Exam 2 - Lecture 4 Flashcards
PAO2 is what in a perfectly healthy adult DIRECTLY after gas exchange?
104 mmHg
After gas exchange occurs, the now oxygen rich blood is considered to be pulmonary ______ blood.
Venous – Because it is returning to the heart
The PAO2 blood becomes pulmonary venous blood, and mixes with what?
bronchiolar admixture blood, which is the pulmonary circulation blood for the tissues in the lungs, and by the time it mixes, it will become 100 mmHg of O2 when it reaches the left atrium
What % of cardiac output is bronchiolar admixture blood?
1%
When does PAO2 become PaO2
When it gets mixed with bronchiolar admixture and becomes 100mmHg
Whats a normal PaO2 for a healthy 20 year old? What is it for a 90 year old?
100mmHg; 80 mmHg
Drops as you age
things go downhill for your lungs after ___ years old and then the rest of your body goes downhill at ____ years old
20;40
What happens to O2 and CO2 if you increase ventilation without increasing blood flow?
Higher O2, Lower CO2
How much dead space for a normal 500mL breath? what portion of the breath becomes deadspace?
150mL, THE LAST PORTION of an inspired breath is the deadspace.
When you inhale 500mL, the 350mL that is actually used for gas exchange gets mixed with
3L of air thats already in the lungs, gets diluted out.
Two types of deadspace are
Anatomical and alveolar
What is anatomical deadspace?
Conducting zones of upper respiratory system
What is alveolar dead space?
alveolar that isnt perfused with blood flow, but is being ventilated.
e.g. pulmonary embolism blocking blood flow from perfusing that portion of the lung.
Which deadspace increases as we age and why?
alveolar
As we lose good alveoli, the others have to work extra hard, which can lead to more dead space. think of the kidney cells with GFR
What is physiological dead space?
Both dead spaces put together!!!!! anatomical + alveolar
VT = ?
this is the equation for tidal volume while accounting for deadspace
VT = VD + VA
E.g. 500 = 150 + 350
VT = VD + VA
What does the D stand for? A?
D = physiological dead space
A = GOOD alveolar ventilation. Bad alveolar ventilation would go under D!!!
VA with a dot above the V means
minute ventilation in alveoli
Whats the equation for alveolar MINUTE VENTILATION?
VA = VT -VD
since its minute, we need to use normal volumes and times them by 12 for each one.
Normal alveolar ventilation per minute is?
4200mL/min
What does VE mean?
Minute total ventilation.
the book will leave the dot above the V off, but it still means minute!
The first 150mL’s we expire will be
deadspace gas, has not been mixed.
O2 = 150mmHg and CO2 = 0mmHg
If we have higher than normal alveolar ventilation, what happens to PAO2 and PACO2
increases PAO2, decreases PACO2
Pulmonary capillary hydrostatic pressure is
7mmHg, favors filtration
pulmonary blood oncotic pressure is
28mmHg, opposes filtration
The interstitial hydrostatic pressure is
-8mmHg, which is more negative than systemic (-3mmHg), favors filtration
more negative due to surrounding negative intrapleural space, does that mean he could ask a question about this pressure during forceful exhalation? Think about that shit.
The interstitial osmotic pressure is
14, which is double from systemic, favors filtration.
What is the only pressure that opposes filtration?
Pulmonary blood osmotic pressure
What is the total outward forces, where filtration is favored?
Total inward forces, where reabsorption is favored?
Net filtration pressure?
29mmHg; 28mmHg; +1mmHg net filtration pressure.
what makes up for the imbalance of net filtration pressure in the lungs?
Lymphatic system are a little extra active.
Whats special about the lymphatic system in the lungs?
They are easily compressed just like the rest of the vessels in the lungs, so its important to keep them open.
Discuss the water solubility of oxygen
its fucking not, so keeping the lungs dry is important for gas exchange.
What deviation from normal pressure does left atrial pressure begin to cause pulmonary edema?
21mmHg
This is partly a trick question, because normal left atrial pressure is 2mmHg.
Pulmonary edema begins at 23mmHg, so it would be a 21 point deviation from normal.
