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Old 02-01-2019, 15:15   #1
ender18d
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Question My Favorite Teaching Case (EKG Practice)

After the EKG thread I'm going to present a new scenario, and anyone interested (regardless of training level) can present a single differential diagnosis item along with items support or speak against that diagnosis. One reason this is a great (real) case for teaching is that there are a large number of realistic possible causes of what happened based upon the history and an EKG just chock-full of badness.

****


You are working in a large tertiary care medical center with separate pediatric and adult EDs. You are assigned to the pediatric side but its late in the evening and not many patients are being brought in, so you decide to be helpful and pick up a handful of adult patients to help manage the over-burdened waiting room. You decide that a 38yo with a reported chief complaint of syncope looks like a nice, easy case you will likely be able to turn around quickly...


Chief Complaint
Syncope

HPI
The patient is a 38yo man with a past medical history significant for hypertrophic cardiomyopathy status post ablation >10 years ago, insulin dependent diabetes, chronic neuropathies, and depression. He has been more down recently due to a breakup and has not been eating much due to poor appetite. He has been suffering near syncopol symptoms that are brief and associated with a sense of impending doom for the past week that he has been trying to brush off. Tonight, in the bathroom, he passed out per family for about 30sec, crashed face first into the floor, and when he awoke he experienced chest pain and palpitations. His chest pain is substernal, non-radiating. Associated nausea, dyspnea and diaphoresis. His symptoms have improved and he now is primarily suffering mild chest discomfort and a sense of impending doom. There was no witnessed seizure activity and he has no history of seizures, no incontinence, no injuries, no post-ictal period.

PMH:
Hypertrophic Cardiomyopathy
Insulin Dep Diabetes
Depression
Neuropathies
HTN
HLD

Surgical History:
Ablation of HOCM >10 years ago

Medications:
aspirin 81 mg oral tablet, 81 mg= 1 tab, PO, Every Day Centrum Men's oral tablet, 1 tab, PO, Every Day Colace 100 mg oral capsule, 100 mg= 1 cap, PO, BID, PRN Effexor XR 150 mg oral capsule, extended release, 2, PO, Every Day melatonin 10 mg oral tablet, disintegrating, 1, PO, PRN, PRN methadone oral liquid (mg/kg), 70 mg metoprolol tartrate 100 mg oral tablet, 200 mg= 2 tab, PO, TID, 3 refills omeprazole 20 mg oral delayed release tablet, 2 caps, PO, BID Xanax 1 mg oral tablet, 1 mg= 1 tab, PO, TID

Family HX:
Diabetes
HTN
HLD
No family history of SCD

Physical Exam:
Triage Vitals all within normal limits
Pale, anxious appearing. No acute distress.
+Faint Systolic Murmur (hard to hear in busy ED), otherwise regular cardiac rate and rhythm. No edema, no JVD
Lungs CTAB with no adventitious sounds
Abdomen unremarkable
Detailed neuro exam unremarkable

You note that an EKG was already done at triage, and now significantly concerned about this patient based upon history you excuse yourself to go to the chart to pick up his EKG. As you leave the room he asks you not to go since he feels like something terrible is going to happen. You find his EKG and start to read it but only have a moment or two before the nurse comes running around the corner and says: "Come quickly he's not breathing!"

****

Based upon this history and EKG, please provide ONE possible cause of this patient's symptoms along with supporting or opposing evidence.
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Old 02-01-2019, 16:14   #2
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My first question is why you would take an adult patient with a complicated PMHx when assigned to the pediatric side...

My item for the differential:
Long QT syndrome - I didn't get out my calipers, but on eyeball it looks to be borderline at best, and the QT interval can be worsened by both methadone and proton pump inhibitor medications. Myocardial ischemia can also contribute, and his history of diabetes and Hypertrophic cardiomyopathy put him at risk for cardiac ischemia - the neuropathies suggest his diabetes has not been very well controlled. Data suggests effexor is not likely contributing, but case reports suggest it might.
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Old 02-01-2019, 16:46   #3
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Quote:
Originally Posted by PedOncoDoc View Post
My first question is why you would take an adult patient with a complicated PMHx when assigned to the pediatric side...

My item for the differential:
Long QT syndrome - I didn't get out my calipers, but on eyeball it looks to be borderline at best, and the QT interval can be worsened by both methadone and proton pump inhibitor medications. Myocardial ischemia can also contribute, and his history of diabetes and Hypertrophic cardiomyopathy put him at risk for cardiac ischemia - the neuropathies suggest his diabetes has not been very well controlled. Data suggests effexor is not likely contributing, but case reports suggest it might.
The most important teaching point of this case is: NEVER BE HELPFUL.

