hydrostatic pressure in systemic vs pulmonary circulatoin

[aspiringmd1015]

in the pulmonary circuit, w/ hypoxic VC, does taht increase or decrease your hydrostatic pressure? As in the peripheral circulation, arteriolar constricting decreases your hydrostatic pressure(seen in times of hemorrhage, to favor absorption)

---

Members don't see this ad.

 

[Macaroon_Berry]

.

 

[aspiringmd1015]

i think its the opposite, thats why you give acetazolamide in pts w/mountain sickness, bc itll get rid of the fluid, apparently due to hypoxic vc and bc of their resp alkalosis getting rid of bicarb.

 

[aspiringmd1015]

Another question: so hypoxic VC is due to low PA02. Apparently in Dead space like conditions like PE, giving supplemental 02 will relieve the hypoxemia, but what i dont understand is, why is there hypoxic VC in PE, when the PA02(alveolar 02) should be normal? the patient's ventilation isnt the issue, the perfusion is, so how would he get hypoxic vasoconstriction?

 

[Macaroon_Berry]

Hmm I'm not sure actually, I just googled it and it seems like hypoxic pulmonary VC does lead to pulmonary edema so there would be increased hydrostatic pressure.. not sure how though..

 

[RnaPolymerase2]

V/Q mismatch in PE is perfusion defect no blood gas exchange decrease blood flow to lungs. This leads to pulmonary hypoxemia which means not enough O2 in blood circulation and peripheral chemoreceptors stimulate and increase alveolar ventilation rate and overtime alveolar O2 is decreased . Remember PE symptoms is shortness of breath especially when active, which leads to hypoxic constriction and increasing lung arterioles resistance and leading to pulmonary HTN.

 

[aspiringmd1015]

increasing alveolar ventilation shouldnt decrease your PA02?

 

[Phloston]

in the pulmonary circuit, w/ hypoxic VC, does taht increase or decrease your hydrostatic pressure? As in the peripheral circulation, arteriolar constricting decreases your hydrostatic pressure(seen in times of hemorrhage, to favor absorption)

Right heart failure secondary to pulmonary arteriolar congestion is due to increased fluid pressure. So yeah it's hydrostatic. That's why you'd get peripheral edema if your right heart fails; that's hydrostatic.

 

[Phloston]

Another question: so hypoxic VC is due to low PA02. Apparently in Dead space like conditions like PE, giving supplemental 02 will relieve the hypoxemia, but what i dont understand is, why is there hypoxic VC in PE, when the PA02(alveolar 02) should be normal? the patient's ventilation isnt the issue, the perfusion is, so how would he get hypoxic vasoconstriction?

You'll vasoconstrict in the lung in a PE probably in response to the trauma it causes. Vasoconstriction is a normal response to trauma. If you lodge a massive embolus there, you're going to get fluid leaking out proximally that will affect local O2 diffusion.

 

[aspiringmd1015]

i see, the reason why im asking is because, they mentioned in i think DIT that w/ a dead space like condition in a V/Q mismatch like PE, you can give supplemental 02, and that WILL increase the patients pa02/relieve the patients hypoxemia, bc of the a/c Hypoxic vasoconstriction thats occuring in dead space like conditions, which doesnt make sense to me bc in dead space like conditions your PA02 is normal, even higher actually a/c to BRS at 150 mmgh instead of 100, so i thought theres no way that would cause VC, bc PAc02 controls Hypoxic VC in the lungs.

 

[Phloston]

i see, the reason why im asking is because, they mentioned in i think DIT that w/ a dead space like condition in a V/Q mismatch like PE, you can give supplemental 02, and that WILL increase the patients pa02/relieve the patients hypoxemia, bc of the a/c Hypoxic vasoconstriction thats occuring in dead space like conditions, which doesnt make sense to me bc in dead space like conditions your PA02 is normal, even higher actually a/c to BRS at 150 mmgh instead of 100, so i thought theres no way that would cause VC, bc PAc02 controls Hypoxic VC in the lungs.

With any lung pathology the parenchyma is going to attempt to close off perfusion to problem areas. Whether supplemental O2 works or not just depends on how bad the problem is. Once the problem becomes bad enough and additional O2 doesn't allow for the net alevolar O2 to adequately sustain arterial O2, it's considered a shunt pathology. Decreased ventilation though generally implies that externally administered O2 will be useless because it can't reach the alveolar capillary beds anyway. But any lung-based pathology could technically cause a shunt.

 

[aspiringmd1015]

okay cool, thanks pholston. Also, a UW question stated that a pt w/hypothermia looks blue bc he has a left shifted curve, so more 02 attatched to HB and less to tissue's, but FA states that you become cyanotic when your hb conc becomes >5g/dl. So im clearly missing something here