Thursday, June 17, 2021

ECG Blog #234 (50) — What is the Unifying Diagnosis?

The ECG shown in Figure-1 was obtained from a man in his 60s, who presented to the ED (Emergency Department) with shortness of breath.

  • How would you interpret this ECG?
  • Clinically — What would you say about this patient?


Figure-1: ECG obtained from a man in his 60s who presented with shortness of breath (See text).



NOTE #1: Some readers may prefer at this point to listen to the 7:20 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-50).


Today’s ECG Media PEARL #50 (7:20 minutes Audio) — Reviews the ECG diagnosis of RVH (with distinction between pulmonary disease vs RVH).

  • NOTE #2: For an 8-page PDF review of RVH — CLICK HERE (These 8 pages appear below in Figures-3, -4, -5 and -6 in the ADDENDUM below).



My THOUGHTS on the ECG in Figure-1:

The rhythm is sinus at ~90-95/minute. The PR interval is normal. The QRS is not prolonged. The QTc is at most minimally prolonged. 

  • There is marked RAD (Right Axis Deviation) — as determined by the tiny r wave in lead I with predominantly negative S wave.
  • There is marked RAA (Right Atrial Abnormality) — as diagnosed by the finding of tall, peaked and pointed P waves in each of the inferior leads. In particular, the P wave in lead II is at least 3 mm tall, and as voluminous of a P wave as you are likely to see.


PEARL #1 (Beyond the Core): Many clinicians may be tempted to interpret the deep negative component of the P wave in lead V1 as consistent with LAA (Left Atrial Abnormality). However, on occasion — the right atrium may become so enlarged as to "flop over", and be viewed by right-sided lead V1 as manifesting electrical activity moving away from lead V1.

  • True LAA typically produces a rounded deep negative component to the P wave in lead V1. The fact that the negative component to the P wave in lead V1 of Figure-1 is pointed, in association with huge pointed P waves in each of the inferior leads suggests to me the likelihood of an extremely large right atrium, but no LAA.
  • NOTE: For more on review of ECG criteria for RAA and LAA — See ECG Blog #75.


Regarding Q-R-S-T Changes:

  • There are tiny q waves in the inferior leads that are unlikely to be of any clinical significance. But the Q wavein lead V1 is significant! (See PEARL #2 below!).
  • Regarding R Wave Progression — There is a predominant R wave in lead V1! (Normally there should be predominantly negativity in this right-sided lead). Of note — R wave amplitude dramatically decreases in size after lead V4 (with no more than tiny r waves + deep, persistent S waves in leads V4-thru-V6).
  • Regarding ST segments and T waves — There is ST segment flattening with slight ST depression in each of the inferior leads, and in leads V1-thru-V4. I'd interpret these ST-T wave changes as suggestive of RV “strain” in both of the lead areas where this finding may be seen ( = the anterior and inferior leads).


PEARL #2: The presence of a qR pattern in lead V1 in a patient with longstanding pulmonary disease is a marker of severe pulmonary hypertension, with increased risk of mortality (Waligóra et al: J Electrocardiol — 50(4): 476-483, 2017).

  • Technically — one might call the qR pattern in lead V1 consistent with incomplete RBBB, because terminal S waves are seen in lateral leads I and V6. My preference (given the totality of ECG findings) — is to attribute this qR pattern to severe RVH with pulmonary hypertension, rather than to postulate a conduction defect.


Putting It All Together:

I've listed ECG findings suggestive of RVH in Figure-2. Considering the History in today's case ( = a man in his 60s, who presented to the ED with shortness of breath) — the combination of the following ECG findings described above for Figure-1 strongly suggest longstanding, severe RVH with pulmonary hypertension.

  • Marked RAD.
  • Marked RAA.
  • Relatively low voltage in the limb leads (though not strictly qualifying for "low voltage" — since the QRS complex in lead III is clearly more than 5 mm in amplitude).
  • Persistent precordial S waves (with predominant S waves seen in leads V4, V5 and V6).
  • RV "strain" in both the inferior and anterior lead areas.
  • Predominant R wave in lead V1.

Follow-Up in Today's Case: This patient was found to have longstanding severe pulmonary disease with marked pulmonary hypertension and right ventricular dysfunction.



Figure-2: ECG findings suggestive of RVH in adults (This subject is the theme of the above 7:20 minute Audio Pearl — and is summarized in Figures-3 through -6 in our Addendum below).


Additional PEARLS Regarding the ECG Diagnosis of RVH:

  • Detection of RVH in adults by ECG criteria is often exceedingly difficult. This is because the left ventricle is normally so much larger and thicker than the right ventricle — that it masks even moderate increases in RV chamber size. As a result, many patients with RVH will not be identified IF assessment of chamber enlargement is limited to obtaining an ECG (an Echo will often be needed to know for sure).
  • In contrast to adults — ECG diagnosis of RVH is often surprisingly EASY in children with congenital heart disease (because the relative size of the RV compared to the LV is not nearly as different in infants and young children as it is in adults).
  • KEY POINT — By the time you see a predominant R wave in lead V1 of an adult — the extent of RVH is usually marked (ie, the patient almost always has end-stage pulmonary disease and/or pulmonary hypertension).
  • There is no single ECG criteria that by itself can reliably diagnose RVH. Instead, a combination of ECG findings is needed — especially when seen in a likely clinical setting (ie, COPD, long-term asthma, right-sided heart failure, pulmonary hypertension).
  • There is only 1 condition in medicine that produces right atrial enlargement without also producing RVH. That condition is tricuspid stenosis, which is rare. Therefore, the ECG finding of RAA that is not the result of slender body habitus — often provides an important indirect clue to the presence of RVH.
  • Technically there is an S1Q3T3 pattern in ECG #1 (albeit the q wave in lead III is no more than a tiny negative deflection). That said, we need to remember that the finding of an S1Q3T3 pattern is of limited sensitivity and specificity for diagnosing acute PE — and, must be interpreted in the clinical context in which it is found. Although we do not know details of the clinical history in today's case (beyond shortness of breath) — I thought the totality of ECG findings in this tracing (especially the huge size of P waves and the predominant R, wave with qR pattern in lead V1) — favored longstanding RVH with pulmonary hypertension as more likely than acute PE (See ECG Blog #233for more on the S1Q3T3 pattern and ECG diagnosis of acute PE).


Final PEARL: The unifying diagosis that explains all of the ECG findings in Figure-1 is severe RVH with pulmonary hypertension. Regardless of whether the shortness of breath in today's case is the result of an exacerbation of this patient's longstanding pulmonary disease and/or superimposed pulmonary embolism — recognition of several (or more) of the ECG findings listed in Figure-2 in a patient with dyspnea should instantlyalert you to the fact that you are not dealing with left-sided heart failure, but rather with a patient having severe pulmonary disease.



Acknowledgment: My appreciation to 유영준 (from Seoul, Korea) for making me aware of this case and allowing me to use this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #77 — Reviews ECG criteria for the diagnosis of RVH and RV “Strain”.
  • ECG Blog #75 — Reviews the ECG criteria for the diagnosis of RAA & LAA.
  • ECG Blog #233 — Reviews the ECG diagnosis for acute PE (Pulmonary Embolism).


An Example of RVH in a 21yo Woman:

  • See My Comment at the BOTTOM of the page in the September 1, 2020 post on Dr. Smith’s ECG Blog (as I comment in detail on the 1st of the 6 cases that Dr. Smith presents).



ADDENDUM (6/17/2021): I've excerpted below in Figures-3-4-5, and -6, — several pages from my ECG-2014-ePub — that summarize the ECG diagnosis of RVH (Right Ventricular Hypertrophy).



