# 52 year old male CC: Seizure

You're working a QRV on a busy weekend, when you get dispatched for a "man down". No transport units are initially available, but a BLS crew from a neighboring town are on their way.

Upon your arrival an officer on scene directs you inside to a man he says, "looks like he had a seizure".

Your patient, a 52 year old male, is seated on the ground with a family member holding a cold washrag to his forehead. He is responsive to verbal stimulus, but isn't making any sense.

His wife introduces herself and fills you in on the story. Apparently, they were watching TV when he suddenly went unresponsive and began, "shaking all over". She also says that he has never had a seizure before and usually is never sick. When you ask about alcohol or drug usage she becomes evasive.

You introduce yourself to the patient and feel for a pulse at the radial. His skin is hot and moist and his radial feels quite fast. He's slowly coming around and smells of cigarrette smoke.

• Pulse: 180 bpm
• BP: 112/64
• RR: 26
• SpO2: 92% r/a
• Lungs: clear and equal bilaterally
• Temp: 99.9 F tympanic
• BGL: 188 mg/dL

The wife states the patient takes something for his cholesterol and hypertension. You attach your monitor and see a narrow complex rhythm at 180 bpm.

The patient is now answering questions appropriately, but with some hesitation. He denies that he's had seizures before and denies taking any drugs.

The BLS crew arrives as you acquire the following 12-Lead:

• What is the patient's rhythm?
• Is the patient's condition related to the rhythm?
• What is your course of treatment?

• Mark says:

Whats is his D stick? Possible hyperkalemia?

• Sugar was normal, will update to reflect the numbers.

• Alex says:

looks like a delta wave is existent. WPW?

• FB says:

Rhythm=sinus tachycardia. Anecdotally I have seen patients have sympathetic surges during and then after seizures (although I would expect his bp to be a little more elevated). I guess we have to be a little worried about toxins but it seems like he’s acting appropriately for having just had a seizure. I don’t think any treatment at this point is necessary. Everything will probably resolve itself in time as long as his symptoms continue to improve. Monitor/transport to the hospital of his choice.

• Mike says:

Sinus tachycardia. Presentation is stable but could deteriorate. Continue to monitor, IV saline bolus and transport. Question as to how long fever was present or any recent out of the country travels

• Robert says:

Upright P waves in I, II, III, and aVf w/ Neg P wave in aVr, Regular rhythm, Fast, Narrow complex. This rules out SVT, Ectopic Atrial tachycardia, and A flutter.
Sinus Tachycardia.
Find out how long the "shaking" lasted. Rule out for why he had a primary seizure? Recent falls, drug use, infection, ingestional error, electrolyte imbalance, etc… I'd question him a little more about cocaine/methemphetamine use given the wife was a little evasive on the drug question.
Treatment: 02 n/c, IV, fluid up to a liter, reassess. If still tachycardic, i'd consider 2-5 mg of versed.

Ok……I'll take a stab at it.  ST @ 176 bpm, normal axis with no ectopy.  There is no ventricular hypertrophy.  I do see evidence of RAE.  I do not see delta waves and the PRI is normal, so WPW or LGL is not suspected.  I do not see multiple PW's or F waves, so A flutter is also not suspected.  There is also evidence of prominent TW's in V3 and V4.  The QTc is normal, and so is the QRS duration, so even though TCA OD can cause tachycardiac, and neurological symptoms including seizures, I wouldn't think this is a TCA OD.  Given that this person is 56 y/o, I would say that he is up there with his sinus rate (220-age).  He is posictal fro a seizure that he has no history of, and the wife dances around the question of drug use.  Is there any white powder around his nose?, or new vena-punctures?  Anyway, If he did do Cocaine, his DBP would be elevated.  I still think this guy did something, and had a siezure because of it.  Any stimulants that would cause this pt to be tachycardic, would also cause the pupils to be dilated.  So, how were his pupils?  Maybe this guy is on an ACE inhibiter to reduce his B/P so he will not have an increase in his DBP through vasoconstriction.  He is showing signs of overload on the Lt artia with P-pulmonale.  this could be secondary to years of smoking, which is exacerbated from tachycardia, reducing preload to the RV, therefore to the LV, thus reducing overall SBP.  Because the patient is suspected of doing stimulants and had a siezure, I would think that it would be appropriate to administer a benzodiazepine to prevent further seizures and bring down his heart rate.  And, of course, O2 via NC @ 4 lpm to help with hypoxia and subsequent pulmonary artery constriction, thus improving right sided output and increasing preload to the LV, which will increase B/P.  So….O2, IV, monitor, 12 lead, transport for further elvauation and treatment.

