Unit 11 Asma Physiology Of Respiration

Front 1

Describe the muscular actions associated with pulmonary ventilation.

Back 1

The lungs can be expanded in two ways: (1) downward & upward mvt. of the diaphragm, and (2) elevation & depression of the ribs / ribcage
Normal, quiet breathing – primarily all diaphragm: inspiration – diaphragm contracts, pulls lower lung surfaces downward expiration – diaphragm relaxes, elastic recoil of lungs, chest wall, & abdominal structures compress lungs & expels air (during heavy breathing, need additional contraction of abdominal muscles)
Rib / Ribcage Mvt. (increases anterior/posterior diameter of the chest cavity by ~ 20%): Inspiration (elevate/raise ribcage) –EXTERNAL intercostals
Sternocleidomastoid – lift sternum upward
Anterior Serrati – lift many ribs
Scaleni – lift the first two ribs
Expiration (depress/lower ribcage) – abdominal recti and INTERNAL intercostals

Front 2

Describe the pressures responsible for moving air in & out of the lungs.

Back 2

Pleural Pressure (-5 to -7.5 cm H2O) – pressure of the fluid in the thin space bwtn. lung pleura and chest wall pleura; slight negative pressure (i.e., suction) due to continual removal of excess fluid into lymphatic channels
Alveolar Pressure (-1 to +1 cm H2O) – pressure of air inside lung alveoli When the glottis is open & no air flows in/out of the lungs, the pressures in all parts of the respiratory tree (including alveoli) equal atmospheric (atmosp.) pressure, which is considered to be zero reference pressure in the airways
(i.e., 0 cm H2O)
Inspiration – to cause inward air flow, pressure in the alveoli must fall below atmosp. pressure; -1 cm H2O in alveolar pressure if enough to pull in 0.5 l of air into the lungs
Expiration - +1 cm H2O is enough pressure to move 0.5 l of air out of the lungs
Transpulmonary Pressure (-7.5 to +1 cm H2O) – pressure difference btwn. inside of alveoli & the outer surfaces of the lungs; measure of elastic forces in the lungs that tend to collapse the lungs at each instance of respiration (i.e., recoil pressure)

Front 3

Describe the effects of surface tension & surfactant on pulmonary ventilation.

Back 3

When water forms a surface with air, water molecules on the surface of the water have an especially strong attraction for each other; the water surface is always attempting to contract (e.g., this contractile tension is what holds raindrops together) Along the inner surface of the alveoli, the water surface also attempts to contract, forcing air out of the air sacs and collapsing the alveoli; net effect is an elastic contractile force of the entire lungs = surface tension elastic force

Front 4

What is surfactant?

Back 4

Surfactant – surface active agent in water, greatly reduces the surface tension of water, thereby reducing the effort of the respiratory muscles to expand the lungs; mixture of phospholipids, proteins, & ions; secreted by type II alveolar epithelial cells

Front 5

What are the effects of surfactant?

Back 5

Effects of surfactant:Surface tension of pure water = 72 dynes/cm Normal fluids lining the alveoli w/o surfactant = 50 dynes/cm Normal fluids lining the alveoli w surfactant = 5 to 30 dynes/cm

Front 6

If an air passage is blocked, what happens to the air sacs?

Back 6

If an air passage is blocked, surface tension in the alveoli tends to collapse the air sacs, creating a positive pressure attempting to push the air out. Amount of pressure generated:
2 X surface tension
Pressure = -----------------------
Radius of alveolus

Front 7

For an average-sized alveolus w. a radius of 100 micrometers and lined w. surfactant what is the water pressure?

Back 7

~ 4 cm H2O pressure (3 mm Hg) If alveoli lined w. pure water ~ 18 cm H2O (about 4.5 X greater)

Front 8

What is the anatomic dead space?

Back 8

Anatomic “Dead Space” (150 ml at rest) = airways from the nares to respiratory bronicholes do not participate in gas exchange

Front 9

What is the sympathetic dilation of the bronchioles?

Back 9

Sympathetic dilation of the bronchioles – few sympathetic nerve fibers, but bronchiole tree exposed to norepinephrine & epinephrine released in the blood due to sympathetic stimulation of the adrenal medulla

Front 10

What is the parasympathetic constriction of the bronchioles?

Back 10

Parasympathetic constriction of the bronchioles – achetylcholine released by the Vagus (X) nerve

Front 11

What are local secretory factors?

Back 11

Local secretory factors – usually cause constriction; histamine & slow reactive substance of anaphylaxis are released from mast cells during allergic rxns.; smoke, dust, sulfur dioxide, acidic elements in smog

Front 12

List and describe the functions
of the respiratory passages.

Back 12

Trachea – air is completly humidified & warmed by the time it reaches the end of the trachea; curved cartilage plates keep the trachea open, smooth muscle btwn. cartilage plates
Primary Bronchi (Rt. & Lt.)
Lobar (Secondary) Bronchi (3 branches on the Rt., 2 branches on the Lt.)
Segmental (Tertiary) Bronchi
* purpose of bronchi is to conduct air to the respiratory zone; progressively fewer cartilage plates, more smooth muscle
Bronchioles – almost entirely smooth muscle
Respiratory (Terminal) Bronchiole (i.e., “respiratory zone”, gas exchange)
Alveolar duct
Alveolar sac & alveoli
Pulmonary venule
Pulmonary arteriole
Lymphatic

Front 13

Describe pulmonary artery pressure.

Back 13

MEAN PULMONARY ARTERIAL PRESSURE = 15 mm Hg
Systolic pulmonary arterial pressure = 25 mm Hg
Diastolic pulmonary arterial pressure = 8 mm Hg
During systole, pulmonary arterial pressure ~ equals rt. ventricular pressure, but once pulmonary valve closes (end of systole) rt. ventricular pressure drops sharply whereas pulmonary arterial pressure falls more slowly as blood flows through lung capillaries

Front 14

Describe pulmonary capillary pressure.

Back 14

Pulmonary Capillary Pressure: = 7 mm Hg; low pressure critical for maintaining a mean filtration pressure of +1 mm Hg, moving fluid out of the capillaries into the pulmonary interstitium

Front 15

Describe blood volume of the lungs.

Back 15

450 ml (9% of total blood volume); ~ 70 ml of pulmonary blood volume flows through the pulmonary capillaries at any given time, the remaining volume evenly distributed bwtn. pulmonary arteries & veins

Front 16

Describe the functions of the three (3) circulatory systems in the lungs.

Back 16

Pulmonary Vessels – pulmonary arterial branches are very short & arterioles have larger diameters than their systemic counterparts, carry partially deoxygenated blood;
arterial vessels are thin & distensible giving the pulmonary arterial tree a large compliance (~ 7ml/mm Hg), large compliance allows pulmonary arteries to accommodate the stroke output of Rt. Ventricle
Pulmonary veins are also short, immediately empty their effluent blood into Lt. atrium, to be pumped by the left heart through the systemic circulation
Bronchial Vessels – small bronchial arteries that originate from systemic circulation carry oxygenated blood to supporting lung tissue, 1-2% of total cardiac output; once this blood passes through the supporting tissues, it empties into pulmonary veins & enters the left atrium (vice the right atrium)
Lymphatics – throughout the lung supporting tissue; remove alveolar particulate matter & plasma proteins leaking from lung capillaries, helping to prevent pulmonary edema
(lymph empties into right thoracic lymph duct)

Front 17

Describe pulmonary venous pressure.

Back 17

Pulmonary Venous Pressure / Lt. Atrial Pressure:
MEAN PULMONARY VENOUS PRESSURE = 2 mm Hg
(ranges from 1 mm Hg {recumbent} to 5 mm Hg {standing})

Front 18

Describe the lungs as a blood reservoir

Back 18

Lungs as a blood reservoir: quantity of lung blood volume can vary as much as ½ normal to 2 X normal

Front 19

How does the Valsalva maneuver affect blood volume of the lungs?

Back 19

Valsalva maneuver – can expel 250 ml of blood into systemic circulation Loss of systemic blood volume due to hemorrhage can be partly compensated for by an automatic shift of blood from the lungs Left-side heart failure, mitral valve failure, stenosis, or regurgitation can dam up pulmonary circulation, increasing lung blood vol. as much as 100%, greatly increasing pulmon. vascular pressures (risk for edema)

Front 20

Describe factors that effect blood flow through the lungs.

Back 20

1) Automatic control due to effect of diminished alveolar O2
2) Hydrostatic pressure gradient

Front 21

What happens when alveolar PO2 is < 73mmHg?

Back 21

When alveolar PO2 < 73 mm Hg (ambient air [O2] < 70%), adjacent pulmonary blood vessels constrict, increasing vascular pressure 5 X; (opposite effect observed in systematic vessels, which dilate in response to low O2 levels);

Front 22

Low O2 levels trigger the release of what from lung tissue?

Back 22

Low [O2] levels trigger release of a vasoconstrictor substance from lung tissue (i.e., hypoxic alveolar epithelial cells…?), effect is to “shunt” blood from poorly ventilated alveoli to better aerated lung areas

Front 23

What is the pressure gradiant in the lungs?

Back 23

~ 23 mm Hg pressure gradient w/in the lungs; pulmonary arterial pressure at lung apex is 15 mm Hg less than pulmonary arterial pressure at heart level, pressure in lung basilar regions is 8 mm Hg greater

Front 24

What happens to blood flow to the lung apices and basilar regions when standing position at rest?

Back 24

* Standing position at rest -- little blood flow to lung apices, but 5 X as much blood flow to lung basilar regions

Front 25

What happens is lung alveolar air pressure is > capillary blood pressure?

Back 25

If lung alveolar air pressure > capillary blood pressure, the capillary closes off & there is no blood flow

Front 26

Describe the three (3) hydrostatic pressure zones of the lungs.

Back 26

Zone 1: no blood flow during all portions of cardiac cycle (alveolar air pressure < local capillary pressure); blood flow occurs in Zone 1 only during abnormal conditions
Zone 2 (lung apices): intermittent blood flow only during pulmonary arterial pressure peaks b/c systolic pressure > alveolar air pressure; (10 cm above heart midlevel to the top of lungs)
Zone 3: (base of lungs): continuous blood flow (capillary pressure > alveolar air pressure during entire cardiac cycle)

Front 27

What happens with the hydrostatic pressure zones of the lungs during exercise?

Back 27

** Exercise: blood flow increase 700-800% in lung apices, converting them from Zone 2 to Zone 3; 200-300% increase in blood flow to lung basilar regions

Front 28

What value must pulmonary capillary pressure rise to?

Back 28

* Pulmonary capillary pressure (7 mm Hg) must rise to a value at least equal to the colloid osmotic pressure (28 mm Hg) of the plasma inside the capillaries before significant edema develops;

Front 29

What is the pulmonary safety factor?

Back 29

Pulmonary Safety Factor = 21 mm Hg

Front 30

Describe the effects of exercise on pulmonary vascular resistance.

Back 30

During heavy exercise, blood flow through the lungs increases by four to seven times normal, this extra flow is accommodated by:
1. increasing # of open capillaries by as much as 3X
2. distending all capillaries & increasing flow rate through each capillary by 2X
3. increasing pulmonary arterial pressure
* (1) and (2) both decrease pulmonary vascular resistance so that pulmonary arterial pressure rises very little; prevents a significant rise in pulmonary capillary pressure, thus also preventing the development of pulmonary edema

Front 31

Describe factors that affect the fluid dynamics of the pulmonary capillaries.

Back 31

Total Outward Force = +29 mm Hg
Total Inward Force = -28 mm Hg
-----------------------------------
MEAN FILTRATION PRESSURE = 1 mm Hg
* creates a slight, continual flow of fluid from the pulmonary capillaries into the interstitial spaces where the fluid is then pumped back into the circulation via the pulmonary lymphatic system

Front 32

What type of pressure do the pulonary capillaries and pulmonary lymphatic system normally maintain and what happens to excess fluid in the alveoli?

Back 32

* Pulmonary capillaries & pulmonary lymphatic system normally maintain a slight negative pressure in the interstitial spaces, any excess fluid in the alveoli is “sucked” into the lung interstitium & carried away by the lymphatic system, keeping the air sacs dry

Front 33

List 2 fators that lead to pulmonary edema

Back 33

Factors Leading to Pulmonary Edema:
1.left-sided heart failure or mitral valve disease (great increase in pulmonary venous pressure & pulmonary capillary pressure)
2.damage to pulmonary capillary membranes due to infection (e.g., pneumonia) or by breathing noxious substances (rapid leakage of plasma proteins & fluid out of the pulmonary capillaries)

Front 34

Death can occur w/in 30 min. to an hour if pulmonary capillary pressure rises to what?

Back 34

25-30 mm Hg above the safety factor
(e.g., left-sided heart failure, capillary pressure = 50 mm Hg)

Front 35

In chronic conditions in which > 2 weeks, with pulmonary capillary pressures = 40-45 mm Hg, what happens to the lymphatic vessels?

Back 35

Lymphatic vessels can expand by 10X to carry away more fluid

Front 36

Describe the functions of pleural fluids

Back 36

1)Provide a slick lubricant for the lungs to slide back & forth w/in the pleural cavity as they expand & contract
2) Negative pressure w/in the pleural fluid (-4 to -7 mm Hg) on the outside of the lungs keeps the lungs expanded and pulled against the chest wall; negative pressure created by constant pumping of fluid into the lymphatic vessels

Front 37

What are the 3 respiratory centers in the neural control of respiration?

Back 37

1. Dorsal Respiratory Group/Medulla Rhythmicity Center 2. Pneumotaxic Area 3. Ventral Respiratory Group (medulla)

Front 38

Describe the role of the dorsal respiratory group/medulla rhythmicity center in the neural control of respiration.

Back 38

1) Dorsal Respiratory Group / Medulla Rhythmicity Center – sets basic rhythm of respiration; inspiration = 2 seconds, expiration = 3 seconds

Front 39

What do inspiratory neurons do?

Back 39

* Inspiratory Neurons set rate; intrinsic excitability, active for 2 seconds then shut off for 3 seconds; “ramp” signal that begins weakly & increases steadily over 2 seconds
Nervous Impulses --à travel along --à Inspiratory Muscles
Phrenic Nerve (diaphragm & external

Front 40

What do expiratory neurons do?

Back 40

* Expiratory Neurons – inactive during normal, quiet breathing; activated during high ventilation rates due to impulses from Inspiratory Neurons; send output to abdom. muscles & internal intercostals to contract & decrease thoracic cavity size

Front 41

Describe the role of the pneumotaxic area in the neural control of respiration.

Back 41

Pneumotaxic Area – upper pons; inhibitory impulses to medullary inspiratory neurons; shuts off inspiration before lungs fully inflated
* limits inspiration, facilitates expiration, & increase breathing rate

Front 42

Describe the role of the ventral respiratory group (medulla) in the neural control of respiration.

Back 42

Ventral Respiratory Group (medulla) – inspiration & expiration; normally inactive, but important for contracting abdom. muscles for forceful expiration

Front 43

Basic rhythm of respiration is ___.

Back 43

* Basic rhythm of respiration is intrinsic; even when all peripheral nerves entering the medulla are sectioned, & the brain stem transected above & below the medulla, the inspiratory neurons of the dorsal respiratory group still emit bursts of action potentials

Front 44

Damage to the pneumotaxic area prolongs inspiration by how long?

Back 44

* Damage to the pneumotaxic area prolongs inspiration by 5 seconds or more, filling lungs w. excess air

Front 45

What is the Hering-Breuer Reflex?

