Exam 2 Flashcards
Schmidt Exam 2 (577 cards)
1
Q
____ determines how much filling the ventricle is going to have during phase 1 of the cardiac cycle.
A
Preload
2
Q
____ fluences how long it takes for the aortic valve to get open as well as how fast it is going to slam shut.
A
Afterload
3
Q
____ is going to give us a different SV by leveling different quantities of squeeze on whatever is in the ventricle.
A
Contractility
4
Q
When we have aortic ____, we have a really high interventricular pressure pumping against a high resistance valve.
A
aortic stenosis
5
Q
With a lot of valve issues, we have compensation of the system via an increase in ____ and ____.
A
heart rate and filling pressure
6
Q
With almost all of these cardiac problems, chronic elevations in ____ are the main things that keeps the heart and body in working condition.
A
filling pressure
7
Q
After an acute MI where the heart is injured, the body’s immediate response to that is what? Why?
A
The body will increase sympathetic tone of BOTH the heart and veins, because it will give us stronger contractions of heart and better filling pressure from the veins.
8
Q
The long term fix for heart failure is going to be a general increase in ___, usually seen in elevated CVP.
A
Psf
9
Q
Reduced contractility = ___ SV
A
Reduced (because we aren’t getting as much out of the heart on each beat)
10
Q
Decrease in SV will manifest as ___ ESV and ___ EF.
A
increased ESV and decreased EF
11
Q
How does increased CVP affect SV?
A
An increase in CVP is increasing the EDV (amount of volume that is going to be in the heart on each beat). So, EDV will increase from 120 mL to 170 mL.
12
Q
What kind of drug would we give if patient has a heart that has reduced contractility but needs something that will keep volume coming out of the heart for a longer period of time?
A
an afterload reducer
13
Q
How does an afterload reducer work?
A
An after-load reducer will get more SV/CO each beat as a result of opening the aortic valve earlier and closing it later. So, it will increase our SV at a lower energy expenditure, since we are pumping against lower pressures.
14
Q
How does external work in an untreated HF patient compare with a HF patient taking afterload reducers?
A
The area of the PV loop is larger in the afterload-treated patient is compared to the untreated afterload patient. So, EW of the treated patient is greater than the untreated patient.
15
Q
People with moderate HF, we can help their heart pump by just reducing ____ and increasing ____.
A
reducing afterload and increasing contractility
16
Q
How does ACE-I’s help HF patients?
A
It is an afterload reducer, it stops scar tissue by inhibiting growth factor, and it prevents messing up electrical conduction pathways. Overall, it slows the heart from scarring over and gets a bunch of useful side effects.
17
Q
2 inotropes that help with HF.
A
Digoxin (cardiac glycoside) and Milrinone (PD3 inhibitor)
18
Q
How do inotropes help with HF?
A
They will increase contractility of the heart, making the heart beat stronger.
19
Q
Why do we have to be careful when giving Milrinone, specifically with HF patients?
A
Milrinone can reduce afterload in addition to increasing myocardial contractility.
20
Q
Normal CO curve peaks at __ L/min with a normal amount of SNS and PNS activity.
A
13 L/min
21
Q
How would the CO curve change if we increase amount of SNS stimulation at the heart?
A
We would have a higher CO, so the curve shifts higher (greater plateau). It will also shift a little to the left (slightly less RAP).
22
Q
On a cardiac output curve, what does a shift on the x-axis to the left and right mean?
A
Shift left = stronger pump. Shift right = weaker pump.
23
Q
Why do we expect a drop in RAP if the CO curve shifts to the left?
A
RAP be reduced from its normal value because the heart is pumping out what is being returned to it faster than it normally does.
24
Q
If the heart isn’t pumping out what is being returned to it as quickly/effectively, then we would expect RAP to ____.
A
increase
25
If we reduce the pumping effectiveness of the heart by just removing the sympathetic tone (no other change), how is CO affected?
The heart still remains a pretty decent pump! CO plateau only drops from 13 to 10L/min. Hopefully, in surgery you won’t need 13L/min. So, just messing with the heart itself doesn’t really do a whole lot!
26
If we were to maximally stimulate the SNS, what are the two effects it would have on the venous return curve?
1. Increase in Psf 2. Increase in RVR
27
If we were to maximally stimulate the SNS, which is more important? The change in Psf or RVR?
Change in Psf is always the most important change! Increased Psf will give us more venous return, increase CO substantially. The increase in RVR is secondary to that.
28
If we were to maximally stimulate the SNS, how would the slope of the venous return curve appear?
Increased SNS activity = increased RVR = reduced slope of the venous return curve.
29
Why does Psf increase when we having increased SNS activity?
Because all the blood vessels will be constricted/tighter than normal.
30
How does a volume infusion affect Psf and RVR?
That will increase filling pressure and increase the width of the blood vessels that are being filled. So, that would cause a reduction in RVR and and increase in Psf. (Another example Dr. Schmidt gave of this was exercising and pulling blood from other parts of the body to where it was needed.)
31
How does a volume infusion affect RAP?
If we put volume in externally or just shuffled it around the body a little bit, one of the side effects of this is that we have a fairly high RAP (even though the heart is working like a very effective pump).
32
When is the only time we would see a healthy person have an increased RAP?
When we have a scenario where we have expanded the circulating volume of the CV system, such as during exercise/working out strenuously.
33
If you need to drastically increase CO, there is really only one way to do it and that is to do what?
Get more blood back to the heart and make the heart a stronger pump. Need to do both, since making the heart a stronger pump in and of itself isn't really that helpful.
34
Increased ___ is more importantly a big determinant than increased Psf.
CVP
35
If CVP is high, then the heart has a problem, and that might be true. Is the CVP the problem or the solution?
The high CVP is the body’s solution to the problem, not necessarily the origin of the problem.
36
A ____ is an accessory pathway that allowed blood to get through the heart through an abnormal channel/open conduit.
AV fistula
37
\_\_\_ is really helpful to keep BP high to help with coronary and organ perfusion. In terms of getting blood to the heart, though, it is an impediment.
SVR (So, if we remove/reduce SVR, it makes it easier for blood to get back to the heart.)
38
What drug specifically works to reduce SVR without affecting Psf?
Hydralazine
39
Does Hydralazine affect veins or arteries or both?
It is an arterial-specific vasodilator. So, it has no effect on the veins.
40
When giving Hydralazine, how is the net filling pressure affected?
If we reduce SVR, the pressure in these blood vessels (between the chokepoint and the heart) will be reduced in that area. That will result in an increased pressure on the other side of the obstruction/squeeze point. It balances out, so the net Psf doesn't really change all that much!
41
How does an AV fistula affect SVR and Psf?
An AV fistula would relax the arteriolar resistance/SVR. Because we put in an extra pathway, overall the Psf doesn’t change a whole lot because it’s just pressure going from one place to another. If we are looking at the pressure as a whole, the pressure as a whole doesn’t change too much.
42
How an AV fistula affects blood getting back to the heart is mediated by a reduction in \_\_\_\_.
Reduction in RVR [We just created another pathway/second option, so resistance of the system is reduced and that is going to make it easier to get blood back to the heart so it can pump it back out again.]
43
With the AV fistula, we don’t see a huge change in pressure but we do see a very large increase in \_\_\_.
CO, because we have just reduced the difficulty of getting blood back to the heart so it can pump it out again.
44
If the heart is looking at pressure in the arteries and sees that it's low, what 2 things does it do to help fix the pressure problem?
It will (1) increase/expand blood volume and (2) increase SNS activity at the heart.
45
What is the initial compensation the body has if someone has an MI?
Increase in sympathetic tone; that will get the failing heart to increase its output to 4-5L (something to keep us alive).
46
The long-term solution the body has if someone has an MI and low CO is?
Blood volume expansion, which helps us with filling of the heart.
47
True or False. When we have a failing heart, that would be analogous to the pressure volume loops we looked at before with reduced contractility.
True. So, SV is low and the compensation by the body is just increased preload, filling pressure, and increased filling of the heart.
48
What do catecholamines do in HF?
Having lots of catecholamines at the heart usually goes hand-in-hand with a lot of catecholamines floating around in the blood. What that does to help the heart temporarily is it will make Psf higher by squeezing veins more than they would normally be squeezed.
49
Advantage of fluid retention over the long haul compared with autonomic/SNS tone.
The advantages of doing this is to unload some of the SNS activity at the heart, and that reduces our chance for arrythmias that are sympathetic-tone related. A lot of the tachy and ventricular arrythmias are better off with a heart that is a little stretched out compared to a heart that has a lot of SNS activity.
50
Why do we need some reserve SNS activity?
. If our sympathetic tone is already at 100% and we are alive (barely), when we get out of the chair we will fall on our face because we have no reserve to help us out when we change our body position. In order to have that flexibility so we can get around throughout the day, we need some reserve SNS activity.
51
What is the CO that is compatible with keeping all the organs alive?
4-5 L/min
52
If we are unable to get to an appropriate CO to maintain life even with increased sympathetic tone, what type of drug can we give to bring up the CO?
Inotrope (dig or milrinone)
53
How does the CO curve appear if we have heart failure?
It is depressed (decreased slope), with CO about 50% of normal.
54
RAP with HF would be ___ mmHg.
+4 mmHg, because the heart isn’t pumping out what is being returned to it.
55
With HF, the main response of the system is going to be to (reduce or increase) venous compliance.
Cv would be reduced. [If we make the veins tighter/less compliant, that will increase filling pressure, RVR and SVR.]
56
How is Psf and RVR affected with mixed vasodilators?
Psf is decreased. RVR is decreased (slope is higher).
57
When do we have decompensated heart failure?
When the CO is below the critical CO level required for normal fluid balance.
58
Are inotropes first line or last line treatment for HF?
Those are usually last ditch drugs. By the time someone is on digitalis or some other inotrope, they will probably be on it for the rest of their natural life.
59
True or False. Decompensated HF is very similar to severe compensated HF.
True.
60
If we have HF and use drugs to increase our CO unsuccessfully, how long does it take for the body to completely fail?
About a week after the MI
61
About a week after an MI, the body can completely fail if CO is not stable. Explain what this complete failure is caused by.
Part of the failure will be related to the excessive filling of the heart/excessive expansion of blood volume. At some point, the additional stretch and additional filling is actually problematic for CO. If we fill the heart too much, then the heart gets all stretched out and can’t pump effectively. So, the body's attempt at compensation actually becomes more of a problem than a solution.
62
With long term CHF, usually our ___ are going to be retaining volume until BP is fixed.
kidneys [Anytime they think that CO or MAP are lower, they will hang onto additional volume.]
63
What type of drug can we give to patients with HF whose kidneys are hanging onto too much volume?
Diuretic [Oftentimes, long-term diuretic therapy might be used in CHF to prevent the kidney from overloading the filling pressures that are stretching the heart apart.]
64
What can happen to the lungs if we have left heart failure and increased Psf?
The Psf is also a gauge of what is happening in the lungs, especially if we have left heart failure. The last thing we want to do is have fluid filling up in the lungs or an overstretched LV. So, a diuretic is often used to prevent water from filling up the lungs and prevent the heart from stretching out any more than it has to be.
65
\_\_\_ is a function of getting O2 to where it is needed.
Cardiac output
66
\_\_\_\_\_ are the top controllers of metabolic needs.
Thyroid hormones
67
What happens if the kidneys are unable to get the heart's CO and BP up to a normal level after an MI?
If we get to a point where we are overstretching things because CO is not normal and BP is not normal, we can get to the point where we hang onto too much fluid and electrolytes and that stretches heart out past the point of it being helpful.
68
If long-term HTN exists, that means the ____ have to be messed up.
kidneys (if they weren’t messed up then we wouldn’t have high BP. So, some problem at the kidney to have high BP.)
69
When we have high BP, there is usually a small elevation in ____ that is unexplainable and a small expansion of \_\_\_\_\_.
CO ; blood volume
70
\_\_\_\_ parallels the expansion in the blood volume.
ECF
71
One component to long-term HTN is a prolonged sustained increase in \_\_\_\_.
SVR (aka total peripheral resistance; In terms of what is causing it, it is probably something with ANS, but exactly what is unknown.)
72
With long-term HTN, we see a \_\_\_% increase in SVR and a 5% increase in ____ and \_\_\_\_.
33% increase in SVR ; 5% increase in blood volume and CO.
73
With elevated SVR, what drug class can we give the patient to help?
Ca channel blockers (we really don’t have a whole lot of CV medicines that will fix elevated SVR! CCBs won't actually help the underlying issue.)
74
How does having HTN going into the OR affect your anesthetic?
They will be more sensitive to anesthetics than someone with normal BP.
75
5 things that can cause a sustained increase in CO.
Nutrient deficiences (ex. Beriberi), AV shunts, hyperthyroidism, anemia, pulmonary disease
76
Why would nutrient deficients cause a sustained increase in CO?
If our tissues are using nutrients in an inefficient manner, we might need to deliver more nutrients to the tissue. (Normally, oxidative metabolism is a very complicated step-by-step process that involves a lot of enzymes; if we uncouple any of those enzymes, we can remove the benefit of oxidative metabolism.)