Figure-3: ECG Criteria for RVH.



Figure-4: ECG Criteria for RVH (Continued).



Figure-5: ECG diagnosis of pulmonary disease and RVH in children.



Figure-6: Example tracings of RVH.

Saturday, June 12, 2021

ECG Blog #233 (49) — Why Did the Patient Die?

The ECG shown in Figure-1 was obtained from a previously healthy 70-year old man, who presented to the ED (Emergency Department) with new-onset dyspnea.

  • Does the anterior T wave inversion represent acute ischemia from Wellens’ Syndrome?
  • If not — What is YOUR diagnosis?


Figure-1: ECG obtained from a previously healthy 70-year old man with new-onset dyspnea.



NOTE #1: Some readers may prefer at this point to listen to the 7:40 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-1. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-49).


Today’s ECG Media PEARL #49 (7:40 minutes Audio) — Reviews the ECG finding of Anterior T Wave Inversion (with emphasis on not overlooking acute PE as the cause!).

  • NOTE #2: Among the topics discussed in this Audio Pearl are the ECG findings with acute PE (See Figure-3 and Figure-4 in the ADDENDUM below) — Wellens' Syndrome (reviewed in ECG Blog #209) — and — Giant T Wave Syndrome (reviewed in ECG Blog #59).




My THOUGHTS on the ECG in Figure-1:

The rhythm is sinus tachycardia at ~115/minute. The PR interval is normal. The QRS is not prolonged. The QTc appears to be no more than minimally prolonged (though this is difficult to assess given the tachycardia). The frontal plane axis is relatively vertical (almost +90 degrees) — but not quite rightward (since the S wave in lead I is not predominantly negative). There is no chamber enlargement.


Regarding Q-R-S-T Changes:

  • There is a Q wave in lead III — and perhaps a tiny q wave in lead aVF. There is a QS complex in lead V1.
  • Regarding R Wave Progression — a tiny initial r wave (positive deflection) is seen in lead V2 — with this R wave gradually increasing in size, until transition finally occurs between leads V5-to-V6.
  • ST segments are coved, with moderate symmetric T wave inversion in leads III, aVF and leads V1-thru-V4. A smaller effect on ST-T waves is seen in leads II, V5 and V6.


Additional ECG Findings Relevant to Today’s Case:

  • An S1Q3T3 pattern is present!
  • S waves persist across all chest leads (with a significant S wave still present in lateral lead V6).
  • Slight ST elevation is seen in lead aVR.



The History is KEY in today’s case: This previously healthy 70-year old man presented with new-onset dyspneaThere is no mention of chest pain. As a result — acute coronary disease would seem to be much less likely. In contrast — acute PE (Pulmonary Embolism) is perfectly consistent with this history! 

  • In association with the history in today’s case — several of the ECG findings noted above in Figure-1 place acute PE as the presumed diagnosis until proven otherwise.



The ECG Diagnosis of Acute PE:

The ECG is far from optimal as an investigative tool for the diagnosis of acute PE. That said — there are times when the ECG, in conjunction with the clinical history — can be extremely helpful in suggesting the diagnosis even before additional testing can be accomplished. The ECG in Figure-1 provides an excellent example of this situation.

  • PEARL #1: The ECG is unlikely to identify patients with smaller PEs. Do not expect to see anything on the ECG of these patients (This may be a “blessing in disguise” — as longterm benefits of anticoagulating such patients are debatable). Sensitivity of the ECG for suggesting the possibility of acute PE is clearly better with large (especially submassive) PEs.


PEARL #2: One of the problems with using the ECG as a diagnostic tool for detecting acute PE — is that there is no single ECG finding definitive for this diagnosis. Instead, acute PE may be suggested by a combination of several supportive ECG findings that occur in association with the right clinical scenario (ie, recent onset of unexplained dyspnea, syncope and/or shock, especially in a patient predisposed or with a prior history of venous thromboembolism).

