Friday, July 25, 2014

Syncope and Bradycardia

An elderly woman had syncope while having a bowel movement.  She had an aortic stenosis murmur.  Here is her ECG:
There is sinus bradycardia
Computer Measurements:
PR interval 174 ms, QRS 106 ms, QT 474 ms, QTc 442 ms, QRS axis 43, T wave axis 53.

The differential of her syncope was listed initially as:
--sick sinus syndrome (because of the bradycardia)
--aortic stenosis
--Valsalva syncope (on the toilet)
What is the most important entity missing from this differential?

Long QT.  Again, the computer fails at measuring the QT interval.  Here is another case I recently posted.

Here is a manual measurement in lead V5.  One measures this be drawing a line along the downward slope of the T-wave until it intersects with the baseline:
From the beginning of the QRS (vertical line) to the end of the T-wave (slanted line) is 15.75 little boxes, each of which is 40 ms.  40 ms x 15.75 = 630 ms
The preceding R-R interval is 1200 ms = 1.2 sec.  The square root of 1.2 is 1.095.  The QTc is then: 630 divided by 1.095 = 575 ms

The computer read a QTc of 442 ms (vs. our manual measurement of 575 ms!!)

Sometimes, what appears to be a prolonged QT is really a QU interval (a U-wave is making it appear as if there is a long QT).  Is that the case here?  No.

Case Progression:

The patient was given 2 g of IV Magnesium.  A Mg level returned low at 1.2 mEq/L.  The patient was admitted to telemetry.  More Mg was given until the level was up to 2.2 mEq/L.

While on telemetry, she had a 12 second episode of Torsade de Pointe.  She also had several runs of Non-sustained VT and many PVCs.  Echo showed only moderate aortic stenosis.

She was found to be on a couple antibiotics that can prolong the QT interval.  More magnesium was given.  There was a plan for isoproterenol infusion should this recur.

See here for full management of Polymorphic Ventricular Tachycardia.

Again, the computer measurement of QT interval fails.  The computer does well at measuring QT intervals of less than 450 ms.   I have been unable to find studies of the accuracy of computerized QT interval when it is long.  But in my very long experience, and paying a lot of attention: when the QT is long, the computer usually fails to register this abnormality.  


1.  You must assess the QT interval visually.  If it appears long, then measure it manually (in the lead in which it is longest).  A QTc interval greater than 500 ms is potentially dangerous.

2.  Acquired long QT is more likely to cause torsade when the patient is bradycardic ("pause dependent").  A longer pause creates a longer QT interval, allowing more time for a PVC to land on the vulnerable part of the T-wave.  Thus, increasing the heart rate with isoproterenol or overdrive pacing prevents Torsade.

3.  Although a slow heart rate results in a shorter QTc (corrected for heart rate), it also leads to a higher risk of Torsade at any given QTc!

Tuesday, July 22, 2014

Are these peaked T-waves the patient's baseline T-waves?

A middle-aged patient presented feeling moderately ill.  He had an ECG recorded.
QRS 102 ms.  There are peaked T-waves. See V4 especially.  The ST segment is horizontal until it abruptly rises to a very peaked T-wave.  The T-wave is "tented" to a point.  It is all but pathognomonic for hyperkalemia.

By history, the patient had no reason to have hyperK on history. A recent previous ECG, done at a K of 4.5 mEq/L, was sought by the residents:
The old ECG also shows very peaked T-waves.  The residents concluded that these were his baseline T-waves.  Were they correct? 

No!  Notice the ST segments in the ECG at presentation are much more flat, and they then rise much more quickly to a peaked T-wave, especially in lead V4. 

Case Conclusion

Residents had already made the comparison and decided that it was not different.  Several minutes later, I saw these two ECGs and immediately saw the difference.   I could see that the new ECG was diagnostic of hyperkalemia, and told the residents that they must immediately start treatment.  As we were walking to his room, and before Calcium could be given, the patient had a v fib arrest while in his room, before his K returned from the lab.  This was a presumed hyperkalemic arrest.  He was immediately defibrillated and given Calcium.  His K returned at 7.0 mEq/L.

Some say you don't need to treat hyperK unless there is QRS widening, claiming that merely having peaked T-waves is not enough.  This is only one case, and anecdotal, but we found no other etiology of arrest in this patient.  The patient had new renal failure as the etiology of hyperK.

1.  Peaking of T-waves occurs in other conditions than hyperkalemia, such as early repolarization.  Comparison with the previous ECG must be done very carefully

2.  I always treat immediately if I think the ECG is affected by hyperK.  I do not wait for the laboratory results

Friday, July 18, 2014

Subacute AnteroSeptal STEMI, With Persistent ST elevation and Upright T-waves

A man in his 60's presented after 4 days of chest pain, with some increase of pain on the day of presentation.  Exact pain history was difficult to ascertain.  There was some SOB.  He had walked into the ED (did not use EMS).  He was in no distress and vital signs were normal.  Here is his ECG:
What is your interpretation?  Obviously there is MI.  How acute is it?

There is atrial fibrillation at a rate of 95.  There is Right Bundle Branch Block with a QR particularly noted in V1-V3 (no rSR', because there is an initial Q-wave; this is diagnostic of infarction in the anterior wall and septum).  The Q-waves extend to V5 and are very wide (80 ms in V2).  There are also inferior Q-waves which can mimic a left anterior fascicular block, as they result in left axis deviation.  There is rather massive ST elevation, and this is not only anterior but inferior (see analysis below).  

The end of the QRS is best seen in lead V1 (and results in a QRS duration of 176 ms).  If one draws a line down to lead II across the bottom, one can find the end of the QRS in lead II.  From there, one can find the end of the QRS in all leads.  This analysis shows that there is ST elevation after the end of the QRS in lead II, III, and aVF, and reciprocal ST depression in aVL.  Thus, this is BOTH an anterior and inferior STEMI in the setting of RBBB.

How old is this antero-inferior STEMI?  

Could it be acute (vs. subacute or days old)?  Although the patient has had pain for 4 days, could the artery have fully occluded only within hours?  Very unlikely.  Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Raitt et al.), such Q-waves are associated with larger MI and worse outcomes (2. Armstrong et al.), the presence of such well developed, wide, anterior Q-wave suggests completed transmural STEMI.  

So this patient likely has a several day old infarction, with persistent ST elevation and persistently upright T-waves.

The wide Q-waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle).  This was common in the days before reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy.  When there is MI extending all the way to the epicardium (transmural), that infarcted epicardium is often inflamed (postinfarction regional pericarditis, or PIRP).  

What complication is the patient with post-infarction regional pericarditis at risk for?

The patient was taken to the cath lab emergently and a 100% mid LAD occlusion was opened but opening resulted in no flow.  The initial troponin I was 23.7 ng/ml and was falling, confirming infarction days ago.

Case Continued

2 days later the patient became increasingly tachycardic, hypotensive, ashen, clammy (in cardiogenic shock) and had a new murmur.  This was the 12-lead ECG. 

Add caption

Not much change, except a slightly faster ventricular response at 110 bpm.  No resolution of ST elevation.  The T-waves are persistently positive.  This remains consistent with PIRP, as was the first ECG.  Notice also how easy it is to diagnose ST elevation in the PVC.

An echocardiogram showed no hemopericardium, but Doppler showed a new small ventricular septal defect with left to right shunting.  This was in addition to a large septal, anterior, and apical wall motion abnormality, and moderately severely decreased LV function.

An intra-aortic balloon pump was placed, and the patient was taken for immediate surgical repair but did not survive.


When there is full thickness infarction, there is epicardial inflammation (post-infarction regional pericarditis), and the myocardium is at risk of "rupture."  The term "rupture" makes it sound like some sort of explosion or massive blowout, but it is usually a small, slow leak that, over time, can cause tamponade and death.  Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock.  If detected early by ultrasound, the patient can be saved.  Our own Dave Plummer of HCMC reported on survival of 2 of 6 patients with STEMI who had free wall myocardial rupture diagnosed by presence of hemopericardium on bedside ultrasound in the ED.(3)

Oliva et al. (4) strongly associated myocardial rupture with postinfarction regional pericarditis (PIRP), and associated PIRP with persistent upright T-waves.  He found 2 ECG patterns of atypical T-wave development in PIRP:
1) persistently positive (upright) T-waves 48 hours after AMI onset. 

2) premature, gradual reversal of inverted T waves to positive (upright) deflections by 48 to 72 hours after MI onset in the presence of well formed Q-waves.


1. Well formed Q-waves with persistent ST elevation, especially in a patient with prolonged pain, should alert to transmural MI with possible post-infarction pericarditis. One should be on the alert for myocardial rupture.  
2. In the case of septal MI, as here, be on the alert for development of a ventricular septal defect.
3. Bedside echo may detect these in a timely way.
4. Additionally, these patients have a high incidence of LV aneurysm with mural thrombus.
5. Although rupture has a high mortality, it is not uniformly fatal


1.  Raitt MH, Maynard C, Wagner GS, Cerqueira MD, Selvester RH, Weaver WD. Appearance of abnormal Q waves early in the course of acute myocardial infarction: implications for efficacy of thrombolytic therapy. J Am Coll Cardiol 1995;25(5):1084-8.

