EKG interpretation:
Sinus at 70/minute
Axis normal (10°)
PR and QRS intervals normal, QT is prolonged in many leads (eg aVL)
No chamber enlargement
A U wave is present after the T wave in several leads (leads V2-3)

The important features to recognize in this EKG is the appearance of a U wave and the diminution of the T-waves, leaving the appearance of a prolonged QT in several leads. The differential of a prolonged QT interval, besides offending medications, are hypokalemia (seen with increasing U waves and diminishing T waves), hypomagnesemia, and hypocalcemia. Alcoholics are already prone to hypomagnesemia, and the addition of several days of gastroenteritis may quickly deplete other electrolytes and cations.

While the patient was being monitored during the initial stages of her evaluation, she suddenly became unresponsive and the following rhythm was captured on the monitor:

She regained consciousness with sinus rhythm on the monitor and stable VS without intervention. Soon thereafter labs resulted:

K – 2.3 mEq/L (3.6 – 5.2)
Mg – 0.6 mEq/L (1.3 – 1.9)
iCa – 0.96 mmol/L (1.1 – 1.3)

Remember that alcoholics who become sick are at risk for prolonged QT, torsade de pointe, and syncope or sudden death!

EKG interpretation
Sinus at 100/minute
Axis is normal
Intervals are normal
Ischemia/infarct – T wave inversion V1-4 with loss R waves (deep Q waves) in the same leads

T-wave inversion in the anterior leads has a broad differential. Deep, or giant, T-wave inversion has it’s own differential including CNS changes (see full differential under Impressive T-wave Inversion on TorreyEKG.com). More minor T-wave inversion can be seen with ischemia, acute PE, evolving or subacute STEMI, and many other causes.

These T-wave inversions in leads with well-formed Q waves suggest a subacute MI, possibly days to weeks old (the Q’s have formed, the ST-segments are back close to baseline, but the T-wave inversion can persist for weeks).

And what is the connection between a recent anterior MI and his presentation with a stroke? Once anticoagulated on heparin, a transesophageal ultrasound showed a large mural thrombus in a dyskinetic wall of his left ventricle.

His level of hypotension seemed unusual for an acute septal MI, especially in an otherwise fairly healthy young man. He had no chest pain, just some shortness of breath.

78/46   110   28   O₂sat 92% on RA   afebrile
lungs – clear bilaterally
cor – regular, no murmur appreciated
extremities – no edema, diminished distal pulses

RUSH (Rapid US in Shock) exam revealed a massively dilated right ventricle. When asked about leg pain, he described significant pain in his right calf for 2 days. Ultrasound of the right popliteal area revealed a non-compressible vein with intramural clot. STAT CT angiogram revealed large bilateral pulmonary emboli. This patient received TPA in the ED and has done well.

While PE has no definite EKG findings, it is a great masquerader…it can present with T-wave inversion anteriorly (small or giant T-wave inversion) and with ST-segment elevation on occasion. Keep PE on many differentials, especially when the EKG findings don’t quite fit with the clinical presentation.

This middle-aged man is a landscape worker in Massachusetts and frequently encounters ticks that he “burns off with a cigarette”. He vaguely remembers a “large round red rash” during the summer. Currently he has no complaints but was noted to be bradycardic at a routine PCP office visit.

Rate and rhythm – narrow QRS complexes at a regular rate of 45/min, with P waves at a regular rate of 72/min; the P waves and the QRS complexes are completely dissociated – this is 3° AV block, or complete heart block.

Notice that the rate QRS complex is 45/min and the complexes are narrow-complex – this implies that this “escape rhythm” is high in the progression of possible escape locations, probably just below the AV node.

This healthy middle-aged landscaper was diagnosed with Lyme carditis with AV node involvement.

Interpretation:
Rate: 114/minute
Rhythm: the overall rhythm is irregularly irregular – either atrial fibrillation…or, the other irregularly irregular rhythm. Multifocal Atrial Tachycardia (MAT).
Intervals: PR seems to vary where it can be easily measured
Chamber enlargement: none
Ischemia and infarct patterns: none

The rhythm is multifocal atrial tachycardia (MAT) as there are definite P waves discernible in front of some QRS complexes, of varying morphology and PR interval.

