Why I’m Not a Neuro Nurse

‘Cause sometimes they’re just a little too freaky.  Too many weird things happen inside that bony vault of ours that we can’t understand, much less fix.  Take a CVA.  Simple thing, right?  No blood flow.  Same as a MI.  One we can fix relatively easily and they’re back out eating Big Macs in 48 hours.  The other renders the person spouting word salad out of a drooping mouth while being unable to feel their left side and many times there ain’t a damn thing we can do to fix that.  No stents, t-Pa only if you know the last normal and even that isn’t a sure bet, usually all we can do is support what is left.

But what really hammered this unlove of neuro was a situation this week at work.  Chicky comes in after having trouble moving their right hand, some drooling and slurred speech.  By the time she hits the ED, everything has resolved itself.  Classic TIA.  Now we all know that having a TIA increases your risk of having a full-blown CVA exponentially, so she gets admitted to us on our stroke protocol for further work-up.  So I’m walking past the room doing my last set of rounds just at shift change when her nurse pops her head out and says, “Can you give me a hand?”

“Sure,” I say walking into the room.  And there she is, Ms. TIA, not moving the right arm and talking a little like a drunken sailor.  But she’s alert and oriented, following commands, just some focal deficits, that are nearly exactly the same as the ones that brought her in.  Her nurse asks, “Do I need to call a RRT?”

“Not yet,” I start.  “Get a good NIHSS assessment going and I’ll page her doc.”

She starts up on that as I go to page the doc.  As I head back in, the nurse looks at me and  says, “She’s completely resolved!  Totally back to baseline.”  Sure enough, 100% neuro intact.  Not a single deficit.  Went from a 2-3 on the scale to a 0 (the higher the number the worse the symptoms), in a mater of 3 minutes.  Completely freaky.

“Well,” I say, “let’s put her back on bedrest and make her NPO, the 24 hour clock just reset itself.”

We were both a little freaked out by it.  I’d never seen that before, to go from having (mild) stoke symptom to complete resolution in a manner of minutes.  Cool, but freaky.  Ms. TIA however, bought herself another 24 hours of bedrest, nothing to eat or drink and a stat trip to the MRI machine.  Yeah, don’t want to do that again anytime soon.

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

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.

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.

Skills?

Yes, I have ‘em.  Occasionally.

The other night was had a guy who dropped his CBG to 36mg/dl.  Par for the course he was a little out of it and coupled with an already existing issue with aspiration, PO intake was not going to solve the problem without possibly creating more problems.  As the nurse flushed his IV she saw it too had gone bad.  Crap.  One nurse tried to start a new IV already, but to no avail.

Enter the Charge Nurse.  Me.  Armed with a 22g IV, an amp of D50 and raw desire I jumped in.  And there it was.  Popping out of his skin 2 inches above the wrist, a nice, bouncy, engorged vein screaming out, “Poke ME!”  So I did.  D50 in, CBG up, crisis averted.  I love it when a plan comes together.

The true validation came the next night when his nurse said to me, “You know Mr 78?  Yeah, that IV you got last night is still in.  And IV resource came today to start another line and got nothing.”

Oh yeah, I gots skills!*

It’s nice when you’re called upon not just for your knowledge, but your technical abilities.  We rely so heavily on our IV team that my skills get rusty, so it is a small celebration when I get a good stick on a relatively dehydrated older gent.  Makes me feel validated that I can do this.  Makes me say, “I love my job!”

*of course it was a one-in-a-million shot, will probably never happen again and when it really comes down to it, starting IVs is not really my strong suit, but sometimes you come in and hit that clutch shot!

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.

Angiography: Live and In-Person

BBC NEWS | Health | Watch an emergency heart procedure

This is far too cool.  Patient is a 36 year old male, with a blockage of his RCA (according to the cardiologist). Risk factors?  Smoking. I lived in England for 3 months and am sure that smoking was not the only risk factor…but.

