This is a quiz. The ECG is pathognomonic. Answer is at the bottom.

Hyperkalemia, with near sinusoidal pattern.  Note very wide QRS, bizarre deep T-waves in V1 and V2, peaked T-waves in V4 and V5, long PR interval this case.

Whenever you see a wide QRS, you must think of hyperkalemia.

The K was 8.7 mEq/L.  It responded to therapy.

Reversible T-wave inversion -- it reverses, then evolves, then reverses when ischemia is gone. Normalization of T-waves, NOT pseudonormalization.

A 62 yo male has had chest pain with exertion for 2 weeks.  He began having chest pain at rest at 2AM, and presented at 7 AM.

Here is his initial ECG:

Sinus rhythm.  There is a QS-wave in V2 (old MI?) and very subtle terminal T-wave inversion in V3, and ST depression in V4-V6, highly suspicous for LAD NonSTEMI.  I believe the extra wave in V1-V3 is artifact. 





This was recorded 2 hours later, after troponin I confirmed acute MI at 0.485 ng/mL:



There is a PVC, but now the terminal T-wave inversion is gone. Some ST depression in V5 and V6 remains.



An angiogram revealed 3-vessel disease and a 90% LAD stenosis, 99% RCA, and 70% ostial right Posterior Descending Artery.  No intervention was done because of consideration of CABG.

This was recorded 9 AM the next day.  A simultaneous echo had very subtle WMA in the LAD territory.

Now there is classic biphasic terminal T-wave inversion (strictly speaking, it is not Wellens' because Wellens' requires preservation of R-waves). There is also subtle new Terminal T-wave inversion in aVF ("inferior Wellens").



On day 2, PCI of the rPDA and RCA was done.  The troponins continued to trend down.  

This ECG was recorded the next AM (day 3):

There is evolution of anterior T-waves, with T-wave inversion in V4 more pronounced now.  T-wave in aVF is now upright.

On day 3, he had the LAD stented.  Troponins bumped to 3.0 mcg/L after the PCI.   This was recorded the next AM:

Now, the anterior T-waves have completely normalized.

Such reversal is usually due to reocclusion (pseudonormalization) and associated with chest pain.  Wellens in the setting of significant troponin elevation usually evolves to deep and symmetric T-waves, then normalizes over weeks to months.  This is an unusual case of T-wave normalization without re-occlusion that occurred in 24 hours.

In unstable angina, with no myocardial cell death, T-waves are more likely to normalize when ischemia is resolved.

Contrast this normalization of T-waves to the pseudonormalization of the last post.

Pseudonormalization of Inferior T-waves

In a few days I will post a twist on pseudonormalization, but wanted to first post this classic case.

This 49 year old male presented after an episode of chest pain. 

There is sinus rhythm.  There are T-wave inversions in II, III, aVF and V4-V6.  This is consistent with inferior and lateral Wellens' type reperfusion T-waves.  There is also a large upright T-wave in V2 (and, in retrospect) I see this as a posterior reperfusion T-wave. 

The first ECG is consistent with a patient who had an occlusion of an artery supplying the inferior and lateral walls, but is now reperfused.

In the ED, his pain recurred and this ECG was immediately recorded, 20 minutes later:

Now the T-waves are upright (not normal, but pseudonormalized).  This is an obvious STEMI, but nicely illustrates the phenomenon of pseudonormalization.  Lead V5 by itself looks normal unless you compare it to lead V5 20 minutes prior.

Pseudonormalization is a phenomenon or reocclusion of an artery that has recently reperfused.  The reperfusion resulted in inverted T-waves (reperfusion T-waves, Wellens' T-waves).  The reocclusion results in the T-wave becoming upright again.  If seen in isolation, one may be lulled into thinking they are truly normal (see V5).

See here for more cases of pseudonormalization.

This also illustrates the importance of serial ECGs.

Bizarre T-wave inversion of Stokes Adams attack (syncope and complete AV block), with alternating RBBB and LBBB

This is a 68 yo male with a history of aortic stenosis, on carvedilol, fell from a ladder approx 20 ft onto concrete, landing face down with likely loss of consciousness.  Upon EMS arrival, pt was still face down in a pool of blood, but was responsive, alert, and neuro intact.  His BP was stable en route, but he was bradycardic in the 30's.


