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. (Reproduced from ECG-2014-ePub).  NOTE - Enlarge by clicking on Figures - Right-Click to open in a separate window.
------------------------------------------------------------
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 – the tracing shows characteristic findings of Brugada Syndrome
  • Cardiology consult should be obtained.
  • ICD (Implantable Cardioverter-Defibrillator) placement is advised.
------------------------------------------------------------
ACKNOWLEDGMENT: My appreciation goes to Dr. Harsha Nagarajarao (of Cardiology Boards) for allowing me to use this tracing.
------------------------------------------------------------

For more on Brugada SyndromeClick on the icon:

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

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. – NOTE – Enlarge by clicking on Figures – Right-Click to open in a separate window.
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:
----------------------------------------------------