Monday, December 4, 2017

ECG Blog #144 (Bradycardia – AV Block – Alternating BBB – High Grade).

The ECG and long-lead II rhythm strip shown in Figure-1 was obtained from a 58-year old man who was admitted to the hospital with a history of chest pain and “fatigue”.
  • How would you interpret the tracing?
  • Is there 3:1 and/or “high-grade” AV block?
  • How many different types of conduction disturbances can you identify?
  • Is there ECG evidence of a cause?
  • What treatment is likely to be needed?

Figure-1: 12-lead ECG with long lead II rhythm strip obtained from a 58-year old man with chest pain and fatigue. NOTEEnlarge by clicking on FiguresRight-Click to open in a separate window.
Interpretation: This is a complex tracing. The easiest way I have found to derive the mechanism for complex arrhythmias such as this one — begins with the simple step of numbering the beats and labeling the P waves (Figure-2).
  • NOTE: The value of using calipers as an aid for interpreting complex arrhythmias cannot be overemphasized. Using calipers allows you to rapidly determine if P wave and QRS rhythms are regular or not, and whether beats are (or are not) likely to be conducting. With minimal practice — you’ll find calipers dramatically increase your speed for interpretation, as well as improving your accuracy. The cardiologist who does not regularly use calipers to interpret complex arrhythmias will miss the diagnosis on more than one occasion …
RED arrows in Figure-2 below indicate all P waves on the long lead II rhythm strip at the bottom of Figure-1. What conclusions can you now draw about this rhythm?
Figure-2: The beats from Figure-1 have been numbered. P waves have been labeled (RED arrows — See text).
Interpretation of Figure-2: Red arrows show regular occurrence of P waves with similar morphology. Thus, there is an underlying sinus rhythm.
  • The reason for slight variation in the P-P interval, is that there is sinus arrhythmia. (NOTE: A special type of sinus arrhythmia, known as “ventriculophasic sinus arrhythmia” — is commonly seen in association with 2nd- or 3rd-degree AV block, and this is probably what we are seeing here).
  • Some beats in Figure-2 are conducting! Note that the PR interval preceding beats #1, 3, 5 and 7 is constant (albeit slightly prolonged beyond 0.20 second in duration). This means that beats #1, 3, 5 and 7 in Figure-2 are all being conducted (albeit with 1st-Degree AV Block).
  • That said — other sinus P waves are not being conducted! We know that some of the other P waves are not being conducted — because there is no QRS complex near many of these other on-time but non-conducting P waves.
  • Since the atrial rate (P-P interval) is regular (or at least, fairly regular) — and since some P waves conduct but others don’t — this means that some type of 2nd-Degree AV Block is present. This cannot be complete (3rd-degree) AV block — because there is some conduction!
QUESTION: Can you think ahead as to which type of 2nd-degree AV block is present in Figure-2? Does this represent Mobitz I? — or Mobitz II? — or high-grade AV block? — or, some indeterminate form of 2nd-degree AV block?
Next STEP: Can you figure out which of the lettered P waves in Figure-3 have a chance to conduct, yet still fail to do so?
  • To clarify which P waves are (or are not) conducting, we have made Figure-3 — in which we label each of the P waves in the long lead II rhythm strip.
Figure-3: We have labeled all P waves in Figure-2 with letters. Which of these P waves have a chance to conduct, yet fail to do so?
Interpretation of Figure-3: As already noted — the P waves labeled a, d, g and j are all conducting (because the PR interval preceding beats #1, 3, 5 and 7 is constant).
  • One should expect the P waves labeled b, e, and h to be able to conduct — because these P waves all occur near the middle of the R-R interval, at a time when no part of the conduction system should still be refractory. The fact that these on-time P waves do not conduct — is what tells us that there is 2nd-Degree AV Block.
  • This leaves us with the P waves labeled c, f, and i. These P waves are not conducting — because no QRS complex follows them. However, these P waves labeled c, f and i never have a chance to conduct — because they occur immediately after beats #2, 4 and 6. That is, the P waves labeled c, f, and i all occur during the absolute refractory period that immediately follows the QRS complexes that precede them.
  • NOTE: The term, “high-grade” AV Block means that more than 1 on-time P wave in a row that has a chance to conduct, fails to do so. We can not diagnose “high-grade” AV block in Figure-3 — because we never see 2 P waves in a row that have a chance to conduct yet fail to do so. It could be entirely possible that IF beats # 2, 4 and 6 were delayed a little bit more — that the P waves labeled c, f, and i would then have a chance to conduct.
QUESTION: What should we call beats #2, 4 and 6?
  • HINT: In Figure-4, we have drawn in horizontal BLUE lines to show that the distance from the onset of beats #1, 3 and 5 — until the onset of beats #2, 4 and 6 is constant. This is just one of many relationships in this this tracing that can be instantly recognized by using calipers.
Figure-4: Horizontal BLUE lines show that the distance from the onset of beats #1, 3 and 5 — until the onset of beats #2, 4 and 6 is constant. How does awareness of this relationship facilitate determining the etiology of beats #2, 4 and 6?
Interpretation of Figure-4: Beats #2, 4 and 6 are escape beats. When sinus P waves fail to conduct — one hopes for emergence of an “escape” pacemaker site that will prevent development of any prolonged pauses. Escape beats most often arise from the AV Node — though they can also arise from elsewhere in the atria, from the bundle of His, or from the ventricles.
  • Escape beats are recognized because they are either not preceded by any P wave — or, because they are preceded by a P wave with a PR interval that is too short to conduct. Since most “escape” pacemakers are at least fairly regular — the R-R interval preceding escape beats tends to be fairly constant. This important clue is precisely what the equally long horizontal blue lines in Figure-4 show.
  • PEARL: It is often difficult to tell which beats in complex AV block tracings are (or are not) being conducted. Knowing that most escape rhythms are at least fairly regular — the finding of one or more QRS complexes that clearly occur earlier-than-expected is a superb clue that such early beats are probably being conducted. The slower beats that are not preceded by P waves, but which are preceded by a constant R-R interval are usually the escape beats (For review of this concept — Click HERE to go to 25:30 in our AV Block Basics Video).
The Concept of an Escape-Capture Rhythm: From a descriptive standpoint — there are several useful ways to classify the rhythm we see in Figure-4.
  • There is group beating. That is, although the ventricular rhythm in Figure-4 is not completely regular — there IS a pattern. This pattern is, that shorter and longer R-R intervals alternate — with shorter intervals (as between beats #2-3; 4-5; and 6-7) being of similar duration — and longer intervals (as between beats #1-2; 3-4; and 5-6) also being of a different similar duration.
  • The rhythm in Figure-4 is a bigeminal rhythm. This is just another way of stating that the pattern of this rhythm repeats every-other-beat.
  • There is Escape-Capture” Bigeminy. As we have discussed earlier — beat #2 is an “escape” beat — because it occurs after a short pause that is longer than the R-R interval that precedes sinus beats. Beat #3 is a “capture” beat — because the on-time sinus P wave that precedes it (ie, the P wave labeled “d) occurs at a moment during the R-R interval when the conduction system has recovered, and is able to conduct this P wave to the ventricles. This is followed by another escape beat (beat #4) — and then another “capture” beat (the P wave labeled “g” is able to conduct). This sequence then repeats.
SYNTHESIS: The rhythm in Figure-4 represents a form of 2nd-degree AV block. There is group beating, with repetitive short-long sequences. If we look at each sequence as beginning with a P wave that conducts (beats #1, 3, 5, 7) — the next P wave in each sequence fails to conduct (b, e, h). Before we can tell if the 3rd P wave in each sequence will be able to conduct — an escape beat arises (beats # 2, 4, 6). But this 3rd P wave in each sequence (ie, the P waves labeled c, f and i) never have a chance to conduct ...