2.  Armstrong PW et al.   Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention.  J Am Coll Cardiol 53(17):1503-9. Apr 28, 2009.

3. Plummer D.  Dick C. Ruiz E. Clinton J. Brunette D. Emergency department two-dimensional echocardiography in the diagnosis of nontraumatic cardiac rupture.  Ann Emerg Med 1994; 23(6):1333-42.

4.  Oliva PB, Hammill SC, Edwards WD. Electrocardiographic diagnosis of postinfarction regional pericarditis: ancillary observations regarding the effect of reperfusion on the rapidity and amplitude of T wave inversion after acute myocardial infarction. Circulation 1993;88(3):896-904.

5. Oliva PB.  Hammill SC.  Edwards WD.  Cardiac rupture: a clinically predictable complication of acute myocardial infarction: report of 70 cases with clinicopathologic correlations.  J Am Coll Cardiol 1993;22(3):720-6

Sunday, July 13, 2014

Bradycardia, SOB, in a Dialysis Patient

A dialysis patient presented with dyspnea and a heart rate of 33.  His medications included amlodipine and carvedilol.  He has a history of hypertension and DM.  His BP was 150/45 (bradycardia leads to long run-off time after each systolic beat, leading to low diastolic pressure).  He appeared comfortable, in no distress.
QRS duration is normal at 97 ms.  What is the diagnosis until proven otherwise?

This ECG shows a junctional bradycardia (either sinus arrest with junctional escape, or severe sinus bradycardia with junctional escape), with retrograde P-waves (see the negative deflection just after the QRS in lead II, and the positive deflection just after the QRS in V1).  Because this patient has LVH and left atrial enlargement, he normally has a negative P-wave in V1 (see below); with retrograde activation, the atrium depolarizes from inferior to superior, changing its polarity on the ECG to upright.

A dialysis patient with bradycardia has hyperkalemia until proven otherwise.  In this case, the K was 7.5 mEq/L.  Notice there are no other signs of hyperK such as peaked T-waves.

Here is his ECG from 2 weeks prior, when his K was 6.5 mEq/L:
It looks nearly identical, except for the rhythm, which is sinus bradycardia

Of course, this bradycardia could be caused by carvedilol and/or amlodipine, or the combination.  And also by sick sinus syndrome.

If the K had not been high, these would have been the likely culprits.


Before waiting for the K level to return, he was immediately given 3 grams of calcium gluconate, with no change.  Another 3 grams were given, still with no change.  Atropine 1 mg was given with no change (as expected).  Given his stability, no further ED treatment was given and he was taken for immediate emergent dialysis.

After dialysis, he returned to sinus rhythm at a normal rate.


Bradycardia should always prompt consideration of hyperkalemia
Bradycardia may be the only ECG sign of hyperkalemia

Friday, July 11, 2014

Repost: a certain pattern of PseudoSTEMI, with or without superimposed STEMI

I posted this on March 1, 2012.   I was inspired by a post by Len Jin Yee to repost.   But this time without the answers.  These are all on a theme, which will quickly become obvious.

Case 1.  A patient presented with an irregular and fast wide complex tachycardia and was electrically cardioverted.  Here is the post cardioversion ECG:
What is going on?  See below.

This  is WPW with secondary repolarization abnormalities.  Notice the very short PR interval and the delta waves, best seen in leads V5 and V6.  This mimics both anterior STEMI and/or left bundle branch block.  

This patient turned out to have Ebstein's anomaly, (a description of which is beyond the scope of this blog) with WPW.


Case 2.  A patient with chest pain
Is it inferior-posterior MI, whether acute or old? There appear to be inferior Q-waves with possible hyperacute T-waves, reciprocal T-wave inversion in aVL suggestive of inferior MI.  There are tall right precordial R-waves with ST depression and T-wave inversion suggestive of concomitant postererior MI.  See below.

In this case, WPW mimics inferior and posterior MI.  There was no superimposed MI of any age.  Note that there are Q-waves in II, III, aVF and that the T-wave in these leads is upright. In a study of 50 patients with inferior Q-waves due to WPW and not due to MI, 47 had an upright T-wave.  The author, Ary Goldberger, suggests that in the presence of a delta wave and Q-wave, the T-wave should be discordant (opposite the Q-wave) as it is in this case, or at least isoelectric.  He suggests that if it is concordant, then one should suspect inferior infarction.  Accordingly, lateral QRS and T-wave should also be discordant.

Other than the study on inferior Q-waves and its implications for diagnosis of inferior MI, I know of no other studies assessing this phenomenon.  I am not sure if, in WPW, there is a predictable pattern. Are the QRS and ST-T complex normally concordant or discordant?  Not sure.


Case 3: A patient with chest pain
There is anterior ST Elevation (V1, V2) with ST depression in inferior and lateral leads.  Looks like a septal STEMI, right?

I think you are catching on that WPW can mimic acute STEMI, with ST elevation and ST depression.  However, if you remember to always evaluate ST elevation and depression in the context of the QRS, and the abnormal depolarization results in abnormal repolarization, you will look at the QRS and recognize how abnormal it is: wide, with short PR interval and delta waves.  The ST-T abnormalities are secondary to the WPW, not primary.


Case 4.  A patient with chest pain

Again, there are delta waves with subsequent inferior ST elevation and reciprocal ST depression in I and aVL, as well as V2.  You are now tuned into this, and realize that the ST elevation is secondary to the WPW, right?      

Wrong!!  This patient has acute inferior STEMI superimposed on baseline WPW.  There is simply too much ST elevation for this to be due to WPW alone.  Here is his baseline ECG for comparison.


Case 5.  A male in his 50's presents with 1.3 hours of chest pain.
Clearly there is WPW, with short PR interval and delta waves.  There are deep QS-waves (negative delta waves) in III and aVF, with concordant T-waves.  T-waves are upright in I and aVL.  Is there old or new inferior MI?  There is ST depression in V3-V6.  There are nonspecific ST and T-wave findings in V4-V6.  Are these all due to WPW, or is there something hiding?

14 minutes later, this was recorded:
Minimal changes

Neither of these ECGs, in my opinion, clearly show ischemia because WPW can so often mimic ischemia.  However, perhaps simply because of worrisome symptoms, or perhaps because they were unaware that these ST-T repolarization changes can be entirely due to WPW, the clinicians took the patient for an angiogram, which showed a 95% stenosis of the first diagnonal with TIMI 2 flow.  It was stented.

8 hours later, post reperfusion, this was recorded:
Many T-waves are now flattened or inverted.

Day 2 ECG: (troponin I peaked at 32 ng/mL)
Inferior T-waves are now clearly upright, lateral T-waves clearly inverted.  So these discordant T-waves in III and aVF, and I and aVL appear to be the normal discordant T-waves that one finds when there are inferior Q-waves due to WPW.  This appears to be a case of pseudonormalization of T-waves, but it is not true pseudonormalization because it is not from re-occlusion, but rather from reperfusion.   In other words, after reperfusion, the T-wave vectors are in the expected direction for WPW, not inverted from normal as is common in reperfusion.

Day 3, after ablation of the accessory pathway:
QRS is normalized except for Q-waves in I and aVL (due to the lateral AMI suffered on this occasion).   Interestingly, the T-waves are inverted in III and aVF, but not in I and aVL; that is to say that there are apparently no lateral reperfusion T-waves.  There are large T-waves in V2 and V3 which may represent posterior reperfusion T-waves (or early repol, but without a comparison from prior non-WPW ECG, this is uncertain).


WPW has abnormal depolarization through a bypass tract, manifesting as a delta wave.  And like other ECG abnormalities that have abnormal depolarization (LVH, LBBB, RBBB, Brugada, hyperkalemia, and others), they also have abnormal repolarization.  "Secondary repolarization abnormalities."  (Not primary, meaning the QRS is normal but repolarization is abnormal, as in ischemia).

Above I showed 5 cases: 
Cases 1-3 are of WPW with secondary repolarization abnormalities that could mimic old or acute MI.
Case 4 shows a baseline WPW, then with MI superimposed on it.
Case 5 is a case in which WPW conceals acute MI. 

Learning points:

1. WPW alters both depolarization and repolarization and can both mimic and obscure acute MI.
2. In WPW with inferior Q-waves (but without new or old MI), the T-wave is usually upright (discordant).  
3. In WPW with inferior Q-waves, a concordant T-wave should raise suspicion for MI, either old or new.
4. I am uncertain as to whether there are other concordance and discordance rules that may help decipher ischemia in the presence of WPW.

Friday, July 4, 2014

Is the LAD really completely occluded when there are de Winter's waves?

A male in his 30's complained of sudden severe substernal chest pain.  He was rushed to the critical care area where they recorded this ECG:
Obvious Antero-lateral STEMI due to proximal LAD occlusion (proximal because it is proximal to first diagonal, resulting in high lateral STEMI with ST elevation in I, aVL and reciprocal ST depression in inferior leads)

The cath lab was activated, and just before going to the cath lab (19 minutes after the first ECG), this ECG was recorded:
There are de Winter's T-waves (ST depression with upsloping ST segment and hyperacute T-waves).