  • We list the ECG findings to look for when considering the diagnosis of acute PE in Figure-2
  • We expand upon these ECG findings in the Addendum below (See Figure-3 and Figure-4).


Figure-2: ECG findings associated of acute PE. There is no single ECG finding that is diagnostic of acute PE. Instead, the diagnosis may be suggested by the presence of at least several of these ECG findings when they occur in the “right” clinical setting (See text).


WHAT are the ECG Findings in Today's Case?

We list below positive and negative ECG findings in today's case that are suggested in Figure-2, when contemplating the possibility of acute PE:

  • Sinus Tachycardia — While not absolutely essential for the diagnosis, a rapid heart rate (usually to at least 90/minute) is a common and expected finding in patients with hemodynamically significant acute PE. The heart rate in Figure-1 is over 100/minute.
  • Acute RV “Strain” — Awareness of ECG evidence of RV (Right VentricularStrain is one of the most important ECG indicators of acute hemodynamically significant PE. Unfortunately, this sign remains all-to-often unappreciated and misinterpreted as coronary ischemia. RV “strain” manifests as ST depression and/or T wave inversion that typically occurs in anterior leads (V1,2,3) — and/or — in inferior leads (II,III,aVF). Abnormal ST-T wave changes consistent with acute PE are seen in both of these lead areas in Figure-1.
  • S1Q3T3 — Whereas the diagnostic value of this pattern is minimal at best, when seen as an isolated finding — a definite S1Q3T3 pattern can be extremely helpful IF seen in association with other ECG evidence of acute PE. Such is the case here.
  • There is no RAA.
  • The frontal plane axis is relatively vertical — but not rightward.
  • Neither complete nor incomplete RBBB is present.
  • There is no tall R wave in lead V1.
  • Persistent Precordial S Waves — Poor R wave progression with persistence of S waves across the chest leads (through to lead V6) — is another ECG sign seen here that is consistent with new or chronic pulmonary disease.
  • ST Elevation in Lead aVR — Among the unappreciated benefits of lead aVR in ECG interpretation, is awareness that acute right heart “strain” (as seen with large acute PE) may often produce ST elevation in right-sided lead aVR. Although subtle — there is ST elevation in lead aVR in Figure-1.
  • Atrial fibrillation is not present.


Putting It All Together: The one unifying diagosis that explains all of the ECG findings noted above in Figure-1, in this 70-year old man who presented to the ED with new-onset dyspnea (but no mention of chest discomfort) — is acute PE.



CASE FOLLOW-UP: A presumed diagnosis of acute PE was rapidly made by the treating clinicians. They promptly initiated thrombolytic therapy. Unfortunately, the patient’s condition deteriorated as treatment was being started. Resuscitation was unsuccessful. Although confirmatory testing was not completed (made impossible by the patient’s unstable and rapidly deteriorating condition) — I believe the circumstances of cardiac arrest within minutes of arrival in the ED, in association with the combination of ECG findings shown in Figure-1 is consistent with massive acute PE as by far the most likely etiology for explaining this patient's rapid demise.


Acknowledgment: My appreciation to Ismail Mahmood (from Babil, Iraq) for making me aware of this case and allowing me to use this tracing.



Related ECG Blog Posts to Today’s Case: 

  • ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
  • ECG Blog #77 — Reviews ECG criteria for the diagnosis of RVH and RV “Strain”
  • ECG Blog #209 — Reviews the ECG diagnosis of Wellens’ Syndrome (What it is — and what it is not! ).
  • ECG Blog #59 — Reviews the causes of Giant T Wave Inversion.



ADDENDUM (6/12/2021): I've excerpted below in Figure-3 and Figure-4 — several pages from my ECG-2014-ePub — that summarize the ECG findings of acute PE (Pulmonary Embolus).



Figure-3: Summary of KEY findings in the ECG diagnosis of acute PE.

