Weakness and Dyspnea with a Sine Wave. It’s not what you think!

I don't have all the clinical data on this patient, and unfortunately the ECGs are of low resolution, but they are good enough.


A middle aged woman presented with weakness and dyspnea.   This was her presenting ECG:
What is the differential diagnosis?  What would you do?

There is a sine wave, which is seen with severe hyperkalemia.  It is sometimes called "Ventricular flutter," and is also reported with Class I antidysrhythmics, which are sodium channel blocking agents.

There are pacer spikes.  I don't know if this was a pacemaker provided in the ED, or if the patient has an implanted pacer.  The pacer seems to initiate each beat and the patient may indeed be pacer dependent at this moment.

Tricyclic antidepressants (TCAs) also block sodium channels, widening the QRS, but I have never heard of them causing a sine wave.  This one from Life in the Fast Lane is the closest I have seen.

Treatment of such a patient would include Calcium to treat hyperkalemia, either (preferably) as calcium gluconate, or, if you are certain you have a very good IV, Calcium Chloride (CaCl) (which can sclerose veins).

Remember that to give the equivalent calcium load as 1 g of CaCl, one must give 3 g of Ca Gluconate.  If a patient has life threatening dysrhythmias from hyperK, I know of no upper limit to the dose of calcium.  See this case of VT from hyperK in which I gave 15 grams (doses, "amps") of Calcium gluconate before the patient stabilized.

For this patient, I would give Calcium at least until the serum K returned or further history made the diagnosis clear or the patient stabilized.   I would give Bicarbonate as a treatment for possible Na channel blockers, with the added benefit that it helps hyperK as well.

Clinical Course

This patient later admitted to taking too much of her Flecainide, which is a Vaughn Williams class Ic antidysrhythmic and thus a sodium channel blocker and thus prolongs the QRS.

3 hours later, this was recorded: I don't know what therapy was given, if any. 
The QRS is less sinusoidal and actually has a QRS and a T-wave, and both are very wide.  We can see that complexes only occur when there is a pacer spike, so the patient appears to be pacer dependent.  There are pauses of almost 2 seconds where the pacer does not capture. 

There is also a very long QT, partly because of the long QRS, but also because repolarization (the JT interval)  appears prolonged.   Although at therapeutic doses, flecainide is a Na channel blocker, at toxic doses, it may also block potassium channels, inhibiting repolarization.

With others, my brilliant colleague at Hennepin, Jon B. Cole, MD, Medical Director of the Hennepin-based Minnesota Poison Control System, wrote this great case report on use of intravenous fat emulsion (IFE) in Flecainide overdose:  http://www.ncbi.nlm.nih.gov/pubmed/22882363

Flecainide has high lipid solubility and a large Volume of Distribution (4.8 L/kg) due to protein binding and lipid solubility, making it a great candidate for therapy with intravenous fat emulsion.  However, there are significant uncertainties about this therapy, particularly for ingested (as opposed to parenteral) route of toxicity: the IFE may increase absorption of toxin from the gut.

As for dosing of IFE, the American College of Medical Toxicology (ACMT) currently recommends administering 1.5 mL/kg of 20% IFE as an intravenous bolus over 2–3 minutes followed by an infusion of 0.25 mL/kg/min for 60 minutes.  The bolus may be repeated if cardiac arrest ensues, and the infusion can be increased if the patient demonstrates clinical deterioration.

Thus, it should only be given if the patient is in refractory shock and does not have enough time to be placed on Extracorporeal life support (this is a case of flecainide toxicity treated with ECLS), the most preferable treatment for cardiotoxic drugs.


Very large doses of IV Bicarb, and 2-4 g IV Magnesium (as a nonspecific therapy for long QT), and IFE only if the patient is in refractory shock and cannot be put on extracorporeal circulation.   Transcutaneous or transvenous pacing may be critical as well.  Get the patient on extracorporeal life support as quickly as possible in cases that are likely to be refractory to medical therapy.

For more on intravenous lipid therapy for overdose, visit: www.lipidrescue.org, and this article from Critical Care (full text)

Here is an older (full text) case report of flecainide toxicity.

A 50-something male with Dyspnea

A middle-aged male presented with dyspnea.  An ECG was recorded.
What is going on?  See below.

