A&P 400 (respiratory system) Flashcards
repsiratory system
___
ppulmonary ventilationdefine
All of the structures involved in breathing (pulmonary ventilation) and external respiration
___
Pulmonary ventilation: airflow to/from the lungs
external respiration define
External respiration: gas exchange between the lungs and pulmonary circulation
respiration also inveolves
Respiration also involves internal respiration
internal respriation deinfe
gas exchange between systemic circulation and the tissues
respiraiton overview
…
homeostasis requires
a steady supply of O2
and constant elimination of CO2
Disruption?
= oxygen starvation & waste buildup
= rapid cell death
which 2 systems work together to make sure that our cells don’t die
respiratory system provides for gas exchange
cardiovascular system transports the respiratory gases
functions of repiratory system
1) external respiration,
2) ventilation,
3) protection (of air),
4) sound prodution,
5)smell/olfactory
extensive SA for gas exchange
move air from exchange surface of lungs along respiratory passageways
protecting respiratory surfaces from dehydration, temperature change, invasion of pathogens
produce sounds for speaking, singing, and other forms of communication
detecting odors via olfactory receptors in the superior portion of the nasal cavity
respiratory tract consists of
Nose
Pharynx
Larynx
Trachea
Bronchi
Bronchioles
Alveoli
what is the respiratory tract
branching passageway that carries air to/from gas exchange surfaces of the lungs
2 divisions of respiratory tract
Conducting portion
Respiratory portion
conducting portion of respiratory tract
(functional division)
Nasal cavity to larger bronchioles
No gas exchange
respiratory portion
(respiratory portion)
Smallest bronchioles (respiratory bronchioles) to alveoli
Where gas exchange occurs
what is another way the respiratory tract can be categorized / termed?
Can also divide into the upper respiratory tract and lower respiratory tract
functionally terming —>
nose, pharynx, larynx, trachea, bronchi, bronchioles
======>conducting portion
WHEREAS
bronchioles –> alveoli
====== RESPIRATORY PORITON
whereas for lower/uppre rt —>
nose/pharynx - Upper RT
larynx, trachea, bronchi, bronchioles, alveoli,
==== LOWER RT
What are anaotmical structures OF UPPER RT
Nose
Nasal cavity
Paranasal sinuses
Pharynx
what are functions OF URT
Filters (e.g. hairs), warms, and humidifies incoming air
Protects delicate lower tract
Reabsorbs heat and water in outgoing air
LOWER RT –> structures
Larynx
Trachea
Bronchi
Bronchioles
Alveoli
functions of LRT
Conducts air to and from gas exchange surfaces
Respiratory epithelia
… varies depending on where in respiratory tract
1) Respiratory mucosa
Lines the nasal cavity and superior pharynx
Also lines the superior portion of the lower respiratory tract
—> larynx, trachea, bronchi, etc.
—> ciliated columnar with goblet cells (mucus secretion)
2) Stratified squamous epithelium
Lines inferior portions of pharynx
—> oropharnx and hypopharynx (laryngopharynx)
—> protect from abrasion during swallowing ingested food
WHY INFERIOR PORTION OF PHARYNX STRATIFIED SQUAMOUS????
B/c food passes here briefly
3) Simple cuboidal or simple columnar
Lines the smaller bronchioles
note ciliated cells?
trap pathogens, propel debris upward
what about where not ciliated?
macrophages
4) Simple squamous epithelium
Forms gas exchange surfaces
Distance between air and blood in capillaries is less than 1 µm
1) RESPIRATORY MUCOSA
whre?
what tpye of cells?
Respiratory mucosa lines nasal cavity through large bronchioles
Pseudostratified ciliated columnar epithelium with mucous cells
Lamina Propria
underlying areolar tissue
(LOOSE CT)
( underneath respiratory mucosa)
supports respiratory epithelium
mucous glands in trachea and bronchi
mucous cells (different from mucous glands?)
b/w the…
Pseudostratified ciliated columnar epithelium with mucous cells
THE MUCOCILIARY ESCALATOR
Flow of mucus/trapped debris (VIA CILIA)
Sticky mucus produced by mucous cell and MUCOUS GLANDS
Traps debris particles
Moved by beating cilia
where does mucociliary escalator sweep the mucous?
Swept toward pharynx
Swallowed (to acids in stomach) or coughed out
Epithelial stem cells replace damaged/old cells
Anatomy of URT
..
nose
Nose is primary route for air entering respiratory system
what is trhe visible portion of nose?
External nose is the portion you can see
what are external NARES
Nostrils or external nares
Paired openings into nasal cavity
what is the structure of the extenral nose
Bony and cartilaginous structures make up the framework of the external nose
bony framework of nose
Dorsum of nose
(bridge) formed by two nasal bones
Maxilla and frontal bones also contribute
Cartilaginous framework of the external nose
NASAL CARTILAGES:
small, elastic cartilages extending laterally from bridge; help keep nostrils open
I.e.
Septal cartilage
Lateral nasal cartilage
Alar cartilage
nasal cavity (BORDERS)
superior border
inferior border
medial border
lateral border
supeior border
Superior border: ethmoid bone
inferior borer
Inferior border: hard palate, made of palatine bones and palatine process of maxillae
medial border
Medial border: nasal septum
latearl border
Lateral border: ethmoid bone, maxillae, lacrimal bones, palatine bones, and inferior nasal conchae bones
The nasal cavity
…
majority of nasal cavity is
Majority lined with respiratory mucosa
what does the nasal cavity anteiroly merge with
anteriorly merges with the external nares
what does nasal cavity posteriorly communicate with?
posteriorly communicates with the NASOPHARYNX through the CHOANAE (AKA internal nares)
choanae etymology
The term is a latinization from the Greek χοάνη, “choanē” meaning funnel.
The choanae ( sg. : choana), posterior nasal apertures or internal nostrils are two openings found at the back of the nasal passage between the nasal cavity and the pharynx
SINGULAR CHOANA
NASAL VESTIBULE
nasal vestibule lined with course hairs for filtering large dust particles
” The area just inside the nostril (nose opening) that leads into the nasal cavity. The nasal vestibule is supported by the cartilage of the nose and is lined with tissue that contains short, coarse hairs.”
functional divison of nasal cavity
Respiratory Region
olfactory portion
Respiratory Region
Larger, inferior region of nasal cavity
Lined w non-keratinized pseudostratified ciliated columnar epithelium with many goblet cells (respiratory mucosa)
Olfactory Region
Smaller, superior region of nasal cavity
Olfactory receptors near superior nasal concha
Have cilia, but no goblet cells
what is respiratory region of nasal cavity lined with (WHAT CELL TYPE???)
NON_KERATINIZED pseudostratified ciliated columnar epithelium
(WITH MANY GOBLET CELLS)
—> I.e.
respiratory mucosa
structure sof nasal cavity
Nasal septum:
Divides right and left nasal cavities
nasal septum formed by
Septal cartilage
Vomer
Perpendicular plate of the ethmoid
structures of the nasal cavity (continued)
conchae and meatuses
Superior, middle, and inferior nasal conchae (bones)
Superior, middle, and inferior nasal meatuses
what is the purpose of meatuses
Passages between nasal conchae
Swirl incoming air to trap small particles
Moves odorants to olfactory receptors
Warms/humidifies air
WHAT ABOUT THE Paranasal sinuses
Frontal, ethmoid, maxillary, and sphenoidal sinuses
Open into nasal cavity
functions of paranasal sinuses
Mucus secreted by sinuses moisten nasal cavity
Resonate sound
Lighten skull
what are NASAL POLYPS (structures related to paranasal sinuses)
outgrowths of mucous membranes
usually found around openings to paranasal sinuses
(not necessarily normal? Can be symptomatic)
what are the NASOLACRIMAL DUCTS?
the LACRIMAL sac drains tears from the eyes
the nasolacrimal duct carries tears from thelacrimal sacof the eye into the nasal cavityNw
basal tears
Basal tears are in your eyes all the time to lubricate, nourish and protect your cornea. Basal tears act as a constant shield between the eye and the rest of the world, keeping dirt and debris away.
reflex tears
Reflex tears are formed when your eyes need to wash away harmful irritants, such as smoke, foreign bodies or onion fumes.
emotional tears
Emotional tears are produced in higher quantities than basal tears. They may be the same amount or more than reflex tears. Unlike, basal and reflex tears, emotional tears can be held back by the individual voluntarily, and they can stop when they want to.
three types of tears
We cry to protect our eyes, to wash out irritants and because, well, we are moved to tears.
“There are three types of tears:
basal tears,
emotional tears
and reflex tears,”
explains David Silverstone, M.D., a professor of ophthalmology at the Yale School of Medicine.
Epiphora
Epiphora is the medical definition for having excess tears or watery eyes.
It’s caused by your eyes producing too many tears, or the tears in your eyes not draining away as they should.
AND SO… what is the purpose of the NASOLACRIMAL DUCTS/system
The purpose of the nasolacrimal system is to drain tears from the ocular surface to the lacrimal sac and, ultimately, the nasal cavity.
what happens if the nasolacrimal ducts are not functioning properly
EPIPHORA
Blockage of the nasolacrimal system can cause tears to flow over the eyelid and down the cheek; this condition is epiphora.
