Code Blue: Just Trying Figure Out What Happened?

[Binz]

I recently started in the ED. I had a patient who came in with Pnuemonia and sepsis. Was on a norepinephrine drip to maintain a MAP>65. Her BP went up, MAP was 80ish. We had to get a stool sample, so me and my preceptor sat her up at the bedside. She started feeling nauseous, felt like she was going to vomit, was very sweaty, and then it's like the life left her eyes. She passed out, became unresponsive. We activated a code and she had to be intubated. I'm just trying to understand how we went from MAP>80, pt talking, eating to intubating. What should I have done/not done? Thank you.

[Elibri]

On 12/10/2019 at 2:13 AM, MunoRN said:

First I should point out that I don't think there was anything wrong with the care you provided, my post came across as more accusatory than intended.

There are reasons to avoid or at least be cautious about feeding patients on high dose pressors, but your patient's dose of 0.05 is a fairly low dose. There are two reasons for this; pressors can contribute to bowel ischemia, and feeding an ischemic gut can cause necrosis and perforation. I know this seems counterintuitive since the purpose of pressors is to improve perfusion, but they don't improve perfusion everywhere in the body. The most visible example of this is that's it's not unusual for the fingers and toes of patients on high dose, long term pressors to become necrotic. The other reason is that digesting food increases the body's metabolic demands by 25% or more, so if you're already struggling to meet the body's metabolic demands then increasing those demands sort of works against you.

I'm always leery of the initial diagnosis of pneumonia and or sepsis in a cardiac patient, since too often it turns out all of their symptoms attributed to pneumonia and sepsis were solely cardiac in nature. Tachycardia, tachypnea, elevated lactate, signs of decreased end-organ perfusion, hypotension, etc can all be explained by HF and other cardiac causes, but also typically trigger a concern for sepsis above all else, which can lead to interventions intended for septic patients that may do more harm than good in HF patients.

I think we're sometimes a bit too quick to get too aggressive with borderline low BG levels, 60 is the low end but is in the normal range for a fasting BG level. I think we also forget how damaging d50 is to vasculature as well.

My guess would be that she was just sicker than she looked while resting in bed, and then the balance between compensation and decompensation suddenly tipped.

Excellent, excellent response. I see too often that we intervene with patients based on standards of care without taking into account the individual patient. This is where the critically thinking nurse comes in and is so important. And, not to go into too much detail about this topic, but this is the expertise we're losing at the bedside. We are hemorrhaging experienced nurses and i feel bad for the newer generation coming in that won't have that mentorship that is so desperately needed. And i must say that you did absolutely nothing wrong in the care that you provided. In fact, this is how we learn. By going back and remaining the thjngs that happened.

[Elibri]

On 12/10/2019 at 1:55 PM, Susie2310 said:

I was thinking that this may have been because of the patient's ejection fraction. It appears to me they used pressors to restore the MAP initially instead of fluid resuscitation.

Yup! Ya gotta fill the gas tank before you start pumping. Using levophed on a septic patient that is by definition profoundly intravascularly dehydrated along with a reduced EF of only 20%, is a disaster waiting to happen, if not carefully managed. There should have been some modest fluid resuscitation at least. Maybe then followed by some lasix. But her EF of only 20% is the key factor here. Anything under 30%, you run the increased risk of arrhythmia's even under normal circumstances, along with dehydration, neosynephrine and (probably) not adequate fluid resuscitation, and you have the perfect storm. But, this is not to say that what was done was wrong by any means. This is simply life, there are so many others determining factors...time being the biggest factor. Could they have intubated to adequately fluid resuscitate her, would the heart have made it through that, would there have been enough time to give her fluids gently but yet adequately to prevent multiorgan failure (which obviously was already happening)? Point is, this lady came in with a low chance of survival. Its why i tell everyone I know that they should never wait to bring in the elderly. They're like children...they compensate, compensate, compensate, until they don't and then they crash.

