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Case #34 Young + Ami = ?


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#1 Mike MacKinnon

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Posted 02 December 2007 - 06:03 AM

This is an actual case which will be about investigation and diagnosis both during and outside the typical scope of HEMS practice. It should be interesting!

1) The Story.

You are called to a local hospital ER to transport a 19 y/o female for "cardiac problems". As you understand it the patient has been in the ER for some time and has been treated for MI. Not much else comes across on the dispatch.

2) On your arrival

You arrive to find a 19 y/o female who is laying on the ER stretcher clutching her chest. The RN at the side of the bed is administering a medication in the IV line and the girls mother is in the room. The mom has a look of absolute panic and fear in her eyes. Before you can ask any questions the attending takes you aside to give you some information.

She tells you that this girl has been into this ER on one other occasion for hypertension and shortness of breath and also into 2 others for the same thing. She wants to let you know that every time they have done a drug screen that has come back negative and today was no different. They have been especially attentive to this family since the father died of a "widow maker" only 2 months previous. Since the facility does not have a cath lab operational at night and she was very symptomatic they decided to send her out to the local "heart" center by air.


3) History (well taken d/t chart)

She has a history of rheumatic fever as a small child after a strep throat infection
Mitral valve regurgitation
She has tested positive for marijuana once in the last year
she is a smoker

4) Obvious Pertinent Physical findings

Vitals: BP: 184/100 HR: 110 Sat: 92% 2l n/c RR: 20

Lungs have crackles bilaterally
Patient is diaphoretic & SOB
Chest pain 8/10 but no history of angina/cp

The ER has already given her:

325 mg ASA
4 L n/c
1 liter of N/S
8 mg of morphine
3 ntg s/l followed by a ntg drip which is now at 12 cc/hr
Metoprolol 15 mg in 5 mg increments

The did complete labs which showed these abnormalities:

CPK 165 U/l
troponin I .96 ug/l
CK-MB 3.25 ng/mL

This is her EKG

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Mike MacKinnon MSN CRNA
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"What gets us into trouble is not what we don't know
It's what we know for sure that just ain't so" - Mark Twain

#2 chris

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Posted 02 December 2007 - 04:04 PM

Alright, I'll go first. Couple of questions. (Well more than a couple)
1. Does she have any peripheral edema? The biphasic T wave in V1 makes me suspicious of ventricular hypertrophy.
2. Did they do a BNP? If so what was that?
3. What were her electrolyte studies? In particular K+, Ca and Mag. Did they do a D Dimer?(Not a great test but warrants further looking if really elevated)
4. Did they CT her chest for PE?
Looking at her EKG, there are some significant findings that at first blush don't correlate. There is a flipped T in I, there is a peaked T wave in III, a positive deflection in AVR, a flipped T in AVL, possible elevation in V1, (hard to see on small EKG size), definitely elevated in V2, and sloped T wave in V3. Maybe Hypokalemia? No global findings like you would see in a case of endocarditis.
Another thing you could ask if they have done is an echocardiocgram to see if her regurg has gotten worse. If she has been there any time at all they could have done a bedside echo.
How many mcgs of nitro is that? Could be 20-40 mcgs. Either way you could increase the dose which would treat her for chest pain and if she is in failure would treat that as well. You could give her some more morphine. With such a crummy sat I would put her on an NRB at 10 lpm.
If she has any peripheral edema I would give her a whiff of Lasix 10-20mg.
One has to wonder with diaphoresis and SOB, 19y/o. Is she on birth control pills? As a smoker she is at increased risk of PE.
Short bedside time and fly to get cath would be my treatment plan to start with.
I hope this is a good start.
Chris
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#3 cardiomedic

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Posted 02 December 2007 - 06:14 PM

I agree with Chris. I would continue current treatment with a high index of suspicion due to the current findings. I would tend to relate the ECG changes to a Wellen's syndrome. See the following two sites for more research.

http://findarticles....406/ai_n9425804

and

http://www.ispub.com.../vol2n2/ecg.xml

If the nitro is at the standard concentration of 50mg in 250mL, then her dose would be at 40mcg/min and that can certainly be increased. Continue to attempt to get her pain free, put on the pads, and get her to interventional care for her probable impending high LAD lesion.

