Exam 2 Flashcards
Schmidt Exam 2
____ determines how much filling the ventricle is going to have during phase 1 of the cardiac cycle.
Preload
____ fluences how long it takes for the aortic valve to get open as well as how fast it is going to slam shut.
Afterload
____ is going to give us a different SV by leveling different quantities of squeeze on whatever is in the ventricle.
Contractility
When we have aortic ____, we have a really high interventricular pressure pumping against a high resistance valve.
aortic stenosis
With a lot of valve issues, we have compensation of the system via an increase in ____ and ____.
heart rate and filling pressure
With almost all of these cardiac problems, chronic elevations in ____ are the main things that keeps the heart and body in working condition.
filling pressure
After an acute MI where the heart is injured, the body’s immediate response to that is what? Why?
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.
The long term fix for heart failure is going to be a general increase in ___, usually seen in elevated CVP.
Psf
Reduced contractility = ___ SV
Reduced (because we aren’t getting as much out of the heart on each beat)
Decrease in SV will manifest as ___ ESV and ___ EF.
increased ESV and decreased EF
How does increased CVP affect SV?
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.
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?
an afterload reducer
How does an afterload reducer work?
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.
How does external work in an untreated HF patient compare with a HF patient taking afterload reducers?
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.
People with moderate HF, we can help their heart pump by just reducing ____ and increasing ____.
reducing afterload and increasing contractility
How does ACE-I’s help HF patients?
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.
2 inotropes that help with HF.
Digoxin (cardiac glycoside) and Milrinone (PD3 inhibitor)
How do inotropes help with HF?
They will increase contractility of the heart, making the heart beat stronger.
Why do we have to be careful when giving Milrinone, specifically with HF patients?
Milrinone can reduce afterload in addition to increasing myocardial contractility.
Normal CO curve peaks at __ L/min with a normal amount of SNS and PNS activity.
13 L/min
How would the CO curve change if we increase amount of SNS stimulation at the heart?
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).
On a cardiac output curve, what does a shift on the x-axis to the left and right mean?
Shift left = stronger pump. Shift right = weaker pump.
Why do we expect a drop in RAP if the CO curve shifts to the left?
RAP be reduced from its normal value because the heart is pumping out what is being returned to it faster than it normally does.
If the heart isn’t pumping out what is being returned to it as quickly/effectively, then we would expect RAP to ____.
increase
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!
If we were to maximally stimulate the SNS, what are the two effects it would have on the venous return curve?
- Increase in Psf 2. Increase in RVR
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.
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.
Why does Psf increase when we having increased SNS activity?
Because all the blood vessels will be constricted/tighter than normal.
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.)
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).
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.
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.
Increased ___ is more importantly a big determinant than increased Psf.
CVP
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.
A ____ is an accessory pathway that allowed blood to get through the heart through an abnormal channel/open conduit.
AV fistula
___ 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.)
What drug specifically works to reduce SVR without affecting Psf?
Hydralazine
Does Hydralazine affect veins or arteries or both?
It is an arterial-specific vasodilator. So, it has no effect on the veins.
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!
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.
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.]
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.
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.
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).
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.
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.
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.
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.
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.
What is the CO that is compatible with keeping all the organs alive?
4-5 L/min
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)
How does the CO curve appear if we have heart failure?
It is depressed (decreased slope), with CO about 50% of normal.
RAP with HF would be ___ mmHg.
+4 mmHg, because the heart isn’t pumping out what is being returned to it.
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.]
How is Psf and RVR affected with mixed vasodilators?
Psf is decreased. RVR is decreased (slope is higher).
When do we have decompensated heart failure?
When the CO is below the critical CO level required for normal fluid balance.
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.
True or False. Decompensated HF is very similar to severe compensated HF.
True.
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
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.
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.]
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.]
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.
___ is a function of getting O2 to where it is needed.
Cardiac output
_____ are the top controllers of metabolic needs.
Thyroid hormones
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.
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.)
When we have high BP, there is usually a small elevation in ____ that is unexplainable and a small expansion of _____.
CO ; blood volume
____ parallels the expansion in the blood volume.
ECF
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.)
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.
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.)
How does having HTN going into the OR affect your anesthetic?
They will be more sensitive to anesthetics than someone with normal BP.
5 things that can cause a sustained increase in CO.
Nutrient deficiences (ex. Beriberi), AV shunts, hyperthyroidism, anemia, pulmonary disease
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.)
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.
____ is a condition that interferes with enzymatic steps for aerobic metabolism.
Beriberi
Beriberi is a deficiency in ____, which is also known as ____.
Vitamin B1 ; Thiamine
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.
What is dinitrophenol?
an uncoupling agent of oxidative metabolism. (It basically does the same thing as thiamine, but has a different chemical name.)
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.
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.
The higher the metabolic rate, the more ___ we need.
CO (This is what happens with hyperthyroidism.)
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.
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.)
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.
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.)
Pulmonary disease would be an example of how we may have an elevated ___ in someone with patchy lungs.
CO
3 things that would cause a huge short-term increase in CO.
Exercise, anemia, anxiety
2 reasons why we would have sustained decreased CO.
removal of limbs and hypothyroidism
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.
____ would cause a short-term decrease in CO.
Shock (all forms!–cardiogenic, neurogenic, hemorrhagic, traumatic, etc.)
Exophthalmos occurs in what thyroid disorder?
Hyperthyroidism (exopthalmos: protruding eyes, eyelids are pulled back)
2 reasons for hyperthyroidism.
Tumor or autoimmune problem
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.)
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)
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!)
Where is thyroid gland found in relation to the crycothyroid ligament?
Inferior (below the ligament)
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)
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.
Hypothalamus secretes a compound called ____.
thyrotropin releasing hormone (TRH)
When is TRH released?
When the hypothalamus decides it needs to increase amount of thyroid floating around.
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)
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.
Thyroid hormones work on a ___ feed back system.
Negative
Thyroid hormones can feed back on the hypothalamus, as well as the ___.
pituitary gland
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.
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.
How does the body create thyroid hormones from tyrosine?
The thyroid gland adds iodine to the tyrosine compound.
Name the different tyrosine-based compounds our thyroid gland makes by adding iodine to it.
Tyrosine > Monoiodotyrosine > Diiodotyrosine > Triiodotyrosine (T3) > Thyroxine (T4)
When we think about thyroid hormone, we are usually going to be referring to ___.
T4 (thyroxine)
The predominant form being produced by thyroid gland is ___.
T4 (So, that is usually what is floating around in the blood.)
100% of T4 that is floating around was manufactured by the ___.
thyroid gland
What % from where is T3 made?
20%: thyroid gland. 80%: reduction of T4 somewhere in tissues
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.
2 ways to make T3.
- Combine one of the monoiodotyrosine with one diiodotyrosine 2. Strip an iodine off a T4
Name of enzyme that strips iodines off T4.
Iodinase
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.)
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.
Where in the body is iodine used?
Thyroid gland (it doesn’t work anywhere else in the body!)
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.)
What is radioactive iodine medically used for?
- 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.)
Radioactive iodine is what isotope number?
131
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.)
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.)
Which is more active? T3 or T4?
T3
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)
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.)
How much thyroid hormone is stored in pituitary gland?
2-3 months worth (In addition to that, there is plenty of circulating thyroid hormone)
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)
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.
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)
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.)
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.)
Thyroid hormone receptors are found outside or inside the cell?
Inside (because we are dealing with a lipid soluble compound)
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.)
The most produced compound that results from thyroid hormone binding to its receptor inside the cell is ____.
Protein
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.)
Glycogen will be broken down to glucose and metabolized through ____ metabolism.
oxidative
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.)
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.)
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)
In hyperthyroidism, insulin release increases or decreases?
Increases (that will help us get the sugar inside the cell where it is consumed)
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)
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.)
How does hyperthyroidism affect CV?
vasodilation; increased CO, HR, and SVR
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.
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.
Something specific with hyperthyroidism is sometimes they exhibit ___ hertz skeletal muscle tremors.
10-15 Hz (Must look really close to see it!)
If you see an unexpected increase in HR there are two things that should come to mind, which are?
valve problems or hyperthyroidism
True or False. MAP of patients with hyperthyroidsim is high.
