Exam III Flashcards
What is the Fowlers test, and what do you need to do it?
Pulmonary function test that looks at how much nitrogen is coming out of the patient via a nitrogen meter with each breath.
All you need is a nitrogen meter, a patient, & a source of 100% O2.
If a normally breathing patient was hooked up to do the Fowlers test, what would you see?
Expect to see normal expired nitrogen content
(74.9% [569/760] for Guyton,
or
79.8% [569/713] for Levitzky who does not take into account water vapor)
On ventilators, we have a capnograph. What are the two values that can be displayed depending on which button you push?
End tidal CO2
or
Partial pressure/concentration (i.e. 569 or 74.9-80% for nitrogen)
How is the Fowlers test done?
Patient hooked up to a closed circuit with a nitrogen meter & a source of 100% O2.
Ask patient to inspire a little deeper than normal (i.e. instead of 500mL, do 1L so we have more air to work with)
As they exhale, the nitrogen meter will pick up the results.
What happens inside the patients lungs during the Fowlers test, and what does the nitrogen meter pick up? (longer card sorry)
When breathing from 100% oxygen source, the patient will dilute this with water vapor which will lower then concentration slightly. However, no nitrogen is being inhaled.
Any nitrogen coming out of the patient is already in the lungs at the start of the test.
The last portion of inspired breath has no nitrogen since there is nothing at the source.
On expiration, the first portion of the breath will have no nitrogen.
As air from deeper areas of the lungs is exhaled, nitrogen sensed by the meter will increase (transitional zone)
^This was already in the lungs at the start of the test.
Eventually, the amount of nitrogen plateaus.
Fowlers test: At the start of expiration, there is no nitrogen sensed by the nitrogen meter. Why?
This is the anatomical dead space. The last portion of inspired air was from a 100% O2 source, meaning no nitrogen should be there. All nitrogen in the lungs will be deep in the alveoli, thus won’t be picked up immediately on expiration.
Why is the Fowlers test done?
Measure anatomical dead space of the lungs.
Fowlers test: What is the transitional phase?
This is the air between the anatomical dead space and the alveoli. The air begins to look like normal lung air (though not as concentrated with nitrogen).
Note: This nitrogen was already in the lungs at the start of the test.
Fowlers test: How do you figure out anatomical dead space?
Find the mid point of the transitional phase.
Find where the time, volume, and midpoint of the transitional phase line up. This gives you your anatomical dead space on the Y axis.
Fowlers test: Why would we want to know what someones anatomical dead space is?
We can factor this into our tidal volumes. Someone with more dead space would require larger tidal volumes to make sure you are ventilating the lungs properly.
What is the normal anatomical dead space of a healthy 20 y/o?
150mL anatomical dead space
Fowlers test: How concentrated is the alveolar plateau?
Depends on how large the inspired breath was (dilution effect)
What is a test that is similar to the fowlers test?
Nitrogen washout test
What does the nitrogen washout test do, and what is required?
Analyzes evenness of ventilation in the lungs.
Requirements: Nitrogen meter + Source of 100% Oxygen.
If you pulled some healthy person off the streets to do the nitrogen washout test, what would be the likely result?
74.9-80% nitrogen on expired air on the FIRST exhalation.
During the nitrogen washout test, what happens as the patient continues to breathe in and out?
There will be less and less nitrogen picked up, as there is no new nitrogen being introduced through inspiration.
During the nitrogen washout test, when is the greatest drop in nitrogen concentration?
Between the first and second breath. At this point, there is the greatest amount of nitrogen available to be diluted.
What concentration of nitrogen is required for the nitrogen washout test to be completed/shut off? How long does this take?
2.5%
Takes way under 7 minutes in a healthy 20 y/o. Normal value for anyone is 7 minutes or less.
Note: Be prepared on the test to figure out how long/how many breaths it takes to get to 2.5%
What is an abnormal result of the nitrogen washout test?
> 7 minutes to get to 2.5% nitrogen concentration.
This would be indicative of a sick set of lungs.
Nitrogen washout test: If nitrogen levels were plotted on a graph, would it be a straight line? Why or why not?
Normally it would not be a straight line, but in Schmidts pptt it is a straight line. This is because they made the Y axis scale up toward the top.
Note: Blue dot = data point from a single breath. Left picture.
Nitrogen washout test: What does it mean when it takes an abnormally long time to get nitrogen below 2.5% concentration?
Air is being directed to different places of the lungs on each breath. If inspired air is directed all over, the washout of existing nitrogen will not be orderly. You might have a little more or less dilution on each breath.
This is the hallmark of a sick lung. Note right picture, 60+ breaths to get down to 2.5% compared to the black line (normal) at around 20 breaths.
What does an abnormal nitrogen washout test mean?
Indicates an unhealthy lung with uneven ventilation.
How many phases of expiration are there on the closing volume/capacity test, and generally speaking, what happens?
4 phases
1 - Dead space is expired, no nitrogen is picked up.
2 - Nitrogen is picked up; transitional period. This is anatomical dead space mixed with alveolar air. More and more nitrogen as expiration continues.
3 - Nitrogen that is picked up levels off. Air from the beginning of phase 3 is from the base of the lung. (Air comes from all parts of lungs, but more and more from the apical region as expiration continues)
4 - abrupt increase in nitrogen levels coming from patient. The start of this phase tells us when the small airways in the base of the lung are starting to collapse.
What does the closing volume/capacity test measure?
How is it done?
Nitrogen coming out of the patient.
Patient starts from TLC and exhales to RV.
They then breathe up to TLC from a 100% oxygen source.
Any oxygen in the lung at this point was there before inhalation at RV.
Patient then expires down to RV, and nitrogen is measured at different time points.
What might the nitrogen washout test look like with someone that has large lungs, or COPD?
Normal tidal volume + large lungs = increases time needed to wash lungs of nitrogen. This is more of the large lung factor rather than uneven ventilation.
(Large amount of nitrogen to be removed)
What is a normal time for the nitrogen washout test?
What about an abnormal time?
Sub-7 minutes = normal
Above 7 minutes = abnormal
In the closing volume/capacity test, what is the general amount of nitrogen that comes out of the lungs from left to right on the graph?
None at first, then more toward the end of the expiration. This is due to the fact that air is coming from different regions of the lung. Depending on where these areas are, you can figure out different properties of the lung.
