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 +1  (nbme22#38)

I understand sleep apnea would cause hypoxia and increase in SNS activity. So treatment would reduce BP and Heart Rate. I was stuck between the two options. Why was the answer blood pressure and not HR? I googled around a bit and found studies that show drop in both HR and BP. I guess BP drops more? Can someone please explain.

madeforupvoting2  CPAP increases intrapleural pressure as the elevated airway pressure is transmitted to other things in the cavity (lung pushes on pleural space/cavity which can then push on other structures). This can lead to compression of veins, including the vena cava -> decreased venous return -> decreased bp (from decreased preload). This is similar to what happens during valsalva (exertion phases) though the positive pressure is provided by a machine pump instead of abdominal muscles/diaphragm. I think heart rate likely increases instead of decrease as a compensatory response. Here’s one site that explains it well (the “free” content is enough and probably already exceeds the depth one might need to know) https://thoracickey.com/extrapulmonary-effects-of-mechanical-ventilation/
apolla24  I guess since changes in HR are such a transient phenomenon and you only have sustained increase in HR when exercising or like acutely experiencing some medical emergency vs BP that can be elevated for long periods of times with no effects. Therefore an improvement in BP is more important. That’s my take.

 +3  (nbme22#45)

Dextro vs Codeine: Both are antitussives, but dextro is more of NMDA agonist that also has opioid agonist activity. Dextro is often abused to get a similar out of body feeling due to its NMDA agonist effect. Codeine on the other other is a full-on opioid agonist. It’s also used as anti-diarrheal, so constipation is very common adverse effect.

Tiotropium is wrong because it’s not an antitussive. Also, it’s an anticholinergic which is (1) contraindicated in elderly unless really indicated, (2) a well-documented anticholinergic effect is constipation.

pparalpha  According to Sketchy and Amboss: dextromethorphan is a weak opioid receptor AGONIST and NMDA receptor ANTAGONIST (it's not an agonist).

Subcomments ...

submitted by gribear(0),

Can someone explain why when you transect the spinal cord superior to the level of sympathetic outflow -- and you get a systemic infection -- the response is alteration of the thermostatic set point?

its_raining_jimbos  So I chose that one because set point is controlled by the hypothalamus (PGE2 and IL-1 mediate fever in the hypothalamus) and the rest of the answer choices involved something below the level that has been transected. Not 100% sure if that’s accurate though. +1  
noselex  Agreed with @its_raining_jimbos -- Fever is mediated by altering set point in hypothalamus. All the other choices, as far as I can tell, involve sympathetic nerves and their effects at target organs. +