Fluid Resusitation?

CWATT

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I feel like the title of this thread is almost an oxymoron. In EMT school we learn to ‘resusitate’ hypotensive patients with fluid because, well... that’s all we had. As Paramedics we have better understandings of underlying physiology and more tools in the toolbox. Someone recently told me they don’t use fluid to ‘resusitate’ patients who are not hypovolemic. This seems like a simple principle; fluid replacement not ‘resusitation’. So the question is, if the hypotension isn’t due to a primary deficit of fluid, why not reach for a pressor (either push-dose or infusion)?

Cardiac — I was recently told a story praising a flight medic for managing a peri-arrest pediatric, cardiac patient by preparing 60ml syringes of saline and administering prn to manage hypotension. Thoguh the Frank-Starling curve does indicate an increase in C/O with increased preload, it’s a parabolic curve and there is a back-side to the slope where fluid-overload actually results in decreased C/O. Moreover, the pediatric population is HR dependent, so why not use push-dose Epi?

Toxins / other — The majority of protocols I see indicate fluid as a first-line treatment for hypotension, usually to the effect of a 20ml/kg bolus PRN. E.g., Calcium-channel blocker OD

Trauma — I know this is going to be a hot-button topic. I actually have a protocol that indictes 500ml saline boluses up to 2L for hypotensive traumatic hemorrhage patients whose bleeding is ‘controlled’ (yes, this includes pelvic fractures). If our goal of therapy for hypotension is to increase perfusion to vital organs and the brain, why are we diluting clotting factors to do so? (My understanding is the counter-argument here is that pressors can’t be ‘turned-off’ immediately).


So fluids, are they the next ‘oxygen’? Rather than every patient getting a bag, should we approach its use as replacement over resusitation or are fluids still our best tool to managing hypotension despite some fairly-well accepted concerns in the setting of trauma?


- C
 
I feel like the title of this thread is almost an oxymoron. In EMT school we learn to ‘resusitate’ hypotensive patients with fluid because, well... that’s all we had. As Paramedics we have better understandings of underlying physiology and more tools in the toolbox. Someone recently told me they don’t use fluid to ‘resusitate’ patients who are not hypovolemic. This seems like a simple principle; fluid replacement not ‘resusitation’. So the question is, if the hypotension isn’t due to a primary deficit of fluid, why not reach for a pressor (either push-dose or infusion)?

Cardiac — I was recently told a story praising a flight medic for managing a peri-arrest pediatric, cardiac patient by preparing 60ml syringes of saline and administering prn to manage hypotension. Thoguh the Frank-Starling curve does indicate an increase in C/O with increased preload, it’s a parabolic curve and there is a back-side to the slope where fluid-overload actually results in decreased C/O. Moreover, the pediatric population is HR dependent, so why not use push-dose Epi?

Toxins / other — The majority of protocols I see indicate fluid as a first-line treatment for hypotension, usually to the effect of a 20ml/kg bolus PRN. E.g., Calcium-channel blocker OD

Trauma — I know this is going to be a hot-button topic. I actually have a protocol that indictes 500ml saline boluses up to 2L for hypotensive traumatic hemorrhage patients whose bleeding is ‘controlled’ (yes, this includes pelvic fractures). If our goal of therapy for hypotension is to increase perfusion to vital organs and the brain, why are we diluting clotting factors to do so? (My understanding is the counter-argument here is that pressors can’t be ‘turned-off’ immediately).


So fluids, are they the next ‘oxygen’? Rather than every patient getting a bag, should we approach its use as replacement over resusitation or are fluids still our best tool to managing hypotension despite some fairly-well accepted concerns in the setting of trauma?


- C
So, you're line of thought is along the right track, but you're dancing around answering your own questions. "Fluid resuscitation" doesn't refer to resuscitating the fluid volume, it refers to resuscitating WITH fluid. Sometimes this is perfectly acceptable. If you are able to measure cardiac output (or any of it's surrogates) you can assess whether or not the patient is fluid responsive. (Reference the passive leg test.)