• mat says:

Atrial tachycardia with 2:1 AV block, more likely type 1 because of the narrow qrs. I dont think the machine is measure the QT accurately, it appears to be rather prolonged.

• Chee Yong Chuan says:

Interesting tracing. It reminds me of the differential diagnoses that we have for regular narrow complex tachycardia, namely: PSVT, Atrial flutter, sinus tachycardia. I was taught that when the heart rategoes faster, the diastolic(repolarisation) component of the cardiac cycle is shortened much more compared to the systolic(depolarisation) component, resulting in the P waves becoming not visible/hidden or burried within the T waves. Hence I would say the first thing to do when approaching a narrow complex tachycardia would be to "scout" for the P waves
This is clear cut, upright P waves can be seen in lead I and II. There is no doubt about sinus tachycardia I think. The question now is whether or not to treat the rhythm, if it is sinus tachycardia, we all know that it is often a compensatory response to an underlying process, hence quite benign!
Although his temperature at the scene was 37 degrees celcius, look out for signs of sepsis as well. It was mentioned that his peripheries were warm and hot. Coupled with altered mental satus and a new onset seizure, one must rule out meningitis!

Blood sugar normal at scene hence unlikely the seizure is due to hypoglycemia.

I agree with the rest that substance abuse should be considered. Especially sympathomimetics.

• Dominick says:

The EKG shows Sinus Tachycardia, as evidenced by clearly defined P-waves in Lead I and several leads. The rate does appear a little high for a natural sinus tach. I would says treat him as postictal for the seizure for now and start looking for other underlying causes. Recent trauma? Drug use? Behavioral changes? Other toxin exposure?

I would say start an IV and administer 1000ml of NS. If he’s been ill, there’s a chance he could very well be dehydrated (which would also become apparent on physical exam). If he’s overdosed or been exposed to toxins, a little bit of saline would dilute the concentration. Also, with the reported illness, one has to consider meningitis or other communicable disease and precautions should be taken to prevent transmission.

In this case, saline alone seems to be the best course of action. As this is quite evidently a sinus rhythm, adenosine would be neither diagnostic nor therapeutic. Barring any other symptoms (such as chest pain, palpitations, hypotension, altered mental status), Cardizem/Metoprolol/Verapamil are all too pharmacologically aggressive — especially in the face of a potential unknown drug overdose. Supportive treatment only for now and try and get to the bottom of it with a thorough exam and patient interview. If there are any changes, address them as they appear and don’t be afraid to conference with medical control over at the receiving facility.

• SAP says:

I agree with sinus-tachy. Looking at his obs, he is mildly hypoxic with an increased RR, and has just experienced a seizure. All of these things could lead to tachycardia. I would apply high concentration O2 until SpO2, RR and HR return to normal. I would monitor the HR to see if the O2 was helping. Transport is warranted due to first occurence of seizure.

En route, I would discuss possible symptoms that may suggest an infective focus, although I’m not expecting to find anything. I would also discuss drug use – both of medications and recreational (current and historical), and make a point of explaining that this may affect his ongoing management. I would explain that it is highly likely that given his current presentation, and his denying of dug use, he is likely to end up with a Dx of epilepsy. I would explain how much of an impact epilepsy can have on people’s lives, eg. effecting what jobs you can do or what vehicle licenses you can hold, and strongly suggest that if there is any history of drug use which might explain the seizure, it would be very much in his best interests to disclose this, particularly bearing in mind the confidentiality we must maintain.

• Hungry says:

The ECG is sinus tachycardia. You can see the p waves clearly in lead 1. The axis is normal, I do not see any ST elevation or depression, there are however peaked t waves. I have encountered patients who have been reported to have seized with no history many times. Quite a few of those times the cause has been related to alcohol withdrawal/delirium tremens/wernickes encephalopathy. I first starting thinking this when you wrote that the wife became evasive with questioning about alcohol or drugs. I think some oxygen, isotonic fluid such as ns, and monitoring will serve this patient best. My protocol allows for thiamine to be given when alcohol withdrawal is suspected.

• UK-SAP says:

I'll hazard at a sinus tachy ECG with a prolonged QT (the computer readings are way off – QT=320ms and QTc=533 by my reconing).  This could have caused a bout of VF, VT or TDP resulting in the seizure.  Prolonged QT could be down to metabolic imbalance, congenital problem or certain medications (including, on reading, methadone). As for treatment, 02 for the low sats, transport to the nearset A+E probably with a pre alert to see whether they want to see him in resus.  Not much else we can give this side of the pond for long QT – is there anything you can give in America?

