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.

Looking 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:

I 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

Question to the Experts

Awhile ago I’m sitting charting when the tele tech comes out of his cubby and says rather excitedly, “93’s rate dropped to 27 and is staying there!”  I pop up, walk over to the room and and see my patient sitting at the side of the bed with a look that says, “What do you want?”

“Do you feel OK?” I ask as I’m slapping a BP cuff around his arm.

“Feel fine.”

“Not dizzy, light-headed?”  I press.

“Nope, nothings changed from when you were here last.”  he says as the BP pops up 144/72.

“Your heart rate dipped into the 20’s and hung there for awhile, that’s all.”  I reply.

Here’s the funny thing though:  he had been doing this for days.  No problems with the low pulse at all.  Peeing fine.  No light-headedness, dizziness, auras or any other weird lack-of-perfusing the brain problems.  Only problem was when he moved about too much, he turned a lovely shade of eggplant purple.

Telemetry was showingwhat appeared to be a slow atrial fibrillation, but with his size, it would not have surprised me it if was a combination of junctional and ventricular escape rather than the a-fib due to the morphology of the QRS complexes.  Even with that in mind though, it could have been a-fib with a bundle branch block.  Then by luck, the morning before he was going to get a pacemaker the tele tech and I were chatting and examining his rhythm when we were able to get this shot.

It starts with a PVC, then a sinus beat and another PVC.  Then it starts to get funky.  The deflection of the QRS complexes shift in every lead except the V-Lead, flipping opposite from what they had been doing.  There wasn’t slowing of the rate that could be coupled to this flip as he had gone lower several times during the night and his strips hadn’t changed like this.  Looking back through, we noticed that he had been doing this all along, but had never captured it on paper.

So why question becomes:  what the hell is going on here?  Am I looking at a junctional/ventricular escape type of rhythm?  Or an intermittent right/left bundle?  And what could be causing this transient shift in axis, especially with no complaints from the patient?

And for what it’s worth, he got a pacer and looked much, much better the next day.  But I’m still baffled.  Any help?

Being Prepared

A 30-something year old male presented to the ED of an outside hospital complaining of palpitations that had been occuring intermittently for about a month.  When he had awoke that morning they were present and had not abated as they had in previous instances, so he went to the ED.  No prior medical history, no medication, no alcohol, tobacco or illegal drug use was reported.  The ED physician contacted a cardiologist at our institution for transport of the patient and admission to cardiology.  The patient’s heart rate was in the 160’s and above, but he was hemodynamically stable, nonetheless an antiarrhythmic drug was started and his heart rate slowed prior to transport.

After an hour and a half transport from the outside hospital the patient arrived and was placed on telemetry.  He was noted to have a rapid heart rate in excess of 190 beats per minute.  Subsequently the following 12-lead EKG was obtained.

As you can see, the heart rate is actually exceeding 200 BPM in this shot.  No P waves are seen as either they aren’t present or the rate is too fast and they blend into the QRS.  But how could a guy who’s rate had been controlled prior to leaving the oustide hospital suddenly ramp up?  Well, if you run out of the drug, in this case procainamide, halfway through transport, you tend to have problems.  Evidently, the medics misjudged the length of transport and left with less than half a bag, which at the rate of the infusion was no going to last them all the way to our facility.  So they ran dry en route and this gent’s heart rate started to go back up as the procainamide wore off.

Needless to say, it was restarted ASAP.  After a loading dose and about 15 minutes on the infusion, his 12-lead looked like this:

So what’s going on with this guy?

If you guessed WPW, you would be correct.  Notice the delta wave that is present, most notably in leads II and III.  Coupled with the rapid rate it is a near classic presentation of WPW.  But what is it?  Wolf-Parkinson-White Syndrome is classified as a pre-excitation arrhythmia where electrical impulses leaving ther SA node travel through an accessory bundle of nerve fibers called the bundle of Kent and travel directly to the ventricle, usually the left, sparking a depolarization before the regular impulse travels through the AV node, or pre-exciting the ventricles.  Notice the short PR interval that leads into the delta-wave of the QRS, this is the electrical stimulus traveling through the accessory pathway to the ventricles.  Typically, the bundle of Kent is present in the fetus, but then is electrically isolated by furhter development, in individuals with WPW, this didn’t happen.  When patients are ina normal sinus rhythm, the haert rate can remain controlled, but in people in atrial fibrillation or atrial flutter, the rapid, chaotic atrial impulses are conducted directly to the ventricles resulting in heart rates up to 300 bpm and usually subsequent arrest.  As you can see there though, just because you’re in normal sinus rhythm doesn’t mean your rate can’t rapidly rise.  Treatment of individuals with WPW can be complicated especiallywhen they present with AFib, as normal pharmacological treament, calcium channel blockers, beta blockers, tend to reduce the conduction through the AV node allowing the impulses through the accesory bundle to maintain and even accelarte the heart rate.  In cases like this patient, antiarrhythmics, like procainamide and amidarone can be used to control the heart rate.  Typically, and in this case, a trip to the EP lab is in order to have the accessory bundle mapped and ablated thereby blocking the pathway.

