A 21 year old who has otherwise been in excellent health, noted the onset of some substernal chest discomfort when taking a deep breath that is new from the day before. He was working as a camp counselor in Wisconsin and presented to the camp nurse who noted his pulse was low. He vehemently denied shortness of breath, cough, fever, chills, rash, prior heart disease of any kind, murmur, or family history of heart disease. His exam, other than a slow, slightly irregular pulse and occassional bounding neck vein, was entirely normal.
He was sent to the local ER. Here's his presenting EKG:
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He was admitted and two hours later, his EKG repeated:
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So, what are the EKG findings and what's the diagnosis?
(Hint: The diagnosis was made by a small hospital that was NOT one of the 50 Best!).
-Wes
18 comments:
Second degree type 2 HB evolving into third degree HB?
Agreed, but throw in occasional 1st degree block, too, on the first EKG - it evolves to third degree AV block. But now the kicker...
...why?
Problem with the first strip. The I/II/III beats are a different sample than the rest of the leads (two beats far apart as opposed to the close-together bests). Aren't they supposed to be 12 different view of the same chronological sample? I realize you said it's not a top-50 hospital.
That said, the first sample shows 2nd degree advanced block (Lead I/II/III have an extended PR interval on the conducted P-waves). You could make a case for some PACs in V1-3 (P-wave atop the T-waves?)
Third degree for the second sample.
Lyme carditis.
First trace: shows periods of second degree AV block, with as many as 3 atrial impulses in a row not conducted (the last QRS complex is likely too close to its preceeding P wave to be conducted. The conduction disturbance appears to be fluctuating because, strangely enough, some premature atrial impulses are conducted. The level of the block is intrahisian or, more likely, suprahisian.
Second trace: Third degree AV block with wider QRS indicative of a ventricular escape focus and suggesting infrahisian level of block.
Taken together the two tracings suggest dynamic involvement of the conduction system at more than one level Combined ECG and clinical findings strongly suggestive of Lyme carditis.
I think it was a third-degree AV block in both EKGs with a new-onset left bundle branch block in the second EKG. How wrong was I?
Third degree AV block implies no AV conduction. But clearly there are at least 2 conducted beats on the first trace.
RWD - Agree w/your logic here... suprahisian block on first trace - NO conduction (with ventricular escape) on the second trace. Now we're havin' fun!
But before breakin' the news, lets keep it goin'....
How would you manage this patient? What tests would you order? Should he be in the ICU? Temp wire? Pacing pads? (He's asx for the most part). Therapy?
Remember, this is what those docs encountered when this patient hit the ER....
Telemetry with pacing pads for 24 hours, just tele if hemodynamically stable until rhythm normalizes. ABX for 7 days. Try not to get bit by ticks for another 11 days.
Patrick -
Any other tests? Could there be another cause? What antibiotic? (Forgot: (and this is the truth), he's allergic to doxycycline)...
Check Lyme ab titers.
Ceftriaxone if he really is doxy allergic (could use ampicllin but given cardiac manifestations, would start IV abx)
Presumably an ECHO showed no structural heart dz?
Since he is relatively asymptomatic, I don't think I'd put pacer pads on him unless he showed pauses or developed sx with his CHB, but would have them at the bedside. Would restrict his activity until determined if he did have pauses or worsening conduction abnormalities.
Can I safely assume because you didn't mention it that there is no hx of thoracic trauma in the past 24 hours, and the CXR shows no pneumothorax and a normal mediastinum?
It screams infective process. I'm sticking with my hand as dealt. I like the lyme titre (is that like a lime rickey?)
And homey don't know ABX. Paramedics don't carry a variety... or any, for that matter.
Thanks to all who contributed to this case discussion. Hopefully it was informative.
Here’s the epilogue:
The case was one of a young camp counselor from the North Woods of Wisconsin who presented with high-degree AV block and complete heart block and complained of only mild chest discomfort. He had been canoeing with campers six week prior. He denied ever seeing any rash or developing arthralgias (joint aches) or fever. He never recalled being bitten by a tick.
He presented to a small rural hospital, who immediately suspected Lyme disease by the history and ordered a Lyme titer using an Elisa titer. This returned positive. To definitively confirm the diagnosis, a Western Blot was performed. This was sent both the day of admission and the following day (not sure why both were sent). The Western Blot on the day of admission was positive and the day after was negative. He was admitted to an ICU setting for 24 hours and observed, An echocardiogram documented normal LV function and normal wall motion and no evidence of aortic pathology.,. He was allergic to doxycycline and was begun on ceftriaxone IV 1 gm q 12h. Because of the cardiac involvement, it was felt parenteral antibiotics should be administered for three weeks. His EKG continued to show intermittent complete heart block for the first three days, but was gradually supplanted by Mobitz II and Mobitz I AV block. He remained asymptomatic and was “bored” by his hospital stay. A PICC line was placed in the right brachial vein and he was discharged home to continue his course of IV antibiotics after the fifth hospital day. An EKG then demonstrated first-degree AV block at 420 msec. I saw him one week after his presentation, and his EKG is shown here.
Lyme disease (Borreliosis) is a bacterial infection with a spirochete from the species complex Borrelia burgdorferi, which is most often acquired from the bite of an infected Ixodes, or black-legged, tick, also known as a deer tick and represents a cause of reversible heart block in the young. Heart block does not tend to manifest acutely, and should be considered in any young patient any time of the year who presents with complete heart block. Only 50% of patients with Lyme disease recall the tick bite or manifest with the acute bullseye-shaped rash, erythema migrans.
More info and links can be found at Wikipedia.
Sorry, the link to his follow-up EKG was miss-typed. Try this one.
I just screened a consult for a 26 yo who is s/p pacemaker for "SSS".
(haven't see him yet or his records from OSH). Our facility referred him to the OSH after he presented to our urgi-care for syncope and while there had a witnessed 12 sec pause on telemetry - EKG during the same visit did NOT show any block. A month prior to the syncope presentation he was seen in the ED for an insect bite with "cellulitis". I've asked his PCP to get Lyme studies. Have you ever seen Lyme carditis lead to 12 seconds of asystole with no prior evidence of conduction abnormalities? Would this presentation be c/w Lyme carditis?
CardioNP
Sinus node involvement has not been described, as far as I am aware, with Lyme disease. Perhaps this is because the sinus node complex has more redundancy (more size) that the anatomically more distinct AV node. This is not to say that it might not be possible, but if the P waves are suppressed at the time of asystole, it would make Lyme disease less likely as the cause of asystole. It is interesting to note, that Jarisch-Herxheimer reactions have occured with the initiation with treatment for Lyme disease, but this does not sound like your patient.
Thanks.
Will let you know if I find out any additional info suggesting Lyme in our pt.
CardioNP
Hey Wes, on the first ECG couldn't you argue that the block was INFRAhisian since it degenerated to 3rd degree block in the same tracing (rather than suprahisian?)?
Without a His bundle electrogram, we can't be sure, but the narrow complex ventricular rhythm in the first EKG should suggest the delay is PROXIMAL the AV node (supra-Hisian).
If you look at the the time between the last two narrow beats on the first tracing, it exceeds the time (i.e., is a slower rate) than the wide complex rhythm seen in the second tracing. It is likely that the rate of the intrinsic automaticity of the ventricle exceeded the rate the AV node could conduct to the ventricle at this time. The presence of the wide complex rhythm, therefore, does not necessarily define the location of the block proximal or distal to the AV node.
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