Physio - Respiration

Front 1

When is intrapulmonary pressure (in the lung) the highest?

Back 1

middle of expiration,forces air out of lungs

Front 2

transpulmonary pressure

Back 2

"collapsing force"; difference between intrapulmonary and intrapleural pressure

P(tp) = P(pul) - P(pl)
~remember intrapleural pressure must always be subatmospheric and lower than intrapulmonary
(less than intrapulmonary, otherwise lung collapses)

Front 3

Tidal volume

Vital capacity

Back 3

The actual respired volume. It varies according to the actual requirements

Vital capacity:(max vol. can be respired) =
Inspir.reserve vol. + tidal vol. + expiratory reserve volume

Front 4

Residual volume

Back 4

The volume remaining in the lungs after a maximum expiration; always there after first breath

Front 5

ANATOMICAL DEAD SPACE

physiological dead space.

Back 5

inspired toward end of inspiration - never reaches the alveoli, but rather just fills inactive parts of respiratory tract (nose, mouth, pharynx, larynx, trachea, bronchi and bronchuli).

So air may reach alveoli and still not participate in gas-exchange, because of other factors (insufficient perfusion in pulmonary cap. OR insufficient diffusion)

Front 6

What are 3 things that must occur for gas exchange?

Back 6

3 factors: ventilation, perfusion (of pulmonary capillaries) and diffusion.

So air may reach alveoli and still not participate in gas-exchange; known as physiological dead space.

Front 7

Dynamic Compliance

Back 7

actual volume of respiration depends on factors like RESISTANCE to airflow, elastic forces of lung tissue, surface tension in alveoli, and friction betw. lung and surrounding tissues.

In chart, during inspiration these counteracting forces (like resistance) increase slope of line, shift to right

Front 8

Respiratory work:

Back 8

how much pressure must be applied to inspire and expire

depends on resistance

Front 9

Attraction forces (favoring collapse) increase when radius of alveoli _______.

Explain what causes this.
What counteracts this?

Back 9

decreases; due attraction forces between water molecules, increases surface tension

SURFACTANT, seperation H2O molecules

Front 10

Approximately _____ of alveolar epithelial cells are so-called _____which produce and secrete the surfactant

Back 10

10%; type II cells

Front 11

What is ~volume of air (at atm pressure) exchanged during respiration?

Volume of blood perfusing pulm.caps during this time? (at rest)
Volume of blood perfusing pulm.caps during exercise?

Back 11

5 L

5 L (@ 15 mmHg)
24L, result of increased blood pressure 28 mmHg

Front 12

functional blood?

nutritional blood?

which has higher pressure and/or perfusion?

Back 12

from R. Ventricle, goes to lungs to exchange gases

from left ventricle via systemic circuit, feed lung tissue itself with O2; higher pressure b/c whole lung needs to be fed

Front 13

Zone at top of lungs?

Zone at bottom of lungs?

HP in these zones?

Back 13

Zone 1: the highest part of lung

If systolic pressure < HP (pushing down), then no blood flow here

Zone 3 (lowest zone, lower HP)
Systolic pressure & diastolic pressure > hydrostatic pressure, so always perfused

Front 14

What effect does increased CO2 have on pH of blood?

Effect of this on O2 dissociation?

Back 14

Lowers it, b/c CO2 is quickly converted to carbonic acid

Lower pH means easier for O2 to dissociate from Hb

Front 15

How does interstitial oncotic pressure in pulmonary capillaries compare with others in body?

Back 15

much higher! (due to surfactant, etc)

So interstitial oncotic pressure is much higher (18 mmHg) compared to peripheral tissues (1 mmHg)
= “leaky capillaries” , pulling fluids out

Although hydrostatic pressure in lung capillary (pushing out), is slightly lower (12 mmHg) compared to other caps (18 mmHg)

Overall pulm.caps push out fluids w/+10 mmHg while other caps push out w/+1 mmHg only (not as leaky)

Front 16

Starling Equation:

Back 16

net pressure =
hydrostatic pressure - oncotic pressure

net pressure =
[ 12 – (-5) ] - [ 25 – 18 ] = + 10 mmHg

Front 17

alveolar vs interstitial edema

Back 17

interstitial edema is the milder form of a pulmonary edema

Alveoli filled with fluid can’t exchange gas any more, and as a result a severe alveolar edema can lead to death by suffocation.

Alveolar edema occurs if interstitial edema (pressure) increases as more fluid enter from capillaries. If this pressure turns positive then the fragile alveolar membranes rupture and fluid oozes out of the interstitium into the alveoli. The result is an alveolar edema.

Front 18

At higher temperature, air holds ______ H2O?

At body core temp, P(H2O) is _______?

At 100 °C pH2O = ?

Back 18

more H2O! so PH2O increases

note: there is P(H2O)max for given temperature; for which P(H2O) cannot exceed


At 37^C, P(H2O) is 47 mmH20

At 100 °C pH2O = 760 mmHg

Front 19

Gases of respiratory importance are highly soluble in ?

Major limitation results from ?

Back 19

highly soluble in lipids

diffusion through the tissue water

CO2 is 20x more soluble than is O2

Distance ~ 1 mm, but this increases w/interstitial edema

Front 20

Respiration is controlled by ________ which adjusts the VENTILATION RATE (increases during exercise) in such a way that the O2 partial pressure in the alveolar air is always 104 mmHg.

How can we increase this PP?

Back 20

respiratory center in the medulla oblongata;

voluntary hyperventilation

extra info:
maximum in dry air would be 159 mmHg, but as alveolar air is saturated w/water vapor it is reduced to 149 mmHg

Front 21

ventilation rate of 18 L/min (human) might occur during _______.

Back 21

exercise; at rest ~4.2L/min

Front 22

Normal alveolar O2

Normal alveolar CO2

Back 22

104 mmHg

40mmHg

Respiratory center maintains an alveolar PCO2 and pO2 by adjusting ventilation rate

Front 23

how conditions in alveoli change if...
if perfusion is low?

if ventilation is low (but perfusion normal)?

Back 23

conditions in alveoli become more like ambient air ((PO2 = 149mmHg, PCO2 = 0 mmHg).


conditions in alveoli become more like blood
(PO2 = 40mmHg and PCO2 = 45 mmHg).

Front 24

Four O2 can bind Hb:
When is affinity for O2 highest? Which O2 binds with most force

Is it harder to remove or dissociate an oxygen when all four are bound? or when only one remains?

Back 24

When 3 oxygen molecules have already bound Hb, affinity is highest; and therefore 4th binds with most force
(The binding of the first O2 increases the binding forces of the remaining three hems.)

harder to remove an oxygen when all four remain bound

Front 25

What causes most of O2 to dissociate from Hb? In other words, what has to happen to get saturation below 50%?

When does this happen?

Back 25

Low pO2 in blood (below 40mmHg)

At low pO2, % saturation (of Hb) is lowest

Usually only during exercise

Front 26

What effect does resting have on oxygen disociation?

Back 26

pO2 in blood at tissues never gets below 40 mmHg, so 75% of Hb remains saturated with O2

Front 27

The binding forces for oxygen to hemoglobin not only depend on the four hems. Four other parameters play an important role too:

Back 27

- pH
- PCO2
- Temperature
- DPG (= concentr. of diphosphoglycerate)
When the metabolism increases more oxygen is needed, and consequently facilitating the release of oxygen is of advantage. A shift of the curve to the right meets this goal.

Front 28

What immediate changes occur in blood during exercise?

How does O2 dissociation curve change?

Back 28

More CO2 produced, so pH goes down (HCO3-).

Body temperature rises

DPG rises (intermediate of glycolysis).

SHIFTS TO RIGHT!
More O2 dissociates.

Front 29

As CO2 expired in lungs, what happens?

What happens to curve?

Back 29

pH rises.
(also body temp is lower than in muscles)

shfits to LEFT

That is why saturation always higher in lungs
@40 mmHg O2, satur. already 90%

Front 30

Intracellular store for O2

Back 30

myoglobin

only one heme

used in muscles for quick uptake of O2

Front 31

CO2 transported in blood mostly as

Back 31

Bicarbonate HCO3- , 70% of time

w/Hb, 23% of time

Front 32

Describe path of CO2

Back 32

-Leaves tissues to ECF, thru capillary wall where enters RBC still as CO2
-CA in RBC, converts W + CO2 --> HCO3- and H+.
- H+ binds to Hb and Cl- uptake drives HCO3- release into plasma

Front 33

Bohr effect has to do with

Back 33

Effect of H+ and CO2 in tissues on release of O2 from Hb.

States that ncreasing conc. of protons and/or CO2 will reduce O2 affinity of Hb. Increasing blood CO2 levels can lead to decrease in pH because of chemical equilibrium between protons and CO2. (more simply CO2 is quickly converted into carbonic acid, so pH down)

Front 34

Haldane Effect.