I have often wondered if de Winter's T-waves really are due to complete occlusion, or to severe, subtotal occlusion.  Perhaps they indicate an open artery with minimal flow and severe subendocardial ischemia, but not total subepicardial ischemia.

Since ACS is so dynamic, with thrombi forming and lysing continuously, and because the ECG and angiogram are rarely simultaneous, it is probable that de Winter's T-waves are recorded in a window when the artery is barely open.

At cath, there was a 99% lesion with some flow.

Here is the first post cath ECG, shortly after opening.
(QTc = 383).  Now there are very subtle Wellens waves

Here is the ECG the next day:
QTc 440.  Well developed Wellens' waves (reperfusion T-waves after opening of LAD occlusion)

de Winter's waves

de Winter et al. (Heart 2009;95:1701–1706, published on 1890 patients who had LAD occlusion.  They found these "de Winter's waves" (ST depression in V1-V6 with upsloping ST depression and a hyperacute T-wave) in 2% of these patients, and stated they were "persistent."

A quote:  "We have observed this pattern as a static ECG pattern lasting from the time of first medical contact until the recording of the pre-procedural ECG and lasting until angiographic establishment of an occluded LAD artery (that is, approximately 60 minutes)"

They gave as an example a patient with chest pain of 91 minutes who had this pattern.  He had an ECG 71 minutes later and the pattern continued.  Then, they say: "The coronary angiogram performed shortly after this registration revealed a fresh occlusion of the proximal LAD artery."  It is in my view that it is very likely that the artery was barely open while the de Winter's waves were present, and closed off entirely by the time of the angiogram which was done "shortly after" the ECG.

My interpretation of this data

de Winter's waves are probably due to severe subendocardial ischemia, with some epicardial ischemia (enough to result in hyperacute T-waves, but not enough for ST elevation.

This is somewhat academic, because these patients clearly need reperfusion whatever the exact thrombotic state of the artery.

Tuesday, July 1, 2014

Head On Motor Vehicle Collision. ST depression. Myocardial Contusion?

A woman in her 40's was involved in a head-on motor vehicle collision.  EMS noted a facial droop. On arrival she was hypertensive but other vitals were normal.  She did complain of back and neck pain, chest pain, and SOB.  She also had a facial droop as noted by medics.  This droop was apparently new.

An ECG was recorded:
This shows diffuse ST depression (diffuse subendocardial ischemia) in leads I, II, aVF an V3 to V6, with reciprocal ST elevation in aVR and V1.  This is diagnostic of subendocardial ischemia or injury.  

The ECG was repeated 36 minutes later:
The findings are improving

Is this:

1. Myocardial contusion?
2. Stress Cardiomyopathy?
3. ACS?
4. Type II (demand ischemia) from stable coronary disease with stress?

She was found on CT to have a subacute middle cerebral infarct.  Other workup and imaging did not show any serious injuries.

She was admitted and underwent serial troponins.  All were negative.  In fact, they were undetectable with the Abbott Architect (contemporary, sensitive, but NOT high sensitivity) troponin I.  Limit of detection (LOD) = 0.010 ng/mL.   All values were less than 0.010 ng/mL.

An ECG was recorded the next AM:
Finding are almost completely resolved, but there is residual ST depression

An echocardiogram was normal with an EF of 82%.

She underwent an adenosine nuclear stress test:

"Myocardial perfusion imaging with pharmacologic vasodilatation demonstrated small to moderate size, mild to moderate intensity reversible perfusion defect involving the distal myocardial segment of the anterior and anterosptal walls with minimal involvement of the apex. There was no breast shift artifact to explain the difference between the rest and stress images. There was 1-1.5 millimeter horizontal ST depression in the inferior and lateral leads during regadenoson (an A2A adenosine receptor agonist that is a coronary vasodilator) infusion along with some chest tightness, nausea, and diaphoresis that resolved during recovery. These findings are suggestive of possible flow-limiting lesion in the distal LAD territory."

This is a notable learning point, other than just ischemia: note that the ST depression was "inferior and lateral" but the ischemia by ultrasound was anterior!  This illustrates a well-known phenomenon that subendocardial ischemic ST depression does not localize.

Thus, she underwent angiography:

There was a critical 95% stenosis of the left main coronary artery.

She then underwent CABG.  The outcome was good.

Final diagnosis:

ST depression due to diffuse subendocardial ischemia triggered by stress in the setting of a very tight, fixed stenosis of the left main.  This was not ACS, not stress cardiomyopathy, and not myocardial contusion.


In spite of severe subendocardial ischemia of the entire heart, all contemporary troponins were negative. This highlights the importance of an ECG in trauma, and the importance of following up on the ECG findings in spite of negative troponins.  What would the result of high sensitivity troponins have been?  We have no idea.

This also shows how diffuse ST elevation with ST elevation in aVR is NOT due to Left Main occlusion.  It is due to left main insufficiency.  Occlusion nearly universally causes death and has the findings of simultaneous STEMI of anterior, lateral, and posterior walls.

For a detailed explanation of ST elevation in aVR, in both STEMI and NonSTEMI

Saturday, June 28, 2014

History of Hypertrophic Cardiomyopathy (HOCM), with Tachycardia and High Lactate

A patient under 40 with h/o HOCM and implantable cardioverter-defibrillator (for secondary prevention of VF arrest that occurred during exertion) presented with chest pain, diaphoresis, and tachycardia.  Earlier in the day, the patient had been physically active, which resulted in dizziness, SOB and diaphoresis.  Then later, there was alcohol consumption associated with further physical exertion.  The patient presented clutching the chest, dizzy, SOB, diaphoretic.  BP was 165/109 (a good example of shock in which the BP is maintained by high systemic vascular resistance).

Here is her ED ECG:
There is a narrow complex (QRS duration =113 ms) tachycardia at a rate of about 160.  There are no definite P-waves.  It appears to be paroxysmal SVT.  There is very high voltage and secondary repolarization (ST-T) abnormalities.
The Bedside Cardiac Ultrasound is shown here:

This shows the very hypertrophic walls, and the consequent very small left ventricular chamber collapsing on itself.  There is very little opporunity for the heart to fill with blood, and probable obstruction of aortic outflow as well.

The patient was given adenosine 6 mg, 12 mg, 12 mg, and 18 mg without any lasting effect.

Lactate returned at 8.3 mEq/L, consistent with shock.

Then an esmolol double bolus (each bolus = 500 mcg/kg) and drip was given, with immediate slowing of heart rate.  The patient was given a normal saline fluid bolus.

The heart rate immediately slowed and here is the ECG at t = 45 min:
Sinus tach with heart rate about 100.  High Voltage and secondary ST-T abnormalities.

The patient stabilized with a BP of 107/58 and pulse of 100 and felt much better.

Later that day:
Sinus rhythm.  LVH with typical repolarization abnormalities.  Though this ECG is diagnostic of LVH, it is not specifically diagnostic of HOCM.  The signatures of HOCM, besides LVH, are tall R-waves in septal leads (septal hypertrophy) and deep S-waves in lateral leads (reciprocal to septal hypertrophy, such as in the ECG from another patient below. 

Here is an example of HOCM with septal R-waves in the right precordium (different patient):
There is massive voltage with corresponding repolarization abnormalities.  There is very high voltage R-waves in right precordial leads, highly suggestive of septal hypertrophy.  The ST segments are depressed, discordant to the large R-wave.  This is unlike most LVH, in which the right precordial S-waves are deep, with discordant ST elevation.)  This is highly suspicious for hypertrophic cardiomyopathy with asymmetric septal hypertrophy (HOCM).   To see this entire case, with ultrasounds, go to this post.

Back to this case:

Interrogation of the IVCD revealed that the heart rate gradually slowed after esmolol (there was no sudden conversion of rhythm to suggest re-entry).  Thus, the initial ECG is believed to have had a rhythm of sinus tachycardia.

Whether sinus tach or SVT, beta blockade is an ideal therapy in this situation, along with fluids.  The LV's pump function is too vigorous, causing collapse.  And the fast heart rate leaves no time for cardiac filling.  The left atrial pressure is too low to allow good preload of the LV.  Therefore, one should increase preload by increasing left atrial pressure (by giving fluids), and both 1) slow the heart rate to allow for better filling and 2) decrease pump function to prevent obstruction of outflow and also allow for better filling (by giving beta blockade, in this case esmolol, as short-acting beta-1 blocker that can be discontinued if there are adverse events).

The high lactate shows how this patient is very volume dependent.  Dehydration can set off a spiral of low stroke volume, then further catecholamine output with consequent increased myocardial contractility, and thus LV chamber collapse, with subsequent obstruction of outflow and worse filling.  The vicious cycle needs to be broken.


The patient did very well and was instructed to not let herself get dehydrated.  It is uncertain if she was discharged on a beta blocker, but this is one potential therapy to help prevent recurrence.

Thursday, June 26, 2014

A 29 year old male with pleuritic chest pain for 6 hours

This case was sent to me by Taylor Sanders of the LSU- Baton Rouge Emergency Medicine residency.

A 29 year old complained of 6 hours of pleuritic chest pain:

QRS: There is rSR' in V1, consistent with RV conduction delay, but the QRS does not appear prolonged and there are no S-waves in lateral leads.  However, this absence of lateral S-wave may be due to terminal QRS distortion from the ST Elevation.

