans inspired air
– Serves as resonating chamber for speech
– Houses olfactory receptors
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The Nose
• Two regions-external nose and nasal
cavity
• External nose-root, bridge, dorsum nasi,
and apex
– Philtrum-shallow vertical groove inferior to
apex
– Nostrils (nares)-bounded laterally by alae
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Figure 22.2a The external nose.
Epicranius,
frontal belly
Root and
bridge of nose
Dorsum nasi
Ala of nose
Apex of nose
Naris (nostril)
Surface anatomy
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Figure 22.2b The external nose.
Frontal bone
Nasal bone
Septal cartilage
Maxillary bone
(frontal process)
Lateral process of
septal cartilage
Minor alar
cartilages
Dense fibrous
connective tissue
Major alar
cartilages
External skeletal framework
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The Nose
• Nasal cavity-within and posterior to
external nose
– Divided by midline nasal septum
– Posterior nasal apertures (choanae) open
into nasopharynx
– Roof-ethmoid and sphenoid bones
– Floor–hard (bone) and soft palates (muscle)
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Nasal Cavity
• Nasal vestibule-nasal cavity superior to
nostrils
– Vibrissae (hairs) filter coarse particles from
inspired air
• Rest of nasal cavity lined with mucous
membranes
– Olfactory mucosa
– Respiratory mucosa
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Nasal Cavity
• Olfactory mucosa contains olfactory
epithelium
• Respiratory mucosa
– Pseudostratified ciliated columnar epithelium
– Mucous and serous secretions contain
lysozyme and defensins
– Cilia move contaminated mucus posteriorly to
throat
– Inspired air warmed by plexuses of capillaries
and veins
– Sensory nerve endings trigger sneezing
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Figure 22.3b The upper respiratory tract.
Cribriform plate
of ethmoid bone
Sphenoid sinus
Frontal sinus
Nasal cavity
Nasal conchae
(superior, middle
and inferior)
Nasal meatuses
(superior, middle,
and inferior)
Nasal vestibule
Posterior nasal
aperture
Nasopharynx
Pharyngeal tonsil
Opening of
pharyngotympanic tube
Uvula
Nostril
Oropharynx
Palatine tonsil
Isthmus of the
fauces
Hard palate
Soft palate
Tongue
Lingual tonsil
Laryngopharynx
Esophagus
Larynx
Epiglottis
Vestibular fold
Thyroid cartilage
Vocal fold
Cricoid cartilage
Trachea
Thyroid gland
Illustration
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Hyoid bone
Figure 22.3a The upper respiratory tract.
Olfactory nerves
Olfactory
epithelium
Superior nasal concha
and superior nasal meatus
Mucosa
of pharynx
Middle nasal concha
and middle nasal meatus
Tubal
tonsil
Inferior nasal concha
and inferior nasal meatus
Pharyngotympanic
(auditory) tube
Nasopharynx
Hard palate
Soft palate
Uvula
Photograph
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Nasal Cavity
• Nasal conchae-superior, middle, and
inferior
– Protrude medially from lateral walls
– Increase mucosal area
– Enhance air turbulence
• Nasal meatus
– Groove inferior to each concha
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Functions of the Nasal Mucosa and
Conchae
• During inhalation, conchae and nasal
mucosa
– Filter, heat, and moisten air
• During exhalation these structures
– Reclaim heat and moisture
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Paranasal Sinuses
• In frontal, sphenoid, ethmoid, and
maxillary bones
• Lighten skull; secrete mucus; help to warm
and moisten air
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Homeostatic Imbalance
• Rhinitis
– Inflammation of nasal mucosa
– Nasal mucosa continuous with mucosa of
respiratory tract spreads from nose
throat chest
– Spreads to tear ducts and paranasal sinuses
causing
• Blocked sinus passageways air absorbed
vacuum sinus headache
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Pharynx
• Muscular tube from base of skull to C6
– Connects nasal cavity and mouth to larynx
and esophagus
– Composed of skeletal muscle
• Three regions
– Nasopharynx
– Oropharynx
– Laryngopharynx
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Figure 22.3c The upper respiratory tract.
Pharynx
Nasopharynx
Oropharynx
Laryngopharynx
Regions of the pharynx
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Nasopharynx
• Air passageway posterior to nasal cavity
• Lining - pseudostratified columnar
epithelium
• Soft palate and uvula close nasopharynx
during swallowing
• Pharyngeal tonsil (adenoids) on posterior
wall
• Pharyngotympanic (auditory) tubes drain
and equalize pressure in middle ear; open
into lateral walls
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Oropharynx
• Passageway for food and air from level of
soft palate to epiglottis
• Lining of stratified squamous epithelium
• Isthmus of fauces-opening to oral cavity
• Palatine tonsils-in lateral walls of fauces
• Lingual tonsil-on posterior surface of
tongue
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Laryngopharynx
• Passageway for food and air
• Posterior to upright epiglottis
• Extends to larynx, where continuous with
esophagus
• Lined with stratified squamous epithelium
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Figure 22.3b The upper respiratory tract.
Cribriform plate
of ethmoid bone
Sphenoid sinus
Frontal sinus
Nasal cavity
Nasal conchae
(superior, middle
and inferior)
Nasal meatuses
(superior, middle,
and inferior)
Nasal vestibule
Posterior nasal
aperture
Nasopharynx
Pharyngeal tonsil
Opening of
pharyngotympanic tube
Uvula
Nostril
Oropharynx
Palatine tonsil
Isthmus of the
fauces
Hard palate
Soft palate
Tongue
Lingual tonsil
Laryngopharynx
Esophagus
Larynx
Epiglottis
Vestibular fold
Thyroid cartilage
Vocal fold
Cricoid cartilage
Trachea
Thyroid gland
Illustration
© 2013 Pearson Education, Inc.
Hyoid bone
Larynx
• Attaches to hyoid bone; opens into
laryngopharynx; continuous with trachea
• Functions
– Provides patent airway
– Routes air and food into proper channels
– Voice production
• Houses vocal folds
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Larynx
• Nine cartilages of larynx
– All hyaline cartilage except epiglottis
– Thyroid cartilage with laryngeal
prominence (Adam's apple)
– Ring-shaped cricoid cartilage
– Paired arytenoid, cuneiform, and
corniculate cartilages
– Epiglottis-elastic cartilage; covers laryngeal
inlet during swallowing; covered in taste budcontaining mucosa
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Figure 22.4a The larynx.
Epiglottis
Thyrohyoid
membrane
Body of hyoid bone
Thyroid cartilage
Laryngeal prominence
(Adam’s apple)
Cricothyroid ligament
Cricoid cartilage
Cricotracheal ligament
Tracheal cartilages
Anterior superficial view
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Figure 22.4b The larynx.
Epiglottis
Thyrohyoid
membrane
Body of hyoid bone
Thyrohyoid membrane
Cuneiform cartilage
Fatty pad
Corniculate cartilage
Vestibular fold
(false vocal cord)
Arytenoid cartilage
Thyroid cartilage
Arytenoid muscles
Vocal fold
(true vocal cord)
Cricoid cartilage
Cricothyroid ligament
Cricotracheal ligament
Tracheal cartilages
Sagittal view; anterior surface to the right
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Figure 22.4c The larynx.
Epiglottis
Hyoid bone
Thyroid
cartilage
Lateral
thyrohyoid
membrane
Corniculate
cartilage
Arytenoid
cartilage
Glottis
Cricoid
cartilage
Tracheal
cartilages
Photograph of cartilaginous framework
of the larynx, posterior view
© 2013 Pearson Education, Inc.
Figure 22.4d The larynx.
Epiglottis
Laryngeal
inlet
Corniculate
cartilage
Posterior
cricoarytenoid
muscle on
cricoid
cartilage
Trachea
(d) Photograph of posterior aspect
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Larynx
• Vocal ligaments-deep to laryngeal
mucosa
– Attach arytenoid cartilages to thyroid cartilage
– Contain elastic fibers
– Form core of vocal folds (true vocal cords)
• Glottis-opening between vocal folds
• Folds vibrate to produce sound as air rushes up
from lungs
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Larynx
• Vestibular folds (false vocal cords)
– Superior to vocal folds
– No part in sound production
– Help to close glottis during swallowing
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Figure 22.5 Movements of the vocal folds.