I am sure there is more to come. She does not fit all of the criteria for Wellen's, that specifically being the ECG changes are usually when the patient is pain free, but with a History of rheumatic fever, there could very well be more going on. I am sure Mike will throw some more at us, so eagerly awaiting what everyone thinks.
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#4 cumedic

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Posted 02 December 2007 - 06:21 PM

Looks like STEMI management is underway, but we should look to precipitating causes as well. Acute mitral valve regurgitation seems likely, and if she's symptomatic we ought to assume the worst (ie, papillary muscle tear/ ruptured chordae tendonae). The rupture will lead to cardiac ischemia, thus we have two concurrent disease processes to treat for: STEMI + AMR.

The EKG shows NS rhythm, left axis deviation, inverted T's in I, AVL, V2, V3, ST elevation in V1, V2, V3.

Along with general O2, IV access, Monitor, Analgesia.

1) Afterload reduction via IV nitroprusside.
2) If she becomes hypotensive, then add dobutamine with nitroprusside. We want to keep afterload pressures low using a systemic vasodilator, while also stimulating cardiac output. Separate lines obviously. Arterial and central lines are prudent, depending on transport time. Consider IABP.
3) Since we can't assume 100% that the MR is the source of the problem, I'd like to hear everyone's thoughts about ASA, heparin, plavix, glycoprotein inhibitors in this case. In a girl her age, the problem is likely not a thrombus, so do we still want to continue standard MI management that works on that assumption, especially if she were to need emergent surgical repair of the valve?
4) The definitive diagnosis of rupture will be via echocardiogram, but I will assume that urgent transport is taking precedence since EMS was called.

Thanks for these cases.

Take care all.
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who is john galt?

#5 Speed

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Posted 02 December 2007 - 06:42 PM

She's definitely got pulmonary hypertension and could stand to be "brought down" a bit. Lasix would seem OK and beneficial, as well as the nitro and morphine. If it's not her thyroid or some other metabolic or toxic state, you'd have to think cardiac, something like PPH? Treat it like bad pulmonary edema. Maybe test with pursed lip breathing, and if that helped maybe a trial of non-invasive CPAP or BiPAP?. It would help the BP too if it showed any positive effect on the dyspnea. Get a destination/plan for a good heart surgeon that can do valves. The Lopressor given earlier is going to cause some bronchoconstriction so some Albuterol may help counteract that, but will be blunted by the beta-blocker as well. If things were getting better as the pulmonary pressure was going down you'd feel a little more confident about a cardiac cause. I wouldn't absolutely rule out any type of occlusive situation. ASA definitely, Lovenox would be safe. If I saw any PVC's after high-flow oxygen I would treat them with Lidocaine (ECG/age OK) after more than about 8-10 a minute, and that might resolve any coronary vaso-spasm as a cause of chest pain too. But I really think it's hypertensive caused chest pain.
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Mike Williams CCEMT-P/FP-C

#6 rjflyn

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Posted 02 December 2007 - 06:44 PM

We are missing some parts here.
Obviously we have a 19 y/o female with a cardiac history, whom smokes. Who on one occasion has tested positive for drugs, who may or may be self medicating with something that a standard drug-screen misses. What are her other medications, did she recently use something that drug screen can miss? Mom may have to be asked to step away briefly so one can ask.

Her lungs are wet, she remains hypertensive and still with pain so increasing the nitro and giving a dose of Lasix along with placing a foley to
monitor output is in order. NRB oxygen is also not going to hurt, I doubt she has any kind of long standing respiratory issues, I would get an ABG first though.

It does not take long to get a chest CT for PE, but if its like here it takes a while to get one read. Oh and while I am thinking of it, I am going to grab a rainbow of tubes for the guys where we are going for the inevitable Zebra tests they are going to do.

Time to burn some JP-8
Rj
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#7 Speed

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Posted 02 December 2007 - 06:47 PM

Sorry, forgot one part: The big Q waves near her septum would make me keep a close eye on her rate, if it started slowing I'd be ready to get aggressive.
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Mike Williams CCEMT-P/FP-C

#8 getoverit

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Posted 02 December 2007 - 07:48 PM

Lots of good responses so far, sorry I don't have much new to add. Chem 8, bnp, clotting times and a d-dimer would be helpful. Question about smoking and birth control pills?
Her sat isn't that bad for pulmonary edema, maybe some BiPAP/CPAP could help along with some diuretic (check K+) . Strong + family history is important cause you can't beat your genes (dad's LAD, rheumatic fever with mitral regurg)! MSO4 and ntg doesn't seem to be touching her pain and I wonder if she'd be able to tolerate an echo or CTA. In any event lovenox probably won't do any harm.
I guess she takes no medications at home. I'd also want to know what the ED had done for her in the past that resolved her similar episodes. do we have her previous 12 leads to compare? cardiac markers are borderline, ekg is ST with left axis, anterior elevation. Definitely needs a interventional cath.
can we get a quick abg? how bad is her murmur? is the MD able to appreciate it as worse than before? what is the description of the chest pain? any aggravating/alleviating factors? how fast was the onset? what was she doing when it happened?
was the medication the RN was administering a the bedside when we walked in the last increment of metoprolol?
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RN, BSN, CCRN


#9 STPEMTP

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Posted 02 December 2007 - 07:55 PM

Couple of things I'd like to know:
Previous visits to this facility: any findings that were suggesting CHF?
Why was a fluid bolus given?
How old was Dad when fatal MI?
Any JVD?
Was a BNP done?
Any change in exercise tolerance or activity levels?
Is pt on BCP?
Does the murmur have an "odd" sound to it?
What was patient doing prior to this episode? Any recognizable cause to symptom onset?
CXR: is cardiac shadow enlarged?
EKG: were any other ekg's, any changes to previous ones?


EKG: High lateral ischemic changes with V2 elevation and questionable V3 elevation, odd that there are no changes in V1 and V4,

Dx: CHF to start, really starting to wonder about vasospasic coronary artery

TX:
STEMI treatments already started, keep them going.
guessing 50mg/250ml prep of NTG Gtt, keep increasing as needed
Increase O2 to mask at 10-15lpm, consider CPAP
Verapamil 5mg IV due to suspecion of vasospasm as cause.
short scene time

What transport time by the way Mike?
Great case
James
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#10 cumedic

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Posted 02 December 2007 - 08:44 PM

And of course I forgot to do the most obvious thing and LISTEN to the patient's heart sounds to backup my suspicion of AMR or ruptured chordae tendonae.

Take care all.
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CUmedic, NREMT-P

who is john galt?

#11 MFlightRN

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Posted 03 December 2007 - 03:10 AM

Given her father's pmhx (widow maker), relatively low changes in cardiac markers, and those 'freaky' T waves in V2 V3, I'd be thinking bout Wellen's syndrome maybe??? :blink:
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Lou-

#12 cumedic

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Posted 03 December 2007 - 03:40 AM

Many folks are mentioning Wellen's Syndrome(Biphasic T in V2/V3 + Angina = Proximal LAD lesion). However, classically the EKG findings occur during a pain free episode. An old EKG to compare may help given that she's had previous admissions.

Other criterion for Wellen's are absence of precordial Q-waves (our patient has them) and no pathologic ST elevation (which our patient also has).

de ZwaanC, Bar FW, WellensHJ. Characteristic electrocardiographicpattern indicating a critical stenosis high in left anterior descending coronary artery in
patients admitted because of impending myocardial infarction, Am Heart J, 1982;103:730-6

Tandy TK, BottomyDP, Lewis JG. Wellens' syndrome. Ann EmergMed, 1999;33:347-51.

