A True Trainwreck:

It’s been an exceptionally long time since I’ve shared one of my “vignettes” from the emergency department. Over the summer, I have had many exciting moments in the ED, but this is by far the most memorable.

One particularly busy night, we get a call from EMS that they’re bringing us a pt in his mid 50s with a probable inferior STEMI. His vitals were normal with the possible exception of borderline hypertension. ASA was given, but no NTG was given due to possible posterior involvement.

We start getting ready for the incoming patient, expecting a quick turnover to cath lab. I don’t think anyone anticipated what happened over the next several hours.

As soon as the pt rolls into the ED, I could tell something wasn’t right. He was pale, extremely diaphoretic, and less responsive than EMS made him sound. This wasn’t any fault of their own, apparently he had just started this as the ambulance pulled up to the hospital. His vitals somehow were still normal, but he still looked sick as can be. Our EKG also confirmed an inferior MI, with significant ST depression in V1/V2, which is suspicious for posterior involvement, and he also had some possible signs of RV involvement. So, we get the ball rolling. The cath lab was activated, the cardiologist was called, and paperwork was getting its due diligence. From what we could get from the patient he had a hx of well controlled HTN, but otherwise no significant medical hx except for a remote appendectomy. He did smoke, however.

So, everything seems to be progressing as expected. The cardiologist is on their way, the patient’s vitals are stable, and he was looking slightly improved. We didn’t have labs back, but at that point his CXR was normal as well. The physician needed to go check on another patient on the other side of the ER, so I stayed in the room with the nurses just to keep an eye on the patient.

Well…for all of you new followers out there, I have the privilege of being the owner of my very own black cloud which always chooses the most inopportune moments to make its appearance. About two minutes after the physician left the room, the patient suddenly becomes obtunded, slumps over in his bed, and then of course the monitor shows him going into a pretty impressive v-fib.

All hell breaks loose. We’re already busy and short staffed, and it always makes these situations harder to control. A code was called, compressions were started, and the doctor comes running in the room. The patient gets shocked with no ROSC and proceeds to get intubated. He get’s epi, get’s another shock, and then has a pulse just as the cardiologist walks into the room. We all take one giant sigh of relief, and start trying to stabilize him for transport to the cath lab. His BP dropped significantly, so he was placed on levophed as well. Right after the levophed starts to hang, he arrests again. At that point, a vicious cycle beings where we get a pulse and then lose it a minute later. He gets an amiodarone bolus/drip, dopamine, and a whole lot of epi. Nothing seems to be working, and 30 minutes into this the cardiologist and ER doc begin discussing calling it. Just as it’s about to be called, we get a pulse-stronger than any of the other times. We wait a minute or so to get everything settled, and then he is whisked off to the cath lab.

Unfortunately, following the general theme of the night, the fun didn’t end there.

About 20-30 minutes later, we get an update from the cardiologist. His cath came back surprisingly not as severe as expected, with diffuse moderate vessel disease but no obvious blockage that would cause his MI. He was going to be scheduled for a CABG in the AM, but his case was still perplexing. It was suggested that maybe the clot dissolved with all the CPR he received, but the cardiologist also thought maybe a pulmonary embolism might be the cause so he sent the pt to get a CTA of his chest.   

About 5 minutes later, the scout image (basically just a CXR) of his CT is available on the computer to view, so I open it just so I won’t forget to take a look at it later. I jumped out my seat as soon as I opened it BECAUSE OF THE MASSIVE TENSION PNEUMOTHORAX HE HAD. I immediately show the ER doc, and we start running to radiology (which isn’t that far away at all), nearly crashing into the cath lab nurse who was running to the ER to grab the doctor. We get into the CT suite and, in a style reminiscent of a Grey’s Anatomy episode, the ER doctor performs a needle decompression (However, unlike Grey’s anatomy he still manages to find the time to wipe down the area with an alcohol prep). After that, instead of dragging him all the way to the ICU, he got transported to the ER for a quick chest tube and then was sent on his way to the ICU. His tension pneumo was the result of several rib fractures secondary to how much CPR he went through. 

