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Code Blue: Just Trying Figure Out What Happened?

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by Binz Binz (New) New Nurse

Binz specializes in Med/Surg.

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BeatsPerMinute has 5 years experience as a BSN, RN and specializes in Cardiac.

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Critical care nurse here! Have some thoughts.. Just gonna throw random things out there. Interesting discussion!

Definitely difficult to offer a good guess without lab values, test results, other useful data.. Shock sounds likely... cardiogenic shock? septic shock? More than one major thing going on? Hard to tell... I'd want to know her CBC, BNP, CMP, Coags, lactic, CXR, 12 lead, urine sample results.. and maybe a CT 

 Maybe I missed it but how old was the patient? Fever shows up a little later in the elderly so if she already had a fever that'd lead me to believe she had a real nasty infection. 

Hypovolemia d/t: blood loss? GI fluid loss? renal loss? decreased CO? Vasodilation (shock) ? 

Acute renal failure? Heart hx/ poor heart function -> prolonged hypoperfusion to kidneys -> renal ischemia and cell death... Infection can cause ARF. Or maybe she had chronic renal issues anyway? Also platelet dysfunction occurs w/ ARF. Was she anemic? Could be a possible explanation for a stool check - maybe they wanted to see if she was bleeding. 

Levophed can really clamp down the vascular system... its often first choice pressor on ICU for low BPs, but I wonder if things should have been done in a different order or maybe a different pressor / BP support therapy would have been best to start with. Really depends on the patient and things can get quite complex. Very hard to tell without knowing more info. Anyway, interesting and educational. Curious what others think. 

 

 

Edited by BeatsPerMinute

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On 12/11/2019 at 5:38 AM, Wuzzie said:

 

That being said. Are there any nursing students out there who would like to tell us about Norepinephrine and it's use in this situation? Please don't copy and paste, tell us what you know! 😊

We are browsing after a full day of cramming for finals.  🙂  brains are quite full at this point.

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10 hours ago, BeatsPerMinute said:

Levophed can really clamp down the vascular system... its often first choice pressor on ICU for low BPs, but I wonder if things should have been done in a different order or maybe a different pressor / BP support therapy would have been best to start with. Really depends on the patient and things can get quite complex. Very hard to tell without knowing more info. Anyway, interesting and educational. Curious what others think. 

 

 

Levo is the first line pressor for septic shock. But it seems that the game plan for cardiogenic shock is changing with new data. It seems that dopamine is no longer favored due to high mortality rates in recent meta-analyses (possibly due to arrhythmias, though I'm not certain). Dobutamine and (I believe) milrinone aren't usually considered appropriate for patients who are hypotensive. Levo is creeping forward in line for cardiogenic shock, though I believe the current best practice is to tailor pressor choice to the particular nature of any individual patient's heart failure. 

I recently had a very knowledgeable intensivist insist on neosynephrine and fluid bolus for an acutely decompensating patient stented for a STEMI (LAD and diagonal) a few hours before. No suspected sepsis at all, slightly bradycardic (50s). This was counterintuitive to me. He cited new data, argued against any beta stimulation in a patient such as that one, and pointed out the move away from dopamine.  I considered making a thread in the ICU forum about current pressor selection guidelines, and would be curious what others are seeing/reading.

In this patient's case, it is unclear what was going on with her heart beyond the low EF and the fact that at least some doctor thought she was overloaded (i.e. that she would benefit from lasix). It's also unclear whether there was a septic element to her shock, since her presentation appears ambiguous enough to trigger a sepsis protocol whether or not she was actually septic. Without more information, I can't effectively second-guess the fluid management or pressor selection. 

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4 hours ago, Cowboyardee said:

In this patient's case, it is unclear what was going on with her heart beyond the low EF and the fact that at least some doctor thought she was overloaded (i.e. that she would benefit from lasix). It's also unclear whether there was a septic element to her shock, since her presentation appears ambiguous enough to trigger a sepsis protocol whether or not she was actually septic. Without more information, I can't effectively second-guess the fluid management or pressor selection. 