77
2 types of metabolism are ___ and \_\_\_. Which one is more efficient and why?
anerobic and aerobic; the more efficient of the two is aerobic metabolism because it allows us to get more ATP out of glucose and fats.
78
\_\_\_\_ is a condition that interferes with enzymatic steps for aerobic metabolism.
Beriberi
79
Beriberi is a deficiency in \_\_\_\_, which is also known as \_\_\_\_.
Vitamin B1 ; Thiamine
80
What happens to metabolism if we have beriberi?
Thiamine is part of the series of enzymatic steps and cofactors that normally allows us to produce ATP very efficiently. If we remove one of those efficient steps, we are left with less efficient metabolism and we will have to deliver more fuel to tissue in order to keep things in balance. So, we end up with sustained increase in CO.
81
What is dinitrophenol?
an uncoupling agent of oxidative metabolism. (It basically does the same thing as thiamine, but has a different chemical name.)
82
Dinitrophenol is found in what? How does it work?
Dietary supplements/weight loss pills. It inefficiently uses glucose, so we have to feed more of the fat compounds into the metabolic compounds and it allows for weight loss.
83
What negative effect does dinitrophenol have on the heart and metabolism?
It screws everything up and increases your metabolic rate; anytime you do that, you are going to increase your risk for heart problems—arrythmias are more common in someone with a higher body temperature and things don’t normally work very well.
84
The higher the metabolic rate, the more ___ we need.
CO (This is what happens with hyperthyroidism.)
85
Thyroid hormone is \_\_\_\_-soluble. How dose that affect its free levels in the body?
Lipid-soluble. So, there isn’t a whole lot of free thyroid hormone floating around in the body.
86
A dangerous extreme form of hyperthyroidism. (2 names)
Thyroid storm or acute thyroid toxicosis (don’t want to happen during surgery because you will have to deliver a whole lot of extra oxygen to the person’s tissues and that can become difficult.)
87
Why do AV shunts cause sustained increased CO?
If we have an AV shunt, we are having blood moving from high pressure side of circulation back to low pressure side of circulation. If it isn’t doing much in terms of delivering nutrients, then it is a part of wasted CO—the heart will have to make up for the blood that isn’t doing a whole lot.
88
When we have regions/patches of the lungs that have poor gas exchange, what does the CV system do?
CV system tries to shut down perfusion of these bad areas;it just clamps off the blood vessels that lead into those areas and basically prevents a pulmonary shunt. (If there is not going to be any gas exchange, it doesn’t make sense to pump blood through there because what comes out of those patchy areas is deoxygenated blood. If we have deoxygenated blood mixing with good blood in the lungs that has undergone gas exchange, we will have a lower oxygen content in the blood coming out of the left side of the heart.)
89
Pulmonary disease would be an example of how we may have an elevated ___ in someone with patchy lungs.
CO
90
3 things that would cause a huge short-term increase in CO.
Exercise, anemia, anxiety
91
2 reasons why we would have sustained decreased CO.
removal of limbs and hypothyroidism
92
Why does amputation of limbs decrease CO?
If we take out a kidney or a lung or limbs, that is going to reduce the amount of oxygen that has to be delivered. That would result in a lower than normal CO.
93
\_\_\_\_ would cause a short-term decrease in CO.
Shock (all forms!--cardiogenic, neurogenic, hemorrhagic, traumatic, etc.)
94
Exophthalmos occurs in what thyroid disorder?
Hyperthyroidism (exopthalmos: protruding eyes, eyelids are pulled back)
95
2 reasons for hyperthyroidism.
Tumor or autoimmune problem
96
Right underneath thyroid gland is our ___ nerves, which control \_\_\_.
recurrent laryngeal ; voice box (If we lose those, we have the potential to lose our voice.)
97
Thyroid gland is extremely vascular; each side has two huge large arteries, the ___ and \_\_\_.
superior thyroid artery and inferior thyroid artery (found on each side of the thyroid gland)
98
The blood flow is usually about ___ times the weight of the thyroid gland, which is about ____ grams.
5x the weight ; 15-25 grams (Most people have larger thyroids than this!)
99
Where is thyroid gland found in relation to the crycothyroid ligament?
Inferior (below the ligament)
100
True or False. There is a lot of muscle lying on top of the cricothyroid ligament.
False (There are NOT a lot of muscle lying on top of that ligament)
101
The ___ is an important sensory area in the brain, connected to lots of different body functions such as?
hypothalamus ; interpreting blood osmolarity or body temp or state of infection.
102
Hypothalamus secretes a compound called \_\_\_\_.
thyrotropin releasing hormone (TRH)
103
When is TRH released?
When the hypothalamus decides it needs to increase amount of thyroid floating around.
104
TRH will make its way over to the \_\_\_, which will release a compound called ___ that acts on the thyroid gland.
pituitary gland ; thyroid stimulating hormone (TSH)
105
If hypothalamus is looking at body temp, once body temp comes to a place where it’s happy, what does the hypothalamus do?
It will reduce release of TRH, which reduces release of TSH and reduces the output from the thyroid gland. Ultimately, the whole cascade gets shut down.
106
Thyroid hormones work on a ___ feed back system.
Negative
107
Thyroid hormones can feed back on the hypothalamus, as well as the \_\_\_.
pituitary gland
108
If thyroid hormones T3/T4 feed back on the pituitary gland, what happens?
On the pituitary gland, there would be a reduction in the # of TRH receptors. That would also shut down the system because it would reduce activity of pituitary gland, reduce the amount of TSH that is released, and in turn reduce amount of thyroid hormone that is released from the thyroid gland.
109
Thyroid hormone is a \_\_\_-based compound. Is there a lot of this found in the body naturally?
Tyrosine; available in plenty of cells in the body. There is hardly ever a deficiency of tyrosine.
110
How does the body create thyroid hormones from tyrosine?
The thyroid gland adds iodine to the tyrosine compound.
111
Name the different tyrosine-based compounds our thyroid gland makes by adding iodine to it.
Tyrosine \> Monoiodotyrosine \> Diiodotyrosine \> Triiodotyrosine (T3) \> Thyroxine (T4)
112
When we think about thyroid hormone, we are usually going to be referring to \_\_\_.
T4 (thyroxine)
113
The predominant form being produced by thyroid gland is \_\_\_.
T4 (So, that is usually what is floating around in the blood.)
114
100% of T4 that is floating around was manufactured by the \_\_\_.
thyroid gland
115
What % from where is T3 made?
20%: thyroid gland. 80%: reduction of T4 somewhere in tissues
116
How do we make T4?
If we have two diiodotyrosine’s, combine those together and strip the iodines off one and just put it on one tyrosine.
117
2 ways to make T3.
1. Combine one of the monoiodotyrosine with one diiodotyrosine 2. Strip an iodine off a T4
118
Name of enzyme that strips iodines off T4.
Iodinase
119
In a first world country, we eat plenty of iodine because it is included in \_\_\_.
table salt (without it being in table salt, there aren’t a whole lot of places where we would get it from our diet. Don’t get a whole lot of it from animals or fruits, so it is important for it to be included in the diet or some other supplement.)
120
Why do goiters develop?
When people don’t have enough iodine, their body has problems producing enough thyroid hormone. So, the thyroid gland is being told to produce something that it can’t since it doesn’t have iodine available to do it.
121
Where in the body is iodine used?
Thyroid gland (it doesn't work anywhere else in the body!)
122
Where in the body is iodinase used?
Anywhere in the tissues! (any cell that is sensitive to thyroid hormone has this enzyme (iodinase) that is available to convert T4 into biologically active T3.)
123
What is radioactive iodine medically used for?
1. slow down overactive thyroid or 2. shrink cancerous tissue (ex: thyroid tumor; we can supply radioactive iodine to be taken up by thyroid gland and then selectively expose it to radiation.)
124
Radioactive iodine is what isotope number?
131
125
If there was a nuclear explosion with radioactive iodine nearby, what can happen? What can you take to prevent it?
Radioactive iodine will be concentrated in the person’s thyroid gland. Remedy: iodine supplements. (We could outcompete that with normal iodine to limit our radiation exposure.)
126
Thyroid receptors are found where?
Everywhere (in our neurons in early development and in fully developed tissue, located in all our muscle, all our fat, it is pretty much everywhere.)
127
Which is more active? T3 or T4?
T3
128
Primarily T\_\_ is floating around the body. Does it have an immediate effect?
T4. If T4 is being delivered to the tissue, then it has to be reduced/processed before it can be in active T3 form. (So, T3 has an immediate effect, NOT T4)
129
If thyroid weighs 20g, what is the blood flow?
20g x 5 = 100 mL/min (If we nick any of the tissue leading into the thyroid or thyroid itself, it has potential to bleed really, really bad because there is so much blood flow going to this organ. It is very vascular and very prone to bleeding.)
130
How much thyroid hormone is stored in pituitary gland?
2-3 months worth (In addition to that, there is plenty of circulating thyroid hormone)
131
What is thyroglobulin?
A glycoprotein that is produced in the thyroid gland to serve as a carrier compound of thyroid hormones. (TH needs a carrier compound since it is lipid-soluble and doesn't dissolve easily)
132
3 carrier compounds of thyroid hormone. Which is the major one?
Thyroglobulin, pre-albumin, albumin. The vast majority of thyroid hormone is carried by thyroglobulin.
133
Is there a more free concentration of T3 or T4 floating in our blood?
T3 (There is a very small quantity of either of these free floating/not attached to anything in the blood! Despite T4 being the predominant version that is present in the CV system, T3 actually has a higher free concentration)
134
Why is there a higher free concentration of T3 than T4?
T4 sticks to thyroglobulin stronger (higher affinity) than T3. (Either way there is very little of both free in the blood because it is lipid soluble and it doesn’t like to be in aqueous solution.)
135
In terms of affinity of thyroid hormone receptors that are present everywhere, thyroid hormone receptors have about 10x the affinity for T\_\_.
T3 (T3 is the biologically active compound whereas T4 is pretty much a precursor; even if T4 does bind to the receptors for a short period of time, usually it is not significantly biologically active.)
136
Thyroid hormone receptors are found outside or inside the cell?
Inside (because we are dealing with a lipid soluble compound)
137
When thyroid hormone binds to its receptors, what happens regarding genes?
increase in gene transcription (This complex moves into the nucleus of the cell and causes gene transcription to happen; pretty much all genes have increased activity when there is more thyroid hormone around.)
138
The most produced compound that results from thyroid hormone binding to its receptor inside the cell is \_\_\_\_.
Protein
139
What pump does thyroid hormone binding to its receptor stimulate/increase the cycling rate?
Na/K/ATPase pump (Exactly how this increases cycling rate with thyroid hormone, I’m not exactly sure how, but it is one of the things that is activated and that is probably the number one increase of energy use through an increase cycling of that pump.)
140
Glycogen will be broken down to glucose and metabolized through ____ metabolism.
oxidative
141
What does body break down to build proteins to allow for a more active cell? (3)
Glycogen, lipids, cholesterol (As a result all these energy compounds being used is, our plasma levels of these energy derivatives oftentimes decrease because they are being consumed in the cells around our body to release energy to build stuff.)
142
If we have a protein that is not needed/not working, we can break it down, take the amino acids apart and turn them into another protein or burn them for energy. That process is called \_\_\_\_.
Catabolism (So, catabolism is breakdown of proteins and anabolism is the assembling of proteins from their component parts.)
143
How does hyperthyroidism affect cholesterol, fatty acids, and blood sugar?
All are decreased (because it is being consumed in all the tissues being affected by thyroid hormone. So, expect a lower body mass)
144
In hyperthyroidism, insulin release increases or decreases?
Increases (that will help us get the sugar inside the cell where it is consumed)
145
How does hyperthyroidism affect SNS stimulation and beta pathways? Treatment?
Increase in activity of SNS, oftentimes increasing beta-agonist pathways (which increases the activity of our cells). Treatment: beta-antagonists (to cut down on some of these effects)
146
Hyperthyroidism does what to O2 and CO2 levels?
Increase oxygen demand. Increase CO2 production. (In hand with that would be an increase in H+ production, oftentimes in the form of lactate.)
147
How does hyperthyroidism affect CV?
vasodilation; increased CO, HR, and SVR
148
Why does hyperthyroidism require increased CO?
To get CO2 to the lungs to be breathed off and to expose blood to oxygen to increase oxygen delivery capacity.
149
How does hyperthyroidism affect energy levels? GI? Musculoskeletal? Body temp?
Patients will have anxiety, insomnia, fatigue. Overactive GI: vomiting and diarrhea. Muscle tremors. Increased body temp and sweating.
150
Something specific with hyperthyroidism is sometimes they exhibit ___ hertz skeletal muscle tremors.
10-15 Hz (Must look really close to see it!)
151
If you see an unexpected increase in HR there are two things that should come to mind, which are?
valve problems or hyperthyroidism
152
True or False. MAP of patients with hyperthyroidsim is high.
False (MAP is normal, despite having an increased SBP)
153
With hyperthyroidism, how is MAP normal with elevated SBP?
