ECG Blog #59 — Giant T - Ischemia -Yamaguchi

No history is available for the ECG shown in Figure 1. That said:

• How would you interpret this ECG?
• What clinical conditions should be considered?

Figure 1:  No history is available. What clinical conditions should be considered?

INTERPRETATION: 

The rhythm is sinus bradycardia and arrhythmia, with an overall heart rate just under 60/minute. All intervals (PR/QRS/QT) are normal. The axis is normal at +50 degrees. Voltage for LVH is present (deepest S in V1,V2 + tallest R in V5,V6 ≥35mm). The most remarkable changes are seen with respect to Q-R-S-T Changes:

• There are no Q waves.
• Transition occurs slightly early (between leads V2-to-V3) – with relatively tall R waves in leads V1,V2.
• There is diffuse, deep symmetric T wave inversion. T wave inversion is almost 15mm deep in leads V2,V3.
• Other subtle-but-real ST-T wave findings include 1-2mm of J-point ST depression in multiple leads – suggestion of ST segment coving in leads I, aVL, V2,V3,V4 – and a hint of ST elevation in leads III, aVR and V1.

Giant T Wave Syndrome

The overall impression is consistent with Giant T Wave Syndrome. Although some T wave inversion is common in many conditions — the term “giant T waves” is reserved for a select number of clinical entities that produce truly deep (>5-10 mm amplitude) T wave inversion. When this clinical picture is seen (as it is in Figure 1) — one should think of the following diagnostic entities.

• Apical (Yamaguchi) Cardiomyopathy.
• Takotsubo Cardiomyopathy.
• Severe CNS disorders (increased intracranial pressure).
• Stokes-Adams attacks (especially when due to severe bradycardia, complete AV block).
• Acute ischemia/coronary artery disease.
• Post-Tachycardia Syndrome (ie, Cardiac "Memory" effect).
• Massive Pulmonary Embolism (acute right heart strain).

Without any history — it is impossible to know which of the above entities is most likely:

• We doubt massive PE (Pulmonary Embolism) — because none of the other stigmata of acute right heart strain are present (no right or indeterminate axis, no right atrial enlargement, no T inversion in lead III, no tall R wave in lead V1). T wave inversion with acute PE is most often limited to right-sided leads (V1,V2,V3 and II,III,aVF) — and is usually not nearly as deep as seen here.

Any of the other entities on the above list are possible.

• Apical cardiomyopathy — is an uncommon variant of the more commonly encountered hypertrophic cardiomyopathy (HCM). The increased voltage seen in Figure-1 is consistent with apical cardiomyopathy (which may produce identical ST-T wave changes as seen in today's tracing). 
• Takotsubo Cardiomyopathy may produce a somewhat localized or generalized Giant T wave pattern, often with a prolonged QTc (dependent on what areas of the heart are affected).
• Anterior ischemia/infarction from high-grade LAD (Left Anterior Descending) coronary artery narrowing/occlusion should be high on the differential list, because of the J-point ST depression, ST segment coving, and subtle ST elevation in leads III, aVR and V1.
• Acute CNS disorders (stroke, subarachnoid or intracranial hemorrhage, seizure, coma, brain tumors, trauma) may produce some of the most bizarre ST-T wave abnormalities. That said — the QT interval will usually be prolonged with CNS disorders and there will often be manifest T wave broadening (neither of which is seen here).
• Finally — a less commonly appreciated cause of diffuse T wave inversion is post-tachycardia syndrome. Diffuse T wave inversion not due to ischemia/infarction may sometimes transiently be seen following conversion of sustained SVT/VT rhythms.

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NOTE: Although many authorities suggest a minimum of ≥10mm for T wave depth sufficient to qualify as "Giant T waves" — for practical purposes (ie, in our experience) — the entities suggested by the above bullets should be considered in cases in which very deep (ie, ≥5mm) but not necessarily "giant" T waves are seen in a number of leads.
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— For more information — GO TO:

• See Section 10.51 on Giant T Wave Syndrome - 
• See ECG Blog #120 ( = Video-16) -

ECG Blog #58 — AV Dissociation vs Block?

The ECGs in Figure 1 and Figure 2 were both interpreted as showing 3rd degree (complete) AV block.

• Do you agree?

Figure 1: Lead II rhythm strip. Is this complete AV block? 

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Figure 2: Lead MCL-1 rhythm strip. Is this complete AV block? 

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INTERPRETATION: We assess both rhythm strips by the Ps,Qs & 3R Approach, looking for: i) Presence (or absence) of P waves (atrial activity?); ii) QRS width (>0.10 sec is wide?); iii) Regularity of the rhythm; iv) Rate; and v) If P waves are present - Are P waves Related to the QRS (Are P waves conducting?).