NarasimhanS, Robinson GM. Wellenssyndrome: A combined variant. J PostgradMed 2004;50:73-74


Take care.
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CUmedic, NREMT-P

who is john galt?

#13 MFlightRN

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Posted 03 December 2007 - 03:52 AM

Many folks are mentioning Wellen's Syndrome(Biphasic T in V2/V3 + Angina = Proximal LAD lesion). However, classically the EKG findings occur during a pain free episode. An old EKG to compare may help given that she's had previous admissions.

Other criterion for Wellen's are absence of precordial Q-waves (our patient has them) and no pathologic ST elevation (which our patient also has).

de ZwaanC, Bar FW, WellensHJ. Characteristic electrocardiographicpattern indicating a critical stenosis high in left anterior descending coronary artery in
patients admitted because of impending myocardial infarction, Am Heart J, 1982;103:730-6

Tandy TK, BottomyDP, Lewis JG. Wellens' syndrome. Ann EmergMed, 1999;33:347-51.

NarasimhanS, Robinson GM. Wellenssyndrome: A combined variant. J PostgradMed 2004;50:73-74
Take care.


Hey now..........I did say 'maybe.' lol....it could be all the Sam Adam's Winter Lager speaking afterall! :rolleyes:
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Lou-

#14 MFlightRN

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Posted 03 December 2007 - 04:17 AM

Many folks are mentioning Wellen's Syndrome(Biphasic T in V2/V3 + Angina = Proximal LAD lesion). However, classically the EKG findings occur during a pain free episode. An old EKG to compare may help given that she's had previous admissions.

Other criterion for Wellen's are absence of precordial Q-waves (our patient has them) and no pathologic ST elevation (which our patient also has).

de ZwaanC, Bar FW, WellensHJ. Characteristic electrocardiographicpattern indicating a critical stenosis high in left anterior descending coronary artery in
patients admitted because of impending myocardial infarction, Am Heart J, 1982;103:730-6

Tandy TK, BottomyDP, Lewis JG. Wellens' syndrome. Ann EmergMed, 1999;33:347-51.

NarasimhanS, Robinson GM. Wellenssyndrome: A combined variant. J PostgradMed 2004;50:73-74
Take care.


After a closer look, and a few more beers, I really don't think we have pathologic Q waves in V1....I see small r waves...a small r wave appears above the isoelectric line. V1 should be more negative than positive. Also, I wonder if the ST elevation in V2/V3 could be from early repolarization??? :blink:
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Lou-

#15 medic31

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Posted 03 December 2007 - 04:56 AM

The pt. doesn't neccasarily have to be pain free for Wellen's as CUmedic mentioned. You will usually see steep t wave inversion or biphasic t's in lead v6 with the painfree type of wellen's pt. I also see small r waves in all precordial leads with the exception of v3 due to the overlap. This pt. appears to present with the less common type of Wellen's where you have the biphasic t's as opposed to the more common steep t wave inversions seen in Wellen's pt's. I would also say that the only lead to show greater than 1 mm elevation is v2 with no other contiguous leads showing the same elevation. All = or < 1mm. I think the Wellen's is a good call for now and would like to see pt. go to cath. I bet on the LAD lesion. just my opinion. cool EKG by the way. B)
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#16 Flightgypsy

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Posted 03 December 2007 - 05:40 AM

Any chance she is one of those rare cases of ALCAPA who has survived this far without diagnosis? The mitral regurge, CHF and RVH would all fit with that as well. Just curious. Agree with the AMI treatments and fast transport. I think an echocardiogram might be good before going straight to cath lab though. I think she is definitely a zebra.
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#17 rfdsdoc

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Posted 03 December 2007 - 06:42 AM

Hey folks from sunny Down Under!

It's that time of the month again to put on our HOUSE MD hat.