If kidney is healthy and MAP is similar to what it would be if they didn’t have a problem, really the only way that is going to happen is the kidney will have to get rid of volume to reduce DBP to make up for the rise in SBP.
154
What happens to SBP and DBP as a function of age and atherosclerosis in order to have a normal BP?
Higher SBP as a function of age and decreased vessel compliance. DBP is reduced via the kidney. So, there is a farther separation between them (higher pulse pressure).
155
Two drugs that can be used to slow down metabolic rate of thyroid gland, which would reduce the amount of thyroid hormone that is being released.
Propylthiouracil and Methimazole (These two drugs are relatively nonspecific.)
156
3 options to "settle down" the thyroid gland from releasing so much TH.
1. Drugs (Propylthiouracil and Methimazole) 2. Radioactive iodine 3. Surgery
157
Why avoid amiodarone if you have hyperthyroidism?
Amiodarone has 30% iodine in the solution (want to avoid giving additional iodine!)
158
What is easier to treat, hyper or hypothyroid? Why?
Hypothyroidism, because you can just give a synethetic TH (Synthroid).
159
3 examples of things that could cause hyperthyroidism.
1. adenoma 2. grave's disease 3. early hashimoto's thyroiditis
160
What is an adenoma?
tumor releases too much thyroid hormone; can cause goiter.
161
What is Grave's disease?
autoimmune disorder that produces antibodies to TSH receptors, causing hyperthyroidism. (These antibodies activate the TSH-Rs on the thyroid gland, acting independent of either the pituitary gland or hypothalamus, causing increased amounts of TH to be released from the gland. That in turn sets all those other things into motion in terms of what we expect to see for clinical features of the problem.)
162
3 things we expect to see in Grave's disease.
1. increase in TH 2. reduced/almost no TRH released from hypothalamus 3. reduced TSH (less TRH because elevated TH is suppressing the releasing factors at the hypothalamus. Less TRH = less TSH, since TSH is in response to TRH)
163
What is Hashimoto's thyroiditis?
autoimmune disorder in which the thyroid gland is targeted and destroyed over time; so, patient has antibodies to the thyroid gland itself causing hyperthyroidism.
164
T3 and T4 levels in early hashimotos is high. Why?
Early on in the disease, there is a lot of inflammation and irritation of the thyroid gland; that inflammation can trigger excessive release of thyroid hormone. So, early = increased T4 and T3 (hyperthyroidism)
165
What happens to T3 and T4 levels in late Hashimotos?
As the thyroid gland is destroyed, it will be less and less able to release sufficient quantities of thyroid hormone. So, there will be lesss T3 and T4. (Late Hashimoto's can cause hypothyroidism).
166
Do you see a goiter with early Hashimoto's? Late?
Early on in Hashimoto’s thyroiditis, when things are being attacked, we would be looking at a goiter because of all the stuff going wrong in the gland. Later on as the tissue is destroyed, there will still be all sorts of scar tissue left over, so that is also going to give us a goiter.
167
Do you see a goiter with Grave's disease?
With Grave’s disease, if we have all these uncontrolled antibodies telling the thyroid gland to release lots of thyroid hormone, that is what it is going to do and it will be enlarged in the process, so that can cause a goiter.
168
5 functions of pulmonary circuit.
1. gas exchange 2. acid-base balace 3. speech 4. enzymes 5. immune response
169
With gas exchange, ___ going into the body and ___ goes out.
Oxygen ; CO2
170
Formula to make carbonic acid.
CO2 + H2O + Carbonic anydrase = H2CO3
171
What makes H2CO3 an acid?
It can fall apart into a proton. (Carbonic acid breaks down into H+ and HCO3- ; reaction takes place fairly easily in solution.)
172
What is carbonic anhydrase used for?
Catalyzes (speeds up) the reaction of turning CO2 + H2O into carbonic acid. Or breaking down carbonic acid into CO2 + H2O (dehydration).
173
Does carbonic acid last a long time?
No. (Carbonic acid isn’t a compound that hangs around too long; it has a short half-life and just falls apart into the proton or bicarb or in the other direction.)
174
Explain why CO2 can essentially be considered an acid.
If we have a bunch of CO2, water, and CA around... the net result of this will push the equation forward and the net result of that is a free proton.
175
By definition, acid base is dependent solely on the concentration of \_\_\_.
Protons
176
How does our respiratory system fix acidosis?
Our body can blow off CO2 and can indirectly get rid of free protons. (Favors reaction going to the left.)
177
Respiratory circuit's acid-base balance is a short or long term fix?
Short (Short-term, we can balance things out by blowing off or hanging onto CO2 to correct whatever acid base problem we have. Long-term, the pulmonary system doesn’t breathe off protons; otherwise, that wouldn’t be good.)
178
If our lungs can’t get rid of protons, the only other place we are going to get rid of them is going to be through the \_\_\_\_.
kidneys
179
If we talk about a system that is producing a lot of CO2 and our body needs to get rid of the CO2, what does our heart and lungs do?
We are going to increase our ventilation—deeper breaths and increased RR. Our CO will also increase, because getting more blood pumped through the lungs will help reduce CO2 also.
180
Acid-base balance is driven by our ___ sensors. Where are they found?
blood gas sensors, found in the aorta at the carotid bifurcation (same area as BP sensors!)
181
What happens to BP is patient is not being ventilated enough and has excess CO2 levels?
BP increases (If our CO2 is high at any blood gas sensors, it causes a reflex increase in CO. That plus increased ventilation helps us get rid of extra CO2. So, if pt isn’t being ventilated enough and they have excess CO2 hanging around, their BP goes up. Likewise, if you blow off a lot of CO2, their BP goes down.)
182
Speech is done via air that is coming out of the system passing through the vocal cords controlled by ?
Skeletal muscles in larynx
183
What important enzyme is found in the respiratory circuit? \*Hint: RAAS.
Angiotensin conversion enzymes (ACE)
184
What does ACE do?
converts ang I to ang II and it also breaks down bradykinin
185
Explain why the nose is an immune component.
A portion of air goes through our nose, which is basically a crude filter. As we are pulling air in, at some point, it will make a hairpin turn inside our head and go down the trachea. All the particulate stuff (dust and larger compounds) don’t make that hairpin turn very well, so it sits in the mucous in our nose and gets collected there instead of going down into the lungs.
186
\_\_\_\_\_ play a big role in chopping up and getting rid of stuff that shouldn’t be in the lungs.
macrophages (As this stuff is chopped up, it is put into smaller pieces that can then be sucked up in lymphatic system.)
187
We secrete ____ so that stuff that shouldn’t be in the respiratory circuit gets stuck in it.
mucous (found in nose and in the lungs!)
188
There is a rich ____ network in the lungs that helps us get rid of all this crap that isn’t supposed to be there.
lymphatic
189
The main muscle of inspiration and expiration under normal resting conditions is the \_\_\_\_\_.
diaphragm
190
The diaphragm made up of what?
2 muscle units connected to each other midline by a tendon
191
Where is the diaphragm fastened in?
Each side of the diaphragm has a little different connecting point on the spine in the abdomen.
192
What part of the diaphragm is the phrenic nerve controlling?
Leaflet or cusp (Each leaflet/cusp is going to be controlled by the phrenic nerve on that side of the body.)
193
If you are healthy and happen to lose one phrenic nerve, what happens to your ventilation?
the remaining phrenic nerve will be able to handle ventilation; it won’t be as efficient to exercise and whatnot, but it will keep us alive.
194
As we contract the diaphragm, it moves ___ and causes more ___ pressure in the thorax. Is this inspiration or expiration?
down ; negative ; inspiration (that will allow us to bring in air from the outside where atmospheric pressure is higher compared to the thorax.)
195
The diaphragm relaxes when we \_\_\_\_.
expire (this will make the internal pressure positive, which is going to move air out of the lungs to the outside, where pressure is lower.)
196
Where are intercostal muscles found? How many do we have?
located in between the ribs; we have two sets of these for each pair of ribs. (12 pairs of ribs x 2 sets = 24 total. Drawn in red)
197
Where are external intercostal muscles found?
On the outside of the ribs with an attachment point on the chest wall.
198
During deep inspiration, what do the external intercostal muscles do and why?
During deep inspiration, the external IC muscle contracts, which will pull the ribcage out to the periphery. That will help us inspire because it is widening the chest wall laterally and increase the volume in the thorax.
199
During normal resting breathing, what are external IC muscles responsible for?
They prevent the collapse of the thorax
200
Where are internal intercostal muscles found?
Between the ribs on the inside.
201
What happens to the ribcage if internal IC muscles are contracted? Does it help with expiration or inspiration?
It will pull ribcage back towards center when it is contracted. That process would help us with expiration.
202
The internal intercostals help with ___ and external intercostals help with \_\_\_.
Internal = expiration. External = inspriation.
203
What are scalene muscles? How many do we have?
The muscles that connect the top of the thorax to the neck. There are 3 sets of these on each side, so 6 total.
204
What happens to the ribcage if scalene muscles contract?
Pull the ribcage up. (If these muscles are pulling the ribcage up while the diaphragm is pulling down, that will help us take deeper breaths.)
205
The ___ muscle connects at the middle of the sternum and the mastoid process on the back of the skull.
sternocleidomastoid
206
What motion does the sternocleidomastoid muscle allow us to?
swivel our head from side to side
207
What happens to the ribcage if sternocleidomastoid muscles contract?
Pull the ribcage up. (If we are pulling ribcage up while the diaphragm is contracting and pulling down again, this will help us take a deeper breath.)
208
The muscles other than the diaphragm are usually thought of as ____ muscles.
accessory
209
The connective tissue that surrounds the lungs is called \_\_\_\_. What does it do?
Visceral pleura. Provide smooth slippery surface for lung to glide up and down in the chest as we move air in and out of the lungs.
210
The inside of the chest wall lining is called the \_\_\_\_. What does it do?
Parietal pleura. Provide a smooth slippery surface so we can get air in and out of lungs without causing a lot of friction and without a lot of pain.
211
In between the two pleura layers is lots of \_\_\_\_.
Mucous (helps the friction be reduced)
212
Where is the costodiaphragmatic recess?
At the very bottom of the chest wall, where the diaphragm connects with the lower ribs.
213
What is the costodiaphragmatic recess filled with?
Usually, it is filled with a little bit of fluid and some mucous, but there is a potential for air there.
214
Trachea is made up of \_\_\_\_, which help give support to prevent our trach from getting crushed and less likely to obstruct the esophagus.
cartilaginous semi-rings (The flexibility of the cartilage is nice so it won’t snap or break if it is under a lot of pressure.)
215
The cartilaginous rings have an opening that is filled with ____ and \_\_\_\_.
connective tissue and smooth muscle
216
If we activate the smooth muscle cells in the cartilaginous rings of the trach, what happens?
Trachea is constricted.
217
If we apply a lot of force to maniphulate the shape of the carlaginous ring opening (connective tissue part), why would this be beneficial?
Coughing (If we need to remove something out of our trachea it is best to have really rapid airflow.)
218
How is air able to move at a greater velocity in the airway?
If we have a divot/split there, then there would be a couple different pathways the air can take. If we have different split points, then the air can move at a greater velocity through those narrower openings compared to if it was just one single circular opening.
219
The trachea has a divot/split from the ____ down.
laryngeal cartilage
220
The tracheobronchial tree has ___ different segments.
24 (Not all parts of the lung have a full 24 segments)
221
The trachea is considered to be generation \_\_\_.
0 (first part before there have been any branches.)
222
How does cartilaginous support appear further from the trachea?
The further from the trachea we are, the more scattered and irregular the cartilage support is. As we move down into the lungs, the cartilage are circular plates that just associate with each other so it’s not as robust of a structure.
223
The first type of airway we wouldn’t find any cartilage in would be the \_\_\_\_. What size diameter is this?
bronchioles, 1 mm
224
Bronchioles are at generation \_\_\_; terminal bronchioles are at generation \_\_\_.
Broncholes = gen 4. Terminal bronchioles = gen16
225
There is not a whole lot of gas exchange that happens in the early generations of the tracheobronchial tree. This zone is called the \_\_\_\_.
Conducting zone (they are just pathways to get the air where it needs to go)
226
Conduction zone is generation __ to \_\_. Respiratory zone is from ___ to \_\_\_.
Conduction zone: 0-16. Respiratory zone: 17-23.
227
\_\_\_\_ are where gas exchange occurs in the lungs.
Alveoli
228
The places where we start to have gas exchange are referred to as the ____ zone.
Respiratory
229
The respiratory zone includes what 3 parts?
respiratory bronchioles, alveolar ducts, alveolar sacs
230
The early parts of the respiratory zones are called the ___ area.
transitional (in between the conduction and true respiratory zones)
231
The first place we have respiration or gas exchange happening that is the \_\_\_\_.
respiratory bronchioles
232
\_\_\_\_ are the terminal end of the tracheal bronchiolar tree. Right before that, we have the \_\_\_\_.
Alveolar sacs ; alveolar ducts
233
What parts of the pulmonary circuit is in the anatomical dead space?
