# Possible Sepsis



## shademt

Arrive on scene for a c/c of high temp. You find the patient semi-Fowler with a N/C set at 6 LPM. B/P is 58/38, HR is 130, RR is 58, and temp 103.5. After being placed on NRB at 15 LPM, no change in RR. How do you treat taking into consideration the low BP with high RR?


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## Wes

At the EMT level without ALS support, PUHA (Pick Up Haul A**) comes to mind.  Get a good assessment in.  What are lung sounds like?   Is pneumonia with sepsis your differential?   I'd think about assisting ventilations with a BVM.

Paramedic level, this guy needs to be on a monitor and definitely needs fluids.  Large bore IV access.   Possibly even considering pressors, especially if you're familiar with early goal directed therapy for sepsis.


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## Anjel

Was the patient anxious? Could you possibly coax them enough to let you try to assist ventilations?  Like Wes said pick up and haul *** to the nearest ALS crew or hospital.

They need fluids, antibiotics, and if they can't get the pressure up and RR down, the pt will need an advanced airway. CPAP really isn't an option with that low of a BP. The pt is going to get tired pretty quick, when breathing once almost every second.


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## Wes

If allowed, I'd seriously consider RSI for this patient.   As an added benefit, we use Ketamine for our induction agent.  Ketamine's hypertensive and bronchodilatory effects would be ideal for this patient.


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## TransportJockey

Nasal tube might be a good choice in this patient... And then if they will tolerate it, sedate them to maintain bag compliance. But this patient would get 2 large bore lines running wide open, possibly pressors, and ventilator assistance. We get to do this often due to having some piss poor rural SNFs in our response area. 

One other thing (lol w/ recent threads, I'm hesitant to say this) you can do as a BLS provider to help R/I sepsis is check a CBG. Most patients in septic shock will have a rather high BGL reading. 
Also asking about urine output would be a good thing. With sepsis, urine output will decrease or stop all together


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## Anonymous

O2 saturation? 

also might lay the patient supine and elevate the feet


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## Wes

What would O2 saturation tell you that the patient's respiratory rate wouldn't tell you?  I'd be more inclined to get an EtCO2 on the patient.

And hasn't the science pretty much shown that Trendelenburg is meaningless?


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## STXmedic

I'll echo a few:

BLS: Get 'em and go. Assist ventilations with a BVM if they can tolerate it. If they won't tolerate it, they will shortly. If the hospital is a good ways away and you can arrange for a ALS intercept, by all means do so. Like Wes said, Tburg is for all intents and purposes worthless.

ALS: RSI if available, if not, BVM (I also like JT's thought on nasal). Two lines and a lot of fluid. Pressors if the fluid doesn't help.

Just based on the information you gave, it sounds like a pretty standard septic shock patient.


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## STXmedic

Anonymous said:


> O2 saturation?
> 
> also might lay the patient supine and elevate the feet



Are you doubting this patient is hypoxic? I know there are a few items in the assessment missing, but with significant hypotension, significantly elevated RR, elevated HR, and 103+ temp, I think oxygen would be a fair assumption... I'd even be willing to take a stab that you'd hear rales when auscultating the lungs.


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## Wes

Agreed.  In this case, oxygen saturation would be just another vital sign to add to the chart.  It's not going to help you with a differential or in treating this patient at this point.

And, assuming the respiratory rate is in the 50s, but the sats are, say, 97%, would you withhold oxygen?


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## Mariemt

How far out are you? If you can't get als intercept and have a ways to go, I'd consider helo


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## Wes

I'm not a flight junkie, but in this case, I'd agree with Mariemt if you're a ways out from a hospital with ICU beds.

Also, another question on assessment of the patient....  How's his mental status?   I've seen several septic patients who are extremely altered, as in hallucinating.


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## Anonymous

Wes said:


> What would O2 saturation tell you that the patient's respiratory rate wouldn't tell you?  I'd be more inclined to get an EtCO2 on the patient.
> 
> *Just Curious*
> 
> And hasn't the science pretty much shown that Trendelenburg is meaningless?



and yes I know Trendelenburg is but the same goes for shock position?


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## Wes

The only difference between Trendelenburg position and shock position is that, in Trendelenburg, the head is also lowered.   So, nope, I don't think the results will be any different.

Just for the sake of discussion, may I ask where you practice and what level you're at?


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## STXmedic

Anonymous said:


> and yes I know Trendelenburg is but the same goes for shock position?



:blink: Huh?...

The "shock position" is trendelenburg... Well, it's a modified trendelenburg. How would modified trendelenburg be useful when trendelenburg is not?


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## Anonymous

Wes said:


> The only difference between Trendelenburg position and shock position is that, in Trendelenburg, the head is also lowered.   So, nope, I don't think the results will be any different.
> 
> Just for the sake of discussion, may I ask where you practice and what level you're at?



Yes I am a basic



PoeticInjustice said:


> :blink: Huh?...
> 
> The "shock position" is trendelenburg... Well, it's a modified trendelenburg. How would modified trendelenburg be useful when trendelenburg is not?



I don't know. I do know one is still taught and one is not and lowering the head has more risks associated with it.


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## Wes

What risks are you concerned about?

And I'd look at this link regarding Trendelenburg:  http://www.ems1.com/ems-products/education/articles/384771-The-Current-Slant-on-the-Trendelenburg-Position


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## DesertMedic66

I thought shock position was now taught as just supine


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## STXmedic

Anonymous said:


> Yes I am a basic
> 
> 
> 
> I don't know. I do know one is still taught and one is not.



They also still teach spinal immobilization, mechanism of injury, the golden hour, and O2 for all. The twos' effectiveness are the same- none.


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## Wes

What's apparently not being taught are assessment skills and critical thinking.


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## NomadicMedic

I think for a basic, it should be this:

1) put the patient in the ambulance. 
2) start an ALS intercept. 
3) if the hospitals closer than ALS, go there.

Am I looking at this from a skewed perspective? ALS can start to manage hypotension with fluid and pressors, but the patient needs to be in a hospital. That should be the number one priority of the basic that's on scene without a paramedic.


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## DesertMedic66

DEmedic said:


> I think for a basic, it should be this:
> 
> 1) put the patient in the ambulance.
> 2) start an ALS intercept.
> 3) if the hospitals closer than ALS, go there.
> 
> Am I looking at this from a skewed perspective? ALS can start to manage hypotension with fluid and pressors, but the patient needs to be in a hospital. That should be the number one priority of the basic that's on scene without a paramedic.



That's how I would run the call. Even if ALS is 10 minutes out and the hospital is 10 minutes out, I'm still going to the hospital.


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## JPINFV

shademt said:


> Arrive on scene for a c/c of high temp. You find the patient semi-Fowler with a N/C set at 6 LPM. B/P is 58/38, HR is 130, RR is 58, and temp 103.5. After being placed on NRB at 15 LPM, no change in RR. How do you treat taking into consideration the low BP with high RR?



Well, considering that you have 3 of the 4 criteria (you need a WBC with manual differential (note: easiest way to clear up a bandemia at my hospital is to order an automatic diff) to get the 4th), and you only need 2 of the 4, your patient is in systemic inflammatory response syndrome, especially with the elevated temp. Give a source (UTI, PNA, etc) and you have sepsis. 

So, yep, sounds like sepsis, which prehospitally is fluids, fluids, fluids, and more fluids.


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## JPINFV

DesertEMT66 said:


> That's how I would run the call. Even if ALS is 10 minutes out and the hospital is 10 minutes out, I'm still going to the hospital.