Here’s a couple of good links for WPW:

Wolf-Parkinson-White Syndrome – Wikipedia

Wolf-Parkinson-White Syndrome – eMedicine

A Little Cardiology Geekery – A Day in the Life of and Ambulance Driver

A Happy Hospitalist: Is Telemetry Overused?

A Happy Hospitalist: Is Telemetry Overused?.

In a short answer: yes.

Does an elder with stable chronic atrial fib being admitted for a UTI need tele?  Nope.  ETOH withdrawal without cardiac history?  Nope.  Too often folks admitted to tele don’t truly need it, and those that may benefit, don’t get admitted (at least right away…).

Happy makes the case of a patient having 12-beat run of SVT.  Remember, supraventricular tachycardia and ventricular tachycardia are 2 very different beasts.  Any good tele nurse should know this.  One is an abberrant rapid rhythm, that when it is self-limited while notable, is not life threatneing (SVT).  The other, is the same way when self-limited, but can be a very bad thing if not (VT).

If it was my patient who had  a 12-beat run of SVT what would I do?  Check them, make sure they’re ok.  Document it and go on my merry way.  If it is something that is happening regularly and with increasing frequency, I might text page the doc an FYI.  But an isolated 12-beat run isn’t even enough to get my heart rate up.

On ther other hand, the delirious UTI patient with a pacemaker on tele who spends the entire night ripping tele leads off may cause me to call the doc for a “d/c tele” order though!

Yikes!

Sphincter-Clenching Case

via ER stories.  It’s pretty damn awesome.

I seem to forget that many times when you have an inferior infarct, odds are pretty good that there is RV involvement.  I remember having an intern literally babysit a patient on the floor one night because she though he was having a RV infarct and was kind of freaked out about it.  She just hung out at the nurses station for hours waiting for the shit to hit the fan, but it never did.  If I remember right, we did a right-sided EKG and it was benign as well.

What bugs me is that during our unit education/skills validation sessions, it’s all LV infarcts.  Which of course means that using nitro is pounded into our heads, but no one stops to ask, “What about RV involvement?”  Sure, it is relatively rare, but it is something that we need to know about.  Granted, LV infarcts are far more common and we need to know how to treat them (at least to keep them alive until they can get cathed…), but I wish the educators would look a little deeper.

EKG of the Week #1

Pretty classic example of failure to sense and failure to capture.

As you can see, the pacer is firing but there is no response from the heart.  No P-waves, no QRS complexes, just lone pacer spikes hanging out.  This is classic failure to capture.  Possible causes of this can be a fractured or dislodged lead, battery failure or electrolyte abnormalities among others.  Luckily in this case the patient has an intrinsic rhythm that is probably perfusing them.

The second item shown is failure to sense.  Notable for this is the pacer spikes in the ST-segments.  Failure to sense is exactly what is says, the pacer is failing to sense the cardiac cycle and inappropriately pacing.  Again, luckily in this case the pacer is not capturing so the inappropriate pacing is not causing issues.  The biggest problem with this failure is inappropriate firing when the heart is not quite yet refractory possibly initiating ventricular arrhythmias.  Causes of failure to sense include lead issues (dislodgement, fracture or poor positioning) or sensitivity issues requires a change to sensitivity.

In this particular case, it appears the patient is in atrial fibrillation, which may be causing issues with both capture and sensitivity.  The erratic electrical signals emanating from the atria may be throwing off the pacer, but many times they are programmed with this in mind.  For nurses the important things to remember is to check on the patient when the pacer is acting up and ensure they are stable.  Past that, with permanent pacemakers, we need to get the cardiolosit involved.  If it the nurse who is running a temporary pacer at the bedside, adjustments to both output and sensitivity may be required to ensure adequate sensitivity and capture (but that’s a whole other ball-game!).

