Cardio in FA 2012

[swamprat]

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Pg 284:

Bedside maneuvers:

Rapid squatting increases venous return and afterload -> Is that because when you squat your muscles contract (skeletal muscle pump) pushing blood out of the veins into the heart kinda like when you exercise? If so, why do you get a increase in afterload? Is that because there is back flow to the arterial side from the veins or because of the increased volume due to a shift from unstressed volume -> stressed volume?

And if thats the case then why does valsalva which decreases venous return (i understand why) not cause a decrease in afterload?

And whats the deal with this hand grip?

 

[MrBeauregard]

Rapid squatting increases venous return and afterload -> Is that because when you squat your muscles contract (skeletal muscle pump) pushing blood out of the veins into the heart kinda like when you exercise? If so, why do you get a increase in afterload? Is that because there is back flow to the arterial side from the veins or because of the increased volume due to a shift from unstressed volume -> stressed volume?

Determinants:
Preload: venous return
Afterload: SVR

Squatting will increase venous return through muscular pump to the heart while also increasing SVR (through the mechanical compression of peripheral resistance arterioles) to increase afterload.

And if thats the case then why does valsalva which decreases venous return (i understand why) not cause a decrease in afterload?

Valsalva increases intrathoracic pressure which decreases venous return to the heart, thus decreasing preload. There is no effect on peripheral resistance arterioles and thus afterload is not affected.

And whats the deal with this hand grip?

Hand grip results in compression of peripheral resistance arterioles and mimics an increase in SVR which then increases afterload. Since the majority of your blood volume is not located in your forearms/hands, contraction will not increase venous return (as it would with squatting).

Someone correct me if I'm wrong.

 

[swamprat]

Thanks that all makes good enough sense for me. One more physio question now that I'm on it: FA 2012 pg 566 V/Q Mistmatch Oxygen therapy.

If V/Q -> 0 meaning you blocked some ventilation by swallowing a peanut lets say, oxygen will not improve PO2.

V/Q -> infinite due to PE, oxygen improves PO2.

Is my reasoning correct in that the PE will allow blood to find another way to see air so you don't have any wasted perfusion just ventilation and that on the arterial side of things you wouldn't have an increase in CO2. Likeware if you have a ventilation blockage the blood passing through the unventilated area will increase the CO2 content of the arterial side and never get a chance to see oxygen so oxygen won't help?

My only confusion to this logic is that if you have an obstruction in a bronchi wouldn't the capillaries constrict shunting blood flow elsewhere to see the oxygen ur delivering.. even though oxygen is perfusion limited the blood would all still be seeing oxygen and a higher concentration of it too.

 

[Morsetlis]

Thanks that all makes good enough sense for me. One more physio question now that I'm on it: FA 2012 pg 566 V/Q Mistmatch Oxygen therapy.

If V/Q -> 0 meaning you blocked some ventilation by swallowing a peanut lets say, oxygen will not improve PO2.

V/Q -> infinite due to PE, oxygen improves PO2.

Is my reasoning correct in that the PE will allow blood to find another way to see air so you don't have any wasted perfusion just ventilation and that on the arterial side of things you wouldn't have an increase in CO2. Likeware if you have a ventilation blockage the blood passing through the unventilated area will increase the CO2 content of the arterial side and never get a chance to see oxygen so oxygen won't help?

My only confusion to this logic is that if you have an obstruction in a bronchi wouldn't the capillaries constrict shunting blood flow elsewhere to see the oxygen ur delivering.. even though oxygen is perfusion limited the blood would all still be seeing oxygen and a higher concentration of it too.

V/Q -> infinite due to pulmonary embolism would NOT be refractory to O2 (the un-oxygenated, un-ventilated blood is dumped back into the system as a physiological shunt), UNLESS it's a small PE and there is blood being rerouted through hypoxic vasoconstriction. If that is the case, you may as well say that the lung is resistant to PE's (which it is, for small ones). But, the lung does not fix itself all the time. And, when it doesn't, you CANNOT fix it through O2 therapy (well, you're going to give them O2 therapy anyway, but that's not the point).

Even though blood may see a higher concentration of oxygen, equal amounts of blood seeing proportionally higher V does NOT compensate for equal amounts of blood seeing proportionally lower V, due to saturation of Hb (this is true, though, for CO2 because of carbonic anhydrase).

 

[Convalaria]

sorry for off-topic, but still speaking about FA and CV system, could someone share thoughts on my thread - http://forums.studentdoctor.net/showthread.php?t=911254

thanks in advance!