A Pacer Puzzler

Sometimes we see things on the monitor that while they look like things aren’t working correctly they actually are doing what they should.  Case in point from awhile ago.

The tech calls me and says, “Your patient in 75, they keep alarming for missing beats and pacer not pacing.  You going to call the doc?” as he hands me the following strips:

#1#2

I looked down, double checked and said, “Nope.  It’s working perfectly.”

In both strips you can see spots where it appears that the pacemaker is failing to pace, after 1st and 7th QRS complexes in strip #1 and after the 4th QRS in strip #2.  In each case you have a spike then a p-wave and nothing until a odd appearing PVC-like beat.  The tech pointed these out and I further reiterated that, “Yes, it’s working just fine.

But I had a cheat, I had read the interrogation report from when the patient had been admitted and knew what mode the device was set for, the tech hadn’t.  This is a pretty good example of a mode known as MVP, or managed ventricular pacing.  Basically this is a mode designed to reduce ventricular dysynchrony by allowing the heart’s natural conduction system to function while providing back-up in case of failure.  Excessive right ventricular pacing has been shown in studies to lead to congestive heart failure, increased incidence of atrial fibrillation, increased left atrial diameter and changes to hemodynamics and ventricular remodeling all of which can have detrimental effect on the patient and their quality of life.

In MVP pacing the pacemaker operates in AAI/R mode, as shown in both strips, with a set duration of time to allow for a ventricular beat.  If no beat arrives in the programmed time span the device will initiate a ventricular beat then return to the AAI/R.  If a beats are frequently dropped, usually 2 out of 4 complexes, the device shifts to DDD/R mode.  It will continue this way for a minute then attempt to return to AAI/R to detect AV conduction.  If beats are still dropped it will remain in DDD/R mode for increasing amounts of time, periodically checking for the return of AV conduction, at which point it will switch back to AAI/R mode.

Let’s break each strip down.

Strip #1:  starts with normal AV conduction in AAI/R mode and almost immediately, a beat is dropped and the device iniates the rescue beat.  It continues for 5 more QRS complexes until there is another dropped beat.  There is normal AV conduction for one more QRS then another dropped beat after which the device switches to DDD/R mode (it was too long to scan).

Strip #2: a little simpler.  4 normal QRS complexes then a dropped beat followed by a PVC, then another dropped beat.  Here you can see the device then switch into DDD/R mode due to dropping 2 out of 4 beats.

So, yes, the pacer was working exactly as it was supposed to.  I explained this to the tech and went on my merry way.  The next time he sees this he’ll stop to ask if they are set to MVP from now on.  Good learning moments come when you least expect them!

Sources:

Sweeney, M., Ellenbogen, K., Casavant, D., Betzold, R., Sheldon, T., Tang, F., & … Lingle, J. (2005). Multicenter, prospective, randomized safety and efficacy study of a new atrial-based managed ventricular pacing mode (MVP) in dual chamber ICDs. Journal of Cardiovascular Electrophysiology, 16(8), 811-817. Retrieved from EBSCOhost.

 Gillis, A., Purerfellner, H., Israel, C., Sunthorn, H., Kacet, S., Anelli-Monti, M., & … Boriani, G. (2006). Reducing unnecessary right ventricular pacing with the managed ventricular pacing mode in patients with sinus node disease and AV block. Pacing & Clinical Electrophysiology, 29(7), 697-705. Retrieved from EBSCOhost.

 

 

 

 

 

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Hypotension Causing Nursing Hypertension

Hypotension Causes: Three Cases Of Severe Hypotension and Their Dramatic Response To Treatment.

I’m almost going to print this up and drop it in a couple of hospitalist’s mail boxes as they completely buggered their management of the hypotensive patient.
So here’s the story…
50-odd year old dude comes in with bilateral foot wounds, both medicine and podiatry are seeing him.  They start antibiotics and aggressive debridement of the said foot wounds.  To complicate matters, dude is “fluffy”.  Y’know, 400+ and we can’t tell if he is edematous or not.  It’s all fluff.  Instead of thinking sepsis, they’re thinking he needs to be diuresed.  Considering a history of CHF, not a bad idea.  But as he’s getting massive doses of IV Lasix, we’re talking drip rates in the 40mg/hour range here, his urine output starts to drop.  It dwindles, then nearly completely stops.  Bad sign, right?

As this is happening, his pressures are following the exact same path, dwindling down to nothing over nothing.  We’re talking 60/doppler and his pulse is dandy.   But here’s the thing:  he is completely alert and oriented, talking a mile a minute watching the Food Network.

This goes on for 4 days and 5 nights.  Yes, 5 fucking nights.  The nursing staff would call the the on-call staff, explain the situation and be rewarded with, “Oh, uh, turn off the Lasix.”  or “Uh, um…give him a 500ml bolus of NS.” The staff leave detailed notes in the progress notes about the situation so that they can be reviewed by the next day’s docs, but still nothing is done.  Maybe some more piddly-ass boluses that do a whole lot of nothing, but produce no net effect.

