question about CHFer

[kokoclose]

Hello excuse my question, but i would like your input . I have a CHFer who came in with hypokalemia of 2.9. Clinically she was overloaded with pulmonary edema on chest xray , but not in respiratory distress. She was not in the ICU so she had no central line access. I went ahead and diuresed her with lasix and Peripheral IV supplementation. But now in retrospect wondering if there was a better way to handle that. Is there a class of diuretics that's better than lasix for these kind of patients. I ask because i was in a bind and was not getting the help from higher level of care. I was nervous about diuresing her with severe hypokalemia and precipitating an arrhythmia.
In the ICU setting I likely would have put her on nitro drip if blood pressure is okay, pressors if she was in shock, and would have felt comfortable diuresing her while throwing line for potassium replacement. I guess what I am asking is how would you approach if this patient was on the medical floors?

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[jdh71]

her gut work ok?

 

[lymphocyte]

Is there a class of diuretics that's better than lasix for these kind of patients.

These patients do great with MRAs like spironolactone. They're often hypokalemic precisely because they have high circulating aldosterone. So, in situations like this, you can pair furosemide with spironolactone if they're not already on it, and, if they are, bump up the dose.

In ATHENA-HF, for example, people in acute heart failure on IV frusemide paired with natriuretic-dose spironolactone (50-100mg) had zero change in their serum K--and it was a safe strategy with respect to mortality and renal function. (It was also a negative trial, but I've always wondered about the hypokalemic sub-group, which has never been studied.)

I try to avoid peripheral IV replacement as much as possible, because the mini-bags are often made up in normal saline. You're delivering a sodium load after giving furosemide, when the kidneys are very sodium avid. Much, much better be to give oral replacement.

 

[sluggs]

Try lasix 40-60 mg po, aldactone 25 mg po, KCL 40 meq po and 4gm mgso4 iv. Recheck lytes in 8 hours. If you need more diuresis, do it again. If HCO3 rises add diamox. If Na rises add metolazone.
If patient not peeing from this, change t0 iv and add albumin.

 

[Instatewaiter]

Try lasix 40-60 mg po, aldactone 25 mg po, KCL 40 meq po and 4gm mgso4 iv. Recheck lytes in 8 hours. If you need more diuresis, do it again. If HCO3 rises add diamox. If Na rises add metolazone.
If patient not peeing from this, change t0 iv and add albumin.

I'm not sure I have a single patient in whom 40 mg of oral lasix reaches threshold for diuresis. Bioavailability of lasix in a patient with pulmonary edema is about 10-20%. Might as well do nothing...

 

[Instatewaiter]

Hello excuse my question, but i would like your input . I have a CHFer who came in with hypokalemia of 2.9. Clinically she was overloaded with pulmonary edema on chest xray , but not in respiratory distress. She was not in the ICU so she had no central line access. I went ahead and diuresed her with lasix and Peripheral IV supplementation. But now in retrospect wondering if there was a better way to handle that. Is there a class of diuretics that's better than lasix for these kind of patients. I ask because i was in a bind and was not getting the help from higher level of care. I was nervous about diuresing her with severe hypokalemia and precipitating an arrhythmia.
In the ICU setting I likely would have put her on nitro drip if blood pressure is okay, pressors if she was in shock, and would have felt comfortable diuresing her while throwing line for potassium replacement. I guess what I am asking is how would you approach if this patient was on the medical floors?

Obviously many ways to skin a cat. Here's my take-


If they are not in extremis, replete K and then diurese . If kinda in extremis, bipap +/- nitroglycerin and aggressive k repletion (PO and iv). Once it starts, start diuresis.

If they are in extremis enough to be in an icu, sodium nitroprusside to temporize. Replete K (iv and PO simultaneously) when it starts, diurese

 

[deleted547339]

Obviously many ways to skin a cat. Here's my take-


If they are not in extremis, replete K and then diurese . If kinda in extremis, bipap +/- nitroglycerin and aggressive k repletion (PO and iv). Once it starts, start diuresis.

If they are in extremis enough to be in an icu, sodium nitroprusside to temporize. Replete K (iv and PO simultaneously) when it starts, diurese

Sodium nitroprusside??? Is it 1970?

 

[Instatewaiter]

Sodium nitroprusside??? Is it 1970?

Haha. So, one of us in this conversation is an advanced heart failure doctor. the other person is you. So there's that. But to explain, these people didn't suddenly take in massive volumes of fluid. Rather the fluid is malpositioned either from splanchnic redistribution or massive increases in afterload. The PA pressures go through the roof. NTP will be a better choice than even lasix in the acute setting.

 

[deleted547339]

Haha. So, one of us in this conversation is an advanced heart failure doctor. the other person is you. So there's that. But to explain, these people didn't suddenly take in massive volumes of fluid. Rather the fluid is malpositioned either from splanchnic redistribution or massive increases in afterload. The PA pressures go through the roof. NTP will be a better choice than even lasix in the acute setting.

Lol. I’ve used it and did took care of more than my share of sick hearts in residency and fellowship - I just don’t see much need for it. I agree, most people don’t understand the difference between hf with a hyperadrenergic state while being essentially euvolemic vs. slowly eating and drinking your way into an overloaded stage.

I manage these folks (the hypertensive crisis type folks) with a few tabs of subling ntg plus bipap followed by an aggressive nitro drip +/- an ace-i.

Was just a little surprised. The only folks I know who use sodium niteoprusside regularly are old CCU attendings who use it diagnostically with a swan already in place. It’s not that I don’t think it could be useful, it’s just that I can do everything I need to do while using safer drugs.

 

[jdh71]

Lol. I’ve used it and did took care of more than my share of sick hearts in residency and fellowship - I just don’t see much need for it. I agree, most people don’t understand the difference between hf with a hyperadrenergic state while being essentially euvolemic vs. slowly eating and drinking your way into an overloaded stage.

I manage these folks (the hypertensive crisis type folks) with a few tabs of subling ntg plus bipap followed by an aggressive nitro drip +/- an ace-i.

Was just a little surprised. The only folks I know who use sodium niteoprusside regularly are old CCU attendings who use it diagnostically with a swan already in place. It’s not that I don’t think it could be useful, it’s just that I can do everything I need to do while using safer drugs.

What is so unsafe about nitroprusside?

 

[Instatewaiter]

Lol. I’ve used it and did took care of more than my share of sick hearts in residency and fellowship - I just don’t see much need for it. I agree, most people don’t understand the difference between hf with a hyperadrenergic state while being essentially euvolemic vs. slowly eating and drinking your way into an overloaded stage.

I manage these folks (the hypertensive crisis type folks) with a few tabs of subling ntg plus bipap followed by an aggressive nitro drip +/- an ace-i.

Was just a little surprised. The only folks I know who use sodium niteoprusside regularly are old CCU attendings who use it diagnostically with a swan already in place. It’s not that I don’t think it could be useful, it’s just that I can do everything I need to do while using safer drugs.

Don't see the need for it? The mechanism is totally different. Thats like saying I don't see the need for dobutamine because I have phenylephrine.

Nitroglycerin is a venodilator . Nitroprusside is an arterial vasodilator. With one you can afterload reduce. The other you cant really. This is vital for those in low output heart failure, those with a low EF and those with severe AS +low EF. If you want I can show you the mechanism with pressure volume loops (pretty sure no one wants that)

Nitroprusside is only unsafe if you aren't experienced using it... which for those outside of cardiology is common. Even many cardiologists don't feel comfortable. But, it is literally the drug of choice in many situations and safer than inotropes, especially in the ischemic. But what would I know... Apparently I'm just an old CCU attending

 

[deleted547339]

Don't see the need for it? The mechanism is totally different. Thats like saying I don't see the need for dobutamine because I have phenylephrine.

Nitroglycerin is a venodilator . Nitroprusside is an arterial vasodilator. With one you can afterload reduce. The other you cant really. This is vital for those in low output heart failure, those with a low EF and those with severe AS +low EF. If you want I can show you the mechanism with pressure volume loops (pretty sure no one wants that)

Nitroprusside is only unsafe if you aren't experienced using it... which for those outside of cardiology is common. Even many cardiologists don't feel comfortable. But, it is literally the drug of choice in many situations and safer than inotropes, especially in the ischemic. But what would I know... Apparently I'm just an old CCU attending

Your condescension precludes further informed conversation.