• Danny says:

Sinus Tach. Normal axis with peaked t waves. Just throwing this out there.. could this be a possible ace inhibitor overdose? Studies have shown that ace inhibitor OD can cause hyperkalemia. Also, chronic use could cause renal failure, leading to the slight increase in body temperature, and the increase in BGL.  Thoughts?

• P. harringt says:

“pre code” Sz. His t wave is spiked. Call a stemi code. He was most likely in v-fib, for a brief moment causing the Sz like activity. Very commen in nursing homes, but not in the text books.

• Tim says:

The rhythm is secondary in this I believe. He is taking meds for “hypertension” and has a bp of 112/64 now??? Vasovagal response (the “looks like he had a seizure”)??? Smells of cigarette smoke sa02 92% resp @26? He needs some fluids (if he doesn’t have a history of chf)and if he isn’t already retaining. Maybe do orthos? Has he had any bloody stools lately? GI??? What does his color look like? I would have to agree with “treat the patient, and not the monitor in this scenario, but being sinus-tach and low bp… possible GI?

• Chris S says:

I agree with UK-SAP with his EKG assessment so I won’t repeat whatâ€™s already there. I also think the QT is prolonged which could have lead to an episode of VT causing the seizure like activity and unresponsive period. Patient could be a chronic alcoholic which would also put him at risk for the prolonged QT interval due to the metabolic imbalances it can cause as stated above. Drug use could also be possible as many stated above. Treatment would be O2, IV, continued EKG monitoring, and transport which hopefully would be uneventful. The patient could also receive some NSS IV to see if that decreases the pulse rate, if it does could help with the differentials. Great EKG canâ€™t wait to see the conclusion.

• Corey Younger says:

2:1 A-flutter

• Corey Younger says:

Disregard my last, didn't look very closely.

• Roy says:

RAte oc 180 is PSVT, is what I was taught….O2, IV of NS, large. bore needle.Adenosine 6 mg rapid IV push…monitor patient followed by another 12mg IV push if his HR does’nt decreaae with the first round…continue to monitor patient….if patient goes down hill, consider Cardioversion after sedation with Versaid 5mg…

• Jack says:

I think his episode is related to the use of an erectile dysfunction drug use. He probably had some sort of sensitive response.

• Brian says:

What about sepsis? Decreased BP, elevated HR, increased temp

• Charlie says:

Like how everyone automatically says ST because that's what the strip says and there's p waves in lead I.  It wouldn't be ST with a rate like that, and don't believe I've ever seen a postictal seizure pt with that kind of rate either.  O2 sat and being a smoker with clear lungs isn't a worry, but Oxygen yes. AEIOU-TIPS. Guessing some type of drug use, recreational or other.

• Dan H says:

SVT causing convulsive syncope which look like epileptic seizures. The SVT could have been triggered by some kind of infection. O2, Monitor, large bore IV, Fluid bolus, ASA, adenosine, transport. If it doesn't convert with two rounds of adenosine he could be a candidate for sync cardioversion.

• Trey says:

I’ve only seen one person mention anything about what happened BEFORE anyone arrived (ref: UK-SAP’s post about VT, VF, etc). What you’re finding NOW may not be what happened to him THEN, which may or may not have caused his syncope, seizure, or whatever transient episode this guy had in the presence of his wife. Yes, his s/s sounds like seizure; and don’t HR’s skyrocket right before and/or after a seizure? Usually from what I’ve seen, yeah, they can and will.

Lest we forget what we didn’t see with our eyes or with a quick EKG tracing and/or 12-lead. I’m not sure what the likelihood of having a transient episode of VT (or God forbid, VF) then converting or transitioning back into a fairly strong sinus tach is.. but I can’t say I’ve heard of it, or at least very often, ya know? I just feel like everyone is saying, “Sinus tach! Sinus tach!” ..and few have noticed the abnormally long QTc. The monitor read normal length, but UK-SAP measured it long.

After a quick refresher on prolonged QTc (yeah, shut up).. it looks like Torsades, VT and VF all fall under the associated risks! Now, would he go back to the 180’s in somewhat of a perfect, yet super fast, sinus tach? No clue.. but these should be considered.

