Sinus at 75/minute
Axis normal, PR and QRS also normal
QT interval is visibly shorter than normal
No LVH
No ischemia or infarct patterns

A decrease in QT interval is seen with hypercalcemia, which fits with the patient’s presentation and known malignancy. This gentleman’s ionized calcium was 2.2.

The ST-segment is short or absent in hypercalcemia and the duration of the QTc interval is decreased. Although it is difficult to give an absolute QTc interval below which hypercalcemia is assured, this value is always <400ms and visually fairly obvious.

Another occasional EKG presentation of hypercalcemia is leftward movement of the apex of the T-wave as in the above example, another example of hypercalcemia associated with malignancy.

Diercks D, et al. Electrocardiographic manifestations: electrolyte abnormalities. J Emerg Med 27:153-160, 2004.

The strip reveals a very rapid (at times approaching a heart rate of 300/minute) and irregularly irregular rhythm with a wide-complex QRS. You must assume that this represents atrial fibrillation conducting through a bypass tract. This is a potentially dangerous situation because rates that approach 300/minute can quickly degenerate to ventricular fibrillation. Additionally, treatment of this rhythm can worsen the ventricular rate by increasing conduction down the bypass tract. Avoid ABCD – adenosine, ß-blockers, calcium-channel blockers, and digoxin. Appropriate treatment includes procainamide and electrical cardioversion. Treatment with amiodarone is effective but controversial as amiodarone has a complex mechanism including actions which block the AV node and have been reported to cause deterioration of bypass atrial fibrillation. It was once recommended by ACLS, but was removed in the 2010 guidelines.

After cardioversion to sinus rhythm the patient’s rhythm strip clearly reveals signs of WPW (short PR interval, prolonged QRS, and a delta wave).

This patient went on to have bypass tract ablation so he wouldn’t have to experience something like this episode again. Note that the signs of WPW are now absent from the EKG.

Baseline is sinus rhythm at 68/minute
Normal axis and intervals
Essentially normal EKG with several strange QRS complexes…

First, if you march the P waves through, they remain constant (note the pen marks of some helpful person). The 4^th and 5^th beats in this rhythm strip are wide-complex and dissociated from the P waves. This rhythm is sometimes called “slow v tach” to indicate the independent (ectopic) ventricular source. This is accelerated idioventricular rhythm (AIVR).

Another helpful feature of this ventricular rhythm are fusion beats as the rhythm phases in and out with sinus rhythm, often at a similar heart rate. In this rhythm strip, the 3^rd and 6^th beats are fusion beats – that is, a combination of the sinus beat and the ventricular beat.

AIVR is well known as a repolarization arrhythmia (especially after TPA or interventional cath). It can also occur in essentially normal patients for no apparent good reason, as was the case in this otherwise healthy young woman.

This EKG has several unusual findings – 1) a significant right axis deviation, 2) upright QRS in lead aVR, and 3) inappropriate R-wave progression in the chest leads. Remember that lead aVR is oriented opposite to other limb leads, and always has a negative P, QRS, and T wave in a normal EKG. The appearance of a negative complex in I and upright complexes in aVR can be seen with switched limb leads…

but notice that the R-wave progression of the chest leads is normal when just limb leads are switched.

This challenging EKG is from a patient with dextrocardia. It is advisable to place the chest leads in the right-sided array to get an improved diagnosis of ischemia and infarct patterns.

The most striking finding on this EKG is the deep T-wave inversions in V2-3 and the biphasic T wave in V4. She was pain-free at presentation and an initial troponin was negative. Three hours later the repeat EKG was unchanged and a second troponin was minimally elevated at 0.12. She was heparinized and admitted to telemetry. She went to cardiac cath the next morning – that revealed 90% proximal LAD stenosis that was successfully stented.

Since these anterior T-wave inversions appeared in the pain-free interval following her chest pain episode, I believe they represent Wellens’ syndrome. Wellens’ may present with biphasic T-waves in the anterior leads or with deeply inverted T-waves in the same leads (original reports actually claimed deep T-wave inversion were the more common finding). We can add this form of Wellens’ to the differential list of deeply inverted T waves (remember: spasm, Takotsubo, CNS event, and rarely PE).

