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CIF > Lungs > Flashcards

Lungs Flashcards

1
Q

Describe the oxidative metabolism.

A

Monosaccharides, FAs, AAs –> acetyl CoA –> citric acid cycle –> NADH + FADH2 + CO2 –> electron transport chain –> ATP

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2
Q

Briefly describe the O2 transport to the tissue.

A

Surrounding air –> alveoli –> pulmunary capillaries –> heart –> aorta –> arteries –> tissue capillaries –> cells

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3
Q

What is necessary for an efficient diffusion?

A

A large area + a small distance => branching

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4
Q

Describe the airway anatomy briefly.

A

Nose/mouth –> pharynx/larynx –> trachea –> LUNG: bronchi –> bronchiole –> alveoli –> alveolar capillaries –> pulmonary venule

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5
Q

Describe the two type of cells found in alveoli and capillaries.

A

Type I cells: gas exchange
Type II cells: produces surfactant

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6
Q

What are the function of bronchioles?

A

They can contrict and dialate

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7
Q

What are the function of cillia and mucus producing cells in trachea?

A

Ensures bacteria and other particles are caught and removed from the airways –> mouth

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8
Q

What are asthma caused by?

A

Decreased contractility in the bronchioles –> resistance to expire air

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9
Q

How can lung volumes be measured?

A

By a spirometer:
Forced expiration volume (FEV) - first max inspiration –> max expiration

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10
Q

What is the residual lung volume, and what are the purpose of this?

A

The volume of air left in the lung after expiration
Puspose: ensures the lungs doesn’t collapse

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11
Q

What is and how big is the tidal volume (TV)?

A

The air inspired/expired at rest, app. 0.5 L

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12
Q

What is the difference between the total lung capacity (TLC) and the vital capacity (VC)?

A

TLC: the total capacity, inc. the residual volume
VC: the actual capacity (TLC-RV)

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13
Q

What happens to the VO2 and ventilation if we look at a trained and an untrained subject?

A

Trained: higher VO2 and higher ventilation

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14
Q

What are the absolute pressures in the intrapleural space?

A

753 mmHg (top), 756 mmHg (middel), 758 mmHg (bottom)

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15
Q

What is the atmospheric pressure?

A

760 mmHg

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16
Q

Describe the P_IP.

A

Less than atmospheric, crucial to keep lungs expanded, gravity and posture –> P_IP gradient from apex to base

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17
Q

What are the intrapleural space?

A

5-35 µm, app. 10 mL fluid surrounding the lungs

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18
Q

What causes the negative pressure in the IPS?

A

The innert pulling of the lungs (towards collapse) and the chest wall pulling away => negative pressure in IPS

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19
Q

How can a collapsed lung be reexpanded?

A

By increasing P_TP, by either:
1) Increase P_alv by pressing air into lungs
2) Decrease P_IP by pulling air out

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20
Q

What is the transpulmonary pressure (P_TP)?

A

The pressure difference between the IPS and the alveoli - keeping the lungs expanded
P_TP = P_alv - P_IP

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21
Q

What is the transmural pressure (P_TM)?

A

The pressure difference across an airway wall - distending the airway
P_TM = P_airway - P_IP

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22
Q

How does the surface tension impact compliance?

A

Accounts for most elastic recoil
High surface tension –> high elastic recoil –> low compliance

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23
Q

How does the type II cells impact the surface tension and compliance?

A

Type II cells produce surfactant –> reduce surface tension –> increased compliance (–> easier to inflate lung)

24
Q

How does surfactant reduce surface tension?

A

It minimizes fluid accumulation in the alveoli –> helps keeping the alveolar size relatively uniform

25
Q

What is compliance?

A

Distensibility (udstrækkelighed)

26
Q

How does lung volume affect the compliance?

A

The bigger the lung volume, the lower the compliance

27
Q

What is the advantage of surfactant?

A

It minimizes surface tension, and increases compliance

28
Q

Give the equation for compliance.

A

C = delta V_L/delta P_TP

29
Q

What is the differnece between obstructive and restrictive pulmonary diseases?

A

O: increased resistance in airways (e.g. emphysema)
R: reduced lung volme, reduced compliance (e.g., fibrosis)

30
Q

How much of O2 is transported bound to hemoglobin?

A

> 98 %, rest dissolved in plasma

31
Q

Describe the O2-Hb dissociation curve.

A

S-shaped due to allosteric regulation of Hb subunits, the plateau provides a safety margin, and the steep part ensures efficient uptake in the lungs and delivery in the tissues
App. 90 % bound to Hb at 60 mmHg, 75 % at 40 mmHg

32
Q

How does pH affect the dissociation curve?

A

Higher pH –> shift to left, and vice versa

33
Q

How does PCO2 affect the dissociation curve?

A

The higher the PCO2 the more to the right the curve is shifted, but not very much

34
Q

How is CO2 transported in the blood?

A

app. 10 % dissolved in plasma, app. 20-30 % bound to Hb, app. 60-70 % as HCO3-

35
Q

What is th Borh effect?

A

Respiratory acidosis shifts the curve to the right
=> Drop in pH and increase of PCO2 decrease the affinity of Hb for O2

36
Q

How does temperature affect the dissociation curve?

A

Higher temp –> shift to right (lower affinity)

37
Q

Describe the pulmonary diffusion capacity (D_L).

A

Describes the impact of thickness of the barrier on flow.
D_L = k * (A* s/a * (sqrt(MW))
A: barrier area, s: solubility of the gas, a: thickness of barrier, MW: molecular weight of gas

38
Q

How is the flow calculated?

A

Flow = D_L * delta P

39
Q

Describe the link between thickness and flow.

A

Increase thickness –> reduce flow
Vice versa

40
Q

How can pulmonary diseases impact the flow?

A

Mainly by reducing the barrier area, or increasing the thickness of the barrier

41
Q

What is CO used to estimate, how and why?

A

Used to estimate D_L, because it’s diffusion limited

Steady state technique: breathe low CO air 12 x –> measure VCO and P_ACO and maybe P_VCO

Single breath technique: maw expiration –> max inspiration of CO/He –> measure He to calculate initial Alv CO content and initial P_AOC –> measure end P_ACO and Alv CO content

VO_CO = DL * (P_ACO - P_VCO)

42
Q

Does CO uptake reach diffusion equilibrium?

A

No
CO flux is low, and Hb quickly binds CO

43
Q

How is DL and CO uptake connected?

A

CO uptake is diffusion limited, CO uptake is proportional to DL over a vide range of DL values

44
Q

Is CO uptake affected by changes in blood flow?

A

No

45
Q

Describe the diffusion properties of N2O uptake.

A

Hb does not bind N2O, diffusion reaches equilibrium at 10 % of length
DL only affects how fat N2O reaches equilibrium, not end capillary N2O uptake/content
Q changes the end capillary N2O content/uptake

=> perfusion limited

46
Q

Describe the diffusion properties of O2 uptake.

A

Reaches equilibrium quickly
Changes in DL affects how fast equilibrium is reached, but not end content
Changes in Q does not change PO2 –> increase in VO2

=> perfusion limited

47
Q

Describe the diffusion properties of CO2 release.

A

Reaches equilibrium quickly

=> perfusion limited

48
Q

What is the difference between the anatomical- and the alveolar deadspace?

A

AN: the air in the respiratory tract that does not reach the alveoli
AL: can happen if e.g., a blood clot causes reduced perfusion

49
Q

What is the physiological dead space?

A

PDS = AN + AL

50
Q

How is the alveolar ventilation (V_A) calculated?

A

V_A = (V_T - V_D)*f
V_T: tidal ventilation
V_D: anatomical deadspace

51
Q

Where in the alveoles are the ventilation highest?

A

At the base, because of posture and gravity

52
Q

Describe how V_A and Q changes towards the apex.

A

Both decreases –> V_A/Q ratio increases

53
Q

How does the lungs counteract alveolar dead space?

A

Alveolar dead space caused by reduced perfusion –> regulated by broncho restriction and redirection of ventilation + reduced surfactant

Alveolar dead space caused by reduced ventilation –> regulated by vaso-constriction and redirection of blood

54
Q

What does hyperventilation and hypoventilation cause respectively?

A

Hyper: CO2 wash out and higher [O2] + higher VA/Q

Hypo: [O2] decrease and [CO2] increase + lower VA/Q

55
Q

How are V_A and P_A related?

A

Inverse: if one increase, the other decrease

CIF (11 decks)

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