Answer:   a) atrial bigeminy with aberrant conduction.

Medics recorded this ECG at time 0 in a patient with chest pain:

There are inferior hyperacute T-waves, with reciprocally inverted hyperacute T-wave in aVL, and a biphasic (down-up) T-wave in V2 and V3, as well as ST depression in I and V4-V6.

"Down-up" biphasic T-waves should always be thought to be reciprocal of "up-down" (Wellens' type) reperfusion T-waves.  (Alternatively, if you see a down-up T-wave, it may actually be a down T-wave followed by an upright U-wave, if it happens very late.)  Thus, this is probably inferior-posterior STEMI, possibly with some degree of reperfusion.

The chest pain began to resolve after NTG (t = 2 minutes):

The inferior T-waves are slightly smaller, and there is less negativity to the T-waves in V2 and V3

Another was recorded at t = 4 minutes:

Now the inferior T-waves are not at all hyperacute and the precordial T-waves are mostly upright.  Clearly, this is a reperfusing inferoposterior MI.  There are down-up T-waves in V4-V6.

Here is t = 13 minutes, with posterior leads V7-V9:

Now there are inverted (reperfusion) T-waves in the inferior leads, with a reciprocally upright T-wave in aVL. The T-waves in V2 and V3 are upright.  There are mostly inverted T-waves in V7-V9, pretty much reciprocal  to (opposite of) V2 and V3.

Here is t = 14 minutes (simultaneous to previous):

T-waves are upright in V4-V6, reciprocal to the inverted T-waves in V7-V9, but not exactly because these are not 180 degrees opposite each other.    V2 and V3 are another example of posterior reperfusion T-waves.

Angiogram showed an open culprit artery supplying the inferior and posterior walls

Usefulness of PVCs from HQMedEd on Vimeo.
K. Wang, MD
Adjunct Professor of Medicine
Inpatient Cardiology and Electrocardiography
University of Minnesota

http://www.med.umn.edu/cardiology/faculty/wang/home.html

A male in his 30s presented with chest pain, cough, and sore throat. 

He had been seen in clinic the day prior for cough x 1 month and sort throat.  A strep test was positive and he was treated with penicillin, and also with acetaminophen and ibuprofen. 

On the day of ED (ER) presentation, he presented with 5 hours of intermittent sudden onset left side chest pressure unrelieved by ibuprofen, with associated vomiting and SOB.  There was some association with moving and palpation, but also some improvement with NTG.  An ECG was obtained immediately:

Sinus rhythm.  There is some inferior and lateral ST elevation that is very subtle, and is associated with a very small amount of ST depression in lead aVL (which we have found to always be associated with inferior MI).  There are large T-waves in II, V4-V6.  There is also a tiny amount of terminal T-wave inversion in lead III (see comparison below).  There is a deformed T-wave in V2

 I was highly suspicious of MI, so an ACS workup was initiated and we recorded a bedside echo (unavailable) which showed no inferior wall motion abnormality (or anywhere else).  He was given aspirin and clopidogrel 600 mg.  Because of the absence of wall motion abnormality, the patient's age, and the atypical pain, we decided to serially evaluate him and not activate the cath lab.  A second ECG was recorded at 37 minutes.

This is identical, except the terminal T-wave inversion in III is gone.

Around this time, the initial troponin returned at 2.0 ng/ml.  Because he had persistent chest pain and persistent ECG abnormalities, we activated the cath lab.  He was taken and found to have open coronaries.  The angiographer was concerned about inadequate opacification of the distal left main and proximal LAD, and did intravascular ultrasound.  He confirmed a plaque with fissure in the distal left main coronary artery.  There was no indication for stenting, but aggressive and prolonged antithrombotic and antiplatelet therapy (to "cool down" the fissured plaque) was instituted for this very high risk lesion.

Here is the ECG after the cath:

The STE and reciprocal ST depression are gone, and T-waves are smaller.  The previously deformed T-wave in V2 is normal now.

Troponin I peaked at 8 ng/ml.  A formal echo showed no wall motion abnormality.  An ECG at 24 hours was recorded:

This confirms inferior and lateral infarction, with increased ST elevation and evolution of T-waves (reperfusion T-waves).

At 48 hours:

Further evolution

The troponins trended down from a peak of 8 ng/ml.

The ECG suggests inferolateral MI.  The T-wave in V2 suggests either posterior or anterior ischemia.  The angiogram is consistent with anterior (LAD) and posterolateral MI (left main supplies the LAD and circumflex), and of inferior MI if the the circumflex is dominant (the cath report did not specify  this).

In any case, what would be considered by most to be a "nonspecific" ECG was highly suspicious and prompted rapid evaluation and management in a young man who might otherwise be thought "low risk" with young age and atypical chest pain.  The finding of reciprocal ST depression in lead aVL confirmed the pathologic nature of the inferior ST elevation.

A male in his 60's with a known history of hypertrophic cardiomyopathy (HOCM) presented for chest pain.  He thought  it was "acid reflux," and it started a few hours prior to his presentation to a non-PCI capable hospital.  He denied any associated symptoms.  His pain was not relieved with NTG.  He had an minimally elevated troponin at the referral institution, (assay unknown).  Here is the first ECG:

There is sinus rhythm with LBBB and high voltage, and all leads have appropriate and proportional discordance EXCEPT for lead V4, which has less than 1 mm of (inappropriate) concordant ST elevation.  Lead V5 also has significantly less discordance than expected.

What should the ECG look like if there is both HOCM and LBBB?  I don't think anyone knows. 

The patient was transferred to a PCI capable hospital where this ECG was recorded:

Now the concordant ST elevation is in lead V5, but since V4 now has a predominantly negative QRS, the difference is a result of lead placement differences between the two ECGs.  V6 has an inappropriately isoelectric ST segment.

An ECG from 5 years previous was available:

This shows inappropriate concordance of less than 1 mm in V4, and inappropriate isoelectric ST segments in V5, so all this configuration is not new for this patient who has known HOCM.

Strictly speaking, none of these meet the first Sgarbossa criterion of 1mm of concordant ST elevation.  In our study of patients with ischemic symptoms and LBBB, of 33 occlusions and 129 without occlusion, we had initially hypothesized that ANY concordant ST elevation (not just 1 mm) would be specific for coronary occlusion.  We did not publish the data (yet), but less than 1 mm of concordant STE occurred too frequently among the control group to be used as a specific criterion for STEMI-equivalent.

Out of an abundance of caution, the cath lab was activated and the coronaries were clean.

The troponin at the referral institution was normal.

The echocardiogram showed:


Normal estimated left ventricular ejection fraction, about 60%.
Left ventricular hypertrophy concentric, marked.
Dynamic left ventricular outflow/subvalvular obstruction (due to HOCM)
Asynchronous interventricular septal motion due to left bundle branch block.

Summary

1. Perhaps HOCM in the setting of LBBB can have concordant ST elevation
2. Concordant ST elevation of less than 1 mm has a specificity less than if it is greater than 1 mm
3. Troponins at or near the 99% cutpoint may give discordant results, especially with different assays.

One very sophisticated reader, Ken Grauer, came up with another interpretation of the last rhythm strip.

Here is the strip:






Here is K. Wang's ladder diagram and interpretation:

Answer: b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats.



What bothered me about this being an accelerated junctional rhythm (interrupted each 3rd beat by sinus capture) - was that the R-R interval for the 1st junctional beat in each sequence (= the R-R between beats #3-4; 6-7; 9-10; and 12-13) is slightly different (shorter) than the R-R interval of the subsequent beat (= the R-R between beats #4-5; 7-8; 10-11; and 13-14) - whereas if this was AV dissociation by usurpation with junctional acceleration I would have expected them to be the same ....

Why couldn't the mechanism be the one I drew - whereby there are PJCs (beats #4,7, 10, 13) that conduct retrograde enough to slow down forward conduction of the next sinus impulse. Admittedly - that next sinus impulse is slowed down to a greater extent than usually occurs with such concealed conduction (perhaps due to switching to some alternate slow conduction pathway ... ).

Just wondering if Dr. Wang might consider my alternate mechanism plausible. In any case - GREAT TRACING - and what IS agreed is that there is AV dissociation from some junctional intervention and no evidence of any AV block. 









Here is K. Wang's Respsonse:

What does this rhythm strip of lead V1 show?

















How about choosing from multiple choice?



b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats
d) Extreme sinus bradycardia and complete AV block with AV junctional escape rhythm



Here is a ladder diagram of the rhythm:



Answer: b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats.

Many of you are probably thinking "Widespread ST elevation! It must be pericarditis!"  And that is certainly high on the differential.  In my opinion, due to much researching for true pericarditis cases (with objective evidence such as effusion or rub or typical evolution of the ECG), I believe that pericarditis is a very unusual cause of ST elevation, and that benign (normal variant) ST elevation is much more common.

In any case, there is no PR depression anywhere on this ECG.  There was no rub or effusion.

The patient had sepsis and hypovolemia.

1) I do not think hyperkalemia was the etiology of the change.  I might be wrong.  It looks like early repolarization to me
2) Contrary to widespread belief, early repol may come and go; it is not always present in any given individual.  See article by Kambara below.
3) Tachycardia, or stress testing, may diminish the ST elevation of early repol.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.
 

In my residency training and beyond, I learned much from Dr. Kyuhyun Wang (here is his bio) and from his Atlas of Electrocardiography.  It has finally been published for all to obtain.

He is especially talented with rhythms, and a wizard with ladder diagrams.  This is his first guest post.  I will ask him for more in the future.

What kind of AV block is this?

Explanation, with ladder diagram, is below

Dr. Smith's Comment:

These two cases (this one and the one on theheart.org is another demonstration of how not every complex that has AV dissociation is demonstrating AV block.  Here is another case posted in June 2011.

A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911.  He had no chest pain.  Medications were aspirin, clopidogrel, metoprolol, and simvastatin.  He was in acute distress from pulmonary edema, with a BP of 180/110, pulse 110.  Here is his prehosptial ECG:

There are inferior Q-waves with ST elevation T-wave inversion.  There is reciprocal ST depression in aVL and I.  There is ST depression in V2 and V3, with biphasic T-waves (down-up).  The computer read is:  *****Acute MI*****

The protocol for prehospital activation in the EMS system that this patient presented to requires 2 elements:

1) Chest pain
2) A computer read of *****Acute MI*****

Only 1 of 2 was present, so there was no prehospital activation.



The patient was transported to the ED.  On arrival, he was hypoxic, with saturations of 92% on room air.  He was in distress, diaphoretic, with signficant work of breathing.  He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema.   Blood pressure was 215/124 and HR 115 (on metoprolol).   Here is his ED ECG:

There is sinus tachycardia.  There are Q-waves in inferior leads, with ST elevation in II, III, and aVF, and reciprocal ST depression in aVL.  There is also ST depression in V2 and V3, now with fully upright T-waves.  Is this acute STEMI?

Of course, papillary muscle rupture and mitral regurgitation should be on the differential here, as in this case, but it is not very likely when the BP is so high.














Is this an acute STEMI?  -- Unlikely!

The prehospital ECG is indeed alarming, and activating the cath lab is certainly not wrong.  The ED ECG is less alarming: acute STEMI generally has an upright T-wave, unless reperfused or reperfusing (analogous to Wellens'), if not through the infarct artery, then through collaterals.  Thus, the absence of an upright T-wave in the leads with ST elevation (or an upright T-wave in leads reciprocal to ST elevation, such as V2 and V3 here) is a strong indicator of an open artery.  In this case, the inferior T-waves are down, and the T-waves that are reciprocal to the posterior leads (recorded in anterior leads) are upright, which suggest reperfusion of both inferior and posterior walls. See this explanation of posterior reperfusion T-waves.

The presence of the Q-waves, and the history of previous MI, are also strong clues that re-occlusion of the infarct-related artery is not the etiology of the symptoms.  Furthermore, the patient has no chest pain (certainly many STEMI do not have chest pain, but it should always make you especially scrutinize the ECG and the clinical situation) and there was severe hypertension.  The hypertension alone is the likely etiology of the pulmonary edema.

So it would be wise to look at the pre-discharge ECG, which was available:

There are Q-waves and ST elevation on this pre-discharge (post-stent) ECG.  The amount of ST elevation and depression is slightly less than on the ECG above, but there is also no tachycardia, which tends to exaggerate ST deviation.

The patient was treated with bilevel positive end expiratory noninvasive ventilation, given 3 sublingual nitroglycerine and started on a nitro drip titrating quickly to 80 mcg/min.  There was immediate relief of dyspnea, and the BP fell to 138 systolic with a pulse of 95 and saturations of 96%.

Before activating the cath lab, it would be useful to obtain another ECG at this point in time, and it is likely to appear very similar to this last one above, in which case the entire clinical presentation could be attributed to to the hypertension/pulmonary edema vicious cycle.

The cath lab was activated.  At angiogram, there was no change in the coronary arteries.  All symptoms were due to a combination of hypertension and fluid overload, and then the vicious cycle of pulmonary edema and SOB causing catecholamine burst, then more HTN and more pulmonary edema, etc.

Inferior LV "aneurysm" morphology


Electrocardiographic "LV Aneurysm" morphology simply means "persistent ST elevation after previous MI."  Not all such ECGs represent anatomic aneurysms (on echo this is "diastolic dyskinesis"), but do generally represent an area of dense akinesis on echocardiogram.  (This patient's previous and repeat echo had dense inferoposterior wall akinesis.)  I have discussed anterior LV aneurysm morphology at length in previous posts (for example, this post), but have not discussed inferior "aneurysm" nearly as much.

First, to be called "aneurysm," the MI must be at least a couple weeks old, so this case does not strictly apply.  Nevertheless, persistent ST elevation immediately after reperfusion is a sign of poor microvascular reperfusion and associated with worse function and higher mortality (and is a more accurate predictor of all kinds of outcomes than is TIMI flow), and also is associated with later persistent ST elevation (but not always).  This patient had had rapid reperfusion of his STEMI 2 days prior (TIMI-3 flow); nevertheless, his troponins rose very high and he had a dense wall motion abnormality.  This is typical of patients whose ST elevation is persistent.

Whereas in anterior "aneurysm," there is virtually always a QS-wave (or only a vestigial r-wave left), in inferior "aneurysm", a QS-wave is relatively less common and a QR-wave is very common.  For this reason, distinguishing acute inferior STEMI from inferior "aneurysm" is significantly more difficult than for anterior "aneurysm."

Nevertheless, in both instances, there are well-formed Q-waves, which is not very common in acute inferior STEMI (though very common in subacute STEMI, which also requires reperfusion therapy).

The patient did very well, and this time was discharged on lisinopril in addition to other medications.

The following is told with full permission of the patient, who is a paramedic who also started, owns and runs with his wife a company for teaching CPR.  He has taught CPR to over 100,000 people.  And he's a wonderful guy.   Here is his story:

Near midnight in December, this 56 yo very healthy and vigorous paramedic was out on a run with a critical case when his partner found him unresponsive in the front seat of the ambulance.  The partner began manual chest compressions immediately and called for help.  He was found to be in ventricular fibrillation and was defibrillated 4 times, unsuccessfully.  After a few minutes of manual chest compressions, the LUCAS device was applied.  Due to jaw clenching, he could not be intubated and so was ventilated with bag-valve-mask.  He received 1 mg of epinephrine and 300 mg of amiodarone and still could not be defibrillated. 