 

[jdh71]

Don't see the need for it? The mechanism is totally different. Thats like saying I don't see the need for dobutamine because I have phenylephrine.

Nitroglycerin is a venodilator . Nitroprusside is an arterial vasodilator. With one you can afterload reduce. The other you cant really. This is vital for those in low output heart failure, those with a low EF and those with severe AS +low EF. If you want I can show you the mechanism with pressure volume loops (pretty sure no one wants that)

Nitroprusside is only unsafe if you aren't experienced using it... which for those outside of cardiology is common. Even many cardiologists don't feel comfortable. But, it is literally the drug of choice in many situations and safer than inotropes, especially in the ischemic. But what would I know... Apparently I'm just an old CCU attending

I was taught cardiac critical care by a guy who trained at your shop who came to where I did fellowship to be part of the heart failure and transplant team. Nitroprusside was beat into me. I've seen it turn around many sick sick hearts. I use it all the time. The first time I pulled it out after showing up as a new attending you would have thought I was trying to kill the patient the way the nurse acted. Refused to give it. Pharmacy is freaking about the cyanide. Luckily the nurse manager was an old UCSF CV nurse and she hung it without blinking for me, and everyone watched the blood pressure go UP. And the patient start making urine. Lol. I didn't spike any footballs, but I knew I scored a bunch of points.

 

[Instatewaiter]

Your condescension precludes further informed conversation.

I didn't really think it was all that condescending...

 

[Instatewaiter]

I was taught cardiac critical care by a guy who trained at your shop who came to where I did fellowship to be part of the heart failure and transplant team. Nitroprusside was beat into me. I've seen it turn around many sick sick hearts. I use it all the time. The first time I pulled it out after showing up as a new attending you would have thought I was trying to kill the patient the way the nurse acted. Refused to give it. Pharmacy is freaking about the cyanide. Luckily the nurse manager was an old UCSF CV nurse and she hung it without blinking for me, and everyone watched the blood pressure go UP. And the patient start making urine. Lol. I didn't spike any footballs, but I knew I scored a bunch of points.

When people start using it, they become converts.

They joke at my current hospital that they can tell when I come on service, bc everyone gets put on nitroprusside

 

[turkeyjerky]

I didn't really think it was all that condescending...

It was, just a little bit.

What're your thoughts on clevidipine? Seems like a good alternative to NTP and easier to use.

 

[Instatewaiter]

It was, just a little bit.

What're your thoughts on clevidipine? Seems like a good alternative to NTP and easier to use.

Not unreasonable especially since nitroprusside got expensive. It is easy/fast to titrate unlike nicardipine. We would use clevidipine for our type A dissections after ntp became more expensive.

For hfpef with severe htn, not unreasonable. For systic heart failure, I still prefer ntp since it lowers pa pressure's better

 

[Dr.CCM]

Not unreasonable especially since nitroprusside got expensive. It is easy/fast to titrate unlike nicardipine. We would use clevidipine for our type A dissections after ntp became more expensive.

For hfpef with severe htn, not unreasonable. For systic heart failure, I still prefer ntp since it lowers pa pressure's better

Is there evidence that in fact lowers PA pressures better than clevi?

What about Milrinone in this patient population?

 

[CCM12]

I think niprid is recommended in the step up approach for management of severe hfref when no adequate uop on 2.5 times the home dose of iv lasix then lasix drip if bp > 90/60
chrome://external-file/nejmra1703100-1.pdf
This is a nice article review about diuretics in hf

 

[Radetzky]

The first time I pulled it out after showing up as a new attending you would have thought I was trying to kill the patient the way the nurse acted. Refused to give it. Pharmacy is freaking about the cyanide.

An example of why its better to have no knowledge of something rather than some knowledge.

 

[Radetzky]

Don't see the need for it? The mechanism is totally different. Thats like saying I don't see the need for dobutamine because I have phenylephrine.