If I was BLS and I saw this upon entering (presumably altered, drastically tachypneic), I'd make the decision there to either call paramedics or transport to the closest hospital depending on ETA including time to package the patient. If I decided that package+move+transport time < paramedic ETA, I wouldn't even bother with an on scene assessment because it wouldn't change anything. NRB, move to gurney, move to ambulance, lights, sirens, camera, action. With a patient in respiratory failure (or really any sick medical patient), EMTs are going to max out their potential interventions pretty quickly, and any additional action, including a "proper assessment" just delays desperately needed medical care. I can get lung sounds in the ambulance. I can get a blood pressure in the ambulance. I can dig through the chart in the ambulance. However none of those are going to change the decision to transport to the closest available emergency department or change the decision to call paramedics.


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## NomadicMedic

It's another one of those "ridiculous EMT class scenarios". How would you manage this patient blah blah blah…

You can blather on and on about Trendelenburg and high flow oxygen, but this patient needs a paramedic armed with a couple of thousand bags and then a hospital. 

This isn't a slam on the OP, it's just another reason why I dislike EMT classes trying to cram a bunch of knowledge into people that really should learn, "the patient is sick, I lack the resources to manage this. I either need a paramedic or the hospital, whichever is closer"


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## Anonymous

Wes said:


> What's apparently not being taught are assessment skills and critical thinking.



Are we not here to learn? 

Apparently you were not taught how not to be condescending. Attitudes like yours are what hinder learning. 

God forbid you ever have a green basic for a partner.


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## NomadicMedic

I think we've all had green basics as partners, and we all do our best to teach them to think and assess patients. 

Unfortunately, it's not taught in most EMT basic programs.


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## Anonymous

DEmedic said:


> I think we've all had green basics as partners, and we all do our best to teach them to think and assess patients.
> 
> Unfortunately, it's not taught in most EMT basic programs.



Teaching someone to think seems futile. Now teaching someone is a little different. 

Why would one not "think" shock position works? It makes sense that it would if you "think about it" Ask anyone outside of healthcare if they think that would work and i guarantee the majority would say yes. 

It is through acquiring knowledge that one realizes it does not work, that has nothing to do with critical thinking skills. Not to mention the Do's and Dont's almost always seem to come full circle in EMS.


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## Wes

For the record, I love teaching and mentoring providers.  I volunteer as both a medic and an EMS educator. I think we do a horrible job of teaching people at the basic level much beyond follow the cookbook. I think we can all master a good assessment, critical thinking, and research.


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## Handsome Robb

VOMIT with an extra line, fluids, dope, diesel and RSI if you've got it otherwise consider NTI depending on distance from te hospital. POC Lactate if you've got it *cough* chaz and DEmedic *cough*. Early notification to the hospital. Consider HEMS for RSI if you've got an extended transport considering after the NTI unless you've got something other than versed you're going to have a rough time sedating him and keeping his pressure from taking a dump even further.

I'd be going emergent with this gentleman, not a huge fan of code 3 transports but is say its appropriate in this guy's case.

I'd also say this is past "possible sepsis".


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## NomadicMedic

I always take any indication of sepsis seriously. My first legitimately septic patient was a 19-year-old female, and she died.

Granted, she was a drug user and her immune system was compromised… But for a 19-year-old to die from sepsis is just a shame.


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## Clipper1

Anonymous said:


> Why would one not "think" shock position works? It makes sense that it would if you "think about it" *Ask anyone outside of healthcare if they think that would work and i guarantee the majority would say yes. *
> 
> It is through acquiring knowledge that one realizes it does not work, that has nothing to do with critical thinking skills. Not to mention the Do's and Dont's almost always seem to come full circle in EMS.



Why would you ask someone outside of healthcare if something medical works?

In this situation critical thinking should tell you it not only would not work but also be harmful to the patient. 

The airway is also already compromised and not secure. Placing a person's head down will make those rapid respirations even more ineffective. 

Placing the head down can also lead to aspiration. This type of PNA along with the cause of the sepsis would probably be a death sentence for the patient. 

Trendelenberg is only a very, very temporary fix. If you have seen it done in the hospital it is only for a minute or two until fluids and pressors are adjusted. During that time a physician will take advantage of the position for a central line. There is also the appropriate suction equipment and probably an NG placed  which may be also to suction. There is intubation equipment and there is the appropriate "high flow" oxygen to give adequate oxygen. A NRBM is not effective at providing the adequate high FiO2 and flow to meet the patient's demand.  

If you do not have fluids or pressors, what happens to the patient when you move them from the trendelenberg position to get them onto another stretcher?

This is not something you have to trial on a patient so you can see them crash for yourself before you believe it. Others have already done that for you.


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## VFlutter

I love Trendelenburg....when pulling heavy patients up in bed. But that is about all I use it for.


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## NomadicMedic

Chase said:


> I love Trendelenburg....when pulling heavy patients up in bed. But that is about all I use it for.



Trendelenburg. The King County fluid bolus.


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## Aprz

Clipper1 said:


> Why would you ask someone outside of healthcare if something medical works?


That's the point he was making.


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## Anonymous

Aprz said:


> That's the point he was making.



Thank you

The point was a lack of knowledge and lack of critical thinking skills are not the same thing.


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## Clipper1

Anonymous said:


> Thank you
> 
> The point was a lack of knowledge and lack of critical thinking skills are not the same thing.



Critical thinking comes from knowledge for medical situations. They go hand in hand.  

This was your earlier post.



Anonymous said:


> O2 saturation?
> 
> also might lay the patient supine and elevate the feet




When a patient's RR is this tachypneic, SpO2 is not going to mean to much except if the person is hypoxic but in this situation the oxyhemoglobin curve will be shifted due to acidosis. That means the SpO2 probably will not be accurate.  As a Basic all you have is a NRB mask and a BVM which means you are very limited.  The patient will probably over breathe the NRB mask since it is not a high flow device and it is doubtful you will be able to over ride the acidosis and rapid respiratory rate without causing the patient more stress if still conscious.


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## Carlos Danger

Early sepsis management is pretty straightforward and non-controversial: improve perfusion with lots of IVF and vasopressors. If you are an EMT, you just need to get the pt to the hospital ASAP, and get an ALS intercept or possibly use HEMS if you have a long transport time.

The only disagreement I have with others in this thread is on early intubation. I would do everything in my power to avoid intubating this patient in the field, at least until the BP has improved substantially. These are the types of patients (especially if he is elderly) who can easily arrest on induction or shortly after. 

Also, as an aside, if I did have to intubate a patient like this, ketamine would not be my first choice. It has direct myocardial depressant effects and can exacerbate hypotension in highly SNS-dependent patients, which could be fatal in a patient like this.


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## Summit

I don't have anything to add...



Halothane said:


> Also, as an aside, if I did have to intubate a patient like this, ketamine would not be my first choice. It has direct myocardial depressant effects and can exacerbate hypotension in highly SNS-dependent patients, which could be fatal in a patient like this.



What would you choose?


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## Carlos Danger

Summit said:


> What would you choose?



A small dose of etomidate.

Ketamine has a tendency to directly depress the myocardium (via a Ca+ blocking mechanism, I believe), but this is normally more than offset by its positive SNS effects (which are due to inhibition of catecholamine reuptake). So the idea is that a patient who is "on the edge" and already maximally SNS stimulated will not have the SNS reserve needed to offset the myocardial depression and may see a further reduction in CO with an induction dose of ketamine. Which of course could be catastrophic in a patient who is already severely hypotensive.