On arrival in the ED, he was in full arrest and undergoing LUCAS CPR.  He had been in arrest for 30 minutes at this point.  O2 saturations were 70% with a waveform.  He was given succinylcholine and intubated and the inspiratory threshold device (ResQPod) was attached to the end of the tube.  Slow ventilations were guided by the timing light on the ResQPod.  Continous cardiac ultrasound revealed good cardiac contraction with each compression.  CPR was very briefly held and the rhythm was ventricular fibrillation with no ultrasonic cardiac activity. 

He was given 1 mg of epinephrine, 3g of calcium gluconate, 100 mEq of bicarb, and 100 mg of lidocaine.  At approximately 40 minutes (10 min in the ED), a 2nd mg of epinephrine (6th overall) and 2 mg of MgSO4 were given.  The monitor confirmed V fib and he was defibrillated again, with conversion to sinus rhythm.  The LUCAS was paused.  There was good cardiac activity on ultrasound and strong pulses. 

With successful return of spontaneous circulation, the cath lab was activated based on the presumption that this would be a coronary event (a greater than 50% probability even without a 12-lead ECG).

A 12-lead ECG was obtained:

Sinus tachycardia.  The QRS is very wide, with a right bundle branch block (RBBB).  The initial r-wave is replaced by a Q-wave in V1 and V2.  There is also left anterior fascicular block.  New RBBB + LAFB is a very bad combination and suggests a huge STEMI, either proximal LAD or left main.

Is there ST elevation in addition to RBBB and LAFB?  To find out, you must find the end of the QRS.  In this case, it is best seen in lead V1, and if you draw a line down to lead II, which is across the bottom of the tracing, you can establish the end of the QRS in II.  Then you can find the end of the QRS is every lead, as below:

This is very similar to a case I posted a couple years ago (one of the most read posts of all time).  You can see that in leads V2, V5, and V6, as well as leads aVR and aVL, there is ST elevation. There is reciprocal ST depression in leads II, III, and aVF.

Case continued:

He had return of ventricular fibrillation immediately after the ECG was recorded (total time in regular rhythm was 2 minutes.)  LUCAS was restarted.  100 mg lidocaine was given.  Defibrillated again, no response.  100 mEq of bicarbonate, 40 U of vasopressin, 1 mg of epinephrine were given.  LUCAS was held briefly and there was wide complex pulseless electrical activity with no cardiac activity seen on ultrasound.  Then the patient reverted to V Fib again.  He was defibrillated again into sinus for only a few moments, then V Fib again.

At this point we realized we were dealing with incessant ventricular dysrhythmias, also known as "electrical storm," a condition seen almost exclusively during severe ischemia/STEMI.  We have had previous success with beta blockade using esmolol (which is short acting and can be turned off if it results in cardiogenic shock), so we gave 40 mg (500mcg/kg) of esmolol in a bolus, and started a 4 mg/min drip (50 mcg/kg/min).  We gave another 3 g of calcium, 1 mg of epinephrine, and 1 mg of atropine. 

A venous blood gas returned: pH = 7.05/pCO2 = 101/pO2 = 25 (venous, remember)/HCO3 = 27.  A lactate returned at 12.8 mEq/L.  Another 50 mEq of bicarb was given.  The patient was defibrillated again after 38 minutes in the ED, and 68 minutes since his arrest.  He converted to sinus.  LUCAS was held.  Cardiac ultrasound showed function with poor ejection fraction.  Therapeutic hypothermia was started. 

A repeat ECG was recorded while waiting for the cath team to arrive:

It appears to be a junctional rhythm at a rate of 55, with one PVC.  Now the anterolateral STEMI is clearly seen.  Interestingly, the ST elevation in V1-V3 is best seen in the PVC, with proportionally excessively discordant ST elevation (ST/S ratio V2 = 4/7 = 0.57, V3 = 4.5/14.5 = 0.31)

He was given aspirin and heparin and taken to the cath lab where a proximal LAD occlusion was opened.  A balloon pump was placed.

There were difficult critical care issues with  shock, low systemic vascular resistance and poor cardiac output, as well as pneumonia. Next day ejection fraction was 25% and peak troponin I was 250 ng/ml.

48 hours after arrest, he was awake and following commands. Within a few days, his wife could not tell any difference from his baseline functioning.  There was complete neurologic recovery.

His ejection fraction 3 months later is 40% and he is able to go 14 minutes on the Bruce protocol stress test (most normal people cannot even do that).  He will be back to work shortly.



Dr. Brian Driver, 4th year emergency medicine/internal medicine resident at Hennepin County Medical Center, gathered a 5-member panel to discuss: Cardiac Arrest: New Innovations and Best Practices.  

Panel members:

• Dr. Brian Mahoney, HCMC EMS director and HCMC site investigator of the ResQTrial.  HCMC EMS has among the highest resuscitation rates in the country (2010 Utstein number, before use of LUCAS, = 49%, overall resuscitation success = 17%)
• Dr. Demetris Yannopoulos, is an interventionalist at the University of Minnesota and is also a prolific cardiac arrest researcher at Minneapolis Medical Research Foundation (MMRF).  He and Dr. Keith Lurie do some amazing work in that laboratory.
• Dr. Mark Sprenkle, of the Division of Pulmonary and Critical Care Medicine at HCMC
• Dr. Gautam Shroff, staff Cardiologist, HCMC
• Dr. Steve Smith of Dr. Smith's ECG Blog and staff emergency physician at HCMC

Dr. Driver wrote this concise summary of the panel discussion:

This case is from my friend Pierre Taboulet, who graciously allowed me to re-post it here.  He has a fantastic EKG site for anyone who reads French, and also a great ECG book (written in French).  He is a cardiologist who practices Emegency Medicine in Paris.

Here is his site: http://www.e-cardiogram.com

What is the diagnosis?  Hint: the T-wave inversions are co-incidental, nonspecific, and not related to the diagnosis.

The image comes from this page. 






This is a translation of Pierre's interpretation: Sinus rhythm.  AV conduction is abnormally short with a PR interval of 80 ms.  As there is no visible pre-excitation (e.g., no delta waves).  The short PR may be due to atrionodal fibers of James or to atrio-HIS fibers ("fibers of Brechenmacher").  This is otherwise known as Lown-Ganong-Levine syndrome.  This anomaly leads to re-entry and episodes of SVT.

Explanation

I a relative novice in these conditions, and have paraphrased and distilled what I think are the essential elements (as I understand them) of a long and excellent article from the outstanding online textbook UpToDate (which needs a subscription).

Lown-Ganong-Levine (LGL) syndrome has a short PR interval, narrow QRS (without pre-excitation), and episodes of palpitations or SVT.  The mechanism of the short PR interval is uncertain, but is most likely due to faster AV nodal conduction, probably due to rapidly conducting fibers in the AV node.  Alternatively, as indicated by Dr. Taboulet's interpretation above, there may also be atrial-HIS fibers known as Brechenmacher fibers that bypass the AV node. Although the syndrome requires palpitations or SVT, it is uncertain if the tachycardia associated with LGL is due to re-entrant dysrhythmias.  

Enhanced atrioventricular nodal conduction (EAVNC) is another condition with a short PR interval, and as I understand the article, can only be distinguished from LGL by electrophysiologic testing.  [K. Wang writes that EAVNC is sometimes called the "greasy AV node."]   It was formerly confused with Lown-Ganong Levine.