Base of tongue
Epiglottis
Vestibular fold (false vocal cord)
Vocal fold (true vocal cord)
Glottis
Inner lining of trachea
Cuneiform cartilage
Corniculate cartilage
Vocal folds in closed position; closed glottis
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Vocal folds in open position; open glottis
Epithelium of Larynx
• Superior portion–stratified squamous
epithelium
• Inferior to vocal folds–pseudostratified
ciliated columnar epithelium
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Voice Production
• Speech-intermittent release of expired air while
opening and closing glottis
• Pitch determined by length and tension of vocal
cords
• Loudness depends upon force of air
• Chambers of pharynx, oral, nasal, and sinus
cavities amplify and enhance sound quality
• Sound is "shaped" into language by muscles of
pharynx, tongue, soft palate, and lips
© 2013 Pearson Education, Inc.
Larynx
• Vocal folds may act as sphincter to
prevent air passage
• Example-Valsalva's maneuver
– Glottis closes to prevent exhalation
– Abdominal muscles contract
– Intra-abdominal pressure rises
– Helps to empty rectum or stabilizes trunk
during heavy lifting
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Trachea
• Windpipe–from larynx into mediastinum
• Wall composed of three layers
– Mucosa-ciliated pseudostratified epithelium
with goblet cells
– Submucosa-connective tissue with
seromucous glands
– Adventitia-outermost layer made of
connective tissue; encases C-shaped rings of
hyaline cartilage
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Trachea
• Trachealis
– Connects posterior parts of cartilage rings
– Contracts during coughing to expel mucus
• Carina
– Spar of cartilage on last, expanded tracheal
cartilage
– Point where trachea branches into two main
bronchi
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Figure 22.6a Tissue composition of the tracheal wall.
Posterior
Mucosa
Esophagus
Trachealis
muscle
Submucosa
Lumen of
trachea
Seromucous gland
in submucosa
Hyaline cartilage
Adventitia
Anterior
Cross section of the trachea
and esophagus
© 2013 Pearson Education, Inc.
Figure 22.6b Tissue composition of the tracheal wall.
Goblet cell
Mucosa
• Pseudostratified
ciliated columnar
epithelium
• Lamina propria
(connective tissue)
Submucosa
Seromucous gland
In submucosa
Hyaline cartilage
Photomicrograph of the tracheal
wall (320x)
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Figure 22.6c Tissue composition of the tracheal wall.
Scanning electron micrograph of cilia in the
trachea (2500x)
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Bronchi and Subdivisions
• Air passages undergo 23 orders of
branching bronchial (respiratory) tree
• From tips of bronchial tree conducting
zone structures respiratory zone
structures
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Conducting Zone Structures
• Trachea right and left main (primary)
bronchi
• Each main bronchus enters hilum of one
lung
– Right main bronchus wider, shorter, more
vertical than left
• Each main bronchus branches into lobar
(secondary) bronchi (three on right, two
on left)
– Each lobar bronchus supplies one lobe
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Conducting Zone Structures
• Each lobar bronchus branches into
segmental (tertiary) bronchi
– Segmental bronchi divide repeatedly
• Branches become smaller and smaller
– Bronchioles-less than 1 mm in diameter
– Terminal bronchioles-smallest-less than
0.5 mm diameter
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Figure 22.7 Conducting zone passages.
Trachea
Superior lobe
of left lung
Left main
(primary)
bronchus
Superior lobe
of right lung
Lobar (secondary)
bronchus
Segmental (tertiary)
bronchus
Middle lobe
of right lung
Inferior lobe
of right lung
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Inferior lobe
of left lung
Conducting Zone Structures
• From bronchi through bronchioles,
structural changes occur
– Cartilage rings become irregular plates; in
bronchioles elastic fibers replace cartilage
– Epithelium changes from pseudostratified
columnar to cuboidal; cilia and goblet cells
become sparse
– Relative amount of smooth muscle increases
• Allows constriction
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Respiratory Zone
• Begins as terminal bronchioles
respiratory bronchioles alveolar
ducts alveolar sacs
– Alveolar sacs contain clusters of alveoli
• ~300 million alveoli make up most of lung volume
• Sites of gas exchange
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Figure 22.8a Respiratory zone structures.
Alveoli
Alveolar duct
Respiratory bronchioles
Terminal
bronchiole
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Alveolar duct
Alveolar
sac
Figure 22.8b Respiratory zone structures.
Respiratory
bronchiole
Alveolar
duct
Alveoli
Alveolar
sac
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Alveolar
pores
Respiratory Membrane
• Alveolar and capillary walls and their fused
basement membranes
– ~0.5-µm-thick; gas exchange across
membrane by simple diffusion
• Alveolar walls
– Single layer of squamous epithelium (type I
alveolar cells)
• Scattered cuboidal type II alveolar cells
secrete surfactant and antimicrobial
proteins
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Figure 22.9a Alveoli and the respiratory membrane.
Terminal bronchiole
Respiratory bronchiole
Smooth
muscle
Elastic
fibers
Alveolus
Capillaries
Diagrammatic view of capillary-alveoli relationships
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Figure 22.9b Alveoli and the respiratory membrane.
Scanning electron micrograph of pulmonary capillary
casts (70x)
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Alveoli
• Surrounded by fine elastic fibers and
pulmonary capillaries
• Alveolar pores connect adjacent alveoli
• Equalize air pressure throughout lung
• Alveolar macrophages keep alveolar
surfaces sterile
– 2 million dead macrophages/hour carried by
cilia throat swallowed
© 2013 Pearson Education, Inc.
Figure 22.9c Alveoli and the respiratory membrane.
Red blood
cell
Nucleus of type I
alveolar cell
Alveolar pores
Capillary
Capillary
Macrophage
Endothelial cell
nucleus
Alveolus
Respiratory
membrane
Alveoli
(gas-filled
air spaces)
Red blood
cell in
capillary
Type II
alveolar
cell
Type I
alveolar
cell
Detailed anatomy of the respiratory membrane
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Alveolus
Alveolar
epithelium
Fused basement
membranes of
alveolar
epithelium and
capillary
endothelium
Capillary
endothelium
Lungs
• Occupy all thoracic cavity except
mediastinum
• Root-site of vascular and bronchial
attachment to mediastinum
• Costal surface-anterior, lateral, and
posterior surfaces
• Composed primarily of alveoli
• Balance–stroma-elastic connective tissue
elasticity
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Figure 22.10c Anatomical relationships of organs in the thoracic cavity.
Vertebra
Right lung
Parietal pleura
Visceral pleura
Pleural cavity
Posterior
Esophagus
(in mediastinum)
Root of lung
at hilum
• Left main
bronchus
• Left pulmonary
artery
• Left pulmonary
vein
Left lung
Thoracic wall
Pulmonary trunk
Pericardial
membranes
Sternum
Heart (in mediastinum)
Anterior mediastinum
Anterior
Transverse section through the thorax, viewed from above. Lungs, pleural
membranes, and major organs in the mediastinum are shown.
© 2013 Pearson Education, Inc.
Lungs
• Apex-superior tip; deep to clavicle
• Base-inferior surface; rests on diaphragm
• Hilum-on mediastinal surface; site for
entry/exit of blood vessels, bronchi,
lymphatic vessels, and nerves
• Left lung smaller than right
– Cardiac notch-concavity for heart
– Separated into superior and inferior lobes by
oblique fissure
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Lungs
• Right lung
– Superior, middle, inferior lobes separated by
oblique and horizontal fissures
• Bronchopulmonary segments (10 right,
8–10 left) separated by connective tissue
septa
– If diseased can be individually removed
• Lobules-smallest subdivisions visible to
naked eye; served by bronchioles and
their branches
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Figure 22.10a Anatomical relationships of organs in the thoracic cavity.
