understanding PPV

[Bubu91]

hello! i ve been reading a lot about ppv the past few days and i have some question regarding it 🙂

1. from what i understood, a high ppv (>13%) means that the patient is hypovolemic AND fluid responsive?

2. the hypovolemic part kinda confuses me because everywhere i ve read it says that high ppv is seen in patients that are hypovolemic, BUT the same article also states that there are patients that have sepsis (distributive hypovolemia) and have a LOW ppv!

what i m trying to say is that can you have a patient that is hypovolemic, with a low ppv? which would mean that he is just not fluid responsive because the ppv is low, and the diagnostic of hypovolemia has to be done with other parameters (urine output etc.)

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[Bubu91]

another way to put my question:
say i have a patient that is hypovolemic, but with a diseased heart aka low ejection fraction that is incapable of increasing it s stroke volume. will this patient have a low ppv because he is on the flat portion of the starling curve? or will he have a high ppv because he is hypovolemic?

 

[engineeredout]

1. from what i understood, a high ppv (>13%) means that the patient is hypovolemic AND fluid responsive?

Short answer, no and no.

Slightly Longer answer: Looking at PPV/SVV/SVI/CVP or any other static variable in isolation is not useful to obtain meaningful clinical outcomes. Saying "The Patient's PPV is 20% therefore they need more fluid" is not likely to get you the answer you want. The patient may require additional fluid, or they may not and the additional fluid may very well be not only useless, but actually harmful. If you are looking for "fluid responsiveness" which is loosely defined as having an increase in cardiac output for a given increase in fluid (IE they are still on the upward portion of the starling curve) then you require dynamic variables, AKA changes over time, to assess that. How has your PPV changed after a fluid bolus. Did it improve? Maybe you could consider them "fluid responsive" in that case. If it hasn't, more fluid probably won't do much, despite whether or not you think the patient is hypovolemic based on PPV alone.

More complicated thinking: Is fluid responsiveness even a clinically meaningful outcome?



Static vs dynamic reasoning can be applied to virtually everything. You have a patient with a lactic acid level of 4.0. Are they getting better or worse? No idea. If their previous lactate was 8.5, you might be feeling okay about their resuscitation. If their previous was 3.8, they got 5L of fluid per CMS and are on levophed, you might want to be concerned that their resuscitation isn't going well. What does a creatinine of 2 tell you without any before or after values? Troponin of .16? Etc...


For more extended answers, I'll direct you to more eloquent explanations behind the use of static variables to predict dynamic results:

PulmCrit- Why we fail at hemodynamics: The flaw of averages & the swan's curse

 

[Hamhock]

Short answer, no and no.

Slightly Longer answer: Looking at PPV/SVV/SVI/CVP or any other static variable

PPV and SVV are NOT static variables.
They are dynamic measures part of functional hemodynamic monitoring.

HH

 

[engineeredout]

PPV and SVV are NOT static variables.
They are dynamic measures part of functional hemodynamic monitoring.

HH

I meant the interpretation of them as static variables is what people end up doing which is not useful, IE looking at a PPV of 20 in isolation is not as helpful as where those numbers go over time with various interventions. I get that by definition PPV/SVV are derived over a certain timeframe/# of cardiac cycles

 

[MarionLampkin]

exactly

 

[drmwvr]

PPV taken out of the context of MAP isn't useful. If the MAP is too low and there is significant PPV and if you fix it with volume, you have your answer. That doesn't mean you have fixed end organ perfusion problems, it just means you raised the MAP and made the PPV go away for a while.