Both syndromes have been found in association with dual AV nodal pathways (which is the anatomic substrate of AV nodal re-entrant tachycardia - AVNRT) and also with concealed accessory pathways (which are distinct and separate from the fast nodal fibers and which is the substrate of AV reciprocating tachycardia - AVRT).  Since a delta wave, by definition, precludes the diagnosis of LGL, only EAVNC has been seen with an overt (unconcealed) accessory pathway.  The most common arrhythmias in these syndromes are re-entrant SVTs (intranodal or orthodromic through a bypass tract).  However, the incidence of  these arrhythmias is not clearly higher than it is in patients without these syndromes (my comment: and there seems to be no clear anatomic reason why they should be).

Furthermore, although the incidence of AVRT may not be higher in these syndromes than in those without them, the heart rate is higher in those who have it because both limbs of the re-entrant rhythm (the fibers specific to LGL or EAVNC which allow rapid conduction through the AV node and the accessory pathway) can conduct rapidly.  Thus, AVRT may be more dangerous in these conditions.  [This does not apply to AVNRT because both limbs of the dual AV intranodal pathway are slow and you would need at least one to be fast in order to have a very fast loop.]

On the other hand, atrial arrhythmias can result in very fast tachycardias in the presence of LGL or EAVNC, as they can be conducted to the ventricles much faster than through the AV node.  Thus, atrial flutter or fibrillation, or atrial tachycardias, can have very fast ventricular rates (similar to atrial fibrillation with WPW), and can result in dangerous ventricular dysrhythmias.


 References

A 78 yo male had a syncopal event and complained of chest pain.

Here are 9 prehospital ECGs during transport:

0 minutes, nondiagnostic

4 minutes, inferior STEMI (subtle).

5 minutes, reperfused, barely shows on the ECG

7 minutes, almost normal again.

15 minutes, more obvious

16 minutes, more obvious, NTG given here

22 min, with V4R, STE gone after NTG and Aspirin

23 minutes, very subtle, resolving

29 minutes, almost entirely resolved

The cath lab was activated prehospital and the patient received an RCA stent and an LAD stent, had a minimal troponin rise, and did well.

This shows how acute coronary syndrome is very dynamic, with arteries opening and closing.  Studies using continuous 12-lead monitoring show that this happens even in the abscence of chest pain.

Here is an interesting case just presented in a conference today.  Thanks to Dr. Simegn, Asinger, Davies, and Bart for their input.

A 69 yo previously healthy woman had very sudden severe dyspnea.  The husband at some point reported that they had been physically active that day, and that the patient had complained of some chest pain one week prior for which she did not take his advice to go to the ER.  She presented in pulmonary edema, hypoxic on high flow O2, and sats were above 90% on Noninvasive Ventilation.  BP was 130/70.  Cardiac physical exam was unremarkable except for very coarse breath sounds. ABG was 6.99/44/201/11 on BiPAP.  Here is her first ECG:

The rate is 143.  There are p-waves, but in lead II there are apparently 2 p-waves for every QRS.  I have measured these with calipers, and they are exactly spaced, so it appears to be atrial flutter.  The second apparent p-wave comes immediately after the QRS and appears to simulate ST elevation (Atrial flutter can frequently mimic ST deviation).   There are also inferior Q-waves with T-wave inversion.   (In fact, there is S1Q3T3).  There is precordial ST depression which could represent subendocardial ischemia from severe tachycardia, hypoxia, etc, or it could be due to inferior posterior STEMI.

What else would sway you to decide whether this is atrial flutter or sinus tachycardia?  Are the notches after the QRS in the limb leads ST segment deviation, or are they flutter waves?  Is this patient having a STEMI?


Considerations include:
1. Lead V1.  In sinus rhythm, the latter part of the p-wave in V1 is always negative, as it represents the depolorization of the left atrium, which is depolarizing away from lead V1.  In atrial flutter, the p-wave in V1 is usually upright.  Here it looks like a normal p-wave.  Furthermore, you don't see an identical wave directly between the p-waves and given that the baseline is pretty steady, it should be there.
2. If flutter, the rate should remain constant in spite of supportive care.

A right sided ECG was recorded 6 minutes later:

The rate is still exactly 143.  Does this confirm atrial flutter?

A bedside echo showed hyperdynamic function and a large RV.  The chest X-ray showed pulmonary edema.  The patient's respiratory status deteriorated and she was intubated.

Step back: what caused sudden respiratory failure with pulmonary edema? 
--Does acute inferior-posterior STEMI alone do this?  Not if the pump function is hyperdynamic.  
--Does atrial flutter alone cause severe pulmonary in someone who was previously healthy?  No.  (However, if this is atrial flutter, it is wise to cardiovert and this can only help the situation.  This was not done.  It appears that the rhythm diagnosis of atrial flutter was not considered.  If it is sinus, cardioversion will not hurt.)
--Does massive pulmonary embolism cause pulmonary edema?  Rarely, if ever.

A CT pulmonary angiogram was negative.

What test is now indicated?  What is the likely diagnosis?

Another ECG was recorded:

Now the rate is down to 120 and it is clearly sinus.  The p-waves are identical to those in the first ECG.  So those, too, were sinus.  Which means the waves after the QRS were indeed ST elevation and depression. There is inferior T-wave inversion and the upright right precordial T-waves are indicative of reperfusion to the posterior wall as well.  There is an infero-posterior STEMI of unknown age.

An otherwise healthy woman in her 20's presented with tachycardia.  She had experienced palpitations and called 911.  Prehospital rhythm strips were at a rate of at least 200 (unavailable) and the medics gave adenosine at both 6 mg and 12 mg with no effect.  She was very stable with no CP, SOB, hypotension or evidence of shock.

Here is the initial ED ECG:

What is the diagnosis (this is pathognomonic)?  See below.  (Notice that the computer incorrectly read ***Acute MI***)

1. The rhythm is irregularly irregular, therefore it is atrial fibrillation
2. The complexes are wide (so one might think of atrial fibrillation with aberrancy, in which case you should see RBBB or LBBB pattern, which is not there)
3. It is very fast (200 bpm)
4. The shortest R-R interval (between complexes 12 and 13) is about 240 ms (very short)
5. The complexes look bizarre and are not uniform, as they would be with simple aberrancy.  Thus, these represent differentially pre-excited ventricular myocardium.

This is atrial fibrillation in the setting of WPW, and is a dangerous rhythm which can degenerate into ventricular fibrillation.  It is more likely to degenerate if the physicians gives AV nodal blocking drugs, especially calcium channel blockers.

Here is another example of this.

How should this be managed?  It can be managed with medications that convert atrial fibrillation to sinus, such as procainamide or ibutilide (and others), but when you have a wide complex very fast tachycardia, it is best to use electrical cardioversion.  It is the safest, and keeps you from having to make a definite diagnosis.   As long as you can manage procedural sedation, which is very easy in the case of cardioversion because you only need seconds of sedation and amnesia, then cardioversion is the safest method.

The pattern was not recognized as pre-excitation, but as atrial fib with aberrancy.  These were very smart and very experienced physicians, but anyone can make a snap judgment followed by premature closure, and this is another reason why electricity is the safest - you don't need to have the correct diagnosis).  Subsequently, the physicians gave the patient first diltiazem and then esmolol, with no ill effect but also little beneficial effect.  It could have resulted in degeneration to ventricular fibrillation.  AV nodal blockade is particularly dangerous when there is a shortest R-R interval of less than 250 ms (as here), and especially if less than 220 ms.  Adenosine is also contraindicated. 


