How come we never talk no more? probably my fault...
Virginia & I had an interesting patient at the 'Port recently. It was the best kind of interesting - lots of EKGs, specialists involved, and no ensuing tragedies. Nice.
It didn't start out promising - a kid who faints (not feints) is not usually the most interesting patient. Kids faint a lot - exhibit A:
So when EMS patched, saying they were bringing a 14 year old girl who had fainted, it didn't really grab our attention, until they mentioned her heart rate was dipping into the 40s during transport.
Ah. I see. Meet you in room 4...
During the evening she had been feeling an upset stomach, describing some epigastric discomfort, as well as nausea. Her parents remember that she looked a little pale before the episode occurred. She was walking into the kitchen when she began to feel faint, and fell to the floor. Her parents, frightened, called 911 immediately.
The ALS crew found her sitting up in a chair, a tissue held up to a small cut on her forehead, but otherwise looking well. Vital signs were normal, and the parents were starting to feel like they had been overreacted in calling 911. While sitting in the chair, however, she suddenly stiffened up her whole body, and then went limp. After being put on the floor, however, she regained consciousness. Although she came around quickly this time as well, everybody decided that calling 911 had been just fine, and she was moved to the ambulance for transport to the ED.
During transport, the medic noticed that her heart rate was slowing down episodically, dipping into the 40's. She still looked pale, and vomited a few times, but her mental status was fine, and she never became hypotensive. A rhythm strip was obtained:
An ECG was also acquired:
The transient episodes of bradycardia did not require pacing or medication. She was brought into room 4, looking a bit intimidated by the number of nurses and doctors around her. She still looked pale, but her speech and mentation were normal. An ECG was obtained in the ED (about 30 minutes after the EMS ECG):
Vital signs were P-100, R-20, BP-127/59, SaO2-100% RA. Her lab work was uninteresting, and a CT of her head show no fractures or bleeding. The cut on her face needed only some Dermabond.
The ECG and rhythm strip obtained by EMS were acquired only a minute apart. The rhythm is interesting, showing a sinus rate of around 120, but with a 2:1 AV block, so that the ventricular rate averages 60. On the rhythm strip we see two episodes of more advanced AV block, with 3:1 conduction, while on the 12-lead we see an apparent Wenkebach pattern in complexes 5-9, with a progressively lengthening PR interval. The QTc, fortunately, appears normal, and there are no signs of pre-excitation, Brugada, or arrhythmogenic right ventricular dysplasia.
The ED ECG shows, first of all, how frakkin' important it is for EMS to grab ECGs in the field, since a number of features had changed on the ED tracing. In the ED there is only a mild 1st-degree AV block (214 ms), and no sign of Wenkebach phenomena. The computer read the QTc as 441 ms, "borderline prolonged," and it does appear to violate the "half the RR interval" rule for a normal QT.
Our patient was transfered to our local quaternary-care center. She was continued on cardiac monitoring during her hospital admission, but 24 hours of telemetry revealed only a single further dropped beat, as well as a resolution of her PRI prolongation. Tests for Lyme, as well as rarer infectious causes of AV block or myocarditis, were negative. She was due to start a Holter study upon discharge, and follow up with a pediatric cardiologist.
|Turns out HIPPA does not apply to dogs, so I can show you a canine Holter monitor.|
1. Was this a seizure or what?
Although the second episode of syncope this young lady had began with an apparent seizure, it was unlikely to represent a primary neurologic process. First of all, the seizure was described as a brief whole body stiffening, follow by loss of tone. While some forms of epilepsy may manifest in this manner, it would be unusual. Also, there was no post-ictal confusion described by the paramedic or parents, making a "true" seizure unlikely. Other historical and exam findings also weigh against a seizure. A good illustration of other factors to consider are found in this article "Seizure versus syncope (PDF download), which features a handy guide:
So this was likely a "convulsive" sub-type of syncope (brief myoclonus due to low blood flow to the brain), following the flowchart above. (In some literature, the convulsive type refers specifically to pallid breath-holding spells in children. I mean it more generally here.)
2. Ok, it's syncope - what kind was it?
Reading the textbooks, there are dozens of terms to describe the various supposed kinds of seizures; micturation, situational, vasovagal, neurocardiogenic, autonomic, reflex... you get the idea. Really, there are only two types of syncope out there, from an EM point of view; cardiac or non-cardiac. Let's start with the second.
"Non-cardiac" does, of course involve the heart, but it's role comes in at the end of a sequence of events which are, as usual in medicine, not well worked out. The standard explanation sounds so weird, it may even be true.
For whatever reason, the body can pool blood excessively in the lower extremities. To compensate, both vascular tone and cardiac output increase substantially. Unfortunately, various pressure receptors in the heart now think the body is hypertensive, and act as if the patient has high intercerebral pressure; the heart rate drops, and cardiac output falls.
The fall in heart rate and blood pressure appear to be mediated by the vagal nerve, at least in part, so people call this vasovaagal syncope. On the other hand, since the sympathetic pathway is also affected, others call this autonomic syncope. Of course, as the picture above shows, the brain has a role in this, so it also called neurally-mediated syncope. If bardycardia, or even asystole (transient), are the main manifestations, it may be termed cardioinhibitory, but if hypotension is prominent, it can be instead called vasodepressor syncope.
Whatever. The important point is to distinguish these benign types from cardiac causes. This kind of "syncope" is caused by a primary problem within the heart, and may not produce all the autonomic symptoms (sweating, warmth, nausea) that normal syncope does. It comes on fast, and can occur even if the patient is seated or supine. This table from a Nadas' Pediatric Cardiology reviews the differences with normal, or "neurally-mediated" syncope:
Remember how normal syncope has a bunch of vague terms to describe the same thing? In contrast, there are 3 distinct types of cardiac syncope, with clearly defined etiologies.
First, there are structural causes (hypertrophic cardiomyopathy, tetrology of Fallot, pericardial tamponade, amongst others).
Next, tachyarrythmias can induce syncope. Examples include long QT, Wolf-Parkinson-White, and Brugada.
|I calculated 411 msec. Normal.|
Last, but certainly not least, we have to worry about bradyarrythmias - sick sinus syndrome, overdose of beta-blockers, and, of course, advanced AV blocks!
3. Finally! So, did the AV block cause the syncope, or vice-versa?
|Salma Hayek is always relevant.|
Sounds like a good question. I'll discuss that in the succeeding post, as well as the reasoning of the cardiologists taking care of our patient.