Here’s what a pacer strip should look like:

Each spike has a corresponding activity, just like it should.

Ventricular Bi & Trigeminy

PVCs are a fairly normal thing.  Sitting right here typing this out, I felt one, it’s kind of like your heart skips a beat.  Usually they are benign, but when you have sustained bursts of sequential runs of PVCs as a nurse we need to do some research and know the reasons why your patient is having these.

First, ventricular bigeminy

In ventricular bigeminy, every other beat is a PVC.  This is usually caused by an irritable foci within the ventricle firing early, in this case, over and over again.

Second, ventricular trigeminy.

As you can see, every third beat is a PVC followed by a compensatory pause and then the cycle starts again.  Once again, an irritable foci within the ventricle is firing off early.

In both cases above, the PVC is followed by a compensatory pause that allows the SA node to rest the cycle.  Also, it appears that in each case, it is a single irritable foci that is firing as the complexes are the same in each strip.  Among the causes of PVCs are:  ischemia, hypoxia, hypokalemia, hypomagnesemia, hypercalcemia, digoxin, cocaine, alcohol, tobacco, cardiomyopathy, MI, mitral valve prolapse and several others.   One of the old school nurses I worked with was saying how back in the day, anytime a patient had more than 6 PVCs a minute, they got started on a lidocaine drip.  Not so much anymore.

If this were my patient, I would double check to make sure they’re maintaining a blood pressure and feeling OK, then make sure their electrolytes get checked.   That is assuming there wasn’t some sort of event, like an MI, occurring.  Typically treatment is either treat the underlying problem, like repleting electrolytes, or do nothing.  Antiarrhythmic medications typically are not used as the side effects can be worse than the problem they are trying to treat!  (See info on the CAST trial for a good illustration.)

The key comes down to this:  how does your patient look?  As with many arrhythmias, sometimes the true measure of what the squiggly lines are saying about your patient is what you patient is telling you.  If they’re doing just fine, then no worries, if not, you need to do some digging!

eMedicine: Prematue Ventricular Contraction

Wikipedia: Premature Ventricular Contraction

Evolution

We don’t often get to see evolving MIs.  Usually they go to cath lab and the ICU so serial EKGs are not available.  In this case, intervention had already been attempted but due to the nature and type of lesion no intervention was possible.  In a case such as this, surgical revascuarlization was the primary modality, but due to multiple co-morbid conditions including age, severe aortic stenosis (valve area in range of 0.55 cm²) and general deconditioning none of our surgeons would touch them.  Notice the subtle changes especially through the precordials.

20:00, Day 1

So, what do we see? First, Q-waves in leads V1, V2 and V3.  Second, ST-elevation in V1 and V2.  Third, ST-depression in V4 (slight), V5, V6 and flipped T-waves in Leads I and aVL.  Also present is probable left atrial enlargement and  Left Axis Deviation with an axis of around -30°.  Based on this you could theorize that the LAD and Circumflex arteries have some sort of lesion.  The patient is actually hemodynamically stable at the moment.  Previous to this, they had been in atrial flutter with a rate of 110-130’s with some instability.  The cardiologist who was on the floor at the time decided to cardiovert the patient, but as we were prepping to do so they spontaneously converted back to sinus rhythm.  Teetering on the knife edge of stability they enjoyed a nice nap thanks to the Versed we had pushed while prepping for the cardioversion.  It was a reminder to follow the checklist, including ensuring that the patient is still in the rhythm you’re going to shock them out of prior to giving drugs and shocking.  The cardiologist in the last rhythm  check notices that it looks different and at that very moment the tele tech comes running in saying, “They’re in sinus!  They’re back in sinus!”

Next, 24:00 Day 1, patient c/o 5/10 substernal chest pain.

Nothing too different, although you could say that there is a slight elevation in V3.  The other leads actually look a little better, especially the lateral leads.  No change to axis.  This was after one SL nitro though, so that dilation may have helped, one reason we try to get a 12-Lead prior to giving nitro.

06:00, Day 2

Now there appears to be ST-elevation in V3.  The lateral leads have calmed down, with just a touch of depression in V5, V6 and I, with flipped T-waves in aVL.