Intercostal
muscle
Rib
Lung
Parietal pleura
Pleural cavity
Visceral pleura
Trachea
Thymus
Apex of lung
Left
superior lobe
Right superior lobe
Horizontal fissure
Right middle lobe
Oblique fissure
Oblique
fissure
Left inferior
lobe
Right inferior lobe
Heart
(in mediastinum)
Diaphragm
Cardiac notch
Base of lung
Anterior view. The lungs flank mediastinal structures laterally.
© 2013 Pearson Education, Inc.
Figure 22.10b Anatomical relationships of organs in the thoracic cavity.
Apex of lung
Pulmonary
artery
Left
superior lobe
Oblique
fissure
Pulmonary
vein
Left inferior
lobe
Cardiac
impression
Hilum of lung
Oblique
fissure
Aortic
impression
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Left main
bronchus
Lobules
Photograph of medial view of the
left lung.
Figure 22.11 A cast of the bronchial tree.
Right lung
Right
superior
lobe (3
segments)
Left lung
Left superior
lobe
(4 segments)
Right
middle
lobe (2
segments)
Right
inferior lobe
(5 segments)
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Left inferior
lobe
(5 segments)
Blood Supply
• Pulmonary circulation (low pressure,
high volume)
– Pulmonary arteries deliver systemic venous
blood to lungs for oxygenation
• Branch profusely; feed into pulmonary capillary
networks
– Pulmonary veins carry oxygenated blood
from respiratory zones to heart
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Blood Supply
– Lung capillary endothelium contains enzymes
that act on substances in blood
• E.g., angiotensin-converting enzyme–activates
blood pressure hormone
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Blood Supply
• Bronchial arteries provide oxygenated
blood to lung tissue
– Arise from aorta and enter lungs at hilum
– Part of systemic circulation (high pressure,
low volume)
– Supply all lung tissue except alveoli
– Bronchial veins anastomose with pulmonary
veins
• Pulmonary veins carry most venous blood back to
heart
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Pleurae
• Thin, double-layered serosa; divides
thoracic cavity into two pleural
compartments and mediastinum
• Parietal pleura on thoracic wall, superior
face of diaphragm, around heart, between
lungs
• Visceral pleura on external lung surface
• Pleural fluid fills slitlike pleural cavity
– Provides lubrication and surface tension
assists in expansion and recoil
© 2013 Pearson Education, Inc.
Figure 22.10c Anatomical relationships of organs in the thoracic cavity.
Vertebra
Right lung
Parietal pleura
Visceral pleura
Pleural cavity
Posterior
Esophagus
(in mediastinum)
Root of lung
at hilum
• Left main
bronchus
• Left pulmonary
artery
• Left pulmonary
vein
Left lung
Thoracic wall
Pulmonary trunk
Pericardial
membranes
Sternum
Heart (in mediastinum)
Anterior mediastinum
Anterior
Transverse section through the thorax, viewed from above. Lungs, pleural
membranes, and major organs in the mediastinum are shown.
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Mechanics of Breathing
• Pulmonary ventilation consists of two
phases
– Inspiration-gases flow into lungs
– Expiration-gases exit lungs
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Pressure Relationships in the Thoracic
Cavity
• Atmospheric pressure (Patm)
– Pressure exerted by air surrounding body
– 760 mm Hg at sea level = 1 atmosphere
• Respiratory pressures described relative
to Patm
– Negative respiratory pressure-less than Patm
– Positive respiratory pressure-greater than Patm
– Zero respiratory pressure = Patm
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Intrapulmonary Pressure
• Intrapulmonary (intra-alveolar) pressure
(Ppul)
– Pressure in alveoli
– Fluctuates with breathing
– Always eventually equalizes with Patm
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Intrapleural Pressure
• Intrapleural pressure (Pip)
– Pressure in pleural cavity
– Fluctuates with breathing
– Always a negative pressure (<Patm and <Ppul)
– Fluid level must be minimal
• Pumped out by lymphatics
• If accumulates positive Pip pressure lung
collapse
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Intrapleural Pressure
• Negative Pip caused by opposing forces
– Two inward forces promote lung collapse
• Elastic recoil of lungs decreases lung size
• Surface tension of alveolar fluid reduces alveolar
size
– One outward force tends to enlarge lungs
• Elasticity of chest wall pulls thorax outward
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Pressure Relationships
• If Pip = Ppul or Patm lungs collapse
• (Ppul – Pip) = transpulmonary pressure
– Keeps airways open
– Greater transpulmonary pressure larger
lungs
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Figure 22.12 Intrapulmonary and intrapleural pressure relationships.
Atmospheric pressure (Patm)
0 mm Hg (760 mm Hg)
Parietal pleura
Thoracic wall
Visceral pleura
Pleural cavity
Transpulmonary
pressure
4 mm Hg
(the difference
between 0 mm Hg
and −4 mm Hg)
–4
0
Lung
Diaphragm
© 2013 Pearson Education, Inc.
Intrapulmonary
pressure (Ppul)
0 mm Hg
(760 mm Hg)
Intrapleural
pressure (Pip)
−4 mm Hg
(756 mm Hg)
Homeostatic Imbalance
• Atelectasis (lung collapse) due to
– Plugged bronchioles collapse of alveoli
– Pneumothorax-air in pleural cavity
• From either wound in parietal or rupture of visceral
pleura
• Treated by removing air with chest tubes; pleurae
heal lung reinflates
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Pulmonary Ventilation
• Inspiration and expiration
• Mechanical processes that depend on
volume changes in thoracic cavity
– Volume changes pressure changes
– Pressure changes gases flow to equalize
pressure
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Boyle's Law
• Relationship between pressure and
volume of a gas
– Gases fill container; if container size reduced
increased pressure
• Pressure (P) varies inversely with volume
(V):
– P1V1 = P2V2
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Inspiration
• Active process
– Inspiratory muscles (diaphragm and external
intercostals) contract
– Thoracic volume increases intrapulmonary
pressure drops (to 1 mm Hg)
– Lungs stretched and intrapulmonary volume
increases
– Air flows into lungs, down its pressure
gradient, until Ppul = Patm
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Forced Inspiration
• Vigorous exercise, COPD accessory
muscles (scalenes, sternocleidomastoid,
pectoralis minor) further increase in
thoracic cage size
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Figure 22.13 Changes in thoracic volume and sequence of events during inspiration and expiration. (1 of 2) Slide 1
Sequence of events
Changes in anterior-posterior and
superior-inferior dimensions
Changes in lateral dimensions
(superior view)
1 Inspiratory muscles
contract (diaphragm
descends; rib cage rises).
Inspiration
2 Thoracic cavity volume
increases.
3 Lungs are stretched;
intrapulmonary volume
increases.
Ribs are
elevated and
sternum
flares as
external
intercostals
contract.
External
intercostals
contract.
4 Intrapulmonary pressure
drops (to –1 mm Hg).
5 Air (gases) flows into
lungs down its pressure
gradient until intrapulmonary
pressure is 0 (equal to
atmospheric pressure).
© 2013 Pearson Education, Inc.
Diaphragm
moves inferiorly
during
contraction.
Expiration
• Quiet expiration normally passive process
– Inspiratory muscles relax
– Thoracic cavity volume decreases
– Elastic lungs recoil and intrapulmonary
volume decreases pressure increases (Ppul
rises to +1 mm Hg)
– Air flows out of lungs down its pressure
gradient until Ppul = 0
• Note: forced expiration-active process;
uses abdominal (oblique and transverse)
and internal intercostal muscles
© 2013 Pearson Education, Inc.
Figure 22.13 Changes in thoracic volume and sequence of events during inspiration and expiration. (2 of 2) Slide 1
Sequence of events
Changes in anterior-posterior and
superior-inferior dimensions
Changes in lateral dimensions
(superior view)
1 Inspiratory muscles relax
(diaphragm rises; rib cage
descends due to recoil of
costal cartilages).
Expiration
2 Thoracic cavity volume
decreases.
3 Elastic lungs recoil
passively; intrapulmonary
Volume decreases.
Ribs and
sternum are
depressed
as external
intercostals
relax.
External
intercostals
relax.
4 Intrapulmonary pressure
rises (to +1 mm Hg).
5 Air (gases) flows out of
lungs down its pressure
gradient until intrapulmonary
pressure is 0.