He was in an adult acute (non-critical) room and his history was not in the EMR and had not been solicited by triage. He was just around the corner close to the peds side though and we had just had a string of code blues and traumas swamping the adult team. I figured this would likely be a simple vaso-vagal case given his age and that he was in an acute room.


Differential:
Long QT (QTc = 652)
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Old 02-01-2019, 17:55   #4
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I'm an nursing student in my senior year, so please be gentle.

Taking into account the possible long QT and the host of other cardiac conditions. I'm thing about early stage of mitral valve prolapse.

Why?

Dyspnea
possible murmur heard
Lack of JVD
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Old 02-01-2019, 18:22   #5
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Quote:
Originally Posted by Shrub View Post
I'm an nursing student in my senior year, so please be gentle.

Taking into account the possible long QT and the host of other cardiac conditions. I'm thing about early stage of mitral valve prolapse.

Why?

Dyspnea
possible murmur heard
Lack of JVD
Glad to have you participate!

Absolutely reasonable to consider a valve problem in a patient with a murmur and acute cardiopulmonary decompensation. Acute valve problems are rare, but for that reason they are often under-considered. And I deliberately did not give a lot of details on the murmur

Mitral valve prolapse in isolation is most typically characterized by a mid-systolic click. It typically only has a true murmur if associated with mitral regurgitation. The of the most dangerous two sequelae of MVP are worsening MR and also a predisposition to arrhythmias. Dyspnea would most likely be caused by MR in MVP.

If we're thinking acute mitral regurgitation 2/2 mitral valve prolapse, that's less likely due to clear lung fields and lack of JVD... acute MR looks much like acute decompensated heart failure. But if we're thinking that my murmur was more of a click and specifically thinking MVP -> arrhythmia, its much more possible.

So we'll throw that on our differential too!

Differential:
Long QT (QTc = 652)
MVP -> Arrhythmia
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Old 02-02-2019, 10:55   #6
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Quote:
Originally Posted by ender18d View Post
After the EKG thread I'm going to present a new scenario, and anyone interested (regardless of training level) can present a single differential diagnosis item along with items support or speak against that diagnosis. One reason this is a great (real) case for teaching is that there are a large number of realistic possible causes of what happened based upon the history and an EKG just chock-full of badness.

****


You are working in a large tertiary care medical center with separate pediatric and adult EDs. You are assigned to the pediatric side but its late in the evening and not many patients are being brought in, so you decide to be helpful and pick up a handful of adult patients to help manage the over-burdened waiting room. You decide that a 38yo with a reported chief complaint of syncope looks like a nice, easy case you will likely be able to turn around quickly...


Chief Complaint
Syncope

HPI
The patient is a 38yo man with a past medical history significant for hypertrophic cardiomyopathy status post ablation >10 years ago, insulin dependent diabetes, chronic neuropathies, and depression. He has been more down recently due to a breakup and has not been eating much due to poor appetite. He has been suffering near syncopol symptoms that are brief and associated with a sense of impending doom for the past week that he has been trying to brush off. Tonight, in the bathroom, he passed out per family for about 30sec, crashed face first into the floor, and when he awoke he experienced chest pain and palpitations. His chest pain is substernal, non-radiating. Associated nausea, dyspnea and diaphoresis. His symptoms have improved and he now is primarily suffering mild chest discomfort and a sense of impending doom. There was no witnessed seizure activity and he has no history of seizures, no incontinence, no injuries, no post-ictal period.

PMH:
Hypertrophic Cardiomyopathy
Insulin Dep Diabetes
Depression
Neuropathies
HTN
HLD

Surgical History:
Ablation of HOCM >10 years ago

Medications:
aspirin 81 mg oral tablet, 81 mg= 1 tab, PO, Every Day Centrum Men's oral tablet, 1 tab, PO, Every Day Colace 100 mg oral capsule, 100 mg= 1 cap, PO, BID, PRN Effexor XR 150 mg oral capsule, extended release, 2, PO, Every Day melatonin 10 mg oral tablet, disintegrating, 1, PO, PRN, PRN methadone oral liquid (mg/kg), 70 mg metoprolol tartrate 100 mg oral tablet, 200 mg= 2 tab, PO, TID, 3 refills omeprazole 20 mg oral delayed release tablet, 2 caps, PO, BID Xanax 1 mg oral tablet, 1 mg= 1 tab, PO, TID

Family HX:
Diabetes
HTN
HLD
No family history of SCD

Physical Exam:
Triage Vitals all within normal limits
Pale, anxious appearing. No acute distress.
+Faint Systolic Murmur (hard to hear in busy ED), otherwise regular cardiac rate and rhythm. No edema, no JVD
Lungs CTAB with no adventitious sounds
Abdomen unremarkable
Detailed neuro exam unremarkable

You note that an EKG was already done at triage, and now significantly concerned about this patient based upon history you excuse yourself to go to the chart to pick up his EKG. As you leave the room he asks you not to go since he feels like something terrible is going to happen. You find his EKG and start to read it but only have a moment or two before the nurse comes running around the corner and says: "Come quickly he's not breathing!"

