Inferior MI

Brady rythms are common with inferior MI.

RCA-Circ involvement, also hits the innervation of the nervous system with nausea and vomiting more than your anterior MI's_ left ventricle.

I never could understand how sick an inferior wall MI could be and come out smelling like a rose with a good ef%, while a huge anterior wall would have only weakness and have a huge EF hit, only not to accept their MI as serious:confused: Why do you have to blow out the heart to a 30 or 25% EF untill you see.. it's time for a change.... anyone else see this?

The inferiors also have tachy- brady as the sino-atrial node can be hit and afib and flutter are as common 48 hours out as a cabg!

We've two massive anterior walls with lateral and inferior extentions on my unit now, one on dobutamine, one a "functional cripple due to lack of reserve, neither ever felt "sick" or "dying" through their stay... while a massive Inferrior had rapid afib, converted with amio, a touch of diuresis with right sided failure and moved out 4 days ago, while my two anteriors are still sitting being closely guarded. doesn't make sense somedays.... the minor anterior walls to me are the hardest to gain compliance for as they just sail through as ticking time bombs... and seem more apt to be non-compliant as their course was simple and early on fixed.... yep, we see 'em later..... keeping up the teaching.

hope this helps, your inferiors are tacky-brady with frequent afib and nausea, your anteriors-lad, main, opm sail free initially. It's not uncommon for your emergent inferiors to present post cath to the ICU with transvenous pacers until 72 hours out until the sinoatrial node either steps back up, or a permanent pacer is put in. and 48 hours out, these guys are on step down when they do their rapid a fib bit... be prepared.

Inferior MI's, esp. those involving the RV actually have a higher mortality than "other" MI's. A couple of big things you can often times see are brady-arrhythmias, brady A-Fib, Junctional rhythms, and some rapid A-Fib also. I think this is especially common because the SA node is commonly affected. With RV involvement, you will often times have profound hypotension, and peripheral edema due to the loss of the right side of the heart. I've seen CVP's of 23 and 25 in patients who have severe RV infarcts, while they had clear lungs, and low BP. JVD will be very prominent often times. Many times the only way to treat them is to drown them and then cautiously diurese them, making sure you don't crump their pressure.

As far as EF's go, they really don't mean much with an inferior MI which is affecting the RV and Rt-side in general, you need to get a specific RV EF, not the typical LVEF which we usually see when basic echo's are done. You may also see some Ventricular Septals shift, and many patients who die from RV infarcts are showned to have a patent Foramen Ovale, as a result of the increased pressure. A big thing that you will see is CP with hypotension, JVD, without rales, and a patient who is brady'ing down on you and having nausea and vomitting. Some of the sickest patients you will ever see, and if re-perfused, they can "Come out smelling like a rose," if not, you may be tasked with making "the Call!!!!"

and many patients who die from RV infarcts are showned to have a patent Foramen Ovale, as a result of the increased pressure. ..QUOTE]

??? PFO's are congenital...not 'pressure' induced.

and many patients who die from rv infarcts are showned to have a patent foramen ovale, as a result of the increased pressure. ..quote]

??? pfo's are congenital...not 'pressure' induced.

actually, they can be pressure induced. go back a while on this forum, and there was a member named "medical zebra" who had one. supposedly related to line insertions, but it was probably more likely related to increased pressures against her ra. do a little search, and you'll see that they are not completely congenital. ever here of a right to left shunt???

here's a decent article to read regarding rv infarcts, and development of pfo's: http://content.onlinejacc.org/cgi/content/full/44/4/793

right-to-left shunt flow through a patent foramen ovale caused by elevation of rv filling pressure is a well-described complication of patients with rvmi and can produce refractory systemic hypoxemia (7). systemically administered vasodilator or inotropic therapy has limited efficacy in decreasing shunt flow, as agents that decrease ra pressure simultaneously reduce the left atrial pressure, leaving the transatrial pressure gradient unchanged. attempts to mechanically close a patent foramen ovale to decrease inter-atrial shunting in rvmi patients have had variable success (33,34). in our study, we observed that 3 of 13 rvmi patients had significant right-to-left shunting through a patent foramen ovale despite breathing at fio2 = 1.0, whereas breathing no consistently reduced the shunt flow and improved systemic oxygenation.

Actually, they can be pressure induced. Go back a while on this forum, and there was a member named "Medical Zebra" who had one. Supposedly related to line insertions, but it was probably more likely related to increased pressures against her RA. Do a little search, and you'll see that they are not completely congenital. Ever here of a right to left shunt???

Here's a decent article to read regarding RV infarcts, and development of PFO's: http://content.onlinejacc.org/cgi/content/full/44/4/793

Thats a decent article, but PFO's are congenital. The quote you put up is talking about a rt-to-lft shunt caused by high pressures in someone with a pre-existing PFO. It's pretty clear.

IF you're trying to say that elevated pressures from an inferior MI can cause some sort of septal-rupture, that would be very very unusual (has it ever happened???). The chamber pressures required to 'blow a hole' through someones septum seems... far-fetched...and the patient would have other problems (death) to contend with rather than a shunt. I think you may have misinterpreted this article.

thats a decent article, but pfo's are congenital. the quote you put up is talking about a rt-to-lft shunt caused by high pressures in someone with a pre-existing pfo. it's pretty clear.

if you're trying to say that elevated pressures from an inferior mi can cause some sort of septal-rupture, that would be very very unusual (has it ever happened???). the chamber pressures required to 'blow a hole' through someones septum seems... far-fetched...and the patient would have other problems (death) to contend with rather than a shunt. i think you may have misinterpreted this article.

dinith,

the blue quote is taken specifically from that article.(not my interpretation) also aha, acls for experienced providers has some info on it, if you can get a copy. it kind of goes over the problems with treating rv infarcts, and how they present. really a good course if you can get into one. i thoroughly enjoy teaching it far more than regular acls. not sure why you are questioning this, the article is the source, not me. you might want to read the article, and see what it has to say. rather than make yet another thread a personal attack.

taken from this site: http://content.onlinejacc.org/cgi/content/full/44/4/793

right-to-left shunt flow through a patent foramen ovale caused by elevation of rv filling pressure is a well-described complication of patients with rvmi and can produce refractory systemic hypoxemia (7). systemically administered vasodilator or inotropic therapy has limited efficacy in decreasing shunt flow, as agents that decrease ra pressure simultaneously reduce the left atrial pressure, leaving the transatrial pressure gradient unchanged. attempts to mechanically close a patent foramen ovale to decrease inter-atrial shunting in rvmi patients have had variable success (33,34). in our study, we observed that 3 of 13 rvmi patients had significant right-to-left shunting through a patent foramen ovale despite breathing at fio2 = 1.0, whereas breathing no consistently reduced the shunt flow and improved systemic oxygenation.

continuing on, one of the risks with ventricular septal shift can be not only septal rupture, but as that septum shift to the left, it decreases the lv filling volume, further complicating the hypotension.

dinith,

the blue quote is taken specifically from that article.(not my interpretation) also aha, acls for experienced providers has some info on it, if you can get a copy. it kind of goes over the problems with treating rv infarcts, and how they present. really a good course if you can get into one. i thoroughly enjoy teaching it far more than regular acls. not sure why you are questioning this, the article is the source, not me. you might want to read the article, and see what it has to say. rather than make yet another thread a personal attack.

.

please dont take this as a personal attack! i'm only trying to clarify this (it's kind of an obligation because we're all nurses(play on words) and shouldn't mis-inform as it reflects on us all)

the quote you posted should be read this way: 'rt-to-lt shunt flow (through a patent foramen ovale) caused by elevation of rv filling pressures blah blah blah... the part of this quote that you've misinterpreted is that you're assuming the pressure is 'causing' a pfo...but it's actually stating the pressure is 'causing' a 'shunt' through the pfo (which is congential). everyone has a pfo (or more acurately an fo) when we're newborns (or just prior to...i think?) and they close up shortly thereafter. the 'p' in pfo means the fo didnt close up ('patent')...it's not all that uncommon. pfo does not mean septal-wall rupture. period.

it's saying high rv pressures are causing the shunt....not the pfo.

look at it like this... take your right ventricle and fill it with gazillions of pounds of pressure...the 'force' of this pressure would eject itself back through the tricuspid valve or up through the pulmonic valve (as they're already pressure escape 'holes' in the ventricle.)...not blow a new hole in the septal wall. it's simple...and common sense.

this is not a personal attack!!!

Actually Dinith, the PFO IS a result of the increased pressure. As the pressure continues to increase, something has to give. The PFO is, more or less, an Atrial Septal "Defect." See pic here: http://www.wellesley.edu/Biology/Courses/111/ForOval.gif

What happens is as the pressure continues to build up, the FO opens, and then the R-to-L shunt occurs. True, these people may already have the predisposed PFO, however, unless they are placed in a situation in which the Rt sided pressures are significantly elevated, the FO never really opens. Actually when doing diagnostic to determine if a patient may or may not have a PFO, a patient may be asked to cough, or pressure may be exerted on the pt's lungs to simulate pulmonary HTN, and then check very closely via Echocardiogram or TEE to visualize the PFO. And oddly enough, we rarely hear about PFO's being problematic unless there is R-to-L shunt, or the patient has a CVA. Supposedly about 25% (suspicions are that the actual %may be higher, as the more investigating that is done, the more often PFO's are found) of the population has a "PFO," however very few of those ever have complications as a result of them. In the situation where a patient has an RV infarct, the increased Rt-sided pressure force open a PFO that would have otherwise remained closed. Therefore, I suppose what I am saying is that the increased pressure makes the "PFO" patent, whereas it otherwise may have never opend up unless the patient coughed very hard, or beared down, and then it would be for very short periods of time.

. Therefore, I suppose what I am saying is that the increased pressure makes the "PFO" patent, whereas it otherwise may have never opend up unless the patient coughed very hard, or beared down, and then it would be for very short periods of time.

Now you're on the right track with this last statement.

And your statement would concur with the fact that PFO's are congenital...and not 'caused' by pressure...but that pressure can cause a 'shunt' through a PR-EXISTING pfo.

Good job.

I was at work last night reading all your comments mostly about pfo's. I am currently employed at a floor specific to pediatric congenital heart defects. It in no means makes me an authority seeing how I just ventured into this field 15 weeks ago. I asked around the unit and the consensus is final. We are siding with Dinith's argument. It is only a congenital defect already existing. Possible to have without being symptomatic. But you can't have an foreamen ovale open once it closes 4-6 weeks after birth. It has to be a patent foreamen ovale in existence. To be absolutely certain, I will ask one of the docs next time I see one. Interesting discussion, though. You all impress me with your knowledge. You make me proud to be a nurse.:balloons: