Or end the shift. Been there, done that, got the poster.
I want some answers!!!
Well, we got ’em. Last week I posted an EKG quizzer. Funny looking 12-lead right? Prolonged QT? Dilaudid, Verapamil? Remember? No? Go check the link to refresh your memory: Friday 12-Lead.
Go ahead, I’ll wait.
OK, so we have signifcant QT prolongation. Or do we?
Is it me or does that T-Wave look kind of funny? Kinda’ looks a little flat-ish.
How about these two?
Hmm…I see a little bit of notching in the T-waves here. Almost like this isn’t just the T-wave we’re looking at. Maybe this will help a little bit: the patient’s potassium level when drawn was *drum roll please* 1.9mEq/L. Yes, 1.9mEq/L. She had gotten some replacement during the days, but obviously it was not enough.
What we have here is actually a QU segment as the U-wave from the hypokalemia has merged into the normal T-wave. More examples of this can be seen thanks to Google’s Book Search from Understanding Electrocardiography. It notes that you start to see dominant U-waves that merge with the T-wave when serum levels of potassium below 3.omEq/L, most notable in leads V2-V6 (as shown above), with the U-waves actually becoming larger than the T-waves when the levels drop to around 1.0mEq/L. Adverse events related to hypokalemia include AV blocks, torsades, V-Fib and cardiac arrest, which is not a surprise knowing how potassium works in the cardiac cycle. Typical causes of hypokalemia include diuretic use, alcohol abuse, loss through the GI tract from vomiting or suction (think NG tube) and some antibiotics just to give short list.
Electrolyte imbalances are also relatively common with pancreatitis, especially when you have vomiting. Our patient was pretty much past the vomiting stage having been NPO for 3 days. Combine that with having NS going at 250ml/hr for the last 2 days and we were flushing her K+ out of the system. Fluids were changed to add K and the rate was reduced. She got several K+ riders during day shift as well. Thankfully the on-call doc didn’t freak out and have us turn the dilaudid PCA off as that would have caused just a bit of a problem based on her usage. Even better was we never had to talk to the EP doc. Small things.
By the time I came back that night, her potassium was edging up to around 3.5 and her QT had normalized out to around 420ms. We get so tuned in to hyperkalemia that sometimes we forget that hypokalemia is just as significant. We were able to keep the potassium within normal for the rest of the stay and to no surprise, her QT intervals stayed normal and there was no recurrence of giant U-waves.
That’s your answer.
Patient was a 30-something year old white female admitted for pancreatitis. History of alcohol and illegal drug abuse and yes, pancreatitis. Currently undergoing fluid resuscitation with normal saline infusing at 250ml/hr.
Medications of note include a dilaudid (hydromorphone) PCA device with dosing of 0.2mg/dose with time lock out of 10minutes and verapamil 80mg PO twice daily.
Telemetry tracing shows normal sinus rhythm in the 70’s with a prolonged QT around 620ms (calcuated QTc of 650ms). QT had increased since start of shift from around 360ms to current.
The following 12-lead is captured:
QT/QTc is measured at 622/671ms by the machine. Quick manual calculation confirms this.
Patient is still asymptomatic and vital signs are stable. She is just pissed you woke her up.
What is the probable diagnosis? What needs to be done? Should we call cardiology? Call and wake up the EP doc? Pacer pads? Let her sleep? Do nothing and pray she doesn’t have a R-on-T PVC?
Answers and discussion to follow in a day or two…
Or, “oh shit! That VT isn’t stopping!”
I’m walking into the nurses station the other night when I hear the “oh shit!” alarm ringing in the tele cave. Y’know the one, that incessant, high-pitched dinging that is saying “Pay attention!” Reflexes trained by my years on a tele floor I look up expecting to see someone bradying down, or maybe some nasty artifact, but instead I see this starting – and it’s not stopping!
A.) Start screaming like a little teeny-bopper freaking out and run in circles?
B.) Shit my pants?
C.) Drop what I’m doing and high-tail it to the room in question?
Believe it or not, C is the correct answer. Sphincter slams shut as I haul ass down the hall. I bust in the room expecting to find a dude laying there, unresponsive, not breathing or generally not doing well. Instead I see dude and his nurse clamly chatting. I breathlessly ask, “Were you shaking the leads?”
“No” she replies, “What’s up?
Dude looks up and says, “Is my heart racing again?”
“Uh, yeah, he’s in VT.” I say, amazed that he’s sitting there calmly chatting. “Do you feel funny or anything?”
“Yeah, my heart feels like it’s going pretty fast. But I’m used to it, it’s happened many times before, no big thing.” he replies nonchalantly, basically amused with the gaping look on my face.
