Respiratory Physiology

Front 1

tidal breath in
dead space
measuring tidal volume/ vital capactiy

Back 1

500 ml
150ml
measure w/: spirometer

Front 2

functional residual capacity

Back 2

amt in lungs after passive expiration, volume at which the pressure of the lungs wanting to collapse = pressure of chest wanting to expand

Front 3

plethysmograph

Back 3

air tight box, based on p1v1=p2v2, decrease in gas volume in the box when the person inhales, increase in pressure in the box

Front 4

gas dilution

Back 4

helium is insoluble in blood, helium concentration in the spirometer = helium concentration in the lungs, can be used to determine residual capacity

Front 5

Ficks law

Back 5

diffusion is proportional to the surface area, gas pressure difference, and diffusing constant and inversely proportional to the thickness

Front 6

diffusion limited

Back 6

C.O; partial pressure does not equilibrate btw gas and blood; amt of gas that gets into the blood is dependent upon the diffusing properties

Front 7

perfusion limited

Back 7

with in 3/4 of a second, the gas has equilibrated with the blood - the only was to increase gas exchange is to increase the blood flow

Front 8

diffusing capacity during exercise (w/ disease)

Back 8

- blood stays in capillary for less time, usually, it is still enough time for o2 to equilibrate
- if diseased, and there is thickening of the alveoli, then it may not be enough time to equilibrate

Front 9

diffusing capacity w. low air o2 (altitude)

Back 9

- less of an O2 gradient - O2 moves into blood more slowly
- steep O2 dissociation curve at low pO2, so pO2 increases more slowly
--> likely to have a failure of equilibration

Front 10

diffusing capacity
-how to measure
-what happens during exercise

Back 10

= DL,includes the thickness, are, and diffusing properties of lung and gas
-use CO to measure - single inspiration and measure rate of disappearance; increased rate of dissappearance (exhale less) = greater diffusing capacity!!
- w/ exercise - increases w/ reqcruitment/ distension of new capillaries (inc SA)

Front 11

transmural pressure

Back 11

pressure difference across a membrane; pressure difference btw inside capillaries and outside capillaries

Front 12

alveolar and extraalveolar vessels

Back 12

when the lung expands, the radial traction of the elastic lung tissue pulls open the large vessels

if alveolar pressure increases, it compresses the alveolar vessels

Front 13

Pulmonary vascular resistance
- changes in lung volume
- changes in BP
- hypoxia

Back 13

- normally, very small
- when BP increases, there is recruitment of new vessels and distension of existing vessels DECREASING the resistance!
- increases at high and low lung volumes
- increases with alveolar hypoxia due to hypoxic vasoconstriction of BVs

Front 14

Zone 1
- blood flow, determinants
- air
-v/q

Back 14

- doesn't happen in life usually
- alveolar pressure is greater than arterial pressure, which is greater than venous pressure
- collapsed lung!
- least blood flow
- least ventilation
-highest v/q, highest pO2, lower pCO2

Front 15

Zone 2

Back 15

-arterial pressure is greater than alveolar pressure, which is greater than venous pressure
-blood flow is driven by arterial/alveolar difference

Front 16

Zone 3

Back 16

- arterial pressure is greater than venous pressure which is greater than alveolar pressure
blood flow is determined by arterial/venous difference
-greatest blood flow
-greater ventilation (due to reduced intrapleural pressure and smaller resting volume)
- lowest v/q (due to greater blood flow)
- lowest pO2
-higher pCO2

Front 17

Airway resistance - general effect of radius

Back 17

increases greatly with decreased radius (r^4) → in medium bronchi, the total cross sectional area is smallest and thus resistance is greatest

Front 18

Airway resistance - small airways vs large

Back 18

in small peripheral airways, have less resistance

Front 19

airway resistance - effect of lung volume

Back 19

– as lung gets more full, it gets larger, and ⇑ elastic recoil, pulls open airways and ⇓ resistance; we breathe at high lung volumes and thus low resistance [people with asthma have ⇑ resistance due to disease, to counteract they breathe at higher blood volumes]

Front 20

airway resistance - effect of tone of brochial smooth muscle

Back 20

sympathetic = bronchodilation (beta 2); parasympathetic = bronchoconstriction

Front 21

airway resistance
-effects of air breathed in

Back 21

air breathed- decrease density and viscosity, easier to breathe, decrease resistance