On exam, he had multiple orthopedic injuries, but no significant head, neck, spinal, chest, or abdominal injuries.  The patient had had no premonitory chest pain or SOB.  His BP was 121/59 and he was well perfused. This was his initial ECG:

There are regular p-waves at a rate of about 90, but they do not conduct.  Thus, there is 3rd Degree AV block with a probable Purkinje escape at a rate of 36; the wide QRS and RBBB pattern (rSR' in V1, wide S-waves in lateral leads) tell us that the escape is from the left bundle, creating an RBBB-like ECG.  [Alternatively, there could be a nodal escape with RBBB].  There are also very wide, bizarre, inverted T-waves.  The QT is 680 ms, and QTc = 527 ms.  There are no ST changes indicative of STEMI.

First troponin returned at 0.11 ng/ml (slightly elevated).  With all his injuries, he spent 2 hours in the ED, and a subsequent ECG is shown here:

Now the escape has an RBBB in the first part of the ECG, and LBBB pattern in the latter part, and the rate is 41.  The escape has alternated to the right bundle [or there is a nodal escape with LBBB].

This is a classic ECG.  A drop attack with third degree AV block is called a "Stokes Adams" attack, and is often associated with bizarre wide inverted T-waves.   A google scholar search comes up with several articles: Giant T-wave inversion associated with Stokes-Adams syncope (sycope due to complete AV block).

The escape rhythm is dependent on the automaticity of the tissue that escapes.  AV nodal escape is the fastest, then HIS bundle, then Purkinje fibers, then ventricular tissue (which results in a slow "idioventricular" rhythm)

In this case, there is either an alternating escape, or a nodal escape with alternating RBBB and LBBB.  If it is the former, then you know that your bundles have appropriate automaticity and can support the rhythm without a stimulus from above.  If it is the latter, then you have the risk of developing block of both the left and right bundles simultaneously, in which case the only escape possible is idioventricular.

Obviously, this is a dangerous situation, and you must place transcutaneous pacing pads and ascertain that they will capture if you need them too.  Alternatively, an internal pacing wire can be placed.

A simple test of capture is nicely done by pacing and observing the heart with bedside ultrasound to be certain of capture.

Case continued:

Fearing possible beta blocker toxicity, glucagon was given in increments up to a total dose of 5 mg, but this was not effective.  Atropone 1 mg was given without effect (this will not work in this situation, ever).  An internal pacing wire was placed in the ED, but not used because, in the interim, dopamine had been started and titrated to 10 mcg/kg/min with an increase in the heart rate to the 50's.  Pacer pads were also placed.


Subsequent troponins rose to a maximum of 8.5, suggesting that ACS may have had a role here.  However, third degree heart block can develop for other reasons than acute MI. 

An echocardiogram revealed moderately severe aortic stenosis with a valve area of 1cm2, with a mean pressure gradient of 50mmHg. There were regional wall motion abnormalities (apex, distal septum and
inferior) but these are difficult to interpret in the setting of LBBB.

Angiography and Ventrilography revealed worse AS, with valve area of  0.74 cm2.  There was no coronary artery disease.

A permanent pacer was placed on hospital day 3.

This is the final ECG:

Perfectly normal paced rhythm.  Note that all precordial QRS are negative.  This is because the pacing lead is placed in the apex of the right ventricle, so that depolarization always proceeds away from the apex of the heart (on the chest, the point of maximal impulse).  Thus, it depolarizes away from all precordial leads.

After many orthopedic procedures, the patient had his aortic valve replaced, and went home.

Altered Mental Status, possible ingestion. What does the ECG show?

A middle aged man was heard to be falling in his apartment.  He was found very agitated, intermittently screaming (and on presentation was intermittently roaring like a lion).  There was no apparent etiology.  He required 10 mg of droperidol for sedation.  He underwent an ECG as a routine part of the evaluation of possible ingestion:



 What jumps out at you?



Answer: There is sinus rhythm with one PAC.  The notable feature is a very long QT interval.  The computer read this as QT = 492 ms, with QTc = 518 ms.  But when the QT gets very long, computers become inaccurate and you must read it by hand. 

