ECG Interpretation Review #53 (Peaked T - Hyperacute - DeWinter - Wellens - aVR)

The ECG in Figure 1 was obtained from a patient who walked into the ED (Emergency Department) with new-onset chest pain.

• Should the cath lab be activated for acute STEMI?
• If so – What do you suspect the “culprit artery” is likely to be?
• How many ECG signs support your impression?

Figure 1: ECG from a patient with chest pain. What are the findings of concern? (Reproduced from ECG-2014-ePub). 

==========================================

INTERPRETATION:  The ECG in Figure 1 is shows normal sinus rhythm. All intervals and the axis are normal. There is no chamber enlargement. There are however, a series of alarming findings that were recognized by the emergency team. Emergency cardiac catheterization was performed within 15 minutes after the patient walked into the ED ― with successful reperfusion of a 100% proximal LAD (Left Anterior Descending) coronary artery occlusion.

     Clues to the need for immediate catheterization and clues indicating localization of the “culprit artery” to the proximal LAD include the following:

• Hyperacute T waves in multiple leads. These are best seen in leads aVL, V2,V3,V4.
• DeWinter T wave complexes ― in which there is 1- to 3-mm of upsloping J-point ST depression in one or more precordial leads that continue into tall, positive symmetrical T waves (DeWinter – NEJM 359:2071, 2008). Although seen in Figure 1 to some extent in all precordial leads except for V1 ― the DeWinter T wave is best manifested in leads V3,V4.
• Loss of anterior R waves (with reduction in R wave amplitude between leads V1-to-V2).
• Marked inferior reciprocal ST depression.
• ST elevation in leads aVR and V1.
• Incomplete RBBB (rSr’ in lead V1; narrow terminal S waves in leads I and V6).

==========================================

DeWinter T Waves: A Sign of Proximal LAD Occlusion:

     Awareness of the relatively uncommon but highly characteristic DeWinter T wave sign is essential for not overlooking the approximate 2% of acute anterior infarction patients who present with this ECG manifestation (Ref 1). Rather than frank ST elevation that usually accompanies acute LAD occlusion ― there is instead the unique DeWinter complex with upsloping J-point ST depression blending into tall upright hyperacute T waves in a number of precordial leads (esp. leads V3,V4 in Figure 1). We emphasize the following key points about this syndrome.

• In patients presenting with new-onset chest pain ― there is extremely high specificity for the DeWinter T wave pattern and acute proximal LAD occlusion.
• Rather than evolution of tall, peaked (hyperacute) T waves into frank ST segment elevation ― the DeWinter T wave pattern was surprisingly static over the next few hours in the DeWinter series of patients.
• None of the patients in the DeWinter series who manifested this ST-T wave pattern had acute left main occlusion on catheterization.
• Despite prompt recognition and intervention ― a significant percentage of patients developed positive cardiac markers for acute infarction. One ECG sign that infarction may have already occurred is loss of anterior r wave amplitude (as is seen in Figure 1).

==========================================

TAKE-HOME POINT: Prompt recognition of the DeWinter T wave sign in patients with new-onset chest pain with immediate mobilization of the interventional cardiology team On-Call is essential for minimizing the extent of acute anterior infarction. 

• As is the case for Wellens’ Syndrome (See Section 10.54 of the pdf in the References below) ― precordial DeWinter T waves is another unique ECG sign with high correlation to acute anatomic coronary occlusion with mandate for immediate intervention.

==========================================
FINAL PEARLS:

     In addition to precordial DeWinter T waves and loss of anterior R wave amplitude between V1-to-V2 ― there are several additional ECG signs in Figure 1 suggestive/consistent with acute proximal LAD occlusion. These include:

• Significant ST segment elevation in leads aVR and V1.
• Incomplete RBBB (that is presumably new).
• Marked reciprocal inferior ST depression.
• Hyperacute T wave in lead aVL.

==========================================

ACKNOWLEDGMENT: My appreciation goes to Andrew Bowman for allowing me to use this ECG and this clinical case.

========================================== 

NOTE: ― Relevant PDFs on ECG diagnosis of acute MI:

• http://tinyurl.com/DeWinter-NEJM ― Link to my dropbox for download of the original NEJM manuscript by Dewinter.
• Link to Section 10.0 from our ECG-2014-ePub.
• Figure 13.3-1 in Blog #126 shows another example of DeWinter T waves.
• Brief Summary of Wellens Syndrome —

========================================== 

ECG Interpretation Review #52 (Wide Tacycardia - Toxins - Hyperkalemia - Ventricular Tachycardia - Sinoventricular Rhythm)

The ECG in Figure 1 was obtained from an acutely ill but alert (and hemodynamically stable) patient.

• Is the rhythm VT (Ventricular Tachycardia)?
• How certain are you of your diagnosis?
• If told that the patient was a 31-year old woman with abnormal renal function who presented in DKA (Diabetic KetoAcidosis) ― Could you come up with an explanation as to why the rhythm in Figure 1 might not be ventricular tachycardia?

Figure 1: WCT rhythm in a 31yo woman with renal disease and DKA. Is this VT? 

INTERPRETATION: The rhythm in Figure 1 is a regular WCT (Wide-Complex Tachycardia) at a rate of ~135/minute. No P waves are seen. The usual differential diagnosis for a monomorphic regular WCT of uncertain etiology is shown in Figure 2:

Figure 2: Common Causes of a Regular WCT when sinus P waves are not seen.

Our reason for listing VT as the first 8 entities in LIST #1 ― is that VT is by far the most common cause of a regular WCT of uncertain etiology – and – that VT should not be missed.

• Assessment of QRS morphology in Figure 1 reveals an exceedingly wide, amorphous QRS complex that does not at all resemble any form of bundle branch block.
• The QRS is entirely negative in lead V6 (deep QS complex) ― and it is entirely positive in lead aVR (monophasic R wave) ― both being features that under normal circumstances identify VT with near-100% specificity.
• There is extreme axis deviation (totally negative QRS in leads I and aVF) ― which also normally conveys near-100% specificity for a diagnosis of VT.

The above said – clinical circumstances in this case differ from the usual setting for VT, and are KEY to recognizing the correct diagnosis. The patient is a 31-year old woman with abnormal renal function and acute DKA. The reason for QRS widening is marked hyperkalemia! (serum K+=9.8 mEq/L at the time Figure 1 was obtained).

• ECG changes of hyperkalemia typically follow a progressive sequence (See ECG Blog #10). Initially ― there is generalized T wave peaking (serum K+ ~5.5-6.5 mEq/L).
• As serum K+ levels approach ~7-8 mEq/L range ― the QRS widens and P wave amplitude decreases.
• Eventually, P waves disappear. Interestingly, the sinus node is still able to transmit the electrical impulse to the ventricles even though no P wave is seen. This is known as a sinoventricular rhythm ― and could be an explanation for how the regular WCT in Figure 1 might reflect sinus rhythm despite the absence of P waves ... 
• Ultimately ― transmission of sinus impulses ceases, and a sinusoidal-widened pattern supervenes. Ventricular fibrillation or cardiac standstill invariably follow.

---------------------------------------------------

BOTTOM LINE: Whether the rhythm in Figure 1 represents VT from marked electrolyte disturbance vs sinoventricular rhythm with QRS widening (and loss of P waves) from hyperkalemia is uncertain. We favor the latter ― because the treating clinician in this case recalled that onset of QRS widening was gradual following an initial ECG in which the QRS was narrow and T waves were peaked. IF the rhythm in Figure 1 had been VT ― we would have expected a much more abrupt onset of the regular WCT rhythm.

