ECG Blog #92 (Basic Concepts-5) – LVH

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     This is my 5th installment of Basic ECG Concepts. Rather than specific cases — the goal of these Basic ECG Concepts is concise review of some less advanced topics that comprise the fundamentals of ECG interpretation. This material is excerpted with modification from my new introductory book to ECG Interpretation = “A 1st Book on ECGs-2014” and/or the expanded 1st-ECG-Book-ePub version (which is out in kindle-nook-kobo-ibooks). Your feedback on this series is WELCOME!

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NOTE: To enhance relevance — some advanced points have been added illustrating selected concepts regarding the ECG diagnosis of LVH (with this more advanced material excerpted from our ECG-2014-ePub). In this way — We hope this post is of interest and value to ECG interpreters of any level.

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LINKS to Previous Basic ECG Concepts:

• Basic Concepts #1 — QRS Terminology
• Basic Concepts #2 — Intervals (PR/QRS/QT )
• Basic Concepts #3 — Axis
• Basic Concepts #4 — Lead Groupings
• Basic Concepts #5 (this post! ) — LVH
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• Basic Concepts #6 — Systematic Approach
• Basic Concepts #7 — Q-R-S-T Changes

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     The 5th Parameter of our Systematic Approach to ECG interpretation (after assessment of Rate – Rhythm – Intervals – Axis) — is determination of Chamber Enlargement (Hypertrophy).

• The reason for delaying assessment of Chamber Enlargement to this point in the process (ie, until after assessment of Intervals) — is that criteria for ventricular enlargement are different IF the QRS Interval is prolonged and the patient has bundle branch block.
• NOTE: We do not discuss here the ECG diagnosis of LVH in the special situation of underlying LBBB — because this is a more advanced concept. (For those interested in this advanced concept — See our ECG Blog #11).

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OVERVIEW on Chamber Enlargement:

     With the parameter of “Hypertrophy” — We assess the ECG for signs of Chamber Enlargement. This may encompass an increase in chamber wall thickness — chamber size dimensions (volume) — or a combination thereof.

• There are 4 cardiac chambers (Figure-1). As a result — our systematic assessment for chamber enlargement should include considerations for enlargement of each of these 4 chambers. That said — We intentionally limit discussion here to review of criteria for ECG diagnosis of LVH (Left Ventricular Hypertrophy). This is the most common form of chamber enlargement — and the one that you’ll most often encounter clinically.
• For those interested — We review ECG diagnosis of atrial enlargement in our ECG Blog #75 — and of RVH (Right Ventricular Hypertrophy) in ECG Blog #77.

Figure-1: There are 4 Cardiac Chambers. These are — the RA (Right Atrium); — LA (Left Atrium); — RV (Right Ventricle); and — LV (Left Ventricle). We limit discussion on Chamber Enlargement in this Blog post to ECG Criteria for LVH (Left Ventricular Hypertrophy). The KEY numbers to remember = 35 & 12.

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Rationale for ECG Criteria on LVH

     The theory for ECG diagnosis of LVH is simple: A thicker and larger LV (Left Ventricle) has more mass. A larger QRS deflection is therefore produced on ECG. We show this schematically in Figure-2:

Figure-2: Schematic illustration for derivation of LVH voltage criteria. Panel A — depicts normal LV (Left Ventricular) and RV (Right Ventricular) wall thickness. Panel B — With LVH, there is an increase in LV mass (larger red arrow in B compared to A). This results in deepening of the S wave in right-sided leads (V1,V2) — and/or an increase in R wave amplitude in left-sided leads (V5,V6,aVL).

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What Happens to the ECG with LVH? Explanation of the rationale for the ECG changes of LVH is best understood by keeping the following points in mind when viewing Figure-2:

• In Basic ECG Concepts #4 — We reviewed the various anatomic lead areas assessed by each of the standard 12 leads on an ECG. Doing so suggests that “left-sided” (or lateral) leads on an ECG — are best thought of as leads I, aVL, V5 and V6 (See Figures 1,2,3 and 6 in Basic Concepts #4).
• In addition to being anteroseptal leads — leads V1 and V2 are also “right-sided” leads. Anatomic placement of the electrodes to record leads V1 and V2 is clearly to-the-right compared to placement for the other 4 chest leads (See Figure-2 in Basic Concepts #4).
• Normal activation of the LV is directed to the left — since this is where the left ventricle lies within the chest cavity (small red arrow in Panel A of Figure-2).
• With the increase in LV mass that occurs with development of LVH — forces directed toward the LV increase (larger red arrow in Panel B). As a result — left-sided leads (V5,V6,aVL) show an increase in amplitude (taller R waves) — and right-sided leads (V1,V2) manifest deeper S waves (due to more activity moving away from the right). As we will see in a moment — the “magic numbers” to recall are “35” and “12”.

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LVH: What are ECG Criteria for Diagnosis?

     The clinical reality is that the ECG is not very sensitive for picking up LVH. That is — many patients with either thickened LV walls and/or LV cavity enlargement do not manifest any ECG sign of LVH.

• Therefore, the ECG is an imperfect tool for assessing LV enlargement. The ECG does pick up many patients with more severe forms of LVH — but it clearly does not pick up all cases.
• An Echo (Echocardiogram) is a far better test (albeit a more expensive one) — for detecting and quantitating thickening of the LV wall and increase in LV chamber size. An Echo is also much more accurate in assessing enlargement of the other 3 chambers (the RA, LA and RV chambers). That said, if certain criteria are met — the ECG may strongly suggest the presence of significant LVH.

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ECG Criteria: There are many criteria in the ECG literature for diagnosis of LVH. None are perfect. In our experience — the most helpful numbers to remember are “35” and “12” — as is pictorially shown in Figure-3. Thus — Criteria for LVH are met in an adult over 35 years of age IF:

• The Sum of the deepest S wave in V1 or V2 + the tallest R wave in V5 or V6 is ≥ 35 mm.
• OR — the R wave in lead aVL is ≥ 12 mm in amplitude.
• AND — LV “strain” is also present in at least 1 lateral lead (See red-green ST-T wave segments in Figure-3).

Figure-3: Schematic illustration of ECG Criteria for LVH. The following caveats should be kept in mind: i) The patient should be at least 35 years of age; ii) Only 1 voltage criterion is needed for diagnosis (ie, 35 or 12); and iii) ST-T wave changes of LV “strain” (red-green segments) should be seen in at least 1 of the lateral leads. NOTE: Each small box on ECG grid paper corresponds to 1 mm of voltage when counting in the vertical direction. Since there are 5 small boxes in each large box — each large box corresponds to 5 mm of voltage — as will become apparent in Figure-5 and Figure-6 when we illustrate counting voltage.

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CAVEATS in ECG Diagnosis: You will not always be able to tell if LVH is present simply from looking at an ECG. A chest X-Ray or Echo may be needed.

• Younger individuals (who are less than 35 years of age) — often have increased amplitude without this being due to a large left ventricle. Thus — the patient should be at least 35 years old for the voltage criteria in Figure-3 to be valid. NOTE: We emphasize that the age “cutoff” of 35 is far from precise. We use this number primarily to recall that younger adults often have increased amplitude of QRS complexes on ECG without this being due to true chamber enlargement. Conveniently — the number “35” corresponds to both the age and voltage criteria for LVH.
• Only 1 voltage criterion (35 or 12) is needed for diagnosis of LVH.
• Clinically — the likelihood of true LV enlargement goes up markedly IF ST-T wave changes of “Strain” are present on ECG in at least 1 of the lateral leads. We schematically highlight the appearance of “strain” in each of the 5 lateral leads within the red-green enclosures in Figure-3 (ie, in leads I,aVL; V4,V5,V6).

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What is LV “Strain”?

     It is difficult to define “strain”. On ECG — there is asymmetric ST-T wave depression — as suggested by the red arrow in Panel C of Figure-4. Perhaps this corresponds to a thickened LV that now outstrips its blood supply. Perhaps not. What counts — is that more pronounced anatomic changes of LVH often produce the ST-T wave pattern that is seen in Panel C (red arrow).