Nitroglycerin is a venodilator . Nitroprusside is an arterial vasodilator. With one you can afterload reduce. The other you cant really. This is vital for those in low output heart failure, those with a low EF and those with severe AS +low EF. If you want I can show you the mechanism with pressure volume loops (pretty sure no one wants that)

Nitroprusside is only unsafe if you aren't experienced using it... which for those outside of cardiology is common. Even many cardiologists don't feel comfortable. But, it is literally the drug of choice in many situations and safer than inotropes, especially in the ischemic. But what would I know... Apparently I'm just an old CCU attending

I thought they both increase NO but through different mechanisms? Why would that have different effects on arterial vs venous? Not doubting, just curious.

 

[aafisahar]

I thought they both increase NO but through different mechanisms? Why would that have different effects on arterial vs venous? Not doubting, just curious.

NTP poisons highly metabolic cells with cyanide. Smooth muscle is highly metabolic in adrenergic crises.

NTG is converted to NO preferably in the venous system.

 

[Tipsy McStagger]

I think niprid is recommended in the step up approach for management of severe hfref when no adequate uop on 2.5 times the home dose of iv lasix then lasix drip if bp > 90/60
chrome://external-file/nejmra1703100-1.pdf
This is a nice article review about diuretics in hf

your link isn't working for me. do you have the title of the article? I'd like to read it. Thanks!

 

[CCM12]

your link isn't working for me. do you have the title of the article? I'd like to read it. Thanks!

Diuretic treatment in heart failure (review article in nejm)

 

[Instatewaiter]

Diuretic treatment in heart failure (review article in nejm)

If that is the nejm pub by Brater from like 1996 I second it. If not, I recommend looking that up too.

 

[Instatewaiter]

Is there evidence that in fact lowers PA pressures better than clevi?

What about Milrinone in this patient population?

Anectdotal. There is a trial ongoing looking at that exact thing. I guess definitive answer in a few years.

Milrinone oneset of action is too long and half life is too long to make as useful as ntp in this circumstance . Note that I never bolus milrinone as some do. Only time might be useful is if very low cardiac output and not enough BP to use ntp. This is a pretty small subset since milrinone tends to drop BP too...

I love milrinone. Tends to be my go to inotrope but as a longer term solution (hours to days instead of seconds to minutes )

 

[kokoclose]

These patients do great with MRAs like spironolactone. They're often hypokalemic precisely because they have high circulating aldosterone. So, in situations like this, you can pair furosemide with spironolactone if they're not already on it, and, if they are, bump up the dose.

In ATHENA-HF, for example, people in acute heart failure on IV frusemide paired with natriuretic-dose spironolactone (50-100mg) had zero change in their serum K--and it was a safe strategy with respect to mortality and renal function. (It was also a negative trial, but I've always wondered about the hypokalemic sub-group, which has never been studied.)

I try to avoid peripheral IV replacement as much as possible, because the mini-bags are often made up in normal saline. You're delivering a sodium load after giving furosemide, when the kidneys are very sodium avid. Much, much better be to give oral replacement.

 

[kokoclose]

Thanks so much makes sense!!

 

[MoMoGesiologist]

Not unreasonable especially since nitroprusside got expensive. It is easy/fast to titrate unlike nicardipine. We would use clevidipine for our type A dissections after ntp became more expensive.

For hfpef with severe htn, not unreasonable. For systic heart failure, I still prefer ntp since it lowers pa pressure's better

I've had a couple attendings say CCB gtt (nicardipine, clevidepine) in HFrEF/LVAD patients is contraindicated. I get how dilt and verapamil are contraindicated, even saw data that nifedipine has negative inotropic effect, but not clear why/how nicardipine or clevidepine is contraindicated in CHF... (I'm usually suggesting it on someone who NTG or NTP is not working and pt is still hypertensive)

 

[chessknt]

Haha. So, one of us in this conversation is an advanced heart failure doctor. the other person is you. So there's that. But to explain, these people didn't suddenly take in massive volumes of fluid. Rather the fluid is malpositioned either from splanchnic redistribution or massive increases in afterload. The PA pressures go through the roof. NTP will be a better choice than even lasix in the acute setting.

Thanks for your posts in this thread. Do you still feel nipride has a role in the hypotensive shocked chf patient if we think it is cardiogenic in nature? The chf docs in my place tend to put these people on diuretics and dobutamine and only use nip ride in the stable ones.

 

[Instatewaiter]

Depends what you consider hypotensive... systolic of 90s? Sure. 70s? Probably not.

