Looking at the V1 rhythm strip, the first five beats are an accelerated idioventricular rhythm (no P waves, wide complex, and regular rate of 70/minute). Just before the 6^th beat you can see the “emergence” of a P wave – this particular P wave is very close to the subsequent QRS, and there is slight variation in the QRS morphology. The 6^th QRS represents a fusion beat (a composite between the ventricular beat and a sinus-conducted beat occurring at nearly the same time). The 7^th through 9^th beats appropriately follow P waves and represent sinus conducted beats. This rhythm represents isorhythmic competition between accelerated idioventricular beats and sinus beats occurring at nearly the same rate.

The reason for this rhythm in this patient is apparent from leads V1-3 (the sinus conducted beats, so they can be interpreted) – the patient is having an acute anterior MI. Periods of accelerated idioventricular rhythm are common during acute infarction and especially during reperfusion following thrombolysis.   AIVR has also been termed nonparoxysmal ventricular tachycardia or “slow v. tach”. It usually does not produce any hemodynamic change, and requires no specific treatment.

This gentleman had chest pain and associated symptoms suggestive of an acute coronary syndrome. His EKG reveals STEMI in leads V₂ – V₅. This is an important pattern to recognize. A RBBB does not perturb the depolarization very much (because the RBBB supplies the much smaller side of the heart), certainly much less than LBBB. Because the depolarization is less altered it is expected that ST-segment changes of acute ischemia or infarct will be recognizable on the EKG.

If there are any questions about the ST-segment elevation in V_2-3 remember that the horizontal tracings on the 12-lead are simultaneously recorded, and that complexes line up vertically. The beginning and the end of the QRS is clear in V₁, and if you follow the end of this QRS down through V_2-3, the ST-segment in these complexes becomes clear – it is not just a wide QRS in these leads!

Another RBBB with acute anterior STEMI – perhaps more clearly seen

This EKG gives the diagnosis…and more!

Rate and rhythm: sinus at 110/minute
Axis: right axis deviation at +120°
Intervals: PR, QRS, and QTc are normal
Chamber enlargement: the tall R wave in V1 and a right axis à right ventricular hypertrophy
ST-segment and T-wave changes: T wave inversion in V1-3 is consistent with right ventricular strain pattern

This EKG is a good example of how the differential of a tall R wave in lead V1 can be helpful (see “Tall R waves in V1” under website section EKG discussion).

Four causes of a tall R wave in V1 with their hints:
RBBB                            QRS ≥ 0.11
WPW type A               delta wave and short PR interval
Old posterior MI      accompanies an old inferior MI
RVH                               right axis deviation

This EKG is from a patient with primary pulmonary hypertension and significant RVH.

Notice the respiratory rate…since the V1 lead is on the chest, the rhythm strip records the chest excursion. The respiratory rate is approximately 24/minute!

I love this EKG! The rhythm is basically 2° AV block, Type II…but with a twist! The P waves are regular with multiple dropped beats. The conducted beats have a constant PR interval, except for the first PR interval of each group that is actually a bit longer. Maybe this is a “reverse Wenckebach”?!

No, actually, the initial slightly longer PR interval is likely non-conducting – the first QRS of each group is probably a junctional escape beat. Notice that the first QRS of both groups is the exact same distance from the preceding QRS, and at a rate consistent with an escape beat. Notice also that the purported escape beats are ever so slightly different in morphology compared to the normally conducted beats.

The underlying rhythm is sinus at a rate of 70/minute. The QRS morphology of the sinus rhythm complex is LBBB (QRS ≥ 120msec, tall monophasic R in V₆). The 4^th and 8^th beats in the rhythm strip above have a similar morphology to the sinus beats but are premature. Notice that the T wave following the sinus beat and before the early beat is different – deformed by a premature ectopic P wave, suggesting that these early beats are PACs.

As a confirmation, you can demonstrate that these early beats are not AV dissociated (eg, the sinus “metronome” is reset by the early ectopic P and subsequent P waves do not appear “on time”). PACs are not fully compensated.

