Relationship between CHF and MI?

[stoic]

Here's the deal -

85 y/o female, healthy other than breast cancer w/o masectomy and high blood pressure. No previous history of SOB or chest pain. No family cardiac history. Family history if DM, but not diagnosed herself.

Presents in ER during AM after night of S.O.B. and slight chest pain.

Triponin slightly elevated, BNP 1100, other labs normal, blood glucose 180, all other labs normal

The lady was admitted with a dx of CHF. After cardiology consult, dx is changed to MI.

My question is why is the BNP so high? Is this a response to the MI? Or could this be failure w/a complicating MI? I'm confused because I was under the impression that a BNP > than 400 was considered severe CHF and with this lady have no prior history of failure symptoms it seems strange that it would first be detected at this level. Where, if at all, does the glucose level play in?

Please educate me.

Dave

PS... the lady is my g-ma, so I'm trying to get as much info as I can.

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[Idiopathic]

Diabetics can have painless MI's, and she may have had one. Troponins certainly suggets an MI 5-7 days ago (right?) and CHF would follow...I think that your grandma had an AMI, progressed into left heart failre (elevated BNP) and now presents with dyspnea as a result of the LHF. ACE-inhibitors first and beta blockers after about two weeks is probably what they prescribed her.

 

[DR]

Dude, you have ischemia to a portion of the myocardium, the heart loses muscle, therefore loses pump (LV) function, goes into temporary (either severe, or mild) failure. It's (myocardial infarction) in the top 3 in the differential for causes of CHF. Remember, technically CHF is not a diagnosis, it's a consequence of some other process...one of which is MI.

 

[DR]

...and actually it's usually beta blockers first, then ACE inhibitors later.

 

[DR]

BTW...
Sorry for the repeat posts, but I just noticed your question regarding the glucose. 2 things: First, she may have a new diagnosis of diabetes; as you probably know those with DM have vascular disease, pretty much by definition (just about). However, she may not have DM, and in fact this may be a stress response to her MI (glucose increases in response to stress...in which an MI most certainly qualifies). Finally, she may have neither...and might have just eaten a little while earlier.

 

[Scarlet_Fire]

late onset insulin resistance is possible and likely given her age, but also the acute stress event itself may be responsible for her elevated blood sugar level to some degree

 

[Idiopathic]

Originally posted by DR
...and actually it's usually beta blockers first, then ACE inhibitors later.

no, no, no...ACE-I is a first line drug, beta blockers only given after patient is more stable. (post-MI, that is)

 

[Eidolon6]

BNP is released in response to increased stretch of the myocardial muscle units. Killing and lysing muscle cells as in ischemia.....releases BNP. Additionally, ischemic and or stunned myocardium stretches, without appropriate Starling response, as a consequence of systole. Utility of BNP measurement is in flux...although in optimized CHF patients, some studies suggest a link to morbidity/mortality. ER physicians have been using the test in some areas....to r/o pneumonia and rule in CHF....which is poor form if you ask me, for various documented reasons. In the acute setting...more money should be weighed on that elevated troponin....

 

[Renovar]

Originally posted by daveswafford
Here's the deal -

85 y/o female, healthy other than breast cancer w/o masectomy and high blood pressure. No previous history of SOB or chest pain. No family cardiac history. Family history if DM, but not diagnosed herself.

Presents in ER during AM after night of S.O.B. and slight chest pain.

Triponin slightly elevated, BNP 1100, other labs normal, blood glucose 180, all other labs normal

The lady was admitted with a dx of CHF. After cardiology consult, dx is changed to MI.

My question is why is the BNP so high? Is this a response to the MI? Or could this be failure w/a complicating MI? I'm confused because I was under the impression that a BNP > than 400 was considered severe CHF and with this lady have no prior history of failure symptoms it seems strange that it would first be detected at this level. Where, if at all, does the glucose level play in?

PS... the lady is my g-ma, so I'm trying to get as much info as I can.

Sorry to hear about your granma. My best attempt to answer your question is this.

BNP is a marker for heart failure. Most cardiologist would definte heart failure as "loss of (or abnormal) left ventricular contractile function resulting in decreased tissue (ie end organ) perfusion." And let's just say that the brain is not one of the organs that tolerate mal-perfusion well. BNP is one of those things that the brain produces when it is chronically under-perfused such as in HF. AMI, on itself, does not cause BNP release.

MI, on the other hand, represents infarction of myocardium mostly secondary to advanced coronary atherosclerotic disease. It is usually diagnosed with EKG changes, enzyme (troponin I, elevated CK AND MB fraction) elevation, and symptoms. 2 out of the above 3 factors positive would be convincing evidence for MI.

The connection between MI and CHF is that former can lead to the latter. If the myocardium is infarcted, it will eventually be scarred down and will lose its myocardial contractile function. In your grandma's case, I would imagine that she must have some degree of mild underlying baseline LV dysfunction, and then have a superimposed MI that acutely decompensated her LVEF. And heart failure symptoms sometimes dont present itself until late stages when the LV dysfunction become markedly decreased.

Glucose level is the last thing she should worry about at this time. In an acute stress setting, such as an MI, it will not be surprising if that represent an acute stress reaction from her adrenal axis dumping out cortisol causing her temporarily elevated glucose. It will be a good idea to get a random level or a fasting level after she recovers from acute setting.

 

[Idiopathic]

Originally posted by Eidolon6
BNP is released in response to increased stretch of the myocardial muscle units. Killing and lysing muscle cells as in ischemia.....releases BNP. Additionally, ischemic and or stunned myocardium stretches, without appropriate Starling response, as a consequence of systole. Utility of BNP measurement is in flux...although in optimized CHF patients, some studies suggest a link to morbidity/mortality. ER physicians have been using the test in some areas....to r/o pneumonia and rule in CHF....which is poor form if you ask me, for various documented reasons. In the acute setting...more money should be weighed on that elevated troponin....

BNP releases as a result of stretch. Increased preload without ischemia would result in BNP release. It is more of a secretory product than a marker for cell death.

 

[stoic]

Thanks for all your replies, folks. I really appriciate the info becuase other than SDN, the only info I'm getting about g-ma is coming from freaked out relatives and it's pretty hard to actually figure out what's going on from them.

Thanks again.

 

[DR]

no, no, no...ACE-I is a first line drug, beta blockers only given after patient is more stable. (post-MI, that is)

I don't mean to nitpick, but I am pretty much correct with my beta blockers first. The first thing you do when someone comes in with an MI is IV lopressor, as long as their LV function isn't crap. It acutely lowers resting heart rate, blocks sympathetic tone, and overall decreases myocardial oxygen demand. Recall your ACLS. ACE inhibitors too may be started in the first 24 hrs, but do not offer any of the above acutely, to decrease immediate mortality (especially reentrant tachyarrhythmias, an important immediate post-MI cause of death). Lopressor can be easily tapered via IV drip to control hemodynamic parameters, whereas ACE inhibitors are longer lasting, and must watch for hypotension...especially after MI when it is the Renin-Angiotensin-Aldosterone system that is maintaining hemodynamic stability. You can indeed start both immediately, but it is the beta blocker that is the first on board in major cardiac centers and CCU's. Both are useful for decreasing risk of repeat MI and mortality in general...over long term. Acutely, beta blocker will save myocardium...when done correctly and pressure is not allowed to dip too low.

 

[Idiopathic]

This case is about a patient who is obviously 5 days post-MI, and now in CHF. Are you saying that you wouldnt give an ACE-I first? I am just trying to rectify what you are telling me with what my most recent clinical lecturer told me.

 

[DR]