The patient's symptoms were severe hypotension and fever and we were told they had an EF of 20 and a history of A-Fib.  The ED MD determined pneumonia/sepsis from the CXR (pneumonia on a CXR has specific visible characteristics), elevated lactate level and elevated WBC, and from the patient's symptoms (some of which likely were not described by the OP).  This appears to be a clear picture of pneumonia/sepsis.  It appears the patient also had serious heart problems.

I agree that we don't know how much of the patient's problems were sepsis/septic shock related and/or cardiac related and that more diagnostic tests and labs and more assessment information would help us to better determine this.

I agree also that if severe cardiac problems existed it is very likely renal problems existed also, and that this may have been included in the plan of care (lasix was given; a pressor was used to increase the patient's MAP, and we were not told that fluid resuscitation took place prior to the pressor being given).

Edited by Susie2310

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59 minutes ago, Susie2310 said:

The patient's symptoms were severe hypotension and fever and we were told they had an EF of 20 and a history of A-Fib.  The ED MD determined pneumonia/sepsis from the CXR (pneumonia on a CXR has specific visible characteristics), elevated lactate level and elevated WBC, and from the patient's symptoms (some of which likely were not described by the OP).  This appears to be a clear picture of pneumonia/sepsis.  It appears the patient also had serious heart problems.

I agree that we don't know how much of the patient's problems were sepsis/septic shock related and/or cardiac related and that more diagnostic tests and labs and more assessment information would help us to better determine this.

I agree also that if severe cardiac problems existed it is very likely renal problems existed also, and that this may have been included in the plan of care (lasix was given; a pressor was used to increase the patient's MAP, and we were not told that fluid resuscitation took place prior to the pressor being given).

I want to add that the priority in the ED was rapidly determining the problem, providing initial stabilizing care, and admitting the patient to the appropriate level of care to receive acute care services as needed. 

Sepsis/severe sepsis/septic shock is a hugely physiologically stressful  medical problem for a patient and is even more so if the patient already has medical problems that affect other organ systems e.g. cardiac and renal.  Patients with decreased physiological reserves such as the elderly are highly vulnerable.

Edited by Susie2310

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5 hours ago, Susie2310 said:

The patient's symptoms were severe hypotension and fever and we were told they had an EF of 20 and a history of A-Fib.  The ED MD determined pneumonia/sepsis from the CXR (pneumonia on a CXR has specific visible characteristics), elevated lactate level and elevated WBC, and from the patient's symptoms (some of which likely were not described by the OP).  This appears to be a clear picture of pneumonia/sepsis.  It appears the patient also had serious heart problems.

I agree that we don't know how much of the patient's problems were sepsis/septic shock related and/or cardiac related and that more diagnostic tests and labs and more assessment information would help us to better determine this.

I agree also that if severe cardiac problems existed it is very likely renal problems existed also, and that this may have been included in the plan of care (lasix was given; a pressor was used to increase the patient's MAP, and we were not told that fluid resuscitation took place prior to the pressor being given).

Yeah, I missed the later posts where the OP recalled the physician looking at the xray and saying it was definitely pneumonia.

For whatever it's worth, some CXRs clearly point to one diagnosis or another, while others are more ambiguous - you can't always tell. Lactate isn't specific to sepsis in a patient already in shock. Elevated WBCs and fever point toward infection, but aren't specific for sepsis either. We see this kind of thing often - a patient who shows up with a chf exacerbation, hypotension, maybe an AKI, along with a uti that may or may not be causing sepsis.

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PeakRN specializes in Adult and pediatric emergency and critical care.

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As a ED and adult/pediatric congenital cardiac intensive care nurse I'll give you a few thoughts.

Patients on pressors/inotropes should not be eating. When patients have limited perfusion your body is going to shunt away whatever blood it can to preserve organ function of the heart, lungs, brain, liver, kidneys, and then other major organ systems. This can result in necrosis of the fingers, toes, nose, gut, et cetera as those organs which are low priority to immediately preserve life take the greatest hit on perfusion.

All pressors work differently, and knowing how a pressor works is really important to understanding the hemodyndamics involved.

