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Flashcards in Lung Physio Deck (27):

Asthma and Emphysema on Spirometry values

These are obstructive, so obviously FEV1 is going way down and FVC is going down and TLC is going up. Causes the ratio to go down as well.

Our RV also goes way up because theres more we can't get rid of, which increases our FRC as well.


Lungs recoil to this passively during expiration



Describe bodily forces around the lung

Inward recoil of the lungs and outward recoil of the chest wall creates pressures.

We are at a negative pressure (transpulmonary) when intraalveolar pressure is lower than ambient pressure. This causes air to come in

We are at a positive pressure to exhale when intralveolar pressure is greater than the ambient pressure.


Discuss when we are at a lower or higher elasticity, compliance, and tendency to collapse.

Emphysema = obstructive = Increased compliance and a decreased elasticity which means a decreased tendency to collapse, opposite for our restrictive conditions like pulmonary fibrosis.


Discuss intralveolar and intrapleural pressures during inspiration and expiration

For air to come in, intralveolar must reflect a proper gradient. We want a negative intralveolar pressure during inspiration, leading to a max of zero at our complete inspiration. To reflect this, our intrapleural pressure needs to drop as well to put negative pressure on the alveoli, so we go from -5 to -8.

For exiting its the reverse.


Discuss the Bohr equation and when we use it

This discusses our physiologic dead space.

VD = VT * [(PaCO2 - PeCO2) / PaCO2]


How does the Bohr equation link to alveolar ventilation?

Alveolar ventilation is how much of our breathing is actually getting to the alveoli, so you have to take your BPM and multiply it by the TV - VD to account for how much is actually getting to them.


Relate compliance to elasticity

Volume change per unit pressure is our compliance which is the inverse of elasticity.


Major source of resistance is:_____

We know this how?

Medium sized bronchos due to r^4 from Poseuille's Equation.

= 8*(Viscosity)*(Length) / pi r ^ 4


Haldane effect?

O2 binding to hemoglobin causes CO2 to release


Discuss the three lung zones, what their PA, Pa and Pv is, Q, V/Q, and PO2/PCO2

Zone 1 is in the top of the lung, PA>Pa>Pv. The capillaries are very compressed up here, leading to a decreased Q. There is more dead space up here, and as such our V/Q is high. PO2 is the highest here and PCO2 is the lowest

Zone 2 is the middle of the lung, Pa>PA>Pv. Blood flow is driven here by the difference between Pa and PA.

Zone 3 is the base of the lungs. Pa>Pv>PA. Blood flow is driven by the difference between Pa and Pv. Q is up here leading to a decrease in V/Q, meaning this is a shunt location. PO2 is the lowest here and PCO2 is the highest.


Discuss how the nervous system affects resistance

Sympathetic stimulates B2 = airway dilate= a decrease in Resistance, albuterol acts as an agonist

Parasympathetic stimlates M3 to constrict leading to an increased resistance. Ipratropium antagonizes this.


Why does a decrease in lung volume lead to an increase in resistance.

LV going down means a decrease in traction leading to more resistance and an increased chance to collapse.


Discuss CO2 transport in the blood

CO2 exists in a directly dissolved form in blood in 7%

93% of the CO2 enters the RBC. 23% of the CO2 binds directly to the Hb. The rest of it with water and CA becomes H2CO3 which splits into H which binds to Hb and HO3- which leaves the RBC as Cl- comes in. This means 70% of your CO2 is in the plasma stored as HCO3-


What is A-a gradient and what causes it to increase/decrease

The difference between PA and Pa (PA - Pa), which is normally your Age/4 + 4Torr.

The A-a goes up with a shunt, V/Q mismatch and diffusion issues


Hypoxemia tree GO

If we don't have an increased A-a gradient, but we still have hypoxemia, then you have to look at how much O2 they are taking in. If they are inspiring less, then their FiO2 is low or their altitude is high, which are both inclusive. If they are inspiring normally, then they are hypoventilating

If we do have an increased A-a, and it is not fixed with straight up 100% O2, then you have a shunt. A right to left shunt will present with decreased PaO2 and a left to right shunt will not have changes in PaCO2.

If your A-a gradient is fixed with the O2, then you have a V/Q mm or diffusion is impaired in some way.


What is LaPlace's Law?

P = 2T/r (alveolar radius)


Discuss Hemoglobin subunits

2alpha and 2betas each with an iron

Fe2+ = Ferrous, we are happy
Fe3+ = metHb = no O2 binding, sadness


Positive coopertivity

More O2 binding means easier to bind


Right shift vs. left shift hemoglobin curve

Right shift is for unloading so we'll have a decreased affinity and decreased pH, but everything else goes up (2,3 - DPG, Temp, PCO2, metabolic needs, 50% Hb capacity)

Left shift = Retention and an alkaline, everything going down causes this.


Fetal hemoglobin

Left shift. 2 alpha and 2 gamma instead of beta so we don't bind 2,3 - DPG as well


CO effect and what we do about it

Left shift and we treat with O2 to compete


PO2 values and how much Hb is bound during them

PO2> 70 = 100% Hb bound
40 = 70% Hb which is our venous supply
25 = 50% which is our P50 set point


Central Respiratory control

Medullay center has a dorsal and a ventral group. The DG receives input from the vagus and glossopharyngeal and then transmits signals to the phrenic which goes to the diaphragm and the intercostals which go to the intercostals. This group controls inspiration and rhythm. The VG deals with forced expiration and increased inspiratory effort. Not active during normal respiration since this is all passive usually. Damage to the medullary center causes respiratory failure.

Pons has a pneumotaxic center (Upper) which deals with inhibiting inspiration and an apneustic center which increases inspiration, located in the lower Pons.

You also have the cerebral cortex which is our voluntary control of breathing


Discuss chemoreceptors

Central chemoreceptors in Medulla respond to the pH in the CSF. Low pH means we're gonna start hyperventilating like crazy.

Peripheral receptors in the carotid and aortic bodies respond to pH also, but they also respond to PaO2 and PaCO2. Acidity, low oxygen and high CO2 are gong to cause hyperventilation.


Excessive stretching of lung stretch receptors caused by excessive inspiration causes what?

Inhibit DG in order to stop inspiration and inhibit apneustic center in order to increase expiration.


Discuss juxtacapillary receptors

Located close to capilaries in the alveolar walls. These guys respond to increased fluid to cause rapid, shallow breathing.