Back 34

In lung hemoglobin gets loaded with oxygen. This pushes CO2 and H+ out of their binding. This CO2 together the CO2 formed from H+ bicarbonate gets expired.

Effect of O2 on CO2 and H+ in lung is called Haldane Effect.

Front 35

Emphysema

Back 35

obstructive lung disease char by destruction of lung tissue around alveoli, making them unable to hold functional shape during exhalation.

Decreased surface area, etc

Front 36

Hamburger Shift

Back 36

also known as Chloride shift

refers to exchange of bicarbonate (HCO3-) and chloride (Cl-) across membrane of red blood cells.

Front 37

Amount of gas dissolved in water phase at equilibrium depends on:

Back 37

-partial pressure of the gas
-soluablity of the gas in water

A gas always diffuses down its partial pressure gradient

pCO2 highest in pulmonary capillaries, therefore it moves out and into alveolar space

Front 38

1. What is normal pCO2 in alveoli?
2. What is normal pCO2 in arterioles?
3. What is normal pCO2 in venous blood?

Back 38

1. 40 mmHg
2. 40 mmHg?
3. 45 mmHg

Front 39

1. What is normal pO2 in alveoli?
2. What is normal pO2 in arterioles?
3. What is normal pO2 in venous blood?

Back 39

1.104 mmHg
2. 95 mmHg (and Hb carries ~200ml O2/L blood)(Hb 95% saturated)

3. 40 mmHg at rest (20 mmHg or less with exercise)(Hb still 75% satur. in venous blood when at rest)

Front 40

1. The _______ consists of several groups of neurons, widely dispersed in the medulla oblongata and the pons


2. ______ and _______of neurons generate the respiratory rhythm

3. The______ terminates the inspiration
The function of the

Back 40

1. respiratory “center”

2. Inspiratory and expiratory groups

Inspiratory neurons dominate. Expiratory neurons get only activated when the respiratory drive increases


3. pneumotaxic center (or central pattern generator, CPG)

Inspiration is an active act. It begins when inspiratory groups generate a signal (increasing AP) that causes inspiratory muscles to contract. Strength of this contraction and depth of inspiration depends on signal strength (frequency of AP's). Diagram above shows that inspiratory groups generate an increasing rate of APs, so-called "inspiratory ramp signal", which, at end of inspiration, is CUT OFF by pneumotaxic center.

Front 41

The function of the _______is not yet completely clear. Under extreme circumstances it seems to prevent or retard the “switch-off” function of the pneumotaxic center

Back 41

apneustic center

Front 42

Hering-Breuer reflex.

Back 42

Protective mechanism for preventing excess lung inflation

Stretch receptors in smooth muscles of wall of bronchi and bronchioli prevent such an overstretch: if a whole lung or part of it gets stretched beyond its physiologcal limits they transmit a signal to respiratory center that causes termination of the inspiration

Front 43

The main stimulus of central receptors (in medulla oblongata) is ______?

Back 43

measure pCO2 via pH of the cerebrospinal fluid (CSF)

CO2 diffuses easily from blood into the CSF,
pH in the CSF mirrors acute changes of pCO2 because of a low buffer concentration in the CSF

Front 44

What happens to gas composition of alveolar air durring inspiration?

Back 44

some of the air to first enter alveoli is from dead space in bronchioles that was not exchanged during last respiratory cycle. this causes an initial reduction in O2 concentration. however, this air then mixes with fresh air and O2 content increases again!

Front 45

1.What is 2,3-DPG?

2. Levels of 2,3-DPG increases during?

Back 45

1. byproduct of glycolysis, present in RBC, which facilitates release of O2 from blood cell

2. increases during...
- during exercise or high activity
- patient has anemia
- at high elevation

But it impairs O2 uptake in lungs? Why?
I don't think its present in high lvl when RBC reach lungs, because most of glycolysis occurs in muscles

Front 46

What is purpose or principle behind the conversion of CO2 to bicarbonate and then to carbonic acid (HCO3-)?

Back 46

- HCO3- dissolves in blood much more easily than CO2

- H+ (from H2CO3) binds to Hb, inhibiting Hb from binding O2, this facilitates release of O2 into tissues! <----Bohr effect!

Front 47

How do Type-I Cells (Peripheral Receptors) respond to increase in CO2, low O2 conc. , and/or low pH?

Back 47

stop K+ efflux, and open Ca++ channels resulting in a release of transmitter via exocytosis

at post-synaptic side the AP is generated; the more nt's received stronger signal generated

Front 48

The main stimuli of Peripheral Receptors are ______?