For example with norepinephrine you get essentially no inotropic effect while at the same time increasing systemic vascular resistance. We give norepi because we need to increase blood pressure so that we can provide adequate perfusion to the organs, however we are also making more work for the heart. You may as a result have no actual increase in cardiac output, and depending on other factors may be increasing the work on the heart without providing any increase in cardiac output resulting in even more stress on the heart. In summary if I give an adult patient with a CO of 1.5 norepi I may easily be making their CO smaller or remaining about the same despite the increased BP.

I'm a bit confused as to why you would give lasix to a patient on pressors who is septic. Fluid balance is of huge consequence in the septic patient, and while we certainly don't want to cause strain from overload in the septic patient generally we preferentially give more fluids rather than trying to diurese the patient. I'd be hard pressed to think of many situations where I want to clamp down vasculature but also reduce intravascular volume, especially early in sepsis management. Lasix is also not really a kidney friendly drug, especially in the setting of poor perfusion. You are asking the kidney to do more work with the same impaired perfusion. If for some reason we really want to diurese a patient with poor perfusion we should be considering CRRT, but that should also be an ICU level care intervention and does not need to be done in the ED.

If I needed to get fluids off of the lungs or reduce cardiac strain I would consider something like a nipride or nitro drip to shunt volume into the vascular space, but this really isn't something that fits with a patient in sepsis and who needs pressors. You could consider milrinone or dobutamine to increase the patient's native cardiac function to reduce the effects of heart failure. You could also consider positive pressure therapy either non-invasive through CPAP/BiPAP or increased MAPs from a somewhat high PEEP and PIP after intubating, which would mechanically force fluids out of the lungs through mechanical pressure though this does nothing for strain and can have some negligible to small decreases on cardiac output. 

I got mentioned by another poster but I didn't see it as part of your posts, but I think it's a really good point. Calcium is hugely important in the management of critical patients. Calcium is what gives us the ability to contract the heart muscle, and build blood pressure. Often in our patients who are hypocalcemic will go from hypotensive to normotensive with only replacement. In calcium in particular we really should be measuring an ionized calcium rather than a total calcium as it gives us a better picture of the patient's extracellular chemistry. Low potassium increases ectopy, while a high K can cause the heart to not squeeze. Low magnesium is huge part of reducing membrane stability and increasing ectopy. 

Lasix is not a treatment for PNAs. While drying out the secretions may have some temporizing preservation of respiratory function it is harmful line the long term management and personally not something I would even consider as a temporizing measure. While PNAs that fluff out do require increased respiratory support it is just a matter of those secretions being dry to start with, if we are going to mobilize them they can't be dry and plugging up the airways this just leads to further respiratory failure.

I would consider some vagal stimulation as being detrimental to her cardiac output. Stimulation in the throat/neck (eating) as well as building pressure in the abdomen (from using the bathroom or trying to hold it in) can all cause a vagal response. Sitting a patient up and shifting their already fragile and likely very dry fluid status isn't helping them either.

A statement from my ED side: I don't care about stool samples. Doubly so in patients that are being admitted. The ICU can get poop, the patient will poop eventually. The floor can get poop, the patient will poop eventually. If we are concerned for bowel ischemia (looking for blood) we shouldn't be feeding them, if we are looking for infection that is life threatening we should be treating them empirically until we get that sample regardless.

A few thoughts on lactates. Lactates are not a specific marker for sepsis, they are a marker of anaerobic metabolism. They can be elevated from sepsis, cardiac failure, respiratory failure, large tumor burdens, having a seizure, and so on. We certainly trend them in our septic patient, but they are only a piece of the puzzle. Same goes for things like elevated white counts. As a note you can definitely die from viral sepsis, so don't consider a low procal always be a good sign.

A few thoughts to take home. Every nurse (and doctor for that matter) has made a mistake at some point. Those who say they haven't are either lying or too dumb to realize the mistakes they have made, both are people you don't want to work with.

All of healthcare is an art whether it is nursing, medicine, pharmacies, therapies, or something else. We all practice to get better. I hope that no one makes mistakes, but more importantly we need to learn from our mistakes and near-misses to get better and provide our patients the best care we can. This is a great opportunity to learn about hemodynamics, pressors, sepsis and so on. If you aren't already I would strongly consider professional membership in the ENA and AACN, and take advantage of the wealth of knowledge and education that is available.

