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Questionable Cause of Death Inquiry: Heart

Can you help us in our search for cause of death?

Very healthy, athletic 49/F presented to ER with nominal symptoms of nausea, fatigue, BP around 88/60, mildly hypotensive, but no pain or chest pain. Rapid HB >120.

No heart history. No family history.

Onset was four days prior, vague chest tightness, saw primary doc before trip out of town, chest X-ray clear. Gave her
Zithromax and albuterol. (patient has prior reported allergy to azithromycin and sulfa). Patient got sick after fist doses of medications, extreme nausea, fatigue upon exertion, threw-up over the weekend and felt that sick for few days. Called doctor on fourth day after flight returned home, reported stopping the Zithro after second dose, doc said doc could proscribe nausea meds. Patient said she wanted to go to ER instead.

ER gave Sodium Choride .9% 1,000ML IV, saline lock, Pepcid, Zofran, EKG, Lab tests, chest x-ray.

X-ray was clean.
Labs were high troponin 7.0, CK-MB 10.7, total CK 298, and high.... ALP, AST, ALT.
Low Sodium, WBC counts within normal range.
NO fever
ER EKG showed: "sinus tachycardia with a right bundle config an isolated ST elevation in V3"

(Note: We are being told today, that at this point, a Right BBB, instead of a Left BBB precludes the need for an angiography and mostly right heart issues like PE or cardiomyapthy should have been followed, however....)

After 2 hours, patient's sinus tachycardia and nausea remained, BP elevated slightly to 91/69 and heart rate dropped to 118. After cardio consult, Cardio took patient immediately to CATH LAB to perform angiography.

After .25mcg of Fentanyl, 1 mg of Versed, and another 4mg of Zofran by IV, she became immediately and progressively hypotensive, her worst numbers of the day within seconds of percutaneous stick to right groin. (81/47) This includes RESP of 77.

(Note: All meds given might cause hypotension as side effect)

He proceeded with angiography left and right, skipped ventriclogram, and finished with aortagram. 100 ml of optispray. Within minutes HR went to 167 and CODED into pulseless electrical activity arrest and progressed to V-tach V-fib arrest.

Angiography was clean.

Emergency ECHO was performed in Cath Lab after arrest to reveal:

LV normal size, normal thickness, but septal dyskenisis, apical akinisis, and severe global hypokenisis, severe systolic dysfuntion estimated near 15% E/F, mural thrombus.

RV: Moderate dilation, severe hypokenisis, flattened septum in diastole consistent w RV volume and pressure overload.

RA: mild enlargement
LA: moderate enlargement.
Pericaridum: normal

(Note: Could this have occurred as a result or two arrests and 30 minutes of Code? A reaction to dye, combined allergens? Or did she have to walk into hospital with this conditions, as they seemed to indicate thru theory of acute myocarditis. Why was Xray done 2 hours earlier and last week clear of size change? Can size change occur as a result of something that happened in that Lab??)

Patient went into cardiac shock was given protocol meds... wide open. She coded about 5-7 more times over the next four hours and died 12 hours after Cath lab in ICU. She was given an IABO balloon pump in cath lab too. She regained semi-consciousness after first round of codes, only to grab at respirator and code again, mostly coma-like for next 8 hours.

(Note: respirator was inserted 24cm by RTT.  4 hours later, xray reading said it was in the right mainstem and advised retracting it 4cm. Should that have been noticed? Could that have caused hypoxy and the continued PEA arrests and trauma?)    

Ultimate diagnoses so far: Nonischemic Cardiomyopathy, possibly viral-myocarditis with tests pending.

There is reason to doubt that's the cause of her death, but it could be what brought her to the ER mildly hypotensive with rapid beat. Ive read that RBBB can be very common and transient. We are being told by several people that you do not do an angiography, ever, when your only indications are Right bundle branch block and elevated troponin. That RBBB almost always rules out CAD and points to CM and PE. No D-Dimer test was done.

We're also being told never go invasive on on young, thin, healthy, somewhat dehydrated women with high liver numbers who is presenting with a possible allergic reaction to Zithromax, with prior allergy issues. We are being told that Right bundle block suggests Pulmonary embolism or right heart issues, like myocarditis or cardiomyopathy for various and many possible causes including immune reactions and that is why they are treated noninvasively until you better understand the cause, that right block and left block on EKG with high troponin indicate two totally separate courses of action and invasive angiography/dye on a hypotensive is the wrong course for right block/troponin.

All opinions, of any kind, much appreciated!

Thank you!    
14 Responses
967168 tn?1477588089
I can't answer your question; I'm only a patient, but I wanted to say I'm sorry for your loss.

I would seek the help of an attorney and let their medical team look over this and let you know if there was an injustice, or at least report this to the medical dept of your state.

I'm sure that's the last thing on your mind, but I came very close to not making it during my ablation; once they brought me back, 1 other time on the count of 0; my heart restarted, and then a 3rd time I converted back myself.  

I would want my family to find a way to make sure whoever was at fault knew they were at fault and somehow make restitution for their suffering.

