Respiratory System Flashcards
Thorax vs thoracic cavity
thorax = boney; includes thoracic cavity & intra-thoracic part of abdominal cavity
thoracic cavity = separated from abdominal cavity by diaphragm
Nasal cavity is b/w what structures
external nares & choanae
has respiratory & olfactory functions
Extent of diaphragm
T7 to T13
Innervation of diaphragm
phrenic nerve
from C5 & C6 ventral primary branches
Fiber direction for external intercostal muscles
caudoventral to craniodorsal
inspiratory
Fiber direction for internal intercostal muscles
caudodorsal to cranioventral’
expiratory
Accessory muscles of inspiration
serratus ventralis & dorsalis cranialis
scalenus
rectus thoracis
abdominals (help support trunk)
Accessory muscles of expiration
transversus thoracis
abdominals
What is the pleura
serous membrane lines thoracic cavity & covers lungs secretes fluid capillary action allows for smooth gliding of lungs against body wall
What is the pleural cavity
potential space b/w pleura
Costo-diaphragmatic recess
from pleura changing directions
lungs do not extend into this space
Line of pleural reflection
continous serous membrane makes an abrupt turn as it travels from he ribs (costal pleura) to the diaphragm (diaphragmatic pleura)
Auscultation triangle
diagonal line from tip of T5 to top of T11
ventral to epaxial muscles
caudal to thoracic limb
avoids heart & trapezius muscles (so that lungs can be heard)
Thoracentesis
needle into 7th to 10th intercostal spaces
must go cranial to ribs, not caudal (arteries & veins)
angle towards body wall to enter space
Clinical relevance of the line of pleural reflection for thoracocentesis
cranial to line = pleural cavity
caudal to line = peritoneal cavity
Type of epithelium for typical respiratory epithelium (TRE)
pseudostratified ciliated columnar epithelium w/ goblet cells
Cell junctions are affected by what
pathogens, autoimmune disease, & cancers
Tight junction
seal
Adherens
attachment (contact inhibition)
Desmosomes
lightly hold cells together
Hemidesmosome
holds cells lightly to basal lamina
Cell types in TRE
goblet, basal, ciliated, neuroendocrine, & brush
height & cell types of TRE change throughout dif regions
Goblet cells
no cilia
nuclei on basal surface
mucus produced & secreted towards apical surface
Basal cells
triangular/polyhedral shape
near basal lamina
contain desmosomes & hemidesmosomes
replace damaged cells
Ciliated cells
columnar
microvilli & vital organelles
escalator of mucus
Neuroendocrine cells
secrete pharmacologically active substances (calcitonin & hormones/chemicals)
diffuse endocrine system
granules face basal side to travel through blood
sense environment
involved in growth of respiratory sys cells
Brush cells
microvilli
sensory receptors for trigeminal nerve
Nasal vestibule is the transition from
skin to respiratory
external keratinized squamous epithelium (w/ or w/out hair) to non-keratinized & thin to cuboidal/ non-ciliated pseudostratified columnar epithelium
Glands, cartilage, & other present in nasal vestibule
serous & sweat glands
hyaline and/or elastic cartilage
nerves, blood vessels, & immune cells (propria submucosa)
Epithelium of caudal 2/3rd of nasal cavity proper (excluding olfactory region)
TRE
Function of nasal cavity
humidification & warming by thin walled veins & glands
Constriction of nasal cavity by
alpha-adrenergic stimulation via sympathetic nervous sys
Other features of nasal cavity
nerves
lymphatic nodules
P450 enzymes for detoxification
Olfactory region epithelium
high pseudostratified epithelium
Cells in olfactory region
olfactory, supporting, & basal
Olfactory cells
bipolar neuron (axon & dendrite) perikarya in basal zone dendrites extend into lumen to sample odorant molecules non-myelinated lamina propria
Supporting (sustentacular) cells
protective
glial-like
occluding/ tight junctions
oval-shaped nucleus is closest towards the lumen
microvilli
wider on apical side & narrower on basal side
anchored to neighboring cells via tight junctions
Basal cell
tight junction
regenerate olfactory cells/ neurons & support/ sustentacular cells
Glands in olfactory region & function
olfactory/ Bowman’s glands
propria submucosa
secrete watery secretion that enhances the solubility of the odorant molecule & cleanse the cilia, allowing for the re-use of receptors for the next odorant molecule to be sampled
Pigmentation of olfactory region
lipofuscin
Location of olfactory region
dorso-caudal portion of nasal cavity
includes parts of ethmoidal conchae, dorsal nasal meatus, & nasal septum
How to olfactory cells allow for the sense of smell
club-like dendritic bulb has 10-30 non-motile cilia that contain olfactory receptors
when an odorant molecule arrives at the site, secretions from the olfactory gland solubilize the odorant molecule, leading to an action potential & odor sensation
axons from olfactory cells reach olfactory bulb of brain & leave as non-myelinated nerve fibers through the cribriform plate of the ethmoid bone
Location of vomeronasal organ
ventral portion on both sides of nasal septum
What is the vomeronasal organ
blind-ended tubes w/ internal epithelial ducts, propria submucosa, & J-shaped hyaline cartilage
Vomeronasal organ opens where
in most species (not horses), incisive duct opens caudal to the upper central incisors
Epithelium of vomeronasal organ
medial side = neurosensory cells, sustentacular/support cells, basal cells, & vomeronasal glands
lateral side = pseudostratified ciliated or non-ciliated epithelium
Function of vomeronasal organ
chemoreceptors of liquid born substances
sexual behavior
maternal instinct
fetal interaction w/ amniotic fluid
Function of muco-ciliary escalator
beat in one direction (towards pharynx) to clear the mucus into the exterior (via sneezing/spitting) or into the GI tract (via swallowing)
