A bradycardic rhythm at 36/minute with P’s before each QRS and another P wave following the QRS that does not conduct. There is also a wide QRS complex consistent with a LBBB.

This rhythm is either 2:1 AV block (a 2° AV block of undetermined type) or atrial bigeminy with blocked PACs. If this is 2:1 AV block, the P waves should be regular…and they are not in this tracing! This is a notorious and well-described masquerader of high-grade AV block. Remember Dr. Marriott’s recommendation “cherchez la P.”

Compare this week’s EKG rhythm strip

…with a similar appearing rhythm that does have regular P waves, and therefore is likely 2:1 AV block

Sinus at 84/minute
Left axis (-50°)
Intervals: PR and QT normal; QRS appears prolonged at 120ms

The interesting feature of this EKG is that it nearly meets the criteria and appearance for LBBB. There is a wide QRS, a tall R wave in V₆, and some secondary repolarization changes like poor R wave progression and the appearance of ST-segment elevation. What isn’t consistent with LBBB is the presence of small Q waves in V_5-6, the “septal Q’s” which indicate early depolarization of the septum by way of the LBBB. This initial, and largely unopposed depolarization wave is left to right, thus small negative waves (Q waves) routinely appear in lateral chest leads, and their appearance assures that the left bundle is present and functioning.

This EKG is severe LVH with voltage criteria and all the secondary changes that begin to accrue – left axis, prolongation of the QRS, repolarization changes in the anterior chest leads. This is one of the most difficult EKG patterns of ST-elevation to differentiate from a STEMI – comparison with an old is helpful and then following the apparent ST-elevation in the anterior leads closely as these repolarization changes are not dynamic and should not evolve as will happen with an acute MI. This pattern is one of the most common causes of “inappropriate” calls to interventional cardiology – often only made clear by repeat EKGs and clinical course. If in doubt, an interventional consult is always the correct answer.

Sinus at 100/minute
Axis: right axis deviation
Intervals: QRS prolonged at 160ms with a tall R in V₁ – RBBB

Now, chamber enlargement?
With a RBBB the usual criteria for both right and left ventricular chamber enlargement are somewhat altered.

R wave in lead V₁ > 15mm suggests RVH, especially with rightward deviation of the axis

LVH criteria become less sensitive (eg not seen as reliably), but if voltage criteria for LVH are met with a RBBB they are quite specific.

In this week’s tracing, the very tall T in V₁ is 18mm, and with the right axis deviation is diagnostic of right ventricular hypertrophy.

EKG interpretation:
Sinus with premature beats in a trigeminal pattern
Axis normal (use the AV conducted beats)
Intervals: normal (again, consider the AV conducted beats)
No chamber enlargement, no ischemia or infarct patterns

OK, this may be getting boring, but repetition is the key!

This premature beat:

1. “resets the sinus node metronome”
2. doesn’t allow the P waves to march through the rhythm
3. is followed by a non-compensatory pause
4. is NOT AV dissociated

These are all ways of saying the same thing – this premature beat is a premature ATRIAL beat!

This rhythm strip actually has four premature beats – all are PVCs (premature ventricular contractions). You can be assured of this diagnosis because the beats are dissociated from the sinus rhythm – that is, the sinus rhythm continues through the rhythm strip, the early complex does not reset the sinus metronome as would an early atrial depolarization. Thus the early beat must be ventricular in origin. Recognizing dissociation of a PVC is simply another way of saying that there is a “fully compensated pause” – the sinus beat comes back right on time.

Sinus rhythm at 66/minute
Axis is 0°
Intervals are normal
Voltage is suggestive of LVH with R waves ≥ 12mm in aVL
Impressive, deep and symmetrical T wave inversion in multiple leads

This striking EKG is typical of an unusual form of hypertrophic cardiomyopathy – apical hypertrophic cardiomyopathy, or Yamaguchi syndrome. This type of HCM is relatively common in the Japanese population, where it was first described, but occurs rarely in other populations (3% of all hypertrophic cardiomyopathy in the US).

This seems a good time to review the causes of “giant inverted T waves”

1. CNS events (particularly SAH)
2. Takosubo cardiomyopathy
3. Wellen’s syndrome (critical LAD lesion during pain-free period) – V_2-4
4. Vasospasm
5. Hypertrophic cardiomyopathy (particularly apical hypertrophy type)
6. Memory T waves with VVI pacing

Siewe D, et al. King of hearts for ace of spades: apical hypertrophic cardiomyopathy. Am J Med 127:31-33, 2014.

Yamaguchi H, et al. Hypertrophic nonobstructive cardiomyopathy with giant negative T waves (apical hypertrophy). Am J Cardiol 44:401-412, 1979.

Pillarisetti J, Gupta K. Giant inverted T waves in the emergency department: case report and review of differential diagnosis. J Electrocardiol 43:40-42, 2010.

This is a regular narrow-complex tachycardia at 130/minute. The differential of this rhythm includes:
1. sinus tachycardia
2. SVT
3. 2:1 flutter

The diagnosis depends on the P wave or atrial activity. Remember Marriott likes to say “cherchez le P.” In this tracing there is something midway between QRS complexes, seen best in the inferior leads, especially lead II. This is a flutter wave and the rhythm is 2:1 flutter! Notice the broad “S wave” at the end of QRS complexes in the inferior leads – actually this is a part of the other flutter wave (occurring at a rate of approximately 300/minute) superimposed on the QRS.

The provider seeing this patient thought that the regular tachycardia was SVT, so Adenosine was given…

Look at all the flutter waves now!

First the rhythm – sinus bradycardia at 36/minute

Second – the inferior leads keep catching my eye…no obvious ST-segment elevation, but the T waves look a bit prominent (hyperacute ?), and then there is the T wave inversion in aVL (remember, reciprocal changes in aVL may be the earliest sign of an inferior MI).

Of course, the correct response would be to repeat the EKG. This was done just 10 minutes later:

Now the inferior STEMI is evident! Note the rhythm change – now sinus at 100/minute, and with more prominent P waves. Not having been there, I can only guess – the original rate was likely due to excess vagal tone (common with inferior MI’s – think pale, diaphoretic, nauseous, bradycardic). The subsequent tachycardia might be due to nitroglycerin administration, or just less vagal tone, or maybe they received atropine.

Keep repeating those EKGs when rhythm or rate changes; you could be looking at an early MI

This EKG reveals a regular rhythm at 30/minute. There are no obvious P waves, although there appears to be irregular fine oscillations of the baseline, consistent with fibrillatory waves. Why would atrial fibrillation
present with a slow and regular ventricular response? Perhaps these ventricular beats are escape beats, occurring because the AV node is completely blocked! This is what complete heart block occurring with atrial fibrillation looks like…

If this patient was taking digoxin it would certainly be important to check a level to rule out toxicity. Digoxin toxicity classically causes two important EKG findings: 1) significant AV block (more than 1° AV block), and 2) increased automaticity (often accelerated junctional rhythm or atrial tachycardias). Typically these two EKG findings occur simultaneously – hence the classic dig toxic rhythms (PAT with block or “regularization” of the a fib due to 3° AV block with accelerated junctional escape rhythm).

PAT with 2:1 block (P waves at 150/minute – too slow for flutter waves, so these are discrete P waves and this is atrial tachycardia)

Another PAT (look hard for the P waves at 150/minute) with 2° AV block, type I

“Regularization of atrial fib” – due to accelerated junctional rhythm at 70/minute with 3° heart block of underlying a fib (note fibrillatory waves in V₁)

What looks like simple bigeminy is actually a slightly more interesting diagnosis. Again, calipers are very helpful!

Notice that the ventricular complexes occur at a regular interval, and that the coupling interval (the space between the preceding QRS and the PVC) is not constant, as would happen with bigeminy. This rhythm is an independent ectopic ventricular rhythm, parasystole. Notice that the 6^th complex is a fusion beat (a combination of the sinus beat and the ventricular beat) – a sure indicator of an independent ventricular rhythm.

Traditionally parasystole is felt to represent a “protected” focus that is isolated from, and thus independent of, the electrical activity of the surrounding myocardium.   Parasystole is of no greater clinical import than PVCs of similar frequency or even bigeminy.