Why does the nitrogen level increase during expiration in phase 3 of the closing volume/capacity test?
As the base of the lung empties, a larger portion of air is coming from the apical portion of the lungs. The apical portion has a higher concentration of nitrogen.
When taking a breath to TLC, what fills first?
What about expiration as it relates to the closing volume/capacity test?
The apex fills first, and the lower portions fill last.
On expiration, the beginning will have no nitrogen, then transitional phase, followed by phase 3.
What is the difference between closing volume and closing capacity?
Same thing more or less.
Closing volume = Air coming out of the patient during phase 4.
Closing capacity = Closing volume + RV
Closing volume/capacity test: What is the point where phase 3 becomes phase 4 mark the start of? (Both in the patient and in the graph)
Patient - small airways at the base of the lung are starting to collapse.
Graph - “closing volume”
What are some causes of phase 4 coming early in the closing volume/capacity test?
Not as much traction
Airways are thinner/more narrow
Closing volume/capacity test: The earlier phase 4 occurs, the ____ off the lungs are.
Worse
Which pulmonary function test does Schmidt think should be a part of every physical, and why?
Closing volume/capacity test.
It’s very sensitive and can detect small changes in tissue behavior. Would be easy to do at a physical, because it only requires a nitrogen meter + a tank of oxygen.
This would allow people to know their lungs suck before it becomes an issue.
Compare the lung volumes/closing capacity between a 20y/o and a 70 7/o?
Standard volumes/capacities don’t change very much
Same: TLC, IC
Very little change: VC
RV increases as we age due to parts of lungs being more difficult to empty as we get older.
At age 20, we ____ _____ any small airway collapse at RV.
Phase 4 is ____.
hardly have any
Phase 4 is small
Blue line = closing capacity
In a 70 y/o, closing capacity/volume is ____ than at age 20. What does this mean?
Much higher
Airways start collapsing before we even get to FRC due to loss of elastic tissue as a function of age.
The more elastic tissue we lose, the ___ elastic recoil we have, the ____ traction we have on small airways.
Why is this important?
Less
Less
Predisposes us to small airway collapse.
In a 20 year old patient, will the small airways collapse normally?
No. A 20 year old doesn’t go below FRC often, and the. closing capacity is well below FRC
T/F
A 70 year old patient will have small airway collapse on every breath.
True: closing capacity exceeds FRC so it is reached on every breath. This increases work of breathing compared to younger people.
What old guy did Schmidt mention is in good shape, but has more work of breathing due to age?
Warren Buffet
What age, even in perfect health, will have small airway collapse with every breath?
55
What is the pleural pressure at RV at the apex of the lung? How about the base?
-2.2 cm H2O at the apex
+4.8 cm H2O at the base
At RV, how full is the apex of the lung? How about the base?
Apex 30%
Base 20% (as empty as the lungs can get before small airways collapse)
At RV, how much air can enter the apex/base of the lung?
The apex can accept 70% more capacity (30->100)
The base can accept 80% more capacity (20->100)
What is the partial pressure of nitrogen in the lung normally?
569 mmHg
If someone took a VC breath at RV from a 100% O2 source, how would the nitrogen content of the alveoli compare between the apex and base?
The nitrogen that was already in the lungs at RV would be diluted.
Since 70% capacity is being added to the apex, and 80% capacity is being added to the base, the base would be diluted slightly more.
The partial pressure of nitrogen in the base of the lungs would be slightly lower than the apex if someone took a VC breath at RV from a 100% O2 source. **
What does a flow volume loop measure?
Top: Expiratory flow rates given different levels of effort between TLC and RV. The higher the curve, the more effort is being given to exhale.
Bottom: Inspiration, same concept
If expiring as hard as possible from TLC to RV, what is the peak expiratory flow rate?
10L/sec
With forced expiratory flow rates, airflow picks up rapidly but then trails off. Why?
Lower and lower lung volumes lead to a lower delta P, which decreases flow rates.
A flow volume loop shows the _______ flow rate between what two lung volumes?
Expiratory flow rate between TLC and RV
What is effort independence?
No matter how much harder we try to push air out of the lungs, the maximum expired flow rate will be capped by something. We won’t expire any faster.
Takes place later in the expiration as there is less and less air to push out, lowering delta P thus decreasing flow.
Right side of graph shows this
What is effort dependence?
If someone tries to exhale faster, it will result in a faster air flow. This happens at the start of expiration when we have plenty of air. Flow is dependent on strength/effort of expiration.
Left side of graph shows this
For our purposes, which flow volume curve do we care about the most?
The maximal effort curve.
Flow volume loops:
How does the flow volume loop compare between inspiration and expiration?
The maximal flow rate happens before the halfway point of expiration assuming maximal effort. Note that if less effort is given, the maximal flow rate will be closer to the end of exhalation (see top of graph).
The maximal flow rate happens exactly at the halfway point on inspiration. Note there is no effort dependence/independence on inspiration, only expiration (See bottom of graph).
What did Schmidt say that the flow volume loop looked like?
An upside down ice cream cone.
Where are the internal intercostal muscles, and what do they do (think pleural pressure)?
Inside and between the ribs. When contracted, they pull the ribs closer together. This reduces the volume in the chest which increases pleural pressure.
If you do a flow volume loop on someone and there is less speed of expiration than expected, what does that indicate?
Problem with the lungs
What is peak expiratory flow rate dependent on?
Elastic recoil pressure: Transpulmonary pressure needs to be +30 cm H2O to fill lungs to TLC.
Pleural pressure: Very positive with maximal effort to push air out of the lungs. Use the diaphragm, internal intercostal muscles, and abdominal muscles to create this pressure.
What happens when the abdominal muscles contract in regard to pleural pressure?
Pushes stuff in abdomen to the bottom of the diaphragm, increasing pleural pressure.
What is an example of a disease that causes awful elastic recoil? What considerations need to be made in the OR?
COPD
Nearly entirely dependent on pushing the air out themselves rather than with elastic recoil. This will collapse the small airways and limit the rate that expiration can occur.
In the OR, there is no internal intercostal/abdominal muscle activity, meaning that patients are entirely dependent on whatever elastic recoil pressure they have.
More time needs to be allowed for expiration in these patients.
When doing a flow volume loop test, what do we care more about? Inspiration, or expiration?
