bri.mcelveen

Ok. So I think it's all coming together, and yes, I do have a strong tendency to overthink things. ONe last clarification: I know that the medulla mediates breathing control. I understand that hypoxia is the drive for a COPD patient to breathe and they can't receive high amounts of O2 or that will decrease the drive. However, in my lecture my instructor stated that in a normal patient, with no issues, that the drive to breathe is high CO2 levels. She said "when we breathe in O2, it travels to the alveoli and is exchanged for the CO2, and then is exhaled and cycle of ventilation is repeated". So when she says "high CO2 level" she means that moment where the O2 and CO2 are exchanged? And at that point, the medulla senses that higher amount of CO2 which makes us exhale it and then breathe in more O2? In a nutshell, I jut need to understand the need/drive for normal person to breathe. Thanks guys!! O2 exam this Friday. Last one of the semester and I wanna rock it! Bri

I understand that COPD is a combination of emphysema and bronchitis. However, I'm trying to piece together a couple things from my lecture. Bronchitis' main component is thick sputum with coughing (productive). Emphysema's main component is air trapped in alveoli resulting in hyperinflation of the lungs. One symptom noted is NON-productive cough. If one has COPD, it stands to reason that both of the aforementioned components would be visible/assessable on a patient. Since a person can have either of these conditions as a stand alone diagnosis, I'm an looking now at emphysema by itself. My powerpoint from school states "inflammation of bronchioles and excessive mucus". Since it's Sunday, I wont get an answer from my instructor until tomorrow. So my question is, is it possible that an emphysema patient can have mucus accumulation with a NON-productive cough and will emphysema affect the bronchioles? So much focus was placed on "air trapped in alveoli" that I am wondering if this is a misprint in the notes. Thanks!

I'm in my second level of nursing school and we are studying perfusion. I know I am going way too deep into the mechanics here, but I am the type of learner that i have to see the ENTIRE puzzle in order to understand the concept. Unfortunately, I'm missing a few of the puzzle pieces and need some plain and simple explanations. While I understand the technical definitions of these words "preload" and "afterload", I am having trouble with the concepts of "which comes first?" and "how does one affect the other". I know that afterload is the pressure that the heart has to beat against in order to eject blood from the left ventricle. The way I see it, if the afterload is high due to obstruction or vasoconstriction, then the preload will be lower b/c cardiac output is decreased due to said obstruction or narrowing and less blood is returning upon venous return. If afterload is normal then preload will be normal as CO adequate to get the blood through the body and back to the heart. If afterload is low b/c of excess vasodilation or decreased pressure and there's not a large amount of pressure to pump against, then the preload could then be too high b/c more blood is filling the heart upon venous return. Now my actual question: how do each of these affect each other? Will low preload cause high or low afterload and will high preload cause high or low afterload? Will high afterload cause low or high preload and will low afterload cause low or high preload? As previously mentioned, I'm sure I'm making this much harder than necessary but I just need a little explanation in "scenario" form to make the puzzle pieces fall into place. Thanks!