Wide Complex Tachycardia and Cyanosis

This case was sent by a former HCMC resident:

A 20-something non-English speaking woman with a history of some sort of congenital heart defect collapsed at home and EMS found her with a regular wide complex tachycardia around 200 bpm. They attempted cardioversion with adenosine, unsuccessfully (dose was uncertain, thought to be 12 mg, but this would be an unusual initial dose).

She was cyanotic and minimally responsive on arrival here, and had a healed sternotomy scar.  There were no records immediately available.

Her blood pressure was normal throughout the case.  O2 sats were 70s and 80s on high flow O2, but there was no evidence of pulmonary edema.  They did notice "clubbing" of the fingers.

A relative was able to state in broken English "single ventricle."

Here is the initial 12-lead ECG:
There is a regular, wide complex tachycardia at a rate of 160, with no P-waves. 
There is a monomorphic Right Bundle Branch block pattern with QRS duration of between 140 - 160 ms (is it difficult to ascertain the exact beginning and end of the QRS)
Is it Ventricular Tachycardia (VT) or SVT with aberrancy?
What else can be said about it?
What should be done?

Full interpretation is at the far bottom of the post


If the patient is unstable, just cardiovert with electricity.  Her altered mental status may be due to hypoperfusion (shock), in spite of the normal blood pressure (non-invasive blood pressures are unreliable in sick patients).  Thus she must be considered unstable, so use electricity 

One might call this patient unstable because of the low saturations, but a patient with a known single ventricle is likely to have cyanotic heart disease and to have baseline O2 saturations that are very low, even on high flow O2.  This is especially true if there is no evidence of pulmonary edema on chest X-ray or bedside ultrasound.  Clubbing is further supportive evidence.
Thus, it is very likely that the patient has uncorrectable hypoxemia due to shunt physiology.

If the patient had been stable (conscious), then there would have been a few minutes to think:

First, if one can easily find old ECGs that are in sinus rhythm, then one can compare the QRS morphology at baseline with this one in tachycardia.  If identical, then this is supraventricular (which includes sinus tachycardia).  To diagnose sinus tachycardia, one can use Lewis leads in order to uncover hidden P-waves.  This takes about 30 seconds.  Here are the instructions for recording Lewis leads.  It is done with the monitor, not the 12-lead.

Second, in most young people without structural cardiac disease, SVT is more likely.  However, this patient does have structural heart disease, so VT is not at all unlikely.

Third, assuming it is truly NOT sinus tachycardia, either adenosine at a higher dose or electrical cardioversion works well.  Even if it is sinus tach, neither of these therapies is terribly dangerous, but they will not benefit the patient.

Fourth, is there any evidence from the QRS that this is SVT vs. VT?  There is a "northwest" axis (between -90 and 180, with a large monophasic R-wave in aVR).  This implies origination at the apex (the ventricle, where VT originates) with propagation towards the base of the heart ("base" meaning upper right). On the other hand, the first part of the QRS (initial depolarization) is very rapid, even in that upright R-wave in aVR.  Look at lead V5: that first part is comprised by the onset of the R-wave to nadir of the S-wave, and it is less than 60 ms.  Thus, SVT with aberrancy is not at all unlikely.

Thus, in a stable patient: As it is easiest, I would try a larger dose of adenosine.

Case continued:

"We intubated the patient, then consulted cardiology and decided to do an electrical cardioversion at 200J biphasic.  This was successful."

"I found records which were limited but suggested congenital heart deformity, and that her baseline O2 sats were in the 70-80% range."

Here is the post cardioversion ECG:
What does this post cardioversion ECG tell you about the initial rhythm?

There is clearly sinus rhythm, with exactly the same QRST morphology as the first.
This proves that the original was indeed SVT with aberrancy.

Airway, Breathing, Circulation (ABC)
We are always taught to use this sequence, but we often get it confused.  Sometimes the issue with the airway and breathing is really a circulation problem (shock with altered mental status).  I would cardiovert first, which will usually solve the problem.   Intubate if it does not.  Also, when the patient is obtunded (stuporous), it is both dangerous and unnecessary to sedate before cardioverting. Our research at HCMC shows these critically ill patients do not remember such events.