That's just my opinion, and it was extremely difficult for me to make the decision to seek legal help; maybe it will help you get the answers if no one here can help you.
712042 tn?1254572809
I can't answer these very detailed questions, and I wouldn't. But I can tell you that you can start by asking for a medical review by the hospital/ER that cared for the patient. I don't know where you are but US states and Canada provinces have mechanisms in place to do peer and quality improvement reviews, to the point of also involving their legal counsel, medical licensure boards and other required reporting of an adverse outcome. No one wants an outcome like this to happen. I'm sure you and your family will be anxious to hear the results of any viral implication and any other post mortem tests performed. Medicine is an art and relies heavily on tests to give the best results in this age of advanced technology. But some things just do not show up, even on the gold standard cardiac cath. My own experience as a healthy, athletic 60 yo with 3 clear heart caths and an arrest, which had a successful resusitation after v-fib to straight line, confirms this. My sincere condolences to you and your family. I hope you find this helpful in your search for answers. Joan.
187666 tn?1331176945
I also found this very interesting to read. But I have no authority to offer answers. But it was fascinating and wish I had the credentials to unravel this puzzle. Perhaps Joan's suggestion will bring the answers you need. If you think of it, perhaps you could post again and let us know what you've learned.
88793 tn?1290230777
I'm very sorry for your loss.  The first few sentences before the Troponin elevated, sound like you're describing my stress test - ECG.  I'm here to let you know my situation only.  I can't understand all your terminologies at your post but it matches many of mine.

RBBB is told nothing serious.  When it comes with elevated ST in V1 & V3, it can be Brugada Syndrome.  While I was at rest after the exercise, my heart keeps stopping and bring the rhythm back by pacemaker pacing.  My original diagnoses was wpw when I was 15 years old.  I scratched my head, how come now he said Brugada variant?   With wpw also can be ST elevated, which is normal.  

Now I also got severe hypokinesis.  Has chest pain but never had Troponin elevated.  Angiogram shows I didn't have any blockage.  All my arteries are opened widely.  What I think it could be....  Only think (no prove or documentation).  Every time when V-Fib or V-tach attacks,  the heart muscle could be short of oxygen supplied so it dies potionly.... It may be depend on how often V-Fib or V-Tach attacks and how long it remains in the straight line.  This is just my guest.  Otherwise how my SEVERE hypokinesis come from?

Avatar universal
Thank you all for your comments and thoughts! What a nice place.

We are asking for a review. From there, we will decide what to do. Apparantly, a week before she told her doc her chest was a little heavy and flu season...was given Zithromax (doc knew she was allergic to erythromycin) and albuterol. She got sick that night, stomach. The Zithro thing had us looking for immune interference allowing a viral myocarditis clearance to attack or something like hyperreactive myocarditis too. Appears a bit in literature. No EOS in labs though. The docs would still have us believe it's an acute viral myocarditis, but heart failure within hours of presentation (in cath lab) w/out the usual harsh last stage symptoms and labs hour earlier don't add up. Neither does the ECG seem to add up with that terrible ECHO after CPR in CATH Lab.

She appeared stable, albeit rapid and hypotensive. no pain, "irritated by nausea". After the fact, with RBBB (right block on ECG) we're suprised no D-Dimer was done to chck for PE, especially after doc visit week before and that consult right before CATH. What also bothered us was no doctor even raised the possibility of dye reaction either, even though arrest occured minutes after dye injection in aorta. They pointed to the ECHO done 30 minutes AFTER Cath and CPR efforts, which showed right side moderate dilation and 10% Ejection Fracion...suggesting that's how she walkd in hours before. Maybe, maybe mot. Can you trust the ECHO was the same heart picture before Cath and after 30 minutes of CPR and respiratory arrest? Esp when X-rays are different before and after? (All we have is the Xray and ECG re heart before CATH). I doubt that Echo is accurate in two hour retrospect. Well, we keep looking...

Good luck with that hypokenisis. That's a tough one to figure out too. I wonder if your blood trends to acid or base..or...anything fairly chronicly elevatedor lowered in your labs but not noticed bc it's within high or low end of normal? You would think that condition would take TIME exposure internally or out, imbalance (or genetics) to get that result. Always check your home, enviroment, consumption habits and the things we all often overlook...and good luck to you!

Avatar universal
Along with all others I send my sympathies to you and your family.

Having read through your posting, the very first thing that came to mind was she died from a form of Cardiomyopathy. Everything you are describing sounds like that to me. Echoes are far and away more accurate than the EKG and X-ray, absolutely no doubt and is considered to be the ultimate determining factor in diagnosing Cardiomyopathies. A high WBC would suggest a Myocarditis right along with the echo findings. The fact that she was complaining about symptoms a week prior to this happening suggests a more chonic problem going on that was just starting to show itself whether that was a Cardiomyopathy or a Myocarditis. One of the primary signs of a cardiomyopathy is hypokinesis. To have an adverse reaction to the dye happens; it even happened to my own father and he almost died as a result. They always ask if you are allergic to dyes before giving them; most people haven't a clue whether they are or not because most people do not go through the types of testings that use the dye in the first place. As far as calling for a hospital review; I think that was a huge mistake. Hospitals will change the records and anything else that can lead to them losing a law suit. You should have gone to a lawyer and have him pull the records because he would have been able to do that without the hospital having time to review the records and pull anything they didn't want you to see. And believe me, they will will do just that.
88793 tn?1290230777
Wow, learn a lot from Grendslori.  Thanks.

