Lungs Flashcards by Sofie Sørensen

Describe the oxidative metabolism.

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

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Briefly describe the O2 transport to the tissue.

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

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What is necessary for an efficient diffusion?

A large area + a small distance => branching

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Describe the airway anatomy briefly.

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

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

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

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What are the function of bronchioles?

They can contrict and dialate

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

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

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What are asthma caused by?

Decreased contractility in the bronchioles –> resistance to expire air

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How can lung volumes be measured?

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

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

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

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

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

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

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

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

Trained: higher VO2 and higher ventilation

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What are the absolute pressures in the intrapleural space?

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

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What is the atmospheric pressure?

760 mmHg

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Describe the P_IP.

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

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What are the intrapleural space?

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

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What causes the negative pressure in the IPS?

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

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How can a collapsed lung be reexpanded?

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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What is the transpulmonary pressure (P_TP)?

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

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What is the transmural pressure (P_TM)?

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

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How does the surface tension impact compliance?

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

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

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

How does surfactant reduce surface tension?

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

What is compliance?

Distensibility (udstrækkelighed)

How does lung volume affect the compliance?

The bigger the lung volume, the lower the compliance

What is the advantage of surfactant?

It minimizes surface tension, and increases compliance

Give the equation for compliance.

C = delta V_L/delta P_TP

What is the differnece between obstructive and restrictive pulmonary diseases?

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

How much of O2 is transported bound to hemoglobin?

> 98 %, rest dissolved in plasma

Describe the O2-Hb dissociation curve.

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

How does pH affect the dissociation curve?

Higher pH --> shift to left, and vice versa

How does PCO2 affect the dissociation curve?

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

How is CO2 transported in the blood?

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

What is th Borh effect?

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

How does temperature affect the dissociation curve?

Higher temp --> shift to right (lower affinity)

Describe the pulmonary diffusion capacity (D_L).

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

How is the flow calculated?

Flow = D_L * delta P

Describe the link between thickness and flow.

Increase thickness --> reduce flow Vice versa

How can pulmonary diseases impact the flow?

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

What is CO used to estimate, how and why?

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)

Does CO uptake reach diffusion equilibrium?

No CO flux is low, and Hb quickly binds CO

How is DL and CO uptake connected?

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

Is CO uptake affected by changes in blood flow?

Describe the diffusion properties of N2O uptake.

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

Describe the diffusion properties of O2 uptake.

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

Describe the diffusion properties of CO2 release.

Reaches equilibrium quickly => perfusion limited

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

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

What is the physiological dead space?

PDS = AN + AL

How is the alveolar ventilation (V_A) calculated?

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

Where in the alveoles are the ventilation highest?

At the base, because of posture and gravity

Describe how V_A and Q changes towards the apex.

Both decreases --> V_A/Q ratio increases

How does the lungs counteract alveolar dead space?

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

What does hyperventilation and hypoventilation cause respectively?

Hyper: CO2 wash out and higher [O2] + higher VA/Q Hypo: [O2] decrease and [CO2] increase + lower VA/Q

How are V_A and P_A related?

Inverse: if one increase, the other decrease