Wednesday, August 8, 2012

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 SyndromeSee ECG Blog #238

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Wednesday, August 1, 2012

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: