Wierd question about the Heart

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I'll put one in for the lungs. Why do premature infants commonly have respiratory distress, especially before 28-34 weeks gestation? (Immature lungs is not a good enough answers for those premeds who would like to try to answer)

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I'll put one in for the lungs. Why do premature infants commonly have respiratory distress, especially before 28-34 weeks gestation? (Immature lungs is not a good enough answers for those premeds who would like to try to answer)

Lack of surfactant? Seems like I remember something like that from gross anatomy.
 
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Lack of surfactant? Seems like I remember something like that from gross anatomy.

Yes, but why?

Surfactant acts to decrease surface tension on alveoli. Without it, they have a tendency to collapse in on themself during expiration. This decreases compliance, increases resistance, increases the work involved in breathing, decreases ventilation, and causes edema in the lung. Due to the edema and also due to the lack of oxygen plus increase in carbon dioxide causes cell death of the pneumocytes in the alveolar walls. An inflammation reaction then causes hyaline membrane buildup in the alveoli further preventing the pneumocytes from maturing, decreasing compliance and increasing resistance.
It doesn't take very long for neonates to die from such a situation and in many cases, no amount of effort can fix the problem. Respiratory distress syndrome or hyaline membrane disease occurs in greater than 50% of neonates born less than 28 weeks gestation but in less than 1/3 of neonates between 32-36 weeks gestation. It is around 25 weeks that surfactant is beginning to be made in the currect form but isn't until around 36 weeks that it reaches the levels that are seen in full term babies.

Heres another one. What type of pneumonia (I'm looking for the bacteria that causes it) is commonly found in those with HIV/AIDS but very rarely seen in those that are not immunmocompromised?
 
Yes, but why?

The surfactant is packaged by the cell into lamellar bodies and extruded into the alveoli. The lamellar bodies then unfold into a complex lining of the alveoli. This layer serves the purpose of reducing the surface tension which would tend to cause the alveoli to collapse in the presence of gas. Without adequate amounts of surfactant, the alveoli collapse and are very difficult to expand. This is why the kid has labored breathing.

Is that what you're looking for?

Heres another one. What type of pneumonia (I'm looking for the bacteria that causes it) is commonly found in those with HIV/AIDS but very rarely seen in those that are not immunmocompromised?

You're asking a clinical microbiologist this? :D

Pneumocystis jiroveci, formerly P. carinii (which was first isolated in rats, but now we know that humans have their own species). I believe that there has been debate over whether it is a fungus or parasite. I think that the fungus people won based on ribosomal RNA analysis.

It's diagnosed with a fluorescent antibody stain that I get to do about once a week at work. :(
 
Yes, but why?

It's not that premature babies don't have sufficient surfactant upon delivery; they do. It's that their type II alveolar cells are still immature and can't replace the pulmonary surfactant. As surfactant levels plummet, surface forces increase in the aveoli and they become harder to inflate/expand, leading to eventual collapse of the lung. Treatment usually entails corticosteriods, which can help the type II cells mature.
 
It's not that premature babies don't have sufficient surfactant upon delivery; they do. It's that their type II alveolar cells are still immature and can't replace the pulmonary surfactant. As surfactant levels plummet, surface forces increase in the aveoli and they become harder to inflate/expand, leading to eventual collapse of the lung. Treatment usually entails corticosteriods, which can help the type II cells mature.

Doesn't it also have to do with the composition of surfactant? i.e. before a certain gestation period there is 1.5 ratio lecithin:sphingomyelin and physicians want to see it up to 2.0 before considering delivery. (glucocorticoids would help improve this ratio)
 
yep. There is 1000X the rate of mesothelioma amongst those who are exposed to asbestos regularly than those who are not.

I know you have questions spicedmanna, come on, give us a few.... :)

:laugh: Okay...

What is pericardial tamponade? What's Beck's Triad? Why the heck would it present with pulsus paradoxus?
 
:laugh: Okay...

What is pericardial tamponade? What's Beck's Triad? Why the heck would it present with pulsus paradoxus?