Figure-4: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE.

Thursday, June 10, 2021

ECG Blog #232 (47) — What is Bigeminy?

You are given the ECG shown in Figure-1 — but without the benefit of any history.

  • What is the cause of the paired beats in the long lead II rhythm strip?


Figure-1: You are asked to interpret this ECG without the benefit of any history (See text).


MSequential APPROACH to this CASE:

Rate & Rhythm: The QRS complex is narrow in all 12 leads — so the rhythm is supraventricular. 

  • NOTE #1: The long lead II rhythm strip at the bottom of the tracing is not continuous with the 12-lead above it. This long lead II rhythm strip encompasses a total of 14 consecutive beats — and shows a bigeminal” rhythm (ie, there are 7 pairs of beats that occur in a repetitive pattern of alternating shorter and longer R-R intervals)
  • We KNOW that there is at least some conduction — as it appears that each of the QRS complexes at the end of each longer R-R interval is preceded by an upright P wave with a constant (albeit prolonged) PR interval.



NOTE #2: At this point in my assessment — I was not certain of the etiology of the rhythm. That said, from a clinical perspective — I thought determining the precise rhythm diagnosis was not yet essential because: iWith regard to initial management of this patient — What counts most is recognition that there is a supraventricular rhythm at a reasonable ventricular rate, with at least a number of beats being sinus-conducted; andii) I could not help but notice the marked ST-T wave changes on the 12-lead that demanded more immediate attention!



PEARL #1: As stated above — the rhythm in Figure-1 is “bigeminal”, supraventricular, and notable in that the 1st beat in each of the 7 pairs of beats is sinus conducted (albeit with a prolonged PR interval). It’s helpful to be aware of the Differential Diagnosis for a bigeminal supraventricular rhythm when there is sinus conduction of the 1st beat in each pair. This differential diagnosis includes:

  • Sinus rhythm with atrial or junctional bigeminy (ie, every-other-beat is a PAC or a PJC).
  • SA ( = Sino-Atrial) Block.
  • Mobitz I, 2nd-Degree AV Block ( = AV Wenckebach) with 3:2 AV conduction.
  • Mobitz II, 2nd-Degree AV Block.


PEARL #2: Although the diagnosis of Mobitz II, 2nd-Degree AV Block would be of immediate concern (because of the need for cardiac pacing) — Mobitz II is highly unlikely in Figure-1 because: i) Among the forms of 2nd-Degree AV Block — Mobitz II is extremely uncommon (ie, In my experience — at least 90-95% of 2nd-Degree AV Blocks are of the Mobitz I type); andii) The QRS is almost always wide with Mobitz II (but the QRS is narrow in Figure-1).


The NEXT Steps in My Assessment:

The limb leads in Figure-1 suggest there has been recent inferior MI:

  • There are Q waves in each of the 3 inferior leads. The largest Q wave is seen in lead III, which manifests a QS complex (ie, all negative QRS). Considering how tiny the QRS complex in lead aVF is — the Q wave in this lead is both deep and wide. In contrast — the q wave in lead II is small and narrow — but the fact that all 3 inferior leads manifest Q waves (with these Q waves being very large in 2 of the 3 leads) confirms that inferior MI has occurred at some point in time.
  • All 3 of the inferior leads manifest at least some degree of ST elevation. ST segments look hyperacute in leads II and aVF (straight ST segment takeoff in lead II; T waves and ST segments being more “voluminous” in both II and aVF). Relatively speaking — the amount of ST elevation in lead III is less, and it is accompanied by fairly deep T wave inversion that is consistent with “reperfusion T waves”.
  • The ST-T wave picture in high-lateral leads I and aVL is almost the mirror-image” opposite of the ST-T wave in lead III. That is — the ST segment in both of these leads is straightened (albeit not depressed) — and the tall, peaked T waves are almost the opposite of the deep T wave inversion seen in lead III.