After dialing up the esmolol, the patient spontaneously converted to NSR and had the following ECG:


After conversion:

Sinus rhythm with short PR interval and large delta waves seen best in precordial leads, and confirming Wolff Parkinson White (WPW) syndrome of pre-excitation down an accessory pathway.  There can be positive, negative, or isoelectric delta waves depending on their own axis.  WPW may greatly change both depolarization (in this case with large upright R-waves in right precordial leads because the accessory pathway is left lateral, depolarizing the ventricle from left to right) and repolarization (see these cases for acute MI mimics due to WPW)

Followup, and what is "Concealed Conduction"?

Her charts revealed 3 previous visits for palpitations, and in all cases the ECG was interpreted as normal.  Here is one of them:

There are very subtle delta waves which I do not believe I would have noticed propectively, but in retrospect look to be real.  The computer read a QRS duration of 106 ms which is borderline long and due to these subtle delta waves.  The PR interval is normal because the delta waves are so minimal.

This is concealed conduction, or nearly concealed.  That is to say, the presence of an accessory pathway is not evident (at least to most observers) on the baseline surface ECG.  (There are times when it is truly concealed, and there are no delta waves even in retrospect).  It is important to know about concealed conduction so that if you suspect WPW as a cause of tachycardia that is now resolved, you will not rule out the diagnosis by a normal baseline ECG.

There are two mechanisms of concealed conduction:

1. Conduction through the accessory pathway is retrograde only (mechanism unclear)
2. The impulse reaches the AV node and gets through to the ventricles before it gets to, and through, the accessory pathway.

The second mechanism applies in this case: Look at the first two ECGs above (those with abnormal conduction). Notice that the R-wave in V1 is very large, as it would be in RBBB.  This is because the impulse is going down a left lateral bypass tract and then proceeding through the myocardium from left to right, resulting in a large R-wave in V1.  Thus, the bypass tract (accessory pathway) is to the left lateral of the left atrium, which is far from the sinus node (right part of right atrium).  When the AV node is conducting fast (such as with anxiety, low vagal tone, high catecholamines, etc.), then the impulse gets to and through the AV node and through the Purkinje system before it makes it down the accessory pathway and therefore there is no (or minimal) delta wave.  On the other hand, if the AV node conduction is slower, then the delta waves will  be evident.

However, even in WPW with concealed conduction, the accessory pathway is always available to cause trouble!  

In both types of concealed conduction, it can result in orthodromic reciprocating supraventricular tachycardia (re-entrant down through the AV node and up through the bypass tract), and this cannot be differentiated from intranodal reentrant (standard) SVT on the surface ECG.

In the second type of concealed conduction, it can result in three abnormal rhythms: First, there can be orthodromic re-entrant reciprocating tachycardia.  Second, there can also be antidromic re-entrant reciprocating tachycardia (which is a regular wide complex tachycardia). And third, if atrial fibrillation develops, then it will manifest as this dangerous wide complex tachycardia.

Why did she not have concealed conduction on the post conversion ECG?   --Because she had received AV nodal blockade with diltiazem and the pathway down the AV node was slow.

Zero hours.  There is STE in V1 and V2, and ST depression in I, aVL, V5, and V6.  Is it normal variant STE?  Or is it anterior STEMI?  As in a recently posted case, ST depression in the lateral leads should not be seen in normal variant STE.  Because of this ST depression, STEMI should be diagnosed until proven otherwise, and the STE equation should not be used; if it were used, with STE60V3 = 2, QTc = 412ms, RAV4 = 20mm, the value would be 20.18 (less than 23.4 would indicate normal variant).  The equation is falsely negative because most of the ischemia is in the septum, not the anterior wall, so that STE in V3 is not high and R-wave amplitude in V4 is not affected.

In this case, there was a previous ECG to compare with (and the patient's last echocardiogram was totally normal as well)

Previous ECG had no ST elevation or depression.  This confirms that the STE is new ischemia and that this is STEMI.

The STEMI was not recognized, the patient was put on a nitroglycerine drip (as well as aspirin, heparin, and clopidogrel), and pain continued.  A subsequent ECG was recorded at 1 hour:

1 hour.  The T-waves in V1-V3 are inverting and in V4-V6 are flattening.  This is some evidence of reperfusion; is it Wellens'?

The ECG has the appearance of Wellens' waves, but the patient is not pain free, so it is not Wellens' syndrome.  Continued pain in the context of definite ischemia is an indication for urgent angiography and PCI.

The patient was still having pain after up-titration of nitro when this ECG was recorded at 2.5 hours after presentation:

2.5 hours.  Wellens' waves are evolving.

Rather than going urgently to the cath lab, an immediate echo was recorded, which showed moderately decreased LV function with an EF of 40%, and a new wall motion abnormality of the distal septum, anterior, and inferior walls, and apex.

The patient was taken for angiogram which showed total occlusion of a type III (wraparound) LAD at the takeoff of a large 1st diagonal.  However, the LAD was filling via left to left and right to left collaterals.  The LAD was opened and stented.

The troponin I peaked at 40 ng/ml.  The collateral circulation explains the Wellens' waves, but it did not fully restore perfusion and so the patient had continued pain.  Collateral circulation was likely fostered by nitroglycerine.

Here is the ECG after intervention

Full evolution of Wellen's waves to "type B" deep symmetrical waves.

What do you think of this ECG?  What do you think the angiogram showed?

Due to the obvious ST elevation, he was given tPA (it was a small rural hospital) and the ST elevation quickly resolved.  The patient had bradycardia, heart block, and hypotension. He was intubated, externally paced, and started on pressors.  There was no pulmonary edema.  What is going on?  See below for answer.















This appears to be a right sided ECG, as the R-waves in I and aVL are not present in V5 and V6 (sorry, I don't have the left sided one).

There is an S-wave in lead I and very large R-waves in V1R to V3R.  As there is an rSR' in precordial leads, is this right bundle branch block?  This is a bit uncertain because lead I appears to have normal QRS duration, but V4R to V6R appear wide.  In any case, is there right  ventricular hypertrophy?  It is difficult to make a diagnosis of right ventricular hypertrophy in the presence of RBBB because both cause an S-wave in lead I and a large R'-wave in V1.  However, in this case the R'-wave in V1-V3 is far larger than with a normal RBBB.  In any case, the R' wave is very large, diagnostic of RV hypertrophy.

ST elevation: There is ST elevation in II, III, aVF with reciprocal ST depression in aVL (inferior STEMI), and ST elevation from V1R to V6R (right ventricular STEMI).  Angiogram showed subtotal occlusion of proximal RCA.  Wedge pressure was 18 (low for a patient in cardiogenic shock).  Echocardiogram showed severe RV hypertrophy with very poor RV function and good LV function but poor LV filling pressures.  It was later discovered that the patient had a history of pulmonary fibrosis and pumonary hypertension.  ST elevation was due to right ventricular STEMI in the setting of severe right ventricular hypertrophy.

This was sent to me by a reader named Aaron.

A 36 yo male smoker presented to the ED with chest pain.  It had started the night before as "indigestion" and had progressed to 8/10 substernal chest pressure radiating to the right shoulder/jaw associated with diaphoresis, nausea, and SOB.

Sinus rhythm.  There is ST elevation in V1 (of 3.0 mm at the J-point), V2, aVR (1 mm, no matter how it's measured), and V4R (1.5 mm at J-point, 2.5 at 60 ms after the J-point), and very subtly in lead III.  There is reciprocal ST depression in I, II, aVL and V4-V6, as well as some very subtle STD in posterior leads V8 and V9 (which also have very low QRS voltage)

Here is his initial ECG, which the tech recorded as a 15-lead ECG (the doctors were not sure why):


Thus, there is a rightward, anterior, and slightly superior ST axis.

Here is a map of leads V1, V2, and V4R.  This is traced off a an actual MRI.