Pericardial tamponade is when excess fluid fills the pericardial sac. I've never heard of Beck's Triad. I've also never heard of pulsus paradoxus. Is it the paradoxical splitting of S2? If it is, then excess pericardial fluid would prevent the right heart from increasing its SV during inspiration (filling would probably be even further impaired) and so the closing of the pulmonic valve would occur before the aortic valve instead of afterwards like it normally would.

I'm just guessing, so I could very well be wrong.
 
Pericardial tamponade is when excess fluid fills the pericardial sac. I've never heard of Beck's Triad. I've also never heard of pulsus paradoxus. Is it the paradoxical splitting of S2? If it is, then excess pericardial fluid would prevent the right heart from increasing its SV during inspiration (filling would probably be even further impaired) and so the closing of the pulmonic valve would occur before the aortic valve instead of afterwards like it normally would.

I'm just guessing, so I could very well be wrong.

Precisely. :) Tamponade is the result of fluid accumulation in pericardial space, constricting the heart and forcing septal deviation. Beck's Triad are the three most common signs: JVD, hypotension (as a result of low stroke volume), and fluid dampening of cardiac sounds. My understanding is that pulsus paradoxus is an exaggerated reponse to what happens to the pulse and BP during inspiration. Normally, when a person inhales, the thoracic cavity expands, decreasing intrathoracic pressure. The right ventricle expands and fills with additional blood from increased venous return. The size of the left ventricle is diminished because the extra blood in the RV will push against the septal wall to the left. This decreases the stroke volume; what accompanies is a fall in systolic BP. That's why when someone inhales, their systolic pressure is lower. Usually it isn't a big deal and it's a small difference. However, during tamponade, the heart is squeezed, so the extra blood that fills the RV will push against the septal wall even more, causing the the LV to become even smaller, further decreasing the stroke volume. This causes a very noticeable diagnostic decrease in systolic BP upon inhalation. The pulse appears to "disappear" during inhalation when there is a concomitant heart beat present. Thus the paradox. Often the degree of pulsus paradoxus can be linked to the degree of fluid accumulation.

The treatment of pericardial tamponade is scary and fascinating! It involves needle pericardiocentesis...long needle puncturing the pericardium to evacuate the fluid.
 
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Not to put a damper on the kickin' party here, but I just wanted to let all of our pre-allo friends know that this type of Jeopardy-lovin pimptastic behavior is not, in fact, encouraged between medical students in any situation. If I come across any of you asking questions like this of me in front of attendings, or even completely alone for that matter, you're going to get a ninja chop in the vagal nerve.

Extra credit points: tell me the physiological mechanism for syncope secondary to a ninja chop in the vagal nerve. ;)
 
It doesn't really matter, and it is just my OCD kicking in, but I keep seeing this word misspelled on multiple posts, in mutiple threads. It's W-E-I-R-D. Weird, not wierd; despite the i before e rule.

Sorry I'm so weird.
 
It's not that premature babies don't have sufficient surfactant upon delivery; they do. It's that their type II alveolar cells are still immature and can't replace the pulmonary surfactant. As surfactant levels plummet, surface forces increase in the aveoli and they become harder to inflate/expand, leading to eventual collapse of the lung. Treatment usually entails corticosteriods, which can help the type II cells mature.

http://aappolicy.aappublications.org/cgi/content/full/pediatrics;109/2/330

The use of steroids in this circumstance is no longer considered appropriate.

Surfactant replacement is the therapy of choice.
 
I don't wanna go to med school anymore. :(

As DoctorFunk said, this kind of energetic pimping session among students is not encouraged in med school. You can do it, but it will make you very unpopular pretty fast. That's probably why everyone is doing it on SDN.
 
Extra credit points: tell me the physiological mechanism for syncope secondary to a ninja chop in the vagal nerve. ;)

CN X is being overstimulated enhancing normal vagal tone. The resulting parasympathetic wave causes widespread vasodilation diverting blood away from the brain if you are in a standing position. This causes the syncope (translation = fainting).

How did I do?

As DoctorFunk said, this kind of energetic pimping session among students is not encouraged in med school. You can do it, but it will make you very unpopular pretty fast. That's probably why everyone is doing it on SDN.

Yeah I thought that it was too easy of a heart question to just let such an opportunity with an aptly-named thread pass.
 
http://aappolicy.aappublications.org/cgi/content/full/pediatrics;109/2/330

The use of steroids in this circumstance is no longer considered appropriate.

Surfactant replacement is the therapy of choice.

hola,
while that article suggests that steriods are inappropriate, they are still used in practice. we try to hold off on the delivery of premies until the mother can get 48 hours of dexamethasone; it's also still taught during second-year courses in med school. (MS3)

ps - blood vessels have purely sympathetic innervation; effect of vagal stimulation is via the heart.
 
http://aappolicy.aappublications.org/cgi/content/full/pediatrics;109/2/330

The use of steroids in this circumstance is no longer considered appropriate.

Surfactant replacement is the therapy of choice.

I think I just got pimped. :oops:

The short-term pulmonary benefits of systemic dexamethasone do not appear to confer long-term benefits. Survival does not improve after dexamethasone administration. Furthermore, data indicating an increased incidence of neurodevelopmental delay and cerebral palsy raise serious concerns about adverse long-term outcomes.
 
ps - blood vessels have purely sympathetic innervation; effect of vagal stimulation is via the heart.

So the HR/contractility/CO bottoms out causing the decrease in blood pressure?

Thanks. I would have blown that one on my exam. :thumbup:
 
hola,
while that article suggests that steriods are inappropriate, they are still used in practice. we try to hold off on the delivery of premies until the mother can get 48 hours of dexamethasone; it's also still taught during second-year courses in med school. (MS3)

True, true and unrelated.

Prenatal steroids decrease the incidence of hyaline membrane disease and are still used for anticipated or potential delivery at 24-34 weeks gestation. A single course is currently used. It is post-natal steroids that are relatively contraindicated. Not to belabor the issue here, but the data showing a poorer developmental outcome was mostly associated with relatively long courses of steroids. There remains uncertainty about short courses and the use of hydrocortisone instead of dexamethasone.

Regardless, the use of postnatal steroids has been drastically reduced in the US and would never be used anymore post-delivery for routine surfactant deficiency. We have multiple types of surfactant to give for that as well as CPAP, etc.
 
I think I just got pimped. :oops:

No way, I didn't ASK you a question, I just corrected your answer. That's teaching, not pimping.:p

Now, if I ask you why surfactant deficiency is more common in males and in Caucasians that would be closer to pimping.:laugh:
 
As DoctorFunk said, this kind of energetic pimping session among students is not encouraged in med school. You can do it, but it will make you very unpopular pretty fast. That's probably why everyone is doing it on SDN.

But this is way different than pimping classmates. This is fun. Its an anonymous forum and if someone doesn't know, they don't have to answer. There is nothing uncomfortable about it. And besides, I got some flattery out of it. :love: Thanks Wizzard
 
No way, I didn't ASK you a question, I just corrected your answer. That's teaching, not pimping.:p

Noted. :D

Now, if I ask you why surfactant deficiency is more common in males and in Caucasians that would be closer to pimping.:laugh:

Hmm...brilliant example.

No idea, though. I suspect it is genetic in nature. I ran across something about surfactant protein (A, B and C) gene polymorphisms in a quick search.
 
Yes, there is mad learning going on here... and because I want to do something with the heart one day I am loving it as a premed... I know the stuff is blowing my mind right now but hey I am glad these people are on this level... shows me that being a doctor is the most prestigous thing on earth.

Ok, here is my question slash concern...

This is a cardiovascular question...

When you exercise heavy your RBC increase in CO2 and thus a decrease in PH causing it to become acidic... why, why does CO2 specifically cause lower PH? where exactly is this coming from in a mechanistic way? As well, is that the true reason why we breath harder to expel more CO2 and thus balance out the PH. please give the lamen term answer... The reason why I am having a problem of understanding why CO2 causes a higher PH is because in order to make the CO2 and H2O the bicarbonate ion has to come into the RBC and react with an H+ ION... I would think this reaction right here would cause an increase in PH even if the result is an increase in CO2... Meaning CO2 isn't even acidic is it?