• Treatment with emergency K+-lowering treatment (calcium gluconate; glucose plus insulin; acute dialysis) resulted in resolution of QRS widening and return of electrically-evident sinus rhythm.

ADDENDUM: Perhaps List #1 in Figure 2 should be amended by addition of an Item #11 = “Something else” to include entities such as hyperkalemia and/or toxin effect (as might be seen with tricyclic overdose, in which marked QRS widening may be seen despite persistence of sinus mechanism).

----------------------------------------------------

ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.

----------------------------------------------------

• See Section 11.0 on Electrolyte Disturbances (in ECG-2014-ePub) ― with the part on Hyperkalemia beginning in Section 11.3.

-------------------------------------------------------------------------------------

ECG Interpretation Review #51 (Chamber Enlargement - LVH - Cardiomyopathy)

The ECG shown in Figure 1 was obtained from a 50-year-old man who presented to the office with dyspnea on exertion. No chest discomfort. He is a chronic smoker with a longterm history of alcohol consumption. The patient says he, “doesn’t see doctors”. He takes no medications. There is no obvious heart failure or wheezing on exam.

• Should the patient be admitted to the hospital because of his ECG?
• What clinical diagnosis do you strongly suspect?

Figure 1: ECG obtained from a 50yo smoker/drinker with dyspnea on exertion. What diagnosis is suggested by this ECG? NOTE - Enlarge by clicking on Figures - Right-Click to open in a separate window.

------------------------------

INTERPRETATION:  The ECG shows sinus rhythm at a rate of about 85/minute. The PR and QRS intervals are normal; the QT is no more than borderline prolonged. The axis is normal (approximately +50 degrees). Beyond this point – a variety of interpretations are possible. We make the following points:

Point #1: There appears to be evidence of at least 3 chamber enlargement:

• RAA (Right Atrial Abnormality) – is diagnosed by the tall, peaked and pointed P wave in the inferior leads (that is >2.5 mm tall in lead II).
• LAA (Left Atrial Abnormality) – is suggested by the deep, negative component to the P wave in lead V1.
• Voltage for LVH (Left Ventricular Hypertrophy) – is diagnosed by the finding of deepest S wave in V1 or V2 + tallest R wave in V5 or V6 ≥35mm.
• True LV (left ventricular) chamber enlargement is strongly suggested (with ≥90% specificity) by the finding of voltage for LVH in an adult over 35 years of age when underlying heart disease is likely – IF there are ST-T wave changes consistent with “strain” (Figure 2). The difficult-to-describe ST-T wave abnormalities seen in leads V5,V6 of Figure 1 are clearly not normal findings in these lateral precordial leads. While they do not quite manifest a typical “Strain” pattern – they do qualify as a “strain equivalent” pattern that overwhelmingly favors a diagnosis of LVH in this patient.

Figure 2: Schematic depiction of LV "strain" and "strain equivalent" patterns. When either is present in addition to voltage for LVH - the specificity of the diagnosis is greatly increased.

------------------------------

Point #2: The QRS complex and ST segments in Figure 1 are not normal:

• There is ST segment coving ("frowny" configuration) with some amount of ST elevation in leads V1,V2 (difficult to be sure where the J point begins in these 2 leads).
• The ST-T waves in leads V4,V5 are clearly abnormal (with appearance of at least some T wave inversion). There is abnormal ST-T flattening in other leads.
• In addition – the QRS complex looks abnormal in Figure 1 (with notching and slurring in several leads). That said – the QRS is really not widened, so no definite conduction defect is present.
• In the absence of a prior ECG – We can not rule out something acute going on (given the ST coving and elevation in leads V1,V2,V3). That said – Our "sense" is that the changes seen in Figure 1 are more likely to be longstanding and not acute.  Supporting this supposition is the lack of reciprocal changes.

