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 Interpretation Review #58 (2nd Degree - 3rd Degree AV Block - AV Dissociation)

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? (Figure reproduced from Case M in ACLS: Practice Code Scenarios-2013-ePub).

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Figure 2: Lead MCL-1 rhythm strip. Is this complete AV block? (Figure reproduced from Case M in ACLS: Practice Code Scenarios-2013-ePub). NOTE - Enlarge by clicking on Figures - Right-Click to open in a separate window.

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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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