Some recommend reading in lead II or V5/V6.  Some say to measure the longest of the 12 QT intervals.  I tend to measure the longest of the 12 QT intervals on the ECG.  I have not measured them all, but at a glance, it looks like V2 and V3 have the longest, and these typically are the longest.  I have blown them up below:

The end of the T-wave has a small hump (wide arrow) which is probably a U-wave and this can make the end of the T-wave appear to be even more delayed than it is.  The narrow arrow more accurately follows the projection of the T-wave to the baseline (horziontal black line).  Using this at the end of the QT interval, I get 540 ms, with QTc as 540/(square-root of R-R interval) = 540/0.91 = 593 ms

(By my eyeballing it, the QT in V5 is also 540 ms.) 

593 ms is dangerously long and may result in torsade de pointes (polymorphic VT), and could be a result of the droperidol, or of metabolic and electrolyte abnormalities, or to many drugs or even be familial.  In any case, it is unsafe to leave it like this, so we gave 2 grams of Magnesium.  A blood gas revealed a pH of 7.75 (entirely a respiratory alkalosis, drawn before intubation and due to his agitation and hyperventilation), which will also cause long QT and torsade.  K was 3.2, which will also contribute.  By this time, we had him on the ventilator and so we intentionally slowed his ventilations to lower the pH.

Repeat pH was normal and Mg was delivered, and we recorded another ECG:

I calculate the QTc at 488 now, which is safe.

The magnesium level returned at 1.2 (low).

Etiology of long QT in this case: 1) hypo Mg 2) hypoK 3) alkalosis  4) droperidol?   5) other drug (we still do not have a diagnosis and the patient is still unable to tell us what meds he is taking)

1) QTc over 500 ms can be dangerous.  When near 600, it is very dangerous.

2) Give Mg, correct to 2.0.

3) Correct high pH (I once had a patient who required mechanical hypoventilation and intravenous HCl to prevent torsade)

4) Correct low K to 4.5.  Hypokalemia causes a large amount of QT dispersion (see #6)

5) Check Ca (normal in this case).  HypoCa causes long QT by lengthening the ST segment without lengthening the duration of the T-wave.  It is uncommon for hypocalemic long QT to result in torsade because it results in only a small amount of QT dispersion.  It is "homogenously prolonged".
6) both QT interval and QT "dispersion" (a measure of the difference, in ms, between the longest QTc and shortest QTc of the 12-leads) are risk factors for torsade.  A QT dispersion of greater than 60 ms is high risk.

Details on measurement of the QT interval can be found here: free full text article.

One should average 3-5 leads, usually take lead II, or the lead that shows the end of the T-wave best, or the leads with the longest QT (which are usually V2 or V3).  Correction for the heart rate must be done, but tends to overestimate the QT interval at fast heart rates and underestimate at low rates, and so other correction methods have been developed.  The U-wave should generally not be included, especially if large, but if small and not distinguishable from the T-wave, the course of action is unclear.

QT dispersion

--Yelamanchi VP, Molnar J, Ranade V, Somberg JC. Influence of electrolyte

abnormalities on Interlead variability of ventricular repolarization times in 12-

lead ECG. Am J Ther 2001;8:117–122.

--Eryol NK et al.  Effects of Calcium Treatment on QT Interval and QT

Dispersion in Hypocalcemia.  Am J Cardiol 91:750-752; March 15 2003.

Droperidol


Droperidol has a black box warning regarding the QT interval prolongation.  Our department has studied this extensively and found it to be a greatly exaggerated danger.

Here is a great recent 2020 paper we wrote on the effect of droperidol on the QT interval. This is all you need to know about droperidol and QT:

The Incidence of QT Prolongation and Torsades des Pointes in Patients Receiving Droperidol in an Urban Emergency Department

Here are two abstracts:

QT Lengthening after Parenteral Droperidol Administration

Stephen W Smith, Marc Martel, Michelle Biros, Marsha Zimmerman and Peter Chase

Hennepin County Medical Center: Minneapolis, MN   SAEM, St. Louis 2002
ABSTRACT
Objectives: Recently, the Food and Drug Administration (FDA) warned of a prolonged QT interval and torsade de pointes as a complication of droperidol (DROP). We sought to determine the frequency of a significantly prolonged QT interval (LQT) in patients who received DROP, and to compare this with the QT interval of patients not receiving DROP. Methods: The EmSTAT electronic patient database was searched from January 1, 1997, through November 30, 2001, for all patients who received DROP. Those who had an electrocardiogram (ECG) ordered at least 30 minutes after administration of DROP were identified. These ECGs were reviewed and the computerized corrected QT intervals (QTc) were recorded. A medication-induced QTc of less than 480 ms is generally considered safe; we defined LQT by QTc greater than 480 ms. Medical records of patients with LQT were further reviewed for previous ECGs, contributing medical conditions, and adverse events. The QTc's of 100 consecutive patients who did not receive DROP were reviewed as controls. Data were analyzed with descriptive statistics and Fisher's exact test. Results: 15,374 patients received 18,020 doses of DROP; 682 had an ECG recorded after DROP, 450 were obtained at least 30 minutes after administration. LQT was found in 17 patients, 1 had left bundle branch block (LBBB), 1 had a paced rhythm, 1 had right bundle branch block (RBBB), resulting in a total of 14 with a normal QRS and LQT (3.1%). Four of these 14 had previously documented LQT not associated with DROP. None had an adverse event related to LQT. Of 100 consecutive patients in the control group, 4 had LQT (4.0%) (p = 0.76) Conclusions: Our study does not support an effect of DROP on the frequency of LQT.

QT Prolongation and Cardiac Arrhythmias Associated with Droperidol Use in Critical Emergency Department Patients

Marc Martel, James Miner, Seth Lashkowitz, Mark Danahy, Joseph Clinton and Michelle Biros

Hennepin County Medical Center: Minneapolis, MN   SAEM Boston 2003
ABSTRACT
Background: QT prolongation and torsade de pointes (TdP) have been reported as a complication of droperidol (Drop). Objectives: To determine the change in the corrected QT interval (QTc) and the incidence of cardiac arrhythmias in critically ill patients who received Drop. Methods: The medical records of all critical care ED patients from 1/1/1997 to 12/31/2001 were hand searched for those who received Drop and an ECG in the ED. Drop dose, ECG time, QTc intervals, and cardiac rhythm were reviewed. ECGs with atrial fib/flutter, right or left bundle branch block, or paced rhythms were excluded. Data was analyzed in 3 groups, patients with an ECG recorded only before Drop, only after Drop, and those with ECGs both before and after Drop. Data was analyzed using descriptive statistics and chi-squared. Results: 11,583 charts were reviewed, 1172 patients received Drop, and 396 had both an ECG and Drop in the ED. 44 patients were excluded due to abnormal rhythm, bundle branch block, or paced rhythm. 96 patients had an ECG only before Drop (mean 33.3min prior), average dose of 2.75mg, and mean QTc of 435.0ms (95% CI 428.1–441.9ms). 186 patients had an ECG only after Drop (mean 25.9min after), average dose of 3.68mg, and mean QTc of 433.3ms (95% CI 427.8 to 438.8ms). 114 patients had ECGs before and after Drop (mean time 28.2min before, 108.8min after), average dose of 2.21mg, and mean QTc of 435.7ms (95% CI 426.7–444.7ms) and 435.8ms (95% CI 427.5–444.1ms) before and after Drop, respectively. The mean ratio of the QTc before and after Drop is 1.005 (95% CI 0.985–1.025). 2 patients had ventricular arrhythmias in the before Drop group, 3 in the after Drop group, and 4 in the before and after Drop group (p = 0.5). 1 patient had an unrecorded event of TdP with a QTc of 466ms after conversion. Conclusions: We detected no statistical difference in the change of the QTc interval or occurrence of ventricular arrhythmias in critically ill patients who received Drop.

Atrial Fibrillation with RVR and Inferoposterior ST elevation (Injury Pattern)

This is an old post from June 2009 that has not received much attention, but should.  Take a look!

This 80 yo woman had been increasingly lethargic for 2 days, and presented hypotensive (SBP =70), pale, and tachycardic.  She had not been complaining of chest pain.  It was uncertain whether she had chronic atrial fibrillation or not.  She was afebrile.  Here is the initial ECG.

There is an irregularly irregularly rhythm (atrial fibrillation) with a very fast ventricular response.  There is an injury pattern, with ST elevation in II, III, aVF, reciprocal ST depression in I and aVL, and ST depression of posterior injury in precordial leads.

 

We did not activate the cath lab.  We suspected GI bleed and this was confirmed with blood on rectal exam.  An ultrasound of the heart showed hyperdynamic function and the inferior vena cava (IVC) confirmed low central venous pressure (IVC was flat).  Had this been a primary cardiac event, the CVP would be high and the IVC distended, and the patient might have also been in pulmonary edema.

She was given blood and fluids until the bedside ultrasound showed good central venous pressure (distended inferior vena cava), but she remained hypotensive and tachycardic, and the ST elevation did not resolve. Thus, we sedated her and electrically cardioverted at 200J (biphasic), but this was unsuccessful x 3.  We then intubated her and started an infusion of amiodarone 300 mg IV, but with no improvement, and a subsequent cardioversion was again unsuccessful.  We then loaded her with 500 mcg/kg of esmolol and started her on a 50 mcg/kg/min drip, after which a fifth cardioversion was successful, and resulted in the second ECG shown here:

The rhythm is sinus (with a couple PACs), rate normal, and all ST elevation and depression is now resolved.

 

The blood pressure came up immediately.  Hemoglobin returned at 7 and WBC count at 29,000.  The troponin peaked at 19, and there was a subsequent inferior wall motion abnormality.  EGD showed duodenal ulcers and erosions which had stopped bleeding.

A stress sestamibi showed no inducible ischemia, so no cath was done. Whether there was thrombus in the infarct-related artery, or whether this was only demand ischemia (Type II MI) is uncertain.  

Convert atrial fibrillation with a rapid response when the patient is unstable; any injury pattern on the ECG constitutes instability.

Though demand ischemia usually shows as ST depression (or nonspecific findings) on the ECG, it may occasionally present with injury (ST elevation).

Young man with syncope while riding a bike [Arrhythmogenic Right Ventricular Dysplasia (ARVD)]

This 31 yo who is otherwise healthy had sudden syncope while riding a bike.  He remembers looking down, then becoming dizzy, then waking up on the ground with his feet still attached to the pedals.  He thought he was unconscious by himself for 45 minutes (!).  Then he awoke and called 911.   He had no prodromal vasovagal symptoms such as flushing, nausea, or diaphoresis. 

He had a several year history of palpitations without syncope, but had one presyncopal epsisode one month prior.  He had been seen by a local cardiologist 3 years prior and had what is described in records as a normal ECG and normal Echo, and had been encouraged to resume exercise.

Here is his presenting ECG in the ED:

Sinus rhythm with some artifact.  QTc may be slightly prolonged; I eyeball it at about 470ms.  This is not long enough to be dangerous.

His symptoms are very alarming.  There are 2 features which are high risk: no prodrome other than dizziness, and onset with exertion.  When a young person who is otherwise healthy presents with high risk syncope, a normal exam, and NSR, it is essential to obtain an ECG not only to look for ischemia, blocks such as LBBB and RBBB, but also for inherited disorders that cause dysrhythmia.  There are 5 that I think of: WPW, HOCM, Brugada, long QT, and Arrhythmogenic Right Ventricular Dysplasia (ARVD), which is a disorder of fatty infiltration of the RV that causes sometimes lethal ventricular tachycardia originating from the RV.  ARVD is quite rare, not often thought of, and very difficult to recognize on the ECG. 

Alas, this young man's presenting ECG shows none of these.

Surprisingly, the first troponin returned at 3.44 ng/ml, the second at 7.48.  Clinicians thought they were dealing with a dysrhythmia due to ACS/NSTEMI, and started heparin and aspirin.  He was admitted to the hospital.

An echo revealed segmental hypokinesis of the apex of the right ventricle only. The contour at this portion of the RV free wall was also unusual, and raised suspicion for ARVD.