To be fair, I think this is mostly theoretical. I don't think there is a lot of research backing it up, but it is mentioned in the anesthesia texts and lots of anesthesia folks will tell you they avoid ketamine in severe shock.


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## Handsome Robb

Learn something new every day. I've always been told ketamine was very hemodynamically stable however I do remember reading to avoid ketamine in septic patients but I didn't see a rationale as to why.

As far as arresting on induction would it generally be secondary to the medications used? Vasovagal response from direct laryngoscopy? Decreased preload from increased intrathoracic pressure? A combination of the any or all of the above? Something I'm missing completely?

I need to get ahold of an anesthesia text.


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## KellyBracket

The RR might be high due to acidosis, even if the SaO2 is normal. If the patient is acidotic, BTW, laying the patient flat, let alone Trendelenburg/shock position, will impair ventilation. Head of bed 30 degrees is probably your best bet.

While the literature on the benefit of crystalloids in trauma is mixed, at best, it's a lot clearer about the benefits of IV fluids in sepsis. Grab a wide-bore IV.


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## Rialaigh

I agree with most of what has been said already. Two large bore IV's, lots of fluid, Im probably starting neo off the bat on this patient if sepsis is suspected immediately. However I am under no circumstances transporting this patient by air, and most likely not transporting code 3. If sepsis is strongly suspected then there is nothing that will be changed by getting to the hospital 30 minutes or an hour later than normal (Assuming you can start pressors and fluids). Especially given the scenario at hand, I would venture to say the survival rate (depending upon age and past medical history) based on the vitals given assuming sepsis is pretty poor. patients that have that severe of hypotension with respiratory failure already are not very likely to survive regardless of what support they receive in the hospital.


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## Carlos Danger

Robb said:


> As far as arresting on induction would it generally be secondary to the medications used? Vasovagal response from direct laryngoscopy? Decreased preload from increased intrathoracic pressure? A combination of the any or all of the above? Something I'm missing completely?



Combination of everything, but mostly just a result of the general depressant effects of most of the IV anesthetics. They pretty much all cause loss of SNS tone, and some have direct vasodilatory and/or myocardial depressant effects. That's not usually an issue with healthy patients, but someone who is severely septic or otherwise critically ill needs all the CO they have. A little neo given at induction can be a huge help.




KellyBracket said:


> The RR might be high due to acidosis, even if the SaO2 is normal.



The likelihood of severe acidosis may be another reason to delay intubation if at all possible. I have heard of cases of severe metabolic acidosis worsening rapidly and causing arrest when patients like this are intubated. Theory being that if the patient is very tachypneic due to severe acidosis, you will not be able to match their minute volume with a BVETT or transport ventilator, and their acidosis can worsen dramatically as soon as you lower their minute volume. 

Have you ever seen anything like that, Dr. Walsh?

I'm not saying we should not provide airway management to someone who clearly needs it. I'm just pointing out some considerations that I think most of us weren't taught in our paramedic programs. At the end of the day, all we can do is follow our protocols and use the meds we have, to the best of our ability.


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## KellyBracket

Rialaigh said:


> .. If sepsis is strongly suspected then there is nothing that will be changed by getting to the hospital 30 minutes or an hour later than normal ...



This patient needs antibiotics and control of the infectious nidus ASAP. While I wouldn't recommend blowing through red lights at warp speed, they need critical care services emergently.

Although STEMI, stroke, and trauma are seen as the "big emergencies," sepsis is where big differences in mortality can be achieved. Although diesel is not a medicine, there is no reason to accept delays in treatment and transport.



Halothane said:


> ...  if the patient is very tachypneic due to severe acidosis, you will not be able to match their minute volume with a BVETT or transport ventilator, and their acidosis can worsen dramatically as soon as you lower their minute volume.
> 
> Have you ever seen anything like that, Dr. Walsh?
> ...



I certainly agree with the principle. We worry about that mostly in bad aspirin overdoses (where even a brief dip in ventilation during intubation can spike the acidosis, and cause cerebral ASA toxicity) or in asthma (where it can be hard to match a young persons ventilatory drive with a machine.


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## Rialaigh

KellyBracket said:


> *This patient needs antibiotics and control of the infectious nidus ASAP. While I wouldn't recommend blowing through red lights at warp speed, they need critical care services emergently.*
> 
> Although STEMI, stroke, and trauma are seen as the "big emergencies," sepsis is where big differences in mortality can be achieved. Although diesel is not a medicine, there is no reason to accept delays in treatment and transport.
> 
> 
> 
> I certainly agree with the principle. We worry about that mostly in bad aspirin overdoses (where even a brief dip in ventilation during intubation can spike the acidosis, and cause cerebral ASA toxicity) or in asthma (where it can be hard to match a young persons ventilatory drive with a machine.



my point was based on the scenario given (obviously age dependent still) I think you would be hard pressed to find a critical care doctor that would advise flying this patient to save anything less than an hour. If the sepsis is this bad already the mortality rate is really really high even with excellent supporting care, a helicopter ride or antibiotics in the field will do nothing to change that.



I do agree that EARLY recognition of sepsis would be a huge game changer in the mortality rates. Many many lives could be saved with minimal long term damage if sepsis was recognized early and treated prior to hypotension requiring pressors.


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## KellyBracket

The helicopter issue is whole 'nother ball of wax. I'll defer to local guidelines, resources, etc., when it comes to answering if a particular should be flown. Choppers are expensive, dangerous, and often of marginal benefit. I think many of us agree on these broad principles.

That being said, if local guidelines allow or dictate flying certain trauma or STEMI patients, then this patient also should qualify. The mortality is high in hypotensive sepsis patients, but it is _precisely_ these sorts of patients that benefit from rapid intervention. Certainly, there is a far greater chance to improve mortality than is seen with, say, fibrinolytics for acute CVA. 

I actually think most CC physicians would choose HEMS for this patient to save an hour. Give me 30 minutes, I'll check with one!


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## TransportJockey

If I picked up this patient from the far south end of my county (or the north end of the next county that we run in since we are closer than their EMS) I would fly them. I'd be looking at almsot two hours with the patient to ANY hospital from that area of the county


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## Carlos Danger

Rialaigh said:


> my point was based on the scenario given (obviously age dependent still) I think you would be hard pressed to find a critical care doctor that would advise flying this patient to save anything less than an hour. If the sepsis is this bad already the mortality rate is really really high even with excellent supporting care, a helicopter ride or antibiotics in the field will do nothing to change that.
> 
> 
> 
> I do agree that EARLY recognition of sepsis would be a huge game changer in the mortality rates. Many many lives could be saved with minimal long term damage if sepsis was recognized early and treated prior to hypotension requiring pressors.



Maybe when it comes to someone truly circling the drain, you've reached a point where nothing that you do is going to help, so why bother with anything at all?

But in general, septic shock patients are some of the sickest people who still have a decent chance to make a full recovery, and even though there may be no magic "door to ___" time like there is with trauma, STEMI, AA, and stroke patients, the right care by the right docs and nurses definitely can make a big difference in these patients. That's why they are generally all transferred to a tertiary facility, and quite often by helicopter. It may be hard to quantify and explain but there is generally a lot more aggressive care going on in a tertiary medical ICU than there is in an ambulance or a small-town hospital, and with these patients things do happen immediately on arrival, just like they do with the other time-sensitive patients.

So while I'm in complete agreement that helicopters are way overused (and even as a flight medic and flight nurse, I regularly made that argument long before it was cool), I think that anytime you have a truly critically ill patient, the most rapid transport by the most experienced CCT folks is a good thing.

There is plenty of room for over-triage of patients like this. There is A LOT of stuff flown "just because" and is complete BS, but this would not fall in that category IMO, not by a long shot.


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## KellyBracket

Okay, I talked to a CC physician, gave her the scenario of a sick septic patient, who has the potential to get to antibiotics and central lines, etc., 1 hour sooner if the helicopter is called. She said "Call the helicopter, no question."

There's a reason they call it _early_ goal-directed therapy; doing the same thereaputic interventions a few hours later doesn't help nearly as much. EMS and EM should own sepsis - and there are CC doctors out there who agree!


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## Rialaigh

KellyBracket said:


> Okay, I talked to a CC physician, gave her the scenario of a sick septic patient, who has the potential to get to antibiotics and central lines, etc., 1 hour sooner if the helicopter is called. She said "Call the helicopter, no question."
> 
> *There's a reason they call it early goal-directed therapy; doing the same thereaputic interventions a few hours later doesn't help nearly as much.* EMS and EM should own sepsis - and there are CC doctors out there who agree!



The scenario given in the first post is anything but *early*. You are in the final stages of sepsis at that point. 

I actually used that article you quoted in a paper I wrote for paramedic class on septic shock. I would like to see more research done on prehospital antibiotics, and whether early intubation and respiratory support increases survival (RSI'ing a patient that has no resp distress yet). A lot more education needs to be done, first basic thing would be requiring ambulances to carry thermometers, theres not a single service near me that does....


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## TransportJockey

Rialaigh said:


> I actually used that article you quoted in a paper I wrote for paramedic class on septic shock. I would like to see more research done on prehospital antibiotics, and whether early intubation and respiratory support increases survival (RSI'ing a patient that has no resp distress yet). A lot more education needs to be done, first basic thing would be requiring ambulances to carry thermometers, theres not a single service near me that does....



Really? Most of the ones in this area do.


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## KellyBracket

Rialaigh said:


> The scenario given in the first post is anything but *early*. You are in the final stages of sepsis at that point.
> 
> I actually used that article you quoted in a paper I wrote for paramedic class on septic shock. I would like to see more research done on prehospital antibiotics, and whether early intubation and respiratory support increases survival (RSI'ing a patient that has no resp distress yet). A lot more education needs to be done, first basic thing would be requiring ambulances to carry thermometers, theres not a single service near me that does....



There is some evidence for early intubation, just to improve the hemodynamic status, but it only comes after a sequence of other actions in the EGDT algorithm. 

I wouldn't consider the patient in the OP's scenario to be in the final stages, actually. First off, we don't know the time course. Second, nothing had been done yet. I wouldn't start getting pessimistic until we had given ≥ 2 liters, dropped a central line, check a CVP, dialed up the pressors, dumped in some broad-spectrum abx, and checked to see if there was any infection that could be cut or sucked out!


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## VirginiaEMT

PoeticInjustice said:


> Are you doubting this patient is hypoxic? I know there are a few items in the assessment missing, but with significant hypotension, significantly elevated RR, elevated HR, and 103+ temp, I think oxygen would be a fair assumption... I'd even be willing to take a stab that you'd hear rales when auscultating the lungs.



Agreed!! I would say this is way you wouldn't want TWO large IV lines running fluids wide open like a previous poster stated. I would try to get the BP up with a pressor and fluid.. We don't carry Dobutamine but that would be a great choice. I would have to use Dopamine.


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## Brandon O

Clipper1 said:


> When a patient's RR is this tachypneic, SpO2 is not going to mean to much except if the person is hypoxic but in this situation the oxyhemoglobin curve will be shifted due to acidosis. That means the SpO2 probably will not be accurate.  As a Basic all you have is a NRB mask and a BVM which means you are very limited.  The patient will probably over breathe the NRB mask since it is not a high flow device and it is doubtful you will be able to over ride the acidosis and rapid respiratory rate without causing the patient more stress if still conscious.



Hard to say what minute volume the quoted RR "means," and how that corresponds to an SpO2 given unknown pulmonary function. So it'd be nice to know, although admittedly partly for pathophys funsies. (Ever feel like you're performing an assessment just for the case presentation later?)

With no attempt to apply it to the actual patient, there ARE some BLS techniques for really maxing out the breathing patient's oxygen supply. If you're using a non-rebreather in the back of your wahmbulance, and that's what you're committed to using, remember that you can supercharge it by running up the flow rate past 15. Just keep turning the valve until it stops; usually this is, oh, well over 40LPM, and the excess flow helps get a spontaneously breathing patient as close to 100% FiO2 as you're likely to get. Sounds like a rocket ship, and don't try it on a portable tank, of course.

You could also try (and this is better if they're not moving a whole lot of volume) a cannula at relatively high flow -- perhaps 15LPM. It's not real comfortable, but if they're obtunded it's no big deal over a short period, and it does a better job of getting oxygen INTO their pharynx if they're not sucking it in very ambitiously (a mask just lets it overflow; a cannula shoots it into their airway under pressure). You can combine cannula and mask as well if you have two regulators.

Finally, if there's obviously gobs of oxygen getting into the lungs, yet their SpO2 remains low (and you believe it), the problem may be V/Q mismatch (shunt) -- O2's inside the lungs but it's not crossing the membrane to enter the blood. PEEP may be helpful, and in principle you can create it using a plain BVM. But this probably wouldn't be very bright for the described patient, who is having hemodynamic troubles as well. (I will remain agnostic here on whether this somewhat sketchy technique is ever a good idea.)

You can also sit 'em up somewhat, although this is subject to hemodynamic limitations as well.

The only thing I'll say about the patient in the scenario is that sepsis is near the very top of the life-threatening emergencies we can help fix, and should be managed with appropriate vigor.


----------



## Clipper1

Brandon Oto said:


> Hard to say what minute volume the quoted RR "means," and how that corresponds to an SpO2 given unknown pulmonary function. So it'd be nice to know, although admittedly partly for pathophys funsies. (Ever feel like you're performing an assessment just for the case presentation later?)
> 
> With no attempt to apply it to the actual patient, there ARE some BLS techniques for really maxing out the breathing patient's oxygen supply. If you're using a non-rebreather in the back of your wahmbulance, and that's what you're committed to using, remember that you can supercharge it by running up the flow rate past 15. Just keep turning the valve until it stops; usually this is, oh, well over 40LPM, and the excess flow helps get a spontaneously breathing patient as close to 100% FiO2 as you're likely to get. Sounds like a rocket ship, and don't try it on a portable tank, of course.
> 
> You could also try (and this is better if they're not moving a whole lot of volume) a cannula at relatively high flow -- perhaps 15LPM. It's not real comfortable, but if they're obtunded it's no big deal over a short period, and it does a better job of getting oxygen INTO their pharynx if they're not sucking it in very ambitiously (a mask just lets it overflow; a cannula shoots it into their airway under pressure). You can combine cannula and mask as well if you have two regulators.
> 
> Finally, if there's obviously gobs of oxygen getting into the lungs, yet their SpO2 remains low (and you believe it), the problem may be V/Q mismatch (shunt) -- O2's inside the lungs but it's not crossing the membrane to enter the blood. PEEP may be helpful, and in principle you can create it using a plain BVM. But this probably wouldn't be very bright for the described patient, who is having hemodynamic troubles as well. (I will remain agnostic here on whether this somewhat sketchy technique is ever a good idea.)
> 
> You can also sit 'em up somewhat, although this is subject to hemodynamic limitations as well.
> 
> The only thing I'll say about the patient in the scenario is that sepsis is near the very top of the life-threatening emergencies we can help fix, and should be managed with appropriate vigor.



Using a device for a way it was not intended will probably not achieve the results you are desiring. Anyone can turn up the NC to blast but then have you look at the way a true hi-flow NC or mask is designed.

Adding PEEP is not going to do anything to meet flow demand.  I believe the ARDSnet studies have also provided evidence that just increasing PEEP without delivery of appropriate flow can actually be detrimental. 

The NRB plus NC is more commonly used for confused patients who might pull off the mask.

You are giving 100% oxygen in hopes of giving an FiO2 of 1.0 *but it is important to use the appropriate device or appropriately use the device used.*  Know your equipment and know how to use it or the basic principles of delivery.  This should also give you a clue about why some things are more "yeah I did that and it sorta worked".


----------



## Brandon O

Clipper1 said:


> Using a device for a way it was not intended will probably not achieve the results you are desiring. Anyone can turn up the NC to blast but then have you look at the way a true hi-flow NC or mask is designed.



Here's a bit of evidence (there's lots more out there, just ask): 

http://www.rcjournal.com/abstracts/2003/?id=OF-03-257

http://www.ncbi.nlm.nih.gov/pubmed/20400000

Obviously it's better to have more appropriate equipment! But if we had all the most appropriate stuff, it wouldn't be EMS, and it sure as heck wouldn't be BLS...



> Adding PEEP is not going to do anything to meet flow demand.  I believe the ARDSnet studies have also provided evidence that just increasing PEEP without delivery of appropriate flow can actually be detrimental.



Hey, I'm not advocating it! Especially for this patient, who's hypotensive and of unclear responsiveness. Although if you do get to where you're using the BVM, "peepy" or otherwise, you'll at least be using 100% O2, so most of these other points will be moot.

It's certainly a double-edged sword, and it's hard to know where you are between those edges without being able to measure pressures. I've never tried to do the BVM PEEP trick on a real humanoid. But it's nice to have tools, and even a difficult and dangerous tool can have value in some situations -- and what makes this one cool is that there's basically no other option for BLS folks (except driving fast... and maybe sticking their head out the side window).



> The NRB plus NC is more commonly used for confused patients who might pull off the mask. . . . You are giving 100% oxygen in hopes of giving an FiO2 of 1.0 but it is important to use the appropriate device or appropriately use the device used



Let's say instead that it's great to have a variety of tools available for increasing FiO2, to understand how they work, and to apply them (individually or in combination) with respect to their strengths and your situational needs. I've done blow-by with a 60LPM mask on patients who wouldn't tolerate anything on their face, for instance.

Notwithstanding any issues of policy or legality (and admittedly those might pertain), the gear doesn't care how it's used; the patient only cares if his problems are solved.


----------



## Clipper1

Brandon O said:


> Here's a bit of evidence (there's lots more out there, just ask):
> 
> http://www.rcjournal.com/abstracts/2003/?id=OF-03-257
> 
> http://www.ncbi.nlm.nih.gov/pubmed/20400000
> 
> Obviously it's better to have more appropriate equipment! But if we had all the most appropriate stuff, it wouldn't be EMS, and it sure as heck wouldn't be BLS...
> 
> 
> 
> Hey, I'm not advocating it! Especially for this patient, who's hypotensive and of unclear responsiveness. Although if you do get to where you're using the BVM, "peepy" or otherwise, you'll at least be using 100% O2, so most of these other points will be moot.
> 
> It's certainly a double-edged sword, and it's hard to know where you are between those edges without being able to measure pressures. I've never tried to do the BVM PEEP trick on a real humanoid. But it's nice to have tools, and even a difficult and dangerous tool can have value in some situations -- and what makes this one cool is that there's basically no other option for BLS folks (except driving fast... and maybe sticking their head out the side window).
> 
> 
> 
> Let's say instead that it's great to have a variety of tools available for increasing FiO2, to understand how they work, and to apply them (individually or in combination) with respect to their strengths and your situational needs. I've done blow-by with a 60LPM mask on patients who wouldn't tolerate anything on their face, for instance.
> 
> Notwithstanding any issues of policy or legality (and admittedly those might pertain), the gear doesn't care how it's used; the patient only cares if his problems are solved.



If someone requires 60 L/m via mask, time to move on to adjusting their toleration for something on their face through pharmacological means.  I doubt if any hospital can have someone hold "blowby" for several hours.  Blowby O2 is an ineffective way to deliver the appropriate FiO2. Room air is surrounding the "blowby". Anything off the patients face also proportionately decreases FiO2 rapidly.  Also note in the article you posted the devices were studied for delivery of FiO2 and not how high the flow goes. That was my point. Regardless of the gear you must understand a few basic principles of delivery.

It is also my understanding from reading these forums and actually seen it done by EMTs on a BLS truck, CPAP provides "PEEP". But, some prehospital devices many not be able to meet both demand and oxygenation.


----------



## Brandon O

Clipper1 said:


> If someone requires 60 L/m via mask, time to move on to adjusting their toleration for something on their face through pharmacological means.  I doubt if any hospital can have someone hold "blowby" for several hours.



Ah, perhaps we're speaking past each other. I had in mind a BLS field situation as described by the OP. Obviously if you have more resources available (better means of airway management, pharmacotherapy, etc), they'll be more effective than any "stretch and squint" BLS solution. On our humble trucks the question is often how effective you can be with what's available, not what would be optimal if you had it.



> Also note in the article you posted the devices were studied for delivery of FiO2 and not how high the flow goes. That was my point.



Could you clarify what you're referring to by "flow"? I'm afraid I'm not catching your drift.



> It is also my understanding from reading these forums and actually seen it done by EMTs on a BLS truck, CPAP provides "PEEP".



I have heard of BLS systems that can deploy CPAP, but they are a rarity.


----------



## STXmedic

VirginiaEMT said:


> Agreed!! I would say this is way you wouldn't want TWO large IV lines running fluids wide open like a previous poster stated. I would try to get the BP up with a pressor and fluid.. We don't carry Dobutamine but that would be a great choice. I would have to use Dopamine.



I _was_ one of the posters advocating running two lines....

The patient may have rales, but the patient also has near nothing in their vasculature. The wet lungs that you'd hear aren't from the patient being fluid overloaded; they're from a fluid shift caused by an increase in membrane permeability (or pneumonia...). The patient still needs fluid, and a lot of it. Pressors aren't going to do you much good if the patient is significantly fluid depleted.


----------



## Clipper1

Brandon O said:


> Ah, perhaps we're speaking past each other. I had in mind a BLS field situation as described by the OP. Obviously if you have more resources available (better means of airway management, pharmacotherapy, etc), they'll be more effective than any "stretch and squint" BLS solution. On our humble trucks the question is often how effective you can be with what's available, not what would be optimal if you had it.
> 
> Could you clarify what you're referring to by "flow"? I'm afraid I'm not catching your drift.
> .



Flow does not necessarily equal FiO2. It seems in EMS a "high flow" device means giving an FiO2 of 1.0.   The FiO2 is dependent upon the minute volume or tidal volume demand. A high flow device is designed to meet that demand. 

*If you actually know the limitations of the oxygen device or how it works you might be more effective at making the most appropriate decision for transporting this patient.* Wouldn't teaching the basics of your equipment be more beneficial to the BLS EMT rather than throwing in stuff which will just exhaust the O2 tanks and not provide adequate FiO2 and/or flow to meet demand?  Call ALS and/or a helicopter. Don't waste time running your O2 tanks dry on a futile delivery method.   The headlines on your Med Directors desk will read "ran out of O2" rather than heroic rigging attempt of an O2 device.   Trying to pull a MacGyver should not supersede education.  Even MacGyver had a strong foundation academically and experience before rigging up things to blow up.

Of course, re-educating the EMT about the "shock position" and time of its usefulness would also be appropriate for a patient such as this.


----------



## Handsome Robb

PoeticInjustice said:


> I _was_ one of the posters advocating running two lines....
> 
> The patient may have rales, but the patient also has near nothing in their vasculature. The wet lungs that you'd hear aren't from the patient being fluid overloaded; they're from a fluid shift caused by an increase in membrane permeability (or pneumonia...). The patient still needs fluid, and a lot of it. Pressors aren't going to do you much good if the patient is significantly fluid depleted.



You beat me to it. No point in "clamping the tank down" if there's nothing for it to clamp down on. The hypotension isn't a result from low cardiac output, it's a result of massive vasodilation and subsequent fluid shift into the interstitial space. 

Dobutamine would not be a good option, in my opinion. It is purely an inotrope and this patient needs vasoconstriction. I may be mistaken but I believe dobutamine can also cause mild vasodilation as well but don't quote me. To be honest it isn't even indicated in this scenario. This isn't a cardiogenic shock, it's a distributive shock.

Levophed would be a good option. Wouldn't be surprised to see the hospital use neo-synephrine or vasopressin either. 

Dopamine at high doses would be my only option. Start at 10 mcg/kg/min and work up from there. 

Hell if you can work it a third line for the pressor would be cool but good luck. This patient is getting a CVC pretty soon after they get to the ER though. 

Someone said it, this patient is potentially very far into septic shock and we are very far behind the 8-ball.


----------



## Carlos Danger

Robb said:


> You beat me to it. *No point in "clamping the tank down" *if there's nothing for it to clamp down on. The hypotension isn't a result from low cardiac output, it's a result of massive vasodilation and subsequent fluid shift into the interstitial space.
> 
> Dobutamine would not be a good option, in my opinion. It is purely an inotrope and this patient needs vasoconstriction. I may be mistaken but I believe dobutamine can also cause mild vasodilation as well but don't quote me. To be honest it isn't even indicated in this scenario. This isn't a cardiogenic shock, it's a distributive shock.
> 
> Levophed would be a good option. Wouldn't be surprised to see the hospital use neo-synephrine or vasopressin either.
> 
> Dopamine at high doses would be my only option. Start at 10 mcg/kg/min and work up from there.
> 
> Hell if you can work it a third line for the pressor would be cool but good luck. This patient is getting a CVC pretty soon after they get to the ER though.
> 
> Someone said it, this patient is potentially very far into septic shock and we are very far behind the 8-ball.
> 
> 
> PoeticInjustice said:
> 
> 
> 
> I _was_ one of the posters advocating running two lines....
> 
> The patient may have rales, but the patient also has near nothing in their vasculature. The wet lungs that you'd hear aren't from the patient being fluid overloaded; they're from a fluid shift caused by an increase in membrane permeability (or pneumonia...). The patient still needs fluid, and a lot of it. *Pressors aren't going to do you much good if the patient is significantly fluid depleted.*
Click to expand...


There are different trains of thought about when to use pressors, and how much fluid should be given first. The EGDT protocol seems a bit unclear on it, assuming you are having a hard time reaching your CVP goal with fluid alone. (I do need to read the paper though; I'm familiar with the protocol but don't think I've ever read the actual paper). And of course there are all the problems that come along with massive fluid resuscitation - could some of those be avoided with earlier use of pressors? Some say that IVC fluid responsiveness and SVV are good indicators, but I'm not sure how well they've really been validated and SVV, while great technology, requires that the patient be intubated and mechanically ventilated. Obviously those aren't options in the field, anyway.

The way I have been trained, and what makes sense to me, and I think is quite applicable to the field, is to keep in mind that the root of the hemodynamic problem here is vasodilation and increased vascular permeability, and the lack of intravascular volume simply follows that. So in a patient who is severely hypotensive and has evidence of lack of perfusion to vital organs, I'd give a bolus of a couple liters quickly, reassess, and give a second bolus, reassess, and give a third, and keep doing that as long as improvements in perfusion were evident. Where this is a little different from what you often see is that if at _any_ point the fluids don't seem to be improving things, I'd be quick to give a vasopressor, whereas many others want to give really massive fluid volumes before going to pressors. If I've given 4 liters of fluid and have seen no or only a very minimal improvement in pressure, and end-organ dysfunction is still suspected, I'd reach for the pressors for sure. 

You are right about dobutamine not being indicated here. Think of dobutamine and milrinone as only being indicated for LV failure; though they work by different mechanisms, both increase inotropy and decreased afterload by arterial vasodilation. I'm don't think the literature shows a clear advantage of any 1 pressor over the others, but I'd rather stick to phenylephrine and avoid the b-stimulation of dopamine or norepi.


----------



## Brandon O

Clipper1 said:


> *If you actually know the limitations of the oxygen device or how it works you might be more effective at making the most appropriate decision for transporting this patient.*



My friend, that is my goal. But let's address the problem by conveying ideas, not just complaining about the problem.

Let me make sure I'm understanding your point... Are you suggesting that, for a sufficiently large minute volume, a device like a non-rebreather may be unable to provide a high FiO2 regardless of the flow rate at the regulator?

This is probably true. But with the maximum rates with typical equipment (40-60LPM with most wall-mounted regs I've seen -- there may be some that limit it lower), the shortfall should be pretty small. A hypothetical minute volume of 60 liters per minute would be quite impressive in any human being, sick or otherwise.

Obviously chasing a high concentration of inspired oxygen is not going to solve a septic patient's problems, any more than sheltering under your desk will protect you from a nuclear blast. But let's give everyone the benefit of the doubt and presume they realize this, since smart folks in this thread have already hit on the other major points such as rapid access to fluid resuscitation, pressors, and so forth. Once all that is in motion, it is very reasonable for a BLS provider to take steps (or at least have options available) to maximize the patient's oxygen tension.


----------



## Clipper1

Brandon O said:


> My friend, that is my goal. But let's address the problem by conveying ideas, not just complaining about the problem.
> 
> Let me make sure I'm understanding your point... Are you suggesting that, for a sufficiently large minute volume, a device like a non-rebreather may be unable to provide a high FiO2 regardless of the flow rate at the regulator?
> 
> This is probably true. But with the maximum rates with typical equipment (40-60LPM with most wall-mounted regs I've seen -- there may be some that limit it lower), the shortfall should be pretty small. A hypothetical minute volume of 60 liters per minute would be quite impressive in any human being, sick or otherwise.
> 
> Obviously chasing a high concentration of inspired oxygen is not going to solve a septic patient's problems, any more than sheltering under your desk will protect you from a nuclear blast. But let's give everyone the benefit of the doubt and presume they realize this, since smart folks in this thread have already hit on the other major points such as rapid access to fluid resuscitation, pressors, and so forth. Once all that is in motion, it is very reasonable for a BLS provider to take steps (or at least have options available) to maximize the patient's oxygen tension.



