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Non-promotional medical education provided as a service to Baxter customers, not intended to be reproduced without the prior written permission of Baxter Healthcare Corporation.
Fluid management education and resources
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Time to read: 2 minutes 22 seconds
What is a dynamic assessment?
A simple way to think about a dynamic assessment of fluid responsiveness is this: challenge the heart with a small amount of fluid, and then observe the heart’s response to that fluid in real time.
There are different ways to assess volume/fluid responsiveness so for today, let’s talk about a dynamic assessment using stroke volume index.
There are two ways to perform a dynamic assessment using SVI: a passive leg raise (PLR) or a rapid IV bolus (250mL administered in 5 minutes or less – OR – 500mL administered in 10 minutes or less).
Essentially, there are three steps to a dynamic assessment.
1. Obtain a Baseline: Measure stroke volume index continuously for 3 minutes with HOB at 45 degrees for a passive leg raise (PLR) or pt. resting in any position for a Bolus.
2. Challenge the heart: Give the heart back a little bit of fluid rapidly. This is accomplished by raising the legs and wedging them at a 45-degree angle after the HOB is in a flat position (PLR) or by giving a small amount of IV fluid (Bolus) rapidly.
3. Look for SVI change: Measure the stroke volume index (SVI) in response to the PLR or Bolus. Did the stroke volume index climb? Stay the same? Go down?
What do the results mean?
A stroke volume index that goes up by 10% or more from the baseline during/after a dynamic assessment indicates the patient is fluid responsive and they are likely to increase their cardiac output in response to a bolus of 500mL of fluid.
A stroke volume index that does not go up by 10% or more indicates the patient is not currently fluid responsive and this should raise questions about the value of further fluid at that time for that patient.
Dynamic assessments help determine if a patient’s cardiac output will increase in response to further fluid. However, it is important to remember that fluid responsiveness is well, fluid. A patient who is not fluid responsive at 1000 for example, may become fluid responsive at 1200.
More on that another time.
May our hearts stay responsive,
Stephanie Griffeth, MSN RN CCRN
Citations for the above summary of a dynamic assessment are here:
Pharmacodynamic Analysis of a Fluid Challenge - PubMed (nih.gov)
What is a fluid challenge? - PubMed (nih.gov)
US_MedDel_2024-0016_ME_V1.0
Time to read: 1 minute 20 seconds
Raising the legs in an average sized adult returns roughly 250cc of blood from the venous capacitance system back to the heart, very quickly.
What is remarkable is that a passive leg raise is highly predictive of how the heart will function in response to further fluid.
If a patient has a 10% or greater rise in stroke volume from their baseline during a PLR, they are considered “fluid” or “volume responsive.”
Simply sitting the patient back up redistributes their blood flow back to their legs with no extraneous fluid given.
It is, as one of my ICU nurse educators says, the only “bolus you can take back.”
The PLR has been well studied and is confirmed to be an excellent diagnostic test with a sensitivity of 88% and a specificity of 92%.
That means as a diagnostic test, it is on par with troponin.
A passive leg raise is an excellent way to determine if fluid will be effective for your patient (or not) at that time. (See the FRESH trial for results that showed patients move in and out of fluid responsiveness).
Reversible, noninvasive, and easy to perform in spontaneously breathing (or intubated) patients when looking at stroke volume index percent change, it is a diagnostic test you can use as often as you can find legs to lift.
May our hearts stay responsive,
Stephanie Griffeth, MSN RN CCRN
For further reading on the PLR, consider these articles:
Will this hemodynamically unstable patient respond to a bolus of intravenous fluids
Passive leg raising for predicting fluid responsiveness: a systematic review and meta-analysis
US_MedDel_2024-0016_ME_V1.0
Time to read: 1 minute 12 seconds
Hypotension is an undesirable physiologic state of being we want to correct swiftly in our patients. Physicians and Providers the world over are consistently faced with the question of whether or not to give fluids in the face of hypotension. Furthermore, if fluids are decided upon, an additional question arises: how much fluid do we give?
