Tuesday, October 22, 2013

ECG Interpretation Review #77 (Chamber Enlargement – RVH – RAE – P Pulmonale – COPD)

The 12-lead ECG shown below in Figure-1 was obtained from a patient with new-onset shortness of breath thought to be due to congestive heart failure.
  • What else do you suspect?

Figure-1: ECG from a patient with new heart failure (See text).

Interpretation of Figure 1:
The rhythm is sinus tachycardia at ~115/minute. The QRS is narrow. As opposed to the usual picture of left-sided heart failure (in which one expects to see LVH with strain) — there is no sign on this ECG of LVH (Left Ventricular Hypertrophy). Instead — the tracing strongly suggests severe pulmonary disease, if not frank RVH (Right Ventricular Hypertrophy):
  • There is marked RAD (Right Axis Deviation) — as determined by the predominantly negative QRS complex in lead I, but positive QRS in aVF.
  • RAA (Right Atrial Abnormality) is present (tall, peaked, “uncomfortable-to-sit-on” P wave in inferior leads that is clearly >2.5mm in lead II).
  • An incomplete RBBB is seen (rsR’ in lead V1; S waves in I,V6).
  • Deep S waves persist through to leads V5,V6.
  • There are nonspecific ST‑T wave abnormalities — albeit not quite RV strain (and no acute changes).

ECG Impression of Figure-1: The combination of marked RAD, definite RAA, IRBBB and persistent precordial S waves all point to a diagnosis of RVH.
  • Clinical Impression: This ECG should make one rethink the premise of left-sided heart failure as the primary cause of this patient’s new-onset shortness of breath. Instead — longstanding/severe pulmonary disease is likely given the combination of findings (possible pulmonary embolism? ).
  • Beyond-the-Core: There is also LAA (Left Atrial Abnormality) — as determined by very deep negative component to the P wave in lead V1. Whether this reflects anatomic enlargement vs increased LA pressure is uncertain.

Chamber Enlargement: ECG Criteria
In recent blogs we reviewed ECG criteria for LAA/RAA & LVH:
This goal of this blog post is to review ECG criteria for diagnosing RVH.

RVH: General Comments
Detection of right ventricular enlargement in adults by ECG criteria is often exceedingly difficult. This is because the LV (Left Ventricle) is normally so much larger and thicker than the RV (Right Ventricle) in adults — that it masks even moderate increases in right ventricular chamber size. As a result, many patients with RVH (Right Ventricular Hypertrophy) will not be identified — IF assessment for chamber enlargement is limited to obtaining an ECG (an Echo is needed to know for sure).
  • NOTE: In contrast to adults — ECG diagnosis of RVH is often surprisingly easy in children with congenital heart disease (because relative size of the RV compared to the LV is not nearly as different as it is in adults).

RVH: Simplified ECG Criteria
ECG criteria for diagnosis of RVH are listed in Figure-2. Several criteria are needed for accuracy.
  • Think of the ECG diagnosis of RVH as similar to making a "Detective" Diagnosis. Rarely will any one single finding clinch the diagnosis. Instead — determination of RVH is made by deduction (ie, from identifying a combination of the ECG findings listed in Figure-2):

Figure-2: ECG criteria for RVH.

Clinical Note: Pulmonary disease without frank RVH is common in longterm smokers. Progression to cor pulmonale (in which there is frank RVH) — represents a relatively late stage in the process. Careful search for the ECG findings in Figure-2 may provide clues to either longterm pulmonary disease and/or associated RVH:
  • Consider Pulmonary Disease IF you see 2 or more of the first 5 criteria listed in Figure-2 (especially if the patient is a known smoker or has other known lung problems).
  • Suspect pulmonary disease plus RVH IF in addition you also see a tall R wave in lead V1 (with or without ST-T wave changes of RV “strain” ).
  • By Definition — By the time you see clear ECG evidence of RVH in an adult — the extent of RVH is usually marked (the patient almost always has end-stage COPD and/or pulmonary hypertension).