Lastly a lot of patients are not compatible with life. If we had made a different decision perhaps we could have bought them a few more minutes, hours, or days... but some patients are going to die no matter what we do. Death is a part of life, and part of healthcare.

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3 hours ago, PeakRN said:

 

I'm a bit confused as to why you would give lasix to a patient on pressors who is septic. Fluid balance is of huge consequence in the septic patient, and while we certainly don't want to cause strain from overload in the septic patient generally we preferentially give more fluids rather than trying to diurese the patient. I'd be hard pressed to think of many situations where I want to clamp down vasculature but also reduce intravascular volume, especially early in sepsis management. Lasix is also not really a kidney friendly drug, especially in the setting of poor perfusion. You are asking the kidney to do more work with the same impaired perfusion. If for some reason we really want to diurese a patient with poor perfusion we should be considering CRRT, but that should also be an ICU level care intervention and does not need to be done in the ED.

If I needed to get fluids off of the lungs or reduce cardiac strain I would consider something like a nipride or nitro drip to shunt volume into the vascular space, but this really isn't something that fits with a patient in sepsis and who needs pressors. You could consider milrinone or dobutamine to increase the patient's native cardiac function to reduce the effects of heart failure. You could also consider positive pressure therapy either non-invasive through CPAP/BiPAP or increased MAPs from a somewhat high PEEP and PIP after intubating, which would mechanically force fluids out of the lungs through mechanical pressure though this does nothing for strain and can have some negligible to small decreases on cardiac output. 

Sitting a patient up and shifting their already fragile and likely very dry fluid status isn't helping them either.

A few thoughts on lactates. Lactates are not a specific marker for sepsis, they are a marker of anaerobic metabolism. They can be elevated from sepsis, cardiac failure, respiratory failure, large tumor burdens, having a seizure, and so on. We certainly trend them in our septic patient, but they are only a piece of the puzzle. Same goes for things like elevated white counts. As a note you can definitely die from viral sepsis, so don't consider a low procal always be a good sign.

 

The patient's blood pressure at the start of care was 70's systolic and 50's diastolic.  This would have been consistent with severe sepsis (hypoperfusion of vital organs, and could also reflect in part the patient's previous apparent history of severe cardiac problems - prior ECHO showed EF of 20 and the patient had a history of A-Fib prior to the sepsis diagnosis).  The MD diagnosed pneumonia/sepsis from the CXR (pneumonia has specific visible characteristics on a CXR), the elevated lactate, elevated WBC, patient's symptoms i.e. fever, severe hypotension, respiratory retractions, all of which taken together provide a clear clinical picture of pneumonia/sepsis.  

The lasix puzzles me also but if there was a need to remove fluid quickly (e.g. symptoms of fluid overload/CHF) it would be an intervention that would rapidly remove fluid and could be given in the ED whereas CRRT would be an ICU intervention (the patient was not in the ICU). It appears that fluid resuscitation was not given to restore the MAP initially but a pressor was used instead - it appears the clinical situation and patient's medical history argued for removing fluids and not adding more fluids i.e. fluid resuscitation; we just don't know the full details.

From personal experience, I can't imagine a patient with sepsis/severe sepsis tolerating a CPAP (which requires wearing a tight fitting face mask and can be uncomfortable and unpleasant to wear if the patient is not about to go to sleep) - in sepsis/severe sepsis/septic shock the patient's system is enormously stressed and they are basically fighting to survive. 

I agree completely with not getting the patient with sepsis/suspected sepsis up.  I have seen this done (the physician wanted to see how the patient tolerated standing - answer was they didn't, at all - with the patient becoming even more profusely diaphoretic and dizzy when they were already very weak and very hot/flushed/diaphoretic with abnormal vital signs).

Edited by Susie2310

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PeakRN specializes in Adult and pediatric emergency and critical care.