  • We cannot determine IF the rhythm in Figure-4 represents Mobitz I or Mobitz II — because we never see 2 consecutive P waves conducting. That is, we cannot tell if the PR interval would lengthen (as it should with Mobitz I AV block) — because we never see 2 consecutively conducted QRS complexes.
  • We also cannot tell if the form of 2nd-degree AV block in Figure-4 represents “high-grade” AV block — because we never see 2 P waves in a row that should conduct, yet fail to do so.
  • The P-P interval in Figure-4 is ~5 large boxes in duration. This corresponds to an atrial rate of ~60/minute.
  • The R-R interval of the escape beats in Figure-4 (ie, the length of the horizontal blue lines) — is ~8 large boxes. This corresponds to an escape rate just under 40/minute. Thus, an important problem here is bradycardia … It is entirely possible that if either the atrial or escape rates were a little faster — that there would be 2:1 (instead of 3:1) AV conduction.
  • If we now change how we look at the repetitive sequences in Figure-4, so that instead of beginning each sequence with a sinus-conducted beat, we begin with an escape beat (ie, with beats #2, 4, 6) — we then have repetitive long-short sequences — which is how the name “escape-capture” was derived.
  • PEARL: It is well to appreciate that “Escape-Capture” Bigeminy (as is seen in Figure-4) is a common manifestation of 2nd-degree AV block.
Remaining Issues: Several questions remain regarding this case. These include:
  • Why is the QRS complex wide?
  • Why are there 2 different morphologies for QRS complexes in the long lead II rhythm strip?
  • What does the 12-lead ECG show? Is there a clue on the 12-lead tracing to the reason why this patient developed AV block?
Addressing the Remaining Issues: To facilitate addressing these remaining issues — We repost a less cluttered 12-lead ECG (Figure-5).
Figure-5: Why does QRS morphology change in the long lead II rhythm strip? How would you interpret the 12-lead ECG? Technical Note: The 12-lead ECG is simultaneously recorded with the long lead II rhythm strip at the bottom. Unfortunately, due to the way in which lead changes are recorded — we do not see beat #2 in leads I, II and III of the 12-lead ECG (but we do see all of the other beats).
Interpretation of Figure-5: Now that we have elucidated the behavior of atrial activity in this arrhythmia — we need to address QRST morphology.
  • Note that there are 2 different QRS morphologies. The QRS complex appears to be widened for both of these morphologies. Looking first at QRS morphology for the sinus-conducted beats (ie, for beats #1, 3, 5 and 7) — the monophasic R wave in lead I for beat #1 — with predominantly negative QRS for beat #5 in lead V1 — with monophasic R wave for beat #7 in lead V6 — are consistent with LBBB as the reason why conducted beats #1, 3, 5 and 7 are wide.
  • Although beats #2, 4 and 6 do not appear to be wide in the long lead II rhythm strip at the bottom of the tracing — a look at simultaneously obtained beat #4 in lead V1, and beat #6 in leads V4, V5 and V6 tells us that beats #2, 4 and 6 are in fact widened. The rSR’ for beat #4 in lead V1 — together with the wide terminal S wave for beat #6 in lead V6 — are consistent with RBBB as the reason why escape beats #2, 4 and 6 are wide.
  • The escape beats could be arising either from the AV Node or the Bundle of His. In either case — escape beats manifest an alternating form of bundle branch block compared to sinus-conducted beats that consistently manifest LBBB conduction.
  • NOTE: Although the term, “trifascicular block” has been discouraged in recent years because of potential ambiguity — this tracing clearly manifests signs of severe and multi-level conduction system disturbance, including: i) 1st-degree AV block (for conducting beats #1, 3, 5 and 7); ii) an indeterminate form of 2nd-degree AV block; and iii) alternating LBBB and RBBB conduction for the escape-capture bigeminal rhythm. Unless some potentially-reversible etiology is found — a pacemaker is likely to be needed.
Are there Acute Changes on the 12-Lead ECG? The final part of this tracing to assess is the ST-T wave changes on the 12-lead ECG. This assessment is especially challenging because of the multiple conduction defects that are present. We proceed as follows:
  • Regarding the sinus beats that conduct with LBBB morphology — the  ST-T wave for beat #1 in lead I manifests a T wave that is inappropriately concordant (upright) with the QRS complex in this lead. Normally, the ST-T wave should be oppositely directed to the last QRS deflection in lead I with LBBB. This finding of inappropriate T wave concordance suggests possible ischemia.
  • Much more remarkable is the persistent ST segment coving and increasingly deeper symmetric T wave inversion for escape beat #4 that is seen as one moves from lead V1-to V2-to V3. The amount of T wave inversion expected in anterior leads with RBBB should be maximal in lead V1. Especially in view of the relatively small QRS amplitude for beat #4 in leads V2 and V3 — this very deep and symmetric T wave inversion is clearly is a manifestation of ischemia, and may represent recent infarction as the precipitating cause of AV block.
  • Finally — the downward “s” wave in lead V2 for the RBBB pattern of beat #5 is fragmented. This suggests scar, and may be consistent with recent infarction.
Conclusion: Admittedly, QRST assessment is challenging on this 12-lead ECG given technical issues and extensive underlying conduction defects. Nevertheless — the findings we highlight above should raise suspicion of recent extensive infarction as the potential cause of AV block.

FINAL Interpretation of this Tracing: Underlying sinus arrhythmia with 1st-degree AV block. Escape-capture bigeminal rhythm, with 2nd-degree AV block of indeterminate severity, but with at least a 2:1 AV block conduction disturbance. Underlying LBBB for sinus-conducted beats — which alternates with RBBB for escape beats. This suggests severe conduction system disease. ST-T wave changes suggest ischemia and/or recent infarction.
P.S.: An “unknown” commenter (below) asked whether the P waves labeled b, e and h might actually be conducting with a very long PR interval? — because the distance from onset of each of these P waves, until the next QRS complex (ie, the distance from b-to-beat #2; e-to-beat #4; h-to-beat #6) appears to be the same! If this was true — then the PR interval “increment” would be extremely long. That is, the relative increase in PR interval for the P waves before beats #1 and 2 would be much more than is usually seen with a typical Mobitz I form of 2nd-degree AV block (ie, the PR interval for beat #2 if “b” was conducting would be over 0.80 second! ). That said, nothing else about this tracing is “typical” — and without additional ECG monitoring strips, we cannot rule out the possibility of dual AV node conduction pathways with change to the slow conduction pathway accounting for the extremely large PR interval increment from one conducting P wave to the next. In this case, the rhythm would be 2nd-degree AV block, Mobitz Type I — with the non-conducting P waves for each Wenckebach cycle being c, f and i. There would still be underlying alternating bundle branch block (from LBBB to RBBB conduction) in this patient with severe conduction system disease. A pacemaker will be needed. Moral: Some complex arrhythmias may have more than a single potentially plausible explanation!    
Acknowledgment: My thanks to Chu Thanh & Nguyen Chi Tinh (from Vietnam) for allowing me to use this tracing and clinical case.
  • For more on AV Blocks — Check out our Video @
  • For more on assessment of ST-T wave changes with BBB — Check out our Video @
NOTE: For any of our ECG Videos — If you click on SHOW MORE that appears under the video on the YouTube page — You will find a timed Linked Contents of all that appears in the video!

Sunday, October 29, 2017

ECG Interpretation Review #143 (ECG Guru - Dawn Altman - Dr. Stephen Smith)

     One of the reasons why I have decreased the frequency of my own ECG Blog posts — is that for the past few years I have actively been commenting on Dawn Altman’s ECG Guru site — as well as on many of the wonderful ECG posts put forth by Dr. Steven Smith on his most excellent blog site. 

For those desirous of additional sources of detailed ECG commentary — I suggest you check out:
I’ve attached below links to more recent posts from both of these sites for which I’ve left detailed commentary. For anyone with a real “passion” for ECG/Arrhythmia interpretation — reading through these posts ought to keep you busy for a good while. Happy reading!
Note: Below the Figure from Dawn’s most recent Instructors’Collection ECG. I’ve added my labels in Figure-1. Detailed commentary by me supplements Dawn’s initial interpretation. Enjoy!
Figure-1: ECG from a 75yo man with new chest pain. How would you interpret this ECG? What is the “culprit” artery? Do you need the bottom ECG to tell? And, WHAT is the rhythm?
Figure-2: Addition of labels to Figure-1 (Please CLICK HERE for my detailed analysis of this case).
For MECG Guru Comments:
For My Comments on Dr. Steve Smith's Blog:
  • Chest Pain & Flu (STEMI vs Localized Myocarditis)  March 18, 2016 -
  • Acute Prox LAD Occlusion (RBBB/LAHB- Lambda) — March 21, 2016 -
  • Pathognomonic ECG (long QT, peaked T — Ca++) — March 24, 2016 -
  • Acute LMain Occlusion (ECG recognition) — March 26, 2016 -
  • Acute STEMI despite Permanent Pacing — April 2, 2016 -
  • Resuscitation Pearls / LCx vs RCA "Culprit" — April 17, 2016 -
  • DeWinter-like T waves — Should NOT be Missed! — April 20, 2016 -
  •    10 Examples to TEST Recognition (Ant. T Waves) — April 23, 2016 -
  •    10 Examples of Inferior Hyperacute T Waves — May 1, 2016 -
  • ECG Distinction between Acute Pvs Chronic RVH — May 27, 2016 -
  • Fusion, Capture beats: "2 Wrongs may make a Right" — June 3, 2016 -
  • RBBB and SElevation (new STEMI vs LAneurysm) — June 6, 2016 -
  • Hyperacute Inferior T Waves or Reciprocal SChanges — June 10, 2016 -
  • Anterior STEMI vs Benign Early Repolarization? — June 17, 2016 -
  • The Computer Missed WPW (re the Concertina Effect) — June 20, 2016 -
  • Terminal QRS Distortion with Acute LAD Occlusion — June 24, 2016 -
  • Acute Inferior STEMI — or IIt? — July 1, 2016 -
  • Acute Anterior Stemi, Saddleback, Early Repol? — July 8, 2016 -
  • Convex SElevation not due to STEMI — July 14, 2016 -
  • WCT in a 12-Year Old — July 20, 2016 -
  • ST Elevation in V1,V2 — RV MI, Brugada or Hyper-K ? — July 24, 2016 -
  • Bifascicular vs Trifascular Block / Acute Changes? — July 30, 2016 -
  • Proportionality of ST-T and the QRS (Ant. STEMI ) — August 5, 2016 -
  • Is this Brugada-1 or a Saddleback? (syncope) — August 10, 2016 -
  • Bidirectional VT vs AVNRT with Alternating RBBB? — August 25, 2016 -
  • RVH vs RBBB vs Both? — Acute PE? (large RV on Echo) — Sept. 1, 2016 -
  • Subtle LCOcclusion or Not? — Sept. 4, 2016 -
  • LAD Occlusion vs Early Repol (interpolated PVC) — Oct. 18, 2016 -
  • Right Precordial T Wave Inversion (benign) — Dec. 5, 2016 -
  • Changing ST Elevation Distribution (Spasm) — Dec. 7, 2016 -
  • Computer Reads "Non-specific" Abnormalities — Dec. 10, 2016 -
  • Cabrera Format at 50mm/sec (a patient with chest pain) — Dec. 29, 2016 -
  • LVH with Marked SDepression + Chest Pain — Jan. 6, 2017 - 
  • Wide Tachycardia with Cyanosis (VT vs SVT ...— Jan. 10, 2017 -
  • LBBB, Chest Pain and Evolving ST-T Changes — Jan. 20, 2017 -
  • Fast SVT in a Child (rate ~220/minute) — Jan. 22, 2017 -
  • Cocaine Overdose and Brugada ECG Pattern — Jan 25, 2017 - 
  • Group Beating & Hyperkalemia (Brugada Phenocopy) — Jan. 27, 2017 -
  • Use of the ECG with Severe DKA (U waves) — Feb. 2, 2017 -
  • Inferior MI, LVH or Both? (a patient with chest pain) — Feb. 5, 2017 -
  • ST Elevation, Neg Troponin but NOT Early Repol! — Feb. 10, 2017 -
  • Subtle Use of Smith-Sgarbossa Criteria with LBBB — Feb. 20, 2017 -
  • Unstable WCT not responding well to Cardioversion — Feb. 23, 2017 -
  • 40yo Man with Chest Pain and "Funny" ST-T Waves — March 1, 2017 -
  • Another 40yo Man with Chest Pain (recurring "theme" ) — March 3, 2017 -
  • Impending LAD Occlusion (recognizing subtle Wellens) — March 9, 2017 -
  • Do Computerized Interpretations Miss Acute STEMIs? — March 10, 2017 -
  •   — Related Post: EMS 12-Lead (on Triaging ED ECGs) — March 11, 2017 -
  • VT vs SVT with Aberration in a 20yo with DKA - March 17, 2017 -
  • T Peaking and "Pseudo-Infarction" with Dehydration - March 19, 2017 -
  • Alternating Fascicular Block Aberrancy (and LSFB! ) - March 31, 2017 -
  • RBBB with Transient ST Elevation (Rhythm?) - April 2, 2017 -
  • Acute or Recent Anterior MI vs LAneurysm? - April 21, 2017 -
  • 16yo Girl with Overdose: LBBB vs WPW? - April 23, 2017 -
  • 40yo Woman with Chest Pain (KEY subtle findings! ) - April 27, 2017 -
  • LVH Pseudo-Infarction Pattern vs Wellens? - May 3, 2017 - 
  • ST Elevation in V1,V2 in a Patient with LVH - May 6, 2017 -
  • TQRSD (Terminal QRS Distortion) - May 13, 2017 - 
  • Dialysis Patient with Bradycardia ... - May 18, 2017 -
  • Acute STEMI in a post-Op Paced Tracing - May 19, 2017 -
  • "Busy at Triage" (subtle-but-real LCx signs ... ) - May 26, 2017 -
  • Chest Pain, GE Reflux and Subtle ST-T Wave Changes - May 29, 2017 -
  • ST Elevation with Reciprocal Change due to ? (MI vs K+?) - June 1, 2017 - 
  • Peaked T Waves in 35yo with DKA/Something Else? June 17, 2017 -
  • Peaked T waves in a 20yo. Anything Else? - June 21, 2017 - 
  • Pulmonary Edema on Echo + Interesting ECG LVH - July 7, 2017 -
  • Subtle ECG Changes in an 82yo with Syncope - July 12, 2017 -
  • The Computer says, "AFib". Do you agree? - August 11, 2017 - 
  • Effect of Adenosine on this Rhythm? (AFlutter? ) - August 23, 2017 -
  • To Thrombolyse after 15 Hrs of Chest Pain? - Sept. 1, 2017 -
  • DeWinter T Waves / AIVR - Sept. 24, 2017 - 
  • A 30yo Woman with Chest Pain. Is her ECG Normal? - Sept 30, 2017 -
  • VT or Supraventricular with LBBB? - Oct. 14, 2017 -
  • Syncope in an Elderly Man ( ? Wellens ? Oct. 25, 2017 -
  • Chest Pain but a Non-Diagnostic ECG ... Nov. 1, 2017 -
  • How to Convince the Cardiologist ??? - Nov. 6, 2017 -  
  • Chest Pain & a "Normal ECG" by Computer Report - Nov. 10, 2017 - 
  • 50yo with Chest Pain (Concept of "Competing Conditions") - Nov 15, 2017 - 
  • 30yo with Chest Pain and this ECG (S1Q3T3; IRBBB,ST) - Nov. 22, 2017 - 
  • About the QTc Interval (Using the Rule of Thumb for QTc) - Nov. 24, 2017 - 