There is sinus rhythm.  There is notable ST depression in V1-V4, maximal in V2 and V3.  At first glance, it appears to be a posterior STEMI.

But one must always read ST and T-wave abnormalities in the context of the QRS.  There is a large R-wave in V1-V3.  One can see a large R-wave in posterior MI, and so one feels as if one's first impression is confirmed.

However, Right ventricular hypertrophy (RVH) also results in large right precordial R-waves and secondary ST and T-wave abnormalities that mimic ischemia.

One should always look for an S-wave in lead I.  And there it is.   There is right axis deviation.  All this is strongly suggestive of RV hypertrophy.

So a cardiac ultrasound was done:

--Pulmonary hypertension: The estimated pulmonary artery systolic pressure is 72 mmHg + RA pressure.
--Right ventricular enlargement .
--Decreased right ventricular systolic performance .
--Right atrial enlargement but the inferior vena cava is small in size.
--Left ventricular hypertrophy concentric .
--The estimated left ventricular ejection fraction is 75 %

--There is no left ventricular wall motion abnormality identified.

The patient ruled out for MI.

Also, the the workup for PE was done and was negative.  Etiology was airway disease.  McGinn (S1Q3T3) is present here but is a very soft sign of PE.  In a large group of dyspneic patients worked up for PE, those without PE had a 3% incidence of S1Q3T3 and those with PE had an incidence of 8%, for very low positive and negative predictive values.  Also, PE does not give large R-waves in right precordial leads. 

Learning Point:

1.  Abnormal ST elevation and/or depression, and/or T-wave inversion (abnormal repolarization), may be primary (due to ischemia, for instance), or these may be secondary to abnormal depolarization (an abnormal QRS, such as LVH, RVH, LBBB, RBBB, and others).

Thus, one must always closely examine the QRS to be certain that it does not harbor abnormalities that explain the repolarization abnormalities.

2.  Right ventricular hypertrophy often results in right precordial ST depression and T-wave inversion that mimics ischemia.  In particular, it mimics posterior STEMI.

Hypothermia and Right Bundle Branch Block, with ST Elevation?

This patient was found outside in the cold, unresponsive, hypotensive, and underwent brief chest compressions by EMS.

Here is his ED 12-lead ECG: 

What do you see?  Description/Answer below.

There is Atrial Fibrillation.  There is right bundle branch block (RBBB), but without the usual rSR', rather with a qR-wave in V1-V4 and aVL, highly suggestive of previous anterolateral MI.  The QRS is 160 ms, or is it longer?  There is a shoulder at the end of the QRS.  What is this?  Is this ST elevation?

The patient's temperature was 30 degrees C (86 deg F).  The "shoulder" is NOT ST elevation, but rather is an Osborn wave in the setting of RBBB.

He was resuscitated and warmed.  A bedside ultrasound showed global hypokinesis but wall motion was not well assessed.  

A repeat ECG was recorded:
The Osborn Waves are a bit more prominent now.  Or is this ST elevation?

Clinical Course

A head CT was negative.  The patient underwent coronary angiography, which showed a chronically occluded LAD.

He did well.  There was no acute MI.

Below are his previous ECG and a follow up after rewarming:

Sinus rhythm and RBBB with qR of old anterolateral MI.  No "shoulder" here.  There is a positive T-wave in the same direction as the R'-wave, which is slightly abnormal and may be due to the old MI.

After rewarming:
No significant difference from the previous.

The ECG in hypothermia 

Rhythm: The most common rhythms in hypothermia are sinus bradycardia, junctional bradycardia, and atrial fibrillation.  Shivering artifact is common.  Atrial flutter is seen in case 1.  At temperatures below 30 C, the patient is at risk for ventricular fibrillation.   In thisstudy of 29 humans cooled to 28-30 C for cardiac surgery, 19 developed atrial fibrillation and 2 ventricular fibrillation.

QRS: Osborn waves are thought to be pathognomonic of hypothermia, but can also be seen in normothermic patients.  "J-waves" or "J-point notching" is very common in early repolarization.   Very narrow Osborn waves were reported in severe hypercalcemia (level 16.3).  Sometimes a short ST segment of hyperCa can be misinterpreted as an Osborn wave (see image below); that is not the case in the aforementioned case report.   J-wave syndromes are proposed to give a unifying pathophysiology to Osborn waves of hypothermia and early repolarization, as well as Brugada syndrome.

Very large and wide J-waves, as in case 1, are almost exclusively due to hypothermia.  The etiology is beyond the scope of this blog, but may be read here.  

Hypothermia and pseudoinfarction patterns: MI or ischemia (either ST elevation or depression) may be mimicked either by 1)repolarization abnormalities (As in Case 2, with ST elevation) or by 2) confusing the J-wave with the ST segment, as in this case in JACC (full text) and this case in Archives of Internal Medicine (no full text).  This latter case also has ST segment depression as a repolarization abnormality.

Other blog cases of Osborn waves

Here is an example of RBBB with anterior STEMI (there are many others if you look at the RBBB "label" down the right side)

Interesting Left Main Occlusion….

Many believe that left main occlusion results in diffuse ST depression with ST elevation in aVR.  This is not true, as I write about in this post: The difference between left main occlusion and left main insufficiency.

A 38 year old male presented with 6 hours of chest pain, and recent chest pain with exertion.  He had no significant past medical history and was on no medications.  He is a non-smoker.  The initial troponin was 1.62 ng/mL.

Here is the initial ECG:
There is diffuse ST depression, with ST elevation in aVR.
This is consistent with coronary insufficiency, but not coronary occlusion.
It could be a tight left main, or a tight LAD, especially with 3-vessel disease.

There is ST elevation in lead III, with an ST axis directly to the left.  Is there inferior STEMI also? 

Such patients have about a 50% chance of needing CABG, as shown in an article referenced and described in this post.  Therefore, Plavix (clopidogrel) should be avoided.

The patient was taken for emergent angiogram:
This is an angiogram of the left main, and it is totally occluded.

How is that possible?  Why is the patient alive?  And why is there ST depression of subendocardial ischemia rather than ST elevation of anterior, lateral, and posterior walls?

Why is this not a STEMI?

The answer lies in the RCA angiogram:
The distal RCA is seen on the left side of the image (we do not see the catheter or the injection at the ostium of the RCA.
There are right to left collaterals which supply the left system with enough flow to keep the patient alive and to prevent subepicardial ischemia (STEMI).  All of the flow seen on the right side of the image is flow in the LAD and circumflex that is supplied by the RCA collaterals.

The apparent inferior STEMI may be due to "Coronary Steal Syndrome": Right to left flow is stealing blood supply from the inferior wall.

The left main was opened and the patient did well.

Most left main occlusions to not make it to the ED alive.

See this previous post for an extensive discussion (same link as above).

How are these cases related?

I saw these two cases on the same day.

This patient had a GI bleed and a massive transfusion:
What is it?

This patient had a history of "frozen shoulders," and had been treated for this elsewhere for quite a while.  He had been seen in the ED 6 days prior for increased shoulder pain, and was referred back to his orthopedic clinic.  He had this ECG recorded because shoulder pain can be a symptom of ACS:
What do you notice?

The first case has a very long ST segment and thus long QT.  This is classic for hypocalcemia; the ionized calcium was 3.0 mEq/L.  This is a common complication of massive transfusion.  One must be vigilant for hypocalcemia.

The second case shows a very short QT with short ST segment.  The computer measured it at 354 ms.   This was a tipoff to hypercalcemia and so we suspected that this patient had cancer as the etiology of his pain.  A chest x-ray (which we were going to get anyway) confirmed a chest mass.  A chest CT confirmed this and also showed otherwise occult spread to the shoulders.  The ionized calcium was 7.32 mg/dL and the total calcium was 15 mg/dL.

Here was the ECG after normalization of Ca in the second (hypercalcemia) case:
The QTc is now 384 ms

Wide Complex Tachycardia in a 20 something.

This was sent by a former resident.  He will remain anonymous because his identity could compromise patient confidentiality.


A 20-something female presented with palpitations and lightheadedness.  She had no previous medical history except for some "in utero tachycardia" which was treated until a very early age.  She has had no problems since and takes no medications.  She has no specific conduction abnormality diagnosis.

Her mother states she is not thinking clearly ("acting as if she is intoxicated").  The patient reports exertional syncope and was syncopal on the way to the triage desk.

Exam: Very large, at 5' 10" (178 cm) tall and 346 lbs. (156 kg).
Pulse: 235
BP: 121/67
SpO2: 98% on room air

Otherwise unremarkable.

There is a regular wide complex tachycardia at a rate of 231. 
There is no recognizable morphology, such as RBBB or LBBB.
The complexes are very wide
The initial portion of the QRS represents prolonged depolarization, arguing strongly against SVT.
So it must be VT or antidromic AV reciprocating tachycardia (AVRT)
There are small waves in lead II across the bottom.  Are these retrograde P-waves?

The rhythm strips, which unfortunately were not recorded, reportedly showed irregularity, with a rate varying from 180-250.

Because of this irregularity, the treating physician was worried about Atrial fibrillation and WPW, and therefore was reluctant to give adenosine.

See here for a discussion of Atrial fib and WPW, and the danger of adenosine and of other AV nodal blockers, and of the safety of these medications if it is NOT atrial fibrillation.

What would cause this rhythm but have some irregularity on the rhythm strip?  Could this be atrial fibrillation?  Is adenosine really contraindicated?

It is very important that you recognized that the ECG shown CANNOT be Atrial fibrillation with WPW.  
1) it is perfectly regular (I even used calipers)
2) When you have atrial fibrillation with WPW, there are multiform QRS complexes.

Clinical Course:

Procainamide was administered.  There was no response.

Labs were normal.  K was 3.5 mEq/L.

Electrical Cardioversion was the next step.  As the BP was stable after some fluids, low dose propofol  (60 mg) was used for sedation.

Synchronization was turned on; here it is:
Are the sync arrows pointing to a T-wave?  Or QRS?  If the point to the T-wave, synchronized cardioversion could result in ventricular fibrillation.
See this post demonstrating dangerous and erroneous identification of the QRS.

Cardioversion was done at 200J biphasic.

Here is the result:
The cardioversion occurs almost halfway through the strip. There is conversion to Polymorphic VT or Ventricular Fibrillation.

There was a pulse, so it must be Polymorphic VT.  The BP was 70 systolic.  She was given 2 g of Mg, and defibrillated at 200 J biphasic.  Here is the result:
Polymorphic VT has deteriorated into Ventricular Fibrillation

After a couple defibrillations, there was conversion back to a wide complex tachycardia:

Color and BP were improving and she was awakening.

Consultant recommends amiodarone and repeat cardioversion.

This was done without success.

She reverted to V Fib again:

Chest compressions were started.  She was given an Esmolol bolus and infusion and then defibrillated again, all during chest compressions:

She is defibrillated into an organized wide complex rhythm, which then becomes a narrow complex tachycardia with occasional wide complexes.

Continued monitor strips:
Finally stabilizes in sinus rhythm

Sinus rhythm.  There is no good indication of underlying pathology.

She remained on the esmolol drip and had no more dysrhythmias.  Cardiac MRI was normal.  Echo was normal.  EP study was done.  See below.

What happened?

Was there an irregular rhythm?  We must take the word of the physician.

Was it atrial fibrillation?  On the initial ECG, it certainly is not atrial fibrillation.   Therefore, if the irregular rhythm was atrial fib, then the patient was flipping back and forth between a rapid atrial fib and a regular wide complex tachycardia.  This is very improbable.  

What else could it be?

It could be what it was proven to be on EP testing: Dual AV nodal pathways and WPW (there is no delta wave, and thus there is 'concealed conduction'.  Read this to understand concealed conduction.

In this scenario, the dysrhythmia is antidromic AV reciprocating tachycardia (AVRT) that goes down the accessory pathway and up either one of two AV node pathways.  The resulting rate depends on which pathway is used.

Here are some schematics that were nicely drawn by the physician:

Dual AV nodal pathways:
Fast pathway: conducts quickly, longer refractory period
Slow pathway: shorter refractory period

Add an Accessory pathway to the mix:

Ablation of the Bypass tract (Accessory Pathway) was completed.

How would I have managed this?

I would have attempted adenosine.  It is not atrial fib with WPW.  If it is VT, adenosine will be safe.   It might work.  If adenosine does not work, then cardiovert.

I believe adenosine would have worked here.