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6 hours ago, Susie2310 said:

The patient's blood pressure at the start of care was 70's systolic and 50's diastolic.  This would have been consistent with severe sepsis (hypoperfusion of vital organs, and could also reflect in part the patient's previous apparent history of severe cardiac problems - prior ECHO showed EF of 20 and the patient had a history of A-Fib prior to the sepsis diagnosis).  The MD diagnosed pneumonia/sepsis from the CXR (pneumonia has specific visible characteristics on a CXR), the elevated lactate, elevated WBC, patient's symptoms i.e. fever, severe hypotension, respiratory retractions, all of which taken together provide a clear clinical picture of pneumonia/sepsis.  

The lasix puzzles me also but if there was a need to remove fluid quickly (e.g. symptoms of fluid overload/CHF) it would be an intervention that would rapidly remove fluid and could be given in the ED whereas CRRT would be an ICU intervention (the patient was not in the ICU). It appears that fluid resuscitation was not given to restore the MAP initially but a pressor was used instead - it appears the clinical situation and patient's medical history argued for removing fluids and not adding more fluids i.e. fluid resuscitation; we just don't know the full details.

From personal experience, I can't imagine a patient with sepsis/severe sepsis tolerating a CPAP (which requires wearing a tight fitting face mask and can be uncomfortable and unpleasant to wear if the patient is not about to go to sleep) - in sepsis/severe sepsis/septic shock the patient's system is enormously stressed and they are basically fighting to survive. 

I agree completely with not getting the patient with sepsis/suspected sepsis up.  I have seen this done (the physician wanted to see how the patient tolerated standing - answer was they didn't, at all - with the patient becoming even more profusely diaphoretic and dizzy when they were already very weak and very hot/flushed/diaphoretic with abnormal vital signs).

Patients in early spesis/severe sepsis/septic shock do not need to be diuesed in the ED. They need volume resuscitation, the pathophysiology of sepsis results in 3rd spacing (which includes the interstial spaces ot the lung) which decreases intravascular volume. Giving lasix in early sepsis isn't going to reduce that 3rd spaced fluid in the lungs, you can't just pull it back into the vascular space simply by reducing the free water volume volume in the intravascular spaces. If you have the desire to really aggressively prevent 3rd spacing during sepsis you can make sure they have optimized osmotic/oncotic pressure and give blood products (especially PRBCs, platelets, and albumin). Lasix is just going to decrease intravascular volume leading to vascular collapse, while doing nothing to address the 3rd spaced fluids.

Pressors are not a replacement for fluids in the setting of intravascular fluid deficit. If you put the patient on a NICOM, Flotrac, trending CVP, trending CO with a PA cath, or doing repeat U/S of the venacava and RV while providing small fluid challenges or passive leg raises they you could argue that more fluids aren't going to help. It doesn't seem that any of those things have been done (nor do most EDs and many smaller ICUs). You could also make an argument for volume replacing with 5% albumin or other colloid, although this isn't supported in the literature.

Many patients don't tolerate CPAP/BiPAP well. A precedex drip, ketamine drip, or a small amount of ativan can all greatly improve tolerance when given with good education and coaching.

 

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28 minutes ago, PeakRN said:

Patients in early spesis/severe sepsis/septic shock do not need to be diuesed in the ED. They need volume resuscitation, the pathophysiology of sepsis results in 3rd spacing (which includes the interstial spaces ot the lung) which decreases intravascular volume. Giving lasix in early sepsis isn't going to reduce that 3rd spaced fluid in the lungs, you can't just pull it back into the vascular space simply by reducing the free water volume volume in the intravascular spaces. If you have the desire to really aggressively prevent 3rd spacing during sepsis you can make sure they have optimized osmotic/oncotic pressure and give blood products (especially PRBCs, platelets, and albumin). Lasix is just going to decrease intravascular volume leading to vascular collapse, while doing nothing to address the 3rd spaced fluids.

Pressors are not a replacement for fluids in the setting of intravascular fluid deficit. If you put the patient on a NICOM, Flotrac, trending CVP, trending CO with a PA cath, or doing repeat U/S of the venacava and RV while providing small fluid challenges or passive leg raises they you could argue that more fluids aren't going to help. It doesn't seem that any of those things have been done (nor do most EDs and many smaller ICUs). You could also make an argument for volume replacing with 5% albumin or other colloid, although this isn't supported in the literature.

