Respiratory Phys Flashcards
respiratory physl is the study of
how oxygen is brought into the lungs and delivered to tissue and how carbon dioxide is removed
what are 6 functions of the respiratory system?
homeostatic regulation of blood gases, protect from microbial infection, regulate blood pH, phonation (speech), olfaction, blood reservoir
what 3 structures comprise the upper resp. system?
nasal/oral cavities, pharynx, larynx
what is after the larynx?
trachea
what 6 structures comprise the lungs?
bronchi->bronchioles->alveoli, smooth muscle, connective tissue, pulmonary circ.
what is the larynx?
the vocal cords
what are the 3 sections of the pharynx?
naso, oro and laryngopharynx
what is anterior and posterior to the trachea and primary bronchi?
anterior: C-shape cartilage
posterior: smooth muscle
what changes from the primary bronchi to the bronchi of the lungs?
C-shaped cartilage to plates of cartilage (smooth muscle remains)
what changes from the bronchi to the bronchioles?
only smooth muscle (no cartilage)
what are the 2 zones of the airways beyond the larynx?
conducting and respiratory zone
what is the conducting zone?
area where gas is brought to gas exchanging region (no alveoli/gas-exchange - “anatomical dead space”)
what is the respiratory zone?
where gas exchange occurs (alveoli)
what is the smallest airway without alveoli?
terminal bronchioles
what airway occasional has alveoli?
respiratory bronchioles (after terminal)
where is generation 0 and 23 of the resp system?
0: trachea
23: alveolar sacs
what incr and decr w each generation level? (2, 2)
incr: # of branches, SA (cross sectional area)
decr: diameter and length
what are the alveoli?
tiny, thin-walled, capillary-rich sacs in lungs where gas exchange occurs
approx. how much blood do capillaries in lungs contain at rest and exercise?
70 mL and 200 mL
what are type 1 alveoli?
flat, epithelial cells
what are 2 functions of type 2 alveoli?
produce surfactant, act as progenitor cells
how can type 2 alveoli act as progenitor cells?
multiply and divide to replace damaged type 1 alveoli
what is the alveolar surfactant and its function?
detergent-like substance made of lipoproteins; reduces surface tension of alveolar fluid
how long is needed for gas exchange to occur at the level of the alveoli?
0.75 (RBC passes through pulmonary capillary system/2-3 alveoli)
what must O2 and CO2 diffuse through?
respiratory memb
what are the 6 layers of the respiratory memb?
alveolar fluid/surfactant, alveolar epi., basement memb of alveolar epi., interstitial space, basement memb of capillary endothelium, capillary endothelium
what is a con of having a thin resp memb.?
easily damaged
what is a pneumocyte?
alveolar cell
what are the 5 steps of repsiration?
ventilation, gas exchange in alveoli, gas transport, gas exchange at tissues, cellular utilization of gases
what is ventilation?
exchange of air between atmosphere and alveoli by bulk flow (O2 in, CO2 out)
what occurs during gas exchange in alveoli?
O2 and CO2 exchange btwn alveolar air and capillary blood by diffusion
what occurs during gas transport throughout the body?
O2 and CO2 circulate through pulmonary and systemic circ by bulk flow
what occurs during gas exchange in tissues?
O2 and CO2 exchange btwn blood in capillaries and tissue cells by diffusion
what occurs during cellular utilization of gases?
O2 is used and CO2 is released
how is ventilation produced? (4)
- CNS sends rhythmic excitatory drive to resp. muscles
- resp. muscles contract rhythmically
- changes in V and P allow for gas movement
- air flows in and out
what are 3 categories of resp. muscles?
pump, airway and accessory muscles
what do the pump muscles do?
make changes in P and V at level of lungs
where are the airway muscles?
upper airways (keep them open)
what are the INS (4) and EXP (2) upper airway muscles?
INS: tongue protruders (Genioglossus), alae nasi, pharyngeal and laryngeal dilators
EXP: pharyngeal and laryngeal constrictors
what do the accessory muscles do?
facilitate respiration during exercise
what are 2 INS accessory muscles?
sternocleidomastoid, scalene
what are the INS and EXP pump muscles?
INS: diaphragm, external and parasternal intercostals
EXP: internal intercostals, abdominals
what are the 5 INS muscles?
acc: sternocleidomastoid, scalene
pump: diaphragm, external and parasternal intercostals
what are the 5 EXP muscles? (4 abd.)
pump: internal intercostals, external and internal abd. oblique, transversus adb., rectus abd.
what is the diaphragm?
dome-shaped muscle that flattens during INS
what occurs when the diaphragm contracts?
forces abdominal contents down and forwards, widens rib cage, incr V of thorax
where are the external intercostals?
within the rib cage
what occurs when the external intercostals contract?
pull ribs upward, incr V of thorax (bucket handle motion)
where are the parasternal intercostals?
near sternum
what occurs when the parasternal intercostals contract?
pull sternum forward and incr anterior-posterior dimension of rib cage (pump handle motion)
what are the 4 abdominal muscles?
external oblique, internal oblique, transversus admonius, rectus abdominis
when are the expiratory pump muscles active?
deeper, faster breathing (exercise) to return lungs to resting position
what occurs when the internal intercostals contract?
pull rib cage down, decr thoracic V
what occurs when the scalenes contract?
elevate upper ribs, incr thoracic cavity
where are the scalenes?
attached on upper rib cage
where are the sternocleidomastoids?
connected to sternum
what occurs when the sternocleidomastoids contract?
raises sternum
when are the accessory INS muscles active?
during exercise or heavy respiration (little contribution to quiet/rest breathing)
what do muscles do during rest INS?
diaphragm contracts, external and parasternal intercostals pull ribs up and out
what do muscles do during forced resp. INS?
stronger diaphragm contraction, accessory muscles recruited (incr thoracic V)
what occurs during rest EXP?
no active contraction of resp muscles (diaphragm relaxes)
what do muscles do during forced resp. EXP?
abd. muscles contract, pushing abd. contents up and diaphragm higher, internal intercostals contract and push rib cage down (decr thoracic V)
what is obstructive sleep apnea?
reduction in upper airway patency during sleep (snoring, apneas, sleep disturbances) due to decr muscle tone or anatomical defects
what 2 regions are involved in the filtering action of resp?
conducting zone/”mucociliary escalator” and macrophages in alveoli
what 2 cells that line trachea are a part of the “mucociliary escalator”?
goblet (mucus-producing) and ciliated cells
what do the cells of the “mucociliary escalator” do?
entrap inhaled biological and inert particles and remove them from airways
what is periciliary fluid?
fluid produced by ciliated cells that forms the Sol layer (low viscosity/density)
what do goblet cells produce?
mucus that forms patchy gel layer above sol layer (high viscosity & elasticity)
how is mucus w/ trapped particles removed?
cilia movements (downward-nasopharynx, upward-trachea) bring mucus towards eso.
what is the last defense to inhaled particles?
macrophages in alveoli (phagocytosis)
what occurs when silica dust and asbestos are inhaled?
macrophages cannot digest these particles and die, producing chemotactic factors that recruit fibroblasts and cause pulmonary fibrosis
what is spirometry?
pulmonary function test to determine amount and rate of inspired and expired air
what is a spirometer?
device used to measure V of air inspired and expired by lungs (amount and rate/time)
what cannot be measured by a simple spirometry test? (3)
residual V, functional residual capacity, total lung capacity
what is the tidal V (TV)?
V of air moved in OR out of lungs during each resp cycle
what is the expiratory reserve V (ERV)?
max. amount of air that can be expelled after a normal expiration (max. voluntary expiration)
what is the inspiratory reserve V (IRV)?
max. amount of air that can be inhaled after a normal inspiration (max. voluntary inspiration)
what is the residual volume (RV)?
V of air remaining in lungs after max. expiration (cannot be expired or measured w spirometer)
what is RV =?
RV = FRC - ERV
what is atelectasis?
complete/partial lung/lobe collapse when alveoli become deflated/collapse (RV)
what are lung capacities?
sum of 2 or more lung volumes
what is vital capacity (VC)?
max. V of air forcibly exhaled after max. inspiration
how do you calculate VC?
VC = TV + ERV + IRV
what is inspiratory capacity (IC)?
max. V of air that can be forcibly inhaled
what do you calculate IC?
IC = TV + IRV
what is functional residual capacity (FRC)?
V of air remaining in lungs at end of normal expiration
how do you calculate FRC?
FRC = RV + ERV
what is total lung capacity (TLC)?
V of air in lung at end of max. inspiration
how do you calculate TLC?
TLC = FRC + TV + IRV = VC + RV
what cannot be measured by a spirometry test?
RV, FRC and TLC (contain RV)
what is tidal volume (Vt)?
total amount of air inspired at each breath (~500mL)
what is total/minute ventilation
total amount of air moved in and out of resp. system per min.
how do you calculate total/min ventilation?
Vt x resp. frequency (breaths per min, bpm)
what is alveolar ventilation (Va)?
amount of air moved into alveoli per min
what is the anatomical dead space (Vd)?
area in upper resp. system that contains air wo/ gas exchange (conduction zone, ~1/3, 150mL)
who do you calculate alveolar ventilation?
Va = (Vt - Vd) x freq. (bpm)
does V in anatomical dead space change with breath size?
no, it is constant
what is the most effective way to breathe to incr alveolar ventilation?
incr depth (decr bpm) rather than incr bpm (decr depth)
what is FEV1?
forced expiratory V in 1 second (FVC in 1s)
what is FVC?
forced vital capacity, total V of air that is blown out after max. INS as fast as possible (VC = IRV + TV + ERV)
what is FEV1/FVC?
proportion of air that is blown out in 1s
normal V for FVC
~5.0L
what does a patient with obstructive lung disease have trouble with?
exhaling all the air from their lungs (slower)
what 3 diseases are associated with obstructive breathing?
bronchial asthma, chronic obstructive pulmonary disease, cystic fibrosis
what is the most reduced w obstructive breathing patterns?
FEV1 (and FEV1/FVC ratio)
what drugs are used to reduce bronchospasms with asthma?
B2 adrenergic agonists
what does a patient with restrictive lung disease have trouble with?
cannot fully inhale/expand their lungs
what might cause restrictive lung patterns?
lung and chest stiffness, weak muscles, or damaged nerves
what is reduced with restrictive lung patterns?
FVC and FEV1
what appears normal with restrictive lung patterns?
FEV1/FVC ratio (both are reduced)
what 3 diseases are associated with restrictive breathing?
lung fibrosis, neuromuscular diseases, or lung tissue scarring
what can be measured using the helium dilution method?
FRC (RV + ERV)
what features of helium makes it useful for the gas dilution technique?
not taken up by vascular system (insoluble in blood) and can stay contained in lungs (reach equilibrium after a few breaths)
what do the variables in C1V1 = C2(V1 + V2) correspond to? (Helium test)
C1, V1: initial conc. and V of He in machine
C2: [He] at equilibrium after a few breaths (lungs + machine)
V2: FRC (V of He in lungs)
what does the helium dilution method only measure?
communicating gas or ventilated lung volume
what are the static properties of the lungs?
mechanical properties when no air is flowing (maintain chest and lung V)
what 4 properties are associated w static mechanics of ventilation?
intrapleural P (Pip), transpulmonary P (Ptp), static lung compliance, ST of lungs
what 3 properties are associated w dynamic mechanics of ventilation?
alveolar P (Palv), dynamic lung compliance, airway and tissue R
what is bulk flow?
movement of gas btwn high to low P
what is Boyle’s Law?
for fixed amount of ideal gas kept at constant temp, P and V are inversely proportional (P1V1=P2V2)
how does expiration demonstrate Boyle’s Law?
compression: decr V and incr P, air flows out
how does inspiration demonstrate Boyle’s Law?
decompression: incr V and decr P, air flows in
what is different btwn Boyle’s Law and the resp system?
not a sealed container (open to atm), air moves by bulk flow
what is the formula for bulk flow?
F = ΔP (= Palv - Patm) / R
what is the pleura?
thin double-layered envelope that cushions btwn lungs and thoracic wall+diaphragm
what does the visceral pleura cover?
external surface of lung
what does the parietal pleura cover?
thoracic wall and superior face of diaphragm
what separates the visceral and parietal pleura?
intrapleural fluid (~10 mL, 5-35 um)
what does the intrapleural fluid do?
allows visceral and parietal pleura to move around while breathing (decr friction)
how does the elastic recoil of lungs and chest wall balance eachother?
lung: tendency to collapse (inward)
chest: tendency to expand (outward)
(not directly attached, intrapleural space)
what is the transpulmonary P (Ptp) responsible for?
keeping alveoli open (P gradient)
what does the intrapleural P act as?
relative vacuum
how does the Pip act as a vacuum?
negative P keeps lungs inflated (always < Patm)
what would occur if Pip = Palv?
lungs would collapse (elastic recoil)
what is Ptp =?
Palv - Pip
why is Ptp always > 0?
Pip is negative and subtracted so the double negative makes Ptp positive (ensures lungs are expanded in thorax)
are Ptp and Palv static or dynamic parameters?
Ptp: static (doesn’t cause airflow but determines lung V)
Palv: dynamic (determines airflow)
what occurs during an INS effort? (8)
CNS sends excitatory drive to INS muscles, contract, incr thoracic V, Pip becomes more neg, Ptp incr (= Palv - -Pip), lungs expand, Palv decr, air flows into alveoli/lungs
what occurs during an EXP effort? (8)
INS muscles relax, chest wall recoils, Pip returns to pre-INS value (incr), Ptp decr, lungs V decr, air in alveoli compresses, Palv incr (> Patm), air flows out of lungs/alveoli
what is airway R usually?
small (small ΔP generates flow ~1 mmHg)
what 2 forces can cause R?
- inertia of resp system
2. friction
btwn what 3 structures can there be R?
- btwn different alveolar sacs (within lungs)
- btwn lung and chest wall (decr by interpleural fluid)
- btwn air and airways (80%)
what is laminar flow?
gas moves linearly (in small airways)
what is transitional flow?
intermission btwn laminar and turbulent flow (branches in bronchial tree, incr R)
what is turbulent flow?
not smooth or laminar (large airways: trachea, larynx, pharynx, high velocity and R)
what does Poiseuille’s law state for laminar flow? (R)
R is proportional to viscosity and length but inversely proportional to radius^4 (highest in small airways)
how does R vary in the tracheal bronchiol tree
low at medium-sized bronchi, decr in resp zone
what is R for a healthy subject approx?
1.5 cm H20/L/s
what is the R in the upper, large and small airways?
upper: 0.6
large: 0.6
small: 0.3
why is R highest in upper and larger airways if r is bigger?
airflow is turbulent or transitional in these airways, R is highly sensitive to non-laminar flow
how is R calculated for airways in series vs parallel?
series: R = R1 + R2…
parallel: 1/R = 1/R1 + 1/R2…
how does airways being aligned in parallel contribute to low terminal R?
each small airway has a high individual R but the sum of all the reciprocal Rs is much lower (large airways in series, incr sum of Rs)
what airways contribute most to R in diseased ppl? 3 reasons why?
small airways; smooth muscle contraction, edema (alveoli and bronchioles), mucus (bronchioles)
what is compliance?
measure of the elasticity and distensibility of the lungs
what is the formula for compliance?
C = ΔV / VPtp
what are the y and x axis for compliance?
∆Vlung vs ∆Ptp
what is dynamic vs static compliance?
w or wo airflow
how is static compliance measured?
at FRC (end of EXP)
does emphysema vs pulmonary fibrosis have higher or lower compliance than normal?
emphysema: higher (stretched/ruptured alveoli)
pulmonary fibrosis: lower (collagen=stiff)
what does dynamic compliance measure?
lung stiffness and airway R against which distending forces have to act (≤ static C)
what is hysterisis?
a system whose response depends on its current state and its HISTORY
what are the 4 regions of P-V graph when inflating a collapsed lung w incr Ptp? (Vl = lung volume)
- stable Vl: hard to inflate collapsed airways
- exponential Vl: airways open and Vl incr
- linear Vl: expansion of open airways (Pip more neg)
- Vl plateaus: max Vl, compliance decr
how is the P-V loop diff in normal vs collapsed lungs?
much smaller and less hysteresis
how is hysteresis apparent in the lungs?
different INS and EXP compliance curves (easier to keep inflated lungs open vs collapsed/narrowed)
what 2 factors determines lung compliance?
- elastic components
2. surface tension
where is elastin and collagen localized in the lungs? (3)
alveolar walls, around blood vessels and bronchi
what 2 components influence the elastic components of the lungs and how?
- elastin (extensible)
2. collagen (inextensible)
what contributes more to lungs elastic behaviour: fiber elongation vs fiber arrangement?
geometrical arrangement of fibers
what does the degeneration of elastin and collagen w ageing cause?
decr lung compliance
what causes emphysema? effects?
elastin destruction (alveolar destruction); incr lung compliance w less elastic recoil (little ΔPtp = large ΔV)
what causes pulmonary fibrosis? effects?
collagen deposition in alveolar walls; decr lung compliance (high Δ Ptp required for ΔV)
surface tension occurs where in the lungs?
air-water interface in alveoli
what effect does incr ST have on lung compliance?
decr (2/3 of lung compliance)
what is surface tension?
measure of the attractive/cohesive forces that pull water’s surface molecules together at an air-liquid interface (H-bonds)
how is the P-V curve of liquid-filled lungs different than a deflated lung?
curve is steeper, no hysteresis, lower inflation pressures
how does alveolar ST influence lung compliance?
water molecules line internal surface of alveoli which creates inward recoil, incr P creates outward F that balances inward ST F
what is Laplace’s equation? ind and dep variables?
P = 2T/r; P: dep, r: ind, T: constant (ST)
what is the effect of different sized alveoli in the lungs?
where ST is constant, smaller r have higher P (small alveoli want to collapses so air can move from high P to lower P/large alveoli)
why don’t smaller alveoli collapse due to incr P?
surfactant in fluid that lines alveoli
what alveolar cells produce surfactant?
type 2
what are 3 benefits of having surfactant in the alveoli?
- decr ST of alveolar fluid
- incr compliance
- stabilizes alveoli
what are 3 components of alveolar surfactant?
phospholipids (dipalmitoyl-phosphatidylcholine, phosphatidylcholine), surfactant apoproteins, Ca ions
how does surfactant reduce ST of water in alveoli?
amphiphilic phospholipids arrange btwn water molecules (hydrophobic: towards air) and reduces H-bonding
how does surfactant stabilize alveoli?
prevents small alveoli from collapsing as thickness of surfactant incr w/ decr in SA and thus decr ST (T) vs larger alveoli (P is equalized and no bulk flow)
what issue do premature infants have w/ their alveoli?
lack surfactant, decr compliance and incr work to breathe (infant resp distress, IRDS)
what areas of the lungs have highest vs lowest ventilation (when standing)?
hightest: bottom
lowest: top
why does the bottom of the lungs have the highest ventilation?
gravity pulls lungs down, decr neg Pip (incr P), less F pulling lungs open, alveoli start more deflated and receive more INS air
what is the relationship btwn ventilation vs Pip?
for the same change in Pip, the change in ventilation is greatest at the base than apex of lungs (logarithmic)
what 2 factors incr P of a gas? (not V)
temp, [gas]
what does Daltons Law state?
in a mixture of gases (air), each gas operates independently (Pt is sum of all Pp)
how do you calculate Pp of a gas?
% of gas in mixture -> decimal/fraction x Pt
what does Fricks Law state? V/t = (A/T) * D * (P1 - P2)
rate of transfer of a gas through a sheet of tissue/time is proportional to A (area), D (diffusion constant), diff in Pp of gas and inversely proportional to thickness (T)
what is D (diffusion constant)?
amount of gas transferred btwn alveoli and blood/time (diffusion)
does CO2 or O2 have greater solubility in liquids?
CO2
what is D also proportional to?
solubility (D = Sol/√MW)
what does Henry’s Law state?
amount of gas that dissolves in a liquid is proportional to Pp of gas in equilibrium w that liquid
if Pp of gas is same as in liquid, what also determines amount of gas in liquid?
solubility ([gas] in liquid = P x Sol)
if Po2 = Pco2, how will the [gas] in liquid differ?
[co2] > [o2] as it has incr solubility
does O2-Hb contribute to Pp?
no, no longer “dissolved in solution” and doesnt contribute to Pp
why is the Pp of water higher in the alveoli than the atmosphere?
air is warmed and humidified in alveoli by mucus membranes
why is Po2 in air > Po2 in alveoli? (3)
- warming/humidification incr Ph2o and decr Po2
- O2 diffuses to blood
- INS air mixes w/ FRV (decr Po2)
how does altitude affect Po2 in alv?
is inversely proportional to alv Po2 (incr = decr alv Po2 )
how does alveolar ventilation (Va) affect alveolar Po2?
incr Va, incr gas exchange until Po2 in atm ≈ alv (incr Po2 in alv)
how does metabolic rate affect Po2 in alveoli?
incr MR, incr o2 consumption in tissues, decr Po2 returning to alv, decr Po2 in alv
what other/4th factor affects alveolar Po2 and Pco2?
perfusion
how does Pco2 in atm affect Pco2 in alv?
barely, Pco2 in atm/INS air is very small
how does alveolar ventilation (Va) affect alveolar Pco2?
incr Va, decr Pco2 (co2 diffuses from blood to alveoli, exhaled)
how does metabolic rate affect Pco2 in alveoli?
incr MR, incr co2 production in tissues, incr co2 returning to alv, incr Pco2 in alv
what % of the capillary length does majority of gas exchange btwn alveoli and blood occur?
~30% (first thrid)
why is it advantageous for gas exchange to occur in the first third of the capillary?
allows more length of capillary to be available for gas exchange if needed (diseased ppl)
whats the difference btwn pulmonary and systemic circulation btwn P and R?
sys: high P, high R (fight gravity)
pulm: low P, low R (fragile system)
why does the pulm circ system have low P and R?
low P: only needs to pump blood to top of lungs, avoid rupturing resp memb or edema formation
low R: shorter and wider vessels (Poiseuille’s law)
what allows the pulm circ to have high compliance vessels? (3)
lots of arterioles w/ low resting tone, thin walls w/ little smooth muscle, can dilate w/ incr BP
can time for blood to pass through pulm capillaries be reduced?
yes, (0.75s to 0.3s) when CO incr
what is the V/Q ratio?
ventilation/perfusion is the balance btwn ventilation and gas exchange in alveoli and pulm capillaries
what is perfusion?
gas exchange btwn alveoli and pulm capillaries (O2 from alv into circ, CO2 from circ into alv)
how does high ventilation affect Po2 and Pco2?
alv levels approach atm levels (incr O2, decr CO2)
how does high perfusion affect Po2 and Pco2?
alv levels approach venous levels (decr O2, incr CO2)
what is the cause and effect of a high V/Q ratio?
cause: capillary occlusion
effect: alveolar dead space (Vd)
what is alveolar dead space?
regions of lungs w/ high V/Q, over ventilated/underperfused, no gas exchange btwn alv and capillary
what is the cause and effect of a low V/Q ratio?
cause: airway occlusion
effect: shunt
what is a shunt?
portion of venous blood that doesn’t get oxygenated/not available for gas exchange and returns to arterial blood
how is regional lung perfusion measured?
inject patient w/ mixture of saline solution and radioactive Xenon while patient holds breath
where is lung perfusion greatest?
base (bottom)
what does lung perfusion depend on? (2)
gravity, posture
where is V/Q ratio highest and lowest in lungs?
highest: base
lowest: apex
what are the V/Q ratios in the base and apex of lungs vs basal/ideal V/Q?
base: 0.6x (decr V/Q: decr Po2, incr Pco2)
apex: 3x (incr V/Q: incr Po2, decr Pco2)
what mechanism matches low ventilation w/ decr perfusion?
pulmonary hypoxic vasoconstriction (due to decr Po2)
what mechanism matches low perfusion w/ decr ventilation?
bronchoconstriction (due to decr Pco2)
what do homeostatic mechanisms do to match ventilation and perfusion?
divert blood and airflow in local/diseased area to healthy areas of lung (vasoconstriction/bronchoconstriction)
How is O2 primarily carried in the blood?
- Dissolved (2%)
2. Bound to Hb (98%)
What are the 4 Hb chains called?
Globins (2 a, 2 B)
What is a heme group?
Porphyrin ring structure w/ ferrous iron (2+) that binds O2 (4/Hb)
what is the approx. Po2 in systemic arterial vs venous blood? in mmHg
arterial: 100 mmHg (towards tissues)
venous: 40 mmHg (away from tissues)
what % of Hb is saturated in systemic arterial vs venous blood?
arterial: 97.5%
venous: 75%
what % of O2 from Hb is dropped off in the tissues?
25%
what is O2 capacity?
max. amount of O2 that can be combined w/ Hb
what is Hb saturation?
% of available Hb binding sites w/ O2 attached
what equation calculates % Hb saturation?
(O2 combined w/ Hb ÷ O2 capacity) x 100
does 100% Hb saturation mean high O2 V in blood?
no, if V of Hb is low, V of O2 is also low
what is the most important determinant of Hb saturation?
Arterial Po2
what 3 factors alter the O2 dissociation curve?
pH, Pco2, temperature
what causes the sigmoidal shape of the O2 dissociation curve?
cooperative binding (allostery)
what is cooperative binding (in context of Hb)?
when 1 O2 binds, Hd undergoes conf change from tense (T) to relaxed (R) state that facilitates further binding of O2 (exposes Fe in heme group)
where on the O2 dissociation curve are the steep and plateau areas? in mmHg
steep: 10-60 mmHg
plateau: 60-100 mmHg
what is the significance of the steep portion of the O2 dissociation curve? (40-60 mmHg)
incr O2 dissociation w/ small decr in Po2
what is the significance of the steep portion of the O2 dissociation curve? (10-40 mmHg)
incr metabolic rate (decr Po2) further facilitates O2 delivery into tissues
what is the significance of the plateau portion of the O2 dissociation curve? (60-100 mmHg)
conditions that decr alv Po2 and thus arterial Po2 won’t affect Hb saturation (% bound to O2 is still high)
what is anemia?
decr Hb in blood (100% sat is still less O2 than normal)
what is polycythemia?
incr Hb in blood or incr V of blood that incr Hb (100% sat is more O2 than normal)
what is the effect of CO poisoning on O2-Hb dissociation curve?
reduction in O2-Hb binding by 33% (CO-Hb) and change from sigmoidal to log shape of curve
how much more affinitive is CO for Hb than O2?
200x
what does the log shape of the O2-Hb dissociation curve bcse of CO poisoning indicate?
decr O2 unloading to tissues as lower Po2 is required
how does incr in Po2blood affect equil btwn deoxy and oxy-Hb?
(use Le Chatelier’s principle)
incr in Po2: incr oxy-Hb
decr in Po2: incr deoxy-Hb (favors unloading)
what does shifts to the right vs left of the O2-Hb dissociation curve mean for O2 aff for Hb?
right: decr O2 aff for Hb (incr unloading)
left: incr O2 aff for Hb
what 4 factors shift O2-Hb dissociation curve to the right?
incr in temp, Pco2, [DPG] and [H+]
where does DPG come from?
end product of RBC metabolism
what are 3 causes for incr [DPG]?
chronic hypoxia, high altitudes, chronic lung disease
what 3 forms is CO2 carried in blood?
dissolved (in plasma or RBC), bicarbonate (maj.) or carbamino compounds (both in RBC)
what enzyme catalyzes the rxn of CO2 + H20 -> H2CO3?
carbonic anhydrase (CA)
what is carbonic acid?
H2CO3
what does carbonic acid react to form?
H+ and HCO3-
what is HCO3-?
bicarbonate
what is the chloride shift?
bicarbonate export from RBC is balanced w/ Cl import to maintain elec. neutrality
what molecule facilitates the exchange of HCO3- and Cl- in RBCs?
anion exchanger
what maintains elec. neutrality in blood so more HCO3- can exit RBCs?
incr in [H+] (decr pH)
what does combination of CO2 w/ amino groups (globins) in Hb produce?
carbaminohemoglobin
is an enzyme required to form carbaminohemoglobins?
no
does deoxy-Hb or oxy-Hb have a higher aff for CO2?
deoxy-Hb
what is the effect of CO2 binding to deoxy-Hb?
decr [deoxy-Hb] shifts equil. to favor more O2 dissociation
what is the benefit of CO2 incr Hb-O2 dissociation?
aids O2 unloading in tissues
how does CO2 transfer into alv due to diff Pco2 affect HCO3- and Hb?
promotes HCO3- (from plasma and RBC) and Hb-CO2 conversion to dissolved CO2
what occurs to the H+ from carbonic acid breakdown in RBCs when HCO3- exits to plasma?
H+ reacts w/ Hb
does deoxy-Hb or oxy-Hb have a higher aff for H+?
deoxy-Hb
what is the benefit of H+ bound to Hb and not dissolved in plasma or RBC?
Hb acts as a buffer for pH (prevents acidity)
how does Hb act as a buffer at peripheral tissues?
O2 drop off forms deoxy-Hb and CO2 pick up forms HCO3- and H+ which reacts w/ deoxy-Hb
how does the equil for HCO3- vs Hb act at the lungs?
HCO3- binds to H+ so Hb-H+ favors dissociation and O2 can bind to deoxy-Hb
what causes respiratory acidosis?
hypoventilation: incr CO2 production wo/ CO2 elimination so Pco2 incr and H+ conc incr
what causes respiratory alkalosis?
hyperventilation: incr CO2 elimination wo/ CO2 production so Pco2 decr and H+ conc decr
what is metabolic acidosis?
incr H+ in blood (ind. of Pco2)
what is metabolic alkalosis?
decr H+ in blood (ind. of Pco2)
what system controls rhythm of breathing?
CNS
what brain structure initiates breathing?
medulla (specialized neurons)
what structures/receptors modify breathing? (5)
higher brain centers (NTs), central and peripheral chemoreceptors, lung stretch receptors, proprioceptors (in muscles/joints), touch/pain/temp. receptors
neuronal networks must establish an _________ rhythm for contraction of resp muscles
automatic
what 3 groups in the brainstem contain resp neurons?
pontine, dorsal, and ventral resp groups
which resp neuron group generates INS and EXP rhythm?
ventral resp group (VRG) in medulla
what group in the VRG initiates INS rhythmic activity?
PreBotzinger complex (PreBotC)
what does the PreBotC excite? via what pathway?
INS resp muscles; polysynaptic
what group in the VRG initiates EXP rhythmic activity?
Parafacial resp group (pFRG)
what does the pFRG excite? via what pathway?
EXP resp muscles; polysynaptic
neuronal networks adjust breathing rhythm to accomodate what 4 bodily changes?
metabolic demands (Po2, Pco2, pH), mechanical conditions (posture, pregnancy), non-ventilatory behaviours (speaking, eating) and pulmonary/non-pulmonary diseases
PreBotC and pFRG neurons drive activity in ________ neurons that excite _____ neurons to rhythmically contract resp muscles
premotor and motor
for INS, the PreBotC activates premotor neurons in the ______ VRG (2 regions)
rostral and parahypoglossal region, pXII
premotor rostral VRG neurons can excite _______ motor neurons in ______ spinal cord and contract the __________ (2 pathways)
PHRENIC/thoracic, CERVICAL/thoracic, DIAPHRAGM/ext. intercostals
premotor parahypoglossal/pXII VRG neurons excite _____ motor neurons in the ________ to control the _______ and ______ _________ ________
cranial, medulla, tongue and upper airway muscles (larynx)
for EXP, the pFRG activates premotor neurons in the _____ VRG
caudal
premotor caudal VRG neurons can excite _______ motor neurons in the spinal cord and contract the __________ ____________ and __________ muscles (2 pathways)
THORACIC/lumbar, INTERNAL INTERCOSTALS/abdominal
are the thoracic motor neurons that innervate INS and EXP muscles the same?
no, different motor neuron pool
t/f: tidal volume and resp rate are fixed
f: can incr or decr based on activation or inhibition of resp networks
what can alter arterial Po2 and Pco2? (4)
sleep, exercise, talking and panting
what is hypoxia and hypercapnia?