The conducting zone (also includes things above the trachea. Ex: larynx)
234
The air in part of the lungs where gas exchange occurs is thought of as \_\_\_\_.
alveolar air (aka alveolar volume)
235
If we have one breath of 500 mL, how much is anatomical dead space? Used for gas exchange?
150 mL dead space. 350 mL gas exchange. (In order to get the 350 where it needs to go for gas exchange, we need the 150 to push it there.)
236
In our large airways, we have a lot of ciliated ___ cells.
columnar
237
What do cilia do in our lungs?
pushes all the gunk from the inside of the lungs back up the trachea, where it can be put back into GI system for recycling and processing.
238
How does the columar cells in the smaller airways different from the ones in the larger airways?
They are smaller in size and their shape tends to be more of a cube (rather than a long column).
239
What happens to the cilia/columnar cells over time if we have really bad lung damage?
What we have at birth is what we are stuck with; they can replenish themselves here and there, but if we wipe all of them out by messing with our lungs really bad, most of our cells that tend to replace them look much smaller than the cells we normally start out with.
240
Goblet cells are also found in the ___ airways and produce \_\_\_.
larger, mucous
241
Deeper in the lung, we find a different type of secretory cell called a ___ cell.
club (aka clara)
242
What do club cells produce? Why is it important?
Surfactant, used to help us breathe. (If we are a preterm neonate, we might not have development of these cells/not have surfactant and that makes it hard for us to breathe.)
243
Lungs will always be filled with fluid and a big portion of that comes from ___ cells.
club (aka clara)
244
True or False. Club cells play a role in getting rid of some of the waste that might be around from macrophages
True (If it is small enough, these cells might take it up. However, if it is a big protein that won’t fit in the cell, that is sent down the lymphatics.)
245
Mast cells in the lungs are involved in ___ and \_\_\_.
inflammation and histamine release
246
Mast cells produce derivatives of \_\_\_.
arachidonic acid
247
Goblet, club, and mast cells are usually found in what type of airways?
large (So, these aren't really found in the alveoli.)
248
True or False. The alveoli aren't very vascular.
False (we have a bunch of blood vessels running through these that are really close to the air inside the unit. So, there is lots of blood flowing through the outside of this thing.)
249
2 types of alveolar cells. Describe them.
Type 1: really thin, elongated, very short distance for gas diffusion to get through easily. Type 2: useful for producing some of the component parts of surfactant, more "square" shaped and thicker.
250
What type of alveolar cell makes the majority of internal alveolar curface area?
Type 1 (They are larger to the extent that they make up 90-95% of the internal alveolar surface area, even though there's technically twice as many Type 2 cells.)
251
Our total lung capacity in a healthy 20-year-old adult patient should be ?
6 L
252
How many lung volumes and capacities do we have?
4 lung volumes: inspiratory reserve volume, tidal volume, expiratory reserve volume, residual volume. 4 capacities: vital capacity, inspiratory capacity, functional residual capacity, total lung capacity.
253
\_\_\_ volume is the normal breath size, which is ___ mL, for a normal 20 year old.
Tidal ; 500
254
With pulmonary system, most things go downhill at what age?
20
255
The amount of air that we have in the lungs in between breaths is \_\_\_, and this is called the \_\_\_.
3 L, functional residual capacity (FRC is the amount of air left in the lungs at the end of a normal expiration or before the beginning of an inspiration)
256
FRC's 2 functions are to?
1. Hold the lungs open 2. This air will be undergoing gas exchange in between breaths. (FRC = 3L total of both lungs)
257
FRC consists of what 2 volumes?
expiratory reserve volume and residual volume
258
If we try to expire as much air as possible out of our lungs, we will be able to expire everything except ___ L.
1.5 L (A portion of this air is in the trachea and airways, so there is no way we can get all that air out because they are fairly rigid structures that don’t collapse easily.)
259
When we try to get all the air out of the deeper portions of the lungs, sometimes we are unsuccessful because?
The pressure we are applying to the thorax is just collapsing some of the small airways that are upstream of these alveoli.
260
What is residual volume (RV)?
volume of gas left in the lungs after maximal forced expiration (prevents lungs from collapsing at very low lung volumes)
261
What is expiratory reserve volume (ERV)?
The amount of air that we can expire out of the lungs, if we start at FRC (normally 3L).
262
Normal ERV is ___ L. Normal RV is ___ L.
1.5 both (FRC = ERV + RV = 3 L)
263
What is tidal volume? How many L?
A normal breath = 0.5L (500 mL)
264
The ____ would be the amount of air that we can inspire in addition to what we bring in on a normal breath.
inspiratory reserve volume (IRV)
265
How much air do we have in our lungs after a normal breath?
3.5 L (FRC 3L + Vt 0.5L = 3.5L)
266
If we inspired a 500 cc breath, we would be at 3.5 L in the lungs, and we should be able to inspire a further ___ L on top of our normal tidal volume.
2.5 L (IRV)
267
What is inspiratory capacity (IC)? How many L?
Combination of regular inspired breath (Vt=0.5L) plus the additional amount we should be able to inspire before lungs are completely full (IRV=2.5L). IC equals a total of 3L.
268
What is total lung capacity (TLC)? How many L?
volume of air in the lungs after a maximal inspiratory effort. RV + Vt + IRV + ERV = 6L
269
Our ____ represents the amount of air that we should be able to inspire starting from RV.
vital capacity (VC)
270
VC is comprised of what 3 volumes? Total L?
IRV + Vt + ERV = 4.5 L (If we were starting in between breaths and push out as much air as possible and then take the deepest breath possible after getting down to RV, we should be able to inspire about 4.5 L of air)
271
How do our lung volumes change when we are lying supine?
When lying supine, our abdominal contents usually push up into the thorax which gives us a lower lung volume compared to if we are upright.
272
What is standard atmospheric pressure?
amount of pressure on us at sea level under normal conditions (The pressure that this is coming from/what is generating this pressure is all of the gas between us and outer space.)
273
1 ATM = ___ mmHg
760 mmHg (This is the amount of weight of all the gases above us pushing down.)
274
How does ATM affect oxygenation?
That pressure is going to give us a push to get oxygen into our blood and transport it where it needs to go.
275
When we are dealing with air moving in and out of the lungs, our outside/room pressure is usually designated as being \_\_\_.
0 (In terms of comparing outside pressure to internal chest pressures, we set room pressure at 0. That is our zero point and we can compare things from there.)
276
If our alveoli were open to the outside environment and no air is moving, the alveolar pressure (PA) would be \_\_\_.
0
277
If I were to contract my diaphragm and drop my chest pressure, our alveolar pressure would be neg or pos?
negative (If we had a path to the outside, that will draw air in because pressure in alveolus is negative compared to what it is in the room.)
278
True or False. If we relax the diaphragm and let it come back up, that will increase the pressure in the thorax and increase the pressure in the alveolus.
TRUE (If the alveolar pressure is higher than room pressure and we have an open pathway, air will move from lungs to the outside environment—expiration.)
279
In addition out outside/room pressure, ____ pressure also determines PA.
pleural (PIP / PPL)
280
What does PIP and PPL stand for?
IP stands for intrapleural pressure and PL stands for pleural pressure (Both are abbreviations for pleural pressure.)
281
Define PIP / PPL.
The pressure between the two sets of pleura (parietal and visceral). Normally, that pressure is negative. When we inspire, we make it more negative than; when we expire, we make it more positive.
282
Pleural pressure usually changes according to the contraction/relaxation of the \_\_\_\_.
diaphragm (when it drops down (contracts), the lung will be pulled down and the parietal and visceral pleura will be pulled apart from one another. So, the pleural pressure will become negative.)
283
\_\_\_ pressure has to do with recoil tension or pressure of the lung tissue.
elastic recoil
284
Normal pleural pressure in between breaths is \_\_\_.
-5 cmH2O (equivalent to -4 mmHg. Inspiration=more negative. Expiration = more positive)
285
Pleural pressure during inspiration changes to \_\_\_.
-7.5 cmH2O (If the lung gets pulled down with inspiration, we are going to have a more negative pleural pressure--no longer be -5cmH2O.)
286
With inspiration, pleural pressure becomes more negative, stretching the lung out as the diaphragm pulls it down. What happens to the alveoli?
It will also pull the walls of the alveoli open as well, causing the PA [alveolar pressure] to become negative. (That will be the stimulus for air to come in and give us our breath.)
287
Our pleural pressure drops from -5 to -7.5 within ___ seconds.
2 (So, it takes 2 seconds to inspire. It takes another 2 seconds to get back to -5 cmH2O after expiration.)
288
If we stretch the inspiration out over 2 seconds, the alveolar pressure becomes the most negative at what point?
Halfway point (What is causing the alveolar pressure to drop is all the stretchy tissue in the lung is being pulled out.)
289
The most negative alveolar pressure gets is \_\_\_. The most positive it gets is \_\_\_.
-1 cmH2O ; +1 cmH2O
290
The thing driving airflow into the lung is ___ pressure.
alveolar
291
What is airflow? measured in what unit?
It tells us what is happening to air with regards to the volume in the lungs. Measured in L/sec.
292
Before inspiration, airflow is ___ L/sec.
0 (because alveolar pressure is 0 and outside pressure is 0.)
293
When does peak inspiratory flow rate occur?
When alveolar pressure is at its lowest; that is when air is coming in at the fastest rate.
294
Lowest and highest airlow rate?
-0.5 L/s ; +0.5 L/s
295
Over a course of 2 seconds, how much volume of air do we have coming into the respiratory system?
0.5 L (The rate at which this thing is filling tends to be at its fastest rate about half-way through inspiration.)
296
What is elastic recoil pressure (PEL/PER)?
The pressure or tension that is exerted on each of the lungs. Helps us create the negative alveolar pressure during inspiration. (Google: the rebound of the lungs after having been stretched by inhalation; the ease with which the lung rebounds.)
297
If we change pleural pressure, that can change ___ pressure.
alveolar
298
Define transpulmonary pressure.
Difference in pressure across the sides of the lung tissue, between the alveolar pressure and pleural pressure. AKA transmural pressure.
299
True or False. Elastic recoil pressure is a type of transpulmonary pressure.
True. (The transmural/transpulmonary pressure is equal to the elastic recoil pressure of the compartment. PTP = PA - PIP = PER)
300
In between breaths, the elastic recoil pressure in the lungs is __ cmH2O.
+5 cmH2O (Alveolar pressure = 0. Pleural pressure = -5. So, the opposing force must equivalent in the opposite direction to balance it out.)
301
If we puncture the chest and increase pleural pressure to atmospheric pressure, what happens to the lungs?
Lungs will deflate. (The pressure that is going to deflate the lungs when I drop pleural pressure to 0 is the recoil pressure that is on all of these springs.)
302
If I open the chest and make that pressure 0 while the lungs still have a recoil tension acting in the opposite direction, our alveolar pressure is \_\_\_.
5 cmH2O (because these springs want to recoil fairly bad. They will be now allowed to do that because there is no negative pressure opposing that.)
303
The really small blood vessels that become smaller when we put more air into the lungs are our pulmonary \_\_\_\_.
pulmonary capillaries
304
Diff between alveolar and extraalveolar changes with inspiration.
Alveolar blood vessels stretch and narrow, so their resistance increases. Extra alveolar blood vessels react opposite; these tend to have an increasing vascular resistance.
305
If we take both alveolar and extra alveolar vascular resistances and add them together, that gives us \_\_\_.
Total PVR
306
Going from FRC to total lung capacity, does the alveolar or extraalveolar resistance change the most?
We have a significant increase in alveolar resistance and a slight decrease in extra alveolar resistance. (So, the alveolar blood vessels would be the culprit of increasing PVR as we increase lung volume from FRC. )
307
Going from FRC to RV, does the alveolar or extraalveolar resistance change the most?
We have a significant increase in extraalveolar resistance and a slight decrease in alveolar resistance.
308
The higher right heart CO, the lower the PVR; that is through a process of increasing ___ and ___ of already recruited blood vessels.
recruitment and distention
309
The place we are going to have the largest perfusion is the base of the lung when we are sitting upright. Why?
because our blood vessels in the base of the lung are fuller/more open and they have higher pressure, which makes blood flow through the base of the lung easier.
310
Where is the gravity dependent region of the lungs?
Wherever there is the most blood flow, where gravity affects it most. (So, if upright it will be the base. If supine, it will be posterior aspect. If prone, it will be the anterior aspect.)
311
4 Passive influences that will increase PVR.
1. changes in lung volume 2. increased interstitial pressure 3. increased blood viscosity/HCT 4. positive pressure ventilation (All these cause compression of vessels)
312
2 Passive influences that will decrease PVR.
1. increased pulmonary artery pressure, LAP, pulm blood volume, CO 2. gravity/body position (All these lead to more recruitment and distention, which will decrease PVR)
313
Someone at high altitude, their HCT will be ___ compared to someone at sea level.
elevated
314
7 things that will actively decrease PVR.