Second, heavy breathing rate expells more CO2 and thus increases PH Again, I am just having a wEird understanding of this mechanism... I think part of the problem might come from the fact that when O2 is entering into the RBC what type of PH change might that cause?
 
Yes, and when people tell you that which medical school you choose is sooooo important, keep in mind that all of us MD wannabes are fed the same material albeit in slightly different ways. So even if we don't know something off the tops of our heads, we know that we should know sooner or later. Everything I've come up with here has been out of board review materials.

When you exercise heavy your RBC increase in CO2 and thus a decrease in PH causing it to become acidic... why, why does CO2 specifically cause lower PH? where exactly is this coming from in a mechanistic way? As well, is that the true reason why we breath harder to expel more CO2 and thus balance out the PH. please give the lamen term answer... The reason why I am having a problem of understanding why CO2 causes a higher PH is because in order to make the CO2 and H2O the bicarbonate ion has to come into the RBC and react with an H+ ION... I would think this reaction right here would cause an increase in PH even if the result is an increase in CO2... Meaning CO2 isn't even acidic is it?

Second, heavy breathing rate expells more CO2 and thus increases PH Again, I am just having a wEird understanding of this mechanism... I think part of the problem might come from the fact that when O2 is entering into the RBC what type of PH change might that cause?

As you already know, the equation is CO2 + H2O to H2CO3 to H+ + HCO3-

If your breathing slows or CO2 can't leave for some reason, CO2 will get backed up and drive the equation to the right by mass action. That's where the H+ (low pH) comes from. Yes the H+ was needed to make the CO2 + H2O in the first place, but now the equation is being pushed back the other way because the CO2 isn't leaving like it's supposed to.

Exercise will also increase lactic acid production. You can try to fix this by blowing off CO2 as well.

Acid will shift hemoglobin O2 binding to the right decreasing O2 affinity, but I don't think you want to go into that stuff here.
 
But this is way different than pimping classmates. This is fun. Its an anonymous forum and if someone doesn't know, they don't have to answer. There is nothing uncomfortable about it. And besides, I got some flattery out of it. :love: Thanks Wizzard

I know - I just wanted to comfort the pre-meds who were worried that med school would be like this all the time. I'm glad that people are doing it online, and not in person! :)
 
This is a cardiovascular question...

Actually, it's a pulmonology/renal question. Whatever - not important.

When you exercise heavy your RBC increase in CO2 and thus a decrease in PH causing it to become acidic... why, why does CO2 specifically cause lower PH? where exactly is this coming from in a mechanistic way? As well, is that the true reason why we breath harder to expel more CO2 and thus balance out the PH. please give the lamen term answer... The reason why I am having a problem of understanding why CO2 causes a higher PH is because in order to make the CO2 and H2O the bicarbonate ion has to come into the RBC and react with an H+ ION... I would think this reaction right here would cause an increase in PH even if the result is an increase in CO2... Meaning CO2 isn't even acidic is it?

Carbon dioxide IS acidic. It's considered a mild acid in the body because, once dissolved, it will form carbonic acid.

Second, heavy breathing rate expells more CO2 and thus increases PH Again, I am just having a wEird understanding of this mechanism... I think part of the problem might come from the fact that when O2 is entering into the RBC what type of PH change might that cause?

Heavy breathing (specifically DEEP breathing) blows off CO2. By blowing off CO2, you're getting rid of an acidic product, which will increase the pH.
 
Yes, and when people tell you that which medical school you choose is sooooo important, keep in mind that all of us MD wannabes are fed the same material albeit in slightly different ways. So even if we don't know something off the tops of our heads, we know that we should know sooner or later. Everything I've come up with here has been out of board review materials.



As you already know, the equation is CO2 + H2O to H2CO3 to H+ + HCO3-

If your breathing slows or CO2 can't leave for some reason, CO2 will get backed up and drive the equation to the right by mass action. That's where the H+ (low pH) comes from. Yes the H+ was needed to make the CO2 + H2O in the first place, but now the equation is being pushed back the other way because the CO2 isn't leaving like it's supposed to.

