Friday, January 11, 2013

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?

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.

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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Tuesday, January 1, 2013

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).
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.
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).
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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