1. PSNS stimulation 2. mACh 3. beta-adrenergic agonists 4. prostaglandin PGE1 5. prostacyclin PGI2 6. NO 7. bradykinin
315
2 things mACh does in the lungs.
1. relax blood vessels to decrease PVR 2. constrict airways (unrelated to PVR) (This is why someone with asthma takes an antihistamine, a mACH antagonist--to help them out with their airway constriction)
316
2 inflammatory agents that actively reduce PVR.
Prostacyclin (PGI2) and Bradykinin
317
11 Active influences that increase PVR.
1. SNS stimulation 2. alpha-adrenergic agonists/sympathomimetics (NE and Epi) 3. PFG2a, PGE2 4. thromboxane 5. endothelin 6. angiotensin 7. histamine 8. alveolar hypoxia 9. alveolar hypercapnia 10. low pH of mixed venous blood 11. HPV
318
\_\_\_\_causes vasospasm and limit bleeding in the periphery; it makes sense it is a vasoconstrictor in the pulmonary circulation as well.
Thromboxane
319
How does the systemic vs pulmonary vessels react to hypoxia and hypercapnia.
They are opposite of each other. Systemic blood vessels relax to hypoxia and hypercapnia; pulmonary vessels will constrict.
320
Normally, the oxygen content in the blood that is arriving to the lungs after being used in systemic circulation has ___ oxygen and ___ CO2.
low oxygen and high CO2 (Obviously. It is being returned to the lung to pick up some oxygen and get rid of some CO2.)
321
If we have bad ventilation to alveloi, we want to reduce the amount of blood flow that is going through these areas of the lung. Why?
If we have blood flow moving through here that mixes with the oxygenated decarbonated blood, then we will have an admixture of the two showing up at the left heart; that would reduce our oxygen content in systemic arterial blood, making us hypercapnic! (abnormally low O2 and high CO2)
322
The body’s defense to perfusing bad alveoli is this mechanism called \_\_\_\_.
hypoxic pulmonary vasoconstriction (HPV). (So, if air in alveoli is hypoxic compared to normal, these blood vessels constrict.)
323
Hypoxic pulmonary vasoconstriction (HPV) if primarily related to \_\_\_.
Oxygen/Hypoxia (Secondary to that would be the elevated CO2 in the alveoli)
324
When we have buildup of CO2 in alveolar air, what happens to the lung's blood vessels?
They will constrict.
325
Dry atmosphere has what 3 primary gasses? % fo each?
N2: 79% O2: 21% CO2: 0.04%
326
How much partial pressure does N2, O2, and CO2 provide if we are at sea level.
N2: 600.3mmHg O2: 159mmHg CO2: 0.3mmHg (Total is 760 mmHg)
327
Denver has an atmospheric pressure of about \_\_\_mmHg, which is lower or higher than sea level? Why?
620-630 ; lower than sea level (760mmHg) because there would be less air on top of us between the surface we are at and outer space.
328
If we are at a place with high atmospheric pressure, how does density of that air change?
Air would be more dense, because all that pressure and weight and effects of gravity will be compressing the air around us.
329
Low altitude = ____ ATM pressure = ____ density.
Low altitude = higher ATM pressure = higher density (So, high altitude = lower pressures = lower density)
330
How does temperature affect density of gas?
Higher temperature tends to decompress gases. If we are at a place with low temperature, we have higher density of gas.
331
Do we have more O2 available with cold or hot air?
Cold (Cold air is more dense! If we have a lot of pressure pushing gas into a container, then we have a lot more gas in that container.)
332
Partial pressure of O2 in denver?
Dever's total atm pressure is 620. O2 is 21% of 620, which is 130mmHg. (Regardless of the altitude we are at, the gas composition in the atmosphere or any altitude is always the same concentration at sea level.)
333
If we think about being at really high altitude either at Everest or in an airplane, the 2 problems we encounter are?
1. low pressure driving the oxygen into our blood 2. less oxygen in that air since higher altitude is less dense. (We can absorb a portion of the oxygen, but there isn’t as much coming into the lungs; that is why they have to pressurize the cabin of planes.)
334
When air is brought into the body, the ___ quickly heats and humidifies the air.
nose (There is also heating in other parts of the incoming parts of the respiratory system, but a lot of the heating/humidification takes place in the nose.)
335
Humidity comes up to about \_\_\_% at body temperature.
100% (the air is saturated with water at body temperature after it has been inspired and that happens pretty quickly.)
336
Adding humidity to the dry gas we are inspiring will do what to the air in our tidal volume?
The humidity added to the inspired gas will displace some of the air we inhald. So, as we attempt to take in 0.5L of the dry air, water or humidity will be added to that and it won’t allow us to bring in a full 0.5L of outside air because there will be more water vapor.
337
What happens to O2 and N2 if we have a substantial amount of water vapor in the air we breathe?
That will dilute the concentration of these other inspired gases. So, we aren’t able to bring in as much oxygen or nitrogen as otherwise would be the case.
338
What does PIO2 stand for?
partial pressure of inspired oxygen (after the inspired gas has been humidified)
339
PIO2 formula.
PIO2 = FIO2 x (PB - PH2O)
340
Water vapor partial pressure (PIH20) is ALWAYS \_\_\_\_mmgH.
47mmHg
341
What does PB stand for?
Barometric pressure
342
FIO2 is ALWAYS \_\_\_%, regardless of whatever altitude we are at.
21% (The concentration doesn’t really change even though the total atmospheric pressure might change.)
343
Partial pressure formula.
Partial pressure = Total pressure x [gas]
344
PIO2 at sea level ?
PIO2 = FIO2 x (PB - PH2O) = 0.21 x (760 – 47) = 149.73mmHg
345
How does composition of gas change from outside air to when it is inhaled/humidified?
Inspired humidified concentrations will be less (diluted). (ex. oxygen partial pressure is 160mmHg, but PIO2 is only 150.)
346
The gas that is most displaced by water vapor is \_\_\_.
Nitrogen (Starts off at 600, drops to 564mmHg when it hits the alveoli.)
347
How does humidity in the air affect inspired gas?
No effect.
348
True or False. The pulmonary artery carries deoxygenated and carbonated blood.
True (So, it has less O2 and higher CO2 than peripheral arterial blood.)
349
Pulmonary arterial blood has an O2 of \_\_\_mmHg and partial pressure of CO2 should be \_\_\_mmHg.
O2: 40mmHg CO2: 45mmHg
350
Fresh air should have an O2 of \_\_\_mmHg and CO2 of \_\_\_mmHg.
O2: 149/150mmHg CO2: 0mmHg
351
When we breathe, oxygen will be absorbed into the blood and CO2 from the blood will enter the alveoli. The net result of this is?
An equilibration of partial pressures of air in the alveoli and the partial pressures of the gases in the blood.
352
As the oxygen is absorbed from the alveolar air, the partial pressure of oxygen in the pulmonary capillary blood goes from ___ to \_\_\_.
40 to 100 mmHg
353
We have a quantity of CO2 that is allowed to leave pulmonary capillary blood; that produces a PCO2 of ___ in the alveolus.
40mmHg (At the same time when that happens, there is also a PCO2 in the pulmonary capillary blood of 40.)
354
What are the partial pressures of O2 and CO2 at the end of gas exchange in the pulmonary capillaries and alveoli?
They are equal! O2: 100mmHg CO2: 40mmHg
355
PAO2, technically, is \_\_\_mmHg, but is hardly ever seen. Why?
104mmHg. Because there is a little bit of admixture from bronchiolar circulation; a small portion of the deoxygenated blood mixes with the oxygenated pulmonary venous blood. The net result is dilution of some of the oxygen that is showing up in the left heart; so, it shows up as 100.
356
Hypoxic pulmonary vasoconstriction—that is probably going to happen whenever we have a lung unit that is \_\_\_.
poorly ventilated
357
What happens to PO2 and PCO2 if airway is blocked?
As airway is blocked, the alveolar pressures and pulmonary veins pressures will be identical to pullmonary arterial blood. PO2 of 40 and PCO2 of 45mmHg. (Since airway is blocked, no oxygen is absorbed and no CO2 is unloaded.)
358
What is the abbreviation for alveolar O2 and CO2 partial pressures?
PAO2 and PACO2
359
3 things that can cause a blocked airway/block alveoli from ventilation?
1. asthma 2. pneumonia 3. infection
360
True or False. A pulmonary embolism will cause a blockage in airway, preventing ventilation.
False (PE will cause a blockage in perfusion. If we have issues with perfusion, we don’t have any blood going through this area but we have normal ventilation.)
361
What are our alveolar gasses if we have a PE?
PE = blockage in perfusion, no affect on ventilation. So, the alveolar gasses will be identical to the fresh air we are breathing in. PO2 of 150, PCO2 of 0.
362
If we throw a PE, the air that we are expiring is going to look different. Why?
Because we are now expiring air that is going to poorly perfused regions of the lung. The expired air would probably have an uncharacteristically high oxygen content and uncharacteristically low CO2 content.
363
If we have areas of lung that are not perfused, what is the lung's response to conserve energy?
Constrict the airways going to that area and divert it to places where the lungs are better perfused. (The blood vessels look at the alveolar gas to decide what to do. So, we could speculate the body might constrict airways in response to abnormally high PO2.)
364
Giving someone too much oxygen for a long time does what to the airways and airway resistance?
You can go into ARDS with inflammation and all sorts of respiratory distress, closing off airways. One of the problems associated with that is increased airway resistance—harder to get air into and out of the lungs.
365
Where in the lung do we have the most ventilation in an upright, healthy 20yo?
Base of lungs (Think of VQ matching. If the perfusion is greater in the base of the lung, it would make sense for us to direct most of the incoming air also to the base of the lung so that we have good matching of ventilation and perfusion.)
366
Where in the lung do we have the most compliance in our airways and alveoli at FRC when we are upright?
Base of lungs (which is why air preferentially goes here!)
367
If gas exchange is going to happen by diffusion, moving down simple pressure gradients, then we will need a lot of ____ for that to happen to keep us alive.
surface area
368
How much alveolar surface area do we have?
190 m2 (approx 200m2, size of tennis court)
369
In the lungs, we can\_t pump oxygen or CO2 because it is dissolved and not easy to grab, so we are just relying on \_\_\_\_, which is why we need a ton of surface area in order to make that happen.
diffusion
370
Benefit of having some alveoli closed off, rather than using 100% of all of them all the time?
If we have some alveoli that are sealed off, if we were to inhale bad stuff, presumably those that are closed wouldn\_t be as affected.
371
Atmospheric pressure is ____ at sea level under standard conditions. (3 ways to list)
760 mmHg, 760 Torr, 1 ATM
372
If there is an equivalent pressure of 0 at the opening of the airway and the alveoli, what happens to air movement?
There is no air movement! (This would be resting, in between breaths; we need a pressure gradient in order for air to move.)
373
What would alveolar pressure be for inspriation and expiration to occur? Positve or negative?
Inspiration: alveolar pressure is negative. Expiration: alveolar pressure is positive.
374
If we hook someone up to ventilator/sealed system, the vent will produce a ___ pressure. What happens?
positive ; If pressure at the top of the system is greater than pressure in alveoli, that will physically force air into the lung.
375
In order for air to go anywhere we need a clean pathway; if we have some of our small airways blocked, what can happen?
The more of those we have blocked off, the more air will be trapped in lungs and can\_t get out; the other way to look at it is it will be hard to fill the lung under those circumstances.
376
True or False. Normally, pleural pressure in between breaths for someone upright healthy and breathing normally is 0 cm H20.
False. PIP/PL = -5cmH2O
377
When we have negative pressure in the chest outside the blood vessels, what happens to the blood vessels and chest pressure?
That negative pressure pulls stretchy/compliant blood vessels open; the result is more negative chest pressure, which turns into more negative vascular pressures because it is easy for these walls here to get pulled open.
378
When we make thoracic pressure more negative, the pressure on all the stuff on the inside of the lungs usually decreases or increases?
decreases (more negative)
379
The degree of alveolar stretch is going to be different depending on what?
where we are in the lungs
380
More negative pleural pressures will cause alveolar pressures to \_\_\_\_.
decrease (Body decides to contract diaphragm and drops pleural pressure from -5 to -6; our alveolar pressure is still at 0 for a very short period of time, then the outside pressure changes the alveolar pressure to -1.)
381
If the thoracic pressure drops and these things are stretchy then the alveolar pressure will drop, and that will help us do what?
inhale (bring in more clean air)
382
We stop inspiring when our alveolar pressure is \_\_\_mmHg?
0 mmHg (at this point, our alveolus if fuller and stretched out.)
383
When our body decides to expire, the diaphragm will relax. What happens to pleural and alveolar pressure?
pleural pressure should drop back down to -5 and our alveolar pressure should go to +1 (The recoil of this alveolus is going to cause an alveolar pressure of +1, because the pleural pressure is no longer negative enough to hold this thing open)
384
After the air has left our lungs after expiration, alveolar pressure will be \_\_\_.
0mmHg (and we will be back at the point where we started--at rest, in between breaths)
385
Recoil pressure vs. Alveoli strech
The fuller/more stretched the alveoli, the more recoil. The smaller the alveoli, the less recoil pressure.