A Primer on Wide Complex Tachycardia

First, use electricity on unstable patients.

What is instability?  Severe shock, cardiac ischemia, or pulmonary edema.

If stable, you can take a bit of time to think.

Differential Diagnosis of Wide Complex Tachycardia

When assessing for the rhythm in wide complex regular tachycardia, these are the assessments I make, though no method is foolproof:

--Sinus with aberrancy -- Aberrancy can be due to toxins (wide complex from the many drugs which have sodium channel blocking effects and prolong the QRS) or to hyperkalemia.
--SVT with aberrancy.  This can be either 1) AVNRT with abnormal conduction to the ventricles, or 2) antidromic AVRT (AV reciprocating tachycardia) with the impulse going down an accessory pathway and up through the AV node)
--Ventricular Tachycardia (VT)

Assess pretest probability:
--Majority of wide complex tachycardia is VT
--If h/o MI, cardiomyopathy, low Ejection Fraction, VT more likely still
Assess the ECG:
--P-waves in front of QRS? --Sinus
--Irregularly irregular? Atrial fib 
                    (VT is regular, except for polymorphic VT which must have a polymorphic QRS)
--Regular? --then: sinus / atrial tach / flutter / PSVT / VT)
--Rate gradually changes or always the same?
              Gradual: sinus or other automatic rhythm (some atrial tachycardias, junctional tach)
              Unchangingreentrant rhythm such as: flutter vs. PSVT (incl AVRT) vs. VT

Wide, monomorphic QRS, and regular without P-waves (or retrograde P-waves)
1. SVT with aberrancy 
           (including antidromic AVRT using an accessory pathway)
2. VT (though it may have P-waves that are dissociated, or retrograde P-waves)

VT vs. SVT with aberrancy

5 Algorithms to differentiate SVT with aberrancy from VT - in my opinion, only Sasaki's is usable in the ED:

1. Brugada
2. Vereckei 1
3. Vereckei 2 (uses aVR only)
4. Sasaki (see below) (Sasaki K.  Circulation 2009; 120:S671) had 86% sensitivity and 97% specificity among 107 cases of wide complex tachycardia.  It has not been validated; this is important: Brugada's rule fared much better in the initial study than in subsequent validation studies.
5. New algorithm (Jastrzebski et al.): more complex but more accurate (full text link):
The ventricular tachycardia score: a novel approach to electrocardiographic diagnosis of ventricular tachycardia. In this very complex scoring system, derived in 512 proven cases of VT and 276 proven cases of SVT, the specificity for a score greater than or equal to 3 was 98%, but with a sensitivity of only 66%.  This is clearly not something that can be easily done in the ED.


Below I have listed what I consider usable features of the algorithms.

If you're not sure, but you are pretty sure it is not sinus tach
Sedate/Cardiovert (or Adenosine)
Adenosine if you suspect SVT:
---Older, with known absence of structural heart disease
---Young age, unless known heart disease
---QRS duration less than 140 ms
---No obvious signs of VT
       concordance, fusion beats, AV dissociation
---Unequivocal rapid depolarization of the initial part of the QRS (e.g., normal LBBB or RBBB)
--safe in VT
--safe in WPW, if regular rhythm
--Unsafe in WPW with atrial fib (irregular, RR intervals less than 250 ms, polymorphic QRS)
--converts reciprocating tachycardia, whether orthodromic or antidromic
    --these depend on the AV node for re-entrance 
--converts one kind of fascicular VT (RV outflow tract VT) 

1) Look for hidden p-waves before each QRS.  Don't miss sinus rhythm.  Use Lewis Leads.
2) QRS duration: VT usually (but not always) has a QRS duration of greater than 140 ms.  A prominent exception is fascicular VT.  The wider the QRS, the more likely it is to be VT.  
3) Is there RBBB or LBBB morphology and is the initial part of that BBB narrow?  Then it is very likely to be SVT.  
4) Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT.   
5) Do a quick look for concordance (in precordial leads, all QRS's in the same direction -- this is not the same as concordance of ST segments in LBBB).  Concordance means there is no RS.  