© 2013 Pearson Education, Inc.
Diaphragm
moves
superiorly
as it relaxes.
Intrapleural pressure.
Pleural cavity pressure
becomes more negative as
chest wall expands during
inspiration. Returns to initial
value as chest wall recoils.
Volume of breath. During
each breath, the pressure
gradients move 0.5 liter of
air into and out of the lungs.
Volume (L)
Intrapulmonary pressure.
Pressure inside lung
decreases as lung volume
increases during
inspiration; pressure
increases during expiration.
Pressure relative to
atmospheric pressure (mm Hg)
Figure 22.14 Changes in intrapulmonary and intrapleural pressures during inspiration and expiration.
Inspiration
Expiration
Intrapulmonary
pressure
+2
0
–2
–4
Transpulmonary
pressure
–6
Intrapleural
pressure
–8
Volume of breath
0.5
0
5 seconds elapsed
© 2013 Pearson Education, Inc.
Physical Factors Influencing Pulmonary
Ventilation
• Three physical factors influence the ease
of air passage and the amount of energy
required for ventilation.
– Airway resistance
– Alveolar surface tension
– Lung compliance
© 2013 Pearson Education, Inc.
Airway Resistance
• Friction-major nonelastic source of
resistance to gas flow; occurs in airways
• Relationship between flow (F), pressure
(P), and resistance (R) is:
– ∆P - pressure gradient between atmosphere
and alveoli (2 mm Hg or less during normal
quiet breathing)
– Gas flow changes inversely with resistance
© 2013 Pearson Education, Inc.
Airway Resistance
• Resistance usually insignificant
– Large airway diameters in first part of
conducting zone
– Progressive branching of airways as get
smaller, increasing total cross-sectional area
– Resistance greatest in medium-sized bronchi
• Resistance disappears at terminal
bronchioles where diffusion drives gas
movement
© 2013 Pearson Education, Inc.
Figure 22.15 Resistance in respiratory passageways.
Conducting
zone
Respiratory
zone
Resistance
Medium-sized
bronchi
Terminal
bronchioles
1
© 2013 Pearson Education, Inc.
5
10
15
Airway generation
(stage of branching)
20
23
Homeostatic Imbalance
• As airway resistance rises, breathing
movements become more strenuous
• Severe constriction or obstruction of
bronchioles
– Can prevent life-sustaining ventilation
– Can occur during acute asthma attacks; stops
ventilation
• Epinephrine dilates bronchioles, reduces
air resistance
© 2013 Pearson Education, Inc.
Alveolar Surface Tension
• Surface tension
– Attracts liquid molecules to one another at
gas-liquid interface
– Resists any force that tends to increase
surface area of liquid
– Water–high surface tension; coats alveolar
walls reduces them to smallest size
© 2013 Pearson Education, Inc.
Alveolar Surface Tension
• Surfactant
– Detergent-like lipid and protein complex
produced by type II alveolar cells
– Reduces surface tension of alveolar fluid and
discourages alveolar collapse
– Insufficient quantity in premature infants
causes infant respiratory distress
syndrome
• alveoli collapse after each breath
© 2013 Pearson Education, Inc.
Lung Compliance
• Measure of change in lung volume that
occurs with given change in
transpulmonary pressure
• Higher lung compliance easier to
expand lungs
• Normally high due to
– Distensibility of lung tissue
– Surfactant, which decreases alveolar surface
tension
© 2013 Pearson Education, Inc.
Lung Compliance
• Diminished by
– Nonelastic scar tissue replacing lung tissue
(fibrosis)
– Reduced production of surfactant
– Decreased flexibility of thoracic cage
© 2013 Pearson Education, Inc.
Total Respiratory Compliance
• The total compliance of the respiratory
system is also influenced by compliance
(distensibility) of the thoracic wall, which
is decreased by:
– Deformities of thorax
– Ossification of costal cartilage
– Paralysis of intercostal muscles
© 2013 Pearson Education, Inc.
Respiratory Volumes
• Used to assess respiratory status
– Tidal volume (TV)
– Inspiratory reserve volume (IRV)
– Expiratory reserve volume (ERV)
– Residual volume (RV)
© 2013 Pearson Education, Inc.
Figure 22.16b Respiratory volumes and capacities.
Measurement
Respiratory
volumes
Respiratory
capacities
Adult male
Adult female
average value average value
Description
Tidal volume (TV)
500 ml
500 ml
Amount of air inhaled or exhaled with each breath under resting
conditions
Inspiratory reserve
volume (IRV)
3100 ml
1900 ml
Amount of air that can be forcefully inhaled after a normal tidal
volume inspiration
Expiratory reserve
volume (ERV)
1200 ml
700 ml
Amount of air that can be forcefully exhaled after a normal tidal
volume expiration
Residual volume (RV)
1200 ml
1100 ml
Amount of air remaining in the lungs after a forced expiration
Total lung capacity (TLC) 6000 ml
4200 ml
Maximum amount of air contained in lungs after a maximum
inspiratory effort: TLC = TV + IRV + ERV + RV
Vital capacity (VC)
4800 ml
3100 ml
Maximum amount of air that can be expired after a maximum
inspiratory effort: VC = TV + IRV + ERV
Inspiratory capacity (IC) 3600 ml
2400 ml
Maximum amount of air that can be inspired after a normal tidal
volume expiration: IC = TV + IRV
Functional residual
capacity (FRC)
1800 ml
Volume of air remaining in the lungs after a normal tidal volume
expiration: FRC = ERV + RV
2400 ml
Summary of respiratory volumes and capacities for males and females
© 2013 Pearson Education, Inc.
Respiratory Capacities
• Combinations of respiratory volumes
– Inspiratory capacity (IC)
– Functional residual capacity (FRC)
– Vital capacity (VC)
– Total lung capacity (TLC)
© 2013 Pearson Education, Inc.
Figure 22.16a Respiratory volumes and capacities.
6000
Milliliters (ml)
5000
Inspiratory
reserve volume
3100 ml
4000
Inspiratory
capacity
3600 ml
3000
Tidal volume 500 ml
Expiratory
reserve volume
1200 ml
2000
1000
Residual volume
1200 ml
0
Spirographic record for a male
© 2013 Pearson Education, Inc.
Functional
residual
capacity
2400 ml
Vital
capacity
4800 ml
Total lung
capacity
6000 ml
Figure 22.16b Respiratory volumes and capacities.
Measurement
Respiratory
volumes
Respiratory
capacities
Adult male
Adult female
average value average value
Description
Tidal volume (TV)
500 ml
500 ml
Amount of air inhaled or exhaled with each breath under resting
conditions
Inspiratory reserve
volume (IRV)
3100 ml
1900 ml
Amount of air that can be forcefully inhaled after a normal tidal
volume inspiration
Expiratory reserve
volume (ERV)
1200 ml
700 ml
Amount of air that can be forcefully exhaled after a normal tidal
volume expiration
Residual volume (RV)
1200 ml
1100 ml
Amount of air remaining in the lungs after a forced expiration
Total lung capacity (TLC) 6000 ml
4200 ml
Maximum amount of air contained in lungs after a maximum
inspiratory effort: TLC = TV + IRV + ERV + RV
Vital capacity (VC)
4800 ml
3100 ml
Maximum amount of air that can be expired after a maximum
inspiratory effort: VC = TV + IRV + ERV
Inspiratory capacity (IC) 3600 ml
2400 ml
Maximum amount of air that can be inspired after a normal tidal
volume expiration: IC = TV + IRV
Functional residual
capacity (FRC)
1800 ml
Volume of air remaining in the lungs after a normal tidal volume
expiration: FRC = ERV + RV
2400 ml
Summary of respiratory volumes and capacities for males and females
© 2013 Pearson Education, Inc.
Dead Space
• Anatomical dead space
– No contribution to gas exchange
– Air remaining in passageways; ~150 ml
• Alveolar dead space–non-functional
alveoli due to collapse or obstruction
• Total dead space-sum of anatomical and
alveolar dead space
© 2013 Pearson Education, Inc.
