Help with anaphylaxis

I don't really understand what you mean by why doesn't "vasodilation cause an increase of BP at the vital organs", but if you have vasodilation then the vessels are relaxed.. and are wider (that's how I picture it in my head) so that the pressure on the vessel walls is decreased.. thus resulting in a lower BP measurement..

I'm not sure if I helped any... :/

I don't really understand what you mean by why doesn't "vasodilation cause an increase of BP at the vital organs", but if you have vasodilation then the vessels are relaxed.. and are wider (that's how I picture it in my head) so that the pressure on the vessel walls is decreased.. thus resulting in a lower BP measurement..

I'm not sure if I helped any... :/

I know I sound a bit confusing, because I do not quite know how ot explain what I mean, but what i really want to know is actually the mechanism of vasodilation and vasoconstriction on the blood pressure. i know constriction increases BP and dilation deceases..but i want to know why? or rather how?

But thanks i get what u said so far:)

Cardiac Output

Scroll about midway down the page on the above link. All I did was google it. Still, it is a nice straightforward explanation (IMO).

Thank you so much! That script explains a lot! :yeah:have a nice day!

Just another question: why would you restrict fluid and Sodium in the diet of a patient with renal failure?

Anaphylactic shock is a type of distributive shock, along with neurogenic and septic shock. In distributive shock states, you have widespread vasodilation. In anaphylactic shock, your patients will look like this:

HR: increased

preload: decreased (preload is your volume)

cardiac output/cardiac index: decreased

afterload: decreased (this includes your systemic vascular resistant - increasing or decreasing afterload affects the vessels. if afterload is decreased that means your blood vessels are dilated therefore you have a drop in BP)

As for why there is no increase in BP to vital organs, think back to the four stages of shock:

1. Initial stage - basically little or no symptoms - you might have some rise in lactate (>2 is bad!)

2. Compensatory stage - this is when your compensatory mechanisms (epinephrine and norepinephrine to increase HR & BP along with the renin-angiotensin-aldosterone system (RAAS) to also help with that). This is the stage that will cause in increase in BP. You will have decreasing urine output, decreased bowel sounds and pale skin due to vasoconstriction (blood going to the vital organs - even though the kidneys are "vital" they aren't included!). You may have some changes in LOC.

3. Progressive stage - this is the decompensation phase, where your compensatory mechanisms begin to fail. HR is still elevated but BP begins to drop, oliguria progresses to anuria, no bowel sounds, skin will continue to be pale and may feel cold/clammy, you will continue to have changes in LOC. lactate will continue to rise.

4. Refractory stage - death is imminent; organs begin to fail due to prolonged hypoxia.

Hope this helps :redbeathe

Just another question: why would you restrict fluid and Sodium in the diet of a patient with renal failure?

With renal failure, you have a decrease in UO because your kidneys aren't functioning properly. This leads to holding fluid on board - you're not eliminating anything. Water follows sodium - it causes fluid retention. If you already have a lot of fluid on board, eating foods high in sodium and drinking a lot of fluids will cause you retain even more fluid. You also need to be careful with potassium because it can begin to build up when your kidneys aren't functioning well. Potassium levels that are too high or too low can cause cardiac dysrhythmias, sometimes lethal. Hope this helps.

Anaphylactic shock is a type of distributive shock, along with neurogenic and septic shock. In distributive shock states, you have widespread vasodilation. In anaphylactic shock, your patients will look like this:

HR: increased

preload: decreased (preload is your volume)

cardiac output/cardiac index: decreased

afterload: decreased (this includes your systemic vascular resistant - increasing or decreasing afterload affects the vessels. if afterload is decreased that means your blood vessels are dilated therefore you have a drop in BP)

As for why there is no increase in BP to vital organs, think back to the four stages of shock:

1. Initial stage - basically little or no symptoms - you might have some rise in lactate (>2 is bad!)

2. Compensatory stage - this is when your compensatory mechanisms (epinephrine and norepinephrine to increase HR & BP along with the renin-angiotensin-aldosterone system (RAAS) to also help with that). This is the stage that will cause in increase in BP. You will have decreasing urine output, decreased bowel sounds and pale skin due to vasoconstriction (blood going to the vital organs - even though the kidneys are "vital" they aren't included!). You may have some changes in LOC.

3. Progressive stage - this is the decompensation phase, where your compensatory mechanisms begin to fail. HR is still elevated but BP begins to drop, oliguria progresses to anuria, no bowel sounds, skin will continue to be pale and may feel cold/clammy, you will continue to have changes in LOC. lactate will continue to rise.

4. Refractory stage - death is imminent; organs begin to fail due to prolonged hypoxia.

Hope this helps :redbeathe

This helped me a lot!! It explains all I needed to know..and they actually asked the RAAS system also in our xam! Thanks a lot!