I have to ask again why you would want an EMT to drain their oxygen tanks blasting a NRB mask at 40 liters.  If a hospital has to resort to that by not having the appropriate equipment or KNOWLEDGE then that is a sad place to take any patient. Also with the suspicion this pt is septic and a NRB is all they have why waste time especially since other interventions are needed?

A sick pt on a ventilator can easily do over 30 l of MV and until other interventions happen.


----------



## FLdoc2011

Levophed is the go-to pressor in septic shock.  From there you can also add on a fixed dose of vasopressin if still not meeting goals.

There is also a role for dobutamine in specific situations.  If you're meeting all other goals (MAP > 65, CVP > 8) but SCVO2 is still low a d assuming not severely anemic, then that's where dobutamine can be added.   Sepsis is not always a hyperdynamic/high cardiac output state, you can get myocardial depression in sepsis as well. 

It was already brought up, but I encourage you to look up the early goal directed therapy and the surviving sepsis guidelines.   There's a decent website with a lot of data including the most recent updates that were published in 2012.   

More and more hospitals are implementing sepsis protocols/bundles that are specifically meant to resuscitate these patients in septic shock in the first 6 hours of recognition and frankly treating these patients in a time sensitive manner like they would a STEMI or stroke alert.   We've even started calling sepsis alerts in the ED and on the floor to address this and focus attention on quickly intervening.


----------



## Handsome Robb

Halothane said:


> There are different trains of thought about when to use pressors, and how much fluid should be given first. The EGDT protocol seems a bit unclear on it, assuming you are having a hard time reaching your CVP goal with fluid alone. (I do need to read the paper though; I'm familiar with the protocol but don't think I've ever read the actual paper). And of course there are all the problems that come along with massive fluid resuscitation - could some of those be avoided with earlier use of pressors? Some say that IVC fluid responsiveness and SVV are good indicators, but I'm not sure how well they've really been validated and SVV, while great technology, requires that the patient be intubated and mechanically ventilated. Obviously those aren't options in the field, anyway.
> 
> The way I have been trained, and what makes sense to me, and I think is quite applicable to the field, is to keep in mind that the root of the hemodynamic problem here is vasodilation and increased vascular permeability, and the lack of intravascular volume simply follows that. So in a patient who is severely hypotensive and has evidence of lack of perfusion to vital organs, I'd give a bolus of a couple liters quickly, reassess, and give a second bolus, reassess, and give a third, and keep doing that as long as improvements in perfusion were evident. Where this is a little different from what you often see is that if at _any_ point the fluids don't seem to be improving things, I'd be quick to give a vasopressor, whereas many others want to give really massive fluid volumes before going to pressors. If I've given 4 liters of fluid and have seen no or only a very minimal improvement in pressure, and end-organ dysfunction is still suspected, I'd reach for the pressors for sure.
> 
> You are right about dobutamine not being indicated here. Think of dobutamine and milrinone as only being indicated for LV failure; though they work by different mechanisms, both increase inotropy and decreased afterload by arterial vasodilation. I'm don't think the literature shows a clear advantage of any 1 pressor over the others, but I'd rather stick to phenylephrine and avoid the b-stimulation of dopamine or norepi.



This is a bad response but per protocol I have to give 2 L of NS before I can jump to dopamine. With that said, I see what you're getting at about basing pressors off of response to IVF boluses, it seems as though we're both still talking in the 2-4L range before starting a pressor. Also, where does the "least invasive way possible" come in to play, especially in the EMS environment when it comes to running pressors through peripheral lines that often are tough to obtain in these patients. If they are responding to fluids hold off on pressors until the hospital can establish a CVC and give it centrally rather than peripherally. 

My question is, and this may sound contradictory to my above statement about "clamping down the container" but, as you said, knowing that the problem behind the hypotension is severe vasodilation would it not be better to start pressors sooner rather than later? Maybe in the 1-2L range rather than the 3-4L? 

Another question I have is what are people's thoughts about antibiotics in the field? If I'm not mistaken they are part of EGDT, correct? Now I'm again going to contradict myself with this study, http://www.ncbi.nlm.nih.gov/m/pubmed/21883637/ , which shows no difference in mortality despite earlier antibiotic administration. The study looks at door-to-antibiotic time of patients that present to triage vs patients that come in via EMS. Not exactly what I was looking for but similar...

Sorry about all the contradictions. I'm kinda thinking out loud at this point from lots of different angles. I need to go to bed.


----------



## RocketMedic

We are getting levophed.


----------



## Carlos Danger

FLdoc2011 said:


> Levophed is the go-to pressor in septic shock.  From there you can also add on a fixed dose of vasopressin if still not meeting goals.
> 
> There is also a role for dobutamine in specific situations.  If you're meeting all other goals (MAP > 65, CVP > 8) but SCVO2 is still low a d assuming not severely anemic, then that's where dobutamine can be added.   Sepsis is not always a hyperdynamic/high cardiac output state, you can get myocardial depression in sepsis as well.
> 
> It was already brought up, but I encourage you to look up the early goal directed therapy and the surviving sepsis guidelines.   There's a decent website with a lot of data including the most recent updates that were published in 2012.



I am going to review those guidelines and read as much of the supporting literature as I can later today.

Regarding levo as the first line pressor, my understanding is that neo was left out of original recommendations due to concerns for excessive splanchnic vasoconstriction, but that subsequent studies have found no difference in outcome between the two. My protocols have always allowed for either, and it is also what we primarily used in SICU for sepsis, along with vaso. IME, neo seems generally easier to use and of course doesn't cause the significant tachycardia that you sometimes see with levo and dopa.


----------



## FLdoc2011

Halothane said:


> I am going to review those guidelines and read as much of the supporting literature as I can later today.
> 
> Regarding levo as the first line pressor, my understanding is that neo was left out of original recommendations due to concerns for excessive splanchnic vasoconstriction, but that subsequent studies have found no difference in outcome between the two. My protocols have always allowed for either, and it is also what we primarily used in SICU for sepsis, along with vaso. IME, neo seems generally easier to use and of course doesn't cause the significant tachycardia that you sometimes see with levo and dopa.



That's sort of the classic/theoretical concern with Neo though I'm not sure how clinically relevant/important that is. 

Ultimately there just haven't been good large studies comparing vasopressors in general.    Levo is currently holds a grade 1B rec in septic shock as it has been what was used in studies.   I think in 2010 there was a head to head between Levo and dopamine with no outcome difference BUT more adverse effects from dopamine so we tend to not go to dopamine first.  

I saw I think it was a small 2008 critical care article comparing levo to Neo with no outcome differences in hemodynamic parameters.  

Ultimately I don't think Neo is a bad choice IF you're running into arrhythmias that may preclude the use of something with some beta agonist activity such as levo and dopamine.    But ultimately it's not the initial recommended recommended pressor so we tend to stick with standard of care and current guidelines unless other clinical parameters preclude that.  

Also,  the first line resuscitation treatment is still fluids... THEN pressors if needed.  Basically keep giving fluid until they're no longer fluid responsive or if fluid impairs gas exhange (pulm edema) and then if still hypotensive/hypoperfusing THEN add a pressor.    

The trick is how do we tell when they ARE or ARE NOT fluid responsive.....   Turns out CVP may not be as good as we thought it was but it's still in the guidelines so we use it,  but there's also passive leg raise,  arterial pulse variation, IVC diameter/variation, and other clinical parameters we're studying.  So ultimately we just don't have a great way of monitoring or predicting responsiveness besides using a combination of the above tools.   

