Hemodynamics question

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I'm a student, of course, and here goes... (thanks to the smart nurse who helps)

Why is afterload increased in cardiogenic shock? I understand the preload, but If blood volume is increased in the heart, and systemic blood pressure is decreased, along with decreased MAP, how can afterload be elevated?

THANKS THANKS THANKS :)

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Specializes in ICUs, Tele, etc..

Hello....Someone's gonna come along and answer this in more detail or will give you a different thread that will show you what happens, there's a thread about CHF, and one of the members who grumbles grumbles(j/k) answered this question very very nicely. But here's a short answer till u find it, you know that the preload is increased because the pump is inadequately pumping....this leads to a decrease in cardiac output becuz ur heart is not pumping well, which would lead to INADEQUATE TISSUE PERFUSION, which is the mainstay definition of shock basically, now the body is gonna try to compensate the underperfusion of the organs leading to ''clamping'' of the vascular system which leads to INCREASED SVR. May it be because of the Renin Angiotensin System, that's why you can have a Cardiogenic shock with bp that is not terribly bad, but then the body is not able to compensate any longer when the heart continues to function the way it is, soooo it becomes a cycle, the SVR will go higher and higher because of the decreased C.O. and in turn the C.O. would continue to go down without intervention because of the SVR getting higher and higher, thus precipitating a cycle that needs to be broken. Hope it helps a little bit.

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Thank you soooo much.

One quick question

Isnt the periphery vasodilated after the short vasoconstriction (compensation)?

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Specializes in ICUs, Tele, etc..

hello, r u asking what happens when it fails? does svr fall down and lead to vasodilation? is that what ur asking? I'm not sure if that is ur question, but the problem with Cardiogenic Shock is the body doesn't know when to stop ''trying'' to compensate to help itself. Anyways here's a really good link kinda extensive on management of Cardiogenic shock/AHF, including hemodynamic parameters and how to handle it, all ur questions will be answered here....

http://www.guideline.gov/summary/summary.aspx?view_id=1&doc_id=6817

hope that helps....hrtprncss

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Hey Y'all

I got put on-call tonight, wound up here. Thanks for the question and right-on the answers from hrtprncss. It does seem contrary to reason that the body would have a mechanism built-in to make it HARDER for the heart to work just at the moment when it's really sick, doesn't it.

You asked about 'afterload' and the (exactly right-on answer) was about SVR and you indicated that you understood they were the same thing. And of course they are different descriptions of ARTERIOLES. That's the part of the body that's constricting onto the blood inside themselves and essentially squeezing the blood out of non-essential organs and major skeletal muscles.

The chemical that the body uses to do this is ADRENALIN. The ol' fight-or-flight hormone.

The meds we give work on the tension of those arterioles: NitroGlycerin/'Tridil' or (rarely) Nitroprusside/'Nipride'. It seems contradictory to be giving these drugs to people that sometimes have pretty low BPs to start with--but that's what Drs Swan and Ganz gave us their catheter for.

So we could 'juggle' our critical patients between pressor drugs (Dobutamine is I think still the drug-of-choice) and dilater drugs. The pressors cause the heart to work harder than it "wants" to--the vaso-dilators make the work easier. So the whole business of "being a pump" is easier.

How'd the body play such a rotten trick, anyhow? Remember that as an evolutionary process, we didn't develope mechanisms to protect us from MI's.

Our predecessors prob'ly had FABULOUS coronary arteries--as you would if you had to chase down and kill every bit of meat you ate.

The body was "taught" by evolution to protect us from dying of TRAUMA. So the body "thinks" that any low-blood-pressure emergency is because we're bleeding. So it "tries" to stem the blood loss by vaso-constricting non-essential aterioles and shunting the blood to vital organs and skeletal muscle.

This really works, by the way, when the problem is getting bit by a gator or gored by a Toyota. But it obviously works against the heart. So the BP gets even lower, right? That's the line of thought that made you ask the question in the first place, right? You saw that the BP going lower makes the arterioles squeeze harder ("thinking" that the bleeding must be really bad!) and the heart gets weaker and the BP goes down and ring-around-the-roses. Thats a 'positive feedback loop' and they are always BAD FOR YOU.

We have to measure the strength of this vasodilation (as elevated SystemicVascularResistance), think critically about it (as 'afterload') and make minute by minute adjustments to it with our IV drugs and break that feedback loop. We actually can GRAB CONTROL OF THE HUMAN BODY!!!! Is that cool or what!!??

Papaw John

PS edit edit...a web site I found about CHF/CardioGenic Shock etc (thousands of links--I didn't look at 'em)

http://www.en/medical.com/article/000158.html

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I'm a student, of course, and here goes... (thanks to the smart nurse who helps)

Why is afterload increased in cardiogenic shock? I understand the preload, but If blood volume is increased in the heart, and systemic blood pressure is decreased, along with decreased MAP, how can afterload be elevated?

THANKS THANKS THANKS :)

You may already have the answer but this might help

http://scalpel.stanford.edu/articles/Cardiogenic%20Shock.pdf

30_003.jpg

Mike

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Yes, thats what I'm asking. I may be confused in thinking that the compensation is only breif. Does the compensation ever fail, and the periphery vasodilate? I think I'm just getting a mind block here. Thanks for your awesome anwers and for taking the time to help!

:balloons:

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Specializes in ICUs, Tele, etc..

Hello again compensation does fail and you know when it fails because it leads to hypotension. Now in regards to your question it would be better answered when you're talking about septic shock. In high output states secondary to an underlying infection, several compensatory mechanisms come into place. Compensatory mechanisms though comes to a point where it's not enough, leading to massive vasodilation of the peripheries and subsequent hypotension...This is when pharmacologic techniques needs to be instituted.

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Specializes in ICUs, Tele, etc..

I should point out that compensatory mechanisms in distributive shock like septic shock is usually an increase in heart rate and stroke volume. Leading to high output states to try to perfuse the organs. But if you see that your patient is still hypotensive that could mean that either there is massive vasodilation going on, or the compensatory response that the heart is just not enough....does that make sense?

hrtprncss

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Ok, I've got it now.

I think I was trying to simulate cardiogenic shock with all other types. Your answer is EXACTLY what I needed to hear. It's no wonder that my second question was confusing. Thank you sooooo much!

My first clinical is tomorrow in CCSD. Wish me luck!

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Specializes in ICUs, Tele, etc..

Good luck on your clinicals:) hope everything works out for you in school....

hrtprncss

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HELP!!!!!! I just had a six hour class today on hemodynamic monitoring for my Critical care rotation and I am very confused.....

How do I tell if the patient is in Cardiogenic, Septic, or Hypovolemic shock by their numbers on the monitor????

Can anyone help with this or am I being to vague????

Sherry :confused:

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