FIGURE 1: — The QRS complex is narrow. The first 3 beats show sinus bradycadia at ~55/minute. The PR interval then noticeably shortens (ie, the PR preceding beats #4,5, and 6 is clearly too short to conduct!). Thus, there is transient AV Dissociation (since P waves are at least temporarily unrelated to the QRS).

• Beats #7 and 8 represent a junctional rhythm at ~58/minute.
• It is because the sinus rate slows (to 55/minute) that a slightly faster junctional rhythm can take over (beginning with beat #4).
• We see NO evidence of any AV block on Tracing A — because P waves never fail to conduct when given a chance to do so (P waves before #4,5,6 don't have a chance to conduct ...).

FIGURE 2: — shows complete (3rd degree) AV Block. Note that the QRS does not necessarily have to be overly wide for there to be 3rd degree AV block.

• The atrial rate is regular (marched out in Figure 3 with RED arrows).
• There is also a regular ventricular rhythm — but P waves at all points in the cardiac cycle fail to conduct despite having adequate opportunity to do so (P waves "march through" the QRS).

Figure 3: Arrows indicate regular atrial activity that "marches through the QRS" in this patient with 3rd degree AV block (See text).

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AV Dissociation vs Complete AV Block

AV Dissociation is not the same as 3rd degree AV block. The term, "AV dissociation" merely means that one or more P waves is not related to a neighboring QRS. AV dissociation may be transient or permanent. It may be due to pathologic conditions such as 2nd or 3rd degree AV block — or it may be a benign manifestation of the simple fact that the sinus node temporarily slows down and is replaced in its pacemaker function by an appropriate AV nodal escape rate between 40-60/minute.

• Always try to determine the cause of AV dissociation - of which there are three: 1) AV block itself (could be 2nd or 3rd degree AV block); 2) Usurpation — in which P waves transiently do not conduct because an accelerated junctional rhythm takes over ("usurps" — as commonly occurs with Dig toxicity); and, 3) Default - in which a junctional escape rhythm takes over by default" (because of SA node slowing).
• Figure 1 is an example of AV dissociation by "default" (slowing of the rate from sinus bradycardia that allows emergence of an appropriate junctional escape rhythm).
• PEARL: In order to confidently diagnose complete AV block — the ventricular rate needs to be slow enough (usually <45-50/minute) in order to guarantee that P waves will occur in all phases of the cardiac cycle, yet still fail to conduct despite having adequate "opportunity" to conduct. This clearly occurs in Figure 3.

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For more information - GO TO:

• ECG Basics of AV Block (in ECG-2014-ePub) - 

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ECG Blog #57 — A Slow AV Block ...

Interpret the lead MCL-1 rhythm strip shown in Figure 1.

• Does this rhythm represent Mobitz I (Wenckebach) or Mobitz II AV block?
• Is a pacemaker likely to be needed?

Figure 1: Lead MCL-1 rhythm strip. Is this Mobitz I or Mobitz II?

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INTERPRETATION:  Neither Mobitz I nor Mobitz II is present. Rather than AV block – the rhythm in Figure 1 is an insightful example of the “mischief” that blocked PACs (Premature Atrial Contractions) can cause, especially when PACs are frequent.

     We have previously reviewed the basics of the 2nd degree AV blocks (See ECG Blog #19 – Blog #20 – Blog #21 – and Blog #22). Essential to the diagnosis that some type of AV block is present are 2 ECG findings:

• Finding #1: A consistent underlying atrial rhythm (usually sinus) – which is established by similar morphology of P waves on the tracing. Occasional PACs or junctional beats may be seen – but constantly changing P wave morphology is much more suggestive of other phenomena (wandering pacemaker; sinus pauses or arrest; multifocal atrial tachycardia) than of “AV block”.
• Finding #2: A regular (or at least fairly regular) atrial rhythm should be seen when some form of AV block is present. Clearly – there may be underlying sinus arrhythmia. In addition – slight variation in regularity of the underlying sinus rhythm may be the result of the AV block itself (known as “ventriculophasic sinus arrhythmia”) – in which the P‑P interval tends to shorten for P waves that sandwich a QRS complex (thought to be due to transiently increased perfusion immediately following ventricular contraction). However, gross variation in the P‑P interval is usually not seen when the primary problem is AV block.

WHY FIGURE 1 is Not AV BLOCK: AV block is not present in Figure 1 – because the above 2 ECG findings are absent. This becomes obvious in Figure 2, in which red arrows highlight each P wave:

Figure 2: Red arrows highlight each P wave in Figure 1.