Back 45

* Inflation Reflex (Hering-Breuer Reflex) – over inflated lungs active stretch receptors w/in bronchi & bronchioles; limits inspiration
Vagus Nerve --à Inspiratory Neurons
INHIBITED

Front 46

CO2 stimulation of the peripheral chemoreceptors is ___ times more rapid than by central stimulation

Back 46

CO2 stimulation of the peripheral chemoreceptors is 5X more rapid than by central stimulation; peripheral chemoreceptors may play a role in “fine tuning” respiration rate during exercise

Front 47

Describe factors that affect respiratory control during exercise.

Back 47

* Most likely a neurogenic response (probably a learned, “anticipatory” response); brain transmits motor impulses to exercising muscles, & simultaneously transmits collateral impulses to excite the medullary respiratory center
* During strenuous exercise, O2 consumption & CO2 formation can increase as much as 20-fold, yet alveolar ventilation increases in step w. increased O2 metabolism, and arterial PO2, PCO2, & pH remain nearly normal

Front 48

Describe the effects of altered CO2 on respiratory control & renal response

Back 48

* H+ ions and CO2 in medullary interstitial fluid & cerebrospinal fluid stimulate chemosensitive area, which in turn excites parts of the respiratory center; (respiratory center itself is not directly affected by changes in blood [CO2] or [H+])
* H+ ions greatly excite chemosensitive area, but H+ ions do not readily cross blood-brain barrier; therefore changes in blood [H+] have less effect than changes in blood CO2 levels
* CO2 stimulates chemosensitive area neurons indirectly by changing [H+]
** CO2 is lipid-soluble, readily crosses blood-brain barrier & combines w. H2O to form H2CO3 (carbonic acid), which dissociates into H+ ions & CO2 **
More H+ ions are released into the respiratory chemosensitive area when blood [CO2] increases than when blood [H+] increases
Marked increase in ventilation rate w. increased PCO2 w/in the normal range (35 to 75mm Hg) due to tremendous effect CO2 changes have on controlling respiration; in contrast, changes in respiration rate are only 1/10th as great w/in normal blood pH range (7.3 to 7.5)
Decreased Stimulatory Effect of CO2 After 1-2 Days due to Renal Adjustment of [H+]
excitation of respiratory center greatest w/in first few hours of increased blood CO2, then gradually declines over 1-2 days to 1/5 the initial effect
* Kidneys increase blood bicarbonate ions (HCO3-), which binds w. & decreases H+ ions in the blood & cerebrospinal fluid; more importantly, HCO3- ions diffuse through blood-brain barrier & combine directly with H+ ions adjacent to chemosensitive area

Front 49

A change in blood [CO2] has a ____ _____effect on controlling respiratory drive, but a ____ _____ effect after a few days’ adaptation

Back 49

Potent acute effect; weak chronic effect

Front 50

Describe the role of the peripheral chemoreceptor system in respiratory control

Back 50

* changes in [O2] have virtually no direct effect on respiratory center itself; indirect effect via peripheral chemoreceptors (carotid & aortic bodies), typically when alveolar oxygen partial pressure (Pao2) drops below 70 mm Hg (altitude of 8K’ {2,438 m})
* Peripheral chemoreceptors stimulated by decreased arterial PO2; particularly sensitive to arterial PO2 of 60 to 30 mm Hg,range in which Hb-O2 saturation decreases rapidly
** Receptors have their own blood supply directly off arterial trunk, exposed at all times to arterial blood, not venous blood **
** Due to having their own blood supply, peripheral chemoreceptor O2 needs can be met by dissolved plasma O2; explains why anemia & CO poisoning, which are accompanied by low arterial [O2] but normal O2 tension/pressure, fail to increase respiration rate **
Carotid Bodies (bilaterally, in bifurcation of carotid arteries)
Hering’s Nerve -à glossophyryngeal nerve --à dorsal
respiratory center in medulla
Aortic Bodies (arch of aorta)
Vagi Nerves --à dorsal respiratory center in medulla
* Increases in [CO2] and [H+] excite the peripheral chemoreceptors & indirectly increase respiration, but the direct effect of these substances on the medullary chemosensitive area is much more powerful, that stimulation via the peripheral chemoreceptors is negligible

Front 51

When does the large part of the total increase in ventilation begin in regard to exercise?

Back 51

* A large part of the total increase in ventilation begins immediately at exercise onset before any blood chemicals have had time to change

Front 52

Describe the pulmonary volumes.

Back 52

Tidal Volume (500 ml) – amount of air inspired/expired w/in a normal breath
Inspiratory Reserve Volume (3000 ml) – extra volume of air inspired over & above tidal volume; inspire w. full force
Expiratory Reserve Volume (1100 ml) – extra volume of air forcefully expired at the end of a normal breath
Residual Volume (1200 ml) – volume of air remaining in lungs after a forceful expiration

Front 53

Describe the pulmonary capacities.

Back 53

Inspiratory Capacity (3500 ml) - IC = TV + IRV; amount of inspired air beginning w. a normal breath to end of maximal inspiration
Functional Residual Capacity (2300 ml) – FRC = ERV + RV; amount of air remaining in lungs at end of a normal expiration
Vital Capacity (4600 ml) – VC = IRV + TV + ERV; maximum amount of air expelled from lungs after of forceful inspiration & expiration
Total Lung Capacity (5800 ml) – TC = VC + RV or TC = IRV + TV + ERV + RV; maximum volume the lungs can be expanded w. the greatest amount of effort

Front 54

Describe alveolar ventilation & the associated resultant air spaces.