14:00, Day2

Kind of ugly now, eh?  Now we have questionable Q-waves in V1-V4 (there is a pip right before the wave drops), but fairly significant ST-elevation in the precordials.  Depression and inverted T’s in the lateral leads has returned.  Again this was during an episode of chest pain.

Later that night the patient started to decompensate fairly rapidly.  They had a drop in LOC accompanied by a drop in SPO2 to the low 80’s on 15L non-rebreather.  Lungs we very wet, obviously filling with fluid.  The nurse called the on-call cardiologist who ordered 80mg of Lasix IV, in addition to the 60mg given previously during the day that only got an output of 200ml.  Everything was starting to shut down.  We ended up calling a RRT to get a doc at the bedside, if nothing more than to see if there was anything within the patient’s advanced directive to help.

About a week prior to this, the patient had gone to the cath lab in the failed attempt mentioned above.  Angiography show a 99% occlusion of the left main and distal disease in the RCA, LAD and circumflex arteries.  The left main lesion was so bad that they interventionalist was unable to even pass a wire through, which means it was very, very tight.  They minimal blood flow the heart and absolutely no reserve.  With that in mind, the doc on the RRT realized that we could not fix the underlying problem that was causing the distress.  She spoke with the patient’s family who in the end realized that the patient didn’t have much longer, and made the patient comfort care.  They ended up expiring about an hour later.

Looking at these EKGs one could argue that the ST-elevation is actually LVH with a strain pattern. It certainly fits the criteria, expecially when considering the patient had endured previous infarctions and had aortic stenosis, but I’m not comletely convinced.  I’m no cardiologist, so I’m going with what I know.  But I am open to other suggestions.  It’s a sad case, especially as the family was still saying how they wanted to talk to the surgeon about open heart surgery the morning of Day 2.  Luckily, we were able to use the means available, notably medication, to give some comfort at the end for the patient, even if we couldnt’ fix what was wrong.

A Never Event?

According to CMS, we experienced a “Never Event” last month.  But the even itself illustrates in my mind the flaws inherent in the whole concept of a “Never Event”.  Theoretically, the idea is agood thing.  There should be events that could occur while a patient is admitted to a hospital.  Some things should never happen:  like wrong blood, surgery on the wrong part of a patient or abduction of a patient of any age.  Some stretch the bounds of rational thought though.  The one that comes to mind is patient falls.

In the hive mind of CMS, patients should never fall.  Once again, theoretically, not to mention from a public relations standpoint, the argument is sound.  What they and the public tend to forget, that unlesss someone it at the bedside 24-7, falls will occur.  You can follow every published guideline out there.  Scheduled toileting, hourly rounds, bed alarms, reduction of the use of medications that can cause or enhance delirium are all really great ideas and have been proven to reduce falls.  But the bottom line is that when our elders, especially those that may have dementia tned to fall.  Add illness, strange environment, odd noises, unnatural schedules and new medications and you cook up a recipe that could conceivably lead to a fall, in spite of any and all safety measures we as caregivers may take.

But people fall.  Sometimes people fall and there is nothing we can do about it.

Exhibit A:

click for larger size

Anyone who knows EKG tracings can immediately grasp the bad things going on here.  But for those who may be a bit rusty, let me break it down for you.  The patient is rolling along in normal sinus rhythm until they get hit with a R-on-T PVC (a premature ventricular beat the falls when the myocardium is not yet fully repolarized, see below) initiating a run of Torsades de Pointes.  Torsades, meaning “twisting of the points” is a life-threatening ventricular arrhythmia that can rapidly devolve into ventricular fibrillation and death.  It is a form of ventricular tachycardia (VT, V-Tach) characterized by the rotation of the complexes around the isoelectric line illustrated by the increasing/decreasing amplitude of the waves in a near sine-wave pattern.  Treatment in an emergent situation is the following of the V-Tach leg of the ACLS algorithms, although usually a bolus of magnesium sulfate can terminate this as well.  Usually though, when we see this though, the proverbial shit has hit the fan.

In this particular case the patient had been ambulating in the hallway and flipped into Torsades.  The red mark is about where we figure when he hit the floor.  Not for sure, but the timing seems about right.  Now what would CMS say about this?  The patient was awake, alert and oriented x 3, ambulating under his own power when he fell.  So it is still a “never event”.  And this is why a one-size fits all labeling makes no sense.