hypoxia: low Po2
hypercapnia: high Pco2
what is the similar effect of hypoxia, hypercapnia and acidosis?
incr in ventilation (incr Po2, decr Pco2 and incr pH)
what are chemoreceptors?
specialized structures that sense changes in Po2, Pco2 and H+/pH (have a key role in chemical control of ventilation)
where are the peripheral chemoreceptors? (2)
carotid and aortic bodies
t/f: the carotid and aortic bodies are the same as the carotid and aortic sinuses
f: carotid and aortic bodies (chemoreceptors) and sinuses (baroreceptors) are different structures w/ different roles
what are carotid and aortic bodies (peripheral chemoreceptors) most sensitive to?
hypoxia (low arterial Po2)
what are 4 characteristics of the carotid bodies?
extremely small, chemosensitive, highly vascularized, high metabolic rate
what allows the carotid bodies to have virtually same Po2, Pco2 and pH as systemic arteries even though they have a very high metabolic rate?
blood flow/perfusion»_space; metabolic rate
what are the 2 types of cells in the carotid bodies?
type 1: glomus cells
type 2: sustentacular cells
what is the function of the glomus cells?
chemosensitive cells that drive ∆ventilation w/ ∆Po2 in arteries (also sensitive to Pco2 and H+/pH)
what is the function of the sustentacular cells?
act as support in CB
what are 4 characteristics of glomus cells that make them neuron-like?
have V-gated ion channels, depolarization causes APs, have intracellular vesicles w/ NTs, stimulation causes release of NTs
what do NTs from glomus cells released in the CB stimulate?
glossopharyngeal nerve (CN IX) afferents
what do glossopharyngeal nerve (CN IX) afferents innervate and cause?
dorsal/ventral resp group in brainstem (PreBotC and pFRG) to incr resp drive to muscles and incr ventilation
glomus cells ____ firing rate in response to low Po2
incr
at what Po2 range (in mmHg) are peripheral chemoreceptors most sensitive?
<60 mmHg (stable btwn 60-120: normal physl levels)
decr in Po2 <60 mmHg will ____ ventilation
incr (drastic)
what occurs when peripheral chemoreceptors incr firing with low INS Po2? (<60 mmHg)
reflex via medullary resp neurons (activate DRG and VRG neurons in medulla) to centrally control activity of respiratory muscles by incr resp rate and tidal volume
what occurs when INS Pco2 incr? (5)
incr alv Pco2 reverses diffusion grad and causes UPTAKE of alv Pco2 and incr arterial Pco2 which will incr ventilation
a range of what Pco2 will causes large changes in ventilation? (in mmHg)
40-46 mmHg (very sensitive)
where are central chemoreceptors?
close to surface of medulla (close contact to blood vessels and cerebrospinal fluid)
what 3 regions regions of the medulla contain central chemoreceptors?
rostral (anterior), intermediate and caudal (posterior)
where are 2 other chemosensitive sites in the brain?
medullary raphe and hypothalamus
what % of central vs peripheral chemoreceptors are responsible for response to hyercapnia?
70% central
what 2 resp groups respond to hypercapnia to change ventilation?
dorsal (DRG) and ventral resp group (VRG)
what is the process for peripheral chemoreceptor detection of hypercapnia? (start w/ inc alv Pco2) (9)
incr alv Pco2, incr art Pco2, incr art [H+] (as CO2 reacts w/ H2O), peri. chemoreceptors incr firing, glossopharyngeal nerves excite DRG and VRG (PreBotC and pFRG), incr resp muscle contractions, incr ventilation (resp. f and TV), alv and art Pco2 return to normal and art [H+] returns to normal
what is the process for central chemoreceptor detection of hypercapnia? (start w/ inc alv Pco2) (10)
incr alv Pco2, incr art Pco2, incr brain ECF Pco2, incr brain ECF [H+], central chemoreceptors incr firing, excite VRG (PreBotC and pFRG), incr resp muscle contractions, incr ventilation (resp. f and TV), alv, art, and brain ECF Pco2 return to normal, brain ECF [H+] returns to normal
what is the step response to metabolic acidosis? (start w/ incr production of non-CO2 acid) (9)
incr production of non-CO2 acid, incr arterial [H+], peripheral chemoreceptors incr firing, reflex via medullary resp neurons, resp muscles incr contractions, incr ventilation, decr alv Pco2, decr art Pco2, arterial [H+] returns to normal
why can hypercapnia but not metabolic acidosis be controlled by central chemoreceptors?
CO2 can easily cross BBB and react w/ H2O to produce H+ but H+ from met. acidosis cannot easily cross BBB (no CO2)
how does strenuous exercise cause hyperventilation?
incr in lactic acid causes metabolic acidosis which is detected by peripheral chemoreceptors to incr ventilation