Back 54

Dead Space Air – inspired air that fills respiratory passages where no gas exchange occurs (e.g., nose, pharynx, trachea); expired first before any alveoli air reaches the atmosphere, making dead space air very disadvantageous for removing expiratory gases from the lungs
Normal Dead Space Volume = 150 ml
Anatomic Dead Space – respiratory passages where gas Exchange occurs (non-alveolar spaces)
Physiologic Dead Space – anatomic dead space and non-functional alveoli due to absent or poor blood perfusion; non-functional alveoli normally < 5 ml by volume in healthy individuals, but can increase to 1-2 l w. some lung diseases

Front 55

Describe the physical principles that affect gaseous diffusion

Back 55

Diffusion – kinetic energy
Net Diffusion – concentration gradient
Gas partial pressures related to gas concentration
Partial pressures of gases dissolved in fluid
Net rate of diffusion in fluids
* For diffusion to occur, there must be a source of energy; kinetic energy, provided by the gas molecules themselves, results in random movement; net diffusion due to a concentration gradient
* Pressure is caused by multiple impacts of moving molecules against a surface, pressure is directly proportional to the concentration of the gas molecules (i.e., “partial pressures” of individual gases)

Front 56

What is the % N2 of atmospheric air?

Back 56

N2 = 79% of atmospheric air

Front 57

What is the % O2 of atmospheric air?

Back 57

O2 = 21% of atmospheric air

Front 58

What is the total pressure of gas mixture at seal level (mmHG)?

Back 58

Total Pressure of Gas Mixture at Sea Level = 760 mm Hg

Front 59

What is the partial pressure of N2 at sea level?

Back 59

PN2 = (.79) X 760 mm Hg = 600 mm Hg at sea level

Front 60

What is the partial pressure of O2 at sea level?

Back 60

PO2 – (.21) X 760 mm Hg = 160 mm Hg at sea level

Front 61

List 6 factors that Determine Partial Pressure of Gas Dissolved in a Fluid:

Back 61

Gas concentration and solubility coefficient of the gas
Solubility of Respiratory Gases at Body Temperature:
Difference between the two partial pressures
Net diffusion of Gases Through Fluids
Relative Diffusion Coefficients of Respiratory Gases in Body Fluids (assuming the diffusion coefficient of oxygen is 1)
Diffusion of Gases Through Tissues

Front 62

What leads to more gas molecules being dissolved without building up excess partial pressure in the solution?

Back 62

* Some gas molecules (especially CO2) are physically attracted to water molecules, leading to more of gas molecules being dissolved w/out building up excess partial pressure in the solution

Front 63

Show Henry's Law in as a formula.

Back 63

Expressed as Henry’s Law:

Partial Pressure = Concentration of dissolved gas/Solubility coefficient

Front 64

What is the solubilty of the following gases at room temperature.
O2
CO2
CO
N2
HE

Back 64

Solubility of Respiratory Gases at Body Temperature:
O2 0.024
CO2 0.57 * CO2 is 20X more soluble than O2
CO 0.018 * PCO2 is 1/20th that exerted by O2
N2 0.012
HE 0.008

Front 65

What is the Net diffusion of gases btwn the gas phase (alveoli) and the dissolved phase (pulmonary blood) is determined by?
Why?

Back 65

Difference btwn. the two partial pressures
If the partial pressure of the gas is greater in the gas phase (alveoli), then the gas diffuses into the pulmonary blood (e.g., O2); if the partial pressure of the gas is greater in the dissolved state of the blood, net diffusion occurs towards the gas phase in the alveoli (e.g., CO2)

Front 66

Why is there net diffusion of gases through fluids?

Back 66

Net Diffusion of Gases Through Fluids: due to pressure differences (i.e., “pressure gradient”)

Front 67

In addition to pressure differences what 5 factors affect the rate of gas diffusion in a fluid?

Back 67

1.Solubility of gas in a fluid – the greater the solubility, the greater the # of molecules available
2.Cross-sectional area of the fluid – the greater the cross-sectional area, the greater the total # of molecules that diffuse
3.Distance – the greater the distance, the longer it takes
4.Molecular weight of the gas
5.Temperature

Front 68

Relative rates at which different gases at the same partial pressure levels diffuse are proportional to their what?

Back 68

Diffusion coefficients

Front 69

List in formula form the net
diffusion of gases through fluids

Back 69

P * A * S
D ---------------------
d * MW
D = diffusion rate
P = partial pressure difference
A = cross-sectional area
S = solubility of the gas
D = distance of diffusion
MW = molecular weight of the gas

Front 70

What 2 things determine the diffusion coefficient of the gas?

Back 70

* Gas solubility & molecular weight determine the diffusion coefficient of the gas

Front 71

What are the Relative Diffusion Coefficients of Respiratory Gases in Body Fluids (assuming the diffusion coefficient of oxygen is 1) for the following: O2
CO2
CO
N2
HE

Back 71

O2 1.0
CO2 20.3 * Although CO2 has a greater molecular wt.
CO 0.81 than O2, it diffuses 20X as rapidly b/c
N2 0.53 of much greater solubility
HE 0.95

Front 72

Respiratory membrane can increase due to what?