I did not label V8 and V9, but they would be on your left behind the lung.  You can see how V1, V2, aVR, and V4R would have ST elevation in either a right ventricular STEMI or with a septal STEMI, and how lateral leads, and even posterior leads, would have reciprocal ST depression.

The combination of precordial ST elevation and ST depression, simultaneously, should alert you to LAD occlusion.  This is frequently seen when there is LV septal involvement.  STE in V4R is confirmatory evidence.   In my early repolarization/anterior STEMI study, I excluded any ECG with any precordial ST depression, considering this to be diagnostic of STEMI because normal variant precordial ST elevation does not coexist with simultaneous precordial ST depression.
  
In this case, the emergency physicians were somewhat puzzled, and the interventionalist was highly skeptical, but took the patient to the cath lab and found an occluded LAD.   It is possible that there was also RV involvement - see explanation below.     


Here is another similar case.


In a 1999 study by Engelen et al. of patients with anterior STEMI, ST elevation of greater than or equal to 3.0 mm in lead V1 was 100% specific (but only 12% sensitive) for septal STEMI.  Smaller degrees of STE in V1 were not nearly as specific.  See more on STE in aVR in anterior STEMI, below.


STE in V4R
Interestingly, here is a paper (published as a letter) describing the results of recordings of V4R in 117 consecutive LAD occlusions and showed that this was associated with septal involvement and also higher risk.

In this study, 39 (33%) had STE of at least 1 mm (at 80 ms after the J-point) in V4R.There were no significant differences between the groups regarding indexes of infarct size.  None of the patients with STE in lead V₄R had echocardiographic evidence of right ventricular dysfunction or dilated right ventricles.  Only the middle anteroseptal segmental wall motion abnormality was significantly and independently associated with STE in lead V₄R. The odds ratio for akinesis (or more severe motion abnormality) was 6.1 (p = 0.036) and for hypokinesis (or more severe motion abnormality) was 12.0 (p = 0.033).  Patients with STE in V4R were more likely to experience the combined end point of primary VF, acute HF, or death (54% vs. 18%) and were also more likely to experience primary VF (21% vs. 2.5%)  and acute HF (39% vs. 17%). In multivariate analysis, STE in lead V₄R on admission electrocardiography remained a strong independent variable associated with acute HF and the combined end point of primary VF, acute HF, or death during hospitalization. 

What does ST depression in V5 and V6 signify? 
This paper addresses this for inferior STEMI, but is relevant here also, I think because it shows how V5, and V6 are reciprocal to V4R, and ST elevation on one side will lead to ST depression on the other:
http://www.cinc.org/Proceedings/2005/pdf/0651.pdf.   In this study of RV MI associated with inferior STEMI, ST depression in V5, V6 had 46% sensitivity and 96% specificity for proximal RCA occlusion.  Sensitivity increased to 58% with a small drop in specificity if STE in V4R was added.   Why are V4R and V5, V6 so insensitive for proximal RCA occlusion?  Would this not always cause RV infarction?  In fact, no.  This is because, in many patients, the RV is supplied by both the LAD and the RCA.  Therefore, the RV is often protected from RCA occlusion by the LAD.  Conversely, LAD occlusion could possibly lead to RV infarct if it is not adequately supplied by the RCA.  Autopsy studies in the '80s by HR Andersen showed this: JACC 1987l10:1223-32 and Br Heart J 1989;61:514-20.  This study used MRI to show the LAD supply to the RV.


How about STE in aVR?
Below is from a quote from part of a piece on aVR which I wrote for Current Emergency and Hospital Medical Reports: "Updates on the electrocardiogram in Acute Coronary Syndromes." DOI 10.1007/s40138-012-0003-1, published online Dec. 23, 2012.

STE in aVR in STEMI 
Not NonSTEMI: STE in aVR during left main ACS is usually NonSTEMI (no occlusion). 





 

When the patient had chest pain, prior to nitroglycerine, what do you think the ECG showed?  See below.














Here is the prehospital ECG, with pain:



Hyperacute anterolateral STEMI


The medics had activated the cath lab and the patient went for angiogram and had a 95% stenotic LAD with TIMI-3 flow.  A stent was placed.

Here is the 3 hour post angio ECG:



The Wellens' waves are receding (this is unusual)

 The next AM, another ECG was recorded:



The Wellens' waves are still present, and not evolving

 A transthoracic echo was entirely normal.  The peak troponin I was 0.364 ng/ml.

The reperfusion was so early that wall motion recovered completely and early.  

For those who depend on echocardiogram to confirm the ECG findings of ischemia, this should be sobering.  I have seen cases of Wellens' syndrome that were ignored because of either negative troponins or normal echo or both and the patient did not get an angiogram and had a bad outcome.

Wellen's syndrome is a Reperfusion syndrome.  All of Wellens' cases in his studies (1, 2) had all of:
1) preserved R-waves
2) resolution of pain
3) restored flow to the anterior wall through either
     a) an open artery or
     b) collateral circulation.

This is a rare case in which we can prove that the Wellens' waves represent spontaneous reperfusion because we recorded a prehospital ECG during pain.  Such a mechanism is supported by the work of Doevendans (3) and Wehrens (4), who both described terminal T-wave inversion (which have the same morphology as Wellens' waves) as the earliest sign of reperfusion from reperfusion therapy.  (I don't know that this connection has ever been formally written about in any original literature, though I have long maintained that this is the pathophysiology of Wellens' waves.)

In my experience, all Wellens' with significant myocardial infarction have evolution from type A waves to type B waves over 6-24 hours' time, so that the presence of type A or type B waves, I believe, are simply a matter of the timing of recording and the rapidity of evolution.  In this case, the duration of ischemia was so brief that there was no such evolution, and there was near-normalization.  When there is extremely brief ischemia, as in this case, or this case, it may entirely reverse, especially in unstable angina (negative troponins).

Lessons:
1. Wellens' syndrome represents a state of reperfusion of the infarct related artery
2. Ischemia may be so brief that Wellens' waves do not evolve
3. Ischemia may be so brief that troponins are borderline or normal
4. Ischemia may be so brief that wall motion normalizes



1. de Zwaan C., Bar F.W., Janssen J.H.A., et al. Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. Am Heart J (1989) 117 : pp 657-665.
  2. de Zwaan C., Bar F.W., Wellens H.J.J., Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J (1982) 103 : pp 730-736.   3. Doevendans P.A., Gorgels A.P., van der Zee R., et al. Electrocardiographic diagnosis of reperfusion during thrombolytic therapy in acute myocardial infarction. Am J Cardiol (1995) 75 : pp 1206-1210.

4. Wehrens X.H., Doevendans P.A., Ophuis T.J., et al. A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty. Am Heart J (2000) 139 : pp 430-436.

A male in his 60's with med h/o only significant for HTN and hyperlipidemia presented for CP and SOB.  On the day prior, he became very SOB and felt like he was going to pass out when he tried to stand up from bed.   This was accompanied by chest heaviness  and followed by left chest pain and a stiff sensation in his neck.  The pain progressed but he went to bed but awoke in the AM with a heavy and "throbbing" chest.  VS were: 122/92, pulse 82, RR 18, O2sat (room air) = 95%  Here is his initial ED ECG:

What is the Diagnosis?

The first troponin returned at 0.092 ng/ml (99% reference 0.034). 


Does the elevated troponin confirm ACS? 


There are both precordial T-wave inversions AND T-wave inversion in lead III.  this is highly suggestive of pulmonary embolism.  There is also S1Q3T3 (this post helps to explain its significance). 

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with APE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

See this post for more detail on the ECG in pulmonary embolism. 

Still more cases are here.