• PEARL: Use of the History may be of invaluable assistance in ECG interpretation. For example, statistical likelihood of LVH goes up markedly — IF the patient is an older adult with longstanding hypertension and/or heart disease. In contrast — true chamber enlargement is far less likely IF the patient is a younger adult who has been previously healthy (and who does not have hypertension or any other kind of heart disease).

Figure-4: ST-T wave appearance of a normal ST segment (Panel A) — compared to the ST-T wave changes of LV “strain” (red arrow in Panel C). As will be seen momentarily in Figure-5 and Figure-6 — the presence or absence of “strain” assists greatly in determining the likelihood of true LV chamber enlargement. NOTE: As one traces the path from a normal ST-T wave (Panel A) — to the asymmetric ST-T wave that is characteristic of LV “strain” (seen in Panel C) — one passes through an “intermediate” stage (Panel B), in which the ST segment flattens but frank asymmetric ST depression is not yet seen. While the correlation is not perfect — patients with this “intermediate” pattern of Panel B are more likely to have true LV chamber enlargement than patients whose ST-T waves are normal (corresponding to Panel A) in lateral leads. In contrast to the asymmetric ST-T wave depression of “strain” seen in Panel C — the symmetric T wave inversion in Panel D is more suggestive of ischemia.

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Distinction between ECG Changes of “Strain” vs Ischemia

     Compare the shape of the ST-T wave in Panel C vs Panel D in Figure-4:

• We describe the sagging ST-T wave depression in Panel C (red arrow) — as consistent with LV “strain” in a patient who has LVH.
• In contrast — the ST segment in Panel D is not depressed, and T wave inversion is symmetric (ie, the slope of T wave descent is about the same as the slope of the T wave rise). Clinically — symmetric T inversion is much more suggestive of ischemia than of “strain”.

BOTTOM Line: The above descriptions of pattern recognition are not perfect. As a result — Clinical correlation is needed. For example — some patients may have both ischemia and LV “strain”, in which case the shape of ST-T wave changes may not be optimally predictive.

• NOTE: Insight to these more refined concepts for the ECG diagnosis of LVH should become readily apparent with review of the tracings we present below in Figures-5, 6, 7 and 9.

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PUTTING It ALL TOGETHER: Is there LVH?

     Consider the tracing below:

• Is LVH present in the 12-lead ECG shown in Figure-5?

Figure-5: Is LVH present in this 12-lead ECG?

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ANSWER to Figure-5: Although there is no long lead II rhythm strip — We can state that the rhythm is at least fairly regular. The upright P wave with fixed PR interval in lead II (green arrow) defines the mechanism of the rhythm as Sinus. We would accept either Sinus Rhythm or Sinus Arrhythmia (as there is slight variation in rate).

• The R-R interval is ~4 large boxes. Therefore the rate = 300/4 ~75/minute.
• Each of the 3 ECG intervals is normal. That is — the PR interval is clearly not more than 1 large box in duration; QRS duration is not wider than 1/2 a large box; and, the QT interval is not more than 1/2 the R-R interval. (For Review of Intervals — See Basic ECG Concepts #2).
• The Axis is normal — since “net” QRS deflection in both lead I and lead aVF is positive. Because “net” QRS amplitude in lead I appears to be slightly greater than “net” amplitude in lead aVF — We estimate the Axis to be slightly closer to lead I (at approximately +30-40 degrees). For purposes of “the basics” — We are happy if you simply said the Axis is “normal”. (For Review of Axis — See Basic ECG Concepts #3).
• KEY Point: The age of this patient is not given. Regardless of his/her age — Voltage in lead aVL is normal (ie, <12 mm). However, IF this patient was ≥35 years old — he/she would have voltage for LVH (20 +23 >35 mm). QRS amplitude would be normal if the patient was a younger adult. NOTE: None of the lateral leads (leads I,aVL,V4,V5,V6) manifest ST-T wave changes of “strain” (as was shown in Panel C of Figure-4). Instead — there is no ST flattening and the T wave is upright in all lateral leads.

