I had a patient who I'd had the previous night, and he had been complaining about not getting much sleep. I got him comfy, got him in a recliner, gave him some coffee and a blanket, he slept, had a ok night. That AM before leaving, I was running a little behind, and he gave me a hard time, saying "hey, you're supposed to be home by now!".
When I came back that night, he was ok, his wife was there nd she was going home. He was being moved to a private room, and I checked his 02 while walking, it was good.
The cardiologist wanted him to get some IV fluid due to a low bp during the day, and a little dizziness. I hooked him up, and over a hour he got a 100 mls. He called me because he was feeling short of breath, and his lungs sounded a little tight. I spoke with his doc and his cardiologist, got 40 of Lasix, gave him that, and told myself I'd be back in 10 minutes.
I came in, and he had just called me.
He was GREY, and sats of 88. Called the rapid response, got some help, he kept saying he was going to pass out, we got him back to bed, called the docs.....etc. etc. gave him another 40 of lasix, got him to the ICU. We hooked him up to the ICU monitor, he coded right away. got him back, coded again(shocked twice). I was there for 2.5 hours while we coded him 5 times, got him to the cath lab, and he coded 2 more times. Ultimately died on the cath lab table.
Figured out he had another MI(he had been admitted with one, and had a balloon pump with a regrafting 4 days prior).
I know I did everything I could, but it still upsets me. I've been taking care of patients for 5 years and have never had anyone code like this before. Just putting this out there. I hope his family finds peace.
Kind of doubt it was another mi. If he just had cabg he could have restenosed but not as likely. Could have been a fatal arrhythmia especially if he had a rca infarct to begin with which would exlain the low bp. I've had a pt in cv post cabg sit in a chair walk arround and almost getting ready to get discharged get into vfib out of the blue. The surgeon oppened the chest and everything was patent. It has been haunting me as he was in his 40s
Actually, this patient had gotten fluid earlier so depending upon an in-depth lung assessment (which the only information given here was "tight") as well as a cardiac assessment, Lasix definitely may have been indicated. And some form of diuretic therapy IS indicated in heart failure management, especially exacerbation which might be caused by right heart failure. Diuretic therapy is driven by kidney function, better to be a bit dry than wet.
100mls is not an amount of fluid I'd particularly look to fluid overload a patient. You do realize that "a bit dry" can be stressful to the myocardium as well correct? Your thinking is a few years behind on the management of acute HF.
And re: orthopnea, that was not listed when the symptoms were discussed, what was stated was " he had been complaining about not getting much sleep". As this pt was post-op for CABG, that is not an uncommon complaint.
Hmmm, a post-CABG patient who is having a difficult time sleeping and needed a recliner to be comfortable. The same patient who later had a cardiac event and coded. I think orthpnea is a reasonable assumption.
Your post jumped to some conclusions that weren't supported by information presented by OP. And as this patient went into an acute situation rather quickly, NTG and ACE inhibitors wouldn't have been indicated, IV inotropes would have been indicated as well as the possible use of Milrinone if the patient stabilized,
Now your jumping to conclusions. Inotropes would be a bad, bad choice for treatment of a typical episode of acute heart failure, which typically presents with HYPERtension, severe SOB due to pulmonary edema, ect. The focus is on getting the load of the myocardium to decrease MvO2 and expand alveolar area to increase gas exchange. Not filling the patients bladder. Inotropes may be indicated for cardiogenic shock, but will likely worsen MvO2 and are a last resort, hence why this patient got a balloon pump, which decreases MvO2 and increases myocardial perfusion.
which unfortunately didn't happen. IMHO the OP was looking for support regarding a situation which deteriorated rather rapidly...not a lecture on presumed heart failure management.
First I never said the OP did a poor job, the MD saddled the OP with a poor choice of treatment. Secondly, see my comments above on learning.
This isn't the time to even think about YOUR shoulda .. coulda. wouldas.
The patient was a fragile cardiac client.We do not have a crystal ball.
I had a patient that was hospitalized for 6 weeks, dressed and ready to go home... died in the bathroom, getting ready to leave.
God calls us when he calls us. We are only his servant in our efforts to provide care... it was your:hug: patients time.
My dad died in the hospital 2 hours before he was to be discharged. He had CHF. The nurse came in and checked on him, he was fine, he teased her because the night before he told her to bring him some wine when she came back to work. He got up and packed his bags and got ready to go home. An hour later, he was gone, sitting up in his bed watching tv. It happened suddenly and he had a DNR..
When it's our time, it's our time.
His nurse felt terrible, I talked to her about it and assured her that we believed she did all she could do.
Nursing is hard work. You never know when you are going to be the last human your patient talks to in their life.
Had that happened yesterday, the nurse asked the pt what he wanted to use his meds with apple sauce or juice, she gave him the med he said thanks, she turned around to answera question family member had asked, before she turned back he was gone (just like that). he was a DNR
OP, I'm sorry you're having to sort through all of these feelings. You did what you felt was right w/the info you had- and orders you had. Yes- you can always learn from lousy events. But people die, no matter what is done to intervene. :heartbeat:heartbeat:heartbeat
thank you all for your comments. I was posting just to mention how quickly someone can go bad. Lasix is usually used in a situation where it is assumed for fluid overload, working on a tele floor. I agree, he may have just had a arrthymia.
Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
This isn't the time to even think about YOUR shoulda .. coulda. wouldas.
The patient was a fragile cardiac client.We do not have a crystal ball.
I had a patient that was hospitalized for 6 weeks, dressed and ready to go home... died in the bathroom, getting ready to leave.
God calls us when he calls us. We are only his servant in our efforts to provide care... it was your:hug: patients time.
:hug:....It's hard when we work so hard and care for someone a long time. I get attached to patients too. I believe we have the power to intervene. The power of the outcome belongs (IMHO) belong to a higher power. I believe when I got that whisper in my ear it was a guradian angel telling me a heads up. Having that "gut feeling" is a gift that can't be taught. A patient that has been in the hospital for an MI with a CABG and a IABP hasn't had the smoothest post op recovery so the odds were against him. Whether it was a massive PE, Pulmonary edema, graft closure, MI, blown septum, blown pappillary muscle you acted appropriately and quickly.....God (or whomever) just had other plans. GOOD JOB!
100mls is not an amount of fluid I'd particularly look to fluid overload a patient. You do realize that "a bit dry" can be stressful to the myocardium as well correct? Your thinking is a few years behind on the management of acute HF.
Hmmm, a post-CABG patient who is having a difficult time sleeping and needed a recliner to be comfortable. The same patient who later had a cardiac event and coded. I think orthpnea is a reasonable assumption.
Now your jumping to conclusions. Inotropes would be a bad, bad choice for treatment of a typical episode of acute heart failure, which typically presents with HYPERtension, severe SOB due to pulmonary edema, ect. The focus is on getting the load of the myocardium to decrease MvO2 and expand alveolar area to increase gas exchange. Not filling the patients bladder. Inotropes may be indicated for cardiogenic shock, but will likely worsen MvO2 and are a last resort, hence why this patient got a balloon pump, which decreases MvO2 and increases myocardial perfusion.
First I never said the OP did a poor job, the MD saddled the OP with a poor choice of treatment. Secondly, see my comments above on learning.
Great. And we all like to learn stuff. But do ya have to be such a **** about it?
100mls is not an amount of fluid I'd particularly look to fluid overload a patient. You do realize that "a bit dry" can be stressful to the myocardium as well correct? Your thinking is a few years behind on the management of acute HF.
Hmmm, a post-CABG patient who is having a difficult time sleeping and needed a recliner to be comfortable. The same patient who later had a cardiac event and coded. I think orthpnea is a reasonable assumption.
Now your jumping to conclusions. Inotropes would be a bad, bad choice for treatment of a typical episode of acute heart failure, which typically presents with HYPERtension, severe SOB due to pulmonary edema, ect. The focus is on getting the load of the myocardium to decrease MvO2 and expand alveolar area to increase gas exchange. Not filling the patients bladder. Inotropes may be indicated for cardiogenic shock, but will likely worsen MvO2 and are a last resort, hence why this patient got a balloon pump, which decreases MvO2 and increases myocardial perfusion.
First I never said the OP did a poor job, the MD saddled the OP with a poor choice of treatment. Secondly, see my comments above on learning.
Interesting. I wasn't aware that loop diuretics are no longer indicated in pulmonary congestion secondary to heart failure (sarcasm). This is of course assuming that this patient had pulmonary congestion, as another poster said the only information we have is that the chest was "tight".
Key word with the orthopnea assumption is: assumption. This patient could have a number of problems that cause loss of sleep, orthopnea being one.
The use of positive inotropes vs. vasodilators depends on the patient's blood pressure. Last we heard from the OP the patient was hypotensive. Administration of vasodilators to a hypotensive patient would be a "bad bad choice" as this would decrease CPP. Current literature recommends loop diuretics, ventilatory therapy, and either inotropes or vasodilators depending on blood pressure, though evidence is lacking for AHF treatment. Not much has been truly proven to improve survival.
I don't think diuretic therapy was a bad choice at all. You do what you can with the information you have. Can't create information and make clinical decisions off of it. Great job OP.
Interesting. I wasn't aware that loop diuretics are no longer indicated in pulmonary congestion secondary to heart failure (sarcasm). This is of course assuming that this patient had pulmonary congestion, as another poster said the only information we have is that the chest was "tight".
It's all about acute vs chronic. There are more important things than filling the patients bladder in an acute (i.e. about to get tubed) event. I suggest you look up any number of resources on sympathetically driven acute heart failure written in the last five years. Later on, the patient might need diureses, but the 15-30 minutes it takes for Lasix to work isn't going to stop a tube.
All that wheezes is not asthma. Learning to differentiate based on other history and physical exam items is key.
Key word with the orthopnea assumption is: assumption. This patient could have a number of problems that cause loss of sleep, orthopnea being one.
Never denied it was an assumption, but it was a fairly safe one based on events wouldn't you say?
The use of positive inotropes vs. vasodilators depends on the patient's blood pressure. Last we heard from the OP the patient was hypotensive. Administration of vasodilators to a hypotensive patient would be a "bad bad choice" as this would decrease CPP.
The OP indicated the patient was hypotensive post-arrest. Which is to be expected. The orginal presentation never mentioned hypotension. Further, the OP gave a second dose of Lasix during the acute event, which would be contraindicated due to hypotension no?
Current literature recommen)ds loop diuretics, ventilatory therapy, and either inotropes or vasodilators depending on blood pressure, though evidence is lacking for AHF treatment. Not much has been truly proven to improve survival.
I don't think diuretic therapy was a bad choice at all. You do what you can with the information you have. Can't create information and make clinical decisions off of it. Great job OP.
One study is not overwhelming evidence.
Creating information vs learning to act in cases of limited information are two different things. You don't need a BNP, chest radiograph and echo to diagnose an acute exaceterbation of HF. You need good physical exam and history skills. It's done thousands of times a day all around the world.
Zaphod, BSN, RN
181 Posts
Kind of doubt it was another mi. If he just had cabg he could have restenosed but not as likely. Could have been a fatal arrhythmia especially if he had a rca infarct to begin with which would exlain the low bp. I've had a pt in cv post cabg sit in a chair walk arround and almost getting ready to get discharged get into vfib out of the blue. The surgeon oppened the chest and everything was patent. It has been haunting me as he was in his 40s