I wish they had displayed a copy of the EKG, but I would venture to guess there was some ST-segment elevation for them to rush him back to the cath lab so quickly.  They show a fluoro shot of the dye being injected then stopping, which gives a great visual representation of what is going on.  You can see how it is pretty much totally blocked.  Then they also show a fluoro shot prior to stenting where you can see the narrowed lumen of the artery. Unfortunately, these shots are pretty much fleeting in nature so to get the best view you would have to pause the video, which I highly recommend.

It’s fun, especially when the patient has a bit of a reperfusion arrhythmia!

via Dr. Wes

Not a Good Thing

It’s how my A&P professor used to classify the problems that could happen to the human body.  It was either OK, or not a good thing.  I’ve learned all sorts of things that surely fall into the latter category, hell, we see that all the time.  Then there times where you foresee the worst possible, but the reality is that it isn’t that bad.  All things considered.

Case in point.  Complete (3rd degree) Atrioventricular [Heart] Block.  Just saying makes my heart rate speed up a bit.  All sorts of bad situations run through my mind.  The ACLS algorithim for bradcardia and PEA jump to the forefront of my memory as I see it pop up on the monitor screen as the “Oh SHIT!” alarm starts ringing for bradycardia.  You run into the patient’s room and they’re sitting there, alert, talkative and having a fine time.  “Do you feel weird?” I ask.

“No, why?” he says.

“Your heart is doing something funny.  Sure you feel OK?”  I continue.

“Oh, that,” totally nonplussed,  “Naw it happens all the time.  I’m used to it.  That’s why I’m getting a pacemaker tomorrow.”  he finishes.

Then I remember the words of my EKG teacher:  sometimes we treat the monitor, others we treat the patient.  The key is to figure out which one is which.

So here’s the first strip:

Atrial rate: 80’s
Ventricular Rate: 60’s
Notice how the P-waves march through without any regard to the QRS complexes, except in beats 2 & 6.  Beat 6 appears to be preceded by a compensatory pause, where the conduction system appears to reset.  One could argue that this may be an extreme case of 1st Degree AV Block, but if you measure the P-P ratio you can see the march of the P’s, into and through the QRS complexes.  While it’s not a complete block, as some impulses do seem to carry through and you do have some time spent in sinus rhythm that I couldn’t scan in, you can tell the conduction system in not well.

Now a second strip:

Again, the atrial rate is in the 80’s, and the ventriclar rate is inthe 50’s.  Notice how the overall strip seemes to be stretching out, or slowing down.  The 5th beat is a PAC, but again, no reset happens.  After that you have a lone P-wave followed by a second P-wave with no QRS to be seen.

Pretty much in this case, the atria and ventricles are not working together at all.  At times there appears to be some synchrony, but whether that is coincidence can’t be seen in short rhythm strips like this.  For some reason I really dig on the heart blocks.  Some of my colleagues have a hard time getting their heads around the concept, but it makes perfect sense to me.  The short of it is that the top of the heart and the bottom are not communicating effectively, kind of like a dysfunctional family, or couple.  (really, AD’s description of the heart blocks is both incredibly informative and hilariously funny, but it makes so much sense.  Maybe I just have a dirty mind though.)  By the time you get to 3rd degree (or complete) heart block, the atria just does its own thing, usually clicking along at the normal rate for the SA node (60-100 bpm) while the ventricle clips along at its own rate, usually either junctional (40-60 bpm) or idioventricular (20-40 bpm).  The ventricular rhythm is determined by which escape pacemaker site is supplying the impulse, the AV node or  the His-Purkinje system.

In cases where the patient is asymptomatic, the are several things nurses can do.  First, keep them on tele for crying out loud.  Don’t let them leave the floor without an ACLS certified nurse.  You say, “Well, duh.”  To which I say, “You think this hasn’t happened?”  Second, either have transcutaneous pacer pads on the patient, or at the very least at the bedside.  Third, make sure they don’t get any nodal blocking agents, like metoprolol or diltiazem.  Once again, “Well, duh.”  Again, “You think, aww screw it…it has happened.”  Fourth, make sure they have at least 1 IV site, that works, preferably 2.  Finally, make sure Cardiology is involved as the ultimate fix is a permanent pacemaker.