So we hook him up to the bedside monitor, and sure enough, there it is VT, rate in the 150’s, BP is 100/53, he’s pink (ok, kind of yellow), warm and dry. No light-headedness, no dizziness, he does admit to a little bit of chest pain, but in reality he’s in better shape that half the floor, except that he’s in this particular rhythm.
Prehospital 12-Lead ECG has a great quote on their wide complex tachycardia page, “If it’s a wide complex rhythm (fast or slow) it’s ventricular until proven otherwise!” And that’s how we were treating it. So we grab some labs, call the ICU team to come assess him and a 12-lead EKG. Should we have called a Rapid Response? Maybe, but we felt we didn’t have to. He was stable. He has had this many times before. And he was sitting there cracking jokes with us.
So here’s the 12-lead:
So what to do now? The ACLS algorithm for tachycardia with pulses starts with determining if the patient is stable. Check. He’s cool. Establish IV access. PICC line left upper arm. Check. Wide or Narrow complex? Duh. Obtain 12-Lead EKG. Check. Expert consultation advised. Check, ICU team is here now. Amiodarone if ventricular tachycardia or unknown, adenosine if SVT with abberancy. Oh, wait…he has a history of WPW and 3 failed ablations. Now what?
This is where expert consultation is really a good idea. In our case, he’s now cracking jokes with the ICU team as well. He’s still rolling along between 145-160 BPM. We grab some labs. Turns out his potassium sucked, magnesium sucked and his calcium critically sucked. The Team decides that amiodarone would be a good idea and getting his electrolytes sorted out might help as well. So we’re hanging amio, mag and they’re calling cardiology. Mind you this is 2130 on a Friday night. Do you think a cardiologist is going to come in at that hour? Nope. She says, “Oh, just have one of the ED docs cardiovert him and call it good.”
He gets packaged and ready to roll to the ICU, ’cause by this time he was pretty much a 1:1 and the nurse had 3 other patients she was already neglecting. Grab the defib off the code cart, because with our combined luck (this nurse and I have a history of codes/RRTs) dude will decide to stop having a pulse once we’re between floors in the elevator.
The rest is rather boring. A little bolus of propofol (yeah, we MJ’d him good!) and the judicious application of 100 joules of DC electricity fixed him right good. One shock and back into sinus. But it was a good thing he was in the Unit as they spent all night getting his ‘lytes repleted.
What could have been a very bad thing ended up being a very, well, fun thing. Too often on our floor a busy night consists of incontinence, wrangling demented patients back into bed 30 times an hour or chasing naked psych patients down the hall, so dealing with a true cardiac issue was a rather refreshing change of pace.
It looks like I’ve broken my streak. I actually had almost 3 months without a Rapid Response or Code Blue on my shift. It’s no more. At least we didn’t have to do CPR on this little 40kg bag of skin and bones, just some airway support and off to the ICU.
But it got me thinking. Thinking led to rooting around in my “book o’ fame” (my morbid collection of EKG strips of “bad things”) which led to me finding a couple of strips related to CPR. Strange how a mind works.
Evidently, per the post-it note, these had been grabbed during a code last year where I did a TON of CPR. Remember kids, a bad thing about being a big strong dude is that you get to do a lot of chest compressions. I’m not dissing the ladies, I’ve seen many a round done by y’all, and you’re fierce, but for some reason whenever there is a code on my floor, yours truly gets roped in to do compressions. Needless to say I had no need to go to the gym after that code.
My tele tech knows my predilection for interesting tele strips so he printed a couple for me.
First, near the beginning of the code:
Second near the end:
In all fairness, they were dead from the get go. Never once did we get a rhythm stable enough for transport, never a pulse, pupils were fixed pretty much from the beginning. Morbid? Probably.
But on to the beat. They say 100bpm is the speed we need to keep when doing CPR. It allows for adequate refilling of the ventricles with blood before the next compression. In the midst of the controlled chaos of a code, keeping that speed can be tough when adrenaline gets the better of us. So what do you do? Keep the beat with a song.
We’ve all heard of “Stayin’ Alive” by the Bee Gees as the “perfect” CPR song. Heck, I have it on my header. My BLS instructor the last time around had a thing for “She’ll Be Coming Around the Mountain”. There is the slightly more darker “Another One Bites the Dust” by Queen that fills the 100bpm measure. Thanks to the American Heart Association, there is a large list of songs that fit the bill of 100bpm. Some notables include: “Kickstart my Heart” by Motely Crue (they would know), “Paradise City” by Guns N’ Roses. “Heart Attack Man” by the Beastie Boys and of all things, “Back to Life” by Soul II Soul. The entire list can be found at Be the Beat, which is a website dedicated to educating kids about CPR, but here’s the playlist.
Will this help me set a new streak? I doubt it. As the rule of three shows, I have 2 to go before a new streak can start…
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:
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
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.
“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?
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:
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!
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.