Amazingly, and against all odds, several weeks later the patient walked out the hospital-alive. He was extremely lucky. Not many people survive cardiac arrests, even in the hospital, and especially with all of the other complicating factors. Not only that, but he walked out without a single neurological deficit.

In Emergency Medicine, we don’t get to celebrate many victories. Even though we provide the best care possible many of our most critical patients are too sick or too injured. Even for those we save, many suffer from complications and debilitating issues for the rest of their lives. To have that one patient, maybe one of the sickest I have seen in a long time, walk out of the hospital as if nothing happened is a victory that I’ll remember probably for the rest of my life. It’s the victories, no matter how small, that remind each of us how rewarding our profession is. 

ECG: quick and dirty

I’ve had countless sessions and lectures on ECGs. I don’t know how many websites I have bookmarked, or how many times my eyes glazed over reading Dubin. I’m also terrible at cardiology. I was on my way to accepting my fate of being horrible at ECGs forever, until I had a life changing session on ECGs taught by a great ER doc. I want to post it here because it was probably the most useful thing I learned in med school, and it will stick with me for the rest of my career. 


1. One ECG is never enough. Always get old ones for comparison. If none available, do another one. Because. One ECG is never enough. 

2. RATE. Look at the number on top of the printed ECG. It’s stupid not to use that number. Yes, you should know the rule, 300-150-100-75-60-50. People say you shouldn’t trust the machine because… well, it’s a machine, and it can make mistakes. This is true. I don’t like to look at their “diagnosis” until I have gone through it myself. But the rate is just a number. Plus you should be able to eyeball it and be able to tell if it’s tachy, brady, etc. If the machine is telling you it’s 200 and if it looks tachy, then it’s probably the right number. 
3. RHYTHM. Is there a p-wave for every QRS and a QRS for every p-wave? Is the p-wave upright in lead II and down in aVR? Good. Done. BOOM. It’s sinus rhythm. ***if you cannot clearly see the p-waves then you cannot call sinus. move on.
4. AXIS. Again, look at the number at the top of the page. If it’s between 0 and +90, then it’s normal axis. If the number isn’t provided, or if your preceptor doesn’t believe in the convenience of machines/technology, look at the QRS complex of lead I and lead II. 
  • up in lead I, up in lead II: normal axis
  • up in lead I, down in lead II: left axis deviation (most common causes are left anterior hemi block and left ventricular hypertrophy)
  • down in lead I, up in lead II: right axis deviation (most common causes are right ventricular hypertrophy…PE)
5. did someone say HYPERTROPHY?
  • look at V1
  • is the R wave tall? (greater than 7mm?) right ventricular hypertrophy.
  • is the S wave tall? (greater than 11mm?) left ventricular hypertrophy.
  6. P-waves
  • look at lead II
  • is it wide? left atrial enlargement.
  • is it tall? right atrial enlargement.
7. PR interval
  • should be between 0.12 sec and 0.2 sec (3-5 small boxes). I used to always get this interval and QRS complex (less than 0.12 sec) mixed up. Think: atria depolarizing + shit getting to ventricles is gonna take longer than ventricles depolarizing. [2 things happening] versus [1 thing happening]. [0.12 sec-0.2 sec] versus [<0.12 sec].
  • long PR interval means there’s some sort of block at the AV node. 
  • 1st deg block. PR interval is long. everything else is normal. cool. 
  • 2nd deg block
  • type I: PR interval progressively gets long. eventually a dropped QRS.
  • type II: PR interval is constant, but randomly dropped QRS. 
3rd deg block “complete block”
  • there is no association between P waves and QRS. they run separately. **QRS does NOT have to be wide. Just look for P wave/QRS complex disassociation. I sometimes get this and 2nd deg type II mixed up. The only difference I try to remember is that PR interval is constant in 2nd deg type II, but is variable in 3rd deg. 
8. QRS complex
  • narrow or wide? 
  • narrow: good. signal coming from somewhere above ventricles. 
  • wide: think BBB (bundle branch block)
  • if the last deflection of QRS is DOWN, then it’s a left BBB
  • if the last deflection of QRS is UP, then it’s a right BBB. super easy. no more of this bunny ears crap. 
9. ST segment
  • always look from J point, and compare with the isoelectric line of T-P segment (NOT PR interval). 
  • elevated/depressed… STEMI… duh. indicates ACUTE ischemic changes. 
  • look for reciprocal changes of the heart. if ST elevation in lateral leads, could see ST depression in the septal leads. PAILS:
  • posterior up, anterior down
  • anterior up, inferior down
  • inferior up, lateral down
  • lateral up, septal down.  
LBBB can look like STEMI. How to tell?
  • disconcordant changes is normal. (QRS and STEMI on opposite sides of the isoelectric line.)
  • concordant changes is abnormal. 
  • massive discordance is abnormal. (STEMI is greater than 5mm)
  • this isn’t that important. Moving on. 
Inferior STEMI. Could right ventricle be involved? 
  • order a 15 lead
  • is STE in lead III > lead II? likely RV involvement
10. T waves
  • is it inverted? indicates recent ischemic changes. 
11. Q waves
  • is it significant? indicates old ischemic changes. will likely be present if followed rule number 1 of reading ECGs. (1 ECG is never enough= look at old ECGs). 
I literally go through this list of 11 points in my head when I’m reading an ECG, regardless of whether or not I have an atrial flutter jumping at my face or if I see a massive anterolateral STEMI. Obviously I needed background knowledge on ECGs and the physiology of the heart before constructing this list, but this basic checklist has been very, very useful to me so far. It might look lengthy, but it doesn’t take a lot of time at all- a patient is not likely going to have all these issues with their heart.    Anyway. I still don’t love ECGs, but it feels pretty wonderful to be able to be able to evaluate it in a systematic manner, and get the theory behind interpreting the scribbles of an ECG reading. I don’t get these moments as much as I would like to, but it’s that crosspoint where my classroom learning actually meets real-life applications that gives me happy brain-gasms for days. I love knowing things and more importantly, knowing why.