FIGURE-2: Review of Specific RVH Criteria
While none of the criteria in Figure-2 by itself is enough to diagnose RVH — seeing several criteria on a single tracing is very suggestive of RVH — especially when seen in a likely clinical setting (ie, COPD, longterm asthma, right-sided heart failure, pulmonary hypertension).
  • RAD (Right Axis Deviation) — is highly suggestive of RVH when seen in association with other criteria listed in Figure-2. Few other conditions produce RAD. Thus, the presence of marked RAD in Figure-1 virtually confirms the diagnosis of RVH.
  • Indeterminate Axis — Alterations in lung volume with emphysema often lead to rightward and posterior axis deviation. As a result — net QRS deflection in both leads I and aVF will be negative. IF ever you see an indeterminate axis — Think RVHCOPDlarge body habitus.
  • RAA (Right Atrial Abnormality) — The tall, peaked, pointed P waves of RAA are easy to recognize (Figure-1). Only one condition produces RAA without RVH (= tricuspid stenosis). Therefore — seeing RAA is an indirect sign that RVH is very likely (See ECG Blog #75 for more on ECG diagnosis of RAA).
  • IRBBB (rSr’ in V1) — The presence of an r’ (r prime) in lead V1 suggests that terminal electrical activity is directed toward the right. While by itself this ECG sign is benign and commonly seen as an isolated finding in otherwise healthy individuals — it supports the diagnosis of pulmonary disease/possible RVH if seen in association with other findings listed in Figure-2.
  • Persistent S Waves — R wave amplitude normally increases as one moves across the precordial leads (as electrical activity moves to the left where the larger LV lies). R wave amplitude usually peaks (is tallest) in V4 or V5 — and then drops off (in V5,V6). Normally, there is not any S wave at all in V5,V6 — since by this time in the depolarization process all electrical activity is traveling leftward. IF more than tiny S waves are still present in V5,V6 — this implies significant rightward activity (Think RVHCOPDlarge body habitus).
  • Low Voltage — Air is not a good conductor of electricity. The large emphysematous chest of a patient with COPD dampens (reduces) voltage.
  • Technically“low voltage” is defined as QRS amplitude ≤5 mm (ie, ≤1 large box) in all 6 limb leads (I,II,III,aVR,aVL,aVF). That said — we also use “low voltage” as a relative term when overall QRS amplitude subjectively appears to be reduced. When you see “low voltage” Think COPD. NOTE: Low voltage may also be seen in hypothyroidism; obesity; pneumothorax; pericardial effusion; and as a normal variant. That said — low voltage is not all that common, so its presence should make you consider the possibility of pulmonary disease.
  • Tall R in Lead V1 — Lead V1 is a right-sided lead. As a result, the QRS complex is normally negative in V1 (electrical activity moves toward the larger LV and away from V1). IF ever the R wave is taller than the S wave in lead V1 — this means rightward forces are increased (which may be an important sign of RVH). Clinically — by the time a tall R wave is seen in lead V1 in an adult with pulmonary disease — the extent of RVH is usually marked (ie, the patient is likely to have end-stage COPD and/or pulmonary hypertension). ECG Blog #81 reviews other potential causes of a Tall R in V1 
  • RV “Strain— Just as LV “strain” is a sign of true LVH — seeing “strain” in right-sided leads (II,III,aVF or V1,V2,V3) strongly supports a diagnosis of RVH.

Schematic FIGURE-3: Example of RVH + RV “Strain
Most of the ECG criteria for RVH that we listed in Figure-2 are present in schematic Figure-3. Specifically — We see RAD; RAA; tall R in V1; and deep S waves in V5,V6.
  • Note also that there is "RV strain" (which is typically seen in inferior and/or anterior leadsboth of which are present here).
  • PEARL: Inferior and/or anterior ST-T wave changes as seen in Figure-3 will often not be due to ischemia — but rather to RVH or pulmonary embolus.

Figure-3: Schematic example of RVH + RV “strain”. This ECG picture with virtually all criteria from Figure-2 is uncommon in adults — and usually indicates marked RVH/end-stage COPD — and/or pulmonary hypertension.

Schematic FIGURE-4: Example of “Pulmonary” Disease
Pulmonary disease (such as COPD) may sometimes be suggested by ECG. Specifically — we look for the presence of at least 2 of the first 5 findings from Figure-2. This concept is well illustrated in schematic Figure-4. Low voltage is not seen — but 4 of the first 5 criteria from Figure-2 are seen! Note:
  • An indeterminate axis (negative QRS in leads I and aVF).
  • RAA (tall, peaked P wave in inferior leads).
  • rSr’ in lead V1.
  • Persistent S waves throughout the precordium.