Could Occam’s Razor - the problem-solving principle that essentially states the simplest solution is usually the correct one - help us when deciding between whether to give fluid or not?
The literature suggests the answer to that could be a resounding yes.
However, in the case of ‘to give fluid or not to give fluid’ when hypotension occurs, the simplest explanation is actually a question: Is my patient fluid responsive, or not?
Whether you agree or disagree, here is a small bite of further reading on the subject for clinical grist:
May our hearts stay responsive,
Stephanie Griffeth, MSN RN CCRN
US_MedDel_2024-0016_ME_V1.0
Time to read: 1 minute 29 seconds
Before we give insulin, we check a blood sugar. Before we give labetalol, we check heart rate and blood pressure. Before we give Tylenol, we check a temperature (and maybe some LFTs but that’s another lecture).
Before we give fluid, we look at blood pressure. This is standard practice, and I have yet to read a study (or take an order) that removes blood pressure from the treatment equation of the ill, critical or otherwise. I think any of us would find such a suggestion silly.
But I do think, as with anything, there are limitations to only (or mostly only) looking at blood pressure as an indicator of a worsening or developing perfusion problem.
Here’s why: the challenge with blood pressure, is the resilience of it. Our bodies are so wired to live, that they will compensate until they crash. So by the time we see a low blood pressure, we know that the body has already been compensating for an indeterminate length of time. We also know from the literature, that blood pressure is one of the last perfusion markers to change when hypoperfusion is present in the body.
So blood pressure changes near last, but we look at it first. No one is suggesting we stop this, but I do wonder if there is room to add to our practice additional perfusion parameters that change ahead of blood pressure? Of course, I am talking about monitoring stroke volume, but also respiratory rate and heart rate.
At the risk of being rudimentary, more on those parameters next week.
May our hearts stay responsive,
Stephanie Griffeth, MSN RN CCRN
P.S. – For further reading, see Convertino’s bleeding simulation study here: https://pubmed.ncbi.nlm.nih.gov/15182742/
US_MedDel_2024-0016_ME_V1.0
Time to read: 2 minutes 14 seconds
In 1944 the Lancet published a study wherein a group of Irish medical students were bled, until they fainted. (I’ll just leave that there and move on for the sake of time).
Their cardiac output, heart rate, blood pressure, and vascular resistance were monitored during the time they were well, deliberately being exsanguinated. Their bleeding is where we pick up the discussion from last week about the challenge with monitoring blood pressure as a primary indicator of perfusion status.
What this study demonstrated (other than what it was like to go to medical school in 1944) was unsurprising on the face of it for those of us in 2024. Our physiology has not changed, and this study has since been replicated with lower body negative pressure suits which are not as interesting but certainly safer.
Cardiac output began to fall immediately and continued to fall without rebounding until reperfusion efforts were started, heart rate began to climb immediately, as did the systemic vascular resistance which we would expect due to our built-in compensatory mechanisms that make our bodies innately resilient.
Now onto the primary point: blood pressure remained steady, until the volunteers fainted.
Stroke volume was not monitored but I submit to you that if the formula for cardiac output is heart rate multiplied by stroke volume, then a rising heart rate automatically mitigates the fall of cardiac output. Therefore, stroke volume (being less affected by heart rate), would have fallen at an even steeper rate than cardiac output.
Stroke volume then, can help you see around the corner on blood pressure as it changes first, ahead of our other vitals.
However, we do not currently monitor stroke volume on every patient. We can then look to heart rate and respiratory rate, knowing that tachycardia and tachypnea occur well before systolic blood pressure begins to fall in the presence of a perfusion deficit. There are a multitude of studies on the value of monitoring respiratory rate early and often, but the biggest challenge with this – and I can say this as a nurse – is getting nurses to count respirations ;). Then again, we all know that sometimes the simplest things, are the hardest to implement.
May our hearts stay responsive,
Stephanie Griffeth, MSN RN CCRN
P.S. – The bleeding study can be found here: https://www.sciencedirect.com/science/article/abs/pii/S0140673600741730
US_MedDel_2024-0016_ME_V1.0