The patient was treated for NonSTEMI, including ACS dosing of heparin and including nitroglycerin, which could be hazardous in pulmonary embolism.  He was admitted to cardiology where he immediately underwent an echocardiogram, which showed RV strain, alerting the clinicians to PE.  A CT pulmonary angiogram confirmed multiple pulmonary emboli.

Strangely, there is no tachycardia and the patient was not on beta blockers.

Lessons:

1. Chest pain with a positive troponin may be due to many causes, not just ACS.  Always consider these. 
2. Precordial T-wave inversion, along with a negative T-wave in lead III, should alert you to the strong possibility of pulmonary embolism.

Sinus rhythm.  ST elevation in I, aVL, V5, V6, with ST depression in V2-V4, diagnostic of posterolateral STEMI.  There are peaked T-waves in V2-V4

A woman in her 50's with multiple medical problems including DM and HTN and Mitral Valve replacement was at home when she began having shortness of breath, substernal chest pain, and diaphoresis for approximately 20 minutes, then called paramedics.

A prehospital ECG was recorded:


Nitroglycerine was given and the pain resolved, as did the ECG (not shown).  On arrival in the ED, she had this ECG recorded:

ST deviation is resolved, but peaked T-waves remain.  QRS duration is 94 ms

On further questioning, the patient then reported that earlier in the day, she was experiencing "cramps" in her chest and abdomen, and took "a bunch" of potassium supplementation (reasoning not certain here).  She was treated for hyperK and the K returned at 8.7 mEq/L.

She did not go to cath.  A workup 6 months previously had an echo with anterolateral and inferior wall motion abnormalities as well as an adenosine sestamibi with reversible inferior and lateral tracer uptake (positive) but at angiogram there had been no significant stenosis (though the degree of minor stenoses and soft plaques was not commmented upon).  The cardiologists had diagnosed her with coronary spasm.

She did undergo another echocardiogram at this visit, which was not different from the previous.

Troponins I (OCD Vitros):

Zero hour: undetectable
3 hours: undetectable
6 hours: 0.024 ng/ml (99% reference = 0.034)
10 hours: 0.018
14 hours: undetectable

These are consistent with unstable angina: a rise and fall with no value exceeding the 99% reference value.  ST elevation may be so brief that it does not result in positive troponins, but a rise and fall profile like this is diagnostic of ischemia in the appropriate setting.

Is she having coronary spasm, or are there nonobstructive coronary plaques that are unstable?  This remains uncertain.

For a related tragic case, click here.

A child between the ages of 5 and 10 was restrained in a motor vehicle collision and sustained multiple chest injuries.  Therefore, an ECG was recorded:

There is sinus rhythm.  The axis is about -50 (left axis), whereas normal for this age is 0 to +90.  So there is left axis deviation.  In V1, there is a tiny r-wave, followed by an s-, an r-, and an S' wave.  Normally there is an RS-wave, and at age 8 the S-wave is more prominent, as in adults.  The QRS duration is 102 ms, which is long for this age (normal, 80-85 ms, see:  Rijnbeek PR.  European Heart Journal (2001) 22, 702–711.  Thus, there is an abnormal conduction delay.  This is probably an atypical RBBB, given that there is an rsrS'.   Furthermore, R-wave progression in children is much earlier than in adults, so the R-wave in V2 should be more well developed.  There are no apparent repolarization abnormalities (ST elevation, depression, or T-wave inversion)  The QTc is 373 ms.

Thus, the ECG is abnormal, and this prompted a troponin measurement, the initial one of which was normal.  The 6-hour troponin was the first detectable and first positive one at 0.044 ng/ml (Ortho Clinical Diagnostics, 99% reference = 0.034 ng/ml).  Serial troponin I  peaked at 0.927 ng/ml. 

A transthoracic echocardiogram showed thinned and dilated right ventricle with poor function and some tricuspid regurgitation. 



A followup ECG 36 hours later was recorded:

The QRS is still prolonged (106 ms) and there are new repolarization abnormalities (T-wave inversion).  The QTc is 396 ms.

Echo was repeated due to the ECG changes and troponin elevation and this showed less tricuspid regurgitation.  There was RV dilation and significant thinning of the apical RV freewall which was akinetic and moved paradoxically.  There was a very small amount of pericardial fluid (blood?--uncertain). There was also some abnormal movement of the septum.

An ECG was recorded at t = 60 hours:

QRS is 107 ms and QTc is 486 ms.  There is bizarre T-wave inversion.

This child did well in the hospital, with no hypotension, tachycardia, or dysrhythmias, and the child was transferred to the care of a pediatric cardiologist.  This is essential, as myocardial contusion with ECG abnormalities can have disastrous outcomes.  See this tragic case.

For a nice review article by Bill Brady on the normal pediatric ECG, look here (full text pdf).

A male in his 40's with no previous cardiac history had presented to a clinic recently with chest burning, had a nondiagnostic ECG, and was diagnosed with reflux. He presented to an ED with 2.5 hours of chest burning a few days later.  His BP was 152/84.  Here is the initial ECG:

Sinus rhythm,  Q-wave in III with minimal ST elevation and minimal ST depression in I and aVL.  There is a suspiciously minimally biphasic T-wave in V6.  This is a nonspecific ECG.

The ECG from the clinic was sought for comparison:

Compared to this one, the ST depression in I and aVL seen above is new and T-waves are nonspecifically different in diffuse leads.

The patient continued to have chest pain of an ischemic quality. The clinical presentation worried the ED physicians, so they performed a bedside ultrasound (parasternal short axis view):


Cardiac Ultrasound Parasternal Short Axis from Stephen Smith on Vimeo.

The curved white line shows the wall (lateral) which has hypokinesis

The wall motion abnormality confirms that these nonspecific T-wave changes are indeed ischemic.  The chest pain is therefore ischemic.  The physicians attempted to control the pain with nitroglycerine, both sublingual and intravenous, titrating to 60 mcg/min, and BP down to 100/57.  Thus, they were trying to treat this "NonSTEMI" medically, as there was no ECG indication for immediate reperfusion therapy.

They recorded a posterior ECG:

Leads "V4" to "V6" are really V7 to V9.  Note the low voltage of posterior QRS because of more distance from the heart and because of air (lung) between heart and ECG leads.  Thus, only 0.5 mm in 1 lead is considered posterior  STEMI.  Here there is no ST elevation.  However, leads V2 and V3 are the same as the first ECG and the T-waves show are not very different.  Thus, the patient has dynamic T-waves.

The echo and dynamic T-waves confirm ACS.  Definite ischemic pain which is refractory to medical therapy is an indication for reperfusion therapy.  It is important to remember that approximately one third of NonSTEMI have an occluded infarct related artery at cath.

Heparin and Clopidogrel were given and the patient was taken to cath (after which the first troponin returned slightly elevated).  He was found to have severe LAD disease and an occluded 1st Obtuse Marginal off the circumflex.  This was opened and stented.  The troponin I (Ortho Clinical Diagnostics) peaked at 45.8 ng/ml (quite high).   Formal echo later showed anterolateral hypokinesis and an EF of 55%.

The artery was occluded and the myocardial territory at risk was very significant, yet the ECG did not have diagnostic ST elevation.  This is common.  Fantastic management led to rapid therapy and salvage of significant myocardium.

A man in his 70's called 911.  When medics arrived, he was in extremis with respiratory failure, able only to say he has a history of CHF.  He arrived in the ED and had pink frothy sputum, was intubated, and had the following ECG:

There is sinus tach with left bundle branch block (LBBB).  There is excessively discordant ST elevation in leads V1 and V2.  The highest ST/S ratio is in V1, with a ratio of 8/30 = 0.27, highly suggestive of LAD occlusion.