Figure-4: Schematic ECG that strongly suggests “pulmonary” disease. 

Return to FIGURE-1: Is there RVH?
Return to the ECG we originally presented in Figure-1. It should now be apparent that RVH is clearly present. Specifically — We see marked RAD; RAA; IRBBB (if not a taller-than-expected r’ in V1); and persistent deep S waves in V5,V6.
  • Awareness that the ECG of this patient shows RVH rather than LVH suggests cor pulmonale (if not pulmonary embolism) as the cause of acute dyspnea. Treatment is very different than it would be for left-sided heart failure.

- For more information  GO TO:
  • See also ECG Blog #73 — for review of LVH criteria -
  • See ECG Blog #75 — for review of RAA/LAA criteria - 
  • For review of the Causes of a Tall R in V1 — See ECG Blog #81 -
ADDENDUM: The following Sections are excerpted from our ECG-2014-ePub. These pages summarize the ECG findings of Acute PE (Pulmonary Embolus).



  1. how much tall (mm)R wave in lead V1 it need to consider RVH ?

  2. Thanks for your comment Mostafa. Rather than any specific numerical criterion — I think it better to consider the combination of factors when assessing for likelihood of RVH on ECG (as I describe in detail on this post). R wave amplitude in V1 might be fairly small (as it actually is in Figure-1 of this case) — but the combination of other ECG findings plus the history (dyspnea) all point to RVH just the same. If there is need for additional certainty — then Echo can provide much additional insight.

  3. Dr. Grauer...

    I've been a fan of yours for some time and I especially enjoy your comments on other websites. If I might suggest something: the increased P terminal force in V1 is actually probably not due to a LEFT atrial abnormality but actually the RIGHT atrium (I know, the concept seems almost blasphemous!). In cases of chronic cor pulmonale due to COPD, the right atrium enlarges to the extent that part of it manages to enlarge and/or rotate into the field subtended by the V1 electrode (normally it's posterior to the RV with only a portion of the auricular appendage on the anterior right border). Jules Constant and other authors have discussed this phenomenon. Also, the pulmonary changes in advanced COPD can cause the horizontal axis to point more posteriorly rather than anteriorly allowing RV hypertrophy to be present with no sign of an increased R wave in V1.

    Thanks for your excellent diagrams and analyses!

    Jerry W. Jones, MD FACEP FAAEM

    1. THANKS Jerry for the kind words! I am aware of the phenomenon you describe in which right atrium enlarges to such an extent that it "flops over" and becomes the reason for a deep negative component to the P wave in lead V1. I DO appreciate your comment — as I should have mentioned this in my interpretation above. Given how dramatic other ECG signs of cor pulmonale are in this tracing — I agree, that right (rather than left) atrial enlargement is the more likely cause of the deep negative P wave component that we see here in lead V1.

      Otherwise — I completely agree that a predominant R wave is not necessarily needed in lead V1 for there to be RVH. The point I was trying to make, was that by the time a predominant R wave IS seen in lead V1 in an adult — that the extent of RVH is severe (and pulmonary hypertension becomes likely). THANK YOU again for your excellent comments!

  4. Why incomplete RBBB in Figure 1, when QRS is less than 0,09 sec?

    1. FIRST — Sorry for my delay in answering! That said — I measure 0.09 second for QRS duration. I call this IRBBB because there IS an rsR' in V1 + narrow terminal s waves in lateral leads I and V6 — and to me, THAT is the definition of incomplete RBBB — :)

  5. Hi Dr Grauer, thank you for your fantastic and enlightening ECG posts! This may be a silly question but, what differentiates the first ECG from a LPHB? With the negative I and avL and positive in all inferior leads. Many thanks! :)

    1. First — SORRY for my delay in answering you! Your question is an excellent one. QRS morphology in leads I,II,III is consistent with LPHB (with possible exception that one lacks the initial small q in lead II (typically with LPHB — both leads II and III manifest a qR morphology). But the MAIN REASON why I would not call a conduction defect (ie, LPHB) is that MULTIPLE OTHER FINDINGS on this tracing are "screaming out" that this patient has severe RVH — so to also postulate a conduction defect is to imagine there are 2 different ECG diagnoses. Much more logical to assume the marked right axis is part of the RVH picture — :)