In starling capillary equation, Q stands for
Flow
QF means
Net flow of fluid
whats the starling capillary equation?
QF = KF x [net filtration pressure]
1mmHg = _cmH2O?
1.36
How to solve for Kf, if given Qf and NFP?
Qf/NFP = Kf
Why does increased capillary permeability cause pulmonary edema?
Proteins leak out and build in interstitium, bringing water with them.
What causes increased capillary permeability in the lungs leading to pulmonary edema?
Infections, O2 toxicity, ARDS, inhaled/circulating toxins
What causes increased capillary hydrostatic pressure, leading to pulmonary edema?
heart failure leading to fluid buildup.
Over administration of fluids according to book, but schmidt says thats mo0re related to decreased colloid osmotic pressure
What causes decreased interstitial hydrostatic pressure, leading to a higher NFP and pulmonary edema?
Rapid evacuation of pneumothreoax/hemothorax, makes pressures in the chest too low
or patient trying to breathe against a closed airway
anything that raises NFP above 1 may contribute to cause
pulmonary edema
A rise in Kf can lead to
pulmonary edema
How low can a PIP go if a patient breathes against a closed circuit?
What age/health status makes this even worse?
What does this lead to?
-50 to -60 cmH2O
Worse in young healthy adults cause their muscles are stronger to generate more negative pressure.
Flash pulmonary edema.
What causes decreased blood colloid osmotic pressure, leading to pulmonary edema?
Schmidt specifically believes over-administration of IV fluids
Protein starvation, Dilution of blood proteins into urine, renal problems (proteinuria)
“Other” etiologies of pulmonary edema include
Insufficient lymphatic drainage, things that put down scar tissue, tumors, high vent settings, high altitude pulm edema, interstitial fibrosing diseases, neurogenic pulm edema, drug overdose
What is neurologic pulm edema?
Excessive sympathetic stimulation caused by neuro issues, leading to excessive pulmonary vasoconstriction, which leads to increased hydrostatic cap pressure and capillary stress failure.
during FRC, the intrapleural pressure at the top of the lung is __, and the bottom of the lung is ___.
-8.5cmH2O; -1.5cmH2O
averages out to -5cmH2O
Where does the lung attach to the bronchi?
At the hilum
Pleural pressures are less negative at the
base
Where is the apex of the lung?
TOP
What do the alveoli look like at the top of the lung?
Wide and full because its much more negative up there.
When fresh air comes into the lung, what is forcing it to go to the lower areas?
The alveoli at the top of the lung are already full because of the more negative intrapleural space.. so when they are more full, the air is going to go where its EASIEST to go, which is to less full alveoili, which is at the bottom with a less negative pressure.
AT FRC, alveoli at the top of the lung are what % full?
what about at the base of the lung?
60%
25%
Is it possible to completely push air out of the alveoli?
no, it would collapse the airway first, 20% is the lower limit.
“PTP is an __________ thats available to put air into the lungs”
Alveolar distending pressure
At FRC, what is the PER at the apex of the lung?
+8.5cmH2O
Which part of the lung requires a higher PTP to move air into it?
top of the lung, since its more full.
whats the difference in compliance for expiration vs inspiration?
The lung is more compliant during expiration than inspiration.
What is the difference of behavior between expiration and inspiration for lung tissue called
hysteresis
In order to get down to RV, the pleural pressure has to
become positive
At the top of the lung at RV, the pleural pressure is ____ and the alveoli capacity % is
+2.2cmH2O; 30%
At RV, the base of the lungs pleural pressure is ___ and the alveoli capacity is ____
+4.8cmH2O; 20% (as empty as possible!)
Which part of the lung has a greater hit on their alveolar capacity when going from FRC to RV?
Top of the lung (60% -> 30%)
At RV, where is air likely to go first? Why?
the top of the lungs that are 30% full, even though it was stated before that air would go to the less full alveoli.
This time its different, because the 20% full alveoli likely have collapsed airways, requiring more effort to get air into them.
What is the compliance of the bottom of the lung when you start to breathe in at RV?
By definition, zero.
“the bottom of the lung has no compliance at all if it isn’t accepting air with collapsed airways. Thats why the slope is 0 at the beginning of RV.”
After breathing in after RV, as lung tissue inflates, the ___ fills, then the walls begin to stretch out and airways open, allowing air to fill the ____ of the lungs too.
top; bottom
Alveoli are _______ to each other, and this is important because why?
Connected to eachother, and this leads to them gradually opening the alveoli around them as they fill with air when pressure grows.
What is not good about RV and the breath we take immediately after? what does it lead to?
V/Q mismatch, because the air is not matching the bloodflow. This is why we dont hangout at RV (parks)
Generally speaking, the higher transpulmonary pressure, the more _____ alveoli will be
distended
Which part of the lung has larger blood vessels?
Bottom
What part of the lung has larger alveoli?
Top
What is Hypoxic Pulmonary vasoconstriction?
HPV occurs when the vascular smooth muscle in the lung detects changes in alveolar gas tensions in a specific spot, causing vasoconstriction to redirect blood flow to alveoli that is properly being ventilated.
E.g. If we have a poorly ventilated region of the lung due to airway collapse, the alveolar gas PAO2 would be low, and upstream vasoconstriction would then occur.
What is special to pulmonary vasculature when it comes to low oxygen levels?
If an area has low oxygen levels in the lungs, the lungs will vasoconstrict in order to direct bloodflow elsewhere.
For the rest of the body, if an area has low oxygen, it will vasoDILATE to get more blood flow to that area.
HPV is MAINLY driven by _______ and secondarily driven by
PAO2 levels; PACO2
All vascular smooth muscle constriction is mediated by ________.
membrane potentials
This is why we give Mag for bronchospasm, to not only block calcium influx into cells but also hyperpolarize the membrane and promote relaxation
All general anesthetics open ____________, which causes what? What does this interfere with?
Potassium channels; relaxation of smooth muscles; interfering with the HPV system.
How does GA reduce SpO2 specific to alveolar deadspace?
As we age, our alveolar deadspace grows. The body compensates through HPV, and we dont waste bloodflow to those areas. When general anesthesia is administered, it takes this regulation offline. The previously constricted vessels now dilate, directing blood flow to areas that aren’t ventilated. This is partly why we need to add extra oxygen.
Schmidt says some of our pharm teachers will say it doesnt affect it all, or some more than others, but he thinks they all do.
What is a detrimental result of hyperoxia?
Airway muscle can also detect changes in gas tension like the smooth blood vessels. If we have a poorly perfused part of the lung, such as a clot, the alveolar gas will just have inspired air instead of a mixture of inspired air and venous gas tensions… It will detect the abnormally high PAO2 levels/Low PACO2 levels, and our airways respond to this by tightening up to match the lack of blood flow.
Hyperoxia causing airway constriction is thought of the ______ for alveolar deadspace ventilation.
Safeguard
What can happen to the capillaries with excessive O2 delivery for an entire day?
Alveolar PO2 would be ridiculously high, turning capillaries into “swiss cheese”, while also constricting airway.
If you want to preoxygenate before intubating, that obviously makes sense, but be careful to not do it excessively in order to prevent
airway reactivity
Whats the primary reflex in the lungs, and whats the primary driver for that reflex?
HPV, low PAO2 levels.
What happens to lung volumes when you lay on your back and what are the SPECIFIC things changing it?
Decreases lung volumes due to abdominal cavity pushing on the diaphragm.
Mesenteric circulation and intestines are “hanging off the back” when we stand, and when we lay down, they will slide up onto inferior part of diaphragm
Whats the FRC difference between standing and lying on our back?
3L -> 2L
What is our ERV in the supine position?
0.5L instead of 1.5L
How does our vital capacity change during supine position?
Total VC does NOT CHANGE!!! still 4.5L
While ERV does decrease by 1L, IRV can handle the extra 1L to replace it.
What patient population experiences a greater impact to FRC while supine?
Obese people
Spirometer is just a _________ (weird quote, but he said it, so..)
upside down water heater lmao
How do we measure vital capacity?
with a basic spirometer, have patient exhale all the way, then inhale all the way.