Pulmonary Function Tests
• Spirometer-instrument for measuring
respiratory volumes and capacities
• Spirometry can distinguish between
– Obstructive pulmonary disease—increased
airway resistance (e.g., bronchitis)
• TLC, FRC, RV may increase
– Restrictive disorders—reduced TLC due to
disease or fibrosis
• VC, TLC, FRC, RV decline
© 2013 Pearson Education, Inc.
Pulmonary Function Tests
• To measure rate of gas movement
– Forced vital capacity (FVC)—gas forcibly
expelled after taking deep breath
– Forced expiratory volume (FEV)—amount
of gas expelled during specific time intervals
of FVC
© 2013 Pearson Education, Inc.
Alveolar Ventilation
• Minute ventilation—total amount of gas
flow into or out of respiratory tract in one
minute
– Normal at rest = ~ 6 L/min
– Normal with exercise = up to 200 L/min
– Only rough estimate of respiratory efficiency
© 2013 Pearson Education, Inc.
Alveolar Ventilation
• Good indicator of effective ventilation
• Alveolar ventilation rate (AVR)—flow of
gases into and out of alveoli during a
particular time
AVR
(ml/min)
=
frequency
(breaths/min)
X
(TV – dead space)
(ml/breath)
• Dead space normally constant
• Rapid, shallow breathing decreases AVR
© 2013 Pearson Education, Inc.
Table 22.2 Effects of Breathing Rate and Depth on Alveolar ventilation of Three Hypothetical Patients
© 2013 Pearson Education, Inc.
Nonrespiratory Air Movements
• May modify normal respiratory rhythm
• Most result from reflex action; some
voluntary
• Examples include-cough, sneeze, crying,
laughing, hiccups, and yawns
© 2013 Pearson Education, Inc.
Gas Exchanges Between Blood, Lungs, and
Tissues
• External respiration–diffusion of gases in
lungs
• Internal respiration–diffusion of gases at
body tissues
• Both involve
– Physical properties of gases
– Composition of alveolar gas
© 2013 Pearson Education, Inc.
Basic Properties of Gases: Dalton's Law of
Partial Pressures
• Total pressure exerted by mixture of gases
= sum of pressures exerted by each gas
• Partial pressure
– Pressure exerted by each gas in mixture
– Directly proportional to its percentage in
mixture
© 2013 Pearson Education, Inc.
Basic Properties of Gases: Henry's Law
• Gas mixtures in contact with liquid
– Each gas dissolves in proportion to its partial
pressure
– At equilibrium, partial pressures in two phases
will be equal
– Amount of each gas that will dissolve
depends on
• Solubility–CO2 20 times more soluble in water than
O2; little N2 dissolves in water
• Temperature–as temperature rises, solubility
decreases
© 2013 Pearson Education, Inc.
Composition of Alveolar Gas
• Alveoli contain more CO2 and water vapor
than atmospheric air
– Gas exchanges in lungs
– Humidification of air
– Mixing of alveolar gas with each breath
© 2013 Pearson Education, Inc.
Table 22.4 Comparison of Gas Partial Pressures and Approximate Percentages in the Atmosphere and in the Alveoli
© 2013 Pearson Education, Inc.
External Respiration
• Exchange of O2 and CO2 across
respiratory membrane
• Influenced by
– Thickness and surface area of respiratory
membrane
– Partial pressure gradients and gas solubilities
– Ventilation-perfusion coupling
© 2013 Pearson Education, Inc.
Thickness and Surface Area of the
Respiratory Membrane
• Respiratory membranes
– 0.5 to 1 m thick
– Large total surface area (40 times that of skin)
for gas exchange
• Thicken if lungs become waterlogged and
edematous gas exchange inadequate
• Reduced surface area in emphysema
(walls of adjacent alveoli break down),
tumors, inflammation, mucus
© 2013 Pearson Education, Inc.
Partial Pressure Gradients and Gas
Solubilities
• Steep partial pressure gradient for O2 in
lungs
– Venous blood Po2 = 40 mm Hg
– Alveolar Po2 = 104 mm Hg
• Drives oxygen flow to blood
• Equilibrium reached across respiratory membrane
in ~0.25 seconds, about 1/3 time a red blood cell in
pulmonary capillary
– Adequate oxygenation even if blood flow increases 3X
© 2013 Pearson Education, Inc.
Figure 22.18 Oxygenation of blood in the pulmonary capillaries at rest.
PO2 (mm Hg)
150
100
PO2 104 mm Hg
50
40
0
0
Start of
capillary
© 2013 Pearson Education, Inc.
0.25
0.50
Time in the
pulmonary capillary (s)
0.75
End of
capillary
Partial Pressure Gradients and Gas
Solubilities
• Partial pressure gradient for CO2 in lungs
less steep
– Venous blood Pco2 = 45 mm Hg
– Alveolar Pco2 = 40 mm Hg
• Though gradient not as steep, CO2
diffuses in equal amounts with oxygen
– CO2 20 times more soluble in plasma than
oxygen
© 2013 Pearson Education, Inc.
Figure 22.17 Partial pressure gradients promoting gas movements in the body.
Inspired air:
PO 160 mm Hg
2
PCO2 0.3 mm Hg
Alveoli of lungs:
PO2 104 mm Hg
PCO2 40 mm Hg
External
respiration
Pulmonary
arteries
Alveoli
Pulmonary
veins (PO2
100 mm Hg)
Blood leaving
lungs and
entering tissue
capillaries:
PO2 100 mm Hg
PCO2 40 mm Hg
Blood leaving
tissues and
entering lungs:
PO2 40 mm Hg
PCO2 45 mm Hg
Heart
Systemic
veins
Systemic
arteries
Internal
respiration
Tissues:
PO2 less than 40 mm Hg
PCO2 greater than 45 mm Hg
© 2013 Pearson Education, Inc.
Ventilation-Perfusion Coupling
• Perfusion-blood flow reaching alveoli
• Ventilation-amount of gas reaching
alveoli
• Ventilation and perfusion matched
(coupled) for efficient gas exchange
– Never balanced for all alveoli due to
• Regional variations due to effect of gravity on
blood and air flow
• Some alveolar ducts plugged with mucus
© 2013 Pearson Education, Inc.
Ventilation-Perfusion Coupling
• Perfusion
– Changes in Po2 in alveoli cause changes in
diameters of arterioles
• Where alveolar O2 is high, arterioles dilate
• Where alveolar O2 is low, arterioles constrict
• Directs most blood where alveolar oxygen high
© 2013 Pearson Education, Inc.
Ventilation-Perfusion Coupling
• Changes in Pco2 in alveoli cause changes
in diameters of bronchioles
– Where alveolar CO2 is high, bronchioles dilate
– Where alveolar CO2 is low, bronchioles
constrict
– Allows elimination of CO2 more rapidly
© 2013 Pearson Education, Inc.
Figure 22.19 Ventilation-perfusion coupling.
Ventilation less than perfusion
Mismatch of ventilation and perfusion
ventilation and/or perfusion of alveoli
causes local P CO and P O
2
2
O2 autoregulates
arteriolar diameter
© 2013 Pearson Education, Inc.
Ventilation greater than perfusion
Mismatch of ventilation and perfusion
ventilation and/or perfusion of alveoli
causes local P CO and P O
2
2
O2 autoregulates
arteriolar diameter
Pulmonary arterioles
serving these alveoli
constricts
Pulmonary arterioles
serving these alveoli
dilate
Match of ventilation
and perfusion
ventilation, perfusion
Match of ventilation
and perfusion
ventilation, perfusion
Internal Respiration
• Capillary gas exchange in body tissues
• Partial pressures and diffusion gradients
reversed compared to external respiration
– Tissue Po2 always lower than in systemic
arterial blood oxygen from blood to tissues
– CO2 from tissues to blood
– Venous blood Po2 40 mm Hg and Pco2
45 mm Hg
© 2013 Pearson Education, Inc.
Figure 22.17 Partial pressure gradients promoting gas movements in the body.
Inspired air:
PO 160 mm Hg
2
PCO2 0.3 mm Hg
Alveoli of lungs:
PO2 104 mm Hg
PCO2 40 mm Hg
External
respiration
Pulmonary
arteries
Alveoli
Pulmonary
veins (PO2
100 mm Hg)
Blood leaving
lungs and
entering tissue
capillaries:
PO2 100 mm Hg
PCO2 40 mm Hg
Blood leaving
tissues and
entering lungs:
PO2 40 mm Hg
PCO2 45 mm Hg
Heart
Systemic
veins
Systemic
arteries
Internal
respiration
Tissues:
PO2 less than 40 mm Hg
PCO2 greater than 45 mm Hg
© 2013 Pearson Education, Inc.
Transport of Respiratory Gases by Blood
• Oxygen (O2) transport
• Carbon dioxide (CO2) transport
© 2013 Pearson Education, Inc.
O2 Transport
• Molecular O2 carried in blood
– 1.5% dissolved in plasma
– 98.5% loosely bound to each Fe of
hemoglobin (Hb) in RBCs
• 4 O2 per Hb
© 2013 Pearson Education, Inc.
O2 and Hemoglobin
• Oxyhemoglobin (HbO2)-hemoglobin-O2
combination
• Reduced hemoglobin
(deoxyhemoglobin) (HHb)-hemoglobin
that has released O2
© 2013 Pearson Education, Inc.
O2 and Hemoglobin
• Loading and unloading of O2 facilitated by
change in shape of Hb
– As O2 binds, Hb affinity for O2 increases
– As O2 is released, Hb affinity for O2 decreases
• Fully saturated (100%) if all four heme
groups carry O2
• Partially saturated when one to three
hemes carry O2
© 2013 Pearson Education, Inc.
O2 and Hemoglobin
• Rate of loading and unloading of O2
regulated to ensure adequate oxygen
delivery to cells
– Po2
– Temperature
– Blood pH
– Pco2
– Concentration of BPG–produced by RBCs
during glycolysis; levels rise when oxygen
levels chronically low
© 2013 Pearson Education, Inc.
Influence of Po2 on Hemoglobin Saturation
• Oxygen-hemoglobin dissociation curve
• Hemoglobin saturation plotted against Po2
not linear; S-shaped curve
– Binding and release of O2 influenced by Po2
© 2013 Pearson Education, Inc.
Figure 22.20 The amount of oxygen carried by hemoglobin depends on the P O2 (the amount of oxygen) available
locally. (1 of 3)
In the lungs, where PO2 is high
(100 mm Hg), Hb is almost
fully saturated (98%) with O2.
This axis tells you how much
O2 is bound to Hb. At 100%,
each Hb molecule has 4 bound
oxygen molecules.
Hemoglobin
100
•
Percent O2 saturation of hemoglobin
Oxygen
If more O2 is present,
more O2 is bound.
However, because of
Hb’s properties (O2
binding strength
changes with saturation),
this is an S-shaped curve,
not a straight line.
80
60
40
20
•
0
0
20
40
60
80
100
PO2 (mm Hg)
This axis tells you the relative
Amount (partial pressure) of
O2 disslolved in the fluid
Surrounding the Hb.
© 2013 Pearson Education, Inc.
In the tissues of other organs,
Where PO2 is low (40 mm Hg), Hb
is less saturated (75%) with O2.
Influence of Po2 on Hemoglobin Saturation
• In arterial blood
– Po2 = 100 mm Hg
– Contains 20 ml oxygen per 100 ml blood
(20 vol %)
– Hb is 98% saturated
• Further increases in Po2 (e.g., breathing
deeply) produce minimal increases in O2
binding
© 2013 Pearson Education, Inc.
Influence of Po2 on Hemoglobin Saturation
• In venous blood
– Po2 = 40 mm Hg
– Contains 15 vol % oxygen
– Hb is 75% saturated
– Venous reserve
• Oxygen remaining in venous blood
© 2013 Pearson Education, Inc.
Figure 22.20 The amount of oxygen carried by hemoglobin depends on the P O2 (the amount of oxygen) available
locally. (2 of 3)
In the lungs
At sea level, there is lots of O2.
At a PO2 in the lungs of 100 mm Hg,
Hb is 98% saturated.
Percent O2 saturation of hemoglobin
100
98%
80
60
40
20
0
0
20
40
60
PO2 (mm Hg)
80
100
At high PO2, large changes in PO2 cause only
small changes in Hb saturation. Notice that the
curve is relatively flat here. Hb’s properties
produce a safety margin that ensures that Hb is
almost fully saturated even with a substantial PO2
decrease. As a result, Hb remains saturated even
at high altitude or with lung disease.
© 2013 Pearson Education, Inc.
95%
At high altitude, there is less O2.
At a PO2 in the lungs of only 80
mm Hg, Hb is still 95% saturated.
Other Factors Influencing Hemoglobin
Saturation
• Increases in temperature, H+, Pco2, and
BPG
– Modify structure of hemoglobin; decrease its
affinity for O2
– Occur in systemic capillaries
– Enhance O2 unloading from blood
– Shift O2-hemoglobin dissociation curve to right
• Decreases in these factors shift curve to
left
– Decreases oxygen unloading from blood
© 2013 Pearson Education, Inc.
Percent O2 saturation of hemoglobin
Figure 22.21 Effect of temperature, PCO2, and blood pH on the oxygen-hemoglobin dissociation curve.
100
10ºC
20ºC
80
38ºC
43ºC
60
40
Normal body
temperature
20
0
Percent O2 saturation of hemoglobin
(a)
100
Decreased carbon dioxide
(PCO2 20 mm Hg) or H+ (pH 7.6)
80
Normal arterial
carbon dioxide
(PCO2 40 mm Hg)
or H+ (pH 7.4)
60
40
Increased carbon dioxide
(PCO2 80 mm Hg)
or H+ (pH 7.2)
20
0
20
40
60
80
PO (mm Hg)
2
© 2013 Pearson Education, Inc.
(b)
100
Factors that Increase Release of O2 by
Hemoglobin
• As cells metabolize glucose and use O2
– Pco2 and H+ increase in capillary blood
– Declining blood pH and increasing Pco2
• Bohr effect - Hb-O2 bond weakens oxygen
unloading where needed most
– Heat production increases directly and
indirectly decreases Hb affinity for O2
increased oxygen unloading to active tissues
© 2013 Pearson Education, Inc.
Homeostatic Imbalance
• Hypoxia
– Inadequate O2 delivery to tissues cyanosis
– Anemic hypoxia–too few RBCs; abnormal or too little
Hb
– Ischemic hypoxia–impaired/blocked circulation
– Histotoxic hypoxia–cells unable to use O2, as in
metabolic poisons
– Hypoxemic hypoxia–abnormal ventilation;
pulmonary disease
– Carbon monoxide poisoning–especially from fire;
200X greater affinity for Hb than oxygen
© 2013 Pearson Education, Inc.
CO2 Transport
• CO2 transported in blood in three forms
– 7 to 10% dissolved in plasma
– 20% bound to globin of hemoglobin
(carbaminohemoglobin)
– 70% transported as bicarbonate ions
(HCO3–) in plasma
© 2013 Pearson Education, Inc.
Transport and Exchange of CO2
• CO2 combines with water to form carbonic
acid (H2CO3), which quickly dissociates
• Occurs primarily in RBCs, where carbonic
anhydrase reversibly and rapidly
catalyzes reaction
© 2013 Pearson Education, Inc.
Transport and Exchange of CO2
• In systemic capillaries
– HCO3– quickly diffuses from RBCs into
plasma
• Chloride shift occurs
– Outrush of HCO3– from RBCs balanced as Cl– moves
into RBCs from plasma
© 2013 Pearson Education, Inc.
Figure 22.22a Transport and exchange of CO2 and O2.
Tissue cell
Interstitial fluid
(dissolved in plasma)
Slow
Binds to
plasma
proteins
Fast
Chloride
shift
(in) via
transport
protein
Carbonic
anhydrase
(Carbaminohemoglobin)
Red blood cell
(dissolved in plasma)
Oxygen release and carbon dioxide pickup at the tissues
© 2013 Pearson Education, Inc.