Advanced NOTE: There is a difference between saying a patient has “voltage for LVH” vs LVH with “strain”. Even if the patient whose ECG is shown in Figure-5 was over 35 years old — lack of “strain” means specificity for true chamber enlargement is low. This is in contrast to the situation we describe in the next example (Figure-6).

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TEST YOURSELF: Is there LVH?  — Is there “Strain”?

     Interpret the 12-lead ECG shown in Figure-6.

• This patient is 60 years old and has a long history of severe hypertension. How does this information influence your interpretation?

Figure-6: This ECG was obtained from a 60-year old patient with a long history of severe hypertension. NOTE: Once again — each large box on ECG grid paper corresponds to 5 mm in voltage.

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ANSWER to Figure-6:  The rhythm is Sinus at a rate just under 100/minute (green arrow showing the upright P wave in lead II). All Intervals are normal. The Axis is normal at approximately +70-80 degrees. It is almost certain that there is LVH because: i) Deepest S wave in V1,V2 + tallest R wave in V5,V6 is much more than 35 mm; ii) ST-T wave changes of LV “strain” are present; and iii) The history is consistent with a diagnosis of LVH.

• Clinical NOTE: Although we have emphasized how the ECG is an imperfect test for the diagnosis of LVH — severe LVH is almost certain to be present in Figure-6 because: i) the patient is an adult of a certain age (60 years old) — and the patient has longstanding severe hypertension; ii) QRS amplitude is dramatically increased (ie, 35 mm for the S wave in lead V2 + 27 mm for the R wave in lead V6 adds up to far more than the required 35 mm criterion for LVH); and iii) Typical changes of LV “strain” are seen in leads V5,V6 (with the ST segments in these leads closely resembling the picture in Panel C of Figure-4).

BOTTOM Line: ECG interpretation is an “art” that incorporates both recognition of ECG findings — and integration of these ECG findings with the clinical history. Although this concept is an advanced one — We hope tracings like the one in Figure-6 provide insight as too how ECG findings may be used clinically.

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Advanced Concept: Diagnosis of LVH using Lead aVL

     As schematically shown in Figure 3 — the voltage criteria we favor for ECG diagnosis of LVH include presence of an R wave ≥12 in lead aVL. In Figure-7, which was obtained from an older patient with hypertension — We illustrate how lead aVL may be used to recognize voltage for LVH when chest leads fail to satisfy required voltage criteria.

• R wave amplitude in lead aVL of Figure-7 — is clearly increased beyond the required 12 mm. That is, the R wave in lead aVL is more than 3 large boxes in height (= more than 15 mm). This satisfies voltage criteria for LVH.
• However — there is no indication at all of voltage for LVH from assessment of QRS amplitude in the precordial leads in Figure-7 (ie, deepest S in V1,V2 + tallest R in V5,V6 is very much less than 35 mm).
• Since only 1 voltage criterion is needed for diagnosis — the presence of a tall R wave in lead aVL (≥12 mm) in Figure-7 satisfies voltage criteria for LVH.

Advanced Point: There is LAD (Left Axis Deviation) in Figure-7 — as is evident from the predominantly negative QRS in lead aVF with positive QRS in lead I. This supports the premise that lead aVL tends to be most helpful as a voltage criterion for LVH in the presence of a leftward axis.

Figure-7: ECG obtained from an older adult with hypertension. Voltage criteria for LVH are satisfied by the tall R wave in lead aVL (≥12 mm) — despite relatively low voltage in the precordial leads.

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NOTE: Don’t Forget to Check the Standardization Mark!

     Most of the time — the ECG will be set to normal standardization. Confirmation that this is the case is easily achieved by recognition of the standardization mark at the very beginning or end of the 12-lead recording (black arrow at the onset of lead III in Figure-8).