Back 72

* Membrane can increase due to edema in interstitial space; fibrosis as a result of pulmonary disease

Front 73

Respiratory gases are all highly soluble in ___, and consequently, highly soluble in ___ ____; major limitation is the rate of diffusion through ____ ____ instead of through the cell membrane

Back 73

Rrespiratory gases are all highly soluble in lipids, and consequently, highly soluble in cell membranes; major limitation is the rate of diffusion through tissue water instead of through the cell membrane
** gas diffusion through tissues is ~ equal to gas diffusion through water (i.e., the relative diffusion of gases in body fluids) **

Front 74

* Alveolar air has different concentrations gases from atmospheric air due to what 4 things

Back 74

1) Alveolar air is only partially replaced by atmospheric air w. each breath (“dead space” air)
2) O2 constantly absorbed into pulmonary blood from alveolar air
3) CO2 constantly diffusing from pulmonary blood into alveoli
4) Dry atmospheric air entering the respiratory passages is humidified before it reaches the alveoli

Front 75

Describe the composition of alveolar air & the factors that control this composition

Back 75

* PH2O (water )vapor at normal body temp. (37oC) = 47 mm Hg; b/c total pressure in the alveoli can not rise above atmospheric pressure (760 mm Hg), the water vapor dilutes all the other gases of inspired air
Alveolar O2 (PO2 = 104 mm Hg) -- alveoli concentration & thus its PO2 is controlled by:
1) rate of O2 absorption into the blood
2) rate of entry of new O2 into the lungs
Alveolar CO2 (PCO2 = 40 mm Hg) – alveolar PCO2
1) increases in direct proportion to rate of CO2 excretion
2) decreases in inverse proportion to alveolar ventilation
* Alveolar air is completely replaced by atmospheric air slowly (after ~ 16 breaths); important for preventing sudden changes in gas concentrations in the blood
FRC = 2300 ml, yet only 350 ml of new air is brought into the alveoli w. each breath
Tidal Volume - “dead air space” (500 ml – 150 ml) = 350 ml

Front 76

Describe the anatomical structure of the respiratory membrane

Back 76

Average thickness = 0.6 micrometers
Total surface area = 70 m2 (~ floor area of 25’ X 30’ room)
Total quantity of blood in pulmonary capillaries at any given time = 60-140 ml
Average diameter of pulmonary capillary = 5 micrometers; forces RBCs to squeeze through; RBC membrane usually touches capillary wall so that O2 & CO2 do not have to diffuse through significant amounts of plasma
1.Layer of fluid w. surfactant lining inside of alveolus
2.Alveolar epithelium composed of thin epithelial cells
3.Epithelial basement membrane
4.Thin interstitial space btwn. alveolar epithelium & capillary membrane
5.Capillary basement membrane (often fused w. alveolar basement membrane)
6.Capillary endothelial membrane

Front 77

Describe the 4 factors affecting rate of gaseous diffusion through the respiratory membrane

Back 77

1.Membrane thickness
2.Membrane surface area
3.Gas diffusion coefficient
4.Partial pressure difference of the gas btwn. the two sides of the membrane

Front 78

Respiratory membrane can decrease due to what?

Back 78

* Membrane surface area can decrease due to emphysema where many alveoli coalesce w. dissolution of alveolar walls; new alveolar chambers are larger than the original, but total surface is often greatly decreased; when total surface area decreases to 1/3 to ¼ normal, gas exchange is significantly impaired even during resting conditions

Front 79

Gas diffusion through respiratory membrane is due to what?

Back 79

* gas diffusion through respiratory membrane ~ to diffusion through water -à CO2 diffuses 20X as rapidly as O2, and O2 diffuses ~ 2X as rapidly as N2
Gas diffusion coefficient dependent on gas’ solubility in the membrane, and inversely to square root of gas molecular weight

Front 80

What are the two factors that determine PO2 and PCO2:

Back 80

1) rate of alveolar ventilation
2) rate of O2 & CO2 transfer through respiratory membrane

Front 81

Describe the ventilation-perfusion ratio (VA/Q)

Back 81

Normal VA/Q – gas exchange is nearly optimal
PO2 = 104 mm Hg (149 mm Hg in inspired air; 40 mm Hg in venous blood)
PCO2 = 40 mm Hg (45 mm Hg in venous blood; 0 mm Hg in inspired air)

Front 82

What is VA/Q=0?

Back 82

VA/Q = 0 – no alveolar ventilation, normal perfusion; alveoli air comes into equilibrium with venous blood partial pressures (PO2 = 40 mm Hg; PCO2 = 45 mm Hg)

Front 83

What is VA/Q=infinity?

Back 83

VA/Q = (infinity) – normal ventilation, abnormal perfusion; alveolar air not carried away, comes into equilibrium w. humidified inspired air (PO2 = 149 mm Hg; PCO2 = 0 mm Hg)

Front 84

What is VA/Q below normal?

Back 84

Physiologic Shunt (VA/Q is below normal) – inadequate ventilation to fully oxygenate blood, & a small fraction of venous blood is not oxygenated (“shunted”)

Front 85

What is VA/Q above normal?

Back 85

Physiologic Dead Space (VA/Q is above normal) – inadequate perfusion to some areas of lungs (e.g., apices); alveolar ventilation is “wasted”, ventilation in anatomical dead spaces is also “wasted”

Front 86

What is abnormal VA/Q in upper lung?

