Inferior and Lateral ST Elevation and A Positive Troponin

A young woman presented with substernal chest pain described as both crushing and stabbing, with radiation to the jaw and left arm and associated with dyspnea.  It was not positional or pleuritic.  She was otherwise healthy except for an unspecified "recent illness" and recent pyelonephritis.  She denied tobacco or other drug use.

Here is her initial ECG:

There is sinus rhythm and normal, though low voltage, QRS.  There is inferior and lateral ST elevation., with large T-waves very suggestive of hyperacute T-waves.  Is this MI?  Pericarditis? Early repolarization manifesting in inferior and lateral leads?

We have found that, in inferior STEMI, there is always some, at least minimal, amount of reciprocal ST depression in aVL (manuscript being submitted).  Of course, if this is inferior STEMI, it is really inferolateral STEMI.  Does inferolateral STEMI also have reciprocal ST depression in aVL?  In my experience, yes.  I have yet to see an inferolateral STEMI without some reciprocal ST depression in aVL, in spite of the lateral ST elevation in V5 and V6.  We will be re-analyzing our data to look at that.


Value of ST elevation in lead II vs. lead III for diagnosis of inferior MI vs. non-MI etiologies of "inferior" ST elevation:

A lot of attention is given to whether the ST elevation in lead II is greater than, or equal to, that in lead III: many claim that, if it is, then it is not inferior STEMI, but rather pericarditis.  First, it is important to point out that baseline inferior ST elevation (early repol of the inferior leads) is more common than pericarditis, and if a patient complains of chest pain, and happens to have baseline inferior early repol, they are likely to get a diagnosis of pericarditis if they rule out for ACS.  In our research (not yet published), we found that STE in lead II was greater than or equal to STE in lead III in 49 of 49 cases of pericarditis, but only 32 of 66 cases of early repol.  Thus, in non-MI etiologies of inferior ST elevation, STE in lead II was greater than or equal to STE in lead III in only 81/115 cases.  In inferior MI, STE in lead II was greater than or equal to STE in lead III in only 6 of 155 cases.  Thus, the sensitivity for inferior MI of lead III greater than or equal to Lead II STE elevation was high, at 96%, but it had only 70% specificity.  This does not compare favorably with any ST depression in aVL, which had 99% sensitivity and specificity.  Thus, do not compare STE in lead II and III; use STD in aVL only.

Clinical Course

The ED physician ordered another ECG and it was unchanged.  He also performed a bedside ultrasound and saw no effusion and could not identify any wall motion abnormalities.  A third ECG (not shown) looked improved.  The initial troponin I returned at 6.1 ng/mL and so, with a dynamic ECG and positive troponin, the cath lab was activated.

The angiogram was normal.  A formal Echo the next AM was normal, with no effusion and no wall motion abnormality.  Although no rub was ever heard, and she did not undergo MRI, she was diagnosed with myocarditis.  She had had fevers and chills and myalgias, and a CRP mildly elevated.

Sarda et al. (free full text) studied patients with apparent MI but normal angiograms ("apparent MI" means they excluded patients who clearly had clinical myocarditis) and investigated them with Indium-111 Scintigraphy antimyosin antibodies, allowing noninvasive diagnosis of myocarditis.  In 2 patients, they found MI, presumably due to reperfused occlusion or to vasospasm.  In 17, diffuse myocarditis was found, and in 18, focal myocarditis was found, and 8 had no tracer uptake.  Thus, 35 of 45 cases were myocarditis.  Among all these patients, only 2 of 35 had any reciprocal ST elevation anywhere on the ECG even though 22 of 35 had regional wall motion abnormalities.

Thus, reciprocal ST depression in aVL is very sensitive and specific for MI, and very unusual in myo-pericarditis.