Exercise will also increase lactic acid production. You can try to fix this by blowing off CO2 as well.

Acid will shift hemoglobin O2 binding to the right decreasing O2 affinity, but I don't think you want to go into that stuff here.

I know this sounds weird... but OK the CO2 in this case is the limiting reagent. meaning the water is in excess and increase in water surely wouldn't cause an increase in H+ (PH)... but, in a wierd way..... it could work that way couldn't it? meaning H2O would actually be the limiting agent and cause higher acid concentrations in the blood.

Ok, and now for this point... the RBC stores the carbonic anhydrase but HCO3- isn't created in the RBC correct? meaning, the bicarbonate ion comes from the plasma? and from the plasma is the equation CO2 + H2O --> HCO3- + H+???

Now, my question is this... when the CO2 leaves the RBC... it won't react with the H2O in the RBC leading to more H+??? Thus, the lack of H+ ions will create a lack of HHb and CO2???? lol, this is making my head spin... and finally all of this will lead to a higher affinity of O2 on Hemeoglobin?

last question... are there anywhere else the H+'s can come from... other than the CO2 + water reaction???

You are awsome and thanks for helping a premed out...
 
last question... are there anywhere else the H+'s can come from... other than the CO2 + water reaction???

Yes. Lactic acid from your muscles will increase body pH. Poorly controlled diabetics will also have excessive acid in their bodies. Certain substances (aspirin, methanol, antifreeze) will contribute to the acid load in your body.

Take home point is: Don't drink antifreeze, kids. Even if it does taste pleasantly peppermint-y. (It supposedly tastes like peppermint schnapps. Don't ask - this is just what I've heard.)

[I'm not even going to ask the inevitable follow-up question. I just wouldn't respect myself if I did.]
 
How did a thread with a simple question (that was answered within 5 seconds in the first two or three posts) turn into a 3-page thread??? :confused:

You are all a bunch of nerds. :p
 
Yes, metabolic acidosis can occur too.

There shouldn't be any limiting reagents in an equilibrium reaction. If you run out of any of the above, you're probably dead. It's probably best to ignore the RBC membrane to understand this material. The ions will move to their required places via transport mechanisms to maintain homeostasis.

BTW CO2 can react with the peptide chain of Hb to also decrease oxygen affinity.

I think that you're making this subject too complicated.

How did a thread with a simple question (that was answered within 5 seconds in the first two or three posts) turn into a 3-page thread??? :confused:

You are all a bunch of nerds. :p

Have I told you that I :love: you lately, baylormed? Let me know if you don't have a Valentine. ;)

Join in the fun!
 
I know this sounds weird... but OK the CO2 in this case is the limiting reagent. meaning the water is in excess and increase in water surely wouldn't cause an increase in H+ (PH)... but, in a wierd way..... it could work that way couldn't it? meaning H2O would actually be the limiting agent and cause higher acid concentrations in the blood.

Ok, and now for this point... the RBC stores the carbonic anhydrase but HCO3- isn't created in the RBC correct? meaning, the bicarbonate ion comes from the plasma? and from the plasma is the equation CO2 + H2O --> HCO3- + H+???

Now, my question is this... when the CO2 leaves the RBC... it won't react with the H2O in the RBC leading to more H+??? Thus, the lack of H+ ions will create a lack of HHb and CO2???? lol, this is making my head spin... and finally all of this will lead to a higher affinity of O2 on Hemeoglobin?

You're thinking about this on a very small, cellular level, and a little too deeply as well. As I've said before, this is not a cardiovascular question. Pulmonology/Renal physiology will teach you much more about arterial blood gases and acid-base balance. (And teach it better too.)

Regulation of the body's pH doesn't occur at the level of the RBC. pH is regulated by the lungs (blowing off CO2) and the kidneys (which produce bicarb).
 
Have I told you that I :love: you lately, baylormed? Let me know if you don't have a Valentine. ;)

Join in the fun!


