This 92-year-old patient was diagnosed with left bundle branch block on ECG, and left ventricular hypertrophy on echocardiogram.  The two conditions are very often seen together, in fact, a majority of LBBB patients have LVH.  Since the two conditions can have similar ECG changes, it is difficult from the ECG alone to determine the presence of LVH when LBBB is present.  If the ECG criteria for LVH are present, it can be assumed that LVH is present, even in the presence of LBBB.  For determining LVH by ECG criteria, the Sokolov-Lyon criteria are commonly used ( S wave in V1 + R wave in V5 or V6 > 35 mm). 

The common criteria for left bundle branch block include:  wide QRS complex, frontal plane axis normal or leftward, negative QRS in V1, and positive QRS in leads I and V6.   LBBB is only found in supraventricular rhythms (not ventricular rhythms).  The ST segment and T wave will be negative in leads with positive QRS complexes, and positive in leads with negative QRSs (discordant).

Left ventricular hypertrophy also widens the QRS, although not often as much as LBBB does.  There will be discordant ST segments and T waves, which is called the "strain" pattern.  It also is easier to diagnose in supraventricular rhythms, because ventricular rhythms usually have large QRS complexes due to the depolarization wave being in one direction across the heart.

For confirmation of LVH, an echocardiogram is recommended.

This ECG also has an interesting rhythm.  The first beat appears normal, the second beat is a PAC.  The third beat appears to arise from a different focus, which would make it an escape beat, but it is very difficult to determine this due to the very tiny P waves.  After a pause, a regular sinus rhythm resumes.  To see the P waves, look at the right chest leads:  V1, V2, V3.  Since left bundle branch block only occurs in SUPRAVENTRICULAR rhythms, it is important to determine the rhythm, and P waves are a definite sign of SV rhythm.  We wish the P waves here were taller.

This ECG was obtained from a 49-year-old man who was a patient in an Emergency Dept.  We do not know his presenting complaint, only that he had a history of insulin-dependent diabetes mellitus (IDDM).  It was noted by the donor of the ECG that the patient had no chest pain, no shortness of breath, and no other cardiac symptoms.  We do not know his hydration or electrolyte status.  There are quite a few interesting abnormalities on this ECG, and the exact interpretation would, of course, depend upon the patient's clinical status.  It would definitely help to be there!

First, we note a sinus tachycardia at a rate of 118 bpm.  This could be due to very many causes, including but not limited to:  dehydration, pain, anxiety, high or low blood glucose, fever, or CHF.  The PR and QT intervals are within normal limits.  The QRS complexes are narrow.  The axis is normal at 0 degrees.  The QRS voltage in the lateral leads is on the high side of normal, but we do not know this patient's body type.  Voltage as read by the ECG can be influenced by a thin chest (making voltage look larger) or a large chest (making voltage lower).

There are T wave abnormalities in the lateral leads:  I, aVL, V5 and V6.  The T waves are inverted, which can have many meanings.  However, when inverted T waves are in the lateral leads, as opposed to the inferior or right chest leads, it is often a sign of ischemia.  The flat, horizontal ST segments can also signify coronary artery disease (CAD).  This patient denied cardiac symptoms, but his age and history of IDDM make it probably that CAD is a factor.  The leads with T wave inversion also have a small amount of ST segment depression.  The right precordial leads, V1 and V2, have a small amount of ST elevation,  This possibly represents a reciprocal change to the ST depression in V5 and V6.

Because we are not at the bedside of this patient, there are many details we do not know.  But these inverted T waves could be ischemic T waves, and this requires that the patient be further evaluated.

As always, we welcome comments, as this ECG probably has more to say!

REFERENCES:  Dr. Ken Grauer,  Life In The Fast Lane, World Journal of Cardiology 

This strip offers something interesting for both your basic-level students and for your more advanced students.  First, it is a good example of sinus rhythm with a premature beat.  The PR interval was measured by the machine at .21 sec (218 ms).    The premature beat is supraventricular - that is, it is not a PVC.  Because of the slightly long PRI in this strip, it's P wave COULD be buried in the preceding T wave.  That would make this a premature atrial contraction (PAC).  

For discussion with your more advanced students, the P wave could, instead, be retrograde, and occurring during the QRS or slightly after it.  That would make the premature beat junctional, or an atrial echo beat. The origin of the premature beat is mostly academic - there is likely no clinical need to determine the origin.  

In looking for clues as to the origin of the premature beat, we would scrutinize the premature beats for "hidden" P waves.  Upright and before the premature beat would indicate a PAC.  Negative P waves before, during, or after the premature QRS would indicate PJCs.  In this strip, the T waves just before the premature beats are slightly deeper than the other T waves.  This could indicate atrial "echo", or reciprocal beats, which requires the presence of dual junctional pathways, in which the impulse turns around, reenters the atria, and causes a new beat.  It can be helpful to look at multiple leads (the more the better) in your search for P waves.  For a look at this patient's 12-lead ECG, go to this link.  

The P wave of a premature beat often penetrates the SA node and "resets" it, causing the next normal beat to occur after a "normal" R-to-R interval from the premature beat. This fact can help us find "hidden" P waves, as well.

Another interesting feature of this strip for your students who are interpreting 12-Lead ECGs, is that this ECG shows the criteria for left ventricular hypertrophy.  See the link above for the 12-lead and discussion.

This ECG is from a man with left ventricular hypertrophy.  LVH causes taller-than-normal QRS complexes in leads oriented toward the left side of the heart, such as Leads I, II, aVL, V4, V5, and V6.  Leads on the opposite side, such as V1, V2, and V3, will have deeper-than-normal S waves.  A commonly-used criteria for determination of LVH is the  Sokolow-Lyon index:     S in V₁ + R in V₅ or V₆ (whichever is larger) ≥ 35 mm (≥ 7 large squares);  and  R in aVL ≥ 11 mm.  There is no perfect ECG criteria for determining LVH. The most accurate way to evaluate the size and thickness of the chambers of the heart is echocardiogram (ultrasound).  Frequently, there is left axis deviation, especially if the hypertrophy is confined to the left ventricle.

The left ventricle can be enlarged for many reasons, some worse than others.  Athletes naturally enlarge the heart, as they work the muscle.  Pathological causes for LVH can include anything that strains the heart as it pushes against increased afterload, such as hypertension and aortic stenosis, and diseases of the myocardium, such as cardiac myopathies.