IMPRESSION: There has been a recent Inferior MI. It is difficult to “date” this infarction in the absence of any history. My “guess” would be recent” (ie, perhaps 6-to-12 hours ago, up to 1-to-2 days ago) — but probably not so acute as occurring within the past 1-to-4 hours or so.

  • I based this “date estimation” on the finding of established Q waves (which are very large in leads III and aVF+ deep reperfusion T waves in lead III (which suggest that at least some time has passed) — yet withpersistence of some ST elevation in all 3 inferior leads (with hyperacute-looking ST-T waves in leads II and aVF).
  • CAVEAT: Anything is possible. On occasion — surprisingly deep Q waves can form in as little as 1-2 hours! Moreover, the course of evolving infarction is not always immediate — but sometimes can be “stuttering” — with spontaneous reopening, followed by re-closure, with this reopening and/or re-closure sometimes occurring a number of times until a final disposition develops. 



The chest leads in ECG #1 are consistent with recent Posterior MI — which is a common accompaniment of inferior MI. This is easiest to appreciate with use of the Mirror Test” that I illustrate in Figure-2 (See ECG Blog #193 — for more on the “Mirror” Test).

  • The mirror-image view of leads V2 and V3 (within the RED border in Figure-2— looks similar (albeit even more dramatic) to what we see in lead III in ECG #1 — namely, a modest amount of ST elevation in association with deep, symmetric T wave inversion. This is consistent with reperfusion T waves in the left ventricular posterior wall location.
  • Application of the Mirror Test in Figure-2 also provides insight into a disproportionate increase in anteriorlead R wave amplitude (that is seen in leads V2 and V3 of ECG #1). When viewed in its mirror-image — this disproportionate increase in R wave amplitude in leads V2 and V3 is seen as deepening Q waves (within the RED border in Figure-2).


Figure-2: To illustrate the Mirror Test — I’ve enlarged anterior leads V1V2V3 — and have placed them next to a mirror-image ( = vertically flipped) view of these leads.


Closer LOOK at the RHYTHM:

Now that we know this patient has had a recent infero-postero MI — it becomes EASIER to interpret the long lead II rhythm strip in ECG #1. For clarity — I have numbered the beats in Figure-3. 

Figure-3: For clarity — I have numbered the beats in the long lead II rhythm strip. WHAT is the cardiac rhythm?



NOTE: Some readers may prefer at this point to listen to the 5:45 minute ECG Audio PEARL before reading My Thoughts regarding the ECG in Figure-3. Feel free at any time to review to My Thoughts on this tracing (that appear below ECG MP-47).



Today’s ECG Media PEARL #47 (5:45 minutes Audio) — Reviews the concept of Bigeminy (which may be due to Atrial or Ventricular Bigeminy, Wenckebach conduction — or other causes).


MSequential APPROACH to Interpreting the RHYTHM:

In addition to recognition of recent infero-postero MI — We have already made some observations about the rhythm:

  • The QRS complex is narrow in all 12 leads — so we know that the rhythm is supraventricular.
  • There is group beating, in the form of a bigeminal rhythm (ie, there are 7 pairs of beats that occur in a repetitive pattern of alternating shorter and longer R-R intervals).
  • PEARL #3: Recognition of recent or acute inferior MI in association with group beating — should immediately make you suspect AV Wenckebach ( = 2nd-degree AV block, Mobitz Type I). This is especially true when each of the relatively longer R-R intervals ends with a conducted sinus P wave that manifests a fixed PR interval (RED arrows in the long lead II rhythm strip in Figure-4).
  • PEARL #4: AV Wenckebach that occurs in association with acute inferior MI is often associated with 1st-Degree AV Block. Therefore, the finding that the PR interval is prolonged for each of the P waves highlighted by RED arrows in the long lead II rhythm strip in Figure-4 further favors the likelihood of Mobitz I as the etiology of this rhythm.
  • PEARL #5: The atrial rhythm should be regular (or at least, almost regular) — IF there is some type of AV block. Therefore, in order to prove that the rhythm in Figure-4 is AV Wenckebach — we need to establish that the underlying atrial rhythm is regular. Use of calipers and looking in other leads facilitates accomplishing this. NOTE: Most of the time when there is AV Wenckebach — those P waves that are not readily visible can be found hiding within elevated ST segments and T waves. For example — YELLOW arrows in lead V1 highlight where P waves within the T wave of the 1st beat in each pair are hiding.