[Elibri]

The more I've read of this thread, it seems likely to me that the patient came in with septic shock, complicated by her HF with EF 20%. Pt at high risk for arrhythmias. Usually these patients receive a defibrillator (AICD) just for that reason alone. also, zofran prolongs QT even further and someone with EF of 20% likely already had some ekg changes and possibly a prolonged QT on ekg. Along with all the other things that have been mentioned. But, still this lady died from acute chf exacerbation and cardiogenic shock sec to pna and septic shock. Great case study.

[Elibri]

On 12/15/2019 at 8:25 AM, PeakRN said:

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.

I hope you are a preceptor, in advanced practice, education, or some sort of role where you can mentor, educate, and support our fellow nurses. Many of us have the same knowledge but the way you explain things and put it into perspective is your talent. If not already, i hope you look into further educating the nurses of our profession. Very well worded and educated response.

[Susie2310]

1 hour ago, Elibri said:

Its why i tell everyone I know that they should never wait to bring in the elderly.

100% agreement; the only problem is that once the elderly patient with decreased physiologic reserves gets there (even when brought in promptly), even with sepsis symptoms - elevated temp, tachycardia, hot, flushed, diaphoretic, blood pressure increasing, tachypnea, new onset of severe weakness, no energy, UTI symptoms - being triaged as an ESI 2 can still mean a significant wait of around an hour (in an empty waiting room) while the patient continues to deteriorate whilst using up their last ounces of strength.

[PeakRN]

1 hour ago, Susie2310 said:

100% agreement; the only problem is that once the elderly patient with decreased physiologic reserves gets there (even when brought in promptly), even with sepsis symptoms - elevated temp, tachycardia, hot, flushed, diaphoretic, blood pressure increasing, tachypnea, new onset of severe weakness, no energy, UTI symptoms - being triaged as an ESI 2 can still mean a significant wait of around an hour (in an empty waiting room) while the patient continues to deteriorate whilst using up their last ounces of strength.

If an ED has ESI 2 patients waiting in the waiting room for any amount of time, but especially over 10 minutes, the leadership needs to restructure how the department flows.

[JKL33]

When people make special note that the WR was empty that doesn't mean that every other patient who had shown up so far was already in the back being treated; it means that there were no patients and none of the nurses were doing anything.

[2BS Nurse, BSN]

18 hours ago, Elibri said:

Excellent, excellent response. I see too often that we intervene with patients based on standards of care without taking into account the individual patient. This is where the critically thinking nurse comes in and is so important. And, not to go into too much detail about this topic, but this is the expertise we're losing at the bedside. We are hemorrhaging experienced nurses and i feel bad for the newer generation coming in that won't have that mentorship that is so desperately needed. And i must say that you did absolutely nothing wrong in the care that you provided. In fact, this is how we learn. By going back and remaining the thjngs that happened.

This!!! "We are hemorrhaging experienced nurses and i feel bad for the newer generation coming in that won't have that mentorship that is so desperately needed". The main reason I wouldn't apply for an inpatient job after graduation! I knew I'd be thrown on a floor without adequate training. I'm finding our young RNs are moving to outpatient within 2 years!

[Cherylflies]

The one test I did not see but might have been mentioned is the ever standard ECG. If the patient had a history of AFIB, one should have been given. Also, in our ED, every patient is considered as r/o cardiac with every dx, too, especially in women, because of the differential symptoms. I agree with all about the pressors, the lactate and was curious if the patient seemed edemic given the dx and lasix? But, I too, think nipride to shunt would have been a better choice. The hardest part was that she was talking to you, which can distract from the 20% EF and the 80 MAP. Both good reasons for more response.

Here's why you will be a great nurse: because you are choosing to learn and re-evaluate to do better every time--which is inspiring. Sorry about your patient.

[organichombre, ADN, BSN, MSN, LPN, RN]

Just off the cuff here folks but who in their right mind is going to get a septic patient up to the bedside to get a stool sample? And why would a stool specimen "have to be gotten"? Stool samples can wait, adequate circulation cannot.

[Blueeyednurse15]

Going off of previous comments it sounds like maybe she was going into septic shock and afib. The meds were masking it but then she had a vasalvagal response and her body just gave out. She was dangling by a thread and the thread broke. When I was a student I had a patient go septic very quickly the meds she was giving masked it and then she died.