R-waves in Lateral leads: the R-waves in I and aVL are minimal, but are well formed in V5 and V6; this is somewhat unusual, and one must entertain the possibility of reversed limb lead placement.  However, when the axis is 90 degrees, because V5 and V6 are inferior to limb leads I and aVL, they may show R-waves when I and aVL do not.   

PR segments: there appears to be some PR depression in leads II and V3.  In lead II, it is partly due to a downsloping baseline.  This PR depression is suggestive of myo-pericarditis, but may also be found in MI.  PR depression of greater than 0.8 mm is generally considered specific for pericarditis, but the data upon which this is established comes from the pre-angiogram era, and cannot be fully trusted.

ST segments: 

There is marked ST elevation in inferior and lateral leads.  Inferolateral STEMI and pericarditis are very difficult to distinguish, and the best means to do so is that with inferolateral STEMI there is virtually always ST depression in aVL, even when there is ST elevation in V5 and V6.  There is no reciprocal ST depression in aVL and this makes inferior STEMI, even with superimposed lateral STEMI, very unlikely. 

The ST axis in pericarditis is rarely to the right of lead II.  An ST axis towards lead II results in no limb lead ST depression except in aVR (which is the opposite of a lead midway between I and II)

The ST axis in inferior STEMI is almost always to the right of lead II (resulting in ST depression in aVL) 

ST depression in aVR is found in all etiologies of inferior ST elevation: pericarditis, early repol and MI.  So this is not helpful.  However, there is ST depression in V1 and V2: is this posterior injury?  Or are these ST segments simply discordant to the R' wave, and a result of the abnormal depolarization ("secondary", not "primary" ST segment abnormalities)?  In general, myo-pericarditis does not have reciprocal ST depression anywhere except lead aVR, but this may be an exception due to the R' waves in V1 and V2.

T-waves: These are prominent, and worrisome for MI or early repolarization.  Early repolarization is possible, but less likely when not also seen in anterior leads.  Slow upstroke and fast downstroke, and relatively short QT favor a non-MI diagnosis as well.  T-waves in II, III, aVF and V4-V6 are very tall relative to the R-wave and QRS.

QTc interval: I do not have the computerized QTc for this case, but my visual inspection puts it at no longer than 380 ms.  In our as yet unplublished study of inferior STEMI, only 7% had a QTc less than or equal to 380ms. 

I was shown this ECG with just the clinical information above.  I responded that this is probably myo- or peri-carditis but that I was worried about the size of the T-waves.   And I often say the "you diagnose pericarditis at your peril."  The fact that the pain was pleuritic and the patient was 29 years old is supportive of pericarditis, but look at this case of a 24 year old woman with chest pain after a night of drinking and vomiting.

The first troponin I returned at 6 ng/mL (significantly elevated).

Another ECG was recorded:
Now there is much more ST elevation in lateral precordial leads.  There is also STE in aVL.  (ST axis is to the left of lead II; this is highly suggestive of pericarditis.  But how much do you want to bet?)
These are dynamic ST segments.  Are ST segments in pericarditis this dynamic?  I don't think we have a lot of data on this.  But this is very worrisome for STEMI, so the patient was taken emergently to the cath lab.

A very reasonable course of action would be a formal echocardiogram to look for wall motion abnormalities.  Absence of WMA would make STEMI impossible and establish the diagnosis of pericarditis without subjecting the patient to an angiogram.

It is also very reasonable to avoid any delay and go directly to the cath lab.

All coronary arteries were clean.

Final diagnosis:  Myocarditis

Tuesday, June 24, 2014

Respiratory Failure and ST Depression: Is there Posterior STEMI?

The ultrasound in this case was recorded by Dr. Robert F. (Rob) Reardon, one of my partners here at Hennepin County Medical Center (HCMC) in Minneapolis, and one of the world leaders in emergency ultrasound.  He is also an editor of this great new textbook of emergency ultrasound (Ma, Mateer, Reardon, Joing, eds.), and one of the authors of the Cardiac Ultrasound chapter (other authors of this chapter are Dr. Andrew Laudenbach (also of HCMC) and Dr. Scott Joing (also of HCMC, and the creator of the outstanding FOAMed site,


A middle-age woman with a history of emphysema presented in severe respiratory distress and respiratory failure.  She was intubated emergently in the ED.  Her venous blood gas after intubation had a pH of 7.16 and pCO2 of 66.  The Chest X-ray was suggestive of pneumonia, but not pulmonary edema.  The following ECG was recorded:
There is sinus tachycardia, and ST depression that is maximal in V3 and V4, suggestive of posterior STEMI, or possibly subendocardial ischemia.  [However, subendocardial ischemia is usually diffuse, and therefore has an ST depression vector towards the apex of the heart (towards V5 and V6.  That is to say, the maximal ST depression is usually in I, II, V5, and V6, with reciprocal ST elevation in aVR.]