Figure-4: I’ve added arrows to Figure-3 to highlight P waves. The RED arrows indicate obvious sinus P waves that conduct with 1st-degree AV block. The YELLOW arrows in lead V1 clue us into the fact that P waves are hiding within the T wave of the 1st beat in each of the 2-beat groups.


PEARL #6: Common things are common! Admittedly — I can not clearly see indication that a sinus P wave is hiding within the T wave under each of the WHITE arrows in Figure-5. That said, these T waves do appear to be “extra” peaked and, by far — the most logical assumption based on precise “walking out” of my calipers — is that another P wave is hiding within the T waves of beats #2, 4, 6, 8, 10, 12 and 14. 


Figure-5: Using calipers suggests that the most logical assumption to make — is that the WHITE arrows I have added to Figure-4 highlight another hidden P wave.


For clarity — I’ve colored all arrows in RED to highlight the location of regular sinus P waves I believe are occurring throughout the long lead II rhythm strip (Figure-6).

  • Isn’t it now easier to appreciate Wenckebach periodicity?

Figure-6: I’ve colored all arrows in RED to highlight where I believe regular sinus P waves occur throughout the long lead II rhythm strip. 



The easiest way to illustrate the mechanism in today’s rhythm — is by drawing a laddergram (Figure-7). 

  • NOTE: For review on how to read (and drawladdergramsSee ECG Blog #188.   

Figure-7: My proposed Laddergram illustration of the Mobitz I, 2nd-degree AV block with 3:2 AV conduction, as described above in today’s case (See text).



Acknowledgment: My appreciation to Bashiruddin Sayeem (from Chittagong, Bangladesh) for the case and these tracings.




  • ECG Blog #218 Reviews when a T wave is Hyperacute (including the 5:20 minute Audio Pearl in this blog post). 
  • ECG Blog #194 Reviews how to tell IF the “culprit” artery has Reperfused, using clinical and ECG Criteria (including the 6 minutes Audio Pearl in this blog post). 
  • ECG Blog #184 — Reviews the “magical” mirror-image opposite relationship with acute ischemia between lead III and lead aVL (including the 2:15 minutes Audio Pearl in this blog post). 
  • ECG Blog #224 — Reviews this important picture to recognize (which resembles in many ways today's tracing = HOW to quickly recognize Mobitz I with Acute Inferior MI). 
  • ECG Blog #193 — Reviews a case of an acute infero-postero MI that illustrates use of the Mirror” Test.



  • ECG Blog #186 — The AV Blocks (including a 4:30 minute Audio Pearl on When to suspect Mobitz I, 2nd-Degree AV Block). 
  • ECG Blog #78 — Shows a case of Atrial Bigeminy, in which every-other-P wave is a PAC that is either blocked or conducted with aberration. 
  • ECG Blog #140 — Another case study of Atrial Bigeminy, showing various forms of aberrant conduction. 
  • ECG Blog #57 — Atrial Bigeminy with blocked PACs that mimics AV block. 
  • ECG Blog #228 — Shows a case of Ventricular Bigeminy (including the challenge of assessing ST-T wave changes with this rhythm). 
  • ECG Blog #206 — A bigeminal rhythm due to a complicated AV Block.
  • ECG Blog #163 — A case if Escape-Capture Bigeminy. 
  • ECG Blog #188 — How to Read (and DrawLaddergrams.