In our study of coronary occlusion in LBBB, we excluded patients with severe hypertension, extreme tachycardia, respiratory failure and pulmonary edema for 2 reasons: 1) they often have false positive ECGs and 2) they need critical care in any case, with or without angiography.  So, although this patient has excessive discordance, it is not necessarily due to coronary occlusion.  In this case, the very high voltage suggests LVH, as does excessively discordant ST elevation confined to leads V1 and V2. 

The cath lab was activated.

After intubation, the BP was 120/70, there was a combined respiratory and metabolic acidosis, and further exam revealed absence of peripheral edema.  The patient was put on a nitro drip.  A bedside echo showed probable anterior, apical, and septal wall motion abnormality, but this is very difficult to interpret by the non-expert because of the dyssynchrony caused by the abnormal activation sequence in BBB.  

The patient was regaining hemodynamic stability and a repeat ECG after supportive care (cannot be found) showed much less ST elevation.

At angiogram, there was no acute culprit lesion, though there was some CAD and a chronic occlusion of the first diagonal.  The troponin I peaked at 10 ng/ml and the post cath ECG was recorded:

Now the highest ST/S ratio is still in V1, but is 4/35 = 0.11.  0.11 is the normal mean maximum ST/S ratio for leads V1-V4 in our control group.  So this discordant STE is now entirely normal.


At cath, there was a low left ventricular end diastolic pressure (LVEDP) at only 6 mmHg, indicating that whatever insult caused the pulmonary edema has rapidly resolved.  Then the pulmonary edema also rapidly resolved.  Subsequent formal echo showed concentric LVH, questionable anterolateral and inferior wall motion abnormalities, dyssynchrony from BBB, and EF of 37%. 

The patient did very well and was extubated the next day.

So what happened?

Was the excessive discordance on the ECG due to physiological stress of respiratory failure, pulmonary edema, tachycardia, and hypoxia (severe demand ischemia), or was there another inciting factor?


It might be better to ask: what initiated the pulmonary edema? 


1) Was it fluid overload leading to pulmonary edema, then a worsening cycle of fluid retention, catecholamines, and vasoconstriction?  Unlikely because of the absence of edema and the low LVEDP.  LVEDP caused by fluid overload does not resolve rapidly.

2) Was it transient ACS with transient ischemia, resulting in poor LV function, then temporarily high LVEDP, then pulmonary edema., then spontaneous lysis of thrombus with resolution and negative cath due to lysis of thrombus?  --Possibly.

3) Or was there a transient dysrhythmia (never recorded) that resulted in poor stroke volume, temporarily high LVEDP, onset of pulmonary edema, then resolution of dysrhythmia, then resolution of pulmonary edema?

The answer is uncertain.  However, the fact that the ECG shows acute current of injury in this case does not necessarily mean coronary occlusion, though transient occlusion or obstruction remains a possibility.  Severe demand ischemia can also cause ST elevation.  See this case.

A male in his 40's with no previous heart history presented with palpitations.  There were no symptoms or evidence of hypoperfusion.  A 12-lead was recorded during the tachycardia:


There is a regular, wide complex tachycardia at rate of 170 bpm, with QRS duration of 124 ms.  There are no p-waves, no AV dissociation, no concordance (QRS in precordial leads are not all in the same direction).  There is inferior axis (all positive in II, III, aVF, and all negative in lead aVR.  There is an initial wide r-wave in V1 and V2 (greater than 40 ms).  There is a left bundle branch block morphology, except that the initial r-wave is wider than 40 ms. What is the diagnosis?


The tachycardia resolved on its own with no therapy.  The post conversion ECG is below. 

There is lead reversal, making it appear as if there are Q-waves in leads I and aVL.  Otherwise it is normal.

Had it not spontaneously converted, what therapy would be appropriate?









Answer: this is RVOT, right ventricular outflow tract ventricular tachycardia, and it is usually sensitive to adenosine.  (I have been waiting for a case of this for years, and here it is!)  This is one of the "idiopathic" (though no longer actually idiopathic) VT types that occur in the absence of structural heart disease.  They generally have a relatively narrow QRS, less than 140 ms, whereas most VT has a QRS greater than 140 ms.  Here is a fine article discussing these and other types of VT in the absence of structural heart disease.

Adenosine would be appropriate here, as it generally is for regular, monomorphic, wide complex tachycardia, as long as you recognize that not all wide complex tachycardia that converts with adenosine is SVT with aberrancy.  This is the exception to that rule. In other words, conversion with adenosine does not prove SVT.  

The 12-lead ECG in RVOT VT has

1. LBBB pattern
2. wide r-wave
3. Inferior axis. 
4. The transition from S-wave to R-wave in the precordial leads depends on how far anterior (RV outflow tract vs. LV outflow tract) the origin of the VT is.

Here is a short quote from the article:

"Patients may be asymptomatic but often present with palpitations, chest pain, dyspnea, presyncope, and even syncope. In general, Outflow Tract Arrhythmia occur more frequently with exertion or emotional stress, and may have a diurnal variation. Women may have an increase in symptoms related to changes in hormonal status. In general, the prognosis of truly idiopathic OTA is benign.  Long-term follow-up studies have provided evidence that the vast majority of patients do not develop structural heart disease or SCD. However, as already noted, a small percentage of patients with very frequent VAs may have LV dysfunction over time, and rare reports have documented cardiac arrest and Polymorphic VT in patients who were initially thought to have “benign” Outflow Tract Arrhythmia."

Here are 2 more relevant posts, which include the approach to wide complex tachycardia: 1)  SVT with aberrancy  2) verapamil-sensitive posterior fascicular VT

There is a wide QRS with a tall R-wave in aVR and V1 and wide S-wave in lateral leads, leading one to believe this is RBBB.  There is ST elevation in V1, and ST depression in V4-V6, suggestive of ischemia/MI.   What is the Diagnosis? --see Below

This is a classic pseudoinfarction pattern -- hyperkalemia, with K of 6.9 due to DKA (pH 7.12, bicarb 6).  In this case the diagnosis was easy because the patient presented very ill with known Type I diabetes and with vomiting, not chest pain.

However, here are two from my files that presented with chest pain:

The peaked T-waves give it away, but the ST elevation in V1 and V2 is a little known pseudoinfarction pattern.  There was no MI here.

Thanks to K. Wang for this EKG.  Again, there was no MI, only hyperkalemia.

In all 3 of these cases, the findings disappeared with treatment of hyperkalemia, and the ECG normalized.

Answer below













The QRS is very narrow (about 70 ms?), so it must be a pediatric ECG. 

Thus, the fact that the rate is 230 bpm does not necessarily mean that it is SVT because infants can have very fast sinus rhythm.  Thus, what appear to be p-waves are indeed p-waves (see leads II and V1).  This is from a febrile 3 month old infant.  The ECG was done because the heart rate was 230 and the differential included SVT vs. sinus tachycardia.  This ECG, and the fact that the heart rate was variable (not constant) confirmed sinus tach.  Note also how the PR interval is very short.  Again, this because all intervals in infants are short. 

Notice also that there is right ventricular hypertrophy.  There is an S-wave in lead I, tall R-waves in leads V1-V3, with late transition to S-waves in precordial leads, and T-wave inversion in right precordial leads.  This is typical of pediatric ECGs because the fetal circulation depends on the right ventricle.  So these are normal findings in the ECG of an infant.


With management of fever and dehydration, the heart rate normalized.

Reminder:
Never trust the computer read.  The computer read is usually very good at determining pacemakers and intervals, but it was way off in this case:  it said: "electronic ventricular pacemaker" and measured the QRS at 202 ms!