• P wave morphology changes in Figure 1 (and in Figure 2). Sinus P waves are seen as a biphasic (small pointed positive followed by rounded negative) deflection preceding beats #1, 2, 3, 4, 5 and 6. In contrast – P waves buried within the ST-T wave of beats #1-thru-6 are triphasic (small negative-then positive-then narrow negative) deflections that clearly look different in morphology than the sinus P waves. These triphasic-deflection P waves arise from an atrial site other than the sinus node.
• Red arrows in Figure 2 make it obvious that the P-P interval varies. In fact there is a pattern to this P‑P variation (alternating short-long cycles) produced by the fact that every-other-P wave is early (premature). The underlying rhythm is atrial bigeminy (every other beat is a PAC).

PEARL: The Commonest Cause of a Pause is a Blocked PAC

     We introduced the concept of “blocked” PACs in ECG Blog #14. Depending at what point within the refractory period a premature beat occurs – a PAC may conduct: i) Normally; ii) With aberrant conduction (if part of the ventricular conduction system is still refractory); or iii) The PAC may occur so early as to fall within the absolute refractory period when no conduction is possible. This is what is occurring in Figure 2 – in which every-other-P-wave is blocked (non-conducted)!

• The commonest cause of a pause is a blocked PAC!  Blocked PACs are far more common than any form of heart block. Although sometimes subtle – blocked PACs can be identified if looked for. Close inspection of T waves at the beginning of a relative pause will usually reveal a notch or other small deformity not evident in the T waves of normally conducted sinus beats.

BEYOND-the-CORE: What is Happening with Beat #7?

     Unlike the PACs occurring within the T waves of beats #1-thru-5 (which are non-conducted) – the PAC that notches the T wave of beat #6 is conducted (ie, beat #7)!

• The reason for QRS widening and the different QRS morphology of beat #7 – is that this PAC conducts with LBBB (Left Bundle Branch Block) aberration. It presumably occurs during the RRP (Relative Refractory Period) – as illustrated in Figure 2 of ECG Blog #14.
• The reason for the longer-than-anticipated PR interval preceding beat #7 – is that the PAC that occurs within the T wave of beat #6 encounters a still partially refractory AV node, resulting in delay of conduction to the ventricles.

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BOTTOM LINE: The commonest cause of a pause is a blocked PAC. Remembering to think of this truism whenever you assess a tracing for possible AV block will prove invaluable in uncovering the real reason for the rhythm disturbance in a surprising number of cases. Blocked PACs occur far more often than any form of AV block.

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- For more information – GO TO:

1) ECG Blogs on AV Block: Blog #19 – Blog #20 – Blog #21 – Blog #22.

2) ECG Blogs on Aberrant Conduction: Blog #14 – Blog #15 –

3) ECG Basics of AV Block (from ECG-2014-ePub) -

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ECG Blog #56 — A Mirror-Image View

You are asked to interpret the ECG in Figure 1. You are told that the patient was just resuscitated from cardiac arrest. This is his post-resuscitation 12-lead ECG.

• In light of this history – How would you interpret this ECG?
• Given that the patient was just resuscitated – What treatment would you recommend?
• What would you expect to see on cath?

Figure 1: 12-lead ECG obtained immediately post-resuscitation. What would you expect to find on cath? 

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INTERPRETATION: There is sinus rhythm at a rate ~85/minute (upright P wave with fixed PR interval in lead II). All intervals (PR/QRS/QT) and the axis are normal. No chamber enlargement. Regarding Q‑R‑S‑T Changes:

• There is a narrow but deep Q wave in lead III – but no other Q waves.
• An rSr’ complex is seen in lead V1.
• Transition occurs early with a relatively tall R wave already by lead V2.
• ST segments show significant coved ST elevation in each inferior lead (II,III,aVF) – as well as in lateral precordial leads V5,V6. ST depression is seen in leads I, aVL and V2.
• Beyond-the-Core: There may be slight ST elevation in lead V1. There appears to be a peculiar downslope to the ST segment in lead V1 that blends into shallow T wave inversion in this lead.