Where does it say 5 days post MI? It says she came in to the ER the morning after a night full of CP and SOB. He says that she ruled in for MI, and also had a high BNP (which is pretty much not useful in the setting of acute MI for reasons we all stated). I agree with you, Idiopathic...an ACE is appropriate, too, given the current literature. So we agree. But the mechanisms of action of ACE inhibitors and beta blockers are different, and the beta blocker would immediately remove many of the factors that are causing the infarct. You wouldn't wait 2 weeks later, is all I'm saying (as you said in your original post)...you'd start some lopressor ASAP. You can start an ACE right away too, but if anything, the ACE has the larger warning attached, which is hypotension. Think of how you dose an ACE; they are usually QD or BID, which means they hang around for a bit. They will definitely reduce cardiac risk over time given their ability to affect remodeling, decrease afterload, etc. etc. But a beta blocker acts to cut right to the core of the cause of myocardial ischemia: cardiac work. Lowers oxygen demand almost instantly when infused, and is so short acting, you can literally tweek it to make sure you don't drop the BP. Waiting 2 weeks until after the MI is not standard of care, and would result in a lawsuit if the patient didn't do well. Talk with the cardio guy who gave the lecture...in an acute MI, they won't urgently call out for captopril/ramipril, or whatever...they will, though, call for IV lopressor (though it is probably already hanging there by the nurse).
So I totally am on the same page with ya; an ACE would be useful as well. Just gotta give the blocker immediately, as well (obviously as long as she isn't in cardiogenic shock, which changes everything about this case, and in which both the ACE and the blocker would be the last thing on your mind at the time!)

 

[Idiopathic]

Originally posted by daveswafford
Triponin slightly elevated, BNP 1100, other labs normal, blood glucose 180, all other labs normal

I gathered from this that no CK-MB was present...troponins disappear after 7-10 days, so this would say to me that the MI was at least three days prior.

 

[PTCA]

I believe that you guys have successfully answered the original question.
I don?t pretend to know anything, being an MS. But since you guys seem to know what you are talking about I felt this might be a good opportunity for me to clarify a thing or two?
In the acute face
ACE-I has an absolute indication if that person has LVF (which she probably does according to history). You are right to argue that b blocker could be crucial since you can vigorously monitor pressure in the CCU. But concerning this particular patient since it is pretty much granted that she has VF (especially if her fraction is below 40%) while it is unknown if she has arrhythmias, she isnt young and her infract could be quite large (if the HF is due to myocardial dismotility and not due to mitral valve dysfunction) do you think that b blocking is still the most beneficial of the two?
Long-term
Would you agree that whether b blocking is a long-term treatment option for her or not will be determined by her discharge ventricular function test?

Troponin drops later than CK-MB, but also rises faster (4h). So could this be a very recent instead of late MI?

Best of luck to your grandma daveswafford. The situation you are experiencing is difficult but I think that you should try to maintain a positive outlook. Many people recover successfully from MI.

 

[PTCA]

Plus, what people where I study are always yelling is that the very first thing for MI is:
Aspirin!(chewed) along with O2 and morphine (IV)
and then rush to revascularization
is it too late for all that as far as this patient is concerned?

 

[DrQuinn]

I think you two are perhaps miscommunicating:

No BB in CHF until they are compensated.

BB definately in MI unless there is reason not to give (i.e. COPD, CHF).

ACE/I in CHF most definately.

ACE/I most likely in most MI patients.


Also, you can bump your troponins in a lot of ways. Got a little afib that converts to NSR? Your trpI will bump up a bit. Got a little PE that you lyse two days later? Your trpI will bump up a bit.
Q, DO

 

[adude]

ASA-definitely should be given to all patients suspected to have acute coronary syndrome
Morphine-only if needed for pain relief
Oxygen-no evidence or theoretical reason for this unless the patient is hypoxic but is generally used on everyone

Revascularization(eg emergent cath or thrombolysis)-only in the setting of ST elevation MI within 12 hours of the onset of symptoms. Although there is some data that early (within 24 hours) cath is of benefit in NSTEMI or unstable angina, and most would procede to this if the patient continued to have pain despite treatment with nitrates and morphine.

In her case the indication for the beta-blocker is acute coronary syndrome and improves mortality in the short term as well as down the line in a secondary prevention sense for someone with CAD. Whether or not her CHF will tolerate it is another issue but if it does it is also beneficial in someone with poor LV function. No matter how low the EF most cardiologists try to use them in stable CHF patients.

 

[Idiopathic]

I am pretty sure that the initial morphine use would be to try and reduce pain to reduce heart rate in an attempt to get as much blood in the coronaries as possible. I know there are more intricate effects, but I think those are not at work here

 

[DrQuinn]

Besides pain control, and relief of anxiety during an ACS, morphine also has preload reducing abilities. I've turned several CHF'ers around with a squirt of Morphine (instead of tubing).

Q, DO