****

Based upon this history and EKG, please provide ONE possible cause of this patient's symptoms along with supporting or opposing evidence.
Given the history of cardiomyopathy and the drugs on board along with the expression of a sense of impending doom in this patient, I would want to take a closer look at the lungs for signs of pulmonary edema. Do we have a PO2 on this patient? Standing by with a dose of digoxin might not be a bad idea.
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Old 02-02-2019, 11:13   #7
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Patient has been feeling down lately. History of depression. Current Effexor use.

There is a terminal R wave in AVR. This can be seen in sodium channel blockade e.g. TCA (tricyclic antidepressants ) toxicity.

Possible Effexor OD or had some old TCA and downed the bottle.

Concern for ventricular arrhythmia from sodium channel blockade toxicity.
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Old 02-02-2019, 12:02   #8
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Quote:
Originally Posted by Trapper John View Post
Given the history of cardiomyopathy and the drugs on board along with the expression of a sense of impending doom in this patient, I would want to take a closer look at the lungs for signs of pulmonary edema. Do we have a PO2 on this patient? Standing by with a dose of digoxin might not be a bad idea.
One of the things I like about this case is that the scenario I've given is actually how it played out. I got to do an H&P then look at the EKG before @#$& hit the fan, and had to develop a quick starting differential based solely on the info I had. Certainly more things were ordered later but for the sake of the scenario, let's work on the differential we have. Later on we can talk about ordering more studies.

There were no signs of pulmonary edema on auscultation and no other signs of acute decompensated CHF.

However you mentioned the history of cardiomyopathy, so I'm going to throw that on the differential. This guy has a history of hypertrophic cardiomyopathy that has *in theory* been corrected, but no treatment is perfect and all of the various procedures used to correct hypertrophic cardiomyopathy are no exception. Hypertrophic cardiomyopathy kills in two primary ways: its an arrhythmogenic condition unto itself and obstruction can occur when a combination of septal hypertrophy and systolic anterior motion of the mitral valve, where the valve flips over and blocks aortic outflow tract.

This obstruction is an important differential to consider because we treat it substantially differently than a normal cardiac arrest: goals are to increase preload (fluids) AND increase systemic vascular resistance (phenylephrine) while sparing any inotropic agents (epi, norepi included) to the extent possible.

So while I had (and still have) a hard time gauging how likely this guy would really be to have obstructive HCM, one can't ignore a history of HCM in a guy with scary-sounding syncope and chest pain.

So the list stands at:
Long QT
Hypertrophic Cardiomyopathy
MVP>Arrhythmia
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Old 02-02-2019, 12:05   #9
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Quote:
Originally Posted by Patriot007 View Post
Patient has been feeling down lately. History of depression. Current Effexor use.

There is a terminal R wave in AVR. This can be seen in sodium channel blockade e.g. TCA (tricyclic antidepressants ) toxicity.

Possible Effexor OD or had some old TCA and downed the bottle.

Concern for ventricular arrhythmia from sodium channel blockade toxicity.
100% agree this is a major consideration for this patient especially considering the wide QRS of unknown chronicity.

Differential:
Long QT (QTc = 652)
Hypertrophic Cardiomyopathy
Overdose, especially TCA
MVP -> Arrhythmia

Anyone want to take the low hanging fruit and see if you can find any ECG signs this hypertensive hyperlipidemic diabetic guy with chest pain could be having a heart attack?
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Old 02-02-2019, 18:51   #10
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I'm unsure of how to explain this.

The qrs complex looks small in amplitude to me which I think means incomplete depolarization along with the long qt syndrome. I'm thinking a partial occluded coronary artery.
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Old 02-03-2019, 05:19   #11
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Quote:
Originally Posted by Shrub View Post
I'm unsure of how to explain this.

The qrs complex looks small in amplitude to me which I think means incomplete depolarization along with the long qt syndrome. I'm thinking a partial occluded coronary artery.
Low QRS amplitude can have a bunch of different causes including ischemia/infarction. It can also be caused by anything ranging from Addison's disease to cardiac tamponade to obesity. Usually the criteria is 5mm in the limb leads and 10mm in the precordials. I can see what you are saying in leads II, and V6 which are right on the edge, but the amplitudes in the other leads are pretty decent. I would be hesitant to read too much into just those two leads but its certainly reasonable to think about.

ischemia can absolutely be a contributor to long QT.