Back 86

Apex – both pulmonary capillary blood flow & alveolar ventilation are considerably less, and perfusion is decreased even more than ventilation; VA/Q as much as 2.5X greater than ideal value, leading to a moderate degree of physiologic dead space

Front 87

What is abnormal VA/Q in lower lung?

Back 87

Base – slightly too little ventilation in relation to perfusion; VA/Q as low as 0.6X the ideal value, leading to a small physiologic shunt

Front 88

What is abnormal VA/Q in Chronic Lung Disease (smoking, emphysema)?

Back 88

1) Small bronchioles become obstructed & alveoli “downstream” are unventilated (VA/Q = 0)
2) In areas were alveolar walls are destroyed but ventilation is still normal, the ventilation is “wasted” b/c perfusion is inadequate
* some lung regions have a serious physiologic shunt, whereas other areas have a serious physiologic dead space

Front 89

Respiration is dependent on what in regard to O2?

Back 89

* respiration is dependent on O2 tension / pressure, not concentration

Front 90

Describe the factors that determine PO2 and PCO2 of the pulmonary blood and of the tissues

Back 90

Lungs – alveolar PO2 – 104 mm Hg, venous blood PO2 = 40 mm Hg; initial pressure difference of 64 mm Hg moves O2 from lungs into the blood
* PO2 of blood entering left atrium (& thus systemic circulation) = 95 mm Hg due to venous admixture;
(~ 2% of the blood is “shunted” from the aorta to bronchial circulation, on leaving the lungs the “shunted” blood has a PO2 = 40 mm Hg; when combined w. oxygenated blood in the pulmonary veins, the venous admixture decreases the overall blood PO2 entering the left atrium)
Peripheral Capillaries into Tissue Fluid & Tissue Cells – systemic capillary PO2 = 95 mm Hg, interstitial fluid PO2 = 40 mm Hg
Interstitial fluid PO2 = 40 mm Hg, intracellular PO2 = 23 mm Hg

Front 91

PO2 at tissue level is determined by what 2 things?

Back 91

(1) rate of O2 transport (PO2 increases w. increased blood flow), and (2) rate of cellular O2 consumption (interstitial PO2 decreases w. increased cellular metabolism)

Front 92

CO2 diffuses ___times more rapidly than O2.

Back 92

* CO2 diffuses ~ 20X more rapidly than O2, so the pressures differences are much less than those required for O2 diffusion

Front 93

Describe the %s of oxygen transported by red blood cells and blood plasma

Back 93

97% transported by RBC combined w. hemoglobin (Hb); 5 ml of O2 per 100 ml of blood
3% dissolved in plasma (O2 has a low fluid solubility coefficient, does not dissolve readily in water); 0.17 ml of O2 per 100 ml of blood

Front 94

Describe the factors that determine PO2 and PCO2 of the pulmonary blood and of the tissues

Back 94

Tissue Cells & Tissue Fluid into Peripheral Capillaries –
intracellular PCO2 = 46 mm Hg, interstitial PCO2 = 45 mm Hg
Interstitial fluid PCO2 = 45 mm Hg, blood PCO2 (arterial end of capillary) = 40 mm Hg --à venous blood PCO2 (leaving capillary) = 45 mm Hg
* rate of blood flow & tissue metabolism affect interstitial PCO2 exactly OPPOSITE to their effects on tissue PO2
1) interstitial PCO2 increases w. decreased blood flow (from 45 mm Hg to 60 mm Hg); interstitial PCO2 decreases w. increased blood flow (45 mm Hg to 41 mm Hg)
2) a 10-fold increase in cellular metabolism greatly elevates interstitial PCO2 at all rates of blood flow,decreasing cellular metabolism to ¼ normal decreases interstitial PCO2 to 41 mm Hg
Lungs – blood PCO2 entering pulmonary capillaries (arterial end) = 45 mm Hg; alveolar PCO2 = 40 mm Hg; initial pressure difference of 5 mm Hg moves CO2 from the blood into the lungs

Front 95

During strenuous exercise extra O2 released w. little further decrease in tissue PO2 due to what 2 things?

Back 95

1) steep slope of dissociation curve
2) increased tissue blood flow caused by decreased PO2 (very small decrease in PO2 released large amounts of extra O2)

Front 96

What is the “Buffer” Effect of Hemoglobin When Atmospheric PO2 Changes?

Back 96

* Hb still maintains nearly constant tissue PO2 b/c. pressures are w/in “steep” part of the curve

Front 97

Why is alveolar PO2 lower than ambient PO2?

Back 97

* alveolar PO2 is lower than ambient PO2 due to displacement of O2 by water vapor & mixing w. CO2 during gas exchange

Front 98

Describe hemoglobin oxygen saturation at various PO2 levels

Back 98

Maximum amount / ideal conditions:
15 g Hb per 100 ml blood
Each gram can bind w. a maximum of 1.34 ml O2
* 20 ml O2 bound to Hb per 100 ml of blood IF Hb 100% saturated

* Systemic arterial blood is 97% saturated w. O2 (19.4 ml O2 per 100 ml blood); venous blood returning to heart has 14.4 ml O2 per 100 ml blood (75% saturated)
* under normal conditions, 5 ml O2 off-loaded to tissues (transported from lungs to tissues) per 100 ml blood
* Systemic arterial blood leaving heart – PO2 = 95 mm Hg, blood 97% saturated w. O2
* Venous blood returning to heart - PO2 = 40 mm Hg, blood 75% saturated w. O2, 25% of the O2 off-loaded into tissues
* During strenuous exercise interstitial PO2 can fall to 15 mm Hg, blood ~ 18% saturated w. O2, 82% of O2 off-loaded to working muscles (15 ml of O2 delivered to tissues vice the normal 5 ml)
Hemoglobin Maintains a Nearly Constant PO2 in the Tissues:
** Hb in the blood automatically delivers O2 to the tissues w/in a tight pressure range of 15 mm Hg to 40 mm Hg
* Upper limit of PO2 = 40 mm Hg b/c if interstitial pressure rises any higher, the amount of O2 needed by the tissues would not be released

Front 99

List the Altitude/ Atmo Pressure (Pb)/ Amient PO2 (PAO2)/ Alveolar PO2 (PaO2)/ Arterial PO2/%Hb-O2 sat for the following:
SeaLevel
8K'
10K'
18K'
25K'
Mt Everest

Back 99

Altitude/ Atmo Pressure (Pb)/ Amient PO2 (PAO2)/ Alveolar PO2 (PaO2)/ Arterial PO2/%Hb-O2 sat
SeaLevel/760mmHg/159mmHg/104mmHg/95mmHg/97%
8K'(2,438m)/ 565mmHg/118mmHg/ 69mmHg/~59mmHg/89%
10K'(3,048m)/ 523mmHg/110mmHg/ 61mmHg/~51mmHg/87%
18K'(5,486m)/ 380mmHg/80mmHg/ 38mHg/28mmHg/55%
25K'(7,620m)/ 282mmHg/59mmHg/ 30mmHg/~20mmHg/28%
29,028'(8,848m)/ 253mmHg/

Front 100

List the factors that “shift” O2-Hb Dissociation Curve:

Back 100

* Hb has LESS affinity for O2, releases more O2 into the tissues
* Bohr Effect – increased CO2 and [H+] (blood more acidic); more metabolically active muscles release greater amounts of CO2 into the blood, increases PCO2 which in turn raises blood H2CO3 (carbonic acid), and thus [H+]; “shifts” O2-Hb dissociation curve downward & to the right, forcing O2 away from Hb & into the tissues
* 2,3-biphosphoglycerate (BPG) – product of BBC metabolism; increases in response to chronic hypoxia

Front 101

Describe the mechanisms by which CO2 is transported by the blood, including percentages.

Back 101

7% dissolved as CO2 in plasma
23% as CO2Hgb (carbaminohemoglobin) – influenced by PCO2
70% as HCO3- (bicarbonate ion)
carbonic anhydrase
CO2 + H2O --------------- H2CO3 à HCO3- + H+ in RBCs,
* carbonic anhydrase “hydrates CO2”, catalyzes rxn. by 5000-fold, allows tremendous amounts of CO2 to react w. RBC water before blood leaves the capillaries
* H2CO3 (carbonic acid) dissociates into:
H+ ions – bind w. Hb in RBC, Hb proteins are powerful acid-base buffers
HCO3- ions – diffuse into plasma while Cl- ions diffuse into RBC -- Chloride Shift

Front 102

List the five (5) steps for treating hyperventilation

Back 102

* In clinical practice, treat hyperventilation by reducing the rate & depth of breathing, and by rebreathing exhaled air
* At altitude it’s difficult to distinguish hyperventilation symptoms from those of hypoxia, so treat as if hypoxia by administering 100% O2 before attempting to decrease rate & depth of breathing

Front 103

State the steps for performing the pause breathing method

Back 103

1.Let lungs fill w. air
2.Hold breath for 2-3 seconds
3.Exhale

Front 104

Discuss the relationship between the loss of atmospheric pressure and the onset of hypoxia

Back 104

* Decreased barometric pressure is the basic cause of all hypoxia problems at high altitude; as barometric pressure decreases, atmospheric / ambient oxygen partial pressure PAO2) decreases proportionately
* Alveolar oxygen partial pressure (PaO2) is even lower due to dilution w. water vapor & mixing w. CO2 during gas exchange
* Acute response to hypoxia – increased ventilation (driven by peripheral chemoreceptors) and increased cardiac output
* Chronic response to hypoxia / acclimatization to low PO2:
1) Increase in pulmonary ventilation
2) Increased # of RBCs
3) Increased diffusing capacity of the lungs
4) Increased vascularity of the perhipheral tissues
5) Increased ability of the tissues to use O2 despite low PO2

Front 105

List the five (5) steps for the treatment of hypoxia

Back 105

1.Administer 100% O2
2.Slow breathing rate (pause breathing technique)
3.Check O2 equipment
4.Descend below 10K’
5.Communicate

Front 106

List 4 causes of hyperventilation

Back 106

1.Psychological and/or physical stress / anxiety
2.Pressure breathing – usually above 39K’, when breathing 100% O2 to maintain PaO2 at or above 60 mm Hg
3.Hypoxia – usually above 10K’ where PaO2 drops below 60 mm Hg
4.Medications (salicylates {asprin}, progestins {birth control pills}, theophylline {asthma inhalers})