Many patients don't tolerate CPAP/BiPAP well. A precedex drip, ketamine drip, or a small amount of ativan can all greatly improve tolerance when given with good education and coaching.

 

Did you read that the patient with pneumonia/sepsis was reported by the OP to have had an ejection fraction of 20 and a history of A-fib?  It appears the patient had serious pre-existing heart problems. It seems reasonable to presume the patient could have been fluid overloaded when they presented to the ED, and that the lasix was given for fluid overload/CHF while the patient was being treated for pneumonia/sepsis.  A number of people who have posted  on this thread have conjectured that this is what happened; hence the reason for lasix being given, not for the sepsis.

I haven't suggested that pressors are a replacement for fluid resuscitation as indeed they are not, but I have been curious as to why fluid resuscitation appears not to have taken place in a septic patient (if you read the OP's early posts you will see he/she states that no fluids were running).  The fact that lasix was given and fluid resuscitation appears not to have been given raises the question as to why the pressor appears to have been given without prior fluid resuscitation  in a septic patient; I conjectured that this may have been cardiac related but without knowing more about the patient's clinical condition and medical history it is not possible to know this.

Edited by Susie2310

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PeakRN specializes in Adult and pediatric emergency and critical care.

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6 minutes ago, Susie2310 said:

Did you read that the patient with pneumonia/sepsis was reported by the OP to have had an ejection fraction of 20 and a history of A-fib?  It seems reasonable to presume the patient could have been fluid overloaded when they presented to the ED, and that the lasix was given for fluid overload/CHF.  A number of people who have posted  on this thread have conjectured that this is what happened; hence the reason for lasix being given, not for the sepsis.

I haven't suggested that pressors are a replacement for fluid resuscitation, but I have been curious as to why fluid resuscitation appears not to have taken place (if you read the OP's early posts you will see he/she states that no fluids were running).  The fact that lasix was given and fluid resuscitation appears not to have been given raises the question as to why the pressor appears to have been given without prior fluid resuscitation  in a septic patient; I conjectured that this may have been cardiac related but without knowing more about the patient's clinical condition and medical history it is not possible to know this.

Yes, I read the history of CHF and Afib.

One of the questions is why is the patient hypotensive and requiring pressors. If we believe that the patient is hypotensive not as a result of sepsis but rather advanced cardiac disease then that needs to be addressed, and norepi isn't the drug for it (or at least not the only drug). If we believe that the problem is the heart's ability to squeeze them we should be giving an inotrope.

Patients with a history of heart failure typically still require some fluid resuscitation during sepsis/severe sepsis/septic shock. If the patient requires volume resusitation, then giving lasix isn't going to help anything.

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24 minutes ago, PeakRN said:

Yes, I read the history of CHF and Afib.

One of the questions is why is the patient hypotensive and requiring pressors. If we believe that the patient is hypotensive not as a result of sepsis but rather advanced cardiac disease then that needs to be addressed, and norepi isn't the drug for it (or at least not the only drug). If we believe that the problem is the heart's ability to squeeze them we should be giving an inotrope.

Patients with a history of heart failure typically still require some fluid resuscitation during sepsis/severe sepsis/septic shock. If the patient requires volume resusitation, then giving lasix isn't going to help anything.

The patient was diagnosed with sepsis/pneumonia  - the patient was severely hypotensive - BP was 70's systolic 50's diastolic at the start of care, with a fever, elevated lactate, elevated WBC, respiratory retractions, and the MD diagnosed pneumonia/sepsis from the CXR and the presenting symptoms and labs.  It also appears the patient had serious pre-existing heart problems, possibly heart failure.  There was a point raised earlier on the thread that it is not possible to know how much of the hypotension is sepsis related and how much is related to the presumed pre-existing cardiac problem.  

For me the questions are, given the patient's diagnosis of pneumonia/sepsis and what we know about the patient:  1) Why was the lasix given to this particular patient?  2) Why was fluid resuscitation apparently not given to this patient?

 

Edited by Susie2310

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