------------------------------

Point 3: The clinical diagnosis that we strongly suspect when we encounter an ECG such as seen in Figure 1 is of a cardiomyopathy (based on the history and ECG findings of abnormal though not necessarily prolonged QRS complex; multi-chamber enlargement; and clearly abnormal ST-T wave morphology).

• We would not necessarily admit this patient to the hospital on the sole basis of this ECG.  We would obviously feel better IF we could find an old ECG showing similar changes.  We'd use clinical judgement in the context of the clinical setting to guide our decision. 
• This patient would most likely be admitted to the hospital IF he presented in the middle of the night to an ED (Emergency Department).  IF he however presented to the office without any objective evidence of heart failure and without any chest discomfort – and his dyspnea was not new, not severe, and associated with a good office oxygen saturation – we would probably feel comfortable managing his presumed cardiomyopathy on an ambulatory basis.  One just has to be there to decide . . .

------------------------------

• See ECG Blog #73  – for more on ECG diagnosis of LVH -
• See ECG Blog #75  – for more on Atrial Enlargement - 

------------------------------

ECG Interpretation Review #50 (Syncope - STEMI - MI - Brugada - RBBB - Early Repolarization)

The ECG shown was obtained from a 62-year-old man who presented to the ED (Emergency Department) with a history of several presyncopal episodes in recent months. His ECG was diagnosed as showing acute anterior STEMI (ST Elevation Myocardial Infarction). 

• Do you agree? 
• What treatment is indicated?

Figure: ECG obtained from a 62 year-old man with a history of presyncopal episodes. 

------------------------------------------------------------

INTERPRETATION: The ECG shows sinus bradycardia at a rate just under 60/minute. All intervals and the axis are normal. There is no chamber enlargement. There may be slight J-point ST elevation in lead I, and some nonspecific ST depression in inferior and lateral precordial leads. That said – the area of most concern clearly relates to findings in leads V1 and V2.

• There appears to be an rSr’ complex in V1,V2.
• There is an elevated J-point in each of these leads – with an unusual type of downsloping ST segment that is especially marked in lead V2. The ST segment terminates in shallow T wave inversion.
• The ECG findings in the Figure are highly suggestive of Brugada Syndrome. First described in 1992 — the Brugada syndrome is important to recognize because of an associated very high risk of sudden death. The prevalence of this disorder is approximately 1/2000 in the general population. Brugada syndrome is a leading cause of sudden death in adults under 40.

------------------------------------------------------------

BOTTOM LINE: Although serial tracings and troponins are advised — the ECG in the Figure is not suggestive of acute STEMI. It is also not representative of RBBB (Right Bundle Branch Block). Instead, especially in view of the history of several recent presyncopal episodes (!) — the tracing suggests Brugada Syndrome. 

• Cardiology consult should be obtained.
• ICD (Implantable Cardioverter-Defibrillator) placement should be considered, pending results of careful evaluation.

------------------------------------------------------------

ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.

------------------------------------------------------------

For more on Brugada Syndrome – See ECG Blog #238 —

—  —

------------------------------------------------------------

ECG Interpretation Review #49 (Chest Pain - STEMI - Culprit Artery - LAD - RBBB - LAHB - AFib - Nodal)

The 12-lead ECG and lead II rhythm strip shown in Figure 1 were obtained from 55-year-old man with “chest pressure”. He is hemodynamically stable.

• What is the rhythm?
• Can you identify the “culprit artery” ?

Figure 1 – 12-lead ECG from a 55-year-old man with chest pressure. 

INTERPRETATION: The first problematic aspect of the tracing in Figure 1 is to determine the rhythm. Given that the patient is hemodynamically stable – there is at least a moment to contemplate what is seen.

