Respiration Flashcards
1
Q
Gas Exchange in Lungs: 2 places
A
- O2 delivery and CO2 removal
- (1) gas exchange at lungs & (2) tissues
- gas exchange in lung to take O2 to tissue where metabolism happens like skeletal muscle
- oxygen first goes to heart and then to body where exchange gases and then non oxygenated blood goes back to heart and lungs
- pulmonary artery carries deoxygenated blood
- pulmonary vein carries oxygenated blood
- in body system is where O2 diffuses out of blood into tissues and that gradient also has to support O2 diffusion
2
Q
Diffusion is key & Fick Equation
A
- how gases move, no pumping
- look at partial pressure of gas
- rate of diffusion = diffusion coefficient permeability x area x partial pressure gradient/distance
- depends on permeability
3
Q
To maximize delivery
A
- increase surface area
- thin membrane for a small distance - thin respiratory membranes
- maximize partial pressure gradient by matching airflow to blood flow
- gases diffuse according to partial pressure gradient
- set up gradient w/in lung to max mvmt of O2 out of lung and into blood
- go from high PP to low PP and difference facilitates that
- humans use 250 mL O2 /min
4
Q
Thoracic Cavity and Muscles
A
- respiratory system in thoracic cavity bounded by diaphragm which is a major muscle for respiration
- upper respiratory system - top of trachea and then mouth and nasal cavity where take air in
- lower respiratory system - trachae and lung w/diaphram and external intercostals, scalinas, sternoclyomastids for breathing in
- diaphram, adb and internal intercostals for breath out
- move air in and out of lungs via diaphragm
5
Q
Muscles of inspiration and expiration
A
- muscles of inspiration - inhale use diaphragm and external intercostales, which is btwn ribs and lift ribs up and out
- sternocleido/sternoclyomastids and stelanous/scalinas for deeper breaths to lift up rib
- muscles of expiration - when exhale your diaphragm relaxes, and muscles help w/more forceful exhalation we have internal intercostals to move ribs down and in and helps to breath out
- also abdominal muscles which push in and up on diaphragm to put pressure on thorasic cavity ; breath out
6
Q
Cavities and Membranes
A
- base of lung is bottom, top is apex
- in L lung there is space carved out like a heart called cardiac notch
- dorsal back and ventral front side and heart sits between
- pleural membranes -
- visceral membrane is on the lung
- parietal membrane is on inside of thorasic cavity
- the membranes are right next to each other and the space between is the intra plural space and is below barometric pressure (pB); NEGATIVE PRESSURE; KEEPS LUNGS INFLATED
- really hard to get two wet plates apart like these membrane
7
Q
Respiratory Tree
A
- conducting zone - larnynx, trachae and then bronchi are divided and have smooth muscle around them so can affect AIR FLOW until you get area of gas exchange in alveoli
- action for gas exchange in alveoli - bronchi branch into smaller vessels called bronchioles which have smoooth muscle around them which can adjust and contract to adjust radius of bronchi to some degree
8
Q
Flow Equation
A
Flow = driving pressure x r4
- driving pressure times radius
9
Q
Asthmatics
A
- smooth muscle contracts and constricts/reduces airways
- flow through bronchi and down into alveoli is proportional to driving pressure we use to move air times the radius to the fourth power which is why things get very dramatic when adjust radius
- small change in radius of bronchi make huge change in air flow which is why keep opena dn reasonably sized is important
10
Q
Alveoli and Capillary Network
A
- alveoli are thin structures and capillary network surrounds each alveoli so capillaries pick up O2 and assoc w/blood flow and each alveoli
- alveoli 200-350 microns in diameter - small w/HUGE SA so they inflate and deflate
- elastic fibers around each alveoli - when inflate we push out elastic fibers; “rebound”, so very little energy required to breath (1-2% of energy budget) mostly inspiration
- when exhale elastic fibers push back and help us push air out
- most of our energy on breathing is inhalation, exhalastion is about free energy at rest
11
Q
Trachea
A
- trachea keep airways clean - goblet cells w/mucous pushed to the surface so cells taht are ciliated beat and try to trap particulate matter in mucous and use cilia to push back into mucous and keep respiratory tract clean/clear
- smooking paralyzes the cilia so hard to keep trachea clean of particulate matter
12
Q
Alveoli Details
A
- Type 1 cells make up structure of alveoli and involved in gas exchange
- Type 2 cells - make pulmonary surfactant which decreases surface tension and helps enlarge alveoli
- capillaries - want intimate association between circulation and blood flow so only 1 row of endothelial cells around
- surfactant is put in water layer which improves stability and easier to inflate (less surface tension and pressure)
- child born too early has respiratory distress syndrome is born too eary and not enought surfactant so hard to breathe - induce surfactant w/cortisol higher
13
Q
Exchange surface of alveoli
A
- rbc in capillary
- lining of pulmonary surfactant of pumonary space and O2 then has to go through alveolar cell w/2 cell membranes one on either side and then goes through capillary endothelial wall which is 2 membranes
- then goes into plasma which is liquid of blood and most of O2 is carried via RBC and goes through that cell membrane too
- total of 5 membranes for O2 to cross before gets carried away
- O2 is very permeable to cell membranes and respiratory membranes are thin
14
Q
Cross sectional area is important
A
- as go deeper into respiratory system the diameter of these get smaller and they also increase in number exponentially
- their cross sectional area > too!
15
Q
Conducting & respiratory zone
A
- number 17 is respiratory zone
- at 17 of airway generation, we get into respiratory zone and the total cross sectional area just sky rockets
- this is how we support our MR w/high need for O2, since all this area to exchange gases
16
Q
Thoracic Cavity and Muscles
A
- diaphragm is big main muscle to separate abd from thoracic cavity
- intrapleural pressure always bit neg since not let alveoli collapse
17
Q
Breathing: Mechanics
A
- at rest, diaphragm is relaxed
- diaphragm moves down and contracts and thoracic volume increases - inhale
- decrease pressure in thoracic cavity which is intrapleural pressure
- suck in air since lower pressure of alveoli and so alv pressure is less than atm pressure
- diaphragm relaxes and rises and thoracis vol decreases - exhale
- > intrapleural pressure but still neg
- > alveolar pressure so greater than baro pressure and air leaves lungs
- 3 pressures to be concerned about - intrapleural pressure is always neg., intraalveolar pressure, and barometric pressure (pB)
- inhalation - diaphragm contracts and moves downa nd we decrease intrapleural pressure to make it more negative, whcih drops intraalveolar pressure which goes neg., so pB greater than Alvp and air flows from high to low, so air flow from pB to outside into the lung like suction
- exhalation - diaphragm relaxes and fills w/air - will increase intrapleural pressure (still neg but less); pressure in thoracic caviety so pressure on alveoli so > intraalveolar pressure, now AlvP > pB so air flows out and thats our exhalation
- pressure pump
18
Q
Diaphragm like pump handle
A
- contracting diaphram until < pressure in lung so Pb > Palv so inhale
- relax diaphram will increase pressure in lungs so Pb < Pa and exhale
- when move pump handle up and rib up then increase anterior-posterior dimensions of rib cage
- bucket handle increases lateral dimension of rib cage
19
Q
Passive expiration and active expiration w/muscles and pic of general inhalation and exhalation
A
at rest before inspiration, move ribs down and drop in intrapleural pressure and can use extra muscles too if need it
- Diaphragm relaxes and comes back up and sets up chamber, more forceful expiration you use abdominal muscles and abdominal muscles
- Pressure changes are responsible for response of alveolar to these pressure changes
Active expiration, during which contraction of the abdominal muscles increases the intra-abdominal pressure, exerting an upward force on the diaphragm. This reduces the vertical dimension of the thoracic cavity further than it is reduced during quiet passive expiration. Contraction of the internal intercostal muscles decreases the front-to-back and side-to-side dimensions by flattening the ribs and sternum.
20
Q
Pressure and Volume Changes while Breathing
normal breath about 500 ml
inhale intrapleural pressure begin at -3 and on inhale get to -6
at inhale alveolar pressure begins low and then increases to bring air in
when Pb = Pa then no net air flow
A
- move 500 mL air in and 500 mL out
- intrapleural pressure - starts negative and when we in bring it more negative
- as exhale it goes back up but still neg
- alveolar pressure - at beginning of inhalation its no diff from atm pressure(pB) but at end of we bring back to pB but differs in middle
- exhale the intrapleural pressure is less neg since compress thoracic cavity and extra air in lung
- alveolar pressure goes up and start forcing air out since alvP > pB
- by end of exhalation forced air out and back to pB in alveolar pressure so equal
- exhale the intrapleural pressure is less neg since compress thoracic cavity and extra air in lung
- deeper breath - bottom graph peak is higher, greater volume
- intrapleural pressure graph goes even more neg and at end of breath goes back to normal so deeper trough not peak
- alveolar graph - alveolar pressure drops more than normal but by end of inhalation still at zero and exhalation is higher peak too
21
Q
Intrapleural pressure is always negative
A
- neg intrapleural presssure - elastic recoil of chest wall tries to pull chest wall outward and that of lung creates inward pull
- if puncture lung - you create a hole and pressure in chest cavity equilibriates to pB and lose neg pressure and lung collapses
- to keep lung inflated you need that neg pressure
- can put cord and generate suction and neg pressure and reflate teh lung