Expiration most of the time, though inspiration can be useful in some cases.
What is the difference between a flow volume loop and an expiratory flow function curve?
It is only the expiratory flow curve that is plotted.
Whatever a patient looks like under maximal exertion (flow volume loop) is important. Why?
Tells us about lungs collapsing. Collapsed lungs will have air come out slower than usual.
What might an expiratory flow function curve look like in someone with COPD? Why?
The maximal flow rate would be less than usual, and the expiration would be longer than usual due to the loss of elastic recoil. There is a curve on the effort independent side of the loop. (right side of the left-most loop)
What is missing in obstructive lung disease?
Elastic recoil
What does the shape tell you about when talking about expiratory flow function curves?
Behavior of tissue
What is the problem in restrictive lung disease?
More scar tissue, more elastic recoil pressure
This makes it difficult to fill with air d/t increased tissue
Expiratory flow rate is reduced.
This is more of a fullness issue rather than elastic issue. The elastic pressure is there, but the air is not. Less air = not as fast expiratory rate.
Which peak expiratory flow is greater - obstructive disease or restrictive disease?
Restrictive flow is greater than obstructive
Which has a greater VC - restrictive or obstructive disease?
Obstructive disease
Order the following RV volumes greatest to least: Normal, obstructive disease, or restrictive disease. Provide volumes.
1) Obstructive 4.5L; d/t fuller lungs at higher pleural pressure, less springs.
2) Normal 1.5L
3) Restrictive 1L
Does obstructive disease have a greater VC than normal lungs?
No, normal lungs have a greater peak expiratory flow rate as well as a greater VC
Order the following TLC volumes greatest to least: Normal, obstructive disease, or restrictive disease. Provide volumes.
1) Obstructive; 8.5L
2) Normal; 6L
3) Restrictive; Just over 4L
What is FVC (forced vital capacity) almost always referring to?
Expired portion of a flow volume loop - we care more about how air gets out of a patient than in most of the time.
Order the following VC volumes greatest to least: Normal, obstructive disease, or restrictive disease. Provide volumes.
1) Normal 4.5L
2) Obstructive 3.5-4L ish
3) Restrictive 3L
The smaller the VC on an expiratory flow function curve, the ____ the disease.
Worse
Normally flow volume curves won’t have volume and airflow plotted like in this graph.. what do they usually do?
Usually have a scale like on maps and you have to eyeball it.
What is one flaw of the flow volume loop compared to an expiratory flow function curve?
RV isn’t plotted, so you wouldn’t know what it was unless you did a helium dilution measurement with FRC/RV.
Without RV, you wouldn’t know where to position the expiratory flow function curve, and wouldn’t know that RV was huge (or small).
Can look at other things for abnormalities instead, such as max expiratory flow rate, the shape, and VC. RV will be missing.
Note: For test day, I bet he will give us a flow volume loop and make us figure out helium dilution/RV.. be prepared for that
What does the forced vital capacity maneuver look at?
Expiratory flow rate (normally.. can look at inspiration, but not often).
With forced exploratory maneuvers, what is the pleural pressure? What about the alveolar pressure?
Given this, why does air flow out of the lungs?
+25 cm H2O pleural pressure
+35 alveolar pressure
There is a pressure gradient (delta P) along the airways. +35 cm H2O within the alveoli, and 0 cm H2O in the environment. This allows for air flow from high pressure to low pressure areas.
(right picture)
Does pleural pressure change as you go up and down the airways? What about alveolar pressure?
Pleural pressure is uniform along the airways, while airway pressure changes (more positive in the alveoli while closer to 0 cm H2O outside of the airways)
The conducting zones (Upper airway) are supported by what? What is the purpose?
Cartilage (firm tissue)
Prevents collapse of upper airways during forced expiratory maneuvers.
Do lower airways have cartilage? What is the implication?
No
They are vulnerable to collapse, as evidenced by blue arrow on right picture.
Pressure in the airway and pleural pressure are the same. If the pleural pressure were to overcome the airway pressure, it would collapse.
How is passive expiration different than forced expiration?
Passive expiration relies only on elastic recoil to push air out, while forced expiration adds effort (positive pleural pressure)
In a normal patient, what is the pleural pressure on passive expiration?
-8 cm H2O
In a normal patient, what is elastic recoil pressure? Does this change with passive/forced expiration?
+10 cm H2O; does not change
Very important to help us get air out of the lung***
In a normal patient, what is the pleural pressure on forced expiration?
+25 cm H2O
In a normal patient, what is the net pressure within the alveoli with passive expiration? What does this mean?
+2 cm H2O
Positive value = outward airflow
Why do the airways stay open on passive expiration?
The pressure within the small lower airways (+1 cm H2O) is greater than the pleural pressure (-8 cm H2O)
Is there a choke point within the airways during passive expiration?
Not normally
With forced expiration, how would emphysema change pressures/chokepoints?
Loss of elastic recoil/tissue in alveoli results in a half normal recoil pressure of +5 cm H2O.
Pleural pressure remains at +25 cm H2O.
This makes alveolar pressure +30 cm H2O instead of +35 cm H2O like normal.
While delta P is still +30 cm H2O, the pressure in the small airways will be lower than normal.
i.e., pressure within the small airways might be +19 cm H2O, while pleural pressure is +25 cm H2O.
This results in collapse of the small airways in a patient with emphysema (obstructive lung disease) on forced expiration.
What can predispose us to collapsing airways?
Narrow airways as seen with asthma or low lung volumes.
What guards us from airway collapse?
Spongy recoil tissue of the alveoli. More tissue = more recoil pressure. Note recoil tissue/springs are in alveoli as well as small airways.
This provides traction on small airways and keeps them open.
What happens if we lose springi-ness of the small airways and alveoli?
What is an example of this?
Traction on small airways would be lost, resulting in airway narrowing. This causes susceptibility to airway collapse.
i.e. COPD/Emphysema d/t loss of elastic recoil and thus loss of small airway traction.
Can upper airways ever collapse?
Not usually, but if someone has loss of upper airway cartilage it can increase the risk of collapse.
What relationship does an ETT have with the trachea? What does this imply?
No matter what size the ETT is, it has to be smaller than the trachea. This leads to higher resistance to airflow (both inspiration and expiration)
What does an ETT do to the flow volume loop?
Cuts the top and bottom off of it due to extra upper airway resistance. (Both inspiration and expiration impacted).
This is fixed (intra- or extra thoracic). It is a continuous problem.
What is the difference between intrathoracic and extra thoracic?
Intrathoracic is in the chest, extra thoracic is outside the chest.
What kind of problems would cause a variable extra thoracic flow volume loop?
Obstruction outside chest
Weak point at top of upper airway, such as missing cartilage
Trachea removed
Paralyzed vocal cords
If there is a weak point in the upper airway, what can happen?
Negative internal airway pressure causes airways to collapse on inspiration, evidenced by bottom of flow loop being flat.
What does open/closed state depend on with paralyzed vocal cords?
Pressures in and around the airway inside of the larynx. If the pressure in the larynx is negative, the cords are pulled closed.
On expiration (especially forced), the chest pressure is increased, which increases airway pressure. This will open the vocal cords/move the obstruction. There is no opposing environmental pressure outside of the thorax.
Note: This applies to NORMAL breathing.
How does the open/closed state of paralyzed vocal cords change with positive pressure ventilation?
The obstruction will be pushed out of the way (i.e vocal cords will be pushed open d/t positive pressure).
Note: Will cause other problems from PPV though.
Name the three variants of the flow volume loop.
Fixed (intra or extra thoracic)
Variable extra thoracic
Variable intrathoracic
What is a variable intrathoracic flow volume loop? Name some diseases that can cause it.
Not present all the time - variable.
Impacts expiration, especially forced. This cuts the top of expiration on a flow volume loop off.
This is due to loss of elastic recoil pressure. Not enough traction to keep airways open on forced expiration.
On inspiration, airways open since thorax pressure is very negative.
COPD, emphysema, asthma
What is FVC?
Forced vital capacity
What is FEV1?
Forced expiratory volume in 1 second with maximal effort
FEV1/FVC gives us what?
A ratio/fraction. We should be able to move 80% of our VC out of the lungs within 1 second during maximal forced expiration in a healthy lung.
Note: NOT TLC; this is talking about VC.
What does it mean if FEV1/FVC is lower than 80%?
Your lungs have a problem.
What does this graph mean?
Looking at how much air is coming out of the lung over time during a forced expiratory maneuver.
Note: RV is left out of this graph.
VC is 4.5L
Read right to left - lots of lung volume removed in 1 second, then trails off.
FEV1/FVC ratio is about 80% here.
This graph shows an airway obstruction. What does it tell you?
FVC lower than normal.
At 1 second, not much air has came out of the lung.
Slower expiratory rate, takes longer to get to RV than normal.
FEV1/FVC ratio less than 50%, which is lower than the normal of 80%.
This graph shows a normal FEV1/FVC ratio overlapped with the blue line, which is airway obstruction. Note differences.
Read left to right in this graph, as opposed to right to left in other FEV1/FVC graphs. Pay attention to this.
Normal:
FEV1 = 3.6L
FVC = 4.5L
FEV1/FVC = 80%
Airway obstruction:
FEV1 = 1.5L
FVC = 3L
FEV1/FVC = 50%
What is the difference between these graphs?
Left: FEV1/FVC ratio graph, read left to right. Can figure out how much air is coming out of the patient, but can’t tell flow rate.
Right: No time axis here, just flow rate and volume. You cannot figure out how much air is coming out of the patient with this. Can tell flow rate with this graph.
What lung disease would have a normal FEV1/FVC ratio, but have a low VC?
Restrictive lung disease. Low VC, low FEV, but in proportion to VC you have a normal FEV1/FVC ratio.
Note: less flow rate d/t lower volumes in restrictive lung disease.
Max flow rate is under 6L/s, while normal is close to 10L/s
What kind of lung does the graph depict? Why?
Restrictive lung disease.
Normal FEV1/FVC ratio
Low VC, low FEV
What kind of lung disease does this graph show?
Advanced emphysema/bad COPD (Obstructive disease)
Note extended amount of time to get air out of lungs, so much so that the X axis of the left graph is cut off.
Only 1.5L out in the first second. Low FEV1/FVC ratio.
With PPV, what is expiration in obstructive lung disease (COPD/Emphysema) dependent on?
Elastic recoil (which they are lacking - need more time for expiration).
What is the hallmark shape/change indicating obstructive lung disease, or a problem getting air out?
Right graph
Note the peak of flow rate, followed by a curved line on the back end.
What are the 5 steps of the PFT algorithm?
1) Is FEV1/FVC <70%? — if lower than 70%, it’s a problem (like obstructive lung disease)
2) Evaluate FVC
3) Helium dilution/spirometry to find TLC/RV — if RV increased, could be obstructive lung disease. Compare to TLC to find out what obstructive disease it is.
4) DLCO measurement, AKA CO diffusion test to measure gas exchange in the lungs — don’t need details here
5) FEV1 reversibility with bronchodilator - administer bronchodilator —– if reversible, could be airway reactivity like asthma. If not, then there is an elastic tissue issue like emphysema.
Brushed over this, know this chart.
What is this?
Flow volume loop plot with FVC. Expiration starts at 5L with both X and Z (two different patients). Graph keeps track of how much patient expires.
Note that it starts at one second, so the two second mark would be FEV1.
What is the FEV1/FVC ratio of X?
FEV1 = 4L
FVC = 5L
FEV1/FVC = 4/5 –> 80%
This is normal.
What is FEV1/FVC of Z?
FEV1 = 3L
FVC = 5L
FEV1/FVC = 3/5 –> 60%
This is low. Could be restrictive lung disease OR someone who is just small.
What does this graph show?
Flow volume loop with different level of effort.
Z = normal FRC breathing.
Y = Little deeper inspiration/expiration than Z.
X = even more so
W = maximal effort inspiration/expiration.
What does “a” stand for on the top of this OxyHgb dissociation curve?
What is the PCO2 of “a?”
a = arterial blood sample. PCO2 on average in arterial blood is 40 mmHg with a higher pH compared to venous blood.
Why does venous blood have a lower pH than arterial blood?
Will this be a left or a right shift on the OxyHgb curve?
Finally, will all venous blood look the same?
It has picked up more CO2
Right shift (lower pH)
For the most part, there is little difference in behavior in different areas of systemic circulation when it comes to venous samples.
What is the optimal hypothetical number for venous saturation of oxygen?