First, does this mean we shouldn’t let patients ambulate?  They might fall.  Second, should we not give medicatons that may cause arrhythmias like this (more below…)?  They might fall.  Third, should we not anti-coagulate patients who are under treament for atrial fibrillation and thus increase their risk of bleeding with a fall?  Painting in broad strokes doesn’t always work.

Unfortunately, the patient had previously been in atrial fibrillation and been anti-coagulated with warfarin for an INR of 3.2.  He had been cardioverted out of a-fib into sinus earlier in the day and was intiating Tikosyn therapy.  The truly unfortunate part is that when he went down, it was like a tree falling in the forest:  straight back off his heels with his head striking the floor.  CT showed a massive cerebral bleed as a result and family chose to withdraw support allowing him to pass.  So this is a huge “never event”, as per CMS, “Patient death associated with a fall while being cared for in a healthcare facility.”  If he had not been ambulating, odds are pretty good that he would have made it out of the code, as there was a spontaneous return to sinus rhythm right after the scanned strip ends, with spontaneous return of circulation as well.  But since he fell in the hallway and hit his head, the deck was stacked.

As for the medication, Tikosyn (dofetilide) is a Class III antiarrhythmic medication that works by prolonging the cardiac action potential duration.  One major hallmark is that it subsequently prolongs the QT segment.  A prolonged QT interval increases the risk of ventriclar arrhythmias as the repolarization of the myocardium happens at different rates allowing myocytes that have already passed their absolute refractory period to depolarize early and possibly causing a re-entrant phenomenon, kind of like a viscious circle.  The FDA actually mandates that anyone being started on Tikosyn gets themsselves a 3 day vacation on a telemetry floor for this very reason.  Usually we monitor the QT/QTc closely in these patients, obtaining a baseline, then 12-lead EKGs 2 hours post-dose to ensure that the QT/QTc is still within limits.

So was this a “never event”?  Probably.  Could it have been prevented?  Probably not.  There were too many variables in play to do so.  Sometimes shit just happens, no matter what we do.

It’s an Infarct

I was taking care of a patient awhile ago, post-angio.  Currently chest pain free, normal sinus, hemodynamically stable, a good outcome.  But then I took a look at the EKG they shot right after his trip to the cath lab.

click to enlarge

So what do we have?  ST-elevation in V1-v4, and flipped T-waves in V5, V6, I and aVL.  Looks nasty, like an anterolateral MI, right?  Maybe some issues with the Left Anterior Descending and Left Circumflex arteries?  Nope.  According to the cath lab report, angiography showed several “hazy” luminal irregularities in the LAD, but nothing stentable.  The patient was kept overnight for aggressive anticoagulation and initiation of statin therapy.

So what’s the deal?  It could be a couple of things.  First, being a taller, young man, this could be a normal variant on his EKG, unfortunately there was no prior EKG to compare it to.  Second, he could have had a vessel spasm causing acute ischemia, but this would be transient and as several EKGs done over a course of several hours showed this same view , it is not a transient phenomenon.  Finally, this could be an example of microemboli showering from a plaque rupture into the distal circulation served by the LAD.

Microembolic showering highlights some contentious issues in coronary artery disease, the issue of the large vessel versus small vessels.  Too often the distal circulation is overlooked in favor of dealing with the larger supply vessels.  We tend to focus on the big pipes, but where the real perfusion happens in the small distal arterioles that supply the myocardium.  One reason is that why can’t adeuately visualize these small vessels.  We can shoot all the dye we want and still see nothing.  This also delves into the scene where the pipes are clear, but the patient is still experiencing chest pain:  the distal portion is not getting enough blood.

Looking at the tracing, one would expect to have either a complete blockage of at least one artery or a subtotal occlusion, not a minimal irregularity.  Whether or not this gent dodged a bullet remains to be seen, but odds are they’ll be back.  Unfortunately.

*UPDATE*  Thanks to great discussion and several well-informed comments I have learned a great deal.  LVH?  Sure thing.  Not too suprising either considering the patient had a long-standing history of hypertension.  A small caveat though:  I’ve only been taught to identify basics on 12-leads, but I am learning.  Things like his help me learn and increase my skills and knowledge, which is why I share these cases for discussion.