A posterior ECG was recorded:
There is ST elevation in posterior leads V7 and V8.  

Although this meets criteria for posterior STEMI (0.5 mm in 2 leads), there will virtually always be some ST elevation in posterior leads when there is ST depression in anterior leads, as these are opposing leads. 

[There is an exception to this rule, and that would be in pericarditis, when there is an ST elevation vector that goes from endocardium to epicardium throughout the entire heart, with an ST elevation summation vector towards the apex.  In such a case, there is diffuse ST elevation, including towards the posterior wall.]

Thus, there is probably posterior transmural ischemia.  Is this ACS with posterior MI?  The presentation of respiratory failure without pulmonary edema is not at all typical for ACS.  The patient apparently has a COPD exacerbation with pneumonia.  She could have 2 pathologies at once, but this is less likely.

An ED cardiac echo was performed at the bedside:

This subcostal view shows poor contractility at the entire base of the heart, and excellent contractility at the apex.  There is no wall motion abnormality in a coronary distribution.

Dr. Reardon made a diagnosis.  What is it?

Reverse Takotsubo!  (See below for description of Takotsubo and Reverse Takotsubo)

Case continued:

The patient was admitted to the Medical ICU.  She recovered.  Her max troponin I was 2.2 ng/mL.  Formal Echo also showed Reverse Takotsubo, with EF of 35%.  Echo 2 months later showed full recovery of EF.

She returned in respiratory distress 5 months after the first presentation, and required intubation again.  Here is her ECG from that visit:
Very concerning for Anterior STEMI
A bedside echo showed what appeared to be an anterior wall motion abnormality.  Cardiology was immediately consulted for a formal echocardiogram.  It showed an EF of 15% with a circumferential loss of function at the mid-section, with preservation of the apex and the base.  (This is called mid-ventricular stress cardiomyopathy).

Again, the troponin I peaked at 2.2 ng/mL.

An angiogram was done and showed normal coronary arteries.

The LV function eventually recovered again.

Stress Cardiomyopathy, Takotsubo and Reverse Takotsubo, and Mid-Ventricular Takotsubo Cardiomyopathy

In Takostubo stress cardiomyopathy, caused by small vessel ischemia from high catecholamine influence, there is poor contractility at the apex, causing "apical ballooning," which has the appearance of a Japanese octopus trap, or "Takotsubo"  Here is a left ventriculogram of Takotsubo SCM.
Standard Takotsubo with Apical Ballooning.
See this case for ECG and Echo video of Takotsubo Stress Cardiomyopathy that Mimics STEMI.

Reverse and Mid-Ventricular Takotsubo Stress Cardiomyopathy (SCM):

Reverse Takotsubo SCM is the term used when the LV dysfunction is of the base, and not the of the apex.  Thus, there is no apical ballooning. As in standard Takotsubo, the dysfunction is circumferential, not in a vascular territory, and not due to ACS.    

Reverse SCM has been described in many stressful situations, just as standard Takotsubo SCM, including sympathomimetic drug abuse, energy drinks, serotonin syndrome, anaphylaxis, high dose epinephrine (adrenaline!), pheochromocytoma, subarachnoid hemorrhage, sepsis, and dobutamine stress.

Reverse Takotsubo may be more common in younger patients, but there is little systematic data on the condition.  One small registry of 103 SCM patients, 20 of whom had reverse Takotsubo, showed that the reverse type had higher incidence of triggering stress (100% vs. 77%), less dyspnea, pulmonary edema, and cardiogenic shock, and less T-wave inversion on ECG.

Mid-ventricular Takotsubo is the term for good function of the mid LV, with poor function of BOTH the base and the apex.  It is less common than either of the other forms.

Of course, if it is SCM that does not have apical ballooning, it does not look like an octopus trap, and therefore perhaps should not be called Takotsubo at all.

There is also a claim of a 4th type, "localized" SCM (with focal wall motion abnormalities mimicking ACS).  The claim is substantiated only by case reports, such as this one, which cannot establish with certainty the absence of a thrombotic coronary lesion.

Take Home Lesson:

When the clinical situation is stress (such as respiratory failure from COPD in this case -- not from pulmonary edema), and the echocardiogram shows circumferential dysfunction, whether at the base, mid-LV, or apex, then stress cardiomyopathy is very likely the etiology of the ECG abnormalities.