Blood plasma
Transport and Exchange of CO2
• In pulmonary capillaries
– HCO3– moves into RBCs (while Cl- move out);
binds with H+ to form H2CO3
– H2CO3 split by carbonic anhydrase into CO2
and water
– CO2 diffuses into alveoli
© 2013 Pearson Education, Inc.
Figure 22.22b Transport and exchange of CO2 and O2.
Alveolus
Fused basement membranes
(dissolved in plasma)
Slow
Chloride
shift
(out) via
transport
protein
Fast
Carbonic
anhydrase
(Carbaminohemoglobin)
Red blood cell
(dissolved in plasma)
Oxygen pickup and carbon dioxide release in the lungs
© 2013 Pearson Education, Inc.
Blood plasma
Haldane Effect
• Amount of CO2 transported affected by
Po2
– Reduced hemoglobin (less oxygen saturation)
forms carbaminohemoglobin and buffers H+
more easily
– Lower Po2 and hemoglobin saturation with O2;
more CO2 carried in blood
• Encourages CO2 exchange in tissues and
lungs
© 2013 Pearson Education, Inc.
Haldane Effect
• At tissues, as more CO2 enters blood
– More oxygen dissociates from hemoglobin
(Bohr effect)
– As HbO2 releases O2, it more readily forms
bonds with CO2 to form carbaminohemoglobin
© 2013 Pearson Education, Inc.
Influence of CO2 on Blood pH
• Carbonic acid–bicarbonate buffer
system–resists changes in blood pH
– If H+ concentration in blood rises, excess H+ is
removed by combining with HCO3– H2CO3
– If H+ concentration begins to drop, H2CO3
dissociates, releasing H+
– HCO3– is alkaline reserve of carbonic acidbicarbonate buffer system
© 2013 Pearson Education, Inc.
Influence of CO2 on Blood pH
• Changes in respiratory rate and depth
affect blood pH
– Slow, shallow breathing increased CO2 in
blood drop in pH
– Rapid, deep breathing decreased CO2 in
blood rise in pH
• Changes in ventilation can adjust pH when
disturbed by metabolic factors
© 2013 Pearson Education, Inc.
Control of Respiration
• Involves higher brain centers,
chemoreceptors, and other reflexes
• Neural controls
– Neurons in reticular formation of medulla and
pons
– Clustered neurons in medulla important
• Ventral respiratory group
• Dorsal respiratory group
© 2013 Pearson Education, Inc.
Medullary Respiratory Centers
• Ventral respiratory group (VRG)
– Rhythm-generating and integrative center
– Sets eupnea (12–15 breaths/minute)
• Normal respiratory rate and rhythm
– Its inspiratory neurons excite inspiratory
muscles via phrenic (diaphragm) and
intercostal nerves (external intercostals)
– Expiratory neurons inhibit inspiratory neurons
© 2013 Pearson Education, Inc.
Medullary Respiratory Centers
• Dorsal respiratory group (DRG)
– Near root of cranial nerve IX
– Integrates input from peripheral stretch and
chemoreceptors; sends information VRG
© 2013 Pearson Education, Inc.
Figure 22.23 Locations of respiratory centers and their postulated connections.
Pons
Medulla
Pontine respiratory centers
interact with medullary
respiratory centers to smooth
the respiratory pattern.
Ventral respiratory group (VRG)
contains rhythm generators
whose output drives respiration.
Pons
Medulla
Dorsal respiratory group (DRG)
integrates peripheral sensory
input and modifies the rhythms
generated by the VRG.
To inspiratory
muscles
External
intercostal
muscles
Diaphragm
© 2013 Pearson Education, Inc.
Pontine Respiratory Centers
• Influence and modify activity of VRG
• Smooth out transition between inspiration
and expiration and vice versa
• Transmit impulses to VRG modify and
fine-tune breathing rhythms during
vocalization, sleep, exercise
© 2013 Pearson Education, Inc.
Generation of the Respiratory Rhythm
• Not well understood
• One hypothesis
– Pacemaker neurons with intrinsic rhythmicity
• Most widely accepted hypothesis
– Reciprocal inhibition of two sets of
interconnected pacemaker neurons in
medulla that generate rhythm
© 2013 Pearson Education, Inc.
Factors influencing Breathing Rate and
Depth
• Depth determined by how actively
respiratory center stimulates respiratory
muscles
• Rate determined by how long inspiratory
center active
• Both modified in response to changing
body demands
– Most important are changing levels of CO2,
O2, and H+
– Sensed by central and peripheral
chemoreceptors
© 2013 Pearson Education, Inc.
Chemical Factors
• Influence of Pco2 (most potent; most closely
controlled)
– If blood Pco2 levels rise (hypercapnia), CO2
accumulates in brain
– CO2 in brain hydrated carbonic acid dissociates,
releasing H+ pH drops
– H+ stimulates central chemoreceptors of brain stem
– Chemoreceptors synapse with respiratory regulatory
centers increased depth and rate of breathing
lower blood Pco2 pH rises
© 2013 Pearson Education, Inc.
Figure 22.25 Changes in PCO2 and blood pH regulate ventilation by a negative feedback mechanism.
Arterial PCO2
PCO2 decreases pH
in brain extracellular
fluid (ECF)
Central chemoreceptors in
brain stem respond to H+
in brain ECF (mediate
70% of the CO2 response)
Peripheral chemoreceptors
in carotid and aortic bodies
(mediate 30% of the CO2
response)
Afferent impulses
Medullary
respiratory centers
Efferent impulses
Respiratory muscle
Ventilation
(more CO2 exhaled)
Arterial PCO2 and pH
return to normal
Initial stimulus
Physiological response
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Result
Depth and Rate of Breathing
• Hyperventilation—increased depth and
rate of breathing that exceeds body's need
to remove CO2
– decreased blood CO2 levels (hypocapnia)
• cerebral vasoconstriction and cerebral ischemia
dizziness, fainting
• Apnea–breathing cessation; may be due
to abnormally low Pco2
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Chemical Factors
• Influence of Po2
– Peripheral chemoreceptors in aortic and
carotid bodies–arterial O2 level sensors
• When excited, cause respiratory centers to
increase ventilation
– Declining Po2 normally slight effect on
ventilation
• Huge O2 reservoir bound to Hb
• Requires substantial drop in arterial Po2 (to 60 mm
Hg) to stimulate increased ventilation
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Figure 22.26 Location and innervation of the peripheral chemoreceptors in the carotid and aortic bodies.
Brain
Sensory nerve fiber in cranial nerve IX
(pharyngeal branch of glossopharyngeal)
External carotid artery
Internal carotid artery
Carotid body
Common carotid artery
Cranial nerve X (vagus nerve)
Sensory nerve fiber in cranial nerve X
Aortic bodies in aortic arch
Aorta
Heart
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Chemical Factors
• Influence of arterial pH
– Can modify respiratory rate and rhythm even
if CO2 and O2 levels normal
– Mediated by peripheral chemoreceptors
– Decreased pH may reflect
• CO2 retention; accumulation of lactic acid; excess
ketone bodies
– Respiratory system controls attempt to raise
pH by increasing respiratory rate and depth
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Summary of Chemical Factors
• Rising CO2 levels most powerful
respiratory stimulant
• Normally blood Po2 affects breathing only
indirectly by influencing peripheral
chemoreceptor sensitivity to changes in
Pco2
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Summary of Chemical Factors
• When arterial Po2 falls below 60 mm Hg, it
becomes major stimulus for respiration
(via peripheral chemoreceptors)
• Changes in arterial pH resulting from CO2
retention or metabolic factors act indirectly
through peripheral chemoreceptors
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Influence of Higher Brain Centers
• Hypothalamic controls act through limbic
system to modify rate and depth of respiration
– Example-breath holding that occurs in anger or
gasping with pain
• Rise in body temperature increases respiratory
rate
• Cortical controls—direct signals from cerebral
motor cortex that bypass medullary controls
– Example-voluntary breath holding
• Brain stem reinstates breathing when blood CO2 critical
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Pulmonary Irritant Reflexes
• Receptors in bronchioles respond to
irritants
– Communicate with respiratory centers via
vagal nerve afferents
• Promote reflexive constriction of air
passages
• Same irritant cough in trachea or
bronchi; sneeze in nasal cavity
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Inflation Reflex
• Hering-Breuer Reflex (inflation reflex)
– Stretch receptors in pleurae and airways
stimulated by lung inflation
• Inhibitory signals to medullary respiratory centers
end inhalation and allow expiration
• Acts as protective response more than normal
regulatory mechanism
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Figure 22.24 Neural and chemical influences on brain stem respiratory centers.