6) Finally, because it is easy to apply, I like Sasaki's rule 

Sasaki's rule

Step 1: Initial R in aVR?  

This means is there a large single (upright) R-wave (not a small r-wave) in aVR.  This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.
--If yes, then rhythm is VT. If no, step 2.  

Not here.  See ECG with line below.  Although at first glance there appears to be a monophasic initial R in aVR, the line shows that there is actually a 30 ms delay.
Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?  See image below.  
--If yes, then rhythm is VT. If no, step 3.  Not here.

Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)
--If yes, then it is VT.   If no, then it is SVT.  "No" here, therefore it is SVT

Although there appears to be an initial R in aVR, there is actually about 30 ms of hesitation before the R-wave initiates.  I have drawn a line at the beginning of the QRS.
Thus, there is also only a 30 ms r- or q- wave at the beginning of the QRS.

This Sasaki rule was quite accurate in derivation, but never validated, at least not to my knowledge.

My interpretation is that the initial deflections are of very short duration and therefore unlikely to be VT.  But I only saw it after knowing the outcome (too biased!)

So I showed the ECG blindly to Ken Grauer (one of the masters, here is his site):

"Bizarre morphology, which of course makes one consider VT — but:
1) check leads (all positive in aVR); and
2) Could very well be supraventricular with some severe form of underlying heart disease (cardiomyopathy; congenital heart disease if young)"

"So I'd really want to know the clinical situation....Several leads looked like they might be supraventricular (ie, very slender narrow initial r-wave in predominantly negative lead I and aVL — rather than being all negative) — slender initial r-wave in V4 with very steep downslope — and the Q in lead III looked like it may be pathologic rather than an all neg axis Q as VT would have."

LVH with secondary ST depression??

This was sent by Michael Macias (Twitter: @EMedCurious), a 4th year EM resident at Northwestern in Chicago.


An elderly man with end stage renal disease and coronary disease presented with chest pain.

Here is his ECG:
See the computer interpretation above.
What do you think?

Dr. Macias' interpretation is here:

Significant elevation in aVR with diffuse ST depression. Hemoglobin was 7.0 g/dL. I thought this was likely triple vessel disease with subendocardial ischemia, but we activated the cath lab given impressive ECG and his history.

Smith interpretation:

The computer reads LVH with repolarization abnormality. There is high voltage, and you expect some discordant ST depression, but this ST depression, although always discordant, is way out of proportion to the QRS voltage. Moreover, the ST depression is NOT maximal in V5 and V6, as it should be with LVH repolarization abnormalities.

So this is ischemic ST depression.

Whether it is diffuse subendocardial ischemia or posterior STEMI is more problematic.

As the STE is most profound in V3 and V4, NOT V5 and V6, posterior STEMI is more likely. However, the STE in aVR (which is reciprocal STE, reciprocal to the ST depression vector towards the apex), is more typically seen in diffuse subendocardial ischemia. ST depression due to subendocardial ischemia is most commonly caused by demand ischemia. One cause of demand ischemia is severe anemia, but a Hgb of 7.0 does not qualify, especially without any tachycardia.

So this must be assumed to be due to ACS.

In fact, the ST depression in V5 and V6 is not all due to ischemia: it is a combination of LVH repolarization and ischemia; the ischemia component is only one portion and so there is less ischemic STD here than one might at first think. This means that the ischemic ST depression is significantly more profound in V3 and V4.

So this is most likely a posterior STEMI pattern, superimposed on LVH. Activating the cath lab is indicated!


100% acute circumflex occlusion, opened.

Learning Points:

1. Again, the computer algorithm cannot be trusted.
2. Posterior STEMI has more ST Depression in V3 and V4. Subendocardial ischemia is maximal in V5 and V6.
3. Know the expected amount of repolarization abnormality in the presence of LVH.  I don't have a calculated ratio.   Below are two examples of LVH with repolarization abnormalities.  These are both baseline ECGs without any active ischemia.  Notice the proportional amount of ST depression, and that it is maximal in V5 and V6.

Why does this young male with chest pain have a tall R in V1, and lateral Q waves?