Lucky for us the gent in question stayed hemodynamically stable through the night and ended up getting a new brigh and shiny pacemaker implanted the following morning.  It could have been far worse, for sure.

Emedicine’s article:  Heart Block, Third Degree

The ECG Blog has a great couple of case studies of this phenomenom, complete with 12-Lead tracings.  The latest, Complete (Third Degree) Atrioventricular Block with Junctional Escape Rhythm, is pretty darn cool, and it has our most common complaint in folks with this, “tiredness.”  Classic.

Dedicated to Sidney Sinus Node and Viginia Ventricle…

Sensational MRSA Headline

How our hospitals unleashed a MRSA epidemic | Seattle Times Newspaper

It says it right there:  MRSA is the fault of hospitals.  If it wasn’t for hospitals, MRSA wouldn’t be so prevalent, wouldn’t be so deadly or such a large issue.  Right.  What a crock of shit.

It mentions nothing abot the over-prescribing of antibiotics.  Nothing of the emergence of the USA300 clone of MRSA in community-acquired infections.  Nothing of the reality that this is based on environmental pressure on the bugs that cause them to acquire resistance in the first place.  No, it’s the hospitals’ fault.

Now I will give due.  We suck when it comes to handling these issues.  And we can do better.  Unfortunately this is a multi-factorial issue and difficult to address whitout pointing fingers.  Wahing hands?  We don’t do it nearly enough.  And nurses aren’t the only culprits.

Physicians can be the most lackadaisical about infection control.

In April 2006, doctors at the UW Medical Center carried personal items from home into sterile operating rooms and dropped them on the floor. These items included backpacks and satchels, made of porous materials friendly to germs. Hospital administrators told inspectors this was “common practice.”

In November 2006, a physician at St. Joseph Medical Center in Tacoma removed his surgical mask during an operation. He had complained it was uncomfortable. Hospital officials told inspectors the physician was a “repeat” violator and had been warned before to keep his mouth and nose covered.

In hospitals, the most common violation is the failure to wash hands upon entering or leaving a patient’s room.

In the worst cases, as few as 40 percent of staff members comply with hand-washing standards. Doctors are the worst offenders, according to confidential hospital records reviewed by The Times.

I’ve lost track of times I’ve seen docs walk into isolation rooms and not don any PPE.  VRE?  MRSA?  C.DIff?  Not a problem, it seems their white coats magically protect them from the all but the worst offenders.  Not to mention becoming a vector in their own right.

While measures like presumptive isolation, isolating anyone who has ever had MRSA, screening everyone on admit my help to slow the rise of the germ in hospitals, it does nothing to prevent it coming from the outside.  All of the MRSA patients I have taken care of, have had it on admit.   It’s why they were there.  In a perfect world, we would have private rooms or all patients.  There would be a fast bedside screening tool for MRSA and other community-acquired resistant germs.  Rooms would be cleaned appropriately and thoroughly.  We would all wash our hands or use foams/gels every single time.  But it’s not a perfect world.  Even in our new unit we have double rooms.  Even though our housekeepers do a pretty good job, there is still the risk of acquiring MRSA from a previous occupant just on odds alone.  It is going to happen.

One problem the article doesn’t address is the rise of the USA300 clone that is present in nearly 97% of community-acquired MRSA infections, most notably in skin and soft tissue infections.  This virulent and nasty strain, with its included Panton-Valentin Leukocidin exotoxin can cause necrotizing fascitis, sepsis and pneumonia.  It’s nasty. But again, like any MRSA, good hand hygeine and terminal room cleaning can help to prevent its transmission inside hospital walls.

While hospitals may have covered up cases and mortality due to MRSA, as shown pretty damningly in the Times article, this not just a focused problem.  It is a multi-systemic issue that reaches across disciplines.  Therefore its going to take a multi-system effort to combat it.