PVCs are fully compensated, another way of saying that they are AV dissociated and do not disturb the sinus metronome (P waves will march through the appearance of the premature beat.)

While this premature beat might look like a PAC, it is fully compensated (AV dissociated) and therefore a PVC!

This should be a striking EKG, and in fact should send shivers down your spine! There are significant ST-segment depressions in many leads (I, II, aVL, III, V_2-6) as well as ST-segment elevation in aVR. This EKG is the classic example of critical left main occlusion, and should be considered a “STEMI equivalent.” This patient should be referred to interventional cardiology, as this patient was! They took him to cath, and indeed found a 99% stenosis of the left main coronary artery; they inserted an IABP to support his pressure and alleviate symptoms, and got an emergent cardiac surgery consult for CABG. The surgery was accomplished and the patient did very well.

Critical occlusion of left main coronary artery.

Wellens described this EKG finding many years ago – ST-segment depression in ≥ 8 leads and ST-segment elevation in aVR. This is particularly specific if there is also ST elevation in aVL.

Lawner BJ, Nable JV, Mattu A. Novel patterns of ischemia and STEMI equivalents. Cardiol Clin 30:591-599, 2012.

This rhythm is a regular wide-complex tachycardia. By definition, this rhythm is ventricular tachycardia until proven otherwise. Fully 70% of WCT is v. tach. Other causes of WCT include SVT with 1) rate-related changes (aberrancy), 2) pre-existing bundle branch block, or 3) antidromic conduction down a bypass tract (WPW).

Some electrocardiographic clues that suggest ventricular tach include QRS concordance (QRS complexes in chest leads all predominantly negative or positive), very wide QRS complexes (eg QRS > 160 msec with LBBB), extreme right axis (-90° to ±180°), and evidence of AV dissociation.

While there are many criteria for predicting v. tach, clinical association is as good as any electrocardiographic criteria. If the patient has a cardiac history, it is v. tach 97% of the time! (Lift up the hospital gown and look for the sternotomy scar!)

And in an emergency, treat wide-complex tachycardia (WCT) per current ACLS protocols.

This youngster was so weak that he had difficulty moving himself around the stretcher. His EKG actually provides some explanation of his situation:
Sinus rhythm at 72/minute
Axis normal (60°)
PR normal (0.16), QRS normal
QT appears to be prolonged, look especially in III and V₃

The ST-segment and T wave changes on this EKG can be explained by hypokalemia. As potassium levels decline U waves appear following the T wave. At the same time T waves will diminish. When severe, the T wave may disappear and a prominent U wave can be mistaken for the T wave, thus one of the reasons that hypokalemia is always included in a differential for prolonged QT interval.

This young man was extremely hypokalemic, with a K⁺ of 1.7mEq. Pediatric endocrinology came up with an interesting diagnosis – thyrotoxic periodic paralysis!   His weakness improved with repletion of his K⁺ and further treatment of the thyroid disorder.

Rate: 100/minute
Rhythm: Sinus rhythm
Axis: Right axis deviation
Intervals: PR, QRS, QTc are all normal
Chamber enlargement: none
Ischemia and infarction: none

The most striking thing about this EKG is the right axis deviation (large Q wave in I) and the generally positive deflection of all complexes in lead aVR (usually P, QRS and T waves are negative in lead aVR). These are clues to switched limb leads.

When the leads were carefully replaced, the resulting EKG is a good example of a normal tracing!

Look closely at the rhythm strip – there are actually three separate (and unrelated) rhythms on this strip. There are P waves (↑) at 75/minute, QRS complexes (●) at 25/minute that are dissociated from the P waves, and pacer spikes (↓) at 70/minute which neither capture nor sense. This is an example of pacemaker failure and underlying complete heart block (the reason this patient had a pacemaker in the first place).

This pacemaker had failed to generate sufficient energy to capture or sense normally – the battery needed to be changed!