The wide-complex beat seen slightly after the middle of this tracing is most likely an aberrantly conducted supraventricular beat based on Ashman’s prediction. Notice the long R-R interval followed by a short R-R interval resulting in a RBBB morphology wide-complex (notice the tall R-wave in V1).

See also: EKG of the Week #42, and
EKG Discussion of Ashman beats

This EKG is common in the ED and worth being comfortable with so that young healthy patients are not inadvertently thrombolysed or referred to interventional cardiology. While there is noticeable ST-segment elevation in lead V_3-5 this pattern is consistent with Benign Early Repolarization.

Notice that the ST-segment elevation occurs in association with large amplitude QRS complexes in the chest leads, and often has a notched, or “fishhook”, appearance at the J point (apparent here in V_4-5).

Another corroborating find in early repolarization is an early R/S transition. Usually, the R/S ratio progresses across the chest leads (V₁ – V₆) with the transition, or R/S closest to 1, occurring in V_3-4. In early repolarization the R/S transition often occurs before V₃ as in this example.

Finally notice that there are no reciprocal changes noted in other leads as would typically be present with ST-segment elevation associated with an acute MI.

Each of these findings, particularly in young healthy men with an appropriately atypical chest pain complaint, suggests benign early repolarization.

This rhythm is a rapid irregularly irregular rhythm at about 170/minute. It is mainly a narrow complex tachycardia, with seven wide beats of a different morphology. This rhythm is rapid atrial fibrillation. The wide-complex beats could be PVCs or, in the setting of rapid atrial fibrillation, Ashman’s phenomenon would suggest these could be aberrantly conducted supraventricular beats.

Ashman’s phenomenon occurs because the repolarization period for any QRS complex is proportional to the R-R interval preceding the complex (bradycardic rhythms with longer R-R intervals have longer QTc intervals). Therefore, when a relatively long R-R interval is followed by a short R-R interval, that third beat may find part of the conduction system refractory – in fact, usually the right bundle (the longest bundle) is the refractory part of the conducting system, and the resulting aberrantly conducted beat will have a RBBB morphology (tall R wave in V1).

and as long as the R-R interval remains short, the aberrancy persists – notice the RBBB morphology with tall R waves in this V1 rhythm strip

— see EKG discussion “Ashman phenomenon” on the home page  (scroll down)

The clinical history and this EKG were sufficient for the consideration of acute pericarditis. There is the suggestion of inferior-lateral ST-segment elevation, but notice the following…

1. The ST-segment elevation, when closely scrutinized, is partly due to PR-segment change from the baseline. This is most clearly seen in leads II and I as PR depression. There is also PR-segment elevation in lead aVR, an additional described sign of pericarditis.

2. In the lead II rhythm strip there is downward trending of the T-P baseline, also known as Spodick’s sign.

Spodick’s sign of pericarditis

3. ST-segment elevation in lead III > ST elevation in II suggests acute ischemia.

References

LeWinter MM. Percarditis – clinical review. NEJM 371:2410-16, 2014.

This EKG is striking in several ways…
Atrial fibrillation with slow ventricular response at 54/min
Right axis deviation
Extreme low voltage in the limb leads

Exam revealed…
VS: 138/68 66 24 O2sat 90% 982
Clear lungs, distant heart sounds, +JVD, 2+ pretibial edema

CXR

Hopefully you were concerned with the possibility of a large pericardial effusion, or even tamponade, with the low voltage on the EKG, some aspects of the physical exam, and then the “waterbottle” cardiomegaly on CXR! The next step in managing this patient was bedside ultrasound (not pericardiocentesis as hemodynamically stable).

Bedside ultrasound revealed no pericardial fluid but a massively dilated right ventricle?!

The rhythm is the most important and possibly difficult thing to assess. The first three beats appear to be sinus at a rate of 50 beats/minute. The rhythm then abruptly changes rate to 33 beats/minute. This patient was symptomatic when she had long periods of a rate of 33/minute. One might assume sinus node dysfunction, but look closer…

This rhythm strip demonstrates something deforming the terminal portion of the T wave that precedes the beats of the slower rate (arrows). The deflect that deforms these T waves is a very early atrial beat, a premature atrial contraction (PAC), that is so early that the conduction system is not yet ready to accept a premature beat – thus what we see here is bradycardia simulated by blocked PACs occurring in a bigeminal pattern.

Remember,
The most common cause of a pause
in sinus rhythm is a blocked PAC!