- lungs naturally collapse unless sitting in neg pressure - geared to collapse since elastic around them
22
Q
Law of LaPlace
A
- in alveoli: thin layer of fluid inside and air inside = surface tension of alveoli (water-air interface) –> this generates pressure that wants to pull alveoli in to cuase it to collapse
- Law of La Place is pressure of alveolus = 2T/r
- smaller the r, the more pressure, the more likely to collapse - less stable
- small alveolus will have more pressure than larger one, so the small blows up the bigger one
23
Q
Pulmonary Surfactant
A
- helps surface tension is a 16 carbon fatty acid + phosphotydylcholine
- overall effect is to decrease surface tension so less likely to collapse
- increase stability of alveoli
- helps keep alveoli dry
- increase compliance of lung so easier to inflate w/pressures we have
24
Q
Compliance Curve - how easily the lung can inflate
“hysteresis” - diff in these curves
A
- hystersis - 2 sep curves due to air-water interface
- change in pressure is alveolar pressure - intrapleural pressure
25
Q
Compliance Curve - how easily the lung can inflate
fibrosis/normal exhalation/emphysema
A
- fibrosis - stiff lung not very compliant, far less volume of air in lung for this change in pressure
- normal exhalation in middle - so look at it in comparison for disease
- emphysema - more elastic lung so more compliant, more air into lung but trouble getting it out and proper exchange
- drop pressure a lot to get air back out
- need bigger pressure differential to push air out of lung
- exhale hard
26
Q
Dead Space
A
- we have alveolar air which is exchange zone and then airway or dead space from trachae
- 150 mL are in dead space and 350 mL are in alveoli; for every breath some is in alveoli and some in dead space
- lung vol total is 5-6 L
- w/each breath you create refresh rate, not overturning all air in your lungs
- 500 mL of air move in and out btwn atm and respiratory system
- 350 mL are actually exchanged btwn atm and alveoli since dead space
- dead space is entire trachae since no gas exchange
- more at higher altitude w/cold air so way to warm before hits lungs
27
Q
Respiratory Cycle in Humans
A
- exhale - 150 mL from dead space and 350 out form alveoli
- inhale - first 150 mL is stale air stuck in dead space form last breath and then 350 fresh air and so 150 mL filled w/new 150 mL of fresh air and then push back out in exhale
- plays role in partial pressure of gases
- 500mL total gets distributed among all alveoli
- in dead space O2 isnt exchanged
- parial pressure of O2 that is fresh is 150 mmHg
- partial pressure O2 that is stale is 100 mmHg
28
Q
Effects of Breathing Pattern on Alveolar Ventilation
A
- normal breath: 12times/min and you get 350 mL fresh air into alveoli each breath which is 4200 mL/min of alveolar ventilation which is functional air for gas exchng not dead space
- if take in 300 mL of breath w/20 rapid breaths still same total pulmonary ventilation but dead space doesn’t change so 300-150 = 150 in alveoli to get alveolar ventilation of 300 which is less since talking shallow breaths even tho more of them
- if slow ventilation breath, total pulmonary ventilation rate is same, fresh air to alveoli is 600 mL per breath which gives higher alveolar ventilation
- respiratory minute volume - RMV: goes up in breath/min and vol/min and alveolar ventilation >
- when exercise depth > and rate of breathing goes up so RMV >
- RMV = breath/min x vol/breath
- we don’t do deep breathing due to high energy cost
29
Q
Action at Lung
A
- blood enters lung via plumonary artery - deoxygenated
- pO2 = 40 mmHg; pCO2 = 46 mmHg
- lung has pO2 = 100 mmHg; pCO2 = 40 mmHg
- blood gest saturated w/O2 in lung and Co2 released
- blood leaves via pulmonary vein to heart and then to gen circulation
- pO2 = 100; pCo2 = 40 mmHg since blood went into equilibrium w/partial pressure of lung
30
Q
barometric pressure and respiratory tract
A
pB = pN2 + pO2 + pCo2 sum of all partial pressures
pO2 = 0.209 x pB (760) so pO2 in air is 159 mmHg
coming into the lung: respiratory tract has saturated air w/water vapor, so in respiratory the O2 has pO2 of:
pO2 = 0.209 x pB - pH20(47) = 149 mmHg when take out water vapor the pO2 headed for lungs has this pressure
6L/min is respiratory min vol
how much O2 are we carrying?/O2 solubility in aq solution
[o2] = 2.5 cc O2 /100 mLs (solubility coeff) x 100/760 (percent O2 in atm) = concentration of O2 we can dissolve in blood is 0.3 ccO2/100mL blood
not enought since we use 250 mls O2/min so we use respiratory pigments!! to get O2 to tissues
31
Q
Fetal Hemoglobin
A
•Fetal hemoglobin has 2 alpha and 2 gamma;
- O2 dissociation is diff; placenta is respiratory organ for fetus so can be fully oxygenated at lower pO2 - since pO2 at which maternal blood is 25% oxygenated
- system allows oxygenation of fetal tissue at low pO2, found in blood entering placenta
- when maternal side in placenta has P02 around 40 or 50 then will unload on the maternal side and the fetal side will bind that O2 and be 100% saturated and then distribute to the tissues; fetal saturates at pO2 available on surface
•Gamma does not bond 2,3 DPG so it really shifts over to the left
32
Q
Respiratory pigments - hemoglobin (Hb)
A
- Hb protein w/2 alpha and 2 beta subunits and 4 heme groups each w/Fe2+ and O2 binds to iron and Hb is oxygenated or deoxygenated
- can bind 4 O2 per hemoglobin molecule
- proteins alpha and beta units determines O2 binding
- Hb present in RBC and rbc made in bone marrow and has fixed amount of Hb
- given Hb/rbc and rbc#, this can increase carrying capacity for O2/ enough Hb in blood that our carry capacity is:
- 20% vol which means 20 mLs/cc O2 per 100 mL
- hematocril - is percent of rbc in blood, so normal ranges for female adult is 38-46% and male is 42-54%
- given # rbc we have, but its the fact that we can carry 4 O2 per Hb that how we survive
- we dont’ adjust Hb per rbc but can adjust # rbc
-
erythropoeitin (EPO) - adjust rbc # w/this hormone from the kidney and responds normally to decrease in pO2, which > EPO
- EPO acts on bone marrow to > rbc #, see in ppl who go to higher altitudes
33
Q
How does O2 bind to Hb? Oxygen Dissociation Curve
A
- sigmoidal curve -due to heme-heme interaction (when 1 O2 on easier for 2nd to come on, etc.) - allosteric effect
- saturated at pO2 in lung (available respiratory surface)
- curve describes how Hb loads O2 and how unloads O2 to deliver it
- at pO2 100 mmHg you are 100% sat (which is po2 at resp surface); at 40 pO2 you are 50% sat
- unloading - as pO2 at tissue falls, more O2 is unlaoded from Hb at that site
- Hb of dotted line see that A >B for affinity
- if change position of curve see both curves saturated close to same level but at pO2 40, HbB unloads a lot more since only at 30% sat w/oxygen so unloaded 70% (70% unsat) so unloads more than A
- so B has less affinity
- po2 50 see that A at 60 sat whereas B is 50% sat
- dissociation curve illustrates affinity - how easily O2 loads/unloads
- O2 coming off depends on pO2
- cc is carrying capacity = amount of O2 blood can carry
- 20 ccO2/100 ml blood
34
Q
Things that can influence O2 dissociation curve
A
- (1)increase in Co2 at tissues causes “bohr effect” - favors unloading of O2 at tissue w/increase CO2 for same pO2; shifts curve to R
- (2) decrease pH causes shift to right of graph and favors unloading sooner
- ex generate lactic acid when working out, facilitates unloading - increase in acid at areas of increase metabolism
- move to R optimizes loading/unloading of O2 to areas selectively
- at tissue there is decrease affinity that favors unloading
- (3) increase in temp causes shift to R; even in ectotherms when working muscle facilitate unloading
- (4) increase 2,3 DPG shift curve to right ; internally regulates rbc
- increases w/> altitude which shifts to R to correct for altitude since at higher alt there < pO2 so we > RMV since need more O2 (gotta work harder for it
- we blow off more Co2, so Co2 levels <, so at tissues would not favor unloading which bad
- so DPG made to force shift to R so O2 is delivered to tissues back to normal position
- vice-versa for all of these
35
Q
CO effects
A
- Co has affinity for Hb at 250 x that of O2; so CO binds sites on Hb where stronger than O2 so fewer O2 bind
- carry capacity < and affinity for O2 goes up a bit too for O2 on there so O2 on there has trouble unloading
- hyperbaric chamber where increase pO2 dramatically so O2 pushes off CO and get more O2 dissolved in blood
- above 760 mmHg
36
Q
2 pigments - hemoglobin and myoglobin
A
- myoglobin -respiratory pigment w/in tissues like skeletal muscle
- binds one O2 - either on or off
- provides an O2 reserve at tissues for when pO2 is really low
- easily sat myoglobin at low pO2; so O2 from circulation to oxygenate skeletal muscle
- myoglobin releases O2 at very low pO2
- compared to hemoglobin which is sigmoidal curve