Where are Peripheral Receptors located?
What are these receptors called?

Back 48

- measure O2, H+, CO2

-Aorta, a. carotis
- known as single cell type (Type-I cells)

Front 49

1. Where would particles (size = 6um) be deposited?

2. Where would particles (size = 1-5um) be deposited?

3. Where would particles (size <1um) be deposited?

Back 49

1. at the bends of the larger airways of nasopharynx (this is known as impaction)

“mucociliar escalator” in the pharynx

2. sedimentation onto the walls of smaller airways (secondary bronchi?)

3. reaches alveoli
(diffusion to surface or exhaled again)

Front 50

What is fate of these vasoactive substance entering lung capillaries:
1. Serotonin
2. Norepinephrine
3. Bradykinin

Back 50

endothelial cells in lung caps can synthesize, activate and inactivate hormonally
active agents, thus also influencing other organ functions in body.

1. removed almost totally

2. cleared to some degree(ACH, epinephrine, and histamine are not removed)

3. inactivated by angiotensin-converting enzyme

Front 51

What is fate of these vasoactive substance entering lung capillaries:
1. Angiotensin I
2. Prostaglandins
3.

Back 51

1. converted to angiotensin II
2. majority of prostaglandins are degraded in the lung

Front 52

What is fate of these substance entering lung capillaries:
1. Leukotrienes
2. Exogenous toxic substances

Back 52

1. degraded by neutrophils

2. removed from blood

Front 53

Atelectasis

Back 53

Atelectasis means absence of gas from parts of or a whole lung.

Front 54

Emphysema

Back 54

Emphysema is called an obstructive lung disease because the destruction of lung tissue around alveoli

It is opposite of atelectasis; it means there is excess air in the lung.
Can develop quickly, or overtime. Alveoli get severely overinflated and rupture, thus forming “super-large alveoli” with their neighboring alveoli. Unfortunately blood supply does not match size of these “super-large alveoli” and they contribute little or nothing to gas exchange. They are just physiological dead space.

Front 55

Open pneumothorax

Back 55

open hole in chest wall, opening up pleural space to the ambient air outside. Recoiling forces of lung cause collapse of lung and space fills w/air sucked in thr. open hole.

Front 56

Tension Pneumothorax

Back 56

hole in pleural space is smaller and works like valve; closes during expiration. Lung collapse and incr. pressure continues to push against mediastinum and healthy lung. Very serious.

Front 57

nutritional circulation for lung originates from ________?

function circulation for lung originates from ________

Back 57

left ventricle! this blood is oxygenated already

right ventricle, this blood is going to lung to get oxygenated..this is called pulmonary circuit
(13 mmHg leaving right ventricle, 5 mmHg returning)

Front 58

Closed Pneumothorax?


3 things that can cause this?

Back 58

hole is in lung itself, air enters pleural space and collapses injured lung

most common type of pneumothorax

inherited weakness of lung tissue, by forced respiration due to obstruction of airways, or ascending from a dive without breathing.

Front 59

Closed Pneumothorax?


3 things that can cause this?

Back 59

hole is in lung itself, air enters pleural space and collapses injured lung

most common type of pneumothorax

inherited weakness of lung tissue, by forced respiration due to obstruction of airways, or ascending from a dive without breathing.

Front 60

Bronchitis

Back 60

mucous blocks airways, becomes a problem during expiration b/c airway constricts; this leads to chronic pulmonary emphysema

Front 61

Frequent causes for pulmonary edemas are:

Back 61

1. Left heart failure or mitral valvular disease --> increase of capillary hydrostatic pressure

2. Damage of pulmonary capillary membrane(e.g. infection, breathing noxious gases) --> increase of permeability

Front 62

Are alveoli functional in patient suffering from interstitial edema?

Back 62

Yes, although the gas exchange may be reduced because of a longer diffusion distance, the alveoli remain functional and gas exchange can occur.

Front 63

Total capacity

Back 63

The maximum air the lungs can hold (= after a maximum inspiration)
~also includes residual volume which can never be expired

Front 64

When is transpulmonary pressure lowest?

Back 64

end of expiration

Front 65

When intrapulmonary VOLUME the highest?

Back 65

At end of inspiration, between inspiration and expiration

known as STATIC COMPLIANCE

intrapulm.vol and intrapleural vol are constant

Front 66

zone 2 is only perfused during

Back 66

systole
(not diastole)