Monday, February 23, 2015

ECG Blog #106 (Sinus Tachycardia - Hyperkalemia - DeWinter T Waves - Heart Rate)

Interpret the ECG shown in Figure 1 — obtained from a middle-aged adult.
  • Are there DeWinter T waves in the chest leads of Figure-1? Is this patient about to occlude his proximal LAD (Left Anterior Descending) coronary artery?
  • OR — Does this patient have hyperkalemia?
  • HINT: What is missing (that should never be missing)?
Figure 1: ECG obtained from a middle-aged adult. Are these DeWinter T waves? Does the patient have hyperkalemia? NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
Systematic Interpretation of Figure 1: There is some baseline movement with slight artifact. The overall rhythm is regular — with upright P waves in lead II, so that the rhythm is Sinus Tachycardia. The rate is ~160/minute (the R-R interval is just under 2 large boxes in duration).
  • The PR interval is normal — and the QRS complex is narrow. The QT interval is probably normal given the exceedingly rapid heart rate.
  • The axis is indeterminate (QRS complexes are nearly isoelectric in virtually all limb leads).
  • There is no chamber enlargement.
Regarding Q-R-S-T Changes:
  • There appears to be a Q wave in lead aVL.
  • Transition is slightly delayed to between V4-to-V5 (as the point where the R wave becomes taller than the S wave is deep).
  • The most remarkable finding on this tracing are the rather tall and peaked T waves, especially in leads V2-thru-V4. In a patient with chest pain — this appearance resembles that of the DeWinter T waves that herald proximal LAD occlusion. There is even suggestion of some J-point ST depression in leads V3,V4 and V5 prior to the steep rise in T wave ascent. In a patient predisposed to hyperkalemia — the T wave peaking seen here should also prompt consideration of this electrolyte disorder.
QUESTION: What is missing from this presentation?

ANSWER: No history was given ...
  • It turns out that this 12-lead ECG was recorded as part of an exercise stress test on an otherwise healthy and asymptomatic middle-aged man. The purpose of this test was to assess exercise capacity. There was no chest pain — and no history of renal disease or other medical problems.
The LESSON to Be Learned: ECGs cannot be intelligently interpreted in a vacuum. If told that this patient was having new-onset worrisome chest pain — We would wonder why he is so tachycardic, and we would clearly be concerned that the prominent T wave peaking might be ischemic or a DeWinter T wave equivalent. We would check serum K+ values as part of our evaluation, especially if the patient had any factors potentially predisposing to hyperkalemia.
  • T wave peaking as seen here commonly occurs in healthy adults during exercise. This T wave change is transient — and resolves after termination of exercise.
  • Rapid-upsloping ST segment depression as seen here in several chest leads is a normal response to exercise.
  • This patient had excellent exercise capacity for his age. His exercise test was entirely normal — and he was cleared to perform vigorous aerobic activity. No laboratory testing was done (as none was necessary).
- For more information  GO TO:
  • For review of the Systematic Approach to ECG Interpretation — Check out our ECG Blog #93
  • For review on DeWinter T Waves — Check out our ECG Blog #53.
  • For review on Hyperkalemia — Check out our ECG Blog #10.

Sunday, January 25, 2015

ECG Blog #105 (ECG Video-Blog-8) Basics of AV Block

This is the 8th installment of my ECG Video BlogThis 58-minute video covers the Basics of AV Block  including Pearls on ECG diagnosis — clinical relevance — and distinction from AV Dissociation.
NOTE: There are advantages to using a video format format. These include:
  • Ability to illustrate concepts not done full justice by the written word.
  • Greater dispersion of my content through Google & YouTube. This material is free for anyone to use.
LINKS to my ECG Video-Blog installments:
     My goal in this 58-minute video series is to review the approach to diagnosing the AV Blocks. This starts with recognizing what AV Block is (and is not— what conditions may mimic AV Block (ie, blocked PACs— and how to distinguish Complete AV Block from AV Dissociation. Focus is on the 3 types of 2nd-Degree AV Block (Mobitz I; Mobitz II; 2-to-1 AV Block— and on how to make a definitive diagnosis of Complete AV Block.
  • Below in Figure 1 — a sample of some issues discussed. I believe this video brings the topic to life!
Figure-1: Slide reviewing the causes of AV Dissociation. The tracing illustrates Sinus Bradycardia with resultant AV Dissociation by "default" (ie, due to slowing of the sinus rate). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
GTO – - on YouTube to view this ECG Video (58 minutes). The "Easy" Link = -
  • Click Here  — for a Timed CONTENTS of Video-Blog #8 on AV Blocks.
  • Please also check out my ECG Video Blog page on Google. The link is easy to remember = -
NOTE: For a Power Point Show (.ppsx) version of my Video Blogs - CLICK HERE. This folder will contain links to download a .ppsx version that allows faster viewing:
    • Download the .ppsx to your computer desktop.
    • The PPT show is without automatic sound. YOU activate only the Audio clips you want.
    • Hover your mouse over the highlighted Audio. You may play and/or pause if/as you like.
    • Feel free to use this .ppsx for teaching with my blessings!