What is it actually closer to?
What is it in the standard healthy person, and why would it be lower?
75% optimal
60% actual (he mentioned this but pivoted to 70%)
70% healthy person; lower with a sick/acidotic patient. More acidotic = less saturated Hgb
When might SVO2 be higher?
If tissue isn’t extracting O2 d/t low metabolic rate (i.e. cold). Will have higher venous Hgb saturation
Regarding OxyHgb affinity values, what is P50?
P50 value refers to the partial pressure of oxygen (PO2) required to bring a Hgb oxygen saturation up to a level of 50%
What is the normal P50 of oxygen under normal conditions?
26.5 mmHg
What characteristics would Hgb have if P50 was right shifted?
Hgb is less prone to saturating with oxygen. More oxygen (PO2) is needed to reach 50% saturation.
Lower affinity = need more oxygen for the same (50%) result
What characteristics would Hgb have if P50 was left shifted?
Hgb more prone to saturating with oxygen. Less oxygen (PO2) is needed to reach 50% saturation.
Higher affinity = need less oxygen for the same (50%) result
The whole blood CO2 content is a combination of how many forms? What are they?
Three forms - all are needed to figure out CO2 content
Dissolved
Carbamino compounds
Bicarb
What is the normal OxyHb saturation of venous blood?
How about the PCO2 of venous blood?
Lastly, what is the whole blood carbon dioxide content in mL CO2/dL venous blood?
OxyHgb: 75% (for our class, 70% if healthy)
PCO2: 45mmHg
CO2 content: 52.5 mL CO2/dL
What is the normal OxyHb saturation of arterial blood?
How about the PCO2 of arterial blood?
Lastly, what is the whole blood carbon dioxide content in mL CO2/dL arterial blood?
97.5% (for our class, we’ll use 100%) OxyHgb saturation
40 mmHg PCO2
Carbon dioxide content: 48 mL CO2/dL
In arterial blood, aside from gas exchange having occurred, why is CO2 in lower concentration than oxygen?
How does this change in venous blood?
Less room for CO2 if there is lots of oxygen floating around (arterial)
Less oxygen, more room for CO2 to be transported.
Why is it important to use both a OxyHgb/CO2 dissociation curve, and not just one or the other?
Oxygenation impacts carrying capacity of blood - they are related to one another.
Why is it that if we have a lot of oxygen that we have “less room for CO2?”
Why is it that if we don’t have a lot of oxygen that we have “more room for CO2?”
R proteins can be Hgb. If it is OxyHgb and saturated with oxygen, there are not as many exposed terminal amine groups for CO2 to bind at.
As OxyHgb becomes DeoxyHgb, more terminal amine sites are exposed, allowing Hgb to do other things like bind to CO2 or buffer protons (HbH+).
Remember the acid/base equation on slide 15 (attached). If you have lots of CO2 producing lots of protons plus Hgb available to buffer said protons, you can fit more CO2 in blood.
What three things can Hgb do?
Bind and release O2
Form carbamino compounds
Buffer protons
What are the three forms of CO2, and what % of CO2 is in each?
Dissolved - 5%
HCO3 - 90%
Carbamino - 5%
Note: While composition is different in venous, Schmidt said to use this composition for both arterial and venous. This is the arterial composition.
How do you calculate dissolved CO2?
Solubility of CO2 x Partial pressure CO2 in solution = amount of CO2 dissolved in sample solution
What is the solubility of CO2?
0.06 mL CO2/mmHg partial pressure CO2/dL blood
What is carbamino, and how does CO2 get carried by it?
Proteins can have a terminal amine group. That is considered a carbamino. Note: Hgb is a type of carbamino group.
Terminal amine + CO2 = carbamino compound.
In good conditions, when lots of CO2 is around the terminal amine group, one proton (hydrogen) falls off of the terminal amine group. The hydrogen ion dissociates into solution.
If more CO2 exists in solution, what will happen to the level of carbamino compounds?
More CO2 concentration = more carbamino compounds
What is the molecular structure of a terminal amine group?
R-NH2
What is the chemical structure of a carbamino compound?
RNH-CO2 + H+
How does bicarb carry CO2? Does anything help this reaction along?
CO2 combines with water, forming carbonic acid (H2CO3).
Carbonic acid isn’t stable, and falls apart into its components. It can go one or two ways depending on the pH.
1) Bicarb + Proton (blood in area that is high in CO2 will create this)
2) CO2 + H2O (Blood in area that is low in CO2 will create this)
This reaction gets help from carbonic anhydrase, an enzyme that pulls the water out of carbonic acid OR puts water and CO2 together for form carbonic acid. It works both ways.
How much mL O2/dL would be in solution if the PO2 was 1mmHg?
0.003 mL O2/dL per mmHg partial pressure of O2
Carbonic anhydrase can speed up the dissociation of carbonic acid into CO2/H2O and vice versa. What does speed of this depend on?
The amount of product/substrate in the area. Can’t have a reaction if you don’t have the pieces
When calculating CO2 in arterial/venous samples, what is the difference in the formula?
No difference other than the PCO2 value of the sample (40mmHg in arterial, 45mmHg in venous)
How many mL/dL of CO2 is in arterial blood with a standard PaCO2?
PaCO2 x CO2 solubility = mL/dL CO2 in arterial solution
Standard PaCO2: 40 mmHg
CO2 solubility: 0.06 mL CO2/mmHg PCO2/dL
40 mmHg x 0.06 mL CO2/mmHg PCO2/dL =2.4 mL CO2/dL arterial blood***
Knowing that 2.4mL CO2 is in the dissolved form in arterial blood with a standard PaCO2, calculate how much CO2 in mL/dL arterial blood would be in each of the following: Carbamino, HCO3, and dissolved.
Give the total CO2 in the arterial system as well.
2.4mL/dL dissolved = 5% of the CO2 in the arterial system
5% is also in carbamino compounds, meaning that 2.4mL/dL is there.
90% of bicarb is remaining.
20 x 5 =100%
so
2.4mL/dL x 20 = total CO2 content
Total CO2 content = 48mL CO2/dL arterial blood
48mL - 2.4mL - 2.4mL = 43.2 mL CO2/dL in bicarb
Why is there so much CO2/dL blood?
It’s very soluble. More dissolved in blood than oxygen, while oxygen is bound to Hgb mostly
In arterial blood, CO2 is carried three ways:
Carbamino - 5%
Bicarb - 90%
Dissolved - 5%
How does this change in venous samples?
Carbamino - 30%
Bicarb - 60%
Dissolved - 10%
Note: He said just know the relationship, but we will use the arterial composition for the purpose of our class.
In venous samples, why is the % of CO2 dissolved higher than in arterial samples?
Have a higher PCO2, so more is in the dissolved state
In venous samples, why is the % of CO2 in bicarb lower than in arterial samples?
More protons in venous blood compared to arterial blood, so protons will consume some bicarb leaving less for CO2 to use
In venous samples, why is the % of CO2 in carbamino groups higher than in arterial samples?
Remember Hgb is a terminal amine group when desaturated. CO2 binds to Hgb and forms carbamino groups this way.
More CO2 = more carbamino
What is the difference between these lines?
Different OxyHgb saturation levels. These are CO2 venous curves at different levels of PCO2.
Deoxygenated blood has more room to transport CO2.
What is this known as, and what is the definition?
The Haldane Effect
The amount of CO2 transport we have is dependent on OxyHgb saturation.
Why don’t we use the same curve for both of these samples?
If you use the same curve, (lower being 100% saturated with O2, upper being 70% saturated with O2), it would be inaccurate.
i.e. 100% saturated blood can’t carry as much CO2, meaning that the CO2 content of the blood would be lower than in desaturated blood.
A second curve is used to show PCO2 levels at different levels of OxyHgb saturation.
A OxyHgb saturation of 100% would allow for how many mL of CO2 content?
2mL CO2
What is the CO2 content in blood that is 70% saturated with oxygen?
52.5mL/dL
What does A, B, and C show?
A - normal V/Q
B - shunt (low V/Q)
C - alveolar dead space (High V/Q)
Is the V/Q constant throughout the lung?
No - different in each area.
If your ventilation is higher than perfusion, how will the O/CO2 content change, and will the V/Q be high or low?
Higher O2 than usual
Lower CO2 than usual
Low V/Q
See B
If an alveoli had no ventilation, but there was perfusion (shunt), what is the VQ?
Zero (0/x = 0)
If your ventilation is lower than perfusion, how will the O/CO2 content change, and will the V/Q be high or low?
Lower O2 than usual
Higher CO2 than usual
High V/Q
See C
If an alveoli had ventilation, but there was no perfusion (alveolar dead space), what is the VQ?
Higher than normal
Assuming alveolar dead space, what is the highest V/Q ratio possible?
Infinity
When sitting in a chair, where is most of the fresh air going? How about blood flow?
Both to the bottom of the lung
What happens to blood flow and ventilation as you go lower in the lungs?
The BOTH decrease
At the bottom of the lung, which is greater? Blood flow or ventilation?
How about the top of the lung?
Bottom - blood flow is greater
Top - ventilation is greater
Again, note BOTH decrease the higher in the lung you are.
What part of the lung in general is under ventilated?
Overventilated?
Bottom (meaning V/Q ratio is lower here than at the top of the lung normally)
Top (meaning V/Q ratio is higher here than at the bottom of the lung normally)
What is the PO2 at the base of the lung?
PCO2?
90 mmHg (lower than average)
Little higher than 40 mmHg (higher than average)
d/t having lower than average V/Q at base of the lung
What is the PO2 at the apex of the lung?
PCO2?
PO2 - 130 mmHg, higher than average
PCO2 - 30ish mmHg, lower than average
Higher V/Q ratio than average
More ventilation will result in a ___ PO2 and a ____ PCO2.
Less ventilation will result in a ___ PO2 and a ___ PCO2.
Higher; lower
Lower; Higher
Alveolar air should have PO2 of
100 mmHg
What is normal alveolar ventilation in mL/min?
4,200mL/min
VT = 500mL
VD = 150mL (anatomical)
VA = 350mL
RR = 12
VA x RR = VA/min
350mL x 12 = 4,200mL/min
Note: on test, be prepared to calculate alveolar dead space and incorporate it here.
What are normal factors that influence ventilation?
Intrapleural pressure
Transmural pressure gradient
Alveolar size
Ventilation/min
What are normal factors that influence perfusion?
Intravascular pressures
Recruitment distention
Resistance
Blood flow
What is the most important/largest factor that can cause problems with V/Q ratio?
Development of alveolar dead space
What do we do that increases alveolar dead space?
What can we do to “put a band aid on it?”
Anesthetize w/ positive pressure ventilation (abnormal for lungs)
More positive pleural pressures cause alveolar dead space.
Increase ventilation to maintain blood gas as more and more alveolar dead space develops.
What’s the difference in these?
Right picture has atelectasis visible in the left lung lobe.
The left picture is an awake patient. The right picture is an anesthetized patient with zero PEEP. (aka ZEEP). No usage of PEEP results in lung collapse.
Note the large decrease in V/Q ratio. This is due to less ventilation relative to perfusion.
What happens over time as the lung is collapsed?
Longer it has been collapsed, harder it is to reopen.
How long does it take for lung collapse on induction without PEEP?
Is this an issue?
Instantly, causing a V/Q mismatch
20 minute procedure on a 20 y/o? Probably not an issue
Longer surgery on a 90 y/o or person in poor health? Apply PEEP as soon as possible, this won’t be good for them.
What is LaPlace’s Law?
If you had a two different sized balloons (spheres) connected via a pipe system and put air down it, the smaller balloon would deflate and move air to the larger balloon.
The pressure of a balloon is dependent on what?
Radius of a sphere
Regarding LaPlace’s law, what formula is used to find pressure of a sphere?
Pressure in a sphere is related to surface tension divided by the radius
AKA
T/r = P1
For a sphere twice as big, it would be T/2r, since the radius is twice as large.
T/r = P1
vs
T/2r = P2
What would the formula above mean for air trying to enter two spheres, one with the first formula and one with the second?
The second sphere would have a lower pressure since the denominator is higher.
T = tension
This would mean air would want to go into the second sphere before the first one. Air would also leave the first sphere to enter the second one. (provided the second sphere is not full)
If you had two balloons of different sizes connected by a series of pipe, how full would the bigger balloon need to be before air would go to the smaller balloon?
80-100% full.
However, eventually pressure exceeds capacity and you can blow them out.
If LaPlace’s law held true to the lungs ,what happens if you have one lung collapsed partially?
Air would move from the collapsed lung to the non-collapsed lung, worsening the bad lung. Will take a lot of pressure to re-recruit the affected lung.
What happens to surfactant concentration as we take a breath?
Unless we produce more surfactant, the biological concentration is reduced as alveoli get larger.
As alveoli get smaller, the biological concentration is increased d/t surfactant not being spread out as much.
LaPlace predicts that ventilation is uneven, fresh air goes to alveoli that are already open, and that closed alveoli just don’t get air. Is this true? Why or why not?
Not true under normal circumstances.
Surfactant protects us by breaking surface tension, distributing pressure needed to fill with air.
In what cases might LaPlace’s law hold true in the lungs?
Surfactant deficiency.
Any respiratory issue ever is known to cause surfactant deficiency.
The “effective surfactant concentration” describes what?
Small surface area with surfactant = more concentrated, making it easier to put air in
Large surface area with same amount of surfactant = less concentrated, making it harder to put air in
Why is it harder to open a lung that has been collapsed for awhile?
Alveolar macrophages eat up surfactant, making it harder to re-open the alveoli.
What information do you need to find the volume of a gas?
Size of the container
Concentration of the gas
If you have a pressure and need to know a volume, how can you find it?
Use concentration of the substance to figure out the volume.
What is physiological dead space?
TOTAL amount of dead space, consisting of alveolar and anatomical dead space.
How much anatomical dead space do we have?
~150mL
What does a healthy 20 y/o physiological dead space consist of?
Little to no alveolar dead space.
150mL anatomical dead space.
What things cause alveolar dead space?
Anesthesia exposure
Ventilators (PPV makes blood flow difficult)
Unhealthy environments
What is an easy way to calculate anatomical dead space?
1mL/lb of ideal body weight
What is mixed expired gas?
Collection of entire inspired breath & what was already in the lungs
(lungs + alveoli + dead space)
What happens with air in alveolar dead space?
Air isn’t being used for gas exchange.. need more ventilation to make up for it
Will anatomical dead space have CO2?
No, but it will have high PO2. Air is getting there, but no exchange is happening.
PE(O2)
What does E stand for?
Mixed expired air
If you put mixed expired gas in a container, what would PO2 be? (think dead space)
Between PO2 of dead space and PO2 of alveolar air
What is the PO2 of alveolar air?
PO2 of dead space?
Alveolar air - 100 mmHg O2
Dead space O2 - 150 mmHg
If you put alveolar air and dead space air in a container, would the PO2 equilibrate closer to alveolar air or dead space air? Why?
What is the actual PEO2?
Closer to alveolar air as there is 350mL of that, vs 150mL dead space
^Careful on test if we end up having more dead space than alveolar air, one thing to think about. Know diseases that would change this.
PEO2 = 120 mmHg
What is PEH2O?
47 mmHg always for water
What is the CO2 in the dead space?
How about the alveolar air?
Finally, if allowed to equilibrate, would it be closer to dead space or alveolar air, and what would the value be?
Dead space CO2 - 0 mmHg
Alveolar air CO2 - 40 mmHg
Closer to alveolar air
PECO2 - 27 mmHg
Oxygen and CO2 mixed expired air numbers are different than atmospheric, but nitrogen is about the same. Why?
We don’t really take up nitrogen, so what we breathe in is what we breathe out more or less. 569 mmHg is in the atmosphere, while we breathe out 566 mmHg
If dead space is developing in the lungs, how will mixed expired air change?
Lower than expected PECO2 d/t less surface area for diffusion
How are the mixed expired air concentrations found?
i.e. PECO2 = 27 mmHg
long card sorry; math
VT = 500mL (portion dead space, portion VA)
PCO2 in dead space should be 0 mmHg
Find alveolar air CO2, need concentration of CO2
PACO2 = 40 mmHg
Partial pressure of gas = concentration x total pressure
Total pressure = atmospheric = 760 mmHg
so
40 mmHg/760 mmHg = 0.053
or
5.3% is the concentration of CO2 in the alveolar air
How do you find how much CO2 in mL is in alveolar air?
The normal concentration of CO2 in alveolar air assuming 40mmHg PCO2 and standard atmospheric pressure is 5.3%.
Alveolar air volume is 350mL.
Concentration x volume = mL
5.3% x 350mL =18.42mL CO2 in alveolar air
If there is 18.42mL CO2 in alveolar air, 150mL dead space, and 350mL alveolar air, what would be the concentration of CO2 assuming alveolar air and dead space air were mixed? (i.e. mixed expired air)
Dead space + alveolar air = 500mL
Now find concentration by:
Volume gas/volume sample
18.42 mL CO2/500mL air = 0.0368
or
3.67% concentration of CO2 in the mixed sample.
Note, concentration in alveolar air went from 5.3% –> 3.67% when mixed with dead space.
How do you find the PCO2 of a mixed sample?
Take concentration x total pressure
i.e.
Concentration: 3.7%
Total pressure: 760 mmHg
3.7% x 760 mmHg = ~28 mmHg
^Note for our class we will use 27 mmHg CO2 in mixed expired air
As we have more dead space, how will PECO2 change?
It will get lower.
What two things in the chest are a barrier to putting air in the lungs?
The lungs themselves - d/t recoil; they like to be empty as can be
Chest wall - depends on lung volume/positioning/heaviness/tightness
I.e someone on their back has more weight on their chest, thus decreasing chest wall compliance
What are the steps to get to PCO2 of a mixed expired sample?
Not sure what concentration is to start, but can use formula for partial pressure of a gas.
Have partial pressure? Can then figure out concentration –> How much CO2 we have –> PCO2 of the total mixed sample –> Divide that by total size of the sample –> This gives the new concentration –> Multiply that by the total pressure = PCO2 of the mixed expired sample
Are the lungs/chest wall in series, or parallel when it comes to compliance?
In series. Both outward and inward recoil determine pleural pressure and lung volume. This decides what our FRC is.
(1/compliance of lung) + (1/compliance of chest wall) = (1/total compliance)
The apex of the lung sits where in relation to the ribs?
Above rib 1
Which way does the chest recoil?
How about the lungs?
Why is this important?
Chest - outward
Lungs - inward
Creates negative pleural pressure normally of -5 cm H2O
Elastic recoil pressure can be abbreviated how?
PER, or Pel
ER/el are subscripts
If you decided to take a saw to a chest, what would happen to the ribs? Why?
They would pop outwards d/t the chest walls natural tendency to recoil outwards.
What happens if lung recoil doesn’t balance chest wall recoil, for example in severe emphysema?
There is less inward recoil of the lung, which allows the chest wall to expand.
The ribs then protrude outwards, leading to larger lungs + barrel chest.
Because of this shift, instead of a -5 cm H2O pleural pressure, people with severe emphysema have a more positive pressure (-2.5 cm H2O) since there is less opposition to the chest wall. Not as much pressure is needed to get air in the lung.
What happens to the lungs if someone gets shanked in the chest and it opens the chest wall? (i.e. pneumothorax/hemothorax)
Air/blood moves in to fill pleural space, making it equal to atmospheric pressure (so equilibrated at 0 cm H2O)
This leads to the lung deflating and difficulty filling with air since there is not a negative pleural pressure.
What is the TLC of emphysema with transpulmonary pressure of 10cm H2O? Why?
6L. Not as much pressure is required to get air in the lungs d/t lack of elastic recoil, leading to chest wall expansion.
Normally 6L TLC takes 30 cm H2O
How do you find lung compliance?
Compliance = delta V/Delta P
VT = 500mL
P1 = -5 cm H2O
P2 = -7.5 cm H2O
Delta V = 0.5L
Delta P = 2.5 cm H2O
Compliance = 0.5/2.5
Compliance of the lungs normally = 0.2 L/cm H2O
What is compliance of the lungs measured in?
L/cm H2O
Upright & at FRC, is the chest wall in the way of breathing?
No
Why are the lungs/chest wall considered a system in series?
What is lower compliance - the components, or total compliance?
When we breathe in, we’re pushing against both elastic recoil of the lungs and the stiff chest wall.
1/n + 1/n =1/total compliance
Total compliance is lower than any single component. (about half)
Definition of resistance?
How hard it is to push something through a conduit
Compliance is a measure of what?
How easy it is (i.e. how much air can you put into the lungs with a given pressure)
Why do we use the formula for a system in parallel to find compliance of the lungs and chest wall if they are a system in series?
Want to know how easy it is to put air into the lungs
In a parallel system, is total resistance higher or lower than individual components?
Lower, as there as more pathways
Formula for parallel system resistance?
1/R total = (1/R1) + (1/R2) etc
What is the normal compliance of the chest wall?
And the lung?
0.2 L/cm H2O - chest
0.2 L/cm H2O - lungs
Find the compliance of the average lung/chest wall system.
Chest wall compliance = 0.2 L/cm H2O
Lung compliance = 0.2 L/cm H2O
(1/0.2 L/cm H2O) + (1/0.2 L/cm H2O = 1/x
5 + 5 = 1/x
10 = 1/x
Multiply both sides by X
10x = 1
Divide both sides by 10
(10x/10) = (1/10)
Total compliance of the system is:
X = 1/10
X = 0.1 L/cm H2O
What does the Bohr equation do?
Helps estimate alveolar dead space
What was the name of the guy who named the Oxyhemoglobin dissociation curve?
Bohr
He also named the Bohr equation, very original
Derive the Bohr Equation.
Just kidding, good luck
What is a common thing with both subtypes of physiologic dead space?
Alveolar and anatomical dead space both do not have CO2 in them since there is no gas exchange
What is a quick way to figure out anatomical dead space?
Fowlers test (review that)
All CO2 coming from a mixed expired air sample comes from where?
Alveoli that are both ventilated and perfused.
What can we do with this?
Scratch out the middle section. No CO2 comes from dead space, so it is not needed.
How do we find the amount of CO2 in a mixed expired sample?
If we know the fractional concentration of CO2 and the volume of air, we can multiple those together to get the quantity of CO2 in mixed expired air.
Size of sample x concentration of CO2 = amount of CO2
^Note that this amount of CO2 HAD to have came from good alveoli
Mixed expired air with CO2 in it had to have came from ____ alveoli.
Good/healthy
How do you find the amount of CO2 in mixed expired air that is coming from the alveoli?
All CO2 comes from good alveoli
Mixed inspired = mixed expired CO2
The most simple formula for finding alveolar deadspace is what?
What is the best formula?
Simple: VT = VDS + VA (rearrange and find VA)
Best: VA = VT - VDS
VA= alveolar ventilation
VT = tidal volume
VDS = dead space
Fractional mixed expired CO2 should be lower than what?
5%
40 mmHg/760 mmHg = ~5%
What would dead space divided by tidal volume give you?
Difference in gas fractions
What tool do we use that can tell us fractional inspired PCO2 if you’re at utopia general?
Fancy ventilators
What’s the easiest way to find fractional inspired PCO2?
Provided there is no shunt, look at a blood gas
What is the Bohr Equation that we need to have in our brains?
These 4
Assuming a healthy person, end tidal CO2 should be = to what?
Arterial PCO2
How can we find mixed expired PCO2 for this equation?
The ventilator can do it
Or
Do the math
^Need PaCO2 (blood gas works)
PECO2 = PaCO2 - (VD/VT) * PaCO2.
Figure out VD/VT
Plug it in to the equation
i.e.
VD = 150mL
VA = 350mL
VT 500mL
150/500 =0.3
PECO2 = PaCO2 - (VD/VT) * PaCO2.
VD/VT ratio = 0.3
40 mmHg - 0.3 x 40
40 mmHg - 12 mmHg
28 mmHg CO2 = PECO2
If you discover someone has alveolar dead space, what happens?
It continues to get bigger - need to give more ventilation to make up alveolar dead space.
Note: Can’t do anything about physiologic dead space.
What kind of dead space does this solve for if you rearrange it?
TOTAL dead space
How can we find alveolar dead space from this?
Subtract anatomical dead space from VDCO2
What is the roof of the mouth called?
Hard palate
What is posterior/inferior to the hard palate?
Soft palate, hangs off the back of the hard palate and can create difficult airway if they have too much tissue.
Note: Soft palate typically is what makes people snore
What is the projection of the soft palate called?
Uvula
What sits right behind the uvula?
Tonsils
What are the two types of tonsils?
Palatine (visible just behind the uvula)
Pharyngeal tonsil, which is in the back of the nose