MRI of the heart was done; here is the final report:

There is focal dyskinesia involving the RV apex and the anterior wall. On the T2-weighted sequence, there is linear increased signal in the RV myocardium suggesting fatty infiltration. There is no definite delayed enhancement in this area. These findings are suspicious for arrhythmogenic right ventricular dysplasia.

Coronary cath was normal.  Troponins trended down. 

Here is another ECG from 3 days later: 

Now there is abnormal T-wave inversion in III, aVF, and V2.  So the patient only has minor criteria by ECG, and only on the followup ECG (see below).

Case Conclusion:

He had an EP study that induced VT at a rate of 252.  Here is the induced VT:

VT at a rate of 252 bpm.  Short QRS for VT (116 ms).  Not a typical LBBB morphology, but induced VT in ARVD need not be of LBBB morphology.

A heart rate like this would stress the heart and lead to troponin release.

An implantable cardioverter defibrillator was placed.

ARVD, also known as arrhythmogenic RV cardiomyopathy, is estimated to have a prevalence of 1 in 5000 adults and is responsible for approximately 11% of sudden death in young adults and 22% in a study of athletes in northern Italy.  The diagnosis is not easy (see below).

Here is a 2017 review article on ARVD in the New England Journal

  

There is a 2010 publication by the Task Force in Diagnosis of ARVD: Diagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria. 

Free full text: https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.108.840827  

There are 6 categories of criteria: 

1) Imaging

2) Pathologic

3) ECG Repolarization

4) ECG Depolarization

5) Arrhythmias

6) Family History.  

ECG and historical Highlights of this publication are (Suspect ARVD with):

1) High risk syncope with no other etiology; Family History

2) Depolarization abnormalities (Major criteria):

        a) Epsilon Waves

        b) Localized prolongation (greater than 110 ms) of the QRS complex in right precordial leads (V1-V3)

3) Repolarization abnormalities in patients of age at least 14 years (because younger patients often have juvenile T-waves)

        a) Minor: Inverted T-waves in right precordial leads V1-V2 

        b) Major: Inverted T-waves in right precordial leads V1-V3 or beyond (major criteria) 

4) Arrhythmias

        a) Major criterion:

                i) VT of LBBB morphology with superior axis (negative or indeterminate QRS in leads II, III, aVF and positive in lead aVL) (major criteria)

        b) Minor criteria:

                i) VT of LBBB morphology with inferior axis (positive QRS in leads II, III, aVF and negative in lead aVL) (minor criteria)

                ii) More than 500 PVCs per hour

5) Finally, it is a progressive disease and patients without ECG abnormalities may develop them over time.

Here is an example of an epsilon wave (image C).  And another example.  Here are some great examples from the post on RV dysplasia (translated by Google translate!) on Pierre Taboulet's great French site:  #1, #2, #3

Here's a great example on Wave Maven.

Here is an explanation od the importance of leads V1 and V2.

Here is another nice example.  I've taken the liberty of blowing up part of the ECG at this link for better viewing.  Look closely at V1-V2:

There are Epsilon waves (small waves at the end of the QRS) and also a slight prolongation of the QRS at the very end. 

Some excellent references on ARVD:

This is a case report with lots of good info, from 2019, but you can only read it if you have a subscription to American J Cardiol:

Holshouser JW and Littmann L.  Usefulness of the Electrocardiogram in Establishing the Diagnosis and Prognosis of Arrhythmogenic Right Ventricular Cardiomyopathy

Other References, from the above article:

1

FI MarcusEpsilon waves aid in the prognosis and risk stratification of patients with ARVC/D

J Cardiovasc Electrophysiol, 26 (2015), pp. 1211-1212

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FI Marcus, W ZarebaThe electrocardiogram in right ventricular cardiomyopathy/dysplasia. How can the electrocardiogram assist in understanding the pathologic and functional changes of the heart in this disease?