Epiphora etymology
late 16th century (in epiphora (sense 2)): via Latin from Greek epi ‘upon’ + pherein ‘to bear or carry’.
And so… WHY DO YOU GET runny nose after crying (rhinorrhea?)
When you cry, tears come out of the tear glands under your eyelids and drain through the tear ducts that empty into your nose. Tears mix with mucus there and your nose runs.
I.e.
They go through the NasoLacrimal Ducts
why does lacrimation take place in response to emotions? (emotional tears)
your limbic system — the part of your brain that regulates emotions — sends a signal to your brain’s message system to activate your lacrimal glands to produce tears.
note about lamina propria
Lamina propria (basement membrane) of nasal cavity has extensive network of vessels
what functions take place in nasal cavity?
Release heat to warm inhaled air
Water from mucus evaporates to humidify inhaled air
as a result of heating mechanism in nasal cavity
Air moving from nasal cavity to lungs:
—-> Heated to almost body temperature
—-> Nearly saturated with water vapor
On the other hand…
during exhalation:
The reverse process occurs during exhalation
—> mucosa reabsorbs heat and water; reduces heat loss and water loss to environment
—> Releases air (with CO2) – taking as much heat/water from released air as possible
WHAT IS something that eliminates these benefits?
Mouth breathing eliminates these benefits
Let’s discuss the pharynx
…
what two systems is the pharynx a part of?
Pharynx is shared by respiratory and digestive systems
what is the colloquial term for the pharynx?
Colloquially referred to as the throat
describe the pharynx
5 inch muscular tube from CHOANA (internal nares?) to cricoid cartilage
what is the pharynx lined with?
Lined with respiratory mucosa
–> except oropharynx and hypopharynx (laryngopharynx) – lined w/ stratified squamous
what is the function of the pharynx?
passage for food and air
resonating chamber for speech
lymphatic tissue (tonsil) to prevent the entry to the body
—> entry?? pathogens? ?
tonsils
(NOTE MALT —> mucosa associated lymphatic tissue)
The tonsils are lymph nodes in the back of the mouth and top of the throat. They help to filter out bacteria and other germs to prevent infection in the body.
A bacterial or viral infection can cause tonsillitis.
Strep throat is a common cause.
three regions of pharynx
1) Nasopharynx
2) Oropharynx
3) Laryngopharynx
Nasopharynx
superior part of the pharynx
Lined with respiratory mucosa
possibly, the oropharynx is the region with
non-keratinized stratified squamous epithelium
yes
“The stratified squamous epithelium of the oropharynx is continuous with the laryngopharynx”
“Anteriorly, the laryngopharynx opens into the larynx; whereas, posteriorly, it enters the esophagus.”
boundaries of the nasopharynx
From choanae to soft palate
what is a unique struture contained by the NASOpharynx
Has pharyngeal openings of the auditory tubes (EUSTACHIAN tubes)
what is another unique structure contained by the nasopharynx
Contains adenoids (pharyngeal tonsils)
adenoid etymology
aden = gland
oid
adenoids define
Adenoids are a patch of tissue that is high up in the throat, just behind the nose.
They, along with the tonsils, are part of the lymphatic system.
The lymphatic system clears away infection and keeps body fluids in balance.
The adenoids and tonsils work by trapping germs coming in through the mouth and nose.
eustachian etmyology
The Eustachian tube is named after the Italian anatomist Bartolomeo Eustachio (also spelled Eustachi and known by the Latin name Bartholomaeus Eustachius) who lived circa 1510-1574.
function of eustachian tubes
The primary function of the Eustachian tube is to equalize air pressure between the atmosphere and the middle ear.
Yawning and swallowing cause contraction of the muscles connected to the Eustachian tube, enabling the tube to open to small amounts of air.
why does airpressure need to be equalized?
The equalizing of middle ear pressure is crucial to the proper workings of the eardrum.
With equalized air pressure, the eardrum can vibrate appropriately and transmit sound.
OROPHARYNX****
middle part of the pharynx behind oral cavity
Lined with non-keratinized stratified squamous epithelium
boundaries of oropharynx
From soft palate to base of the epiglottis
glottis vs epiglotttis
The glottis opens into the windpipe and is responsible for the production of sound.
While the epiglottis is a cartilaginous flap on top of the glottis that prevents the food from entering the larynx.
Laryngopharynx
inferior part of the pharynx
Lined with non-keratinized stratified squamous epithelium
(NOTED ABOVE)
laryngopharynx boundaries
From epiglottis to cricoid cartilage
Anatomy of LRT
…
LARYNX
Cartilaginous tube that surrounds/protects glottis (“voice box”)
Connects the pharynx with the trachea
—> Anterior to C4 – C6
note term
laryngeal skeleton
what are the three large cartilages that make up the larynx
1) Epiglottis
2) Thyroid Cartilage
3) Cricoid Cartilage
an important note
even though epiglottis and laryngopharynx are at the same level, they are different structures
epiglottis itself is part of larynx
however, the laryngopharynx is simply at the same level of the epiglottis
1) EPIGLOTTIS
projects superior to glottis, forms lid over it
During swallowing the larynx elevates, the epiglottis folds back over glottis, and blocks entry into respiratory tract
2) THYROID CARTILAGE
Prominent anterior surface is laryngeal prominence (Adam’s apple)
Thyrohyoid ligament attaches it to hyoid bone; other ligaments attach it to epiglottis and smaller cartilages (e.g. cricoid)
thyroid etymology
shield shaped
3) CRICOID ETYMOLOGY
Forms complete ring around larynx
With thyroid cartilage, protects glottis and larynx
provides attachment for laryngeal muscles/ligaments (muscles that control voice pitch, sound production, and so on)
cricoid etymoloy
ring-shaped
what is the landmark use for a treacheostomy?
Cricoid cartilage (directly above “)
what is a tracheostomy for?
A tracheostomy is a surgically created hole (stoma) in your windpipe (trachea) that provides an alternative airway for breathing
tracheotomy vs tracheostomy?
The term “tracheotomy” refers to the procedure to make an incision (cut) into the trachea (windpipe).
The temporary or permanent opening itself is called a “tracheostomy.”
However, the terms are sometimes used interchangeably.
why would a tracheotomy be necessary>
Medical conditions that make it necessary to use a breathing machine (ventilator) for an extended period, usually more than one or two weeks.
Medical conditions that block or narrow your airway, such as vocal cord paralysis or throat cancer.
Other catilage structures (three other minor cartilaginous structures of larynx)
Arytenoid cartilages (2)
Corniculate cartilages (2)
(elastic cartilage)
Cuneiform cartilages (2)
arytenoid catilages function
change position & tension of vocal cords via synovial joint w cricoid cartilage
cuneiform cartilages function
support vocal folds and lateral epiglottis
what is the glottis
where air passes through larynx
what does glottis consist of?
Made of VOCAL FOLDS
and RIMA GLOTTIDIS
(opening between folds)
glottis=
“the part of the larynx consisting of the vocal cords and the opening [Rima glottidis] between them. It affects voice modulation through expansion or contraction.”
rima define
a long narrow opening, esp between the vocal cords and the cartilages at the back of the larynx.
“Rima is Latin for a narrow cleft, crack or slit”
Vocal Folds
(Also known as the vocal cords)
VOCAL FOLDS = tissue folds that contain vocal ligaments
how are sound waves produced?
Vibration of VOCAL FOLDS produce sound waves
how are the vocal folds opened and closed?
Opened/closed by rotation of ARYTENOID cartilages
PHONATION define
Phonation = sound production from larynx
Vibration of vocal cords produces sound waves
ARTICULATION define
modification of sounds by tongue, teeth, and lips
where does amplification (part of articulation?) occur?
Amplification and resonance occur in pharynx, oral and nasal cavities, and paranasal sinuses
how do sound dynamics take place? and what role does larynx play in sound dynamics?
3 components:
producing sound
pitch
volume
1) Producing sound
bands of elastic ligaments stretched between laryngeal cartilages
muscles contract
= cartilages move
= pulls ligaments tight
= stretched vocal folds out into airway
= rima glottidis narrows
= air passes through folds and they vibrate
= sound
2) Pitch
Depends on tension of vocal folds
taut = rapid vibration = pitch
Androgens = thicker & longer vocal folds = lower pitch
3) Volume
Depends on the pressure of air
ventral, ventricular
late Middle English: from Latin ventriculus, diminutive of venter ‘belly’.
late Middle English: from Latin venter, ventr- ‘belly’ + -al.
ventricular folds of larynx
The ventricular folds, also known as the vestibular or false vocal folds are located above the true vocal folds and separated from them by the laryngeal ventricle
They are commonly referred as “false” vocal folds as they historically have been thought not to be directly involved in the production of “normal” voice.
ventricular folds funtion
aka false vocal cords
above true vocal cords
Space between = RIMA VESTIBULI
Useful for holding breath against thoracic cavity pressure
rima vestibuli vs rima glottidis
..
epithelium of larynx
depends on location:
1) superior to vocal fold
= non-keratinized stratified squamous epithelium (RECALL, UP TO CRICOID, LARYNGOPHARYNX IS STRATIFIED SQUAMOUS)
2) inferior to vocal fold
= pseudostratified ciliated columnar epithelium with goblet cells (respiratory mucosa)
THE PASSAGE OF AIR **
Trachea
—> Main Bronchi
—> Lobar Bronchi
—> Segmental Bronchi
—> Bronchioles
—> Terminal bronchioles to pulmonary lobules
passage of air via…
The trachea, bronchi, and bronchial branches convey air to and from lung gas exchange surfaces
trachea (windpipe) — at levels of…
Starts at C6 and ends at T5 by branching into bronchi
5 inches long
1 inch in diameter
esophagus vs trachea?
Lies in front of the esophagus
note the trachial cartilages
Has 15–20 C-shaped tracheal cartilages
what is function of tracheal cartilage?
Prevent collapse and overexpansion
allow esophagus to expand slightly into tracheal space
why does esophagus expand into trachea?
The hyaline cartilage in the tracheal wall provides support and keeps the trachea from collapsing.
The posterior soft tissue allows for expansion of the esophagus, which is immediately posterior to the trachea.
CARINA OF TRACHEA
ridge at the base of the trachea that separates the openings of the right and left main bronchi
carina define
a cartilage situated at the point where the trachea (windpipe) divides into the two bronchi.
etymology:
“keel”
note significant feature of structure/function of trachea (in the region of CARINA)
highly innervated mucosa
very sensitive cough reflex to prevent choking
—> prevent food/debris reaching bronchi
how are ends of c shaped tracheal catilages connected?
ELASTIC LIGAMENTS
as well as, TRACHEALIS (muscle)
what does contraction of trachealis do?
Contraction of trachealis narrows trachea; restricts airflow
why/when does tracheal diameter change?
Trachealis = how
why?
Tracheal diameter changes often, mostly controlled by sympathetic stimulation which increases airflow
note again tracheal cartilage shape/structure vs swallowing and esophagus
Tracheal cartilages are incomplete posteriorly allowing for expansion when swallowing
layers of mtrachea
mucosa
sub-mucosa
fibromuscular membrane
adventitia
1) mucosa (of trachea)
pseudostratified ciliated columnar epithelium with goblet cells (respiratory mucosa)
2) sub-mucosa (of trachea)
loose CT with seromucous glands
seromucous glands
release a mixture of mucus and antibacterial compounds. This mixture also serves to humidify and warm the air before it gets to the lungs.
3) fibromuscular membrane (with smooth muscle & elastic CT – INCLUDING TRACHEALIS mm)
(layers of trachea)
allow tracheal diameter change during inhalation/exhalation
4) adventitia (CT)
(layers of trachea)
binds trachea to other organs
Bronchi
..
main bronchi (s. bronchus)
aka primary bronchi
First division of bronchi
Right and left bronchus go into each lung
how do right and left main bronchi differ?
(Due to position of heart)
Right bronchus wider, at a steeper angle, and shorter than left
= foreign objects in trachea often go into it
why right/left bronchi different?
“The left lung has to accommodate the heart, which is positioned slightly towards the left side of the thoracic cavity. This anatomical arrangement causes the left bronchus to be more horizontal and curved to navigate around the heart.”
do bronchi have cartilaginous rings as well?
Have complete cartilaginous rings
note internal lining of bronchi
Lined with respiratory mucosa
Lobar Bronchi
(aka SECONDARY bronchi)
one lobar bronchi goes to each…
one goes to each lobe of the lung
(5 FIVE lobar bronchi)
—> 3 lobes on right
—> 2 lobes on left
(superior, middle, inferior lobes on right)
(superior, inferior lobes on left)
cartilage vs smooth muscle for lobar bronchi?
Smooth muscle encircles lumen and increasingly replaces cartilage
lobar bronchi internal lining
Also lined with respiratory mucosa
Segmental bronchi
(aka TERTIARY bronchi)
HOW MANY PER LUNG?
Each lung has approximately 10 segmental bronchi
what does each tertiary bronchus supply?
Each one supplies triangular shaped unit of lung
(BRONCHOPULMONARY segment)
bronchopulmonary segments
divisions of each LOBE
“A bronchopulmonary segment is a portion of lung supplied by a specific segmental bronchus and its vessels”
“These arteries branch from the pulmonary and bronchial arteries, and run together through the center of the segment.”
“Veins and lymphatic vessels drain along the edges of the segment.”
BRONCHIOLES
cartilage vs smooth muscle?
No cartilage; thick smooth muscle
what does HYALINE cartilage do for BRONCHI and TRACHEA
A layer of hyaline cartilage supporting the tracheal rings surrounds the submucosa.
The hyaline cartilage layer is sturdy but flexible and prevents the collapse of the trachea during expiration.
bronchioles – histology (LINED WITH…)
Ciliated simple columnar epithelium w goblet cells
& Ciliated simple cuboidal epithelium w/o goblet cells
(club cells or Clara cells)
recall:
simple cuboidal/columnar lines smaller bronchioles
Club cells (Clara cells)
Club cells, also known as bronchiolar exocrine cells,[1] are low columnar/cuboidal cells with short microvilli, found in the small airways (bronchioles) of the lungs.[2] They were formerly known as Clara cells.
broncholdilation
Sympathetic nervous system (NE/E) causes bronchodilation
—> increases airflow
bronchoconstriction
Parasympathetic nervous system causes bronchoconstriction
—> Decreases airflow
—> Histamine, asthma attack, allergies
extreme bronchoconstriciton
Extreme bronchoconstriction can occur during allergic reactions such as ASTHMA
lobes –> bronchopulmonary segments –> lobules
3 lobes (right lung)
+ 2 lobes (left lung)
= 5 lobes
right primary bronchus
= steep, wider, shorter
left primary bronchus
= angled, narrower, longer
(angled and longer to get around heart, narrower b/c less space)
In general, each lung has 10 segments
(TEN BRONCHOPULMONARY SEGMENTS)
Internally, each lobe further subdivides into hundreds of lobules.
bronchioles
—> TERMINAL BRONCHIOLES
—> Respiratory bronchioles
Bronchioles open into short segments called terminal bronchioles, which are thin-walled branches of the bronchioles.
Terminal bronchioles transition into respiratory bronchioles.
Respiratory bronchioles are lined by two types of epithelial cells:
(SAME AS bronchioles)
—> ciliated columnar cells and club cells (also known as Clara cells)
___NOTE THAT CLASS NOTES SAY THAT TERMINAL BRONCHI HAVE NON-CILIATED cells –> macrophage action instead
what do terminal—>respiratory bronchioles lead to?
Terminal bronchioles lead to PULMONARY LOBULES (for gas exchange)
i.e.
one main bronchus per lung
2 + 3 lobar bronchi per lobe
10 segmental bronchi (on each side) per BRONCHOPULMONARY segment
then many terminal/respiratory bronchioles PER lobule
terminal bronchioles
Many terminal bronchioles
Each terminal/respiratory bronchiole supplies a pulmonary lobule
Smooth muscle (no cartilage) = airway patency vulnerable to muscle spasms
terminal bronchioles –> LINING (histology
Non-ciliated simple columnar epithelium
macrophages remove debris (no cilia to move mucous)
respiratory bronchioles…
(according to class notes)
Many, many respiratory bronchioles
Simple cuboidal & simple squamous epithelium
—> AGAIN DIFFERENT FROM ABOVE
(follow classnotes)
respiratory bronchioles are…
First place where external respiration can occur, although limited
external vs internal repiration
Internal respiration occurs in the body tissues, where cells release carbon dioxide and take in oxygen from the blood.
External respiration occurs in the lungs or gills and occurs when the body takes in oxygen from the atmosphere and releases carbon dioxide.
review… (THE BRONCHIAL TREE)
Trachea: larynx to main bronchi in mediastinum
Main bronchi: one to each lung; cartilage rings are complete
Lobar bronchi: 3 in right lung, 2 in left; one per lobe
Segmental bronchi: branch to give rise to bronchioles
(one per bronchopulmonary segment)
Bronchioles
Terminal bronchioles
Respiratory bronchioles
review anatomy
Structural Division:
Upper Respiratory Tract
vs.
Lower Respiratory Tract
*
Functional Division:
Conducting Region
vs.
Respiratory Region
URT
nose, nasal cavity & pharynx
LRT
larynx, trachea, bronchi & lungs
Conducting region
nose, pharynx, larynx, trachea, bronchi, bronchioles, & terminal bronchioles
respiratory region (where gas exchange occurs)
respiratory bronchioles, alveolar ducts, alveolar sacs, & alveoli
gross anatomy of lungs
..
Each lung divided into lobes
Right lung (3): superior lobe, middle lobe, inferior lobe
Left lung (2): superior lobe and inferior lobe
(Each lobe has multiple bronchopulmonary segments)
—> 10 on right?
—> 9 on left?
right lung vs left lung
(SIZE)
Right lung is slightly shorter d/t liver
Left lung is 10% smaller d/t heart
how does lung form lobes?