 

[jw3600]

I always thought of NTG as a venodilator and an areteriodilator. As in it can reduce pre and after load. Should I change my thinking?

 

[jdh71]

I always thought of NTG as a venodilator and an areteriodilator. As in it can reduce pre and after load. Should I change my thinking?

nitroglycerin isn't doing much peripheral arterial vasodilation, so you should probably change your thinking on it

this is also the reason its stupid to flog patients with hypertensive urgencies/emergencies with it

 

[Hamhock]

nitroglycerin isn't doing much peripheral arterial vasodilation, so you should probably change your thinking on it

this is also the reason its stupid to flog patients with hypertensive urgencies/emergencies with it

I probably disagree...but it depends on what you mean by "hypertensive urgencies/emergencies".

If you mean acute and crashing sympathetic pulmonary edema with SBP >200 (EMCrit Podcast 1 - Sympathetic Crashing Acute Pulmonary Edema (SCAPE)), then NTG infusions should not be dismissed. There is more venodilation, but there is some arteriodilation also.

"SCAPE" patients will rapidly trend towards normotension (or even hypotension) with just NTG infusion both because the removal of the dyspnea/sympathetic surge but also because of the arteriodilation. Rarely do I ever have to use more than high-dose NTG infusions for SCAPE...longer term "CHF pulmonary edema" is a different game.

On the other hand, NTG infusion for things like ICH, renal failure, etc is not so useful and more arteriodilating medications are used.

HH

 

[jw3600]

Being a resident is already hard enough. Modern medicine is so controversial sometimes I don’t know even know why I try lol.

 

[jdh71]

I probably disagree...but it depends on what you mean by "hypertensive urgencies/emergencies".

If you mean acute and crashing sympathetic pulmonary edema with SBP >200 (EMCrit Podcast 1 - Sympathetic Crashing Acute Pulmonary Edema (SCAPE)), then NTG infusions should not be dismissed. There is more venodilation, but there is some arteriodilation also.

"SCAPE" patients will rapidly trend towards normotension (or even hypotension) with just NTG infusion both because the removal of the dyspnea/sympathetic surge but also because of the arteriodilation. Rarely do I ever have to use more than high-dose NTG infusions for SCAPE...longer term "CHF pulmonary edema" is a different game.

On the other hand, NTG infusion for things like ICH, renal failure, etc is not so useful and more arteriodilating medications are used.

HH

 

[jdh71]

Being a resident is already hard enough. Modern medicine is so controversial sometimes I don’t know even know why I try lol.

It's really a toxic personality problem in my opinion. Especially in critical care. And it won't be all of your attendings just a few. But those few zealots are all about one way of doing things (their way) while everyone else is not only wrong but killing people and mother**** everyone else doing anything different. Many ways to skin a cat. A patient is an individual case not an anonymous N in a randomized trial yeah? You do your best. Have a rationale. Advocate.

 

[WheezyBaby]

I've had a couple attendings say CCB gtt (nicardipine, clevidepine) in HFrEF/LVAD patients is contraindicated. I get how dilt and verapamil are contraindicated, even saw data that nifedipine has negative inotropic effect, but not clear why/how nicardipine or clevidepine is contraindicated in CHF... (I'm usually suggesting it on someone who NTG or NTP is not working and pt is still hypertensive)

I've heard the regarding the contraindication. To my understanding its based on the negative inotropy. Regardless, back when I looked into it, physiology studies demonstrated increased cardiac output with cardene despite the negative inotropy secondary to the afterload reduction. Wouldn't mind ISW's blessing on that comment though

 

[MedicineZ0Z]

When people start using it, they become converts.

They joke at my current hospital that they can tell when I come on service, bc everyone gets put on nitroprusside

What relative contraindications are there in those patients?

 

[Instatewaiter]

Are you talking about nicardipine? In that case borderline blood pressure and aortic stenosis. They've actually studied in low EF doesn't appear to be terribly deleterious although again there are better options

 

[Laryngophed]

I will say, I was a little taken aback in a LFLG AS patient on nipride. But someone dropped “the Clinic” and “observational study” and magically it was okay. It truly is an interesting concept, but definitely something that gave me pause. And I titrations inotropes ans vasoactive agents all day, erryday.