:D I don't know what to say, I'm very honored. **blushes**
 
How did a thread with a simple question (that was answered within 5 seconds in the first two or three posts) turn into a 3-page thread??? :confused:

You are all a bunch of nerds. :p

Just wait another year - you'll sound just like this, without knowing how it happened.

Please remember: when hanging out with other med students, do NOT do the "walk-by diagnosis" thing. My classmate and I went to the beach last summer, when suddenly he nudges me and says "the guy in the red bathing suit over there? Bell's palsy!" Then, we spent the next five minutes debating whether the woman in the blue bathing suit was just very tanned or had Addison's disease. And, yes, people heard us and gave us weird looks.
 
Just wait another year - you'll sound just like this, without knowing how it happened.

Please remember: when hanging out with other med students, do NOT do the "walk-by diagnosis" thing. My classmate and I went to the beach last summer, when suddenly he nudges me and says "the guy in the red bathing suit over there? Bell's palsy!" Then, we spent the next five minutes debating whether the woman in the blue bathing suit was just very tanned or had Addison's disease. And, yes, people heard us and gave us weird looks.

The younger brother of the politician on Heroes...Bell's Palsy (yes I had that exact conversation two weeks ago).

Wizard = doesn't tell parents that he's in medical school = detached caregivers during childhood, also stuck orally-fixated and exhibits denial and projection as defense mechanisms

In case you haven't seen this...

[YOUTUBE]http://www.youtube.com/watch?v=un4ULrgVYMY[/YOUTUBE]

You will live this scenario as a medical student. I identify with the intimidator.
 
Yes, metabolic acidosis can occur too.

There shouldn't be any limiting reagents in an equilibrium reaction. If you run out of any of the above, you're probably dead. It's probably best to ignore the RBC membrane to understand this material. The ions will move to their required places via transport mechanisms to maintain homeostasis.

BTW CO2 can react with the peptide chain of Hb to also decrease oxygen affinity.

I think that you're making this subject too complicated.



Have I told you that I :love: you lately, baylormed? Let me know if you don't have a Valentine. ;)

Join in the fun!


First thank you so much... the only reason why I called it cardiovascular is because in my examkracker book that is the section the material came up in... Again, I am only dealing with the heart lungs and blood for this section so that is why I was focusing on it so much... LOL that is where the first question came from as well...

Now, I am a Chemistry major so sorry I got a little deep into the subject but Believe me you all helped so much in what you where explaining that I totally get the concepts now... I mean the take home message was that increase of CO2 decreases PH because of the IONS and Carbonic Acid forming.

Lastly, the rate limiting reaction could occur, while yes the reaction is in equalibrium that is only via the reaction mechanism... if more of a substance is available then more amounts of it will be produced to it limiting reagents capacity... Obviously the limiting reagent is CO2 but I was just being a nerd and saying that if you had way too much CO2 and very little water... an actual increase of water would be the main culprit for causing acidosis.... I know I know... LOL I hear the birds chirping but I gotta be able to contribute some braniac knowledge...

Especially for my oh so bad initial question...

Again, thanks this thread was actually productive and I am going to put the important parts in my diary over on the MCAT thread...
 
As well, is that the true reason why we breath harder to expel more CO2 and thus balance out the PH.

Probably an even better answer is to minimize an R/Q missmatch. Because as we exercise, we increase cardiac output, ventilation (R) must increase as well to maintain proper oxygenation. The removal of CO2 is only half of the answer.

g
 
Probably an even better answer is to minimize an R/Q missmatch. Because as we exercise, we increase cardiac output, ventilation (R) must increase as well to maintain proper oxygenation. The removal of CO2 is only half of the answer.

g

Yes, that is probably "why" the body responds in this way, but the true reason is that the central chemoceptors in the brain are very sensitive to change in pH, so if there is an increase in pCO2, pH goes down, and the chemoceptors increase their firing to increase the amount of ventilation to lower the CO2, so at least as far as the brain is concerned, pH (or CO2) is what causes change in ventilation.
There are also peripheral chemoreceptors located close to the heart (I think in the aorta and carotid artery) that are sensitive to change of pO2 in the blood and they also are responsible for affecting ventilation.
 