"Why not reach for a pressor" I'll counter with, "why not reach for fluids?" Unless you know the exact cause of hypoperfusion, fluids probably won't hurt, and like you said, the starlings law does suggest a benefit, to a point. A 500ml bolus is quick and easy. 1 liter also doesn't take too long. Beyond that, especially if you're giving saline, a pressor might be better.
 
(cont...)

As far as sepsis, we already know that these patients benefit from fluids, but also need pressor support.

And trauma/uncontrollable hemorrhage, well, if you're not doing permissive hypotension, then what are you doing.
 
Some of the stuff I've read over the past year or so about sepsis is that while patients do benefit from fluids, it's also only good to a certain point. Same goes for the Early Goal Directed Therapy ideas regarding shotgunning broad-spectrum antibiotics for patients that may not actually need it. Think about influenza... those patients can easily meet Sepsis criteria and since the "bug" is viral... antibiotics aren't going to work, yet we blast 'em with broad-spectrum abx anyway.

I suppose what I'm getting at is that we should really start thinking about what the patient actually needs instead of simply applying a protocol that someone mandated because it worked in a certain set of patients and thought it a good idea to apply more broadly.
 
I suppose what I'm getting at is that we should really start thinking about what the patient actually needs instead of simply applying a protocol that someone mandated because it worked in a certain set of patients and thought it a good idea to apply more broadly.
RT. I can't count the number of times I heard our ED physicians say yesterday "lets just start the sepsis bundle so we don't get dinged" on people who the sepsis bar fired on, even though they obviously weren't septic. It doesn't help the patient, is not good medicine, and may worsen the patient's condition. Not everything is sepsis; a young person with viral symptoms can easily run a low-grade fever and bump up their heart rate from their baseline of 80 to over 100 due to anxiety/flashing lights/white coat syndrome and all of a sudden meet sepsis criteria.

Just yesterday, an ICU midlevel ordered a 30 ml/kg fluid bolus on a lady from a SNF who was hypertensive with a normal lactate and borderline procalcitonin in respiratory distress requiring intermittent BiPAP. Documented history of CHF, BNP of 2800, gave 40 of Lasix earlier, but lets give this fluid bolus because "she meets sepsis criteria". I wonder how that went...
 
RT. I can't count the number of times I heard our ED physicians say yesterday "lets just start the sepsis bundle so we don't get dinged" on people who the sepsis bar fired on, even though they obviously weren't septic. It doesn't help the patient, is not good medicine, and may worsen the patient's condition. Not everything is sepsis; a young person with viral symptoms can easily run a low-grade fever and bump up their heart rate from their baseline of 80 to over 100 due to anxiety/flashing lights/white coat syndrome and all of a sudden meet sepsis criteria.

Just yesterday, an ICU midlevel ordered a 30 ml/kg fluid bolus on a lady from a SNF who was hypertensive with a normal lactate and borderline procalcitonin in respiratory distress requiring intermittent BiPAP. Documented history of CHF, BNP of 2800, gave 40 of Lasix earlier, but lets give this fluid bolus because "she meets sepsis criteria". I wonder how that went...

I’m sure that went swimmingly.
 
So I intentionally didn’t include Sepsis in my original post because those people require both fluids and pressors; the systemic infection causes an initial spike in pro-inflammitory cytokines which increases capillary permeability allowing the plasma to second space into interstitial tissues. Pressors will counterbalance this mechanism but these patients also require fluid replacement. I know there was a time when clinitians attempted ‘fluid resusitation’ but it is now widely accepted that fluids + pressors is the most appropriate treatment.
 
Cardiac — I was recently told a story praising a flight medic for managing a peri-arrest pediatric, cardiac patient by preparing 60ml syringes of saline and administering prn to manage hypotension. Thoguh the Frank-Starling curve does indicate an increase in C/O with increased preload, it’s a parabolic curve and there is a back-side to the slope where fluid-overload actually results in decreased C/O. Moreover, the pediatric population is HR dependent, so why not use push-dose Epi?

Really is situation, or pathophysiology, dependent. Most pediatric patients are not going to be on the downward slope of the curve on presentation. Remember even when patients are grossly volume overloaded they are usually intravascularly euvolemic or even hypovolemic. Push dose Epi may not necessarily be the best option for a patient with severely depressed cardiac function. Pressure does not equal perfusion. These patients have an insanely high SVR already, increasing afterload to maintain a pressure usually decreases CO more than anything else.

"Specifically, in those patients demonstrating signs of cold and dry shock, judicious use of isotonic fluids in 5-10 cc/kg aliquots may be required to augment preload with diligent attention to signs of volume overload such as worsening tachypnea, bibasilar crackles and increasing hepatomegaly. This is necessary prior to the administration of any form of sedation as suboptimal preload may predispose this patient to cardiovascular collapse. However, the opposite holds true for the patient presenting in a wet state, as more volume administration may worsen respiratory symptoms leading to respiratory failure and need for mechanical ventilation."

Awesome article.
https://www.mayoclinic.org/medical-...d-mechanical-circulatory-support/mac-20430722


pediatrics-fig-4-lg.jpg
 
Cardiac — I was recently told a story praising a flight medic for managing a peri-arrest pediatric, cardiac patient by preparing 60ml syringes of saline and administering prn to manage hypotension. Thoguh the Frank-Starling curve does indicate an increase in C/O with increased preload, it’s a parabolic curve and there is a back-side to the slope where fluid-overload actually results in decreased C/O. Moreover, the pediatric population is HR dependent, so why not use push-dose Epi?

Really is situation, or pathophysiology, dependent. Most pediatric patients are not going to be on the downward slope of the curve on presentation. Remember even when patients are grossly volume overloaded they are usually intravascularly euvolemic or even hypovolemic. Push dose Epi may not necessarily be the best option for a patient with severely depressed cardiac function. Pressure does not equal perfusion. These patients have an insanely high SVR already, increasing afterload to maintain a pressure usually decreases CO more than anything else.

"Specifically, in those patients demonstrating signs of cold and dry shock, judicious use of isotonic fluids in 5-10 cc/kg aliquots may be required to augment preload with diligent attention to signs of volume overload such as worsening tachypnea, bibasilar crackles and increasing hepatomegaly. This is necessary prior to the administration of any form of sedation as suboptimal preload may predispose this patient to cardiovascular collapse. However, the opposite holds true for the patient presenting in a wet state, as more volume administration may worsen respiratory symptoms leading to respiratory failure and need for mechanical ventilation."

Keep in mind that most significantly sick kids will present with dehydration in addition to their underlying medical problem. Even when kids start to dehydrate they continue to be very poor at concentrating urine, and it's not uncommon for us to bolus many kids with 60mL/kg (in smaller aliquots of course) before they start to produce urine for us. There are even studies that have shown that there isn't the risk of kidney damage that we used to be concerned for in otherwise healthy kids who are po ad lib and on aggressive maintenance fluids (thus the whole maintenance is 4-2-1 or 10-5-2 less PO thing we used to calculate). Add into this that kids who are sick are probably going to be tachypneic, crying, drooling, sweating, and a variety of other 'insensible' fluid losses that are far greater than in adults proportionally.

Kids can lose stroke volume and pressure independent of heart rate. They tend to tach up before their other hemodynamics change, but that doesn't mean that a kid with a normal heart rate can't drop their pressure or tank their stroke volume. Keep in mind that if kids are not driving up their heart rate we need to be investigating the cause rather than simply trying to remedy with chronotropes. Things I would consider in kids who are bradycardic or not appropriately increasing their heart rates would be hypoxia, neonates who need stimulation or are generally being naughty, being cold, CV anatomy disorders (anomalous coronary arteries, transposition, hypoplastic right hearts, sinal node dysfunction, and so on), toxidromes, or other disease processes. Kids with bradycardia who don't have a obvious etiology deserve a workup not dissimilar to adults; this includs EKGs, trops, chem panels, thyroid levels, toxicology studies, ECHOs, cards consult, and so on.

Also keep in mind that kids especially can present in vasodilatory shock and that being warm does not preclude hypoperfusion nor the need for fluids or pressors.

While I think that there is a time for PDPs, I don't think that peds is one of them. If a kid is so sick to need pressors we should be considering that very carefully (though rapidly) and administering drugs in a very controlled and planned manner.
 
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