When we're looking for ischemia or infarction, the first place we look is the ST segments and then the T waves. I've zoomed in a bit and highlighted some ST segments here and while this is not quite meeting STEMI criteria I find it very concerning that this patient has ST elevation in two contiguous leads (III, AvF) with reciprocal changes in I and AvL. This pattern is suggestive of possible inferior MI. We're not quite a millimeter, so I may not be activating the cath lab just based on this EKG, but its concerning. The elevation in AvR is also potentially concerning for left main disease as we're right around a millimeter. AvR isn't as specific as traditional STEMI criteria and can be a marker for subendocardial ischemia, so again, not spinning up the cath lab yet but worth a look.


Differential:
Long QT (QTc = 652)
Acute Coronary Syndrome
Hypertrophic Cardiomyopathy
Overdose, especially TCA
MVP -> Arrhythmia

In addition to the highlighted ST segments I've attached a highlighted version of the ECG pointing out some features. Does this suggest one last differential item to anyone?
Attached Images
File Type: jpg IMG_2469.jpg (89.3 KB, 20 views)
File Type: jpg IMG_2469 (1).jpg (96.1 KB, 19 views)
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Old 02-03-2019, 09:41   #12
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Okay my gut is bringing me back to pulmonary function i.e. pulmonary hypertension/PE. Some of the highlighted changes in the ECG I think supports this differential - prominent S wave and lead I, invertedT lead III. TallR in VI. I will go out on a limb and suggest aRV MI.

So did you spin up the Cath Lab in time? I'm just guessing this patient dodged the bullet thanks to your attention and clear dDx
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Old 02-03-2019, 11:44   #13
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Originally Posted by Trapper John View Post
Okay my gut is bringing me back to pulmonary function i.e. pulmonary hypertension/PE. Some of the highlighted changes in the ECG I think supports this differential - prominent S wave and lead I, invertedT lead III. TallR in VI. I will go out on a limb and suggest aRV MI.

So did you spin up the Cath Lab in time? I'm just guessing this patient dodged the bullet thanks to your attention and clear dDx
Yes the S1Q3T3 and also the right bundle branch block (which we must presume is new without comparison) suggests right heart strain and therefore in context of chest pain, dyspnea, and syncope concerning for pulmonary embolism.

Agree the ST changes suggest the possibility of right side MI.

So lets call that good for our differential and cap it at:

Differential:
Long QT (QTc = 652)
Acute Coronary Syndrome
Pulmonary Embolism
Hypertrophic Cardiomyopathy
Overdose, especially TCA
MVP -> Arrhythmia


Rejoining the action, you respond to the nurses call and find your patient unresponsive and apneic in the room. You quickly check a pulse and find an extremely rapid, weak and thready pulse. You perform a head tilt-jaw thurst and begin bagging the patient effectively as you transfer him to a resuscitation bay. On arrival in the bay you note that he now no longer has pulses and begin CPR. Your nurse cannot immediately get an IV so you get IO access. You start a full run of POC labs off the IO but remember that some labs are not reliable from IO. Your patient is connected to a Lifepack and on your first pulse check he is pulseless and the attached strip represents what you see on your monitor. (unfortunately I did not get a chance to copy the real strips, but this is a good approximation)

1. What is your interpretation of the strip?
2. Which item(s) on our differential are most likely now?
3. What are your next most important steps?
Attached Images
File Type: jpg strip.jpg (20.3 KB, 14 views)
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Old 02-03-2019, 13:19   #14
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This just got serious! Dx - pulseless ventricular tachycardia

Treatment plan is 2 phase with the first phase focusing on establishing a normal rhythm:
1. Breakout defibrillation paddles
2. Administer lidocaine IV bolus
3. Administer digoxin IV bolus
4. Administer sodium bicarb IV bolus

Second phase is determine the proximal cause for tachycardia.

Obtain angiogram
obtain transesophageal echocardiogram
balloon angioplasty to resolve infarct.
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Old 02-03-2019, 14:20   #15
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Originally Posted by Trapper John View Post
This just got serious! Dx - pulseless ventricular tachycardia

Treatment plan is 2 phase with the first phase focusing on establishing a normal rhythm:
1. Breakout defibrillation paddles
2. Administer lidocaine IV bolus
3. Administer digoxin IV bolus
4. Administer sodium bicarb IV bolus

Second phase is determine the proximal cause for tachycardia.

Obtain angiogram
obtain transesophageal echocardiogram
balloon angioplasty to resolve infarct.
Some of this I love, some could be improved.

Anyone else want to take a stab?
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