386
Define transmural/transpulmonary pressure.
The difference in pressure on two sides of a container (ex. Alveolus). When we have changes in that pressure across the wall, that is going to result in air either moving into or out of the container.
387
Does transmural pressure describe normal breathing or positive pressure breathing?
Both (this number is universal)
388
Normally, during a breath, our pleural pressure drops to \_\_\_.
-7.5mmHg (over 2 seconds, does not happen instantaneously)
389
Highest and lowest peak of alveolar pressure? At what point do these peaks occur?
-1 and +1 mmHg. Happens midway through inspiration and midway into expiration, respectfully.
390
\_\_\_\_ (L/s) correspeonds to the pressure gradient.
Airflow
391
When does the biggest pressure gradient occur with breathing?
Midway on inspiration and midway on expiration, because that is where our alveolar pressure is lowest and highest respectively.
392
Lung diagnostic pressures specifically measure what part of breathing?
expired gas coming out of the lungs (Expired air in pulmonary function tests are denoted as being positive air movement. So, +0.5=peak expiration and -0.5=peak airflow.)
393
Over the 2 seconds, we should get in how much volume?
0.5L (Vt--tidal volume)
394
During inspiration, a lot of air comes in during the midpoint, but not the beginning or tail end of inspiration. Why?
There isn't much of a pressure drop in the alveoli at first. As we go along, the pressure becomes more negative and air comes in faster. Once it starts filling up, the rate at which air is coming in slows; it is still coming in, but the rate/speed is dropping. Up at the top (2 sec), eventually we wouldn\_t be putting any more air in at all.
395
Inspiration: Expiration ratio of normal breathing vs mechanical vent.
Normal is 1:1 (Equal time spent). Vent is 1:2 (put air in quickly, let air sit there and equilibrate for twice as long.)
396
The 2 pressures causing air movement.
alveolar pressure and the thing making alveolar pressure change is pleural pressure.
397
Compliance formula.
\_V/\_P (\_V =end volume _ starting volume. \_P =end pressure _ starting pressure.)
398
Normal lung compliance at FRC in someone healthy and upright.
0.2 L/cmH2O (\_V/\_P = 0.5 L / 2.5 cmH2O. 0.5L is how much air is going in and coming out. The pressure change that we need to generate in order to get that volume in and out is 2.5 cmH2O, pleural pressure difference.)
399
Describe pleural pressureand alveolar pressure at beginnging and end of expiration.
When we relax the diaphragm: increase in pleural pressure, which causes alveolar pressure to be more positive; that pushes air out. When the alveolar pressure is back down to 0 again, expiration ends.
400
\_\_\_\_ are where gas exchange will happen.
Pulmonary capillaries (To provide blood flow to all those pulmonary capillaries, we need a lot of blood vessels to facilitate blood getting to capillaries and blood getting back to left side of the heart.)
401
How is the lung positioned in reference to the heart?
If we are in the upright position, we are going to have parts of the lungs that are above the heart and portions of the lung that are at or below the level of the heart itself.
402
From base to apex of lung, how long/tall are the lungs?
35 cm
403
Is BP higher in the apex or base of lung?
Base (Think about gravity! The higher up we are, the lower the BP and the lower we are, the higher the BP.)
404
Blood vessels in the ____ are more full, less resistance, wider diameter, more easily perfused.
Base (Because intervascular pressure is going to be higher in the lower portions of the lung and lower towards the top. The fuller the vessel, the higher the internal pressure.)
405
In order to perfuse alveoli, the vascular pressure will have to be ____ than alveolar pressure.
higher
406
\>100% Blood flow/alveolus occurs in what part(s) of the lung?
lower and "really" lower parts of the lung. (further down the ling = more gravity = more perfusion pressure.)
407
Least blood flow/alveolus % occurs at what part of the lung? what rib level?
The upper lung, at rib 2. (further up the ling = less gravity = less perfusion pressure.)
408
Describe the pressures and perfusion in Zone 1 of lung.
Alveolar pressure is higher than both arterial and venous BP (higher than BP all the time); it is impossible for us to perfuse that portion of the lung without adding blood pressure.
409
Zone 1 only exists in \_\_\_\_.
pathology (there is NO zone 1 in healthy persons!)
410
Describe the pressures and perfusion in Zone 2 of lung.
Intermittent perfusion; occurs when arterial pressure is higher than alveolar pressure. The higher the arterial pressure, the more perfusion.
411
The most likely time for intermittent perfusion (zone 2) to occur is ?
During systole or when pulmonary arteriole pressure is high.
412
Describe the pressures and perfusion in Zone 3 of lung.
Continuous perfusion; both arterial and venous BPs are higher than alveolar pressure all the time. That would happen in the lower regions of the lung.
413
Describe the pressures and perfusion in Zone 4 of lung.
Similar to zone 3, but at the VERY bottom of the lungs. (Continuous perfusion, arterial and venous BP \> alveolar pressure at all times.)
414
Where does peak blood flow occur?
Right above the very base of the lung (zone 3)
415
How does the weight of the lung affect perfusion in zone 4/the VERY bottom of the base?
The weight of the lung will clamp down some of the blood vessels at the base of the lung\_this causes a little lower blood flow at the very base of the lung.
416
Do we use all our pulmonary blood all the time?
No (If we shut down our alveoli randomly, we shut down blood flow associated with the alveoli; it doesn\_t make sense to put blood flow into alveoli that isn\_t getting fresh air because it wouldn\_t oxygenate that blood.)
417
2 reasons why we would recruit more alveoli.
Increased CO. Increased metabolism (whenever we need to absorb more oxygen, we need to recruit more alveoli!)
418
The process of increasing the number of blood vessels that our lungs are using for gas exchange is called \_\_\_\_.
recruitment
419
More recruitment = ____ vascular resistance
less (If there is more tubes for the heart to pump through, it becomes easier for heart to pump blood through each of those tubes.)
420
Diff between Zone 1 and having closed/shut down alveoli.
Usually, these closed alveolar and blood vessels are scattered; they are not aggregated all together in a continuous patch in the lung. Zone 1 occurs when there is a significant patch that is not perfused at all.
421
Where in the lung do blood vessels have the least resistance?
Base (The fuller they are, the wider they are; the wider they are, the less resistance they have. The fuller vessels are found at the base of lung.)
422
PVR ___ when we have an increase in CO.
decreases (So, if we exercise and use more of our pulmonary blood vessels and put more blood through existing used pulmonary blood vessels, our PVR actually drops.)
423
PVR formula.
PVR = (MPAP - LAP) / CO
424
If we have an independent increase in MPAP without any other changes, the PVR \_\_\_.
increases (Parallel relationship! So, if we have a drop in MPAP, that would coincide with a drop in PVR.)
425
If we have a unilateral increase in LAP without any other changes to MPAP, PVR \_\_\_.
decreases (Inverse relationship! So, if we have a drop in LAP without any other changes to MPAP, then that would be an increase in PVR.)
426
If we change CO, how is that going to affect PVR?
Anytime we increase CO without having any change in pulmonary arterial pressure or LAP, that would give us a reduction in PVR.
427
True or False. If we have a high blood flow, we have a fairly low PVR. If we have a lower blood flow, we have an exponentially higher PVR.
TRUE (The lower the right heart CO, the higher the PVR. If we are in right HF, the worse the CO from right heart is, the higher PVR\_which is going to make the job of the right heart much more difficult and energy intensive.)
428
How does the systemic and pulmonary circulations respond to low O2/high CO2?
Systemic: relax vascular beds. Pulmonary: constrict vascular beds. (They are opposite! The increased vascular resistance with pulmonary blood vessels is to prevent perfusion of under-ventilated alveoli. )
429
Normal PVR for pulmonary circuit = ___ peripheral resistance units (PRUs)
0.14 PRU (Delta P = 16-2 = 14. CO estimated to 100. So, 14/100 = 0.14, about 1/7th of SVR.)
430
LAP is an estimate of ___ pressure, which will always be much higher than the actual LAP.
wedge
431
Alveolar volume at RV vs TLC.
Alveoli are smaller at RV and larger at TLC. (As we fill these alveoli up with air, it will stretch the blood vessels that are associated with the walls of the alveoli.)
432
\_\_\_ blood vessels are integrated as part of the capillary alveoli.
Alveolar (These tubes would all be capillaries that are sandwiched into alveoli.)
433
What happens to alveolar blood vessels as alveoli fill with air?
More air in the alveoli will stretch out its walls; all these blood vessels that are integrated in the wall will also stretch out and lengthen, their internal diameter will be reduced. So, they become longer and more narrow.
434
What happens to alveolar blood vessel resistance as alveoli fill with air?
The higher the volume in our alveoli, the higher the resistance of these alveolar blood vessels.
435
What happens to alveolar blood vessel size and resistance as alveoli release air?
If we were to take air out of the lung, our alveolar blood vessels would be shorter and wider, the lower our alveolar resistance will be.)
436
If we are pulling lungs open by filling alveoli up with air, what happens to the larger blood vessels neighboring the alveoli? What are these larger blood vessels called?
These larger blood vessels are called extraalveolar blood vessels; they will also be pulled open as we inspire toward high lung volumes. (So, as alveoli fill up with air, alveolar vessels get smaller and stretched out whereas the extraalveolar vessels get pulled open! They respond opposite of each other.)
437
As we move towards higher lung volumes, our extra-alveolar vascular resistance \_\_\_\_. Why?
decreases, because these larger blood vessels are pulled open as alveoli are filled with air and the inner diameter/circumference increases.
438
When we actively force air out of the lungs, we generate more positive pleural pressure. Will this constrict or relax extraalveolar vessels?
Constrict (Anytime we physically force air out of the lungs in a way that is not natural, we are going to compress our extra-alveolar blood vessels and increase their vascular resistance.)
439
When do we have the lowest total PVR?
At FRC (normal resting point, in between breaths)
440
The total PVR is a combination of ___ and \_\_\_.
Alveolar and extraalveolar resistance
441
PVR elevated at very low lung volumes and very high lung volumes. Why?
If we physically go to lower lung volumes, our extra-alveolar blood vessels are being constricted or compressed. At abnormally high lung volumes, our alveolar blood vessels are experiencing an increase in vascular resistance. Both scenarios will create increased PVR.
442
If we use positive pressure ventilation, what happens to our extraalveolar vessels?
That would compress our extra-alveolar blood vessels even as we are inflating the lung.
443
\_\_\_\_ pressure is the physical pressure of the gas in the alveoli. How does it change during the respiratory cycle?
Alveolar pressure. In between breaths, PA is 0mmHg. With inspiration, it becomes negative. With expiration, it becomes more positive.
444
What is PTP?
Transpulmonary pressure (Describes the pressure difference across a wall, usually the alveolar pressures and pleural pressures.)
445
At the base of the lung, we have high pressures in the blood vessels due to what?
the weight of the blood being underneath the heart.
446
When would you expect to see pulsatile flow in zone 2?
When arterial pressure (Pa) is higher than alveolar pressure (PA).
447
What phase of the cardiac cycle does NOT allow blood flow in zone 2 of the lungs?
When the heart is filling (diastole). So, as BP is decreasing, that would tend to give us reduced blood flow.
448
Arrange the speed of blood flow in the lungs from slowest to fastest.
Slow= top of lung (rib 2) \< middle lung \< zone 4 (very bottom of lung) \< zone 3 = Fast
449
Why does speed of blood flow taper off in Zone 4?
The weight of the lung tends to be compressing blood vessels at the very base of the lungs.
450
How does PVR affect the alvolar and extraalveolar vessels in RV vs FRC?
At RV (low lung volumes), alveolar vessels have ↓ vascular resistance, because they become shorter and wider. The extraalveolar vessels have ↑ resistance. In FRC, it is the opposite--alveolar vessels have ↑ resistance, whereas extraalveolar vessels have ↓ resistance.
451
How does the right heart affect pulmonary vessel PVR?
When we have a lot of blood coming out of the right heart, our PVR tends to be lower. So, ↓R♥ CO = ↑pulmonary PVR
452
What is the "conundrum" that patients have to deal with regarding heart failure and PVR?
If patients already have a crappy output from the R♥, then the PVR will be high. However, a high PVR will make it harder for the R♥ to push blood to the lungs.
453
When we have a lot of blood coming from the R♥, do the lungs recruit more or less blood vessels?
More! (So, when we have more blood vessels, we tend to have more pathways the blood can go through—that makes it easier for blood to move through the lungs.)
454
Why do we have distention of pulmonary blood vessels if the R♥ has more CO?
When we have distention of existing used blood vessels, that will make them wider, which tends to reduce their PVR. So, when we have an increase in CO, it makes it easier on the heart to pump.
455
When we calculate the amount of gas we are bringing into the lungs, we have to correct for \_\_\_\_. What is the formula?
Water vapor (PIO2 = FIO2 (PB-PH2O)
456
PO2 and PCO2 in the pulmonary artery, pulmonary vein, and alveoli, assuming no obstruction to perfusion or ventilation.
