Syncope and a Possible Type 2 Brugada Morphology

A young man had 10 seconds of syncope without a prodrome.  He had had it once before.  Exam was normal.

This ECG was recorded:
There is rSr' in both V1 and V2, with a "saddleback" in lead V2, and the "beta" angle is wide.  It meets, or at least nearly meets, criteria for type 2 Brugada.

Having just written on this topic, I knew that this could be the result of lead placement that is too high.

V1 and V2 should be placed at the 4th intercostal space.  Placing them at the 3rd can result in false positives for Brugada.

I asked the tech if she was sure she had placed them correctly.

She returned saying that she had placed them one interspace too high, and handed me this ECG recorded at the right interspace:

The rSr' is gone and the saddle is gone as well.

Learning point:

Beware lead placement in the diagnosis of right ventricular conduction delay (rSr") and in the finding of Brugada pattern ECG.

Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. Why?

A middle-aged male had a V Fib arrest.  He had not complained of any premonitory symptoms (which is very common).   He had a history of CAD with CABG.  Here was his initial ED ECG:
There is atrial fibrillation with a rapid ventricular response.  There is profound ST depression especially in I, II, V2-V6.
ST depression is common BOTH after resuscitation from cardiac arrest and during atrial fib with RVR.

The patient was cardioverted.  Here is the post cardioversion ECG:
ST depression, with ST elevation in aVR persists.

Does this patient have ACS?  Should he necessarily go to the cath lab?

Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion.

One must wait a short time (perhaps 15 minutes?), and repeat the ECG, to see if the apparent ischemia persists.

This was done.  A third ECG was done about 25 minutes after the first:
This shows resolution of all apparent ischemia.

The patient thus did not need immediate angiography.

An echocardiogram showed:

Left ventricular hypertrophy concentric .
The estimated left ventricular ejection fraction is 58 %
Aortic stenosis, mild, 9.0 mmHg mean gradient. 1.50 cm^2 valve area.

Troponins were minimally elevated, consistent with type 2 MI from low flow state of cardiac arrest and high demand state of atrial fib with RVR.

The patient underwent angiography later (the next day) and there was no culprit lesion.  He did not have ACS.

He recovered and had an ICD implanted.

Learning Points:

1. Ventricular fibrillation is not only caused by acute coronary syndrome.   There are many other etiologies, including scarring from previous MI, medications, drugs, LVH, and channelopathies.  We found that 38% of out of hospital ventricular fibrillation was due to STEMI.  The remainder were due to other etiologies, (including NonSTEMI ACS).  But approximately 50% were due to non-ACS etiologies.

2. ST depression (with reciprocal ST elevation in lead aVR) is common shortly after BOTH resuscitation from ventricular fibrillation AND after cardioversion from atrial fibrillation.

3.  One should wait a short time (15 minutes?) to record another 12-lead ECG to ascertain whether there is ongoing ischemia and probable ACS, or whether the ST depression is transient only.

4. Not all patients with ventricular fibrillation necessarily need emergent angiography.  Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.


Scott NL. Mulder M. Bart B. Smith SW.  Correlation of STEMI in Resuscitated Non-traumatic out-of-hospital Cardiopulmonary Arrest patients with Initial Rhythm and Cardiac Catheterization Findings (Abstract 580). Academic Emergency Medicine 17(s1):S194; May 2010

Acute chest pain, bradycardia, and hypotension

A middle-aged male complained of acute onset of chest pain.  He was diaphoretic, weak, lightheaded, but alert.    Blood pressure was 60/palp with a pulse of 40.  was given aspirin and a 500 ml normal saline bolus.

Here is the prehospital 12-lead:
There is bradycardia and some kind of AV block.  P-waves are difficult to discern, so the exact nature of the block is unclear

There is obvious inferior STE.   Reciprocal ST depression in aVL confirms inferior STEMI, and ST depression in lead I is a good indicator that this is an RCA occlusion.

In inferior MI due to RCA occlusion, one should always look to lead V1 for ST elevation indicating right ventricular infarct also.

Here, there is ST depression in V1 and V2, but ST elevation in V3.  This is odd and one must suspect that leads V1 and V3 are reversed.

The ST depression in V2 shows extension to the posterior wall.

The cath lab was activated by the medics.

The patient arrived alert and conversant.   BP was in the 40's to 60's, with pulse in 30s to 40s.