• Normal standardization is designated by a rectangular standardization mark that is 10 mm (=2 large boxes) tall.
• On occasion — ECG complexes may be extremely large and extend beyond the space provided for one or more leads on the tracing. Selection of Half Standardization reduces waveform amplitude by half — with result that the entire complex in each lead will again fit on the ECG recording paper and be seen.
• These concepts are illustrated in Figure-8 — in which the Top Panel is a blow-up of leads III and aVF recorded at normal standardization.
• IF instead, these ECG leads were recorded at half standardization — actual QRS amplitude would be twice that shown = 10 vs 5 in lead III; and 26 vs 13 in lead aVF (Lower Panel in Figure-8).

Figure-8: Blowup of leads III and aVF to illustrate the appearance of a normal (top) and half (bottom) standardization mark. Actual voltage is twice that shown when the ECG is recorded at half standardization. 

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NOTE: On rare occasions — You may see double standardization, in which actual QRS amplitude is half the amount shown. This might be used in cases when QRS amplitude is dramatically decreased (as it might be with a large pericardial effusion). Double standardization is recognized by a rectangular standardization mark that is 20 mm (=4 large boxes) tall. As stated — Use of double standardization is rare.

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Advanced Point: LV “Strain”?  — Ischemia?  — or both?

     As alluded to earlier — Confusion often arises as to whether associated ST-T wave changes that are seen in a patient with increased QRS amplitude represent ischemia or “strain” — or both? The best way to explore this concept is by side-to-side comparison of a clinical example (Figure-9):

• In both Panel A and Panel B of Figure-9 — deepest S wave in V1,V2 + tallest R wave in V5,V6 easily satisfy voltage criteria for LVH.
• In Panel A — ST-T wave appearance in leads V5,V6 strongly suggests LV “strain” (there is asymmetric ST depression with slow sagging downslope). While we could not exclude the possibility of ischemia (there is after all, some J-point ST depression — especially in lead V4) — in the absence of a history of chest pain, we would suspect the changes in Panel A predominantly represent LVH with “strain”.
• In contrast, for Panel B — ST segments are coved in V3-through-V6. In addition, there is 1-2 mm of J‑point ST depression (below the PR segment baseline) in leads V4,V5,V6 — with T wave inversion that is deep and appears to be much more symmetric (especially in leads V4,V5). This appearance is more suggestive of ischemia.
• In particular — lead V3 in Panel B looks ischemic (pure LV “strain” virtually never produces ST coving and symmetric T inversion this far anterior).
• Lead V6 in Panel B — has an intermediate appearance between “strain” and/or ischemia.  Given that this patient is “older” and has a history of heart disease and decidedly meets voltage criteria for LVH — We would interpret this tracing as, “LVH and “strain” and/or ischemia.” Clinical correlation and comparison with prior tracings would be needed to determine IF an acute ischemic process might be ongoing.

Figure-9: Comparison of the precordial lead sequence from 2 older patients with heart disease and obvious voltage for LVH. Voltage criteria for LVH are easily satisfied in each tracing. ST-T wave changes in Panel A look more like LV “strain”. On the other hand — ST-T wave changes in Panel B are more suggestive of LVH with possible ischemia as well as “strain”.

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Final NOTE: For readers wanting more — We approach ECG diagnosis of LVH from slightly different perspective in our ECG Blog #73:

• We also cite several additional voltage criteria for LVH in Blog #73. That said — in ~90% of cases when it is possible to diagnose LVH by ECG, use of the numbers “12” and “35” as described in this Basic ECG Concepts #5 is all that you need to do so.

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— For more information — GO TO —

• Material and Figures #1-thru-6 have been excerpted from our newest publication = “A 1st Book on ECGs-2014” and/or from the expanded 1st Book ePub version (available in kindle-kobo-nook-ibooks).

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• More advanced material and Figures #7,8,9 have been excerpted from ECG-2014-Pocket Brain and/or from the expanded ECG-2014 ePub version (available in kindle-kobo-nook-ibooks).

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• Please check out Free Download of our expanded GLOSSARY of ECG-related terms. 

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