Describe stroke of cilia
forward (power) stroke followed by a backward (recovery) stroke
No contact w/ mucus on recovery stroke
Energy from mitochondria
Damage to muco-ciliary escalator due to toxins or other defects results in
cilia unable to remove bacteria, allergens, & dust trapped in the mucus bilayer (gel & soluble layers)
Structure of muco-ciliary escalator
9 peripheral & 2 central microtubules
peripheral tubules held by nexin protein to prevent sliding & ensure unity
inner & outer dynein protein arms of the peripheral generate a sliding motion using ATP
Cause of primary ciliary dyskinesia
immotile ciliary syndrome or Kartagner syndrome
autosomal recessive genetic disorder -> defect in coding of the dynein protein
Result of primary ciliary dyskinesia
excessive mucus build up -> chronic respiratory & middle ear infections
sitrus inversus totalis
sitrus ambiguous or heterotaxy syndrome
reproductive failures
inner, outer, or both dynein arms affected
Diagnosis & treatment of primary ciliary dyskinesia
electron microscopy of nasal/ bronchial epithelium
no treatment, but remove from breeding
Horses are obligate nasal breathers w/ a long soft palate. What diseases commonly affect them
dorsal displacement of the soft palate, laryngeal hemiplegia, & pharyngeal collapse
Epithelium of nasopharynx & larynx
TRE excluding epiglottis & vocal folds
Lamina propria of nasopharynx & larynx has what
loose CT & seromucous glands
Epithelium of epiglottis
oral side & tip = stratified squamous epithelium (non-keratinized)
tracheal side = TRE
Glands & cartilage of epiglottis
no glands
elastic cartilage
Epithelium of vocal folds
stratified squamous epithelium (non-keratinized)
Glands & cartilage of epiglottis
none
Club cells/ bronchiolar exocrine cells
no cilia
secrete glycosaminoglycan
stem cell
metabolize xenobiotics
club cell secretory protein is a biomarker
contain tryptase & activate hemagglutinin of influenza A
Trachea epithelium
lumen lined w/ TRE & supported by c-shaped hyaline cartilaginous rings
Structure of trachea allows for what
semi-flexible & semi-collapsible tube
permits bending/ rotating of neck w/out affecting ventilation
Glands & cartilage of trachea
sero-mucous/ sub-mucosal glands
hyaline cartilage
Trachealis muscle & function w/ swallowing
smooth muscles
faces esophagus on dorsal side, allows for shape change of trachea when food passes through the esophagus
trachea can flatten & expel air when coughing
cartilage provides rigidity to prevent collapse
Tunica adventitia of trachea has
loose CT & longitudinal elastic fibers
Hyaline cartilage of trachea has
chondrocytes, matrix, & type II collagen fibers
Tracheal collapse
“goose honk” coughing
common in toy breeds
sound occurs primarily in expiration
50% collapse = 16x increase in airway resistance
Treatment of tracheal collapse
medical management is a temporary fix
surgical treatment w/ a stent is necessary
Epithelium of bronchi
TRE w/ goblet cells
Cartilage of bronchi
in pieces/ plates
Intra-pulmonary bronchi changes how
height decreases & glands become sparse
Bronchi & trachea smooth muscle comparison
bronchi has more
Bronchioles epithelium
simple columnar/ cuboidal epithelium (ciliated or non-ciliated)
+/- goblet cells
Smooth muscle of bronchioles
circular & oblique fascicles
Glands & cartilage of bronchioles
none
Functional blood
pulmonary trunk & left/right pulmonary veins
gas exchange
Nutritional blood
bronchial artery branches supply pulmonary lymph nodes, bronchi, & bronchioles w/ oxygenated blood
Smaller airways do not need nutritional blood b/c
do fine on just functional blood
Deoxygenated blood from the nutritional blood goes where
into pulmonary vein, mixing w/ oxygenated blood
Pulmonary art
thin
deoxygenated blood
low pressure
both internal & external elastic laminae
Bronchial art
thick
oxygenated blood
high pressure
only internal elastic laminae
Pulmonary vein
thin
only external elastic laminae
Pulmonary lymphatics
thin
valves
no erythrocytes
Pulmonary hypertension
may affect veins or arteries
results from inflammatory lung disease (asthma or COPD) that leads to thickening of the pulmonary artery branches
could occur from a left atrioventricular valve defect that backs blood into pulmonary veins
Terminal bronchiole is considered what portion
conducting portion
no alveoli or gas exchange
Epithelium of terminal bronchiole
simple cuboidal epithelium (ciliated or non-ciliated)
no goblet cells
Glands & cartilage of terminal bronchiole
none
Smooth muscle in terminal bronchioles
greatly reduced
directly below the lining epithelium
Respiratory bronchiole is considered what portion
respiratory portion or transitional zone
Epithelium of respiratory bronchiole
simple cuboidal epithelium (few ciliated)
no goblet cells
some alveoli
Type I alveolar epithelial cells
squamous cells only nuclei well seen cover 95% of alveolar area very thin blood-gas barrier tight junctions
Type II alveolar epithelial cells
large round cells/ cuboidal granular cover 5% of alveolar area mostly in corners of alveoli produce surfactant act as stem cells for Type I AEC
Pathological conditions like chronic inflammation may result in thickening of the respiratory membrane, leading to
decreased efficiency of gas diffusion
Alveolar macrophages are found where
in air spaces w/in alveoli
Function of alveolar macrophages
guard against invading pathogens & their products
Appearance of macrophages when they ingest foreign bodies (dust particles or bacterial products) or dead cells
foamy cytoplasm
may be due to the processing of internalized materials w/ the help of enzymes present in lysosomes
Are there other immune cells in the lungs except for alveolar macrophages
no, unless there is a danger signal (bacteria) -> neutrophils
Surfactant
contained is osmiophilic lamellar bodies
reduce surface tension
allow alveoli to stay open
Epithelium of pleura
simple squamous epithelium (mesothelium) w/ underlying CT & vessels
Pleuritis
may result in pain & affected individuals could sense gliding of their lungs against the body wall in the affected area
Respiration processes involve
ventilation (movement of air)
diffusion
transportation
tissue delivery & return
At higher elevations, how does amount of air & % composition change
amount of total air decreases
% composition stays the same
Air composition at a higher altitude may accentuate certain pathological conditions or physiological performances like
patient w/ lung disease moved to a higher elevation may not be able to perform strenuous activities & experience breathing difficulties
healthy human/animal may have sub-optimal performances when moved to a higher elevation w/ less O2
Upper respiratory tract includes
nares, nasal conchae, pharynx, larynx, trachea, & principle bronchi
Species w/ most & least pliable nostrils
horse - most
pig - least
Function of upper respiratory tract
conditions air
warms it to body temp
entraps inhaled substances in mucus
Nasal conchae (turbinate bones) function
create laminar (slow) slow help trap dust
Other accessory structures of upper respiratory tract
auditory tube, guttural pouches, vomeronasal organ, nasolacrimal duct, & paranasal sinuses
As airways branch, what happens
total cross-section area increases & resistance to flow decreases
Ventilation definition
process of inhaling & exhaling air to acquire O2 & expel CO2
Ventilation is dependent on
pressure differences b/w atmosphere & inside of thoracic cavity
Neg pressure ventilation
created by respiratory muscles
Expiration is usually passive, but can be affected by
pathological conditions like heaves or physiological conditions like strenuous exercise
requires aid of abdominal muscles
Pos pressure ventilation
created by O2 devices used when anesthetizing an animal
VE = VT * f
VE = total amount of air breathed per min VT = volume of each breath during normal breathing f = respiratory frequency; # of respiratory cycles per min
Dead space
no gas exchange
conducting portion
respiration wasted
Anatomic dead space
nostril, mouth, trachea, auditory tube, guttural pouches, & paranasal sinuses
Equipment dead space
endotracheal tube
Alveolar dead space
poor or no perfusion of alveoli
caused by hydrostatic pressure failure, embolus, emphysema, or pre-capillary constriction
Function of dead space
eliminates heat (panting in dogs)
Drawback of dead space
shallow & higher frequency breathing is not desired due to the increase in the amount of total ventilation wasted in the dead space
could lower the amount of effective gas reaching the alveoli
VEdot = VAdot + VDdot
VEdot = tidal volume per min VAdot = alveolar ventilation per min VDdot = dead space ventilation per min
Primary symbols
physical quantities to be measured
uppercase
Name these primary symbols:
P, V, S, F, Q, R, & D
P = pressure V = volume S = saturation w/ O2 F = fractional conc of gas Q = blood volume R = resistance D = diffusing capacity
Secondary symbols
indicated location of gas
Name these secondary symbols:
a, V, & A
a = arterial V = venous A = alveolar
Final symbol
refers to the gas being measured
Describe these symbol modifications:
dot above
bar secondary symbol
prime sign after secondary symbol
dot = quantity measured w/ respect to time
bar = mean or mixed sample
prime sign = end of a structure/ end of expiration or inspiration
Respiratory cycle
one inspiration & one expiration
except horses have two of each
Respiratory pattern waveform
smooth & symmetrical
Complementary breathing cycle (sigh)
deep rapid inspiration & expiration
not seen in horses
created using a breathing bag
Types of breathing
abdominal = most common (except during peritonitis) costal = rib movement (not during pleuritis)
Eupne
normal, quiet breathing
Dyspnea
difficulty breathing
Hyperpnea
increased depth & rate
Polypnea
rapid & shallow (panting)
Apnea
temporary cessation in breathing
Tachypnea
excessive rapidity of breathing
Bradypnea
abnormal slowness of breath
Respiratory frequency
# of respiratory cycles/min indicates health status of animal
What increases respiratory frequency
pregnancy, digestive tract fullness, lying down, & diseases
What decreases respiratory frequency
low temp & sleeping
Normal sound of lungs is due to
air movement through tracheobronchial tree (turbulent air flow)
Adventitious lung sounds are
extrinsic to normal breath sounds
Crackles
edema & exudates
Wheezes
airway narrowing
Lung volume
air w/in lung or breath
all are measured except residual volume (only assessed)
Tidal volume (VT)
volume of each breath
Inspiratory reserve volume (IRV)
extra volume that can still be inhaled after a normal breath (VT)
Expiratory reserve volume (ERV)
extra volume that can still be expired after a normal breath (VT)
Residual volume (RV)
amount of air remaining in lungs after most forceful expiration
Lung capacity
combination of volumes
all are inferred
Inspiratory capacity (IC)
VT + IRV
Functional residual capacity (FRC)
ERV + RV
Vital capacity (VC)
IRV + VT + ERV
Total lung capacity (TLC)
IRV + VT + ERV + RV
VC + RV
IRV + VT + FRC
FRC is affected by
position, sex, diseases, & body condition
only source of O2 during apnea
Ex of restrictive lung diseases & what they are characterized by
fibrosis, muscular diseases, sarcoidosis, & chest wall deformities
fibrotic processes in lung parenchyma -> restrictive inspiration
Volumes & capacities indicating restrictive lung disease
decreased VC, TLC, RV, & FRC
Ex of obstructive lung diseases & what they are characterized by
emphysema, chronic bronchitis, & asthma
inflammation of bronchioles & bronchiolar smooth muscle that contracts upon expiration -> restrictive expiration
Volumes & capacities indicating restrictive lung disease
decreased VC
increased TLC, RV, & FRC
Atmospheric pressure
760 mmHg at sea level
At higher elevations, why does atmospheric pressure decrease
less air
Gauge pressure
pressure measured against atmospheric pressure at a particular location
Absolute pressure
atmospheric pressure + gauge pressure
Dalton’s law
total pressure = sum of individual gases in a mixture
Boyle’s law
pressure & volume are inversely proportional
Charle’s law
w/ constant pressure, volume & temp are directly proportional
Moles law
at constant temp & pressure, volume of a sample of gas is directly proportional to the number of moles of gas in the sample
Ideal gas law
pressure is directly proportional to moles & temp of gas
pressure is inversely proportional to volume of gas
When PAW < PB, what happens
PAW = pressure w/in airways; PB = atmospheric pressure
air flows in until PAW = PB
When PAW > PB, what happens
PAW = pressure w/in airways; PB = atmospheric pressure
air flows out until PAW = PB
Breathing creates what pressure
neg pressure
A ventilator creates what pressure
pos pressure
Transpulmonary pressure gradient (PAW - Ppl) is important for what
(PAW = pressure w/in airways; Ppl = pressure in pleural cavity)
inspiration & expiration
if Ppl increases (ex: pneumonothorax), then lungs do not expand
Function of thin film of fluid in pleural cavity
allows pulmonary/visceral pleura & parietal pleurato have a vacuum-like seal but still be able to slide
How is neg pressure created in the pleural cavity
chest wall & alveoli try to recoil
What happens to intrapleural pressure & alveolar transmural pressure during inspiration
intrapleural: becomes more neg
alveolar transmural: increases
During inspiration, what do the alveoli do
expand so pressure w/in them decreases
air flows in until pressure w/in alveoli = atmospheric pressure
What happens to intrapleural pressure & alveolar transmural pressure during expiration
intrapleural: becomes less neg
alveolar transmural pressure: decreases
During expiration, what do the alveoli do
alveoli return to normal size by elastic recoil
air flows out until pressure w/in alveoli = atmospheric pressure
What aides in lung recoil
elastic & collagen fibers
surface tension of alveolar fluid lining/ air-fluid interface
When water molecules at the air-liquid interface pull towards each other to try to collapse the alveoli, what counteracts this
surfactant molecules cut the H bonds of water to nullify this effect due to surface tension
Law of LaPlace states that what feature of alveoli should be true if they have a smaller diamter
have high pressure & thus be likely to empty or burst into a larger alveoli
What keeps small alveoli from popping
surfactant molecules in a higher density compared to large alveoli, which helps to equalize the pressure
Describe alveolar interdependence
recoil effect of surrounding alveoli can pull the collapsing alveoli back to stabilize it
Alveolar interdependence is altered by what
emphysema since many alveoli are destroyed
Compliance
opposite of elasticity
What diseases affect compliance
emphysema: increases
fibrosis: decreases
Poiseulle’s law
resistance is directly proportional to viscosity of gas & length of airway
resistance is inversely proportional to pi*r^4
Compare pressure b/w pulmonary & systemic circulation
pulmonary < systemic
Why is it advantageous that the pulmonary system has a lower pressure
less work for the heart
thin blood-gas membrane/ alveolar respiratory membrane can be protected
lower chance of edema
Compare density of capillaries b/w pulmonary & systemic
pulmonary has a dense capillary network around alveoli
Describe pulmonary vessels
neg pressure
sm amount of smooth muscle & vasomotor n’s
great distensibility & compliance
Compare hypoxia in pulmonary vs systemic
pulmonary = vasoconstriction (to redirect blood flow towards other alveoli that are well ventilated) systemic = vasodilation
Describe recruitment & distension
meets demand of increased blood through the lungs w/out an increase in arterial pressure
results in a decrease of pulmonary vascular resistance
Why is the equation for pulmonary vascular resistance an estimation
blood is not a Newtonian fluid
pulmonary blood flow is pulsatile
Alveolar vessels are found where
w/in wall of alveoli
What happens to alveolar vessels as the alveoli expand
capillaries are crushed & pinched
Alveolar vessels on pulmonary vascular resistance graph
high PVR from FRC -> TLC
Extra-alveolar vessels are found where
in the corner of alveoli
What happens to extra-alveolar vessels as the alveoli expand
get pulled open
Extra-alveolar vessels on pulmonary vascular resistance graph
high PVR from RV -> FRC
When is pulmonary vascular resistance the lowest
during FRC
Hypoxic conditions affect pulmonary vascular resistance according to what relationship
directly proportional to the amount of smooth muscle present in the wall of the pulmonary art & branches
Which species are more susceptible to hypoxic vasoconstriction
cattle & pigs
Where is hypoxic vasoconstriction more likely to occur
high elevations
Brisket edema is the word for hypoxic vasoconstriction in cattle due to high elevations; what are the clinical signs
right ventricular hypertrophy, dilation, & failure
distension of system veins & edema of brisket region
low exercise intolerance, tachycardia, jugular pulse, & pulmonic 2nd heart sound
Brisket edema treatment
return to low elevation
O2 therapy
Exercise induced pulmonary hemorrhage occurs when
horses exercise at a high intensity, which increases blood flow/ pressure & leads to RBCs entering the alveoli
Treatment of exercise induced pulmonary hemorrhage
nasal strips - hold tissue around nasoincisive notch open so horse can breathe better, which decreases the pressure
furosemide - diuretic drug that decreases total body fluid & pressure exerted by flood flow
Zone 1 where PA > Pa > Pv
no blood flow
seen w/ blood loss & +ve pressure ventilation
absent in healthy lungs
Zone 2 where Pa > PA > Pv
optimal hydrostatic pressure w/ intermittent flow
Zone 3 where Pa > Pv > PA
due to gravity, has continuous flow w/ distended capillaries
When does pulmonary fluid clearance increase
exercise (increased lymph flow) or left sided heart ailure
Steps leading to clinical edema
lymphatic capacity exhausted
proteoglycan bridges break
fluid enters alveoli & bronchioles
Why is pulmonary edema fluid foamy
mix of air, edema fluid, & surfactant molecules
Causes of pulmonary edema
decreased plasma oncotic pressure (hypoproteinemia/ inflammatory lung disease)
increased vascular permeability
inflammation
lymphatic obstruction
Lung edema impedes what
ventilation & oxygenation
Where is pleural fluid reabsorbed
through stromata (holes) on parietal pleura
Hypoxia
specific region or whole body is deprived of O2 at the tissue level
Hypoxemia
abnormally low level of O2 in the blood
Hypoxemia results from
hypoventilation diffusion impairment low P1O2/F1O2 R -> L shunt VQ mismatches
What happens in hypoventilation
alveolar ventilation rate decreases to an abnormally low rate, then PAO2 decreases & PACO2 increases
Causes of hypoventilation
respiratory center depression (inflammation & morphine/barbiturates)
peripheral nerve injury (chest wall injury & dislocation of vertebrae)
neuromuscular disease
lungs resisting inflation (airway resistance, mucus, large endotracheal tube, dense gas, & deep diving)
Hypoventilation A-a gradient & 100% O2 therapy
normal A-a gradient
responds to O2 therapy
What happens in diffusion impairment
decreased diffusion leads to decreased oxygenation
Causes of impaired diffusion
exercise
low P1O2 or low F1O2 (at high altitude)
abnormal lung (due to a pathogen) w/ a thickened alveolar gas-exchange area
Diffusion impairment A-a gradient & 100% O2 therapy
increased A-a gradient
responds to O2 therapy
Normal physiologic shunts
bronchial circulation
thebesian veins
Pathological shunts
arterial-venous anastamoses absolute intra-pulmonary shunts patent ductus arteriosus foramen ovale interventricular septal defects
R -> L shunt A-a gradient & 100% O2 therapy
increased A-a gradient
does not respond to 100% O2 therapy
Why do R -> L shunts not respond to O2 therapy
limit to amount of O2 that can be carried by Hb
Normal lungs have an average V/Q ratio of .8 to 1.2, but certain parts of the lungs differ b/c why
gravity results in units w/ poor perfusion
low compliance of alveoli results in units w/ poor ventilation
V/Q = 0
complete occlusion of an airway
shunt
V/Q < .8
lungs are affected
V/Q > 1.2
pulmonary vessels are affected
V/Q = infinity
total occlusion of pulmonary circulation
dead space
When are V/Q mismatches accentuated
under pathological conditions
V/Q mismatch A-a gradient & 100% O2 therapy
increased A-a gradient
responds to O2 therapy
Physiological response to V/Q mismatches
hypoxic vasoconstriction brisket disease right side heart failure pulmonary embolism COPD asthma pneumonia
Clinical intervention for V/Q mismatches
anesthesia
O2
External respiration
exchange of O2 & CO2 at the alveolar respiratory membrane or blood-gas exchange area
Internal respiration
individual cells of tissues that receive O2 & eliminate CO2
Kinetic motion allows for what
diffusion of O2 & CO2
What happens to gas at 0 K or -273 degrees C
no kinetic motion
gas volume = 0
Composition of gas in the air
N2 = 78% O2 = 21 % Ar = .93 % CO2 = .3 %
Air breathed in has what partial pressure once you take into account that the air is humidified
713 mmHg
partial pressure of H20 = 47 mmHg
Partial pressure is dependent on
conc of dissolved gas
solubility coefficient
Is CO2 or O2 more soluble
CO2
Since O2 is less soluble, what is required for diffusion across the membrane
higher pressure gradient
Under high pressure when scuba diving, N2 gets dissolved in the blood; if a diver comes up too quickly, what happens
N2 forms bubbles in various body tissues -> decompression sickness or bends
When helium is mixed w/ O2, the air is lighter so there is less what
airway resistance
Fick’s law of diffusion
diffusion coefficient is directly proportional to solubility & inversely proportional to molecular weight of the gas
Area of diffusion is increased in what pathologic conditions
emphysema
Thickness of diffusion barrier is increased in what pathologic conditions
sepsis, lung edema, & lung inflammation
What effect does providing an increased % of O2 have on gas diffusion
increase P1; overcomes thickness of membrane
RBCs spend .75 sec in the capillaries to get oxygenated, so any increase in thickness does what
increases the distance & tine of diffusion -> reduces oxygenation
Hyperbaric O2 therapy involves what
O2 administered under high pressure (3-4 atms)
Hyperbaric O2 therapy is useful for treating what conditions
anaerobic bacterial infections wound healing stroke heart conditions CO poisoning cerebral edema gas embolism bone infections COPD
Hyperbaric O2 therapy increases the dissolved fraction of O2 in the blood, which is important b/c
overcomes limitation of O2 carrying capacity of Hb by raising the O2 portion carried in the plasma
Humidification is essential for what
getting inspired air ready for effective gas exchange
for upkeep of mucociliary function
As body temp increases, what happens to vapor pressure & PO2
vapor pressure increases
PO2 decreases
Why does water boil at decreased temps when there is increased elevation
decreased atmospheric pressure, so heat is able to counteract the atmospheric pressure faster
Percent of O2 bound to Hb
98.5%
Percent of O2 dissolved in plasma
1.5%
Hemoglobin is the main component of RBC’s & has what components
1 globin
4 heme
Globin in adult vs fetal
adult: 2 alpha & 2 beta chains
fetal: 2 alpha & 2 gamma -> greater affinity for O2
Site for O2 binding on the heme
Fe2+
Nitrate poisoning makes Hb unable to transport O2 by
converting Fe2+ -> Fe3+
Carbon monoxide poisoning occurs b/c
CO occupies the same site as O2 & has 200 times greater affinity
Treatment for CO poisoning
100% O2, CO2, & fluids
O2-Hb binding is reversible & follows what law
law of mass action
As O2 partial pressure increases, does O2 binding to Hb increase or decrease
increase
Describe allosteric conformational change properties of Hb
once the 1st O2 binds, then it is easier for the rest of the O2 to bind
O2-Hb saturation curve starts flattening at what saturation
90% saturation
At normal PaO2 of 100 mmHg, Hb has what saturation
97.5% saturation
PaO2 < 60 mmHg is considered hypoxemic b/c
this is 90% saturation
any decrease beyond this leads to a significant reduction in O2
PaO2 = 25 mmHg has what saturation
50% saturation
PvO2 = 40 mmHg has what saturation & occurs when
72-75% saturation; occurs in tissues under extreme exercise/ hypoxia conditions
Each gram of Hb combines w/ how many mLs of O2
1.34 - 1.39 mL
Why is a range given for the mLs of O2 that a fully saturated Hb holds
presence of impurities may result in lower O2 binding
If patient becomes anemic due to a reduction in Hb conc, what happens to the O2-Hb curve
shape almost stays the same, but total O2 content will be reduced
Right shift O2-Hb curve means
Hb affinity for O2 decreases
delivery of O2 is facilitated
Left shift O2-Hb curve means
Hb affinity for O2 increases
delivery of O2 is difficult
Bohr effect
increased PCO2 or decreased blood pH reduces the affinity of Hb to O2
right shift
Why are pH & PCO2 related
CO2 can combine w/ H2O to produce H2CO3 & H
rxn is favored in RBCs b/c they have carbonic anhydrase
2,3 DPG is a product of glycolysis w/in RBC’s that has what effect on the O2-Hb curve
right shift
When does production of 2,3 DPG increase
in anemia & at high altitudes
Effect of 2,3 DPG is reduced when blood is
stored
Why must a CO-oximeter be used to diagnose CO poisoning
regular pulse oximetry does not distinguish b/w HbO2 & HbCO
PaO2 levels may look normal w/ CO poisoning, but tissues still experience what
hypoxia
left shift
O2 therapy can help treat CO poisoning b/c
O2 knocks CO off from Hb
Why are fluids & 5% CO2 also necessary when treating CO poisoning
stimulate peripheral chemoreceptors to increase drive for ventilation
ensures that CO will be expired
CO2 is produced where
in metabolizing tissues
CO2 is removed b/c
high levels -> confusion, coma, death, & acidosis
low levels -> alkalosis
Why is hydration rxn favored in RBCs
have carbonic anhydrase
Acetazolamide, a carbonic anhydrase inhibitor, is used to treat
glaucoma & metabolic acidosis
Why does Cl- move into RBCs after the hydration rxn occurs
to maintain electrical neutrality as HCO3- leaves
H+ formed are buffered by
oxyhemoglobin
CO2 is eliminated in the alveoli b/c of
partial pressure gradient
hydration rxn in reverse
Modes of CO2 elimination
dissolved in plasma
transported as HCO3-
bound to hemoglobin
at lung alveoli
Describe haldane effect
reverse of Bohr effect
for a given PCO2, the content of CO2 increases as PO2 levels decrease (loading of CO2)
as PO2 levels increase, CO2 delivery increases
CO2 dissociation curve
steep
no cooperativity/ allosteric effect
lacks a plateau
Acid
donate [H+] to soln
Base
accept [H+] from soln
Buffer
mix of weak acid & its conj base
Strong acid/ base
dissociate completely in a soln
Weak acid/ base
do not dissociate
Relationship b/q pH & [H+]
inverse & exponential
Acids/ bases made by the body
food, digestion, & cellular metabolism (CO2)
Normal blood pH
7.35-7.45
Acidemia
blood pH < 7.35
Alkalemia
blood pH > 7.45
Define acidosis/ alkalosis
physical processes & chemical rxns that progress into acidemia or alkalemia
Normal PCO2
40 mmHg
High PCO2
acidosis
Low PCO2
alkalosis
ATOT
total weak non-volatile acids
High ATOT
acidosis
Low ATOT
alkalosis
High SID
alkalosis
Low SID
acidosis
Function of buffers
exchange strong acid or base for a weak one
help prevent deleterious effects of increased or decreased [H+]
For Henderson-Hassalbalch eq, what do the kidneys/ lungs manage
kidney - base [HCO3-]
lung - acid PCO2
Addition of a strong acid into a buffer yields
weak acid & salt
Addition of a strong base into a buffer yields
weak base & water
Bicarbonate buffer system (pK = 6.1)
NaHCO2 & H2CO3
independently regulated by lungs & kidneys
Phosphate buffer system (pK = 6.8)
NaH2PO4 & Na2HPO4
major intracellular buffer
tubular fluid in kidneys
Protein buffer sys (pK = 6.6 if ox & 8.2 if deox)
carboxyls give up H+ & amino groups accept H+
Hb has imidazole groups
Anderson-Devenport nonogram
normal PCO2 line plotted w/ intersections at pH = 7.4 & HCO3- = 24 mEq/L
Top left corner on Anderson-Devenport
respiratory acidosis w/ increased renal H+ excretion & retention of HCO3-
Bottom left corner on Anderson-Devenport
metabolic acidosis w/ decreased PCO2 & H+
Top right corner on Anderson-Devenport
metabolic alkalosis w/ increased PCO2 & H+
Bottom right corner on Anderson-Devenport
respiratory alkalosis w/ decreased renal H+ excretion & retention of HCO3-
Describe the central controller DRG
in dorsal medulla
inspiratory activity
basic rhythm of breathing
Input & output for DRG
input: vagus & glossopharyngeal n
ouptut: phrenic n to diaphragm
Describe the central controller VRG
in ventral medulla
expiratory & some inspiratory
inactive during normal, quiet breathing
active during exercise/ heaves
Input & output for VRG
input & output: vagus n
innervates intercostal & abdominal m
Function of pontine respiratory centers & their names
modify output of medullary centers
apneustic & pneumonotaxic center
Location of pontine respiratory centers
pons & medulla
Pontine respiratory centers input & output
input: chemoreceptors, lungs, cortex, & other receptors
output: diaphragm & respiratory m
Vagus n has neg feedback signals
Apneustic center does what
stimulates inspiratory neurons of DRG & VRG
over-stimulation -> apneusis
Pneumotaxic center does what
stimulates inhibitory signals to DRG & VRG
fine tunes inspiration & expiration
increased signals increases the respiration rate
Central chemoreceptors are found where
ventral surface of the meddula
Central chemoreceptors respond to what by doing what
pH of ECF or CSF
if decreased pH, then inspiratory neurons are stimulated
leads to increased tidal volume & frequency of breathing
Peripheral chemoreceptors are found where
in carotid bodies at the bifurcation of common carotid art & aortic bodies near the aortic arch
Carotid bodies are innervated by
glossopharyngeal n
Carotid bodies are fast adapting receptors that respond to
decrease in PO2 & pH; increase in PaCO2
Aortic bodies are baroreceptors that sense changes in
partial pressures of O2 & CO2
Cell types in aortic bodies
Type I: contain dopamine
Type II: sustentacular/supporting
Pulmonary stretch receptors are slow adapting & respond to what
increase in lung volume beyond a certain limit & inhibit inspiration (Hering-Breuer reflex)
Irritant receptors in the airway epithelium are rapidly adapting pulmonary stretch receptors that respond to
gases, dust, & cold air
Impulses from irritant receptors travel where
in vagus n to cause bronchoconstriction & hyperpnea
J receptors are endings of non-myelinated c fibers in the wall of the alveoli that respond to
injected materials in pulmonary circulation
Impulses from J receptors travel via what nerve, sense what, & result in what
vagus n
lung edema
rapid, shallow breathing & dyspnea
Bronchial C fibers are similar to J receptors & are supplied by
bronchial circulation
Bronchial C fibers lead to
rapid, shallow breathing, bronchoconstriction, & mucus
Nose & upper airway receptors are found where
nose, nasopharynx, larynx, & trachea
Nose & upper airway receptors respond to
mechanical & chemical stimuli w/ sneezing, coughing, & bronchoconstriction
Joints & muscle receptors stimulate
ventilation
Gamma system is found where & sense what
diaphragm & intercostals - sense elongation of muscle spindles
How does the gamma system respond to elongation of muscle spindles
controlling the strength of contraction
important in sensing airway obstruction & efforts to overcome the resistance
Increased arterial blood pressure leads to what responds in arterial baroreceptors
hypoventilation or apnea through stimulation of aortic & carotid sinus baroreceptors
Decreased arterial blood pressure leads to what response in arterial baroreceptors
hyperventilation
Pain leads to
apnea -> hyperventilation
Heat leads to
hyperventilation
Compare fetal to adult circulation
Fetal: parallel, mixing of arterial & venous blood, placenta for gas exchange, anatomic shunts, & increased Hb O2 affinity
Adult: in series, no mixing of arterial & venous blood, lungs for gas exchange, shunts are abnormal, & decreased Hb O2 affinity
Describe gas exchange in the fetus
simple diffusion of simple molecules in the placenta
transfer of O2 depends on uterine arterial PO2 levels
Placenta has passive & active transport
passive - glucose transport
active - AAs & ions
Fetal Hb has a higher affinity for O2 than adult Hb; some species also have what in relation to Hb
higher Hb conc in fetal blood (human, sheep, & cows)
Relative to body mass, fetuses have a higher cardiac output than adults, which helps to
deal w/ hypoxia
Ruminant fetal Hb
increased O2 affinity is an intrinsic property
Pigs & horses fetal Hb
do not have it
Primates fetal Hb have the inability to do what
bind 2,3 DPG
In fetal circulation, is blood flow increased in the placenta or the lung
placenta
Pulmonary vascular resistance & Pa are higher in fetus or adult
fetus
Fetal lung is in a psuedo-glandular stage at birth w/ what type of cartilage
eosinophilc hyaline cartilage (does not have proteoglycans like adult lungs)
Important signals that a fetus experiences after birth
hypoxia & hypercapnia
fetus cools & fetal fluids evaporate
sensory input from mother
Describe the first breath
great inspiratory effort
not all alveoli open at first
surfactant is important
Carotid bodies in a newly birthed animal start to function & sense what
decrease in O2 & increase in PCO2
As lungs expand in a newly birthed animal, pulmonary vascular resistance
decreases
What vessels rupture upon birth
umbilical vessels
When to fetal shunts close
aortic pressure > Pa & LA pressure > RA pressure
Avian embryo is wrapped in
fetal membranes & chorioallantosis (CAM)
in contact w/ egg shell
Egg shell internal & external sides
external: hard layer of CaCO3 coated by a thin cuticle
internal: two soft membranes
What connects the environment w/ the CAM & what does it allow for
10,000 pores
diffusion
As the embryo in the egg grows, what happens
increase in CAM
increase in O2 affinity for Hb
increase in cardiac output & hematocrit values
increase in diffusion gradient
Heat stress in an egg leads to
hyperventilation & decrease in PCO2 -> decrease in HCO3- levels -> affects normal amount of CaCO3 -> poor eggshell quality -> dehydration of developing chick embryo
Describe the trachea of birds
size & shape varies across species
full circular cartilage
hyaline cartilaginous rings appear as double rings (telescoping)
wider & longer than mammals, but resistance is about the same
Large tracheal dead space is compensated by what in birds
1/3rd respiratory frequency
VT 1.7x larger
lg expansible volume
greater compliance of respiratory system (decreased work & energy of breathing)
Birds lack an epiglottis & use what to produce sound
syrinx (instead of larynx)
Describe the bronchial tree of birds
primary: extra pulmonary & intra pulmonary
secondary: 4 groups
tertiary: parabronchi
Basic unit of gas exchange in the bird
parabronchi
Air sacs are connected to what & function as
lungs & long (pneumatic) bones
bellows -> move air
do not exchange gas
Lungs of birds are
fixed in dorsal part of the body & cannot expand
Name the air sacs in birds
2 cervical 1 clavicular 2 cranial thoracic 2 caudal thoracic 2 abdominal
Describe neopulmonic parabronchi
in some species
accounts for 10-12 % of total lung volume if present
meshwork
Describe paleopulmonic parabronchi
present in all birds
unidirectional air flow
always in contact w/ fresh air
Each volume of air in birds w/ paleopulmonic parabronchi is
eliminated via 2 cycles of respiration
Arrangement of capillaries in paleopulmonic parabronchi
air capillaries are surrounding by blood capillaries
Paleopulmonic gas exchange is
cross-current & highly efficient as it allows for an increase in percent of O2 capture & elimination of CO2
A thin blood-gas exchange area in paleopulmonic parabronchi is advantageous according to
Fick’s law
Type IVc collagen in the basement membrane of paleopulmonic parabronchi provides what
strength needed to keep the thin gas exchange area stable
Yaks live where O2 content is 33-66%, so they have what advantages
larger heart & lungs
persistence of fetal Hb
other genes for hypoxia & metabolism under low O2
Yaks do not do well in
temps above 59 degrees C or elevations below 1000 ft
How do fish breathe
using gills
extract dissolved O2 in water
countercurrent flow
Mammalian diving reflex
bradycardia -> from 125 bpm to 10 bpm
peripheral vasoconstriction -> more blood can be used by heart & brain
Diving adaptations of seals to manage the pressure changes
compliant chest
ability to collapse alveoli followed by terminal bronchioles
cavernous sinuses to prevent rupture of middle ear
presence of cartilage in bronchioles & sometimes alveoli to help in collapse/re-inflation of alveoli
specialized surfactants to make re-inflation easier
Seals deal w/ N2 narcosis how
collapse lungs & hold air in dead space
switch to anaerobic metabolism
elastic aorta keeps blood pressure constant
Other adaptations of seals
aortic bulb & slender abdominal aorta lg heart w/ glycogen store increased muscle myoglobin increase O2 in lungs, muscles, & blood increased hematocrit values lg spleen lungs have great rigidity & elasticity deep divers have small RV
Name the 3 forces that affect the settling of particles
sedimentation
inertial force
Brownian motion
Sedimentation
deposition due to gravity & mass of particles
go to nasal cavity & tracheobronchial tree
Inertial force
due to velocity
go to nasal cavity, pharynx, & tracheobronchial tree
Brownian motion
property of small particles
go to small airways & alveoli
Respirable particles
less than 10 micrometers
could end up in blood-gas exchange area
Non-respirable particles
more than 10 micrometers
retained in dead space & processed through the mucociliary escalator
Upper respiratory tract clearance
for regions cranial to alveolar duct
mucociliary escalator pushes particles to the pharynx, which are then sent to the GI system & deposited in the feces
Low respiratory tract clearance
for particles w/in alveoli
absorptive sites near alveolar ducts where particles accumulate & are cleared through lymphatics
fluid flow towards bronchiolar epithelium & cleared by mucocilary escalator
insoluble & microbial particles are phagocytized by alveolar macrophages
alveolar epithelial cells engulf particles & clear them through desquamation & mucociliary escalator
cleared to lymph nodes to be phagocytized
Panting is a response to increased core body temp that does what
increases dead space ventilation to cool off
increases glandular secretions or vascular transudate
Inhalation & exhalation through nose
least cooling
resting dogs
running at slow speed in cold temps
Inhalation through the nose & exhalation through the nose & mouth
most cooling
exercise
resting at > 30 degrees C
Inhalation & exhalation through the nose & mouth
greatest alveolar ventilation
exercise
resting at > 30 degrees C
Purring results from
highly regular, alternating action of the diaphragm & intrinsic laryngeal m
frequency is 25x/sec
oscillating mechanism w/in CNS
Phases of purring
glottal closing
initiation of glottal opening & sound production
complete glottal opening (decreases resistance & increases air flow)
Purring may provide better ventilation during
shallow breathing
Sneeze reflex
foreign objects/irritation of nose mucosa
strong inspiration & vigorous expiration through the nose
defensive
Aspiration/sneeze reflex
foreign object/irritation of pharynx
series of inspiratory efforts (reverse sneezing)
Swallowing reflex
food/drink pushes down on the soft palate
epiglottis bends to close the larynx
respiration continues once the bolus is in the esophagus
Filtration of lungs
particulate matter & blood clots can be handled in the lungs
Pulmonary intravascular macrophages
present in horses, cats, cattle, & pigs
increases susceptibility to pulmonary inflammation
Lungs are a major source of arichiodonic acid metabolites, which are a site for
synthesis, metabolism, uptake, & release
Angiotensin-converting enzyme is produced where
pulmonary epithelium
converts Angiotensin I -> Angiotensin II
maintains blood pressure
Nonspecific lung defense mechanisms
surfactant proteins A & D host defense particles mucociliary escalator cough/sneezing alveolar macrophages TLRs
Specific lung defense mechanisms
surface IGs
pulmonary dendritic & T cells
intranasal vaccines