This is a scary ECG and activating the cath lab is certainly not wrong.  However, analysis of aVL is very accurate in predicting an non-MI etiology of this ST elevation, and if an emergent high quality echocardiogram can be done while the ECG has ST segment elevation, it could rule out STEMI and save this patient a trip to the cath lab on an emergent basis.  (If done after resolution of ST elevation, there could be reperfusion with recovery of wall motion, although recovery of wall motion does not often recover immediately.)

Cardiac arrest: even after the angiogram, the diagnosis is not always clear

A woman in her 40's who was healthy, except for hypertension, was at work when she suddenly complained of neck and shoulder pain and then collapsed.  It was witnessed, and CPR was performed by trained individuals.  She was found to be in ventricular fibrillation and was defibrillated 8 times without a single, even transient, conversion out of fibrillation.

Fine ventricular fibrillation

She received 2 mg epinephrine, 150 mg amiodarone and underwent chest compressions with the LUCAS device.

She arrived in the ED 37 minutes after 911 was called, with continuing CPR.  She was immediately intubated during continued compressions, then underwent a 9th defibrillation, which resulted in an organized rhythm at 42 minutes after initial arrest. The following 12-lead ECG was recorded at 11 minutes after ROSC.  The patient had a combined respiratory and metabolic acidosis (as we commonly find in those with prolonged arrest), and a K of 4.1, at the time of the ECG.  Mg was 1.6.

The rhythm is nearly regular, but there are no P-waves (it is too regular to be atrial fibrillation).  One might be tempted to think this complex is very wide, that the entire complex, as seen in lead II, is QRS.  However, the QRS is barely wide, if at all.  The remainder of what appears to be QRS at first glance is due to ST segment deviation.  (See image with lines below).  The tall R-wave in lead V1, with S-waves in V5 and V6 is consistent with RBBB or incomplete RBBB, depending on the exact QRS duration.  Once the end of the QRS is correctly identified, then the presence of ST deviation becomes apparent: there is ST elevation in aVR and V1, and diffuse ST depression (in I, II, III, aVF and V3-V6). 

Here is the annotated ECG from above, with lines drawn.

The end of the QRS is best seen in leads V4 to V6.  I have drawn a line through the end (actually, my software missed it so that the real end is a fraction of a box to the right). I extend this line down to the lead II rhythm strip at the bottom, so that I know on lead II where the end of the QRS is.  Then I can draw 4 other lines to find the end of the QRS in all leads.  Here is another excellent example of this.

So, in this patient with incessant ventricular fibrillation that has been converted, there is now a supraventricular rhythm with RBBB.  There is ST elevation in aVR, but also in V1, and diffuse ST depression.  STE limited to aVR is due to diffuse subendocardial ischemia, but what of STE in both aVR and V1? 

[Many would say that such ST elevation in aVR is diagnostic of left main occlusion.  I repeat that ST elevation in aVR is not diagnostic of left main occlusion.  Here is an article I wrote: Updates on the ECG in ACS.  The last section is a detailed discussion of the research on aVR in both STEMI and NonSTEMI.  If you want to understand aVR, read this.]

The additional ST Elevation in V1 is not usually seen with diffuse subendocardial ischemia, and suggests that something else, like STEMI from LAD occlusion, could be present.  In left main occlusion, by blocking flow to both the anterior wall (LAD) and posterior wall (circ), the ST depression of posterior ischemia could theoretically diminish the ST elevation of anterior ischemia and leave only V1 with significant ST elevation (Nikus, et al. see below).  I have never seen this, but it is possible.  Alternatively, it is a variant of diffuse subendocardial ischemia, with STE in V1 reciprocal to ST depression in inferior and lateral leads.

The ST elevation in V1, with RBBB pattern and inverted T-wave also suggests Brugada syndrome, but does not fit with the remainder of the ECG.  

Cardiac arrest can cause diffuse subendocardial ischemia, usually transient (it often resolves as time goes by after ROSC).  The patient was resuscitated for 50 minutes, and then this ECG was recorded:

Sinus rhythm.  ST segment abnormalities are almost all resolved.