Front 22

Compliance - what its determined by

Back 22

- elasticity
-interdependence of alveoli
- surface tension (causes hysteresis)

Front 23

Surfactant

Back 23

– reduces intermolecular attraction btw molecules on the surface of the liquid; surfactant preferentially reduces surface tension in small alveoli

Front 24

La Place & effect of surfactant

Back 24

Pressure = surface tension/ radius) so, large alveoli don’t collapse due to large radius which ⇓ pressure and tendency to collapse, small alveoli have a greater chance to collapse due to small radius, but don’t because the surface tension is also small due to surfactant (P=2T/r)

Front 25

Compliance, definition

Back 25

change in lung volume for a given pressure change, Δv/ Δp,

Front 26

Breathing cycle: rest

Back 26

alveolar pressure = 0= atm =no air moving in or out; + transmural pressure (= alveolar pressure – intrapleural pressure) keeps lungs open (+ transmural pressure is expanding force) negative intrapleural p due to lung/ chest wall opposing forces;

Front 27

Breathing cycle, inspiration

Back 27

– increase volume, decrease pressure in lung (alveolar p is negative =less than atm), pulls air in.
End of inspiration: lungs expand, increase elastic recoil causing more negative intrapleural pressure – greater transmural pressure

Front 28

Breathing cycle, expiration

Back 28

there is increased (+) pressure in the lungs compressing the air in alveoli, increased transmural pressure

Front 29

Breathing, forced expiration

Back 29

- during forceful expiration, as volumes decrease, flow becomes independent of effort because of dynamic compression of lung; intrapleural pressure and alveolar pressure increase equally, flow is determined by recoil of lung

Front 30

anemia
effect on
-concentration of O2
-PaO2
-saturation O2

Back 30

- decreased H
- reduces the concentration of O2 (less for it to bind to)
- does not affect PaO2 – because the arteries equilibrate with alveolar gases and alveolar gases remain the same
-saturation remains the same because available Hb is fully saturated
-ventilation is unaffected

Front 31

hypoxia effect on
- concentration of O2
-paO2

Back 31

reduces concentration of O2 and reduces PaO2 (because alveolar partial pressure decreases)

Front 32

CO effect on
-concentration
-pa02
-saturation

Back 32

- CO binds Hb more strongly
- reduces the concentration of O2 in blood
- reduces saturation of O2
- does not affect partial pressure of O2 in blood (no change in alveolar O2)
- no affect on ventilation (since pO2 is normal)

Front 33

Hypoxia, early stage

Back 33

- vasodilation (to ⇑ blood supply, doesn’t help if there is a physical blockage upstream; can be detrimental – might be ⇑ blood to non ischemic areas – stealing blood from ischemic areas)
- w/ ⇓⇓ o2, glycolysis is source of atp, lactic acid accumulation, ⇓ pH (metabolic acidosis)

Hint 33

Vasoactivity
source of atp

Front 34

Hypoxia, late stage

Back 34

- atp is depleted, Na/K pump can’t function
-Na accumulates in cell, H20 follows
- Na/Ca exchanger doesn't work (no Na gradient)
-Ca++ accumulates in the cell
-Ca++ enters the mitochodria, inhibiting ATP production
-F1F0 synthase becomes a hydrolase
-apoptosis

Hint 34

- Pump/Channels affected
-what accumulates where?
- mitochodrial activity

Front 35

inspiratory center
- where it is
- what its function is
- where it gets input from
-lesion below
- output

Back 35

dorsal respiratory group
- controls basic breathing rhythm
- receives info from peripheral chemorecptors via CN IX, X and info from mechanoreceptors in the lung via CN X
- sends output via phrenic nerve to diaphragm
-lesion below: no respiration

Front 36

pneumotaxic center
-where it is
-what it does
-what happens when stimulated
-what happens if lesioned below

Back 36

- rostral 1/3rd of pons
- switches off inspiration, regulating rate/volume of inspiration; fine tuning of respiratory rhthym
- when stimulated, it causes rapid, shallow breathing
- lesioned below: prolonged inspiration =apneuses

Front 37

apneustic center
- where
- what it does

Back 37

- lower pons
- excitatory effects on inspiratory area
- lesioned below: short breaths