Ultimately I'd rather over resuscitate someone with fluids and have to intubate/mechanically ventilate them for pulm edema than under resuscitate leave in a state of shock with possible permanent end organ damage.  I can always get the fluid back off later once they're out of shock.


----------



## Anonymous

What is this patient's SpO2?


----------



## Wes

With a patient in extremis like this, why does it matter?   Would you withhold oxygen if they had a high saturation?   Any reason NOT to oxygenate a patient in septic shock?


----------



## Carlos Danger

FLdoc2011 said:


> The trick is how do we tell when they ARE or ARE NOT fluid responsive.....   Turns out CVP may not be as good as we thought it was but it's still in the guidelines so we use it,  but there's also passive leg raise,  arterial pulse variation, IVC diameter/variation, and other clinical parameters we're studying.  So ultimately we just don't have a great way of monitoring or predicting responsiveness besides using a combination of the above tools.
> 
> *Ultimately I'd rather over resuscitate someone with fluids and have to intubate/mechanically ventilate them for pulm edema than under resuscitate leave in a state of shock with possible permanent end organ damage.  I can always get the fluid back off later once they're out of shock.*



Good point.


----------



## Rialaigh

TransportJockey said:


> Really? Most of the ones in this area do.



Yeah, no thermometers on any service I know of anywhere near here except critical care interfacility transport. 




KellyBracket said:


> There is some evidence for early intubation, just to improve the hemodynamic status, but it only comes after a sequence of other actions in the EGDT algorithm.
> 
> *I wouldn't consider the patient in the OP's scenario to be in the final stages, *actually. First off, we don't know the time course. Second, nothing had been done yet. I wouldn't start getting pessimistic until we had given ≥ 2 liters, dropped a central line, check a CVP, dialed up the pressors, dumped in some broad-spectrum abx, and checked to see if there was any infection that could be cut or sucked out!




OP's scenario is entirely age and history dependant. If this is 75 year old grandma with a cardiac and respiratory history then yes, to make a broad generalization (not an absolute) this is is end stage sepsis, she's not recovering, she's not ever coming off the vent after you put her on, and sooner or later she's not going to make it. I would have to say a VAST minority of patients in this age group with any kind of "normal" american medical history would have any positive outcome.

Now if this is 42 year old female or male with limited medical history and otherwise relatively healthy it's a whole different ball game. Fact is most of the sepsis patients you pick up fall in the first category. 

There will always be exceptions but its a very age and history dependant scenario. 



I am very interested in solutions or initiatives for early goal directed therapy and what hospital ER's and EMS agencies can do to increase the recognition of sepsis in time to prevent permanent lasting effects (ultimately death).


----------



## Handsome Robb

Rialaigh said:


> Yeah, no thermometers on any service I know of anywhere near here except critical care interfacility transport.



Really? We carry temp-a-dots, regular oral thermometers like mom has, a temporal thermometer and the continuous temperature probe for the MRx. 

Also have a pediatric fever protocol, it's bet specific, option for PO liquid Tylenol or PR suppositories. We don't treat fevers in adults. 

I agree with your assessment about the different demographics of patients and their mortality in this scenario.


----------



## DesertMedic66

Robb said:


> Really? We carry temp-a-dots, regular oral thermometers like mom has, a temporal thermometer and the continuous temperature probe for the MRx.
> 
> Also have a pediatric fever protocol, it's bet specific, option for PO liquid Tylenol or PR suppositories. We don't treat fevers in adults.
> 
> I agree with your assessment about the different demographics of patients and their mortality in this scenario.



We don't carry any kind of thermometers on the ambulance (county doesn't require us to). The fire departments do carry them (county requires it).


----------



## Rialaigh

Robb said:


> Really? We carry temp-a-dots, regular oral thermometers like mom has, a temporal thermometer and the continuous temperature probe for the MRx.
> 
> Also have a pediatric fever protocol, it's bet specific, option for PO liquid Tylenol or PR suppositories. We don't treat fevers in adults.
> 
> I agree with your assessment about the different demographics of patients and their mortality in this scenario.



I wish we carried them, you kinda look like an idiot when you show up at the ER with a unresponsive nursing home patient and say "last seen normal last night, vitals are fine" and the ER gets a rectal temp of like 92 degrees or something.....happens pretty frequently....

Would love to have it for Tylenol admin for pedis as well


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## Handsome Robb

DesertEMT66 said:


> We don't carry any kind of thermometers on the ambulance (county doesn't require us to). The fire departments do carry them (county requires it).



That's kinda backasswards. 




Rialaigh said:


> I wish we carried them, you kinda look like an idiot when you show up at the ER with a unresponsive nursing home patient and say "last seen normal last night, vitals are fine" and the ER gets a rectal temp of like 92 degrees or something.....happens pretty frequently....
> 
> Would love to have it for Tylenol admin for pedis as well



The only ones I really trust are the "mom" ones textually ", we use probe covers and cidex the hell out of them afterwards, or the MRx attachment. It actually works pretty well if you have a patient hold it under their tongue if they aren't to the point of putting in esophageally or rectally.

The temp-a-dots confuse my two brain cells and the temporal one always spits out anywhere from 97.8-98.4 99.9% of the time. You'll get a crazy low or high reading then 98.0 three times then a crazy high or low reading again. They just aren't consistent. 

I think it's hilarious how much kids like our liquid Tylenol. They always are all about it. It smells nasty though.


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## Rialaigh

On the sepsis topic does anyone have any good articles about Levophed vs. Neo, I did a google search and waded through a few articles but I am hoping for something a little more well written and in depth. The hospital in my area uses Neo as first line (from what I have seen) for most ICU hypo tension. The ER generally uses dopamine for everything....

Just curious if there is research out there that you guys have stumbled across about the negative chronotropic effects of Neo and safe HR ranges for sepsis patients? I know thats delving more into ICU micro management of sepsis but I am curious.


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## Carlos Danger

Rialaigh said:


> On the sepsis topic does anyone have any good articles about Levophed vs. Neo



There is tons of stuff on Pubmed on the topic of pressors in shock, but the only two articles I found that compared the two drugs head to head clinically in humans were these. I think the pdf's for both of these were available for free:

*Comparison of phenylephrine and norepinephrine in the management of dopamine-resistant septic shock.* Indian J Crit Care Med. 2010 Jan;14(1):29-34

*Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial.* Crit Care. 2008;12(6)

This article provides a good overview / review of the clinical usage of vasopressors & inotropes in septic shock:

*Inotrope & Vasopressor Therapy in Septic Shock*

I still haven't really gotten to the guidelines; been busy doing family stuff and studying for a pharm exam that is scheduled on my first day back from break.


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## Rialaigh

Halothane said:


> There is tons of stuff on Pubmed on the topic of pressors in shock, but the only two articles I found that compared the two drugs head to head clinically in humans were these. I think the pdf's for both of these were available for free:
> 
> *Comparison of phenylephrine and norepinephrine in the management of dopamine-resistant septic shock.* Indian J Crit Care Med. 2010 Jan;14(1):29-34
> 
> *Phenylephrine versus norepinephrine for initial hemodynamic support of patients with septic shock: a randomized, controlled trial.* Crit Care. 2008;12(6)
> 
> This article provides a good overview / review of the clinical usage of vasopressors & inotropes in septic shock:
> 
> *Inotrope & Vasopressor Therapy in Septic Shock*
> 
> I still haven't really gotten to the guidelines; been busy doing family stuff and studying for a pharm exam that is scheduled on my first day back from break.



Thank you for the articles  Its good reading, always nice to expand the knowledge base just a little and have a better understanding of why


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