    Thursday, January 22, 2015

    ECG Blog #104 (My ECG Guru Comments-2) - AV Blocks/AV Dissociation

    As a source of tracings for practice and/or teaching — I have decided to LINK all ECGs I have commented on as Contributing Expert for ECG Guru ( This may take me several weeks to complete ... I will post the relevant tracing and case on my ECG Blog according to subject — with direct link to MComment on the ECG Guru.
    • NOTE: The ECG Guru is dedicated to providing free resources for ECG Teachers and their StudentsSearch the ECG Guru site if you ever are in need of cases on a particular subject.
    INDEX of Topics Covered / LINKS to my ECG Blogs:
    • ECG Blog #103 — Acute MI ECGs (Comments #848; 838; 823; 819; 801 ).
    • ECG Blog # 104 (Coming soon ... ) — AV Blocks/AV Dissociation.
    •    ECG Blog #105 — AV Block Basics Video (
    • ECG Blog # XXX — on Bundle Branch Blocks ... (Coming soon ... ).
    •    ECG Blog #96 — bbb video
    • ECG Blog # XXX — Wide Tachycardias ... (Coming soon ... ).
    • ECG Blog # XXX — Narrow Tachycardias ... (Coming soon ... ).
    • ECG Blog # XXX — XXX ... (Coming soon ... ).
    ECG for Comment #828  on the ECG Guru (Instructor Collection — posted 9/16/2014):
    This ECG was obtained from an 84-year old man who became dizzy and fell. He was not injured in the fall. Subsequent ECGs showed progressive slowing that clearly required insertion of a pacemaker.
    • How would you interpret this 12-lead ECG — given that this 84-year old man presented with syncope?
    • Is there complete AV Block?
    • Is there complete AV Dissociation? Are you certain?
    • What happens at the end of this 12-lead ECG?
    Figure-1: ECG obtained from an 84-year old man admitted for syncope. (Our gratitude to Sebastian Garay for use of this case and all tracings.).

