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
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
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.
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
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.