Was this:
1) ACS with ischemia and spontaneous reperfusion?  Or
2) The ischemia of an ECG post-arrest?
Only an angiogram can tell for certain.  Or can it?

The patient was taken for an angiogram and had an 80% LAD lesion, but it could not be definitely determined whether this was an acute thrombotic lesion or a chronic stable lesion.  It was stented.


Here is the post cath ECG

T-wave inversions consistent with anterior MI, but not diagnostic.

The troponin I peaked at 8.1.  An echocardiogram on day 3 showed no wall motion abnormality (but of course, these can resolved with reperfusion, and the more time it has to resolve from "stunning", the more likely it is to be resolved).

Also, anterior MI could result from 1) ACS, but also from 2) severe ischemia due to combination of a hemodynamically significant LAD stenosis + severe hypotension during cardiac arrest.  In spite of all the evidence, we are still left in the dark!


Here is a 24-hour ECG:

Developing T-wave inversions, still consistent with anterior MI, but not revealing of its mechanism

Here is a 48-hour ECG:

Now there is a very long QTc, at 571 ms.  Does the patient have a long QT disorder, or is this post-ischemia?

Outcome

It could not be determined definitively whether this was primary ACS with arrest, or primary ventricular fibrillation with subsequent demand ischemia.

Therefore, to be safe, an internal defibrillator was placed.

The patient was discharged neurologically intact.

References:

1.  Smith SW. Updates on the Electrocardiogram in Acute Coronary Syndromes. Current Emergency and Hospital Medicine Reports (2013) 1:43–52. 

2. Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiol. 2008;41(6):626–9.

Missed myocardial infarction with subsequent cardiac arrest

A 50 year old male presented to his physician's office with "heartburn".  The physician recorded this ECG, interpreted it as normal, and sent the patient home on an antacid.

See explanation below.

The patient went home and, in front of his wife, he collapsed.  He underwent immediate CPR, was found to be in ventricular fibrillation, and was successfully resuscitated.  I do not have the post-resuscitation ECG.  He underwent coronary stenting (uncertain which artery).  He underwent months of rehabilitation and was able to return to work part time.

Could this have been avoided?

1.  A 50 year old with "heartburn" is a high risk complaint.  There is no way to tell the difference between GI etiology of chest pain and MI. Therefore, even with a normal or non-diagnostic ECG, a 50 year old male patient should undergo serial ECGs and troponins and be admitted to a monitored bed until MI or ACS can be ruled out.  This is obviously a very big topic in itself. 

2. Did the ECG offer unseen hints?  Yes

Leads III and aVF have ST depression with down-up T-waves.  Such T-waves are almost always reciprocal to ischemia in the region of aVL (although aVL looks normal here), and in a patient with chest pain are nearly diagnostic of ischemia.  The upright portion of the T-wave in aVF is very large compared to the QRS size.

These findings mandate that the patient at least get serial ECGs.

If these remain unchanged, then serial troponins.  An emergency cardiac ultrasound could be very useful.  And if definitive signs of ischemia develop, the immediate antithrombotic, antiplatelet, and anti-ischemic therapy is indicated, including an immediate angiogram, if symptoms and ECG findings do not resolve.

Lesson:

1. Chest pain should never be assumed to be from a GI source, even if you think the ECG is normal.
2. Ischemia on the ECG can be very subtle and is easily missed.  Accurate interpretation requires a lot of skill, practice, and experience.   Appreciation of these subtle ECG findings could have helped to avoid a cardiac arrest and its resulting permanent disability
3. Down-up biphasic T-waves are usually reciprocal to up-down biphasic T-waves in the opposing lead and are almost always ischemic
4. T-wave size must be evaluated in the context of QRS size.

Oertle, Paul

Middle Aged Woman with Asystolic Cardiac Arrest, Resuscitated: Cath Lab?