Pulm artery: PO2 40, CO2 45. Pulm vein: PO2 100 CO2 40. Alveoli: PO2 150 CO2 0.
457
As gas exchange is occurring in the alveoli, how do PO2 and PCO2 levels change?
What happens with the pulmonary venous blood should be similar to what is happening in the alveolar air as the gas exchange is happening. To start with, it is PO2 of 150 and PCO2 of 0. As we absorb some of that oxygen, we bring our alveolar PO2 down to about 100 mmHg. For the PCO2, we have enough diffusion of CO2 from the blood to bring our PCO2 in the alveolar air up to 40.
458
True or False. Some discrepancy between how much the partial pressures are changing has to do with the fact CO2 is less soluble than oxygen in aqueous solution that we have in the body.
FALSE! CO2 is much MORE soluble than O2
459
\_\_\_\_ tends to be a spacer gas; it isn’t very soluble and there is not a whole lot for it to bind to in the blood. So, where does it go in the body?
Nitrogen, it tends to stay in the alveoli.
460
Benefit of having nitrogen stay in the alveoli, rather than attaching to Hgb?
Nitrogen is able to help keep the lungs/alveoli from collapsing; it holds them open.
461
If we replaced nitrogen with an absorbable gas, such as oxygen, in the alveoli, what would occur?
The alveoli would become quite a bit smaller as that gas is absorbed. (Nitrogen, which cannot be absorbed, is used to hold the alveoli open. So, if we don't have something to prop open the walls, the alveoli will become smaller.)
462
The ___ is what drives the movement of gasses from one place to another.
partial pressure gradient (If there is no pressure difference, then we don’t have any more movement of the gas.)
463
In between the pulmonary capillaries and alveoli is a small gap of space. What is the purpose of this gap? Why is it bad for fluid to be here?
It is a space for dissolved stuff to hang out in. If there is fluid in this space, that could be an impediment for gas exchange. (Under healthy conditions, this gap is very, very small!)
464
What are the normal values for the following: PCAP, πCAP, PINT, πINT.
PCAP = 7mmHg πCAP = 28mmHg PINT = -7mmHg πINT = 14mmHg \*\*πCAP is the same as in systemic capillaries!
465
Systemic capillary interstitial pressure (PINT) is higher or lower than pulmonary? Explain why.
Systemic PINT is -3, compared to pulmonary PINT of -7; it is more positive. Systemic PINT is generated by the action of lymphatic system pulling all the extra fluid out. In the lungs, the lymphatic system does a good job when everything is working correctly and we also have a pleural pressure of -5 cm H20 in between breaths. So, interstitial hydrostatic pressure (PINT) has to be more negative because lymphatics and pleural pressure are both negative.
466
A high pulmonary interstitial colloid osmotic pressure (πINT) of 14 mmHg implies what?
A high πINT would imply that under normal healthy conditions, there are quite a lot of dissolved proteins or colloids that hang out in pulmonary interstitium, right outside the blood vessel.
467
Even if we have a ton of colloids and proteins hanging out outside the pulmonary capillaries and alveoli, it's not usually an issue. Why?
There is enough balance by lymphatic system to basically suction all that extra fluid up and keep this space here really small, despite the fact there are a bunch of proteins.
468
In general, proteins are at a fairly high concentration inside of the cell. Why?
Because that is where proteins are made and that is where they function.
469
If the cells of the alveoli become infected and break down, what happens?
If we infect one of these cells and break down the walls of the cell, all of these proteins can potentially be hanging out in the interstitium or in the alveolar water layer; we already have a lot of proteins there to begin with. If we dump even more because our cells are dying, that is going to pull blood out of the capillary and into the interstitium or the alveolar water layer. This can cause a fluid shift and become an impediment for gas exchange.
470
If the ____ pressure is not in equilibrium, then proteins aren’t being swept away at the same speed they are being produced, causing a potential fluid shift.
interstitial protein osmotic pressure (πINT)
471
3 things that can affect the interstitial protein osmotic pressure (πINT).
-immune system -infection -toxic chemicals
472
4 clinical problems that can present with increased capillary permeability.
-ARDS -oxygen toxicity -inhaled or circulating toxins -sepsis/bad infection
473
2 clinical problems that can present with increased capillary hydrostatic pressure.
-↑ LAP resulting from LV infarct or mitral stenosis -overadministration of IV fluids
474
1 clinical problem that can present with decreased interstitial hydrostatic pressure.
Too rapid evacuation of pneumo- or hemothorax.
475
5 clinical problems that can present with decreased colloid osmotic pressure.
-protein starvation/digestive problems -dilution of blood proteins by IV solutions -renal problems resulting in proteinuria -liver failure -bone marrow issues
476
5 known etiologies/factors that can predispose patient to pulmonary edema.
- ↑ capillary permeability - ↑ capillary hydrostatic pressure - ↓ interstitial hydrostatic pressure - ↓ colloid osmotic pressure - insufficient pulmonary lymphatic drainage
477
How does capillary permeability affect the amount of proteins hanging outside of pulmonary blood vessels?
If we have big openings in our capillaries, all these proteins that are hanging out on the inside of the capillary would have the opportunity to leak out. So, ↑ capillary permeability = more proteins hanging out.
478
What is Kf in the starling capillary equation? What affects this number?
Kf is the capillary filtration coefficient; describes the permeability characteristics of the membrane to fluids. Anything that increases area of capillary or increases the permeability of capillary could affect that variable.
479
Pro and Con of a failing left heart in regards to higher Psf.
Pro: higher filling pressure (Psf) can help the L♥ do its job. Con: it is going to increase the BP in venous and arterial pulmonary capillaries.
480
With L♥ failure, do the pulmonary arteries or veins get affected first?
What happens first and the real bad thing here is increased blood pressures on the venous side of the capillary. Then as they get really bad, the pressures also increase on arterial side of capillary.
481
The body has more control over the arterial or venous side of the pulmonary capillary? Why?
More control of the arterial side, because if we have high pressure on this side of capillary, then the body can relax blood vessels between the right heart and arterial side of vessel. The venous side of the capillary doesn’t really have that same ability because there are no blood vessels immediately upstream that we can dilate out; the capillary can’t really do much. So, if increased BP on the venous side of capillary, we're stuck with it!
482
If we have an increase in pressure in the capillary, is that good or bad? Why?
This is bad, because increased capillary pressures would favor fluid movement from the capillary into the interstitium, which is bad for gas exchange. \*\*This is why people with left heart function tend to have pulmonary edema.
483
How does hypervolemia secondary to too much NS affect capillary oncotic pressures?
The capillary oncotic force would decrease as we increase volume with crystalloid. So, we will be less able to hang onto fluid within the pulmonary capillary. Can cause pulmonary edema!
484
How does breathing affect pulmonary interstitial pressures?
Breathing can make PINT more negative. (If we inspire, the diaphragm drops, which drops the pleural pressures. So, PINT drops to a lower number.)
485
Semi-conscious young, healthy adults who thinks they're choking. They react by taking a really strong, deep breath. What happens to their pleural pressures and pulmonary capillary interstitial pressure?
If we inspire really hard against a closed airway because we are semiconscious when we shouldn’t be, then the struggle against the closed airway can make pleural pressure really really negative, -40 cm H2O. If PPL goes from -5 to -40, then their PINT of -7 will go well beyond -10, -20, if not lower. This would cause flash pulmonary edema.
486
True or False. If PPL is really positive, you have potential for tons of fluid to move from capillary to interstitium very quickly.
FALSE! If PPL is really NEGATIVE, then patient is at risk for pulmonary edema.
487
Semi-conscious young, healthy adults who thinks they're choking. They react by taking a really strong, deep breath. What do you do to prevent flash pulmonary edema?
Sedate the patient to get them to stop inspiring so hard or open the airway or both. (Ideally, you want to fix the airway problem because if it is occluded for too long then they aren’t getting any air. This would be a good way to treat this; so, fix that and it will resolve this on its own or you could sedate the patient.)
488
Diaphragm is comprised of what 3 things?
2 leaflets/cusps (which are individual muscles) and 1 central tendon.
489
How does positive pressure ventilation (PPV) affect lymphatics?
With PPV, we are filling and emptying the lungs in a way where alveolar pressures are always going to be higher than in between breaths. We are forcing air into the lungs pushing on it, which can obstruct the lymphatics.
490
How does PPV affect pulmonary capillary interstitial pressures?
PPV can potentially obstruct the lymphatics. If that is occurring, then PINT would become more positive. (Remember that lymphatics are a portion of what causes PINT to be negative!)
491
How does PPV affect pulmonary arteries and veins?
Our pulmonary arteries and veins tend to be very collapsible; they don’t have a whole lot of structure to them, their walls are very thin, and they are easily compressed. So, in addition to pushing on the alveoli, they will push on the pulmonary arteries and veins also.
492
3 things that PPV will affect.
1. lymphatics--will obstruct 2. PINT--will increase 3. pulmonary arteries and veins--will compress
493
↑PINT caused obstructed capillaries will cause fluid to stay in capillaries or leave?
↑PINT favors blood staying in the capillaries.
494
What occurs if pulmonary veins collapse?
That could potentially cause ↑BP proximal to the occlusion. This would be bad in terms of trying to get fluid to stay out of the interstitium and out of the alveoli; it would be difficult for blood to leave the pulmonary veins, so it builds up in the alveoli.
495
What occurs if pulmonary arteries collapse?
It would be useful to prevent fluid from building up in the lungs because it would occlude blood flow from the lungs, which is something you obviously wouldn't want to do.
496
Does PPV help with preventing or pushing fluid out of the lungs?
Maybe. It might, might not!
497
The blood has to get back to right heart via \_\_\_\_, and if there is an occlusion in the area of the heart then you could have problems with that. The result of that is \_\_\_.
The blood has to get back to right heart via pulmonary veins. Occlusion can result in potentially fluid building up in the lungs.
498
The walls of the lung units are thickest at what part of the lung?
The base/bottom of the lung are thickest. (This means that there is more blood and blood flow in the base of the lung!)
499
If patient is in prone position, where is the dependent region of the lung?
Dependent region is the part of lung closest to the floor! So, if patient is prone, the dependent region would be the anterior part of the lung.
500
What does good ventilation and perfusion matching mean?
If there is a lot of blood flow through a certain part of the lung, then we want a lot of airflow at that part to match the blood flow.
501
What is the main reason why the behavior of the tissues at the top of the lung vs the bottom of the lung are different.
The main reason for the difference in behavior is due to a gravity-related pleural pressure gradient that runs along the edges of the lungs and affects the behavior of the tissue inside of the nearby lung units.
502
Difference b/t alveoli size and pleural pressures at RV vs FRC.
Left is RV. With RV, the alveoli at the apex of the lung are only slightly larger than alveoli in the base. The PTP pressure at the apex is -2.2 and at the base, it is +4.8. Right is FRC. With FRC, the alveoli are significantly larger in the apex than at the base. The PTP at the apex is very negative (-8.5) and the alveoli at the base is -1.5.
503
How much air is in the system at RV vs FRC?
RV: 1.5 L FRC: 3 L
504
Alveolar pressure in a static lung = \_\_.
0mmHg (no air going in or out of it)
505
Transpulmonary pressure at the apex of a static lung at FRC.
PTP = PA – PIP PPL = -8.5. PA = 0. So, PTP = +8.5
506
What is transpulmonary pressure in a static lung with normal average pleural pressure?
PTP = PA – PIP PA = 0. PPL = -5. So, PTP = +5.
507
If we think about the lung suspended in the chest, the lungs basically connect with the ____ and hangs off that connection point in the chest. What is the significance of how the lungs are found in the chest?
Mediastinum. The fact that the lungs will be pulled down because of gravity gives us a much more negative than average PPL at the very top of the lung and more positive at the base because of all the pressure from gravity.
508
What is pleural pressure and transpulmonary pressure at the apex and base of a static lung at FRC?
Apex: PPL = -8.5 PTP = +8.5 Base: PPL = -1.5 PTP = +1.5
509
When we are at FRC, the alveoli at the base of the lung are \_\_\_% filled. At the apex, it is \_\_\_% filled.
Base: 25% Apex: 60%
510
How is PTP affected with inhalation?
Think of PTP as opposite of PPL! So, if PPL becomes more negative when we inhale, then PTP becomes more positive.
511
\_\_\_\_ is a function of how much volume change are we having and what is the change in pressure that allows us to do that.
Compliance
512
Difference b/t high and low compliance.
If we get a lot of volume in for a small amount of pressure, that is describing a tissue that is very compliant. If we get less volume in using greater amounts of pressure, that tissue is less compliant.
513
Which is more compliant--A balloon already 90% filled OR a balloon already filled 10% and blowing it up to 100%?
More compliant would be the balloon pre-filled with 10%. So, this balloon would be more accepting of volume and require less pressure to inflate.
514
On a pulmonary ventilation chart comparing volume% and PTP, how does the slope of the curve differ at low PTP vs high PTP?
At lower PTP, the tissue is more compliant and has a steeper curve. As PTP increases, the tissue becomes less compliant and the slope becomes to flatten out. At 40 PTP (max), when the alveoli are completely full, the slope is flat.