I agree with you that the central chemorecptors control ventilation. I'm just saying an increase in Q (exercise induced) must be accompanied by an increase in ventilation. It should also be noted that the respiratory system is not the only organ responsible for the control of pH in the exercising person. Since the removal of CO2 in the lungis diffusion limited, and increased Q decreases the amount of time the CO2 can diffusion. Therefore, the remainder of the excess H+ is buffered by bicarb.

G
 
Ok, I just shadowed a heart surgeon again and here is the list of drugs he told me to look up and explain what they do... Now, I looked up each drug and wrote about it... but in the context of actually open heart surgery and why there was a mixture of this drug given at once I am not completley sure. Meaning I understand the individual parts but not the combination per se. I understand the protamine and heparin situation completely. As well, he asked me but I didn't include the retrograde cardiopalagia (spelling I know). I know he said that it is called retrograde because they are putting it through the artieries and not the veins and this was do to the rigidness of the arteries rather than the viens but there was something about the possibility of losing or returning the drug because it was the artieries that I wasn't quit catching. Cardiopalagia I know what it does and we already had that disscusion.... was wondering if you all could elaborate.

Here is what I wrote below...


*************************************

Here is something quick I wrote to the Dr. that I shadowed regarding the experience and / homework he gave me to complete in case I wish to ever shadow him again in the future... check in out and feel free to critique.. i put it in this thread because I know that for the lecture # 7 this short little right up will make it even easier to understand that heart at first. The drug information isn't probably important.

The medications uses yesterday were as follows,

Lidocaine 2% is a local anesthetic agent that affects the neuronal membrane of the tissue it interacts with by inhibiting the ionic fluxes that initiate and conduct impulses.

Verapamil (HCL) is a calcium ion influx inhibitor. Meaning, this drug affects the calcium ion that moves across the cell membrane. First, Verapamil dilates the main coronary arteries and prevents spasm of the coronary artery. This increases myocardial oxygen delivery in patients. As well, A clinical application for this especially in surgery is probably due to the inhibition of calcium ions to move about cell membranes causing an elongated refractory period of the AV node and thus slows AV conduction.

Nitroglycerine (vasodilators) relaxes and dilates peripheral arteries and veins. Dilations of veins promotes peripheral pooling of blood and decreases venous return to the heart. This in coordination reduces left ventricular end diastolic pressure and pulmonary capillary wedge pressure also known as preload. As well, dilatation of coronary arteries also occurs.

Protamine can be an anticoagulant when given alone. As well it is strongly basic. However in the presence of heparin which is very acidic a salt is formed and the anticoagulant activity of both drugs is lost. Neutralization of heparin occurs with 5 minutes after intravenous administration. As a side note the initial Heparin that was used in the first phase was due to the ongoing surgery and necessity of having the patient not coagulate and cause blood clots while being operated on. The Protamine is sort of the turning off switch for when the surgery is being finished and patient needs to again have the ability to coagulate and thus begin the healing process.


As well, the human heart has four chambers. The two upper Atriums and two lower ventricles. The left atrium starts the systemic circulation with leads to a strong push of blood from the left ventricle to the aorta. The aorta branches off to three main parts all leading through the workings of the body. The first artery to branch off is the Brachiocephalic artery, this artery turns immediately into the right subclavian artery and the right common carotid artery. Then the next artery is the left common carotid artery and it is followed by the third artery which is the left subclavian artery. Of course all arteries lead to the pushing of blood away from the heart and veins lead to the return of blood to the heart. the major return repository leading back to the heart is the inferior vena cavae and the superior vena cavae. Two things should be noted about the return of blood to the heart. One there is little to no pressure that is involved in veins and two the oxygen level is completely depleted by the fact the blood has just returned from a grand tour of the body exchanging gases along the way. So as the blood returns to the vena cavae it is deposited into the right ventricle and pushed into the pulmonary system, first the right and left pulmonary arteries which have little or no oxygen, so that it can go into the lungs and collect more oxygen thus returning to the heart again via the pulmonary veins entering into the left atrium and then collecting in the left ventricle. This is known as the pulmonary system.
 
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