19yo with AMI. Youngest I had was a 21yo with AMI/STEMI, given tenecteplase with no results so I had to do scary 45 min flight transfer to the nearest CTU where he died 3 days later in cardiogenic shock.

Doens't look good for this lass as well as she is in acute LVF, hypoxic and hypertensive.

Setup for RSI. Give more oxygen till you are ready. Push the Nitro drip more and some fentanyl or more morphine. Could try some CPAP or BIPAP but I fear she will not tolerate it and may distress her more. Tube her for the transfer..maximises oxygenation and minimises myocardial oxygen demand. Secure her Airway and Breathing prior to uplift so you can focus on her C for the whole transfer time.

Would not give verapamil as already has had metoprolol and could send her into brady/cardiogenic shock with a lethal drug interaction.

Talk to the receiving cardiac team and fax EKG to them. Decision on lysis should be made in consultation in this setting. depends on a few variables such as transport time, duration of chest pain since onset , planned provisional treatment on transfer etc. I know she has only one good lead with ST elevation and the contiguous ones are borderline but she is 19 yo and has the most to benefit from lysis as early as possible unless primary PTCA is possible in under 2-3 hours.
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Minh Le Cong
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RFDS Cairns base , Queensland, Australia

#18 fiznat

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Posted 03 December 2007 - 08:21 AM

Please excuse the first time poster...

Perhaps this question is too late now, but there is a part of me that just does not want to believe that a 19 year old is actually having primary acute coronary syndrome. Though there are risk factors present (hx of hypertension, family history, smoking), the age really bothers me - perhaps more than it should in an arena such as this where zebras tend to be the norm. Is that wrong?

There are other things I wonder about:

-Did the pain/presentation change at all with the NTG? It seems she's received a bunch by this point.

-After the NTG, Morphine, and lopressor, why is the blood pressure still so high?

-Why give a liter of NS to a patient with wet lungs and hypertension?

-On the ECG there seems to be fairly limited ST segment changes (limited in anatomy, I mean), with no recroprical changes. The biphasic T wave is simply "weird" to me, and I wonder if this isn't some pathology other than straight AMI.

-I don't know much about labs but I did some web searching and it doesn't seem that the reported values are all that extreme? ...Or at least maybe not in line with the rest of her presentation?

-Diaphoretic, SOB, lowish O2 sat, wet lungs, 8-10 chest pain--- and a resp rate of 20?


Again, please excuse the (most likely basic) questions. I am a new paramedic and frequent reader of these forums, looking to learn more.
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#19 Dunkle

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Posted 03 December 2007 - 11:30 AM

First-- PMH? Enjoying any medication? Allergies? Surgeries?
I'd agree that Anterior MI is in my differential as well as PE, myo/pericariditis, RBC problems (low or deformed), Printzmetal Angina, Septal rupture/communication/chordae tend rupture.
Things that won't hurt--
Heparin, Gaba 2b3a I, consider lytics. Agree with current posts-- are the current tx helping? Any EKG changes? Body systems- A&O? Urine output? Skin? GI?
Labs- CBC, CMP, BNP, Trop, possible CRP or Sed Rate, Coags, lactate, *ABG*, Rad studies- CT Pulm, CXR (at the very least). H&H stable? Morph ok? Any CO exposure? Prego?
managment- High flow o2 and possible intubation, need some pressure. Continue NTG and Morphine. Looking at our AADO2 gradient will tell us alot. Quick echo if available.
1. Airway and Breathing
2. Bolus 500cc NS
3. Heparin, 2b3a i, ?lytics?, BB, MSo4, NTG > if indicated.
4. Transport to nearest facility for cardio intervention
5. Rest, enjoy ETOH and sunshine!

Thanks.
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#20 Dunkle

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Posted 03 December 2007 - 11:33 AM

oops--- missed the crackles in the lungs---
minus the saline
consider dobutamine or add a little dopamine and increase the ntg.
Don't want to increase MVO2. hmmm....
interesting case.
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