Front 38

expiratory center

Back 38

ventral respiratory group
- usually, respiration is passive, only use expiratory center during active breathing

Front 39

Central Chemoreceptors
- where are they

Back 39

Ventral latera surface of medulla

Front 40

Central chemoreceptors
-what they respond to

Back 40

- respond to CO2 (rapid change) and H+ (slower change) --> major sensor for co2

Front 41

Central chemoreceptors
-BBB

Back 41

- BBB is permeable to CO2, CO2 enters CSF, combines w/ H20 → H2CO3 → H+ + HCO3 → increases H+ in CSF which stimulates central chemoreceptors, which stimulates inspiratory center [CO2 - necessary inbetween for stimulation]

Front 42

Increase PCO2 and the chemoreceptor response

Back 42

- immediate response is done by the peripheral chemoreceptors
- more drastic response is due to the central chemoreceptors (3/4 of response)
- 1/4 of response is due to peripheral chemoreceptors
- central receptors adapt, so prolonged effect is due to the peripheral receptors

Front 43

Peripheral Chemoreceptors

Back 43

-relays info to inspiratory center via CN IX and X
- carotid body responds to: pH, pCO2, and pO2
-aortic arch responds to pCo2 and pO2

Front 44

Peripheral Chemoreceptors and pO2 changes

Back 44

- only in cases of severe hypoxemia do the chemoreceptors respond to pO2 changes. pO2 must be less than 60mmHg for there to be a response

Front 45

Hering breuer reflex

Back 45

- distend airway due to increased transpulmonary pressure or inflation
- causes stimulation of the dorsal respiratory grp and decreased breathing

Front 46

Joint/muscle receptors

Back 46

increased mvmt in joints/ muscles, increased breathing

Front 47

Irritant receptors

Back 47

-rapidly adapting
- located in the epithelium of the extrapulmonary airways
- irritant, mechanical stimulation, pulmonary congestion, lung inflation/ deflation
- causes constriction of bronchi and inc breathing, cough, mucous secretion, expiratory constriction of larynx

Front 48

J receptors & C fibers

Back 48

- J = airway and blood vessel; C fiber = alveolar wall
- non myelinated
- respond to increased interstiial volume (congestion - l. sided heart failure), chemical injury, microembolism
→ rapid, shallow breathing, bronchial constriction, decreased HR (bradycardia), mucous secretion

Front 49

Carotid body chemoreceptor:structure

Back 49

type I cells: sense pO2 change
type 2 cells: support cells
lots of capillaries - blood supply

Front 50

Altitude, effect on:
- PaO2
- Saturation O2
- concentration O2
- ventilation

Back 50

- PaO2 decreases because PAO2 is decreased
- Saturation O2 is decreased (less O2 is available to bind)
- Concentration O2 is decreased
- ventilation is increased (because carotid body is stimulated by low O2)

Front 51

COPD, effects on:
-PaO2
- saturation
-concentration
-ventilation

Back 51

- low PaO2, A-a gradient due to V/Q disparity
- low saturation
-low concentration
- low ventilation, due to the disease

Front 52

hypoventilation, effects on:
-PaO2
- saturation
-concentration
-ventilation

Back 52

- low PaO2, low saturation, low concentration, low ventilation

Front 53

Hypoxia, ventilation response

Back 53

-during hypoxia, you have rapid stimulation of chemoreceptors
- chemoreceptors adapt and ventilation returns to normal
- people who live at high altitudes have a decreased response to hypoxia

Front 54

Control of breathing during exercise
(phases of control)

Back 54

phase I: abrupt anticipatory increase in ventilation
phase II: gradual increase in ventilation due to carotid bodies
phase III: steady state matching of ventilation to metabolism below anaerobic threshold - no chemical stimulus, increased ventilation may be due muscle mvmt, unknown

Front 55

Apnea

Back 55

cessation of air flow for a minimum of 10 seconds

Front 56

hypopnea

Back 56

30-50% reduction in airflow for a minimum of 10 seconds

Front 57

Ventilation during slow wave sleep

Back 57

hypoventilation, slow regular breathing

Front 58

ventilation during REM sleep

Back 58

breathing is shallow and irregular
loss of tone in all respiratory muscles except the diaphragm