Finally on Day 5 (yes, Day 5) as his kidney function is truly in the shitter (creatinine is like 4.0), his ‘lytes are all wacky, his H/H is crap, he barely has any albumin, he hasn’t made urine in 4 days and has been getting goofy at night needing higher amounts of O2, someone decides to actually DO something.  2 units of packed cells, albumin q8, a couple of decent fluid boluses and dopamine.  Finally.

And as if by magic, he gets a blood pressure.  A real blood pressure, like 120’s/80’s.  He slowly starts to make urine.  His O2 need starts to go back to baseline and he’s no longer goofy.  Podiatry decides that now that he is stable it is time to do surgery to lop off the now gangrenous foot and get on with definitive care.

Here’s the thing:  we could have fixed him on night 1 had the on-call doc been willing to look and realize something was not right.  Could we have called a Rapid Response?  Yes, but he wasn’t truly in need of it.  He was relatively stable, with the exception of no blood pressure and no urine.  Besides, we figured that we could manage him on the floor without the ICU.

No one seemed to be cognizant of the fact he was in septic shock from those nasty feet of his.  That is until a prog note was written post-surgery that basically said, “acute on chronic renal failure and septic shock.”  Finally someone got it.

Another for the Record Books

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7.5L of urine output in 24 hours.

Yes, a little over 300ml of urine every hour.  And this wasn’t a patient with some weird endocrine dysfunction or SIADH, but a patient in decompensated CHF.

He came in with sausages for legs and 3+ pitting edema to his armpits (quite nearly…).  The cardiologists throw some Lasix at him, but according to the Laws of the House of God (lasix dose = age + BUN) it wasn’t even close.  Sure he was peeing, but still edematous.  Start up the ACE inhibitor and a little bit of Coreg, but he’s still wiped out walking to the bathroom and looks like the Michelin Man’s long-lost homeless relative.  So what’s next?  Just a touch of dobutamine.  6 hours later it was like a faucet had been turned on.

By the time we were done with him he had legs again, could stalk the hallways looking for food without being short of breath and leave our fine institution.  I’m sure he’ll be back.

Biventricular Pacemakers

One of our EP docs has been doing a roaring business in bivent pacers lately.  Between upgrades to existing pacemakers and new bivents we’ve been seeing these frequently.  On top of that, when we moved, our telemetry provider upgraded our system and software so we could actually see bivent pacing.  I figured that a quick primer on bivents was in order.

What is a biventricular pacemaker anyway?  It is what it says.  There is a lead in each ventricle, pacing each ventricle.  Historically, pacemakers have been one sided only, usually the right ventricle (RV) and/or right atrium (RA) due to ease of access.  You pop into the venous system, float a wire into the right side and you’re good to go.  The difficulty ramped up in reaching the left ventricle (LV) generally, the veins of the coronary sinus are harder to access and of a smaller caliber.  Thanks to advances in catheter size and mobility, this has gotten easier.

But why do this?  In heart failure, espcially dilated cardiomypoathy, the dilation of the heart makes the ventricles, well, floppy.  They get big and stretched out and consequently the condution system gets stretched out as well.  What begins to happen is that the RV and LV start beating out of time (or asynchronously), which in the end makes the heart work harder to achieve the output needed.  The harder workig heart stretches more, which make it work harder to maintain output and on and on down the spiral.  Cardiac resynchronization therapy (CRT) with the use of bivent pacing enables the heart to start beating in time once gain.

I know that I’ve way oversimplified this, but I’m going for core concepts here.  But talking about CRT allows me to post up some great strips that I’ve picked up to demonstrate visually what is happening.

click for largerLooking closely, you notice a couple of things.  This is both a bivent and a dual chamber pacer.  Notice the spikes before the P wave and then the double spikes leading into the QRS complex.  We’re able to see both the RV and LV leads firing.  So instead of having only 1 lead firing in the RV and having the conduction impulse cross via cell-to-cell contact, each side of the heart is being paced, thereby getting better contractility and a better ejection fraction (EF).

Here’s the same patient:

click for largerI changed the tracing speed to 50mm/s to better illustrate the 2 separate ventricular spikes.

In many cases, this is coupled with a defibrillator (CRT-D) for the prevention of sudden cardiac death due to ventricular arrhythmias that folks with severe heart failure can be prone to.  And it is proven to work.  In the MADIT-CRT trials, there was a “29% reduction in death or heart failure interventions when comapred to traditional implated cardioverter defibrillators.”  (h/t Dr. Wes)

Yes, there are risks, there are patients this doesn’t work for and the cost is pretty steep (I’ve heard in the range of $45,000 for the device alone…) but it appears to do what it is intended to do.

Here’s a couple of resources for some in-depth information:

Cleveland Clinc: Biventricular Pacemaker

About.com: Cardiac Resynchronization Therapy

WebMD: Cardiac Resynchronization Therapy

When You Lose

You get used to seeing your frequent flyers, knowing their idiosyncrasies, learning their stories, sharing in their pain and struggle and once they are gone it almost leaves and empty void.  We lost one of those a couple of weeks ago, and I’m still dealing with it as it hit far too close to home.

Part of that was she was young.  My age young.  My wife’s age young.  With a family, children, hopes and dreams.  Another part was that we had brought her back once before.  The progression of her disease was insidious, things compounding into one another, each adding to the vicious cycle, adding momentum, gaining speed as she careened towards the final dance.  The heart failure brought about due to peripartum cardiomyopathy got worse.   The ray of hope that a heart transplant provided was shut out as her kidneys failed and the transplant folks never accepted her inability to lose those last 10 pounds.  I don’t think they realized that losing weight requires exercise and that it’s near impossible to exercise when your ejection fraction is 15%.

She had been on our floor for some time, then went to the ICU as she was no longer stable enough to be with us.  Dialysis at the bedside, levophed to keep her blood pressure high enough to perfuse the brain and what was left of her heart.  She told one of the aides that she wanted to come out to us, instead of our sister floor, when it was time to leave the ICU.  Her kids would come to visit, family too.  And finally it was enough.  She decided that she was done.  She was done with the fight that she had been fighting for so long.  How much of her youth had been spent dealing with this disease?  How much time away from her family had it robbed from her?  She had spent more time in the hospital this year than she spent at home.  So without telling anyone except the docs and nurses, she stopped everything and slipped away.  Selfish?  Maybe.  Maybe it was the action of someone who was just done.

I came back from time off and noticed that the location was no longer next to her name…never a good sign when someone was as sick as she was.  I asked and learned the truth.  I played with the idea of going to her service, but felt odd about it.  It didn’t feel right to intrude upon her family’s’ grieving in that fashion.  I still managed to say good-bye in my own way.

As a health-care provider, death is around us all the time.  I’ve eliucidated my views on death many times, and believe that it is a part of our journey, but when it happens to someone that you know, someone that you’ve taken care of, someone whose life you’ve saved, someone who is close in age to the wife you love, it hits far too close.  I know that she is somewhere better, freed from the shackles of her disease, resting peacefully now.

Pooling for Patients

Since we’re a cardiac floor we have a large contingent of frequent flyer patients.  Most common are our CHFers and chest paineurs, along with the occasional COPDers.  Some of them are very nice folks, they’re respectful and pleasant, others just downright nasty.  You learn their quirks.

One guy who has “adopted” us as his new tune-up clinic is actually one of the nicer of our bunch.  He’s a CHFer who has very tenuous grasp on the idea of a low sodium diet, which invariably leads to his admission for fluid overload/CHF exacerbation.  We’ve tried really hard to teach him that eating at Wendy’s, eating bacon and movie theater popcorn is not the best elements of a low sodium diet, but it doesn’t seem to stick.  The last time he was in though we decided to have a little fun.  Looking back at his previous admission I looked to see what is BNP level was.  BNP, or brain natriuretic peptide is a protein secreted by the ventricles of the heart due to excess stretch brought on by fluid overload of the myocardium.  It’s a good indicator of the fluid status of a patient in acute decompensated heart failure.  We use it to determine how bad the failure may be.  It’s not always the best nor the most accurate, but it works pretty well.  If the level is under 100pg/ml it is considered normal.  Values above that show increasing levels of heart failure.  Our daignostics cut-off at 4500pg/ml, but at that point, the number really is maningless:  it’s high.

Looking to have some fun I announce, “OK, Larry is in the ED, I’m pretty sure he’s going to get admitted.  Anybody want in on a pool for his BNP level?  It’s a buck to buy in, the closest gets the pot.”

“Who?” asks Charlie, “Do I know him?” she continues.

“Yeah, he’s the one with the crush on Tanya.” I said.  Which wasn’t far from the truth, he’s a young guy and when he’s admitted and Tanya is on, he comes and hangs out by the nurses station.  He usually lives inthe 1500s range when he’s admitted.

“He’s the one who eats at Wendy’s right?  Put me down for 1850.”  Charlie says.

I put in for 1500.  No one else wanted in.  I think they kind of thought it was a bit weird that we were pooling on our patients.

Sure enough Larry comes up.  And his BNP?  1225pg/ml.  I won, being the closest, but I didn’t have the heart to take Charlie’s money.  Maybe next time.

Trial of Gene Therapy for Heart Failure

First trial of gene therapy for advanced heart failure shows promising results

Kind of cool.  We know that gene therapy and further advances in modulating the body’s response to disease is going to change the way we practice medicine, it’s just a matter of time.  Now that Phase II trials are starting, we might get more concrete information if this really works.

Here’s another article about the trial: UC San Diego Medical Cente rOffers Gene Therapy Clinical Trial for Advanced Heart Failure

And last but not least, a licnk for the investigational drug: MYDICAR

via Digg