J Electrocardiol, 42 (2009), pp. 136.e1-136.e5

Article

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RNW Hauer, MGPJ Cox, JA GroenewegImpact of new electrocardiographic criteria in arrhythmogenic cardiomyopathy

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FI Marcus, WJ McKenna, D Sherrill, C Basso, B Bauce, DA Bluemke, H Calkins, D Corrado, MG Cox, JP Daubert, G Fontaine, K Gear, R Hauer, A Nava, MH Picard, N Protonotarios, JE Saffitz, DM Sanborn, JS Steinberg, H Tandri, G Thiene, JA Towbin, A Tsatsopoulou, T Wichter, W ZarebaDiagnosis of arrhythmogenic right ventricular cardiomyopathy/dysplasia: proposed modification of the task force criteria

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WC Roberts, N Kondapalli, SA HallUsefulness of total 12-lead QRS voltage for the diagnosis of arrhythmogenic right ventricular cardiomyopathy in patients with heart failure severe enough to warrant orthotopic heart transplantation and morphologic illustration of its cardiac diversity

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JE Madias, R Bazaz, H Agarwal, M Win, L MedepalliAnasarca-mediated attenuation of the amplitude of electrocardiogram complexes: a description of a heretofore unrecognized phenomenon

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A Southeast Asian with Tachycardia and Hypotension after taking a dangerous herbal medication (Bidirectional Ventricular Tachycardia from Aconite Poisoning)

I published this case in Annals of EM 6 years ago.  I figure it's ok to put it here now after all these years, especially since one cannot even read an abstract of it.  The reference is below, so as not to give away the diagnosis.

This 59 year old Hmong woman presented with palpitations, nausea, vomiting, weakness, and numbness.  She had intended to take "Hmong Medicine number 9" but unwittingly took "Hmong medicine number 12."  When she realized her mistake, she knew that she would die, and her family called 911. Her BP was 65/40.  Lungs were clear and exam was otherwise unremarkable.

This was her initial 12-lead ECG:

The family showed EMS the herbal root from which the patient ate shavings:

What is the rhythm????





Answer: Bidirectional Ventricular Tachycardia.   There are alternating ventricular beats; the frontal and transverse axes alternate because there is alternating right bundle and left bundle branch block morphologies.  This is, of course, not because there is actually RBBB and LBBB, but because the origin of the ventricular beat alternates from right ventricle (LBBB) to left ventricle (RBBB).

We treated her with esmolol without any effect.  No therapy helped her, but she did spontaneously convert to NSR 8 hours later.  A Chinese PharmD and herbal specialist identified the root as aconitum Carmichaelii.

Bidirectional Tachycardia is rare, and usually associated with digitalis toxicity.  It has been reported to be unresponsive to electrical cardioversion and lidocaine, but responsive to flecainide.  Aconite (also known as monkshood, or wolfsbane) seems to trigger automaticity by direct activation of inward sodium channels during phase II of the cardiac action potential; thus, flecainide, which blocks these sodium channels appears to be effective in rats.

I had some great questions on this from Beth Bilden, toxicologist:

1.     1.  In a patient with a wide comlex dysrhythmia accompanied by hypotension (both likely caused by the unidentified toxin), I would have been tempted to give sodium bicarb which probably would have made things worse. My answer: Although the QRS is wide, it is not wide because of delayed conduction; it is wide because of bundle branch blocks morphology which indicated a focus of dysrhythmia in the ventricle, not a delay in conduction.  Therefore, bicarb would not be indicated and was not given.  In fact, the best treatment for this (flecainide), when taken in overdose is reversed with sodium bicarb!

2.  

      2.  Esmolol was used for rate control, right?  If so, was a calcium channel blocker considered rather than a beta blocker since a sodium channel blocking toxin/toxicant would decrease inotropy and a sodium channel blocking agent had not been excluded from the differential?   My answer: Again, I don't think the ECG is consistent with a sodium channel blocking agent.  I have to admit, I had no idea what the toxin was and thus what I should do, so I tried esmolol, knowing I could shut it off if it did not work.  No one else knew what to do, so she was only observed overnight and (very luckily) survived.   Obviously, if I saw a case of this now, I'd know the differential and have a much better idea how to treat it.  As would all of you readers!

Here is another case of bidirectional tachycardia.  And another.

Smith SW et al.  Bidirectional Ventricular Tachycardia Resulting From Herbal Aconite Poisoning (Case Report). Annals of Emergency Medicine 2005; 45(1):100-101.