    Sunday, January 18, 2015

    ECG Blog #103 (My ECG Guru Comments-1) - Acute MI Tracings

    As a source of tracings for practice and/or teaching — I have decided to LINK all ECGs I have commented on as Contributing Expert for ECG Guru ( This may take me several weeks to complete ... I will post the relevant tracing and case on my ECG Blog according to subject — with direct link to My Comment on the ECG Guru.
    • NOTE: The ECG Guru is dedicated to providing free resources for ECG Teachers and their Students. Search the ECG Guru site if you ever are in need of cases on a particular subject.
    INDEX of Topics Covered / LINKS to my ECG Blogs:
    • ECG Blog #103 Acute MI ECGs (Comments #848; 838; 823; 819; 801 ).
    • ECG Blog # 104 (Coming soon ... ) — AV Blocks/AV Dissociation.
    •    ECG Blog #105 — AV Block Basics Video (
    • ECG Blog # XXX — on Bundle Branch Blocks ... (Coming soon ... ).
    •    ECG Blog #96 — bbb video
    • ECG Blog # XXX — Wide Tachycardias ... (Coming soon ... ).
    • ECG Blog # XXX — Narrow Tachycardias ... (Coming soon ... ).
    • ECG Blog # XXX — XXX ... (Coming soon ... ).
    ECG for Comment #848  on the ECG Guru (Instructor Collection — posted 1/16/2015):
    This ECG was obtained from a patient presenting to the ED (Emergency Department) with new-onset chest pain. Unfortunately No follow-up is available ...
    • How would you interpret this ECG — given that the patient has new-onset chest pain?
    • What is the "culprit" artery likely to be?
    Figure-1: ECG obtained from a patient with new-onset chest pain.
    ECG for Comment #838  on the ECG Guru (Instructor Collection — posted 11/16/2014):
    This ECG was obtained from a patient with chest pain. Unfortunately  additional details are not available ...
    • How would you interpret this ECG — given the not unexpected history of chest pain?
    • What is the "culprit" artery likely to be?
    • Do the ECG findings shown here suggest LMain "disease"?
    Figure-1: ECG obtained from a patient with chest pain.
    ECG for Comment #823  on the ECG Guru (Instructor Collection — posted 8/29/2014):
    This ECG was obtained from an 88-year old woman who presented to the ED (Emergency Department) in cariogenic shock. She apparently had been "ill" for several days prior to arrival in the ED.
    • What would you expect to find on cardiac catheterization? (Cath films are shown at the above link on ECG Guru).
    • Is all that you see on her ECG likely to be new?
    Figure-1: ECG obtained from an 88-year old woman who presented in cardiogenic shock. What would you expect to find on cath?
    ECG for Comment #819  on the ECG Guru (Instructor Collection — posted 11/16/2014):
    This ECG was obtained from a patient found to have LMain occlusion on cath. Unfortunately  additional details are not available ...
    • Interpret the ECG. How many abnormal findings can you detect?
    • Comment on the cath findings.
    • Can one distinguish on ECG between proximal LAD vs LMain occlusion?
    Figure-1: ECG obtained from a patient with LMain occlusion. Are you surprised by this cath finding?

    ECG for Comment #801  on the ECG Guru (Instructor Collection — posted 7/5/2014):
    The computer interpreted the rhythm for this tracing as, "AFib with PVCs"Unfortunately  additional details are not available ...
    • Do you agree with the computerized interpretation of the rhythm?
    • What else is going on?
    • Which arm should you check first on the patient? (ie, What is the likely source of the artifact?).
    Figure-1: ECG with lots of artifact ... Is the rhythm AFib (as the computer says)? What else is going on?

    Tuesday, December 23, 2014

    ECG Blog #102 (Addendum to ECG Video-7 ) – Wide Tachycardia in a Patient with Chest Pain

    BE AWARE: This is a highly advanced ECG post that supplements my ECG Video-7. The essential concepts to master were presented in the Video. But for those of you who want more  this post hopefully takes assessment of this fascinating case to a new level! Your feedback and comments are welcome!
    In ECG Blog #101 ( = ECG Video-7— We presented the case of a 70-year old woman with new-onset chest pain and the WCT (Wide-Complex Tachycardia) seen in the ECG shown in Figure-1. We posed the following questions:
    • What is the rhythm in the long lead II shown in Figure-1?
    • Is this VT? If you think it is — How certain are you of your diagnosis?
    Our animated Answer to these questions was covered in detail in our ECG Video-7
    • Our purpose in this follow-up ECG Blog #102 — is to address the point highlighted by one of our followers (Алексей Рукин) — regarding the value of meticulous comparison of the WCT tracing in Figure-1 with the post-conversion ECG.
    Acknowledgment: My appreciation to Dr. Sa’ad Lahri (Cape Town, South Africa) for providing me with the case and tracings for ECG Blogs #101, 102.
    Figure-1: Initial 12-lead ECG and long lead II rhythm strip obtained from a 70-year old woman with chest pain. Is this VT? How certain are you of your rhythm diagnosis? (Figure reproduced from ECG Video-7). NOTE — Enlarge by clicking on Figures — Right-Click to open in a separate window.
    Discussion of Figure 1: Summary of ECG Video-7
    Although the 70-year old woman in this case was hemodynamically stable at the time the tracing in Figure-1 was obtained — she was having chest pain. Therefore — a quick decision needed to be made as to whether immediate cardioversion was indicated.
    • Definitive rhythm diagnosis need not be made initially. Instead — the emergency providers in this case rapidly recognized from the long lead II rhythm strip that the predominant rhythm was a regular WCT without normal sinus P waves. Statistical odds that this rhythm was VT (Ventricular Tachycardia) — were at least 90%. In a 70-year old woman with new chest pain — the appropriate decision was immediate cardioversion. This resulted in conversion to sinus rhythm (as we will see momentarily in the post-conversion tracing in Figure-3).
    • PEARL: Total time to arrive at the decision to immediately cardiovert this patient given the above history and the ECG shown in Figure-1 should be no more than seconds …
    One of the major points emphasized in ECG Video-7 — was the presence of a number of additional clues in Figure-1 that increase the likelihood that the rhythm is VT to virtually 100%.
    • Feel free to take one more look at Figure-1 to see how many of these clues you can identify. Our answers follow below — which we illustrate in our labeled Figure-2.
    Figure-2 We have labeled Figure-1 to illustrate additional clues that make diagnosis of VT a virtual certainty.
    Discussion of Figure 2: Proof that the Rhythm is indeed VT
    As emphasized in ECG Video-7 — atrial activity is present (at least some of the time) in the long lead II rhythm strip. RED arrows highlight sinus P waves that we see. While the rapid rate, QRS widening and ST-T wave abnormalities prevent us from marching out P waves throughout this entire long lead II rhythm strip — regularity of the P waves we do see (red arrows) — suggests that there is an underlying sinus rhythm at a rate of ~130/minute.
    • Among the most helpful clues for confirming that a wide tachycardia is VT — is the presence of one or more of 3 related ECG signs. These are: i) AV dissociation; ii) Capture beats; and iii) Fusion beats. All 3 of these ECG signs are present in Figure-2 — which proves this rhythm is VT.
    • AV Dissociation is present in Figure-2 — because there is an underlying sinus rhythm (suggested by the red arrows) that is unrelated to the wide tachycardia (ie, the P waves = [red arrows] that precede beat #3 and follow beats #7,8,15 are not being conducted).
    • The QRS complex is narrow for beats #2, 10, 19 and 23. Each of these beats is preceded by a sinus P wave. Therefore — beats #2,10,19,23 are all Capture Beats (in which a sinus P wave occurs at just the right point in the cycle to get through the AV Node and “capture” the ventricles).
    • Beat #11 is a Fusion Beat. We recognize this because both QRS and T wave morphology of beat #11 is intermediate between sinus-conducted beats (like beat #10) and ventricular beats (like beat #12). That beat #11 is a fusion beat is perhaps best seen within the BLUE rectangle in lead aVF. (IF beat #10 and beat #12 “had children” — the offspring might be expected to look like beat #11, which represents “fusion” between the morphology of beats #10 and #12).
    KEY POINT: — Assessment of QRS Morphology and determination of Axis during tachycardia are 2 additional features that confirm (with virtual certainty) that the rhythm is VT. To facilitate assessment of QRS morphology in each of the 12-leads on this tracing — We have placed a V above those beats that are ventricular in each lead.
    • Note how simultaneous recording of a long lead II rhythm strip below the 12-lead ECG facilitates determination of which beats are sinus conducted (ie, capture beats) — and which beats are ventricular ( = the several short runs of NSVT = NonSustained VT).
    • The presence of extreme Axis Deviation (ie, the finding of an all negative QRS in either lead I or lead aVF) is rare with supraventricular rhythms. Thus, the all negative QRS complex within the GREEN rectangle in lead I of Figure-2 by itself virtually proves the rhythm is VT.