  • RBBB, Missed Occlusion on ECG, What is the Rhythm? - Nov 25, 2017 - 
  • Subtle Abnormality in a 54yo with Chest Pain - Nov. 27, 2017 - 
  • Post Cardiac Arrest ECG (Acute MI vs something else?) - Nov. 30, 2017 
  • Why the Inf. ST Depression? What's the Rhythm? - Dec. 1, 2017
  • 30yo with Pulmonary Hypertension and this ECG - Dec. 13, 2017 -
  • Challenging Wide Rhythm (Syncopal patient) - Dec. 16, 2017 -
  • Wellens' ST-T Waves or Something Else? - Dec. 18, 2017 -
  • Serial Tracings tell the Tale (Cancellation Effect) - Dec. 23, 2017 -
  • Not a "STEMI", but NOT Normal! (Ed Burns, LITFL) - Dec. 27, 2017 -
  • Subtle Findings in a Patient with Chest Pain - Dec. 29, 2017 -
  • There is nothing subtle about this ... Right? - Jan. 2, 2018 - 
  • Acute MI or Something Else? - Jan. 5, 2018 -
  • SElevation: STEMI vs Early Repol vs Pericarditis? - Jan. 8, 2018 -
  • Use of Terminal QRS Distortion (acute stemi- AIVR) - Jan. 11, 2018 -
  • Chest Pain and ST Elevation (old inf MI? Pericarditis?) - Jan. 17, 2018 -
  • Repolarization Variant? LVH? and/or Acute STEMI? - Jan. 24, 2018 -
  • STEMI? Need for Acute Cath? — or Not? - Jan. 26, 2018 - 
  • The Importance of Comparison Tracings (subtle! ) - Jan. 28, 2018 -
  • Artifact in a Dialysis Patient (Not hyperacute ST-T ! ) - Jan. 30, 2018 -
  • Subtle Changes in a Patient with CP (but no doubts! ) - Feb. 1, 2018 - 
  • Acute LCOcclusion despite Non-Diagnostic ECG! — Feb. 5, 2018 -
  • Cardiac Trauma — Now ST Elevation (on Pericarditis) — Feb. 7, 2018 -
  • LBBB + CP — Is there Acute Coronary Occlusion? - Feb. 11, 2018 - 
  • Subtle Abnormality (in leads III,T inversion in aVL) - Feb. 15, 2018 -
  • What's the Temperature? (from an unresponsive woman) - Feb. 19, 2018 -
  • Hyperacute ST-T Waves in an evolving STEMI - Feb. 22, 2018 -
  • RBBB with Subtle Ischemic Changes ... - Feb. 24, 2018 -
  • Diffuse SDepression + SElevation in aVR - Feb. 28, 2018 -
  • Anterior ST Elevation: To Activate or Not? - March 5, 2018 -
  • Alcohol Withdrawal + a very Long QTc - March 8, 2018 -
  • Seizure + a somewhat long QTc Interval - March 9, 2018 - 
  • A Pattern To Recognize! ( = Acute PE! ) - March 12, 2018 -
  • LBBB Criteria Redefined? Acute STEMI? - March 14, 2018 -
  • Not Wellens, but V1,V2 Too High on Chest March 16, 2018 -
  • STEMI vs Pericarditis/Early Repol - May 14, 2011/March 18, 2018 -
  • SVT & Retrograde Atrial Activity (AVNRT vs AVRT?) - March 20, 2018 -
  • You had 2 Hours to Save this Patient (missed STEMI ) - March 24, 2018 -
  • Tale of 2 STEMIs- Step-by-Step (computer report) - March 27, 2018 -
  • NOT an OMI despite HUGE Anterior S Waves! (Superb! ) - April 4, 2018 -
  • Regular Wide Tachycardia due to HyperKalemia! - April 6, 2018 - 
  • ST Elevation + Hyperthyroidism + LVH + Repol April 9, 2018 - 
  • U Wave Inversion — Clinical Significance ... - April 14, 2018 -
  • RBBB with HyperKalemia — Anything Else? - April 16, 2018 -