DEEP FISSURES
Each lung is cone shaped and divided into lobes by deep fissures
right lung fissures
Right lung
horizontal fissure between superior/middle lobes;
oblique fissure between middle/inferior lobes
left lung fissures
oblique fissure between superior/inferior lobes
gross anatomy of lungs
(cone shaped)
Apex (tip) extends to superior border of first rib
Concave base rests on diaphragm
Cardiac notch—left lung; accommodates pericardium/heart
Root of lungs
dense connective tissue; fixes positions of bronchi, major nerves, blood vessels, and lymphatics
CONTAINS HILUM (?)
Hilum (of lungs)
medial depression on each lung
Allows passage of main bronchus, pulmonary vessels, nerves, lymphatics
hilum etymology
‘little thing, trifle’
“a depression or fissure where structures such as blood vessels and nerves enter an organ”
grooves on surface of lungs?
Grooves on surface of lungs mark positions of great vessels
PLEURA (p. plurae)
recall:
“Pleura, pericardium, and peritoneum are all examples of serous membranes.”
Visceral pleura
Parietal pleura
pleura are
serous membrane sacs surrounding the lungs
Visceral pleura
covers outer surfaces of lungs
Parietal pleura
covers inner surface of thoracic wall; extends over diaphragm and mediastinum
Pleural cavity
(same principle as pericardial cavity)
potential space between visceral and parietal layers of pleural sac
Contains pleural fluid that reduces friction of the lungs against the wall
Conditions involving the pleural cavity
(Any may cause partial or complete lung collapse)
Pneumothorax
Hemothorax
Hydrothorax
Empyema
Pneumothorax
pleural cavity fills with air
common cause is chest trauma
Hemothorax
pleural cavity fills with blood
Hydrothorax
collection of serous fluid
m/c cause is cardiac failure
pleural effusion
and
pericardial effusion
pericardial effusion —> cardiac tamponade (?)
pleural effusion —> hydrothorax
Empyema
em = in
puon = pus
Pus in the pleural cavity
m/c cause is pneumonia
partial or complete lung collapse (?)
Any may cause partial or complete lung collapse
=
Pneumothorax
Hemothorax
Hydrothorax
Empyema
lung collapse
“A collapsed lung occurs when air escapes from the lung. The air then fills the space outside of the lung between the lung and chest wall. This buildup of air puts pressure on the lung, so it cannot expand as much as it normally does when you take a breath. The medical name of this condition is pneumothorax.”
Pulmonary lobules contain:
A terminal bronchiole
Venule, arteriole, lymphatics, capillaries
Multiple alveolar sacs
pulmonary lobules are…
Pulmonary lobules are wrapped in elastic CT
(expand and return to original size when filled with air)
note
Each terminal bronchiole branches into multiple respiratory bronchioles
Respiratory bronchioles lead to
alveolar ducts,
which lead to alveolar sacs made of alveoli (sing. alveolus)
external respiration occurs in
respiratory bronchioles and alveoli
Pulmonary alveoli
~150 million alveoli (singular, alveolus) per lung; give lungs an open, spongy appearance
Surrounded by extensive capillary network for gas exchange
pulmonary alveoli – surrounded by
Surrounded by elastic fibers—expansion/recoil aids air movement
Each alveolar duct ends in clusters of alveoli (alveolar sacs, or alveolar saccules)
alveolar sacs vs lobules
A primary pulmonary lobule is defined as the lung unit distal to the respiratory bronchioles. It is significantly smaller than an acinus, and is composed of alveolar ducts, alveolar sacs and alveoli.
Alveolar epithelium
(Three major cell types)
Type 1 Pneumocytes
Type 2 Pneumocytes
Roaming alveolar macrophages
Type 1 Pneumocytes
simple squamous epithelium
thin, delicate, sites of gas diffusion
Type 2 Pneumocytes
produce surfactant: oily secretion; reduces surface tension of water in alveoli to prevent collapse
Roaming alveolar macrophages
locate and phagocytize particles that could clog the alveoli
Blood air barrier
where gas exchange occurs between blood and alveolar air
aka alveolar–capillary membrane or respiratory membrane
three layers of blood-air-barrier
1) Alveolar cell layer (epithelium)
2) Fused basement membranes (alveolar and capillary)
3) Capillary endothelium
Blood air barrier…
Minimal distance separating air and blood (average ~0.5 µm) allows for rapid diffusion
Large total surface area (70 - 100 m2 ) also allows for a large amount of diffusion
CLASS TWO
….
pulmonary ventilation (breahting)
air movement in/out of lungs
Maintains ALVEOLAR VENTILATION
–> air movement in/out of alveoli
respiraiton
Two integrated processes: EXTERNAL respiration and INTERNAL respiration
external respiration
exchange of gases between blood, lungs, and external environment
gas diffusion occurs across BLOOD AIR BARRIER between alveolar air and alveolar capillaries
INTERNAL RESPIRATION
occurs between blood and tissues
Absorption of oxygen from blood into tissues
Release of carbon dioxide by tissue cells into blood
respiration vs ventilaiton
Respiration and ventilation are two different things. Ventilation is mechanical and involves the movement of air. Respiration is physiologic and involves the exchange of gases in the alveoli (external respiration) and in the cells (internal respiration).
how do abnormalities affecting external respiration affect internal respiration?
Abnormalities affecting external respiration affect gas concentrations in interstitial fluids and cellular activities
hypoxia
Hypoxia = low tissue oxygen levels
Severely limits metabolic activities
anoxia
Anoxia = no oxygen supply
Much of damage caused by heart attacks and strokes is the result of localized anoxia
physiology of pulmonary respiration
..
Pressure
Molecules in a gas bounce around independently
When contained, collisions with container wall cause pressure
More collisions = higher pressure
Boyle’s law and pressure
Boyle’s law
= More collisions occur when molecules are in smaller container
= Pressure is inversely related to volume (P = 1/V)
I.e.
Decreased volume = more collisions = higher pressure
Increased volume = less collisions = lower pressure
Pressure and diffusion
diffusion:
the net movement of molecules from an area of greater concentration to an area of lesser concentration
I.e.
Molecules move down their concentration gradient
**
Likeiwse with pressure:
—> Gases will move from an area of high pressure to low pressure
—> Gases will move down their pressure gradient
what is direciton of air into or out of lungs determined by?
Atmospheric pressure and intrapulmonary pressure
Atmospheric pressure is the pressure of air around us
Intrapulmonary pressure is the pressure inside respiratory tract, usually measured at the alveoli
where is intrapulmonary pressure measured?
@ ALVEOLI
therefore, pulmonary ventilation is determined by
Pulmonary ventilation involves changing volume of the thoracic cavity
which structures alter the shape and space in the thoracic cavity?
Movements of the DIAPHRAGM and RIB CAGE (E.g. levator costarum)
—> change the volume of the thoracic cavity, which expands or compresses the lungs (changes lung volume)
Change in volume = change in pressure (Boyle’s Law)
the steps involved in pulmonary ventilation
Start of a breath
During inhalation
During exhalation
(Volume and Pressure Changes During Pulmonary Ventilation)
Start of a breath
Pressures inside and outside thorax are identical; no air movement
Expanding thoracic cavity expands lungs:
(DIAPHRAGM contracts, increases space in lungs –> also note action of levator costarum and other mm.)
what happens when thoracic cavity expands
Parietal pleura attached to thoracic wall; visceral pleura to lungs
Pleural fluid forms bond between layers d/t surface tension
DURING INHALATION
Thoracic cavity enlarges
Increased volume causes decreased pressure
Pressure inside lungs drops below atmospheric pressure (Poutside > Pinside)
Air moves into lungs from an area of high pressure to low pressure
DURING EXHALATION
Thoracic cavity decreases in volume
Decreased volume causes increased pressure
Pressure inside lungs increases above atmospheric pressure (Poutside < Pinside)
Air is forced out of the lungs from an area of high pressure to low pressure
in other words, during inhalation intrapulmonary pressure is…
negative
Negative intrapulmonary pressure pulls air into lungs
—> Intrapulmonary pressure < atmospheric pressure
and during exhalation, intrapulmonary pressure is
POSITIVE
Positive intrapulmonary pressure pushes air out of lungs
Intrapulmonary pressure > atmospheric pressure
respiratory muscles
May be involved with inhalation (inspiratory muscles) or exhalation (expiratory muscles
breathing can either be
quiet or forced
quiet breathing
Quiet breathing is normal breathing
forced breathing
Forced breathing is laboured breathing
quiet breahting occurs via
Active inhalation via primary inspiratory muscles
Passive exhalation via elastic recoil of tissues, not by muscle action
what about forced breathing
Force breathing requires accessory respiratory muscles
I.e.
requires contribution from all repsiratory muscles (?)
–> also, exhalation is no longer passive
inspiratory muscles
primary vs accessory inspiratory uscles
primary inspiratory muscles
Primary inspiratory muscles used for quiet inhalation
ACCESSORY inspiratory muscles
used for forced inhalation
primary inspiratory mm
Diaphragm
external intercostals
what is the ratio/percentage of contribution of diaphragm vs external intercostals (PRIMARY inspiratory muscles)
Diaphragm does ~75 % of movement
—> Flattens floor of thoracic cavity
External intercostals do ~25 % of movement
—> elevate ribs and pull out
Note now the ACCESSORY inspiratory muscles (during forced inhalation)
Sternocleidomastoid
Scalenes
Pectoralis minor
Serratus anterior
what exactly do the accessory inspiratory muscles do?
Increase speed/amount of rib movement to move more air when needed (tissue oxygen demands not met by primary inspiratory muscles)
In other words,
when you are very active, your regular “QUIET” inspiration is not providing adequate oxygen to tissue
—> forced inhalation is required to create greater speed/amount of rib movement to generate greater pressure difference, to let more air into the lungs, more quickly
expiratory muscles
There are no primary (“quiet”) expiratory muscles
Quiet exhalation is a passive process done by elastic recoil
during quiet exhalation
Diaphragm relaxes
—> dome moves superiorly
External intercostals relax
—> ribs move down
Passive elastic recoil caused by:
—> stretched elastic fibres
—> inward pull of surface tension from alveolar fluid (??)
inward pull of surface tension from alveolar fluid
??
accessory expiratory mm
Internal intercostals
—> depress ribs (?)
transversus thoracis
—> depress ribs (?)
external oblique, internal oblique,
rectus abdominis
what do abdominal muscles do during forced exhalation
Abdominal muscles push diaphragm upward
—> possibly via decreased abdominal cavity volume pushing organs against diaphragm (?)
Decrease thoracic cavity volume quickly
Allow greater pressure change and faster airflow out of lungs
FACTORS AFFECTING PULMONARY VENTIATION
Surface Tension
Compliance
Airway Resistance
1) Surface tension
Water molecules attracted to each other more strongly than to air molecules
—> “this is why soap bubbles collapse inward and burst” (?)
Thin layer of alveolar fluid coats luminal surface of alveoli
—> Responsible for 2/3 of elastic recoil of lungs
—> Must be overcome during each inhalation
Surfactant (from type 2 pneumocytes)
—> reduces surface tension below simple water
what substance is responsible for reducing surface tension in lungs?
Surfactant (from type 2 pneumocytes)
when is surfactant first produced in developing fetus?
Surfactant is not produced until 24th – 28th week of development
Note (N)RDS
Recall:
premature infants have decreased surfactant
= ^ surface tension = alveoli collapse = great effort to open alveoli with each inhalation
This leads to something called RDS (respiratory distress syndrome)
Tx of (N)RDS
Tx: intubation, ventilation, artificial surfactant
2) COMPLIANCE (factors affecting pulmonary ventilation)
Compliance = the ability of the lungs and chest wall to expand
what happens during increased compliance
lungs & chest wall expands easily
elastic stretches easily and elastic recoil is not strong making exhalation more difficult
Seen with some OBSTRUCTIVE LUNG DISEASES
—> Like EMPHYSEMA
increased lung compliance – emphysema
Compliance is increased in obstructive lung disease like pulmonary emphysema, less in asthma and at a minor degree in chronic bronchitis.
In emphysema, the elastic recoil is decreased (as a result of increased compliance – or rather, decreased elastic recoil CAUSES increased compliance) and the P-V curve is shifted up and left. This is due to the loss of elastic tissue as a result of alveolar wall destruction.
What about decreased compliance
lungs & chest wall difficult to expand
This is restrictive lung disease
–> Pulmonary fibrosis (asbestosis, TB, etc.)
–> Pneumothorax
–> Pleural effusion
–> Chest wall injury or trauma
–> Scoliosis
–> Respiratory distress syndrome (RDS)
–> Obesity and pregnancy
restrictive lung diseases
Restrictive lung diseases - fibrosis and interstitial lung disease: In interstitial lung diseases, the lung and/or chest wall compliance has become decreased. Therefore there is an increased tendency for the lungs to collapse.
why is INCREAESD compliance causing OBSTRUCTIVE lung disease
decreased elastic recoil means that air is no exiting as effectively
–> I.e. it is obstructing continued passage/cycling of air
why is decreased compliance related to RESTRICTIVE lung disease?
low compliance means there is restriction of tissue to even let air in to begin with.
In other words, even if recoil mechanism is intact in itself, the fibrosed tissue of lungs simply don’t expand to begin with
3) AIRWAY RESISTANCE (factors affecting pulmonary ventilation)
..
airway resistance is
the resistance of the respiratory tract to airflow during inhalation and exhalation
under normal circumstances, during inhalation & exhalation, what happens to the resistance within the bronchioles?
d/t pressures:
—> Bronchioles expand during inhalation = decreased resistance
—> Bronchioles narrow during exhalation = increased resistance
which type of lung diseases are characterized by INCREASED airway resistance?
Obstructive lung diseases
E.g.
Asthma
Chronic Obstructive Pulmonary Disease (COPD)
—> Chronic bronchitis
—> Emphysema
a final review of restrictive lung disease definition
Restrictive lung diseases include diseases that make it hard for the lungs to expand and fill with air (low compliance)
final review of obstructive lung disease definition
Obstructive lung diseases include disease that make it hard for people to expel air from the lungs (increased resistance)
—> increased airway resistance
—> increased compliance / reduced recoil
**
EXTRA:
WHY DOES COPD (e.g. chronic bronchitis) INCREASE AIRWAY RESISTANCE?
—> Expiratory flow limitation is a key characteristic in chronic obstructive pulmonary disease (COPD). Increased airway resistance occurs due to bronchoconstriction, destruction of elastic tissue in the airways, and mucus hypersecretion from goblet cells caused by irritation of the epithelium.
ALSO:
“More severe degrees of emphysema resulted in a marked increase in total airway resistance due almost entirely to the increase in the peripheral airway component.”
(?????)
E.g. obstructive lung disease
Chronic Obstructive Pulmonary Disease (COPD)
E.g.
-> Chronic bronchitis
-> Emphysema
Asthma
Again – examples of RLD
Pulmonary fibrosis (asbestosis, TB, etc.)
Pneumothorax
Pleural effusion
Chest wall injury or trauma
Scoliosis
Respiratory distress syndrome (RDS)
Obesity and pregnancy
again – OLD e.g.
COPD (Chronic bronchitis, Emphysema)
Asthma
COPD is
General term for progressive disorder of the airways that restricts airflow and reduces alveolar ventilation
which two types of COPD frequently occur together?
Chronic bronchitis
+
Emphysema
Chronic bronchitis
Long-term inflammation and swelling of bronchial lining; leads to overproduction of mucus
Frequent cough, lots of sputum can clog airways, increasing resistance, reduced efficiency
—> INCREASED AIRWAY RESISTANCE
Cigarette smoking most common cause
—> Also other environmental irritants
Emphysema
Chronic, progressive condition
Alveolar walls are damaged
—> Loss of elastic tissues increases compliance
Loss of respiratory surface area restricts oxygen absorption (shortness of breath, intolerance of physical exertion
Strongly linked with CIGARETTE smoking
note pattern
emphysema increases 2) COMPLIANCE
chronic bronchitis 3) INCREASES AIRWAY RESISTANCE
—> both contribute to the OBSTRUCTIVE nature of the lung disease
ASthma
aka asthma bronchitis
Characterized by conducting passageways that are extremely sensitive to irritation
Airways respond by constricting smooth muscles along bronchial tree, edema/swelling of mucosa, increased mucus
Breathing difficult; resistance markedly increased
triggers of asthma
Triggers include allergies, toxins, exercise
Breathing patterns
..
Eupnea
normal variation in breathing rate and depth (12 to 18 breaths per minute)
Apnea
temporal cessation of breath (sleep apnea)
a-
-pnoe
dyspnea
painful, difficult, or laboured breathing (shortness of breath, SOB)
Tachypnea
rapid breathing rate (> 20 breaths per minute)
bradypnea
Bradypnea is a symptom in which your breathing rate is lower than expected for your age and activity level.
costal breathing
upward & outward movement of chest during contraction of intercostals
diaphragmatic breathing
abdomen moving outward when contracting diaphragm
(b/c contraction of diaphragm reduces volume of abdominal cavity while increasing volume of thoracic cavity
modified breathing patterns
..
coughing
deep inspiration, closure of rima glottidis & strong expiration blasts air out to clear respiratory passages
sneezing
muscles of expiration spasmodically contract, pushing air out of nose and mouth
hiccupping
spasmodic contraction of diaphragm & quick closure of rima glottidis produce sharp inspiratory sound
yawning
significant amount of inhaled air followed by quick exhalation
valsalve (maneuver)
forced expiration against closed rima glottidis
(increases abdominal pressure)
sobbing
many convulsive inhalations (where rima glottidis prematurely closes, letting in only a little air) & a long exhalation
lung volumes and pulmonary function tests
..
lung volumes
..
how are respiratory voluesm measured?
SPIROMETER
spiro- = breath
what shows the results of spirometer?
spirogram
What is Spirogram? Spirogram is the graphical record of lung capacities and lung volumes using a spirometer.
which groups are lung volume larger generally?
males
taller people
younger people
terms related to lung volume
tidal volume
inspiratory reserve volume
expiratory reserve volume
residual volume
minimal volume
tidal volume
Amount of air moved in or out of lungs during single respiratory cycle at rest (normal quiet breathing)
Averages 500 mL
what percentage of tidal volume actually reaches respiratory zone?
(I.e. zone where gas exchange can actually take place)
70% reaches respiratory zone for external respiration (350ml)
30-35% remains in conducting airways = anatomic (respiratory) dead space (150ml)
anatomic (respiratory) dead space
Dead space is the volume of air that is inhaled that does not take part in the gas exchange,
because it either remains in the conducting airways or reaches alveoli that are not perfused or poorly perfused.
It means that not all the air in each breath is available for the exchange of oxygen and carbon dioxide.
inspiratory reserve volume
Amount of air you can breathe in beyond tidal volume
(with forced inspiration)
expiratory reserve volume
Amount of air you can exhale beyond tidal volume (after normal (quiet?) exhalation)
(forced exhalation (?))
residual volume
Amount of air left in lungs after maximal exhalation (1200 mL)
presumably after forced exhalation
minimal volume
Amount of air in the lungs if they were allowed to collapse
Included in residual volume
Cannot be measured in a healthy person
–> collapsed lung is medical emergency
lung capacities
..
lung capacities can not be
Lung capacities cannot be measured directly but are calculated by taking sum of various respiratory volumes
terms related to lung capacities
inspiratory capacity
vital capacity
functional residual capacity
total lung capacity
inspiratory capacity
VT + IRV
tidal volume + inspiratory reserve volume
—> I.e. volume of air with forced INHALATION
“Amount of air you can inhale after normal exhalation” (??)
vital capacity
ERV + VT + IRV
expiratory reserve volume + tidal volume + inspiratory reserve volume
I.e.
“Maximum amount of air you can move in or out of lungs per cycle”
functional residual capacity
ERV + residual volume
I.e.
Amount of air remaining in lungs after complete quiet cycle
total lung capacity
Vital capacity + residual volume
Total volume of lungs
total lung capacity in male vs female
Averages 6000 mL in adult males, 4200 mL in adult females
Pulmonary function test
(PFT)
Pulmonary function tests (PFT) measure volume, capacities, and rates of flow
Force Vital Capacity (FVC) (test)
measures how much air you can forcibly exhale after taking a deep breath
Forced expiratory volume (FEV) (test)
This is the amount of air expired during the first, second, and third seconds of the FVC test (FEV1, FEV2, FEV3)
Forced expiratory flow (FEF) (test)
This is the average rate of flow during the middle half of the FVC test
Peak expiratory flow rate (PEFR) (test)
This is the fastest rate that you can force air out of your lungs
effects of aging and smoking on lungs
..
respiratory function vs age
All aspects of respiratory function decrease with age
As elastic tissue deteriorates, vital capacity decreases
Arthritis stiffens rib joints, reducing compliance and maximum respiratory minute volume
(features of) emphysema is normal for…
Some degree of (features of) emphysema is normal for people over age 50
Extent varies widely with exposure to cigarette smoke and other irritants
Respiratory function declines more with more years of smoking
Lung cancer
aggressive class of malignancies
Derived from epithelial cells in conducting passages, mucous glands, alveoli
when are SSx of lung cancer present?
Signs/symptoms often not present until tumors restrict airflow or compress adjacent structures
—> Chest pain, shortness of breath, cough/wheeze, weight loss
which cancer causes most deaths per year
lung cancer
Causes more deaths per year than any other type of cancer
how often is lung cancer as a result of cigarette smoking
85–90 percent of lung cancer cases are direct result of cigarette smoking
what effect does smoking have on lung tissue
..
cigarette smoke contains
Cigarette smoke contains several carcinogens (cancer-causing agents)
what do mucous and cilia do in normal respiratory epithelium?
Mucus and cilia in normal respiratory epithelium clean inhaled air
what do carcinogens do?
Irritants/carcinogens in smoke cause progressive series of changes in the epithelium
dysplasia
Cells damaged, and functional characteristics change
Cilia damaged and paralyzed—causes local buildup of mucus
Epithelium becomes
less effective at
protecting deeper,
delicate parts of
respiratory tract
Metaplasia
Tissue changes structure
Stressed respiratory surface converts to stratified epithelium
—> Protects underlying layers but not deeper parts of tract
—> May be reversed if stimulus is removed
before further damage
neoplasia and anaplasia
Neoplasia: Growth of abnormal cells forms a cancerous tumor (neoplasm)
Anaplasia: most dangerous stage
—> loss of differentiation/specialization of cells
—> Cells become malignant and metastasize to other parts of body
is dysplasia reversible?
yes
is metaplasia reversible?
yes
is neoplasia and anaplasia reversible?
no (?)
DAY 3
….
Gas laws
principles that govern the movement and diffusion of gas molecules
Boyle’s law (gas law)
(P1V1=P2V2)
Pressure and volume have an inverse relationship
determines direction of air movement during pulmonary ventilation
____ is a mixture of gases
the atmosphere
total atmoshpere pressure at sea level
760 mm Hg
what is PARTIAL PRESSURE
Partial pressure (P) = pressure exerted by single gas in a mixture
Dalton’s law
All the partial pressures of gases added together equal the total pressure exerted by the gas mixture
where else does Dlaton’s law apply?
also applies to gas in the respiratory tract
what varibale changes gas mixture
LOCATION ( in respiratory tract)
Gas mixture inside respiratory tract varies by location
air when inhaled (location)
Inhaled air gets moistened and warmed
air in alveoli (lcation)
In alveoli, it mixes with air remaining from previous breath
what about exhaled air (location)
Exhaled air mixes with air in anatomic dead space
how does (changing) gas mixture affect partial pressures of (changing) components?
As gas mixture varies, so do the partial pressures of its component gases
Henry’s law
At a given temperature, the amount of a particular gas in solution is directly proportional to the partial pressure of that gas above the liquid
(*Also dependent on the solubility that gas in the solution)
“Henry’s law is a gas law that states that the amount of dissolved gas in a liquid is directly proportional to its partial pressure above the liquid.”
HENRY’S LAW AND BREATHING:
“The main application of Henry’s law in respiratory physiology is to predict how gasses will dissolve in the alveoli and bloodstream during gas exchange. The amount of oxygen that dissolves into the bloodstream is directly proportional to the partial pressure of oxygen in alveolar air.”
External respiration & pressure
..
blood in pulmonary capillaries
Blood arriving in pulmonary capillaries has lower PO2 and higher PCO2 than in alveolar air
—> Oxygen has been used in the tissues
—> Carbon dioxide has been created in the tissues and released in the blood
Diffusion between alveolar gas and pulmonary capillaries:
Increases blood PO2 (oxygen enters blood)
Decreases PCO2 (carbon dioxide leaves blood)
respiratory gas movement –> diffusion?
The actual exchange of gases occurs due to simple diffusion.
“Gas exchange during respiration occurs primarily through diffusion. Diffusion is a process in which transport is driven by a concentration gradient. Gas molecules move from a region of high concentration to a region of low concentration.”
Internal respiration & presure
..
what happens to PO2 of blood leaving lungs (via pulmonary veins)
PO2 of blood leaving lungs in pulmonary veins DROPS SLIGHTLY***** when it mixes with blood from capillaries around conducting passageways;
still higher than PO2 of interstitial fluid
Oxygen diffuses to interstitial fluid
PCO2 in tissues (internal respiration)
PCO2 higher in tissues/interstitial fluid than in blood
Carbon dioxide diffuses from tissues into blood
What do we do with the oxygen transferred into cells?
cellular respiration
= using oxygen inside the cell to create ATP
Gas transport in blood
..
Oxygen transport in blood
—> Each 100 mL of blood leaving alveoli carries ____
~20 mL oxygen
what percentage/amount of O2 is dissolved in plasma? (when transported in blood)
Only ~0.3 mL (1.5 percent) is dissolved in the plasma
what about the remaining 98.5%
Remaining 19.7 mL (98.5 percent) is bound to
is bound to IRON IONS in heme units of hemoglobin (Hb)
Each hemoglobin molecule is made of four
globular proteins
each globular protein with
with one heme unit
each heme unit
iron ion
Thus, how many O2 molecules can each Hb molecule hold?
4 heme units
4 molecules of O2
what is oxyhemoglobin? (HbO2)
a bright red substance formed by the combination of hemoglobin with oxygen, present in oxygenated blood.
why is carbon monoxide dangerous?
Carbon monoxide (CO) is dangerous because it also bind to heme units, making them unavailable for O2 transport
—> HIGHER AFFINITY FOR HEME UNITS —> harder to get off
Hemoglobin saturation
Percentage of heme units containing bound oxygen at any moment
Oxygen-hemoglobin saturation curve
graph showing hemoglobin saturation at different partial pressures of oxygen
WHAT DOES SHAPE OF oxygen-hemoglobin saturation curve REPRESENT??
Shape reflects hemoglobin’s increased affinity for oxygen with each oxygen molecule bound
—> Increases steeply until it plateaus near saturation
—> Hemoglobin is > 90 percent saturated with oxygen when PO2 is above 60 mm Hg
what is saturatin of hemoglobin in blood when entering SYSTEMIC CIRCUIT
~97 % saturated
PO2 is 95 mm Hg
Hb saturation of blood LEAVING tissues
Hemoglobin in blood leaving body tissues is ~75 % saturated
PO2 is 40 mm Hg
WHAT ABOUT BLOOD IN ACTIVE (SKELETAL) MM?
—> what is the Hb saturation like?
Hemoglobin in blood in active muscle is only ~20 % saturated
Large amounts of oxygen being released to tissue
PO2 is only ~15–20 mm Hg
how is Hb saturation measured?
why is it measured?
measured to determine respiratory function
measured using a PULSE OXIMETER
pulse oximeter deifne?
an oximeter that measures the proportion of oxygenated hemoglobin in the blood in pulsating vessels ********Ie»»»»> ARTERIES,
especially the capillaries of the finger or ear.
what is ideal hemoglobin saturaiton?
An ideal hemoglobin saturation or SpO2 is between 96% and 99%
—> recall this measurement is from arteries —> not veins
what Hb saturaitons (from oxygenated blood) is problematic?
An SpO2 of 90-95% requires investigation
An SpO2 of 80-89% requires urgent medical treatment
An SpO2 of < 80% is potentially fatal
SpO2 ????
Serum Pressure = Sp
Shifting the oxygen-hemoglobin saturation curve
A shift in the curve represents a change in the affinity for O2
a shift to the right (red curve) means oxygen is being more easily released from hemoglobin
a shift to the right (blue curve) means oxygen is more tightly bound to hemoglobin
WHAT IS SHIFT IN O2-Hb Saturation curve caused by?
1) pH changes
2) temperature changes
3) changes in the partial pressure of CO2 (PCO2)
4) changes in the concentration of 2,3-bisphosphoglycerate (B P G)
1) Blood pH and shift in O2-Hb Saturation curve
..
via which EFFECT does blood pH affect O2-Hb saturation curve?
via BOHR EFFECT
bohr effect
H+ binds to hemoglobin & alters it, decreasing the Hb affinity for O2
pH decreases (ACIDIC): saturation curve shifts to the right
(lower affinity)
pH increases (BASIC): saturation curve shifts to the left
(higher affinity)
2) TEMPERATURE vs O2-Hb saturation curve
Higher temperature leads Hb to release oxygen more readily (lower affinity)
Especially important in
active tissues
(generate heat)
3) PCO2 vs O2-Hb Saturation curve?
Increased PCO2 will shift the curve to the right
(DECREASED AFFINITY)
NOTE THAT 1) & 3) actually enhance one another –> interdependeant
recall that increase in CO2 causes decrease in pH —> both subsequently LOWER the affinity for O2
consider that 2) is ALSO closely related to 1) & 3)
In ohter words, all three are interdependent in a way
—> pH, temperature, CO2
I.e. INCREASE in metabolism
==== INCREASE in temperature (e.g. exercise)
+ increase in CO2
—> DECREASE in pH
ALL = DECREASE IN O2 AFFINITY
FETAL HEMOGLOBIN
…
fetal Hb structure
slightly different structure compared to adult Hb
fetal Hb affinity for O2 compared to adult Hb
It has a higher affinity for O2 (a left shift)
what is the function of higher affinity for O2 in fetal Hb?
This higher affinity allow fetal RBCs to pull more oxygen from the mother as it binds it more strongly
how much more O2 does featl Hb carrry compared to adult Hb?
Carries up to 30% more oxygen compared to adult hemoglobin
note again – carbon monoxide
Has a higher affinity for Hb than O2 (200x higher than O2)
Therefore, even small concentrations of CO decreases O2 carrying capacity
carbon monoxide poisoning and HYPOXIA — SSx
headache,
dizziness,
weakness,
nausea,
vomiting,
chest pain,
confusion
Carbon Dioxide transport
..
where is CO2 genreated?
in peripheral tissues
how is CO2 generated?
Carbon dioxide is generated by AEROBIC metabolism
whre does CO2 need to go?
needs to be transported to the lungs for removal
how is CO2 transpotrted in bloodstream?
THREEE WAYS&&&&&
1) Dissolved in plasma (~7 %, limited solubility in plasma)
2) Bound to hemoglobin in RBCs (~23 %)
—> Resulting compound is carbaminohemoglobin (HbCO2)
3) Converted to bicarbonate ion, HCO3− (~70 %)
carbaminohemoglobin
This carbaminohemoglobin is formed by the reaction between carbon dioxide and an amino (-NH2) residue from the globin molecule,
a compound of hemoglobin and carbon dioxide, and is one of the forms in which carbon dioxide exists in the blood.
what happens to majority of CO2 in blood ????
(70%)
Converted to bicarbonate ion, HCO3− (~70 %)
BICARBONATE BUFFER SYSTEM
(in response to rise in pH)
CO2 + H2O
—-> H2CO3 (hydrogen donor = acid)
—-> H+ + HCO3-
—-> HCO3- goes to kidneys
(in response to fall in pH)
HCO3- + H+
—-> H2CO3
—-> CO2 + H2O
—-> CO2 goes to lungs
note agian conversion of CO2 to CARBONIC ACID (H2CO3)
(i.e. CO2 + H2O)
Most carbon dioxide entering blood (~70 %) converts to carbonic acid (then Bicarbonate ion)
WHICH*** ENZYME causes conversion of CO2 + H2O into CARBONIC ACID?
CARBONIC ANHYDRASE
carbonic anhydrase
Carbonic anhydrases (CAs) catalyze a reaction fundamental for life: the bidirectional conversion of carbon dioxide (CO2) and water (H2O) into bicarbonate (HCO3−) and protons (H+)
anhydrase
anhydrous + -ase
what then happens to cabronic acid?
dissociates into bicarbonate and hydrogen ions
H2CO3 ↔ HCO3– + H+
and what about bicarbonate (HCO3-) ions?
Bicarbonate ions (HCO3–) exchanged (leave cell) for an extracellular chloride ion (Cl–)
WHERE DOES HYDROGEN ION GO
(AFTER CARBONIC ACID BECOMES HCO3- + H+)
Hydrogen ion (H+) binds to Hb, forming HbH+
Why (?)
—> Hb molecules function as pH buffers
CHLORIDE SHIFT
PROCESS WHERE Bicarbonate ions (HCO3–) exchanged (leave cell) for an extracellular chloride ion (Cl–)
where does bicarbonate ion go?
pissed out if excessive
As long as renal function is maintained, excess bicarbonate is excreted in the urine fairly rapidly.
so again, H2O + CO2 —> H2CO3 —> H+ & HCO3-
—> WHAT HAPPENS TO H+ ??
—> WHAT HAPPENS TO HCO3- ??
H+ binds to Hb —> HbH+ (Hb acting as a pH buffer)
HCO3- leaves cell via CHLORIDE SHIFT (Chloride ion enters RBC, HCO3- leaves cell)
—> pissed out if excess
HALDANE EFFECT ???
Deoxygenation of blood increases its ability to carry CO2
Conversely, oxygenated blood has a reduced capacity to carry CO2
This helps RBCs exchange CO2 for O2 in the lungs (external respiration) and exchange O2 for CO2 in the tissues (internal respiration)
Haldane effect (wiiepdia)
The Haldane effect is a property of hemoglobin first described by John Scott Haldane, within which oxygenation of blood in the lungs displaces carbon dioxide from hemoglobin, increasing the removal of carbon dioxide. Consequently, oxygenated blood has a reduced affinity for carbon dioxide.
so let’s review form the start (THE (3) WAYS OF CO2 tranpsort in blood)
—> When CO2 ENTERS from tissue
1) CO2 diffuses into bloodtream
2) 93% diffuses into RBC
3) 7% DISSOLVES in plasma
4) of the 93%, 23% binds to Hb (CARBAMINOHEMOGLOBIN = HbCO2)
5) the remaining 70% converted to CARBONIC ACID — via Carbonic anhydrase
6) the carbonic acid dissociates into H+ & bicarbonate ion (HCO3-) — This is done via bicarbonate buffer pathway
7) the H+ then binds to Hb (Hb acts as pH buffer)
8) the HCO3- leaves RBC (in exchange for Chloride ion entering) — done via process called CHLORIDE SHIFT
9) HCO3- is pissed out if excess
chloride shift
Chloride shift (also known as the Hamburger phenomenon or lineas phenomenon, named after Hartog Jakob Hamburger) is a process which occurs in a cardiovascular system and refers to the exchange of bicarbonate (HCO3−) and chloride (Cl−) across the membrane of red blood cells (RBCs).
gas exchange —> AT THE ALVEOLI
1) Hb + O2 (from alveoli)
2) HCO3- ENTERS RBC (REVERSE reaction)
—> HCO3- + H+ —> Carbonic acid (H2CO3)
3) H2CO3 —> CO2 +H2O
4) thus, CO2 DIFFUSES to alveoli and out lungs
—> Note that this reverse process is best to counter-act drop in pH (bicarbonate BUFFER pathway)
5) ADDITIONALLY, the carbaminohemoglobin releases the CO2
—> CO2 from HbCO2 is released out of lungs
RESPIRATORY CENTRES AND REGULATION
..
respiratory centre
..
where is the main component of automatic respiration located?
MEDULLA
which part of brain modifies signals of the medulla?
Spontaneous rhythmic discharge of MEDULLARY NEURON is modified by neurons in the PONS
medullary respiratory centre (consists of)
1) Dorsal respiratory group/inspiratory center (DRG)
2) Ventral respiratory group (VRG)
3) Pre-Botzinger Complex
Pontine respiratory group (consists of)
1) apneustic centres
2) Pneumotaxic centres
apneustic etymology
pneumotaxic etmyology
a- (un)
-pneustikos (breathing)
pneumo- (lung/breath)
-taxis (arrangement)
the medullary (lower) respiratory centre
Most basic control
what do pacemaker cells in the MEDULLA OBLONGATA effect* ??
Pacemaker cells in medulla oblongata generate cycles of contractions in DIAPHRAGM
the significance of respiratory rhythmicity and MEDULLARY centres
Paired respiratory rhythmicity centers establish pace of respiration by adjusting pacemaker cells and coordinating other respiratory muscles
Dorsal respiratory group (of Medullary respiratory centre)
Mainly concerned with inspiration
Inspiratory center of DRG controls lower motor neurons to primary (QUIET) inspiratory muscles (external intercostals, diaphragm)
—> intercostal nn to external intercostals
—> phrenic nn to diaphragm
During normal breathing, active for 2sec, inactive for 3sec
which group of medullary respiratory centre is responsibly for quiet (primary) inspiration ?
Dorsal respiratory group
how many seconds is DRG active, vs inactive
During normal breathing, active for 2sec, inactive for 3sec
what feedback causes DRG respones to vary?
Dorsal respiratory group varies response through input from:
—> Chemoreceptors detecting O2, Co2, and pH (via CO2) levels in blood/CSF
—> Baroreceptors that detect pressure/stretch monitor stretch of lung wall
2) VENTRAL respiratory group (VRG) of medullary respiratory centre)
Mainly associated with forced breathing
Functions only when breathing demands increase and accessory (SECONDARY) respiratory muscles are involved
WHAT activates VRG?
the DRG
—> via feedback that indicates loss of homeostasis that DRG can not resolve on its own (?)
3) Pre-Bӧtzinger complex in medulla (3rd component of MEDULLARY respiratory centre)
Rhythm maker that send input to DRG
Essential to all forms of breathing but poorly understood
WHAT ELSE DOES THE VRG control?
MUSCLES OF EXHALATION
—> (Accessory)
—> recall there are no primary exhalation mm
PONTINE RESPIRATORY GROUP
— what do??
IT MODIFIES **** (medulla nervous output)
Transmit nerve impulses to the DRG
Modifies the rhythm of breathing by adjusting nerve output from the medullary respiratory centers
what are the TWO NUCLEI in the pons
1) APNEUSTIC CENTRE
2) PNEUMOTAXIC CENTRES
1) apneustic centres
what do they do?
Promote inhalation by stimulating DRG
WHAT STRUCTURE GIVES FEEDBACK TO APNEUSTIC CENTRES?????
VAGUS NERVE
Degree of stimulation adjusted based on sensory information from the vagus nerve about lung inflation
2) PNEUMOTAXIC CENTRE
what do they do???
Inhibit apneustic centers
Promote passive or active exhalation
—> opposite to apneustic centres
ALSO – what does increased pneumotaxic output do??
shortens inhalation duration (= faster respiratory rate)
i.e. pneumotaxic either
INHIBITS INSP
or SHORTENS INSP
—> faster respiration**
pneumotaxic output —> WHAT ABOUT DECREASED RATE?
Decreased output slows pace and increases depth of respiration
pneumotaxic +++
faster breathing
pneumotaxic —
slower breathing
regulation of repsiratory centres
…***
what locations does feedback/input come from to regulate respiratory centers
1) Cerebral cortex (LANGUAGE, MEMORY, EMOTION, REASONING)
2) Hypothalamus (HUNGER/THIRST, SEX DRIVE, BP, TEMP, MOOD)
3) Limbic system (EMOTION, SEXUAL STIM, MEMORY)
4) Chemoreceptors
5) Baroreceptors (mechanoreceptors)
6) proprioceptors
1) cerebral cortex
voluntarily change or stop breathing
to keep out gases or water
what does incerasing PCO2 & H+ in blood do?
H2O + CO2 –> H2CO3 –> H+ & HCO3-
increasing PCO2 & H+ in blood strongly stimulates DRG and sends impulses down nerves to resume breathing
increasing PCO2 & H+ in blood strongly stimulates DRG and sends impulses down nerves to resume breathing
WHICH NERVES???
phrenic nerve
& intercostal nerves
i.e. if you hold your breath till you faint
if you hold your breath until you faint, you will then resume breathing
(intercostal and phrenic nerve reflex)
chemoreceptors
Central and peripheral chemoreceptors detect chemical changes in the blood/CSF
most important factor / chemoreceptor
Under normal conditions, PCO2 is the most important factor influencing respiration
what percentage rise of PCO2 in arteries doubles RESP RATE
Rise of only 10 percent in arterial PCO2 doubles respiratory rate
PO2 ?
PO2 levels have to drop below 60 mm Hg before triggering respiratory centers
CENTRAL CHEMORECEPTORS
Central chemoreceptors located in the medulla oblongata of CNS
function of central chemoreceptors?
monitor PCO2 and H+ in cerebrospinal fluid
PERIPHERAL CHEMORECEPTORS
Peripheral chemoreceptors are a part of PNS
—> monitor PCO2, PO2, & H+ in blood
location of periheral chemoceptors?
aortic bodies
carotid bodies
chemoceptors in aorta
aka aortic bodies
in wall of aortic arch close to aortic baroreceptors
aortic bodies via WHICH NERVE???
VAGUS NERVE (CNX)
chemoreceptors in carotid
aka carotid bodies
—> in wall of L/R common carotid arteries, close to carotid sinus baroreceptors
carotid bodies via WHICH NERVE???
part of glossopharyngeal nerve (CN IX)
HYPERCAPNIA
“too much”
kapnos = “smoke”
A slight increase in PCO2 (and thus H+) is called hypercapnia
hypercapnia mc d/t
hypoventiliation or obstructive diseases like COPD
what happens in response to hypercapnia
stimulates central and peripheral chemoreceptors
DRG activated, and hyperventilation occurs (rapid & deep breathing)
—> wasn’t DRG only concerned with quiet breathing (????)
—> perhaps b/c DRG stimulates VRG (which activates accessory breathing muscles)
—> Helps expel excess CO2
HYPOCAPNIA
A decrease in PCO2 (<40 mmHg) is called hypocapnia
Most commonly caused by hyperventilation (eg. anxiety)
what happens in response to HYPOCAPNIA
central & peripheral chemoreceptors not stimulated
no impulses sent to DRG
DRG sets its own pace until CO2 accumulates and PCO2 increased to 40 mmHg
what about in response to decrease in OXYGEN?
Hypoxia
A decrease in PO2 (100-50 mmHg)
peripheral chemoreceptors stimulated
DRG activated, inspiration occurs to bring in more O2
BAROCEPTORS (mechanoceptors)
HERING-BREUER REFLEX
detect lung expansion with stretch receptors (baroreceptors) in walls of bronchi & bronchioles
send inhibitory signal to DRG via vagus nerves (CN X)
activated when tidal volume > 1500ml (remember, TV = 500mL at rest)
—> Called the Hering-Breuer reflex
PROPERIOCEPTORS
Ventilation increases even before the need for O2 increases
proprioceptors of joints and muscles activate DRG
upper motor neurons in primary motor cortex also activate DRG
VARIATIONS IN VENTILATION & RESPIRATION DURING EXERCISE
..
Pulmonary ventilation adjusts to meet body’s changing oxygen needs
__
what varies?
__
respiratory rate
adult vs child average/resting rate
___
respiratory minute volume
___
as cardiac output increases
___
O2 diffusing capacity during exercise
___
NOTE INITIAL ABRUPT BREATHING INCREASE VIA NEURAL CHANGES
(perhaps even before increased activity)
___
VS.
gradual breathing increase with moderate exercise due to chemical & physical changes
..
___
Varies number of breaths/minute (respiratory rate)
and volume moved per breath (tidal volume—VT)
___
Respiratory rate (f)= Number of breaths/minute
Normal adult resting range: 12–18 breaths/minute
Average for children: 18–20 breaths/minute
___
Respiratory minute volume (VE) = Volume of air moved per minute
respiratory rate x tidal volume = RESPIRATORY MINUTE VOLUME
___
pulmonary perfusion increases
___
O2 diffusing capacity increased 3X the rate at rest (rate that O2 diffuses from alveolar air to blood)
—> d/t more pulmonary capillaries maximally perfused
___
1) Proprioception
2) limbic anticipation
3) primary motor cortex
___
1) decreased PO2
2) increased PCO2
3) increased temperature