anonymous asked:

Coming from curiosity of a scribe in the ED, what exactly is Troponin? I know the difference and know it comes into play with nstemi/stemi. But I've seen people with elevated troponin walk out of the ED same day and diagnosed with "stress". Ive also seen elevated troponin in a teenager, oddly, and they were rushed to a cath lab. Basically, what is troponin?

Troponin is an enzyme leaked from damaged heart muscle. You can see elevations with heart attacks, pericarditis, endocarditis, and heart muscle strain (like when it’s working too hard in acute heart failure, A fib, sepsis, or severe hypertension). Generally a heart attack will cause a much larger increase in the levels than “strain” would. 

External image

Strain or stress is not just diagnosed by troponin. It depends on what the EKG, and most importantly, the patient, looks like. Some folks with bad CHF will routinely have a slightly elevated troponin level. Strain vs. MI a complicated decision that’s not always based on cut and dry rules.

Also - troponin doesn’t really make a difference in designating STEMI vs. NSTEMI (ST Elevation vs. non). Those designations are based on what the EKG looks like. 

Watch on

Family guy Stewie hates it here

Very interesting STEMI. Textbook signs and symptoms when we got on scene. Enroute to the ER, he coded. Shocked him, he came back talking, then 30 seconds later coded in vfib again. Shocked him again, came back, talking and responsive. Coded AGAIN, vfib, shocked him again and he came back out of it and stabilized. At the scene he showed mild elevation. Gave nitro and aspirin. Shortly after he coded. Medic pushed Amio that seemed to help stabilize him out after coming back from the third shock.

I have jagged edges
and I am made of thorns
however there is no rose
attached to my stem
I’m not sure that I belong
in someone else’s arms
but I’m also not sure
I belong in my own
I guess I’m still searching for home
since I wasted so much time
believing you were a light house
when you were just luring me
away from where I need to be
most days I wish to be alone
but then other days 
mostly when I’ve had too much to drink
I think of you
and then I change my mind