This is another post written by Brooks Walsh, with some editing by Smith.

Ken Grauer, who is truly an ECG guru, also had a hand in the analysis of this ECG.  Visit his extremely informative site here: ECG Interpretation


A teenage male was brought to the ED with 1 week of a left-sided pleuritic chest pain and cough.  He had a modest hypoxia, and a temperature of 99.9.   He had no documented cardiac disorders.

An ECG was obtained:
There is borderline sinus tachycardia. 
The R waves in V1 are abnormally tall, with R/S ratio greater than 1. 
There are also deep (though narrow) Q waves in I, aVL, V5, and V6.

Why does he have these tall R-waves in right precordial leads and Q-waves in lateral leads?  Could he have a previous lateral and posterior myocardial infarction (now classified as inferobasal)?

Several conditions can cause the increased R/S in V1:
  • WPW? But no delta waves to suggest WPW.
  • Posterior MI? But young age, and no supportive ST/T changes in V1-V3.
  • (I)RBBB? But no no rSR’ pattern in V1, no deep lateral S waves
  • RVH? But no S waves in I, aVL, or V6, and no right axis deviation or right atrial abnormality
  • Hypertrophic Cardiomyopathy (HOCM) with Septal Hypertrophy - voltage is inadequate
  • Lead Misplacement - checked and ok.

On the other hand, the pattern of a tall R in V1, and deep Q waves in I, aVL, and V5, V6 is classic for Duchenne’s muscular dystrophy (DMD)

In fact, records revealed that he is known to have Duchenne muscular dystrophy

The CXR suggested aspiration pneumonitis (± pneumonia), consistent with multiple prior hospitalizations, and explaining the patient's chest pain.

These ECG features were found in the majority of patients with DMD in the seminal 1968 paper by Slucka:
From Slucka. Type “a” was most common, seen in 64/106 DMD patients.

More recent studies (example, example, example, and example) have shown more variability in the presence of either tall R waves or deep lateral Q waves in DMD patients. Nonetheless, these “distinctive” features are considered to be classic.

The tall R waves in V1 and the deep lateral Q waves are thought to reflect myocardial fibrosis in the posterobasal and lateral myocardium. Although these changes represent disease progression in the myocardium, they have not been shown to be age-related, perhaps because ECG changes occur quite early in life, proceeding clinical or echocardiographic signs. Although DMD patients do develop a progressive and inevitable left ventricular cardiomyopathy, the classic ECG changes do not seem to be correlated with echo findings (such as reduced EF or increased LV size), or with the presence of dilated cardiomyopathy.

Only the ECG Diagnoses Acute Coronary Occlusion. Do not be Fooled by a Negative High Sensitivity Troponin.

This case was sent by Peter Hammarlund, 2nd year Internal Medicine/Cardiology resident (and self-proclaimed ECG nerd) at Helsingborg Hospital, Sweden.  

Peter frequently sends me great cases like this, but I never post them because the Swedish standard, explained below, is very difficult to interpret.

This time I could not resist.

Especially interesting is the troponin data and the manipulated images seen below.


Hi Steve,

I was involved in this highly interesting case just the other week.

A previously healthy young man (in his 20s), who smokes two cigarettes a day and has a family history of MI (his father had his first MI in his early 50s), was brought to our ED by ambulance with severe central chest pain without radiation for one hour. The pain was not relieved by Nitroglycerine and only slightly relieved by morphine. 

Smith comment: do NOT use morphine until you are either: 
1) committed to the cath lab (or other definitive diagnostic modality, such as CT for dissection or PE)
2) CERTAIN that the pain is not due to serious pathology. 

Case continued

He was tachycardic, but his vitals were otherwise initially normal. 

The initial high sensitivity troponin T was 5 ng/L.
(99% reference is 14 ng/L, or less than 15 ng/L; Level of detection is 5 ng/L).

I was working in our CCU when the cardiology consultant (who was sitting right next to me) got a phone call from the ED doctor taking care of the patient. While he presented the case to the consultant we looked at the prehospital ECG (attached as EKG1, time 7.53 am) and the ED ECG (attached as EKG2, time 8.10 am). 

At the moment (time 10.45 am) the patient was in the radiology department performing a CT aorta, but right after the CT he developed shortness of breath and only had a saturation of 88% with 15 L/min of O2.

I was immediately very worried about the patient when I saw the ECGs.

What do you say? My answer is below.

Note on technique: These are recorded at the Swedish standard of 50 mm/second.  So all intervals appear twice as wide as you are accustomed to!  Furthermore, there is only one average complex per lead.
What do you think?

Here is my answer, after a quick glance:

Hyperacute T-waves are developing over 17 minutes in V2-V4.  LAD occlusion or at least dynamic thrombus.

As an afterthought just this minute before posting, I compressed the ECGs to 25mm/sec.  The difference becomes much more obvious to me:
Peter's Detailed Comment on the ECG interpretation:

The ECG at t = 0 (prehospital ECG) shows sinus rhythm with a minimal ST depression in V3-V4 as well as minimal ST depression in the lateral leads. No significant ST depression is seen in the inferior leads although there is a TWI in lead III that could be non-specific. However, the T wave in V2 looks abnormally large with a hyperacute appearance. Young people might indeed have large T waves in the anterior leads, but the T wave is in fact as large as the whole QRS complex. The positive T wave in V1 could indicate an early sign of anterior ischemia. Although many of these findings may be considered non-specific the appearance is highly unusual in a previously healthy 28 yo man. With a complaint of ongoing chest pain, this is worrisome.

The ECG at t = 17 min (1st ECG in the ED) shows no significant change in V2, but the T wave in V3 is now also hyperacute and the T wave in V4 is also a bit taller. Since the QRS complexes don’t look exactly the same, some of the ST-T changes may be due to different lead placement, but the dynamic change in V3 is too abnormal to ignore. The ST depression in the lateral leads are now gone – could this be pseudonormalisation? There might even be a tiny bit of ST elevation in aVL, and development of slightly downsloping ST segment in the inferior leads (at least aVF and III). Although neither of these ECGs are clearly diagnostic of MI alone, the dynamic changes in combination with a presentation consistent with ACS is highly worrisome.

Smith comment: The ST depression is due to early, and possibly incomplete, LAD occlusion, which is often called "de Winter's T-waves" a type of hyperacute T-wave.  17 minutes later the artery is completely occluded and the ST depression has become ST elevation.  

There should NEVER be ANY ST depression in the precordial leads of a young man.

Peter's response:

You are of course spot on. Me and my colleague saw this immediately, and since these ECGs were recorded 2½ hours before the consultant got the phone call we were very worried about the patient. 

EKG3 (not shown) was recorded 2.5 hours later (Smith comment: treatment was very delayed!) during the consultation and the diagnosis was now obvious with a huge anterolateral STEMI.  The providers had not noticed the ST depression nor the diagnostic T-waves.

Echo hadn't been performed initially, but showed EF 40% and akinesis of the anterior wall. CT of the aorta was of course normal. CT of the lungs showed bilateral infiltrates with gravitational distribution, that initially were interpreted by the radiologist as infectious, but in retrospect were considered to be flash pulmonary edema. 

The patient went for coronary angiography that showed an almost complete occlusion in the distal part of LM with a stenosis extending into the proximal part of the LAD

During PCI the patient needed CPAP and small doses of norepinephrine. He was fully revascularized and was initially admitted to the ICU, but could be moved to the coronary care unit the next day. A formal echo a couple of days later showed EF 50%. The hospitalization was prolonged, due to the development of fever and a small pericardial effusion (postinfarction syndrome?), but otherwise the patient did OK. 

This case was up for discussion the next day in our clinic, and I pointed out the subtle, but real dynamic changes, that might have been picked up, not delaying the diagnosis for another 2½ hours.

Many of my colleagues still considered the initial ECGs to be practically normal, although I pointed out that these findings might be considered non-specific if the patient was presenting with e.g. cellulitis in the leg, but highly worrisome in this particular case, since the patient was having ongoing chest pain. 

Another thing that made the case a bit more complicated was that the initial hs-Troponin T was only 5 ng/L (positive at < 15 ng/L, level of detection at 5) i.e. not positive, but just above the level of detection. This was when the chest pain had been going on for a little more than one hour. 

I think that the ED physician might have been fooled by this. The next troponin measurement in the ICU (6 hours after the onset of chest pain) showed a level of >9998 ng/L. 

In retrospect this was indeed a tricky case, but as I pointed out to my colleagues we should learn from it rather than just call it tricky and convince ourselves that it was unavoidable. 

Regarding the use of your formula: I believe if you use it on the 2nd ECG it comes out positive with a value of 23.678 (if I measured correctly using 2.5 mm of STE at 60 ms, QTc of 428 and RV4 of 14 mm) clearly indicating subtle STEMI.  (A value greater than 23.4 is nearly diagnostic of LAD occlusion in the right circumstances)

Here I have superimposed the ECGs so that you can see the evolution more clearly.  The darker lines are the second ECG at time = 17 minutes after the first:
Notice the significant increase in T-wave amplitude in V3 and V4.
Notice also the new but subtle ST Elevation in I and aVL, with reciprocal ST depression in lead III.

The formula is negative in the 1st ECG due to minimal STE at 60 ms after the J-point in lead V3.
(Remember that 60 ms in this recording format is 3 little boxes, not 1.5)
The formula is positive in the 2nd ECG.
Referring to: Formula for differentiating normal STE from STE due to LAD occlusion

Here it is compressed:

Take home points: 
1) Young people do have MI.
2) Beware hyperacute T-waves
3) Beware any ST depression in precordial leads
4) Do not mask your diagnosis with Morphine (or other opiates)
Serial ECGs would probably have made the difference in this case. 
5) Echo is very helpful in these situations.
4) Don't rely on the first troponin, even if high sensitivity (if there is a short time from the onset of chest pain to the blood testing) 


Comment on the formatting:

In Sweden the different leads usually are presented in the so called Cabrera sequence, which basically means that lead aVR is replaced by -aVR (i.e. aVR with switched polarity, which gives the lead an “up-side-down” appearance) and that the limb leads are presented in a anatomically contiguous order (aVL = -30°; I = 0°; -aVR = 30°; II = 60°; aVF = 90° and III = 120°). This means that the inferior leads are presented next to each other (vertically) and that the high lateral leads (aVL and I) are placed next to each other with -aVR in between. This makes it easier to spot ST-T-changes localized to a specific anatomic area of the heart (at least if you are used to the formatting).

In this case the recordings also have another feature. The tracings that are recorded with a paper speed of 50 mm/s are so called signal-averaged ECGs. There is only one complex presented in each lead, which is an artificially created “mean value” of several ECG complexes. The point of this is to eliminate artifacts. 

On the right side (not shown here) we display short rhythm strips at a paper speed of 12,5 mm/s (thereby looking twice as fast as usual if you’re accustomed to a paper speed of 25 mm/s).  

Persistent Chest Pain, an Elevated Troponin, and a Normal ECG. At midnight.

A middle aged male presented at midnight after 14 hours of constant, severe substernal chest pain, radiating to his throat and to bilateral jaws, and associated with diaphoresis.  It was not relieved by anything.  The pain was not positional, pleuritic, or reproducible.  He had no previous medical history.  The blood pressure was 110/60.  Physical exam was normal and there was no murmur.

I delved into his reasons for arriving so late after onset, thinking that perhaps the pain had only recently increased, or that it had been intermittent until now, but he confirmed that it was 14 hours of constant pain and it was his significant other who insisted that he go to the ED.

Here was his ED ECG:
I read this as normal
--One might say there is ST depression in II, III, and aVF, but this is merely an atrial repolarization wave.  
--You can see the PR segment sagging down, such that the PQ junction is also depressed.  Thus, there is no elevation of the J-point relative to the PQ junction.
--ST segment deviation is measured at the J-point, relative to the PQ junction
--("Inferior" ST depression would have told us that there is unseen ST elevation in aVL and be a strong clue to high lateral MI)
Click here for a couple posts on Atrial Repolarization

He was given an aspirin and a troponin was drawn.  If this is MI, then after 14 hours, the troponin should be elevated.

The troponin I returned at 4.1 ng/mL (ULN = 0.030 ng/mL), diagnostic of myocardial injury.

We recorded a posterior ECG:
V4-V6 are moved around to the back and are really V7-V9.
The "criteria" for posterior STEMI are 0.5 mm STE in one lead.
There is zero ST Elevation.
There are tall R-waves in V2, which could be a sign of old or well developed posterior MI
However, the ECG shows no evidence of acute MI whatsoever.

We gave ticagrelor and heparin and sublingual nitro, with plans to start a nitro drip, but the BP dropped to 80/50 before the drip was started.

The pain was unrelieved.

What do you want to do?

The elevated troponin is diagnostic of myocardial injury. Is it acute or chronic?

There was a normal creatinine and no evidence of heart failure and no other reason for chronic injury, so it must be acute.

Acute myocardial injury: 

Is it myocardial infarction, or perhaps myocarditis?
If it is MI, is it type 1 or type 2?
Is it STEMI or NonSTEMI?  
Is it acute persistent occlusion?

The patient had no hypertension, no tachycardia, a normal hemoglobin, no drug use, no hypotension/shock, no murmur of aortic stenosis.

The patient had been on a long drive, suggesting possible pulmonary embolism (this was unlikely given absence of tachyardia, hypoxia, or any other feature of PE), so we sent a d dimer.  [We also looked at his aortic root by both parasternal and suprasternal views, and the aorta was normal.]  The d dimer returned below the level of detection, ruling out PE and making dissection very unlikely.

So this was not a type 2 MI.  And was not a PE or dissection.

A bedside echo showed good LV function but was inadequate to assess wall motion.  We attempted Speckle Tracking Strain Echocardiography but could not get clear enough images without contrast.

We could not rule out acute epicardial coronary (large artery) occlusion.

What do you want to do now, considering you will need to awaken the hospital's only catheterization team, which must be alert for the next long day in the cath lab?

I called the cardiologist on call and we agreed that we needed to activated the cath lab.

The patient was found to have an acute 100% occlusion of the circumflex proximal to 2 obtuse marginal branches.  It was opened and stented with a door to balloon time of about 120 minutes (this is long for STEMI, but very short for a high risk Non STEMI).

A post cath ECG is shown:
No significant change

The third troponin, drawn before the artery was open, returned at 6.2 ng/mL.
The 4th, after the opening of the artery and release of troponin from the cardiac circulation, was 99.9 ng/mL

So this was a very large MI!!

The formal contrast echo the next morning was difficult technically but showed an inferior wall motion abnormality.  It is unclear if this is "inferobasal" which is the new echo term for Posterior.

Learning Point

Acute coronary occlusion may occur with no ECG findings whatsoever.  Some NonSTEMI require emergent cath lab activation to save viable myocardium at risk.  A patient who has a high clinical suspicion of MI should go to the cath lab.  This is not just my opinion, but the opinion of the American College of Cardiology and American Heart Association.

This is from the 2014 ACC/AHA guidelines.  Earlier versions are more specific. "A subgroup of patients with refractory ischemic symptoms or hemodynamic or rhythm instability are candidates for urgent coronary angiography and revascularization."

Here are the European Guidelines:
Timing of invasive strategy:  Immediate invasive strategy (less than 2 h) in Very-high-risk NSTE-ACS patients (i.e. with at least one very-high-risk criterion according to Table 13 (pasted below) have been generally excluded from RCTs. Owing to a poor short- and long-term prognosis if left untreated, an immediate (i.e. less than 2 h from hospital admission, analogous to STEMI management) invasive strategy with intent to perform revascularization is recommended, irrespective of ECG or biomarker findings.

This includes:

1. Patients with ACS and hemodynamic instability
2. Patients with ACS and acute pulmonary edema
3. Patients with ACS and electrical instability
4. Patients with ACS and refractory chest pain or refractory ischemic ECG findings, usually ST depression

A patient who presents with chest pain and an otherwise unexplained elevated troponin has acute MI.  If the pain is refractory to medical management, no matter what the ECG shows, the patient should go emergently to the cath lab.