    Regarding QRS Morphology: The 3 KEY leads for assessing the presence and type of BBB (Bundle Branch Block) are leads I, V1 and V6. Aberrancy almost always manifests QRS morphology consistent with some form of conduction defect (ie, RBBB with or without a hemiblock; or LBBB). Therefore — the presence of QRS morphology that is inconsistent with some type of conduction defect makes aberrant conduction or preexisting BBB less likely (although it does not completely rule it out). 
    • In Figure-2 — the wide terminal S wave in lead V6 is consistent with RBBB. However, the amorphous and widened R wave in lead V1 that ends with an S wave rather than an R’ is not at all suggestive of RBBB — and, the all negative QRS in lead I is unlike any form of BBB. Thus, QRS morphology strongly suggests the rhythm is VT.
    A Reason for VT? A final clue that this rhythm is VT is contained within the RED rectangles shown in leads II and III of Figure-2. Note the subtle-but-real small q waves and suggestion of hyperacute ST elevation (especially in lead II) in this 70-year old woman who presented with new-onset chest pain. 
    • As was later confirmed on cardiac catheterization — this patient had acute occlusion of a dominant LCx (left circumflex) artery — so, her acute inferior STEMI (ST Elevation Myocardial Infarction) clearly provides a “reason” for her episodes of NSVT. 
    • Even though the QRS complexes seen in leads V1,V2 of Figure-2 are ventricular — the shape of the ST depression seen in these leads suggests acute posterior involvement consistent with these cath findings. 
    Assessment of the Post-Conversion Tracing: What Can Be Learned?
    As mentioned earlier — this patient was promptly cardioverted — which resulted in conversion to sinus rhythm, as shown in the post-conversion ECG (in Figure-3).
    • What can be learned from the post-conversion tracing?
    Figure-3: Post-conversion tracing.
    Discussion of Figure 3: The Post-Conversion Tracing
    The post-conversion tracing shows restoration of sinus rhythm (upright conducting P waves in lead II at the tachycardic rate of 115-120/minute). We note a number of subtle findings:
    • There is RAD (Right Axis Deviation) — with an rS predominantly negative QRS complex in lead I. This may reflect LPHB (Left Posterior HemiBlock) — especially if it is a new finding in this 70-year old woman who is found to have acute LCx occlusion.
    • There is IRBBB ( = incomplete RBBB) — given the predominant R wave in lead V1 plus narrow terminal s waves in leads I,V6 — but no QRS widening.
    • The ST elevation that we saw in leads II,III in Figure-2 seems to have resolved. Small inferior q waves persist.
    • Localized ST depression (in leads V2,V3,V4) persists, with disproportionately tall anterior R waves. This is consistent with acute posterior involvement.
    • Small q waves of uncertain significance are seen in leads V5,V6 (septal q waves — vs infarction q waves from acute LCx occlusion?).
    • There appears to be slight-but-real ST elevation in lead V6 (especially when compared to if anything, slight ST depression in lead V5). Thus synthesis of ECG findings from capture beats in Figure-2 plus analysis of the post-conversion tracing in Figure-3 are consistent with acute infero-postero-lateral STEMI (confirmed by cath findings of acute dominant LCx occlusion) — that resulted in runs of NSVT.
    Figure-4: Comparison of post-conversion QRS morphology (within red rectangles) to the 12-lead ECG during the wide tachycardia.
    Discussion of Figure 4: Comparison of VT with the Post-Conversion ECG
    Given successful treatment of this patient — We enjoy the luxury of being able to dissect her initial ECG ( = Figure-1) by direct comparison with the post-conversion tracing (Figure-3). We do this in Figure-4 — in which QRS morphology after conversion to sinus rhythm is shown within RED rectangles in each of the 12 leads.
    • Making this lead-by-lead comparison suggests a fascinating finding — namely that all narrow complexes on this tracing probably represent some slight degree of fusion rather than being pure “capture” beats. Therefore — rather than representing a series of short runs of NSVT — we strongly suspect continuous VT throughout the entire long lead II rhythm strip seen in Figure-1!
    • Note the middle complex within the GREEN rectangle in lead I of Figure-4. This middle complex is narrow and all negative. It’s shape is precisely what one would expect to see if the post-conversion sinus rS complex in lead I (within the RED rectangle) occurred at the same time as the all negative QS VT beat did. It makes much more sense that the all negative narrow QRS within the GREEN rectangle in lead I is a fusion beat — because it is so rare for sinus beats to manifest an all negative QRS in lead I. In contrast — the predominantly negative rS complex in lead I of the post-conversion tracing is perfectly consistent with a LPHB pattern, which is not at all unexpected given acute occlusion of a dominant LCx artery.
    • Similarly — there are other subtle differences in morphology during and after VT in other leads that suggest all narrow beats in Figure-1 probably represent fusion complexes (ie, loss of the small initial r wave in lead aVL during VT for beat #10 — and loss of the initial small q wave in lead V6 during VT for beat #23). 
    • CLICK HERE — for download of a pdf review on assessment of the regular wide tachycardia (excerpted from my ACLS-2013-ePub). Detailed discussion of QRS morphology, axis during tachycardia, and other discriminating criteria is included.