• The QRS complex looks slightly widened. Assessing QRS duration in leads where the complex appears to be widest (ie, leads V4,V5,V6) – we estimate QRS duration at 0.11 second (just over half a large box). That said – QRS morphology looks to be supraventricular (as we’ll discuss momentarily).
• The rhythm is not sinus. There is no upright P wave in lead II. In fact – there are no P waves anywhere … There are fine undulations of the baseline – although we can’t be sure if this represents baseline artifact, fine “fib waves”, or both.
• The rate is ~100/minute.
• The rhythm is not completely regular. This tracing provides an excellent example of how easy it is to be fooled into thinking a rhythm is regular when one does not measure (with calipers) consecutive complexes. Admittedly – variation in R-R interval from beat-to-beat is minimal – and there are a number of consecutive beats with the same R-R interval. But there is some variation.

-------------------------------------------------------

BOTTOM LINE: What is the Rhythm?

We are not certain what the rhythm in Figure 1 is based on this single tracing. Additional rhythm strips would be needed to know for sure. The differential diagnosis includes:

• Fascicular Tachycardia or VT (Ventricular Tachycardia).
• Accelerated AV Nodal (Junctional) Rhythm.
• AFib (Atrial Fibrillation).

We favor AFib with a controlled but regularized ventricular response as the most likely etiology of this rhythm – given supraventricular appearance, irregularity, and absence of P waves.

• We doubt the rhythm is VT or fascicular tachycardia – given its supraventricular appearance (See below).
• We can’t rule out the possibility of an accelerated junctional rhythm – given the “almost regularity” of the rhythm.
• We fully acknowledge that we are not certain of the rhythm.
• Given that this patient is at the moment hemodynamically stable – there are much more pressing problems than determination of the rhythm!
• Additional rhythm strips will almost certainly clarify rhythm diagnosis.

-------------------------------------------------------

What is Going On with the Rest of the Tracing? 
QRS morphology in Figure 1 suggests RBBB (Right Bundle Branch Block).

• The QRS complex is widened. Although a typical rSR’ pattern is not seen in lead V1 - the QR pattern that is seen serves as a “right bundle equivalent” in a patient who has lost the small initial positive r wave deflection due to septal infarction.
• S waves are seen in left-sided leads I and V6 (although admittedly the S in lead I is not nearly as wide as is usually the case with RBBB).

In addition – there is LAHB (Left Anterior HemiBlock), as determined by the rS complexes in the inferior leads producing a markedly leftward axis. The presence of RBBB/LAHB qualifies as “bifascicular block”.

     Of most concern – the ECG in Figure 1 suggests ongoing evolution of a large acute STEMI (ST Elevation Myocardial Infarction):

• Q waves are seen in septal leads V1 and V2.
• There is significant ST segment elevation in leads V1-thru-V4. There is also ST segment coving and elevation in lead aVL. ST elevation in lead V3 shows straightening of the ST upstroke and elevation of the J point by at least 4mm.
• There is also ST segment elevation in lead aVR.
• Reciprocal ST segment depression is clearly seen in each of the inferior leads (II,III,aVF).
• There appear to be hyperacute T waves in the inferior and lateral precordial leads.

IMPRESSION: The ECG shown in Figure 1 suggests acute proximal occlusion of the LAD (Left Anterior Descending) coronary artery causing an extensive anterior STEMI. Acute reperfusion is urgently needed for this patient.

• ST elevation in leads V1-thru-V4 suggests antero-septal involvement.
• ST elevation also in lead aVL suggests involvement of the 1st Diagonal Branch of the LAD.
• Septal necrosis with extensive damage is suggested by: i) RBBB (especially in view of the loss of the initial positive r wave deflection in lead V1 with this RBBB); ii) Q waves in leads V1,V2; iii) ST elevation in lead aVR; iv) presumably new bifascicular block (RBBB/LAHB); v) AFib. 
• This patient is at high risk of developing complete heart block and/or cardiogenic shock.

-----------------------------------------------

ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.

---------------------------------------------------- 

NOTE: - Relevant PDF on ECG diagnosis of acute MI:

• Link to Section 10.0 from our ECG-2014-ePub.

----------------------------------------------------