Wellens noted that unstable angina with this EKG pattern frequently (75% of his patient series) developed an extensive anterior MI with days to weeks of presentation. This finding correlates with angiography in the modern era that typically demonstrates a critical lesion in the proximal LAD.

Rhinehardt J, Brady WJ, Perron AD, et al. Electrocardiographic manifestations of Wellens’ Syndrome. Am J Emerg Med 20:638-643, 2002.

Tandy TK, Bottomy DP, Lewis JG. Wellens’ Syndrome. Ann Emerg Med 33:347-351, 1999.

There are several reasons to be reassuring about this rhythm.

There is something regular occurring throughout the rhythm strip – in this case, there is some remnant of the sinus beat (as marked above). Also note that the O2 pleth continues undisturbed throughout the period of the questionable arrhythmia. This is a good example of artifact simulating ventricular tachycardia.

Another worrisome rhythm…

This rhythm strip is slightly more difficult to define because the O2 pleth has some artifact throughout the strip. However if you use calipers or mark R-R on a piece of paper you will again find remnants of persistent sinus rhythm through the apparent ventricular tachycardia…artifact NOT ventricular arrhythmia.

This is another example of Ashman’s phenomenon occurring during atrial fibrillation with rapid ventricular response. Ashman’s requires an irregular pattern of QRS complexes. Repolarization of any QRS complex is proportional to the previous R-R interval. Therefore when a relatively long R-R is followed by short R-R the QRS ending the short interval may find a portion of the conduction system still refractory (not yet fully repolarized). The RBBB is predictably the portion of the conducting system that is slowest to repolarize, therefore the beat following the short interval is aberrant with a RBBB morphology. If subsequent beats occur rapidly they will also find the RBBB still refractory and continue with RBBB morphology.

V1 lead from this EKG show the RBBB morphology with wide QRS and tall R wave in V1.

Also see “Ashman’s Phenomenon” in EKG Discussion for more examples of this common rhythm finding.

Wide-complex tachycardia in a gentleman with a cardiac history including prior MI – think no further about the etiology of this rhythm…this is V tach.

What to do? Remember ACLS protocols (and common sense) – this gentleman is having chest pain. With his history, wouldn’t you like to see what is going on under all that wide-complex tachycardia? Besides, although his vital signs are currently stable, do we ever let people with active chest pain sit about with a heart rate of 180? Seriously, even though he seems very stable, this rhythm needs to be treated aggressively – electricity is the right answer.

After cardioversion…

Now his acute inferior MI is easily observed, and he is quickly taken to the cath lab!

This rhythm is 2° AV block Type I, Wenckebach. While it is easily recognizable (I hope!), the actual criteria, or electrocardiographic findings, are worth reviewing.

1. progressive lengthening of the PR interval until a P wave is blocked
2. progressive shortening of the RR interval until a P wave is blocked
3. the RR interval containing the blocked P wave is shorter than the sum of 2 PP intervals

When Type I 2° AV block does not precisely follow these relationships it is typically due to underlying sinus arrhythmia, which alters the RR interval, which in turn will affect the RP and PR intervals of subsequent beats.

Because of the periodic pauses, the rhythm shows “group beating,” a finding that frequently leads to consideration of the diagnosis of Wenckebach phenomenon.

Another example of this rhythm

Typical ventricular paced complexes – since the pacing lead is inserted into the right ventricle the current of depolarization proceeds from right to left ventricle effectively producing a wide QRS with LBBB morphology.

Today’s EKG is 100% ventricular paced with a fairly narrow and normal appearing QRS complex. This patient has a biventricular pacemaker with one lead in the RV (also his ICD lead), and a second wire into the coronary sinus (thinner lead extending further to the left heart wall). This pacer produces simultaneous biventricular activation and is often used now in patients with significant heart failure.