False (MAP is normal, despite having an increased SBP)
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.
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).
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.)
3 options to “settle down” the thyroid gland from releasing so much TH.
- Drugs (Propylthiouracil and Methimazole) 2. Radioactive iodine 3. Surgery
Why avoid amiodarone if you have hyperthyroidism?
Amiodarone has 30% iodine in the solution (want to avoid giving additional iodine!)
What is easier to treat, hyper or hypothyroid? Why?
Hypothyroidism, because you can just give a synethetic TH (Synthroid).
3 examples of things that could cause hyperthyroidism.
- adenoma 2. grave’s disease 3. early hashimoto’s thyroiditis
What is an adenoma?
tumor releases too much thyroid hormone; can cause goiter.
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.)
3 things we expect to see in Grave’s disease.
- 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)
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.
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)
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).
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.
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.
5 functions of pulmonary circuit.
- gas exchange 2. acid-base balace 3. speech 4. enzymes 5. immune response
With gas exchange, ___ going into the body and ___ goes out.
Oxygen ; CO2
Formula to make carbonic acid.
CO2 + H2O + Carbonic anydrase = H2CO3
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.)
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).
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.)
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.
By definition, acid base is dependent solely on the concentration of ___.
Protons
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.)
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.)
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
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.
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!)
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.)
Speech is done via air that is coming out of the system passing through the vocal cords controlled by ?
Skeletal muscles in larynx
What important enzyme is found in the respiratory circuit? *Hint: RAAS.
Angiotensin conversion enzymes (ACE)
What does ACE do?
converts ang I to ang II and it also breaks down bradykinin
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.
_____ 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.)
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!)
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
The main muscle of inspiration and expiration under normal resting conditions is the _____.
diaphragm
The diaphragm made up of what?
2 muscle units connected to each other midline by a tendon
Where is the diaphragm fastened in?
Each side of the diaphragm has a little different connecting point on the spine in the abdomen.
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.)
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.
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.)
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.)
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)
Where are external intercostal muscles found?
On the outside of the ribs with an attachment point on the chest wall.
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.
During normal resting breathing, what are external IC muscles responsible for?
They prevent the collapse of the thorax
Where are internal intercostal muscles found?
Between the ribs on the inside.
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.
The internal intercostals help with ___ and external intercostals help with ___.
Internal = expiration. External = inspriation.
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.
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.)
The ___ muscle connects at the middle of the sternum and the mastoid process on the back of the skull.
sternocleidomastoid
What motion does the sternocleidomastoid muscle allow us to?
swivel our head from side to side
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.)
The muscles other than the diaphragm are usually thought of as ____ muscles.
accessory
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.
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.
In between the two pleura layers is lots of ____.
Mucous (helps the friction be reduced)
Where is the costodiaphragmatic recess?
At the very bottom of the chest wall, where the diaphragm connects with the lower ribs.
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.
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.)
The cartilaginous rings have an opening that is filled with ____ and ____.
connective tissue and smooth muscle
If we activate the smooth muscle cells in the cartilaginous rings of the trach, what happens?
Trachea is constricted.
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.)
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.
The trachea has a divot/split from the ____ down.
laryngeal cartilage
The tracheobronchial tree has ___ different segments.
24 (Not all parts of the lung have a full 24 segments)
The trachea is considered to be generation ___.
0 (first part before there have been any branches.)
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.
The first type of airway we wouldn’t find any cartilage in would be the ____. What size diameter is this?
bronchioles, 1 mm
Bronchioles are at generation ___; terminal bronchioles are at generation ___.
Broncholes = gen 4. Terminal bronchioles = gen16
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)
Conduction zone is generation __ to __. Respiratory zone is from ___ to ___.
Conduction zone: 0-16. Respiratory zone: 17-23.
____ are where gas exchange occurs in the lungs.
Alveoli
The places where we start to have gas exchange are referred to as the ____ zone.
Respiratory
The respiratory zone includes what 3 parts?
respiratory bronchioles, alveolar ducts, alveolar sacs
The early parts of the respiratory zones are called the ___ area.
transitional (in between the conduction and true respiratory zones)