Front 59

obstructive sleep apnea

Back 59

-repetitive episodes of upper airway collapse during sleep
- asphyxia until brief arousal from sleep to "reopen" airways
-daytime sleepiness, restless sleep

Front 60

work of breathing in restrictive lung disease

Back 60

much more work is needed to overcome the elasticity of a stiff lung; normal work to overcome resistance

Front 61

work of breathing in obstructive lung

Back 61

more work is used to overcome the viscosity of the lung and chest wall (resistance)

Front 62

VO2 max

Back 62

maximal oxygen consumption
- there is a linear increase in whole body O2 utilization w/ increasing exercise intensity until a point in which there is a plateau of O2 consumption, even if there is increasing workload
- higher in men
-decreases with age
- genetic component
=CO *av difference for oxygen in the whole body

Front 63

anaerobic threshold

Back 63

abrupt increase in plasma lactate accumulation (50-70% VO2 max)
optimal training - just below threshold
not due to insufficeint O2

Front 64

substrate metabolism during exercise

Back 64

liver glycogen & muscle glycogen can contribute modest amts of calories
triglycerides can supply many many calories
- higher intensity work, more energy is derived from carbohydrates than fat

Front 65

glucose homeostasis during exercise

Back 65

- onset - supression of insulin release, increase gluconeogenisis, glyconeolysis
- glucagon levels increase, stimulating hepatic glucose output
- epinephrine is released increasing peripheral FAs

Front 66

Fatigue

Back 66

- @ modest levels of activity = depletion of muscle glycogen
- at high levels of activity = accumulation of organic acids

Front 67

- anabolic steroids
- growth hormone
- blood doping
-cocaine
- creatinine

Back 67

- anabolic steroids do enhance competitive activity, less readily fatigue, many bad side effects
- growth hormone - no benefit, malformation of joints
- blood doping - increasing Hb, beneficial effects on exercise/ erythropoeitin - stimulates RBC production (thrombosis)
-cocaine - percieved possitive effects, no actual (+) effects
-creatinine - may have (+) effects in intermitent high intensity activities

Front 68

What determines blood flow in capillaries?

Back 68

Difference btw alveolar and capillary pressure

Front 69

partial pressure of a gas

Back 69

pressure of the gas as if it occupied the total volume in absence of other components

Front 70

normal Hb concentration

Back 70

15

Front 71

O2 binding capacity

Back 71

1.39ml O2/gHb

Front 72

what affects CO2 carrying capacity?

Back 72

lower O2 concentration = increased CO2 carrying capacity

Front 73

anatomical shunt
-when its normal
-characteristics

Back 73

-bronchial arterial blood (perfuses bronchials, doesn't get ventilated)
-coronary arteries that directly reenter the heart
- abnormal a-v connection
- CANNOT be abolished via 100% O2!

Front 74

v/q inequality
- areas with high V/q

Back 74

areas of high v/q cannot "make up" for areas of low v/q because of linear shape of O2 dissociation curve - Hb is already saturated
- low v/q areas will "dilute" blood with normal oxygenation

Front 75

Effect of decreased O2 concentration in blood

Back 75

increased CO2 carrying capacity

Front 76

fat causes..

Back 76

decreased compliance in the chest wall

Front 77

high altitude

Back 77

low pO2, causes hyperventilation which causes reduced pCO2 which causes alkalosis !

Front 78

O2 dissociation curve

Back 78

-steep at lower pO2, implying that a large concentration of O2 can be withdrawn from the Hb by the tissues without a large drop in pO2 (keeping the gradient going INTO the cells) - low pO2, Hb will readily dissociate
-flat at the top of the curve (where arterial blood is) --> some change in pO2 will not affect concentration that much

Front 79

CO2 dissociation curve

Back 79

steep-ish; really big change in concentration --> small change in pCO2

Front 80

Pulmonary Stretch receptors

Back 80

- slowly adapting
- Lung stretch receptors in intrapulmonary airways
- distend airway due to increased transpulmonary pressure or inflation
- causes stimulation of the dorsal respiratory grp and decreased breathing (herring breurer)
- bronchodilation
-increased HR
-decreased peripheral resistance

Front 81

gamma efferent system

Back 81

sensation of breathlessness dyspea