A middle-age woman with h/o hypertension was found down by her husband.  Medics found her apneic and pulseless, began CPR, and she was found to be in asystole.  With ventilations and epinephrine, she regained a pulse.  She was never seen to be in ventricular fibrillation and was never defibrillated.  She was hypotensive in the ED and her bedside echo showed a normal RV and LV.  BP gradually rose.  She was completely comatose (GCS = 3) and pupils were midposition and fixed.  Later in the case there was some respiratory effort but no improvement in pupils or any other aspect of the neurologic exam.  Two prehospital 12-lead ECGs looked similar to this ED ECG:

This shows diffuse ST depression (I, II, III, aVL, aVF, V3-V6) with reciprocal ST elevation in lead aVR.

This ECG is diagnostic of diffuse subendocardial ischemia.  

To quote an email from Francis Fesmire, a great expert on Emergency Cardiac Care:  "The new 2013 STEMI guidelines moved away from defining STEMI as "ST elevation >= 1 mm in two leads or new or presumably new LBBB" as in previous guidelines and just use the term STEMI with a general definition of the concept of identifying STEMI on ECG (page e379, under section 2.1).  Note that they finally have laid to rest the “new or presumably new LBBB” as a criteria for STEMI.  Also note that they allow ST depression c/w posterior MI to be a STEMI equivalent.  Finally, they also allow one to consider elevation in aVR to be a STEMI equivalent providing that it is associated with multilead ST depression...." 

In other words, this ECG, in the right clinical scenario, qualifies for a STEMI-equivalent and is an indication for activating the cath lab.

I am not in complete agreement with the recommendation for aVR, because:

1) diffuse subendocardial ischemia is more likely to have non-ACS causes than traditional STEMI ECGs [they are frequently caused by stress cardiomyopathy (usually due to small vessel vasocontriction due to catecholamines) and also by demand ischemia] and 

2) when due to ACS, STE in aVR is very infrequently due to coronary occlusion (there is a mistaken belief that ST elevation in aVR with diffuse ST depression is associated with left main occlusion and this is not true!).  Rather it is due to coronary insufficiency due to a tight left main or 3-vessel disease with inadequate coronary flow.

Patient course

We did not activate the cath lab, but discussed with cardiology the possible non-urgent need for an angiogram within a few hours.

Because the patient had asystole, was resuscitated without difficulty, and had no neurologic function, suspected a cerebral hemorrhage was suspected as the etiology of the arrest, specifically subarachnoid hemorrhage.  She went for a head CT and had a severe subarachnoid hemorrhage (SAH) due to ruptured aneurysm.  Unfortunately,  but not surprisingly, the patient died a neurologic death.

What is the utility of a head CT in cardiac arrest? 

We studied this and published the abstract below in 2010.  We found intracranial hemorrhage in 2% of non-traumatic cardiac arrest patients, and in 4 others the presence of cerebral edema changed management.  Those who had STEMI and underwent CT had a prolonged door to balloon time compared to those without a head CT.    

Kurkciyan et al. in Vienna found that 27 of 765 (4%) of out of hospital cardiac arrests (OHCA) were due to SAH.  In 25 (93%), the initial rhythm was asystole or PEA.  Of these, ischemic ST depression was found in 52%.  What they do not tell us is the percent of OHCA that were in PEA/Asystole; then we could calculate the percent of OHCA with asystole/PEA which were SAH.  If they had a comparable percent to our data (56%), then 428 of 765 had PEA/Asystole and 27/428 (6%) had SAH.  So still a small percent of PEA/Asystole presents as SAH.  In 23 of 27 cases, the diagnosis was suspected on clinical grounds; 39% had a prodromal headache.  Only 1 of 27 survived, after 45 days in the hospital, with a cerebral performance category of 2; this patient had ventricular fibrillation. No patient with PEA/Asystole survived.  I believe that the most likely etiology of arrest is brain stem compression, apnea, hypoxia, then asystole, and that it is ventilation, along with chest compressions, that leads to successful cardiac resuscitation.