I remember long time ago, my dad wants to sue the doctor in a general hospital (government hospital) because of my brother died.  He called the lawyer once my brother passed away.  The lawyer acted immediately.  He was my father closed friend and also our business consultant.  The hospital replied "Patient file lost in transit".

Shipjack said at the post above : WBC counts within normal range.

Avatar universal
Pika, that sounds about right. Where your father's friend made his mistake was to not notify the hospital and then he should have sent a paralegal to the records department so there would be no time to review the records or to lose them in transit. They would have had to turn them over as is.
88793 tn?1290230777
The case didn't go ahead.  We thought the lawyer can't do anything, what can a normal people like us can do?  Now, I'll let my children know it is a paralegal team can act for us to retrieve a dead patient record at the hospital.  Can a paralegal team retrieve our records in a private consultant doctor's (MD) office?
Avatar universal
The paralegal would be working under the direction of a lawyer only. You would still have to sign the normal consent forms with your lawyer.;
Avatar universal
One more thing I forgot to say: the medical records at your hospital, doctor's office etc and LEGALLY yours. You may have copies but the hospital or doctor's office can charge you for the paper used to print your records up for you. You can go get a copy of your records any time you want.
159619 tn?1538184537
Wow, a terrible story and I am sorry about your loss. I'm a bit confused, are you looking for grounds to a law suit? Having read you posts, I don't really see anything that looks like negligence on the part of the medical staff, but I'm not a doctor or lawyer.

A couple of things, viral cardiomyopathy makes sense based everything in your post and what I've read elsewhere. Also, an x ray is not accurate when looking for chamber size of the heart, but will show a dilated heart as a whole. An EKG is also a very poor way to determine chamber size of the heart. An echo is the only way to get a chamber measurement and that's not always accurate either. The only 100% accurate way to measure chamber size is with a volume test and I doubt that this was a priority at the time given everything else going on. I have not been able to find anything that associates CPR or angiography with a change in the modeling of the chambers of the heart.

Also, a RBBB is almost never symptomatic and usually of no prognostic value and I doubt if it was involved in the outcome in any way. RBBB can even be considered a normal variant, as in my case. It's the LBBB that can cause rhythm issues.

I have also looked at the warnings and interactions of Zithromax and there is no listed effect on one's immune system so I would not think it played a role either, even if she were allergic the symptoms would have been different.

This is a very difficult situation and you need to speak with someone much more learned than most of us on this forum.

Good luck,

690060 tn?1247845341
That's such a tragic story, shipjack.

A central point involves why the cath was performed.

There existed anterior (V3) STEMI, elevated cardiac enzymes, and nausea in a female. (Pika was highlighting the STEMI, too.)

This is just my guess, but I'd suggest you look at HERO-2. "in the setting of an anterior STEMI, the presence of an RBBB, whatever its onset, is associated with a higher risk of death". I haven't read the whole article, but an OR >~3 seems alarming.

IOW, they likely did not consider the RBBB alone, but did attach a lot of weight to it in the setting of possible MI.

(The full text of the underlying study is also online.)

But, how to distinguish between acute myocarditis and MI? The usual way since long ago is apparently a cath. E.g.:
"Myocarditis simulating acute transmural myocardial infarction"

I don't know if that's changed, although presumably they'd be looking to stent rather than use fibrinolytic methods these days.

By 'EOS' I'd assume you're referring to eosinophilic myocarditis, but without the test numbers indicating that, maybe you'd want to look at lymphocytic myocarditis instead. Still, can the cell mediated inflammation be localized to the myocardium and not show up as elevations in the serum test? I don't know.

Is there any Hx or Fx of auto immunity of any kind?

Can acute lymphocytic myocarditis account for changes in heart size that are that rapid? I don't know, but as you know inflammation can be quick.

AFAIK the cause of SCD from viral myocarditis would normally be due to a re-entrant VTach / VFib. Being re-entrant means slow conduction. So then you'd also want to look at whether purulent myocarditis causes severe hypokinesis.

Why was an antibiotic originally prescribed anyway? As prophylaxis against 2ndary bacterial infection? Does this relate to possible sepsis/hypotension?

Anyway, good wishes to you and I hope you find some peace of mind through your investigations.

P.S. You can find stats on the possibility of correctly identifying (infectious or immune) myocarditis post-mortem. The chances are not 100%, IIRC. However, the chances when a patient first shows up are much less - it's difficult to do.

P.P.S FWIW, the d-dimer test would probably be affected by the mural thrombus.

690060 tn?1247845341
2 quick additional notes:

for PE they'd normally expect sharp chest/lung pain

also, there is no mention of the thromboprophylactic used before the PCI, such as bivalirudin or a LMWHeparin - so that's another drug to consider, especially since you associated a negative change at that time

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