• Aharon Oppenheimer says:

I think that is a speed drugs, stimulant, maby
Aharon

Wow, there are an awful lot of comments…..many of which are different some of which are just awful….lol.  I'd like to make further observations and comments if I may.  first of all, I'd like to dispute the fact that the pt's QTc is over 550ms.  A 12 lead ecg machine is just that…..a machine.  Some things it does well, where as other things it's not very good at.  It is notorious at interpreting rhythms wrong, to the point that some services shut that function off and force thier medics to interpret it themselves.  What a computer does very very well is math and measurements.  A 12 lead ecg is very good at measuring PRI, QRS, Axis, and QTI/QTc.  I do believe this to be accurate.  The pt's QTc is measured at 0.42 sec which is normal.  This patient is in a ST.  He does have some interesting TW's in V3 and V4 which may indicate his serum K+ may be elevated.
The pt's CBG is 188mg/dL, which is not normal.  i would be concerned if it was 28 more though.  Dehydration can cause an increase in the pt's blood sugar, as well as tachycardia.  It could also cause syncope, which in turn may cause seizure activity when the pt becomes unconscious from the lack of blood supply to the brain.  But, the siezure activity itself also will cause a pt's BS to increase.
Someone mentioned that the patient is hypotensive……..how is this?  The pt's B/P is 112/64 which is about as normal as you can get. I get it….in comparisson with what his B/P normally is.  The pt's MAP is 80 mmHg, which is good as long as the pt's CPP is not greater then 20 mmHg…..which I doubt.  If the pt is on some sort of stimulant, I'd say that his DBP does not show vasoconstriction, which would increase the DBP….hmmmm….ACE inhibitor?
The patient has clear bilateral lung sounds with a RA SpO2 of only 92%.  This is NOT because he is a smoker.  I smoke and my SpO2 is 98-99% on any given day.  Especially if I were tachypneic @ 26/min.  That would bring in more O2 and blow off more CO2.  This is also not the pt's norm.  If they were a COPDer to the point of a hypoxic drive and a "normal" SpO2 for them of low 90's or upper 80's, he would be on home O2 by now or at least respiratory meds.  The pt is tachypneic because of the blood shunting away from his alveoli, and the fact that his blood is zipping by the alveoli so fast that there is less time for the exchange.  The pt become hypoxic because of the tachycardia, not the other way around.  If a person has a seizure, they are not breathing if it is a full blown tonic clonic epileptic type siezure.  That's why they're confused and positictal when they stop and wake up.  The patient does need O2, but not high-flow.  4 lpm via NC will suffice because it is not a breathing problem….it's a circulation problem.  Most people believe that this is an OD problem, but what did he take….hmmmmm.  Sometimes only blood work will tell if we can't get a good enough history or the patient and family are being evasive or telling fibs (hahaha…I said Fibs).  which brings me to another point.  If this person's QTc is normal, there is no ectopy, no ST elevation or even depression.  At a rate of 176 this patient has a pretty healthy heart given that his sinus rate is 176 and he isn't even showing ischemia…..this is a negative stress test….really….lol.
I think it's an OD of some sort of stimulant which caused the tachycardia.  And the pt is on an ACE inhibitor which is preventing us from seeing an increase in his DBP.
Am I the only one who see the 3 p's in the inferior leads? Indicating RAE secondary to Pulmonary artery vasoconstriction.  It could be my imagination, or the PW's being ontop of the TW's. I think this is diagnostic for RAE though.  We'll see.
reguardless, the patient had a siezure and is OD'd on some sort of stimulant.  I think first O2 will help, a fluid bolus (TY Dominiick) 1L but at 250 mL boluses with a reassessment in between.  Of course ECG and ECG 12-Lead.  Finally, I would strongly consider a Benzo for treatment of stimulant induced tachycardia and provention of future siezures.

• forsythfd922 says:

Sounds like a seizure, possibly from DT’s or other Rx? If he’s an alcohol addict as indicated by his “evasive” wife, he may also be addicted to other drugs. Rhythm is bordering on SVT/ Atrial tach since the “P” Waves are disappearing into the “T” Waves. Patient is coming around though, so I’d play low key. Don’t want to mix our drugs with his drugs unless necessary. Wish I knew more info on his meds/ compliance, instead of the traditional “something for blood pressure and something for cholesterol….”. IV-NS 250 cc bolus with repeat prn, O2 via nasal cannula, repeat 12-lead on ER arrival. Transport to rule out Withdrawal/ OD. Oh, and what were his pupils doing? ðŸ™‚

• UK-SAP says:

Nick, I agree, the patient is not hypotensive, and also the oxygen sats are certainly abnormal in the absence of a known respiratory problem/meds. I’m not great on bms in mg/dl but I believe that is around 10 mmol/l which though high isn’t markedly elevated.
Again I agree on the most part that the computerised values on ecgs are usually good, however I’m fairly sure this one is wrong. A rough rule of thumb is the qt should be half the rr (very rough mind you!) – in this case it’s markedly more. Doing the calculation in lead III where the end of the t is clear using the formula qtc = qt / square root rr. Qtc = 0.32s / square root 0.36s = 0.32 / 0.6 = 0.533s or 533ms
I think the reason your seeing p waves in the t waves is due to the long qt.
I do see your point re. ?stimulant od but I’m not totally convinced. I certainly wouldn’t be giving benzo (not that I can anyway ðŸ™‚ ) without more evidence / admission of use.
Ian

• Rob M. says:

The patient is in a sinus tach, albeit very fast given the are-related maximum HR (220-52=168), but likely explained by the seizure activity.  The skin temperature & moisture is also likely related to the seizures as the body temperature of 99.9F is elevated, but not enough to cause me to think the PT is suffering from some sort of infection.  The BP is acceptable, the SPO2 is a bit low, & the RR is a bit high, but again, considering the PT is post-ictal, its not entirely surprising.  Supplemental O2 by NC will suffice for now to help the PT's sats & hopefully the RR as well.  The BGL is slightly elevated at 188, but not enough for me to be concerned about DKA.  I've seen similar cases of patients who have had seizures & were found in tachycardic rhythms (generally SVT) & were determined to be on either cocaine or amphemtamines.  This PT could very well be a user of illicit drugs such as cocaine or amphetamines or could abuse alcohol which could've caused the seizure activity.  However, we should not take his wife's hesitance to answer questions about drug & alcohol use as a positive (its a clue), we have to push (nicely) her to tell us yes or no, explaining that it will only be to his benefit that we know.  Scan around the room & see if there are any clues that the PT uses drugs or alcohol, do we see mirrors & razors, needles & syringes, empty bottles or cans, spoons with residue, etc.  Most users I encounter in their homes are not too careful to hide their habits.  As the PT is answering questions appropriately, I'd likely check the PT's Cincinatti Stroke Scale as CVA & intracerbral hemmorhages are also in my list of differentials.  Since we have him answering, I'd also push to get the drug/alcohol info from him directly.  Turining back to treatments, a fluid bolus might also help control the patients heart rate.  Unless the rhythm changes, I don't forsee using adenosine on this patient, nor would I be using versed unless he were to have another seizure.  In my jurisdiction, this case, with all of its intricacies, would boil down to a VOMIT with a good assessement & HPI to pass on to the ED.  Unfortunately there's not much else they allow us to do around here.

UK-SAP – I'm sorry Brother, but I do not agree with your calculartions.  First of all, I wouldn't use lead III as the lead to get the QTI from.  In lead III the end of the TW is not clear because it is prolonged by the PW.  Lead I is a much better lead to see where the PW begins, and the end of the TW can be better approximated.  The computer is calculating the QTI as being 0.248s.  You can see in one of the middle complexes of lead I that the computers calculation of the QTI is pretty accurate, so I believe that the QTc is also correct.
Danny stated above that this could be an OD of an ACE inhibitor, which I agree with him.  ACE inhibitor OD can cause syncopy, tachycardia, siezures and an increase in serum potassium levels.  V3 and V4's TW's look mighty uncomfortable if you were to sit on them…..lol.
Let me clarify the use of a Benzodiazepine – I would try a Benzo, after all other treatments were exhausted, unless the patient began to have another siezure…then I would give it right away.  It would also depend on what I find in my assessment and reassessment after all other interventions.

• techno_medic says:

Roy. Are you.serious. a rate of.180.is.psvt. there are many other causes.of.He 180. Stach ( like this pt) a fib vtach a tach. Mat. To.say an.ecg is.something based of rate without looking at p waves, qrs duration and all.the other things we commonly look at when we look at ecg and 12 leads. As for this pt. S tach. I do.see some prolong wtf but I was.never one.for measuring by hand. If it was pro long that caused a run of v tach I.would monitor my pt. And be ready for changes. Maybe have Mag ready
As for this pt. Iv access. Ns bolus as long as no contradiction. Maybe ativan 1mg for preventing further seizures and sedation. My thought some tox like cocaine or meth or x. Like to see his pupils. Some of that fake pot I have seen can cause seizures flushed skin and s tachometer
Also look.for.infection. as possible cause
Def would not give adenosine or cardize.

• DEBMedicRNEMTPRN says:

Alkaloid