Higher brain centers
(cerebral cortex—voluntary
control over breathing)
+
–
Other receptors (e.g., pain)
and emotional stimuli acting
through the hypothalamus
+
–
Peripheral
chemoreceptors
Respiratory centers
(medulla and pons)
+
+
Central
chemoreceptors
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Stretch receptors
in lungs
–
+
Receptors in
muscles and joints
–
Irritant
receptors
Respiratory Adjustments: Exercise
• Adjustments geared to both intensity and
duration of exercise
• Hyperpnea
– Increased ventilation (10 to 20 fold) in
response to metabolic needs
• Pco2, Po2, and pH remain surprisingly
constant during exercise
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Respiratory Adjustments: Exercise
• Three neural factors cause increase in
ventilation as exercise begins
– Psychological stimuli—anticipation of exercise
– Simultaneous cortical motor activation of
skeletal muscles and respiratory centers
– Excitatory impulses to respiratory centers
from proprioceptors in moving muscles,
tendons, joints
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Respiratory Adjustments: Exercise
• Ventilation declines suddenly as exercise
ends because the three neural factors shut
off
• Gradual decline to baseline because of
decline in CO2 flow after exercise ends
• Exercise anaerobic respiration lactic
acid
– Not from poor respiratory function; from
insufficient cardiac output or skeletal muscle
inability to increase oxygen uptake
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Respiratory Adjustments: High Altitude
• Quick travel to altitudes above 2400
meters (8000 feet) may symptoms of
acute mountain sickness (AMS)
– Atmospheric pressure and Po2 levels lower
– Headaches, shortness of breath, nausea, and
dizziness
– In severe cases, lethal cerebral and
pulmonary edema
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Acclimatization to High Altitude
• Acclimatization—respiratory and
hematopoietic adjustments to long-term
move to high altitude
– Chemoreceptors become more responsive to
Pco2 when Po2 declines
– Substantial decline in Po2 directly stimulates
peripheral chemoreceptors
– Result—minute ventilation increases and
stabilizes in few days to 2–3 L/min higher than
at sea level
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Acclimatization to High Altitude
• Always lower-than-normal Hb saturation
levels
– Less O2 available
• Decline in blood O2 stimulates kidneys to
accelerate production of EPO
• RBC numbers increase slowly to provide
long-term compensation
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Homeostatic Imbalances
• Chronic obstructive pulmonary disease
(COPD)
– Exemplified by chronic bronchitis and
emphysema
– Irreversible decrease in ability to force air out
of lungs
– Other common features
•
•
•
•
History of smoking in 80% of patients
Dyspnea - labored breathing ("air hunger")
Coughing and frequent pulmonary infections
Most develop respiratory failure (hypoventilation)
accompanied by respiratory acidosis, hypoxemia
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Homeostatic Imbalance
• Emphysema
– Permanent enlargement of alveoli; destruction
of alveolar walls; decreased lung elasticity
• Accessory muscles necessary for breathing
– exhaustion from energy usage
• Hyperinflation flattened diaphragm reduced
ventilation efficiency
• Damaged pulmonary capillaries enlarged right
ventricle
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Homeostatic Imbalance
• Chronic bronchitis
– Inhaled irritants chronic excessive mucus
– Inflamed and fibrosed lower respiratory
passageways
– Obstructed airways
– Impaired lung ventilation and gas exchange
– Frequent pulmonary infections
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Homeostatic Imbalance
• COPD symptoms and treatment
– Strength of innate respiratory drive different
symptoms in patients
• "Pink puffers"–thin; near-normal blood gases
• "Blue bloaters"–stocky, hypoxic
– Treated with bronchodilators, corticosteroids,
oxygen, sometimes surgery
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Figure 22.27 The pathogenesis of COPD.
• Tobacco smoke
• Air pollution
Continual bronchial
irritation and inflammation
Chronic bronchitis
• Excess mucus production
• Chronic productive cough
Breakdown of elastin in
connective tissue of lungs
Emphysema
• Destruction of alveolar
walls
• Loss of lung elasticity
• Airway obstruction
or air trapping
• Dyspnea
• Frequent infections
• Hypoventilation
• Hypoxemia
• Respiratory acidosis
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α-1 antitrypsin
deficiency
Homeostatic Imbalances
• Asthma–reversible COPD
– Characterized by coughing, dyspnea,
wheezing, and chest tightness
– Active inflammation of airways precedes
bronchospasms
– Airway inflammation is immune response
caused by release of interleukins, production
of IgE, and recruitment of inflammatory cells
– Airways thickened with inflammatory exudate
magnify effect of bronchospasms
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Homeostatic Imbalances
• Tuberculosis (TB)
– Infectious disease caused by bacterium
Mycobacterium tuberculosis
– Symptoms-fever, night sweats, weight loss,
racking cough, coughing up blood
– Treatment- 12-month course of antibiotics
• Are antibiotic resistant strains
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Homeostatic Imbalances
• Lung cancer
– Leading cause of cancer deaths in North America
– 90% of all cases result of smoking
– Three most common types
• Adenocarcinoma (~40% of cases) originates in peripheral
lung areas - bronchial glands, alveolar cells
• Squamous cell carcinoma (20–40% of cases) in bronchial
epithelium
• Small cell carcinoma (~20% of cases) contains lymphocytelike cells that originate in primary bronchi and subsequently
metastasize
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Homeostatic Imbalance
• Lung cancer
– Early detection key to survival
– Helical CT scan better than chest X ray
– Developing breath test of gold nanoparticles
– If no metastasis surgery to remove
diseased lung tissue
– If metastasis radiation and chemotherapy
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Homeostatic Imbalance
• Potential new therapies for lung cancer
– Antibodies targeting growth factors required
by tumor; or deliver toxic agents to tumor
– Cancer vaccines to stimulate immune system
– Gene therapy to replace defective genes
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Developmental Aspects
• Upper respiratory structures develop first
• Olfactory placodes invaginate into
olfactory pits ( nasal cavities) by fourth
week
• Laryngotracheal bud present by fifth
week
• Mucosae of bronchi and lung alveoli
present by eighth week
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Figure 22.28 Embryonic development of the respiratory system.
Future mouth
Pharynx
Eye
Frontonasal elevation
Foregut
Olfactory placode
Olfactory
placode
Esophagus
Stomodeum
(future mouth)
Laryngotracheal
bud
Trachea
Bronchial buds
4 weeks: anterior superficial view
of the embryo’s head
5 weeks: left lateral view of the developing lower
respiratory passageway mucosae
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Liver
Developmental Aspects
• By 28th week, premature baby can
breathe on its own
• During fetal life, lungs filled with fluid and
blood bypasses lungs
• Gas exchange takes place via placenta
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Homeostatic Imbalance
• Cystic fibrosis
– Most common lethal genetic disease in North
America
– Abnormal, viscous mucus clogs passageways
bacterial infections
• Affects lungs, pancreatic ducts, reproductive ducts
– Cause–abnormal gene for Cl- membrane
channel
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Homeostatic Imbalance
• Treatments for cystic fibrosis
– Mucus-dissolving drugs; manipulation to
loosen mucus; antibiotics
– Research into
• Introducing normal genes
• Prodding different protein Cl- channel
• Freeing patient's abnormal protein from ER to
Cl- channels
• Inhaling hypertonic saline to thin mucus
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Developmental Aspects
• At birth, respiratory centers activated,
alveoli inflate, and lungs begin to function
• Two weeks after birth before lungs fully
inflated
• Respiratory rate highest in newborns and
slows until adulthood
• Lungs continue to mature and more alveoli
formed until young adulthood
• Respiratory efficiency decreases in old
age
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