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IMPRESSION: The picture is consistent with acute infero-latero-postero STEMI (ST Elevation Myocardial Infarction) from acute RCA (Right Coronary Artery) occlusion. There may also be RV (Right Ventricular) involvement. Immediate cardiac catheterization is indicated in this post-resuscitation patient who may have arrested because of acute RCA occlusion that hopefully will be amenable to acute PCI (PerCutaneous Intervention). We emphasize the following points:

• Acute inferior MI – is suggested by ST elevation in each of the inferior leads. ST segments have a “hyperacute” appearance – with broadening of the peak of the T wave in lead aVF; ST segment flattening in lead III – and straightening of the ascending limb of the ST segment in lead II. Taken together – this picture is highly suggestive of an acute inferior infarction.
• Support that the inferior MI is acute is forthcoming from the presence of reciprocal ST depression (seen best in leads I, aVL and V2 ).
• ST segment elevation in lead III is clearly more than in lead II. This finding is typically seen when there is acute RCA occlusion. Support of acute RCA occlusion is forthcoming from the marked ST depression seen in reciprocal lead aVL.
• The RCA typically supplies the right ventricle – as well as the inferior and posterior walls of the left ventricle. As a result – one may see any combination of infero-, postero-, and/or right ventricular infarction when there is acute RCA occlusion. Clinically – one should always be on the “lookout” for evidence of RV (Right Ventricular) and posterior infarction whenever you see acute inferior ST elevation.
• Acute Posterior MI — is suggested in Figure 1 by: i) Early transition (producing sudden appearance of a predominant R wave by lead V2); ii) Positive “Mirror Test”, especially in lead V2 (See Figure 2); and iii) the findings noted in i) and ii) occurring in the setting of acute inferior infarction.

Figure 2: Flipping the ECG in Figure 1 upside-down produces a mirror image of the electrocardiogram. The anterior leads (V1,V2,V3) now provide an ECG picture of what is occurring in the “mirror-image” posterior wall. The positive “Mirror Test” is best seen in flipped-over lead V2 in this example – which now manifests a deep Q, ST elevation and T wave inversion suggestive of acute posterior MI (red arrows).

• Acute RV MI – may also be occurring. Definitive diagnosis of acute RV MI requires right-sided leads, which should show progressively increasing ST elevation as one moves across the right precordium (usually peaking by lead V3R to V4R). Lacking right-sided leads in this case – We can only surmise the possibility of acute associated RV infarction based on: i) the finding of acute infero-postero MI with likely acute RCA occlusion; and ii) subtle presence of ST elevation in lead V1 of Figure 1 – but not in V2,V3 (whereas with anterior MI from acute LAD [Left Anterior Descending] occlusion there is usually ST elevation in at least several anterior leads).
• Lateral Precordial ST Elevation – is also present in Figure 1. That is – there is subtle but real ST segment coving in both leads V4 and V5, with slight elevation of the J point in lead V5. The ST segment is more elevated in lead V6, and takes on a hyperacute appearance in this last lateral precordial lead. That said – it is not certain that ST elevation in V5,V6 represents acute “lateral” infarction – since this could also be a reciprocal change resulting from acute posterior infarction (lead V6 almost being situated anatomically opposite to anterior precordial leads).
• The finding of acute infero-postero-lateral MI should make one consider the less common (~10-15%) anatomic variant of a left-dominant circulation – in which the circumflex artery is larger-than-usual, and extends to supply the inferior and posterior walls of the left ventricle. The RCA is a relatively smaller vessel in patients with left-dominant circulation. However, despite awareness of this anatomic variant – We still suspect the “culprit artery” in this case to be a proximal RCA (rather than left circumflex) occlusion given: i) marked ST segment elevation in lead III > lead II; ii) significant reciprocal ST depression (rather than ST elevation) in lead aVL; and iii) suspected RV involvement (suggested by the finding of ST elevation in lead V1 but not in V2,V3 in the setting of incomplete RBBB).
• Beyond-the-Core: As noted in our Descriptive Analysis (above under Interpretation) – there is a peculiar downslope to the ST segment in lead V1 that blends into shallow T wave inversion in this lead. This appearance at least superficially resembles Brugada syndrome (See ECG Blog #50). Criteria for true Brugada syndrome are not met – because there is not at least 2mm of ST elevation with this downsloping ST segment shape in at least 2 anterior precordial leads. Nevertheless, since this patient is manifesting an acute STEMI and was just resuscitated – the ST-T wave appearance in lead V1 is at least worthy of follow-up (Click HERE for more on Brugada Syndrome).

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CONCLUSION: Unfortunately we do not have cath follow-up on this case – so our suspicion of acute RCA occlusion is unconfirmed as the “culprit artery”. That said, regardless of what the culprit artery might be – acute cath is indicated in this post-resuscitation patient who clearly manifests an acute STEMI that hopefully was treated with timely reperfusion.

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Link to Section 10.0 for pdf download on the ECG Diagnosis of Acute MI (from our ECG-2014-ePub).

• ECG Changes of Acute MI – begins in Section 10.1 - 
• Discussion of the Coronary Circulation (and determining the "culprit" artery) – begins in Section 10.16 - 
• Mirror Test (Posterior MI) – begins in Section 10.33 -

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