515
At FRC, if the alveoli are only 20% filled and 20cmH2O PTP is applied, how much does the alveoli fullness increase?
It goes from 20% all the way to 90%, a 70% increase! \*\*This increase is significant due to having more compliance at lower volumes.
516
At FRC, if the alveoli are 90% filled and 20cmH2O PTP is applied, how much does the alveoli fullness increase?
It goes from 90% to 100% filled, only a 10% increase. \*\*The reason why it increases only by 10% is because at higher volumes, the alveolar tissue has low compliance.
517
How does PPV affect the right heart?
The R♥ has to push all the blood through these lungs. If there is a ton of positive pressure pushing on the blood vessels, that will really make things difficult for the R♥ because of the increased workload. So, use the lowest possible pressures!
518
At FRC, where in the lung does the majority of fresh air preferentially go to first?
Majority of fresh air preferentially goes to the areas of the lung that are most compliant, where alveoli are less full, and has the most blood flow. This would be the base of the lung.
519
On the pulmonary ventilation curve, what does the slope of the curve represent?
Compliance (The steeper the slope, the more compliant. The flatter the slope, the less compliant.)
520
At FRC, is the top of the lung more or less compliant than the base?
The apex of lung is less compliant. The base of lung is more compliant.
521
How does pleural pressure affect the fullness of alveoli?
The more positive the pleural pressure, the emptier the alveoli. The more negative the pleural pressure, the fuller the alveoli. \*\*Note how alveoli at apex of lung (PPL = -8.5) at FRC is significantly larger than at the base (PPL = -1.5).
522
Pleural pressure gradient in the lungs are driven by \_\_\_.
gravity
523
Is the alveoli at the base of the lungs fuller/larger at FRC or RV? At the apex?
At FRC, the alveoli at the base and apex are both larger than the alveoli at the base and apex of the lung in RV, respectively.
524
Comparing the two together, the alveoli at the base of the lung are only \_\_\_% less full than the base alveoli at FRC.
5% (The way we have that 5% pushed out of the alveoli is we have applied positive PPL to push that 5% out of the alveoli.)
525
Why can't we drop our alveolar fullness any lower than 20%?
Because there is only so much air we can squeeze out of our alveoli before the small airways leading into that alveoli collapse.
526
What happens to alveoli and alveolar pressure when we forcefully expire as much as possible?
When we forcefully expire, this is going to push on the alveoli to help it empty out by pressing on the walls of the alveoli and make PA positive, which will push the air out.
527
When we forcefully expire, how does that affect the small airways leading into the alveoli?
If we push on these hard enough, some of this pushing pressure has a potential to push on the airway, which, at some point, will collapse the airway and prevent us from getting any more air out.
528
If pleural pressure at the base of the lung at RV becomes more positive, what happens to the fullness of the alveoli at the base?
If we push any harder, and make PPL more positive than +4.8 at the base of the lung, it doesn’t change the fullness of the alveoli at the base of the lung at all. The most empty the alveoli can get is 20%!
529
What alveoli will have the potential to become trapped depends on \_\_\_\_.
Lung volume. \*\*If we are at a really high lung or alveolar volume and we push on this (more positive pleural pressure), we are going to be able to get quite a bit of air out of here.
530
True or False. When we have high lung or alveolar volume, the small airway is basically a continuation of the alveolar unit.
TRUE \*\*So, if we have a fairly high alveolar volume, then the attached airway will be really wide!
531
If the alveolus has been pulled open by negative pleural pressure or forced to accept volume in here, the small airways tend to do what?
The small airways tend to widen as alveoli fill with volume. \*\*Remember that the small airways are like a continuation of large alveolar units!
532
Explain why larger/fuller alveoli are less likely to collapse than smaller/emptier alveoli.
Larger alveoli will have larger/wider airways attached to them. Smaller alveoli have smaller/more narrow airways, which make them more likely to collapse.
533
What is the pleural pressures at the apex and base of the lung at RV?
Apex: -2.2 Base: +4.8
534
The higher the transpulmonary pressure, the higher or lower the alveolar volume %?
Higher \*\*Remember PTP is essentially opposite of PPL. So, The higher (more positive) the PTP, the lower (more negative) the PPL, the higher/fuller the alveolar volume %.
535
Describe PTP and PPL on expiration.
On expiration, we are pushing air out of the lungs/alveoli. So, PTP will be lower (more negative) and PPL will be higher (more positive).
536
The alveoli at the top of the lung at RV are more empty than they were at FRC. Why?
At FRC, the PPL at the top is -8.5 and at RV it is -2.2. RV's pleural pressure is more positive, meaning there is isn't as much pressure to hold the alveoli open or fill them up!
537
At RV, the alveoli at the apex of the lung is \_\_\_% full.
30% So, at RV: apex is 30% and base is 20% of total possible capacity.
538
True or False. If we have a PPL of anything that is positive or if we have a PTP that is negative, that would give us the ability to put a little bit more air into alveoli.
False! Putting air into the alveoli (inspiration) would require PPL to be negative and PTP to be positive.
539
Where in the lung are alveoli more compliant at RV?
The apex
540
When we are at really low lung volumes (RV) and inspire, where in the lung will the fresh air preferentially go to first? Why?
The apex, because at RV, the apex has more compliance than the base of the lung--easier for air to go there.
541
Describe the compliance of the base of the lung at RV.
The slope is essentially flat; zero compliance! If we were to increase PTP from +4.8, we would get no volume into the lung for quite a while. If we make PPL 0, we still wouldn’t have a whole lot of air coming into the base of the lung. We would have to actually get all the way over to somewhere around here [pointing/arrow] until we get any air coming into the base of the lung.
542
If we are changing transpulmonary pressure without any change in volume to the alveoli, what is the compliance?
ZERO compliance (This is what occurs at the base of the lung at RV!)
543
What happens to alveoli if they are collapsed for too long?
They will be difficult to open back up! It will be harder for the alveoli/lung to re-inflate. Eventually, if they are collapsed for long enough then that part of the lung is going to eventually disappear.
544
Is there a difference in tissue characteristic between inflating and deflating the lung?
Yes. Lung volume increases correspond to the curve that is on the right and lung volume decreases (expiration) is the curve on the left; that is why they have two lines in there.
545
True or False. PTP of 0 would be equal to a PPL of 0. So, PPL of 0 surrounding the base of the lung. We can assume that as soon as we make PPL more negative, we could probably get air into the lungs at that point.
False! If we are working from really low lung volumes and we do have some collapsed areas of the lung, we actually have to apply a little extra pressure just to prop open those airways back up after they collapsed. What we would have to do is make PPL substantially more negative than it is in order for any air to start going into the base of the lung.
546
How much extra pressure is needed to open up a collapsed alveoli?
4-5cmH2O (in a young, healthy adult). More might be required for elderly patients, smokers.
547
How can we prevent alveoli from collapsing?
Using PEEP on the ventilator to keep a little bit of volume in the lungs.
548
If we are at lower lung volumes (RV) and we are still upright, fresh air would preferentially be going to the top of the lung. What happens as we put more and more into the lungs?
It tends to open up the lungs as it goes down. At some point, we will get enough air into the lungs to reopen the base of the lung. When that reopening has taken place, once those airways and alveoli there open back up, then air will start preferentially going to the base of the lung. This is due to the pleural pressure gradient!
549
Significance of alveoli sharing common walls.
These shared walls connect alveoli together, forming continuous pathways for blood to go through. So, if we are able to start putting air into the middle of the lung here, this is going to pull these other connected alveoli open and help get air into the lower collapsed areas of the lung.
550
What happens to alvolar walls in COPD or emphysema?
Some alveolar walls are lost and alveoli get really big; they don’t have the same types of connections that a healthy person has. If we don’t have as many walls that are attached to each other, we can have an issue getting collapsed areas of the lungs to open back up, resulting in a patchy collapse.
551
Pro and Con of using PEEP to keep extra volume in lungs.
Pro: Prevent alveolar collapse Con: Potential circulatory problems in the lungs, R♥ overload/increased workload
552
Why is transpulmonary pressure used rather than pleural pressure when looking at pulmonary ventilation curves?
Because PTP are applicable to normal breathing and PPV, whereas pleural pressure does not necessarily apply to PPV.
553
Looking at PACO2 (alveolar) and PAO2 (alveolar), ____ is dependent on how much ventilation we have.
partial pressure
554
If we were bringing in completely fresh air from the outside with no blood flow, what would our PAO2 and PACO2 be?
If we had no blood flow but plenty of fresh air coming in, we wouldn’t be absorbing any oxygen out of the alveolus. Therefore, the PAO2 and PACO2 should be equal to what is coming in. So, if PO2 coming into the alveoli is 150, then PAO2 should also be 150. If PCO2 coming into the alveoli is 0, then PACO2 is also 0. \*\*Written in blue on drawing.
555
If we were to have no ventilation of this alveolus but we did have perfusion of this alveolus, what would our PAO2 and PACO2 be?
The alveolar PACO2 should be 45 mmHg, the equivalent of PCO2 partial pressure arriving at this location via the pulmonary arteries. PAO2 would be 40 mmHg, again, the equivalent of PO2 of the pulmonary arteries.
556
\_\_\_\_ is a way for us to measure a number of our lung volumes and capacities.
Spirometry
557
How does a spirometer work?
There is an upside down tank that is pretty full of air, with an opening at the bottom of the tank. The patient is connected by a tube to this machine and as they inspire and expire, the quantity of air inside of the upside down water heater it changes. With inspiration, the tank moves down because it is drawing air out of the tank, sucking in the water. With expiration, it fills the upside down tank with more air, pushing the tank up.
558
What does a large tracing mean on a spirometer?
Large tracings signify more movement, greater inspiratory and expiratory volumes.
559
Normal spirometer can calculate all lung volumes and capacities except?
Residual volume. Therefore, spirometers cannot measure total lung capacity or functional reserve capacity.
560
Patient is hooked up to a spirometer and takes a deep breath and exhales as much as possible. What did the spirometer record?
The patient's vital capacity (VC = TD + IRV + ERV)
561
Is emphysema an obstructive or restrictive pulmonary disease? COPD?
Both are obstructive airway disorders, associated with the loss of elastic tissue and some of the elastic tissue not being connected very well on the inside of the lungs.
562
What lung volumes differ in obstructive lung diseases compared with normal? How are they different?
With obstructive lung disease (ex. Emphysema, COPD, etc.), we can see more than a doubling in the RV vs someone who is completely healthy. Also, they would have a smaller ERV.
563
What do we need in addition to a spirometer to measure residual volume?
We would need extra attachments to it and an indicator dilution setup.
564
4 qualities of an ideal indicator for measuring residual volume.
1. cheap 2. non-reactive 3. non-toxic 4. not absorbed in blood stream
565
The most commonly used indicator for spirometers is \_\_\_.
Helium, because it is fairly inert, doesn’t react with a whole lot of stuff, doesn’t explode when it is exposed to flame, and is probably one of the cheapest of the noble gases.
566
List the noble gases. (6)
1. Helium 2. Neon 3. Argon 4. Krypton 5. Xenon 6. Radon
567
\_\_\_\_ is a noble gas but can actually be radioactive.
Radon
568
Outside of smoking, ___ is the most common source of lung cancer.
Radon (A lot of people ran radon tests if they had a basement if you someone had lung cancer. Sometimes people look for radon leaking in from the outside.)
569
We don’t want a gas indicator that will be absorbed into the blood stream when measuring residual volume. Why?
We want the indicator gas to stay in the gas form; we don’t want it disappearing. Otherwise, it will screw up our measurements and we won’t be able to keep track of it.
570
When measuring RV/FRC using spirometry and indicator dilution setup, before the test there was 10% helium and only 5% after the test. Why?
During the test, the helium is going to be diluted out because you added more space (patient's breath) in the system.
571
Formula for a concentration.
volume of the compound that we are interested in/total volume
572
If a 10 L container has 10% helium, what is the volume of helium in that container?
volume of the compound that we are interested in (X)/total volume 10% He = [He] Total volume = 10L So, [0.1] = X/10 L → X = 1 L He
573
Before the FRC test, there 10% He in a 10L container. After the test, there is only 5% He. How much is the new total volume of the container? What does the difference between the original and new volume mean?
Before test: 10% He = [He] Total volume = 10L So, [0.1] = X/10 L → X = 1 L He After test: 5% He = [He] Total volume = Y So, [0.05] = 1L He/Y → Y = 1 L/0.05 = 20 L So, the amount of volume that is in the patient is the difference—10 L of air in the patient.
574
We would expect composition of dead space gas to look pretty close to what we are \_\_\_.
inspiring
575
The gas that is in the lung after equilibration is going to have some ___ that is missing and some ___ that it didn’t have on the way in.
The gas that is in the lung after equilibration is going to have some oxygen that is missing and it will have some CO2 that it didn’t have on the way in.
576
What we expired during the entire breath, that will be a combo of ___ and \_\_\_.
dead space gas and alveolar gas
577
True or False. The amount of air we have in our dead space it is not available for gas exchange.
TRUE