SAH with cardiac arrest is nearly universally fatal, especially if there is PEA/Asystole.  The combination of sudden increased intracranial pressure with loss of spontaneous circulation results in near total loss of cerebral perfusion.  The blood pressure produced by chest compressions is inadequate to perfuse the brain when ICP is high.



References


Mulder M. Scott NL. Bart BA. Sprenkle M. Bachour FA. Smith SW. Early Post-resuscitative Care Of Adult, Non-traumatic Cardiopulmonary Arrests Is Rarely Affected By Routine Head Computed Tomography Session VII: Best Original Resuscitation Science.  Circulation 122:Abstract 101.  Presented at American Heart Association.  Chicago November 2010.

Background: The role of early head CT in the management of non-traumatic out-of-hospital cardiopulmonary arrests (NT-OHCA) is unclear.

Objectives: To evaluate the diagnostic value of early head CT and its potential drawbacks in NT-OHCA.

Methods:  Between June 2007 - July 2009 all NT-OHCA patients aged >18, transported to our hospital, an urban, level one trauma teaching hospital were included. Data collected included demographics, initial rhythm, EKG, emergency department (ED) CT and outcomes.  The study population was grouped into those who did and did not have an early CT. The data was analyzed in relation to initial rhythm, outcomes and changes or delay in treatment.

Results:  In total 201 NT-OHCA were transported to our ED during the study period; 125 (62%) were successfully resuscitated and admitted to the hospital, of which 86 (69%) had CT. Initial rhythm in those with CT was VT/VF in 33/86 (38%), PEA/asystole 48/86 (56%), and unspecified 5/86 (6%). Evidence of cerebral edema was found more commonly in patients with PEA/asystole 20/48 (42%) vs. VT/VF 4/33 (12%), p=0.006.  In-hospital mortality for patients with cerebral edema was 20/20 (100%) in patients with PEA/asystole and 1/4 (25%) in VT/VF, p=0.002. Fifty-five of 125 (41 VT/VF, 11 PEA/asystole and 3 unspecified) resuscitated patients survived to discharge. CT detected intracranial hemorrhages in 2/86 (2%) of patients. Significant changes in clinical management as a direct result of head CT were uncommon; occurring in 5/86 (6%) resuscitated NT-OHCA patients. Fourteen (16%) of the 86 patients who had CT also had immediate cardiac catheterization for acute ischemic changes; 7 of which had primary percutaneous coronary intervention (PCI). Door to balloon time (DBT) was 96 minutes for 7 patients with ST elevation myocardial infarctions (STEMI) who had CT prior to PCI vs. 75 minutes for 11 patients who did not have CT, p=0.058.

Conclusions: Head CT is common in NT-OHCA.  Cerebral edema is more common in patients presenting with an initial rhythm of PEA/asystole than in VT/VF and is associated with higher mortality.  Management is rarely affected by routine use of early head CT. In those who required urgent PCI, CT was associated with a (non-statistically significant) 21 minute longer mean DBT.

Kurkciyan et al., abstract

http://www.sciencedirect.com/science/article/pii/S0300957201003811

Objective: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest. Design: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features. Results: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome. Conclusions: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.

K. Wang Video: Differential Diagnosis of a Variety of Conditions (37 minutes).....

Regular Narrow QRS tachycardia
Regular Narrow QRS bradycardia
Pauses
Paired QRS
Changing QRS Morphology
ST Elevation in the Precordial Leads

Polymorphic Ventricular Tachycardia

A woman in her 40's presented with multiple "spells" in the past week, with increasing frequency.  She feels lightheaded, then becomes unresponsive.  It usually lasts about one minute then resolves.  She has had no chest pain.  She has a history of seizures as a child but there is no seizure activity during these spells.

The monitor shows this:

Ventricular Tachycardia, polymorphic
(courtesy of LITFL)

During this rhythm she was awake, protecting her airway, with pallor, diaphoresis and cool extremities.  Pulses were present.  There was no respiratory distress.

A 12-lead ECG was recorded:

VT, and it is "Polymorphic" VT because there are multiple morphologies to the complexes.  Rate again approximately 220.  Polymorphic VT is either torsade (associated with a long QT interval)  or not torsade (QT not long, often due to ischemia)

On the monitor, she spontaneously converted to a different rhythm, and another 12-lead was obtained:

There is bigeminy.  Narrow complexes are preceded by P-waves.  The QRS associated with the sinus beats has right bundle branch block (RBBB), and do not appear to have very long QT intervals (I calculated 400ms QT divided by the square root of the preceding R-R interval = 460ms).  The intervening Ventricular complexes (PVC's) look very bizarre with a long QT.  The PVCs have large ST elevation (II, III, aVF) with reciprocal ST depression (aVL, precordial), suggesting inferoposterior STEMI, but this is clearly a mimic because the intervening sinus complexes have no ST elevation.

She went back into tachycardia:

Polymorphic VT again.

What should be done?

First, what kind of VT is this?  Polymorphic VT.  PMVT is defined as a wide complex ventricular rhythm at rate over 100 with rapidly changing QRS axis and/or morphology.


Polymorphic VT

Etiology
Polymorphic VT is either torsades de pointe (associated with a long QT on the baseline 12-lead ECG) or non-torsades (usually associated with ischemia or other organic heart disease).  The presence of QT lengthening on the baseline 12-lead ECG is not always obvious.  Torsade de pointes means "twisting of the points" and refers to the changing axis around an isoelectric line. 

Morphology of the PMVT (i.e., presence of twisting of the points) alone cannot distinguish PMVT due to long QT (torsades) from that due to other etiologies (non-torsades).  It is virtually impossible to distinguish pulseless PMVT from ventricular fibrillation, and studies have shown that the majority of pulseless rhythms that appear to be torsade (with "twisting of the points") are really ventricular fibrillation.  This distinction has no implications for immediate management (defibrillation) but it does have important implications for preventing further dysrhythmias.

Torsades Etiologies of PMVT
1. Acquired: due usually to drugs.  The list is long.  Also due to electrolyte abnormalities, especially hypoK and hypoMg.   Corrected QT interval (Bazett correction = QT divided by the square root of the preceding R-R interval in milliseconds) is usually great than 600 ms.  Torsades in acquired long QT is much more likely in bradycardia because the QT interval following a long pause is longer still.  Thus, torsades in acquired long QT is called "pause dependent": if there is a sinus beat after a long pause (which creates a longer QT interval), then an early PVC ("early afterdepolarization," EAD) is much more likely to occur during repolarization and to initiate torsades.  The usual sequence is: sinus beat, then early PVC, then a long pause because the PVC was early, which then results in a particularly long QT, then another PVC with "R on T" that initiates torsades.

2. Congenital, especially Congenital Long QT Syndrome.   Unstable PMVT due to congenital long QT is much more rare.  (In 26 years of EM and 125,000 patients, I have never seen a case of torsade PMVT due to congenital long QT).  Congenital causes of torsade include "catecholaminergic PMVT," in which there is no visible QT lengthening on the 12-lead, but it is believed to have a similar etiology.   Preventive therapy of Congenital long QT includes use of beta blockers (same with catecholaminergic PMVT, as in both of these, beta stimulation provokes torsade); this is in distinction to acquired long QT, which may be treated with beta stimulation (isopreterenol). 

I have not found any recommendations to use beta blockers for acute management of torsade in this group, but it is nearly impossible to tell if isoproterenol will make things worse, or better, for any given patient with congenital long QT (see comment by our electrophysiologist at the end).   It seems that most symptomatic patients with congenital long QT present after syncope, or resuscitated v fib, and rarely present with continuing torsade or instability.  Thus, the management of these patients is primarily recognition and prevention of future syncope and sudden cardiac death, usually with an implantable debribrillator in addition to beta blockers.  Torsades from Congenital long QT can be induced by use of QT prolonging drugs.


Non-Torsade Etiologies of PMVT
Most commonly due to ischemia.  These will almost always be overt, severe episodes of ischemia, with chest pain and/or unequivocal ischemic ECG abnormalities. Also due to pre-existing cardiomyopathy.

Management of polymorphic VT
Most torsade is self-limited.  If it does not spontaneously convert, then it needs defibrillation if the patient is unstable.  If it does convert, then it is likely to recur, and therapy is aimed at preventing recurrence.

Therapy of Acute Episodes of Torsades:
1. Cardioversion or Defibrillation if active, especially if unstable
2. Removal of offending agent in acquired long QT
3. Correction of hypoK, even to slightly supranormal levels
4. Administration of 2-4g of MgSO4 even if the Mg level is normal (a drip of 3-10 mg per minute may be useful)
5. Only if it is acquired long QT: beta-adrenergic stimulation with isoproterenol
6. If these do not work, then overdrive pacing, usually at a rate of about 100 to prevent any pauses, will almost always work (transcutaneous pacing is fine for temporary relief as a bridge to transvenous pacing).
7.  Lidocaine may also be of benefit because it can suppress the PVCs (early afterdepolarizations) which initiate torsade if they occur on the T-wave.
8. Amiodarone is of questionable benefit, and possible harm.  By itself, it lengthens the QT interval, though without greatly increasing the risk of Torsades
9. Do not give beta blockers unless the patient carries a diagnosis of congenital long QT.  Just the opposite: isoproterenol.
10. If it is congenital [congenital long QT, or catecholaminergic PMVT (which has a normal QT interval)], then acute beta blockade may be indicated.  I would try esmolol first, as it can be turned off.  However, it does not have beta-2 blockade and it is unclear to me if this is important and/or necessary.  If esmolol does not work, then IV propranolol should be given.  Propranolol and Nadolol are the best long term beta blockers for congenital long QT and the beta 1 selective metoprolol is not very effective.  Whether this is due to the beta selectivity is not clear to me.

Here is a fascinating case of congenital Long QT with Torsade. There is a great discussion of the role and function of beta blockade in congenital long QT.

Therapy of Acute Non-Torsade PMVT: Similar to Monomorphic VT
1. Cardioversion or Defibrillation if active
2. Correction of electrolyte disorders, especially hypoK or hypoMg
3. Prevention of further episodes with lidocaine or amiodarone, possibly a beta blocker such as esmolol (which you would avoid in any acquired long QT Torsades).
4. Anti-ischemic therapies, up to and including revascularization
5. Implantable Cardioverter-defibrillator may be necessary even with successful revascularization

Back to our Case
Cardioversion is indicated only when the patient is in torsade, and will only work temporarily, as the patient goes in and out of the rhythm. Prevention of further episodes is essential.

In this case, we only see a long QT on the PVCs, but not in the native RBBB beats.   Often the torsades is "pause-dependent" and can only be seen in a complex that follows a long pause.  There is no chest pain, and we do not have evidence of ischemia on the sinus ECG complexes.  For polymorphic VT to be due to ischemia, there is usually some unequivocal ECG findings of ischemia.  So all this is suggestive of torsades, but not diagnostic.   The patient was not on any known medication that lengthens the QT interval.  She has only a history of Graves disease and reports that she has been off all medications.

When not in VT, her BP is elevated at 190/80 with a palpable pulse of 90 and oxygen saturations of 99.

An initial K returned normal.   Mg level was unknown at this point.

At t = 12, 2 grams of IV Magnesium were given.
At t = 13 minutes, 150 mg of amiodarone was given
At t = 15 minutes, 100 mg of lidocaine was given

At t = 30 minutes, there was no improvement and esmolol bolus and drip were given.  [This would in fact be contraindicated for Torsades, but reasonable if this were ischemic PMVT.  Although a bedside cardiac ultrasound had poor contractility, suggesting Non-torsades PMVT, Torsades is much more likely without clear ischemia on the ECG.]   Isoproterenol should be given.

The cath lab was activated. Another 2 grams of IV Magnesium was given.

t = 64 minutes: K returns at 2.4 mEq/L (initial value was mistaken).   This suggests Torsade even more strongly.  KCl given in central line.  Amiodarone drip started.  Rectal aspirin given.

t = 79 minutes: Procainamide 1500 mg over 2 minutes given.  (Procainamide may be useful in Non-torsade PMVT, but is likely to lengthen the QT and make Torsades more unstable.  It also is a strong negative inotrope and could be hazardous with poor LV function.)

t = 97 minutes: patient taken to cath lab:

The patient was taken to the cath lab and a pacer was placed.  The rhythm was captured with overdrive pacing and then slowed.  There was diffuse coronary disease, but no culprit lesion (no acute coronary syndrome).  Troponin was negative.

It was found that the patient was on methadone and was methadone toxic.  It is one of the many medications that causes a long QT.  This was Torsade de Pointes due to long QT due to methadone and hypokalemia.

Here is the 12-lead during pacing:

During Pacing

Here is another with the pacer turned off, the next day:

Sinus with RBBB and very long QT

And then on the fourth day:


T-wave inversions, QT still long

Because of the extraordinarily long half life of methadone, it took days for the QT to shorten.  Ultimately, the patient did well.



Comment on use of isoproterenol in congenital long QT:

I asked our electrophysiologist (Rehan Karim) this question:

"I want to be certain I have this straight:
For congenital long QT, beta blockade is indicated chronically, and for a patient with recurrent VT who is in the hospital, one would NOT give isoproterenol.

Only acquired long QT is "pause dependent" and improved with a faster heart rate, and beta blockade is NOT indicated. Rather isoproterenol is indicated (and overdrive pacing).
Can you correct me on this?"

In other words:

Do you use isoproterenol for overdrive pacing in patients who are going in and out of Torsades due to congenital long QT?

If so, how does that square with the use of beta blockers in congenital long QT?

Here is his answer:

"I wish things were clear enough to put everything in an algorithmic format… but unfortunately that’s not the case."

It really depends what type of congenital long QT you are dealing with, and even if you know – things are not as straight-forward.

Here’s an example:

Congenital Long QT type-3 is a sodium channel mutation (SCN5A) – which is the same gene as Brugada syndrome.

Long QT type 3 do have pause dependent Torsades. However, beta blockers are still used in this situation (after of course atrial pacing has been instituted to prevent bradycardia) – this is primarily for the effect of beta blockers on decreasing the QT dispersion.

Even more complicated… class I-B sodium channel blocker (Mexiletine) is used sometimes for LQT-3.

To my knowledge the beta blockers are not probably as effective in LQT-3 as in other forms – but are still used.

Therefore, I do not think it is possible to come up with a Yes/No answer with the knowledge we have at this time – things have to be taken in clinical perspective.

If someone clearly is having pause dependent torsades, and is not being paced – I will NOT use beta blocker, but rather try to increase the rate by using isoproterenol.

Dr. Karim added:
this is one of the confusing topics – in fact, most of the genetic arrhythmias / chanellopathies are quite challenging to manage clinically. We are so much used to seeing data from thousands of patients in cardiology trials – and then we get into such situations where the disease burden is not huge enough to give us data other than registries from large clinical centers.

Atrial Flutter with Inferior STEMI?

A 40-something year old male presented with tachycardia.

Computer analysis: Atrial Flutter with Inferior ST Elevation MI.

The computer (and physicians!) frequently fails to recognize that the flutter waves alter the baseline and can thus mimic ST elevation.  All ST elevation in this case is due to the flutter waves.

It is even more common that atrial flutter mimics ST depression.  See this case, and this case.