An ECG was recorded 11 minutes after the first:
Now it is clearly 3rd degree AV block.
There is clearly ST elevation in V1 (and now also V2) confirming right ventricular involvement, and confirming that prehospital leads were reversed.  This is such a large RV infarct that the ST elevation extends all the way to V3, which is often called a "Pseudoanteroseptal MI" (See more cases of pseudoanteroseptal MI)

A right sided ECG was immediately recorded (limb leads are not changed):
3rd degree heart block.  There is ST elevation in V2R (identical to V1 on regular 12-lead) extending all the way out to V6R

A bedside echo was done:

There is bradycardia.  The RV is massively dilated due to RV failure from RV infarct.

He was given ticagrelor and heparin.  He was given 25 mg of ketamine and transcutaneous pacing was begun.  Capture was achieved at 114 mA at a rate of 70.  Systolic BP rose to 110.

Capture was verified by bedside echo:

He went for angiogram which showed occlusion of the proximal RCA, proximal to the right ventricular marginal branch to the RV.

It was opened and stented.

The patient did well.

Learning Points

1.  Occlusion of the proximal RCA may result in hemodynamically significant RV MI.
2.  These occlusions also frequently lead to complete AV block because of blood supply to the AV node from the RCA
3.  RV MI can lead to RV failure and dilatation
4.  Fluids are indicated, as cardiogenic shock due to RV failure responds to fluid loading and does NOT result in pulmonary edema
5.  Transcutaneous pacing can be verified with bedside ultrasound.
6.  Rapid reperfusion of RV MI results in a good outcome

Ventricular Fibrillation, Resuscitation, and Hyperacute T-waves: What does the Angiogram show?

An elderly person collapsed and was found to be pulseless.  He had immediate bystander CPR.  An AED was placed and one shock was given within 5 minutes of arrest.  He immediately awoke.  EMS arrived and recorded these ECGs:

Time = 0
Sinus rhythm. Inferior and lateral ST elevation, with hyperacute T-waves in V4-V6.
1 min later
No definite difference.

He was stable en route to the ED.  On arrival, he was awake and complained of only mild aching left chest pain.  He stated that prior to his collapse, he had been walking briskly and was feeling short of breath, but not having any chest pain. He does have a history of CAD with a stent, and takes clopidogrel, but he did not take it on this particular day.

He had this ED ECG recorded, 13 min after first
There is inferior ST elevation with reciprocal ST depression in aVL, diagnostic of inferior injury.  The hyperacute T-waves in V4-V6 are diminished and there is less ST elevation.

The cath lab was activated.  He was given aspirin and heparin.

Prior to transport, another ECG was recorded. This one is 25 min after first prehospital, and 12 min after the first ED ECG:
There is nearly complete resolution of all injury pattern

Angiogram showed no culprit, but did show severe 3 vessel disease, with 100% chronic LAD and RCA occlusions, and chronic 75% circumflex.  All territories were supplied by collaterals from the circumflex!

An immediate Echo showed distal inferior and distal septal, anterior, and apical wall motion abnormality, with EF of 55-60%.

The patient was prepared for CABG.

Here is an ECG 15 hours after first:
Some reperfusion T-wave inversion in V5 and V6.

Troponin I peaked at 0.59 ng/mL.

ECG recorded 24 hours after first
More pronounced reperfusion waves in V3-V6 (Lateral Wellens' waves)

The patient underwent successful CABG.

Here is an ECG recorded after CABG:
There was some inferior injury that occurred from bypass.  This is not unusual.

So what happened?

1. The patient had demand ischemia from walking with severely restricted coronary flow.
2. The ischemia resulted in ventricular fibrillation.
3. The extreme low flow state of arrest, along with extremely poor coronary flow after resuscitation, resulted in transmural ischemia (subepicardial ischemia) with ST elevation and hyperacute T-waves.

So this is Type 2 MI with ST elevation (we avoid the term "type 2 STEMI", as STEMI is a term associated with ACS)

Giant Inverted T waves in an Elderly Patient

This is another contribution from Victoria Stephen.  Victoria is a third year EM Registrar from at the University of the Witwatersrand in Johannesburg, South Africa, and a great asset to FOAMed.  Follow her on Twitter: @EMcardiac.


A 91 year old presented to the ED of a small hospital with a history of sudden onset syncope. A family member thought she was having a seizure. She reported no chest pain or dyspnoea when conscious. The patient had a history of hypertension which was poorly controlled.

She appeared alert and well-oriented. Her initial BP was 184/90, HR 41 BPM. An ECG was recorded in the ED:
There is second degree heart block with a HR of 41 BPM. The QRS complex is 144ms indicating an infranodal escape. There is an RBBB configuration with a LAFB, indicating it may be originate from the left posterior hemi-fascicle. The QTc is significantly prolonged at 535 ms. There are deep wide bizarre looking T waves seen in virtually all the leads, but most notably in the precordial leads.

She had a CT of the Brain which showed no intracranial bleed. Her renal function was normal and the electrolytes including calcium and magnesium were normal. Two troponin I were increased at 140 ng/L (0.14 ng/mL) and 70 ng/L (0.070 ng/mL) on consecutive days, (negative is less than 40 ng/L for this assay). 

Two days later she was referred to a regional hospital where she was admitted to the CCU with the following ECG:
Complete Heart block still present, HR 33 BPM, QTc prolonged, 503ms. T waves are now upright in leads I and AVL.

An informal bedside echo done by a cardiologist showed a normal ejection fraction with no regional wall motion abnormalities. In view of the positive troponins and the T wave inversions she was taken to the cath lab for angiography, as well as for a pacemaker. No obstructive coronary artery disease was present. She subsequently developed runs of VT while in the lab which were too transient to determine the specific type of VT. A transvenous pacing wire was inserted for temporary pacing and the decision was made to bring her back for a permanent pacemaker.

Here is the ECG post venous pacemaker:
Notice the T-wave inversion is present in spite of the ventricular pacing, which should result in discordant T-waves (opposite the QRS).  Concordant T-waves of this dimension indicate ischemia that cannot be hidden by pacing.

And here is the ECG post permanent pacemaker, recorded 7 days after the first ECG:
This is a single chamber pacemaker. HR 62 BPM. The T waves are upright in in the inferior leads and biphasic in the precordial leads.


This patient suffered a Stokes-Adams attack, which is a sudden loss of consciousness due to a high grade atrioventricular block. Seizure like activity is commonly seen in this form of syncope. Two very different arrhythmogenic mechanisms have been shown to induce the abrupt loss of cardiac output causing the syncope. At the onset of complete heart block, asystole can occur for a brief period before a new pacemaker has kicked in. Either 1) the AV node may act as the new pacemaker, leading to a junctional or narrow escape on the ECG,  or 2) infranodal tissue will take over the pacemaker role.

The second arrhythmia which can abruptly occur during complete heart block (CHB) is Torsade de Pointes (TdP).  TdP is an example of a triggered dysrhythmia. Triggered dysrhythmias are heart rate dependent and are either triggered by a fast or slow heart rate. TdP is triggered by slow heart rates. (This is why overdrive pacing to a higher rate works in terminating TdP) In some patients, at the onset of complete heart block, there is an abrupt decrease in heart rate as well as prolongation of the QTc. The resulting pause plus a well-timed PVC then triggers the onset of TdP. Both asystole and TdP following CHB are often brief, allowing the patient to regain consciousness.
The giant inverted T waves are not common in CHB, but are commonly seen in CHB complicated by Stokes-Adams attacks. Their presence is not fully understood but has been associated with TdP and stress cardiomyopathy occurring after the onset of Complete Heart Block. Stress cardiomyopathy is a spectrum disorder characterized by transient left ventricular systolic dysfunction clinically, ST elevation or T wave inversions on the ECG, and regional wall motion abnormalities on echo which are induced by a catecholamine surge. Takotsubo cardiomyopathy is a specific form of stress cardiomyopathy. This paper demonstrates takotsubo cardiomyopathy developing in patients with complete heart block, preceding TdP:

Stress cardiomyopathy has been seen frequently in a myriad of different critical illnesses, particularly in subarachnoid haemorrhage, which often is associated with giant inverted T waves on the ECG:

Troponins can be elevated in stress cardiomyopathy and demonstrate a rising and falling pattern like an acute myocardial infarction. It is very difficult to differentiate SCM from MI; it often produces a PseudoSTEMI pattern that is very difficult, and sometimes impossible, to distinguish based on the ECG, though there are some guidelines.   Even echo can be misleading: the takotsubo apical ballooning can also be seen in acute STEMI.

If there is ST elevation, and the differential diagnosis is acute coronary occlusion vs. SCM, an angiogram is usually required.  

However, in this setting of Stokes Adams attack with CHB and bizarre T-wave inversion, emergent angiogram is not necessary.


Complete Heat Block accompanied by giant inverted T waves is associated with Stokes-Adams attacks.

A prolonged QTc with CHB is at risk of torsades. Treat any associated electrolyte abnormalities that may be present.

Torsade de Pointes is triggered by bradycardia, a prolonged QTc and an abrupt change in heart rate, which creates a pause.

Inverted T waves are often seen in stress cardiomyopathy syndromes. Stress cardiomyopathy is a diagnosis of exclusion after formal echocardiography with or without angiography. 

Other references:

Mechanisms of syncope and Stokes-Adams attacks: 

Giant T wave inversion: 

Cardiac and non-cardiac causes of T-wave inversion in the precordial leads: