ECG Diagnosis of RVH

Detection of right ventricular enlargement in adults by ECG criteria is often exceedingly difficult. This is because the left ventricle is normally so much larger and thicker than the right ventricle in adults that it masks even moderate increases in right ventricular chamber size. As a result, many patients with RVH won't be identified IF assessment for chamber enlargement is limited to obtaining an ECG (an Echo is needed to know for sure). Think of the ECG diagnosis of RVH as similar to making a "detective" diagnosis. Rarely will any one finding clinch the diagnosis. Instead determination of RVH is most often made by deduction (ie, from identifying a combination of ECG findings from the Table below):

KEY: None of the above criteria is enough by itself to diagnose RVH. But several of these criteria (when seen together on a single tracing) is very suggestive of RVH especially when they occur in a likely setting (ie, COPD, right-sided heart failure, pulmonary hypertension). Suspect pulmonary disease IF you see 3 of the first 5 criteria. Suspect pulmonary disease plus RVH IF in addition you see a tall R wave in lead V1 (with/without ST-T wave changes of RV strain). RAD is very suggestive of RVH when seen in a likely setting in association with other criteria (few other conditions produce RAD).

Indeterminate Axis Alterations in lung volume with emphysema lead to rightward and posterior deviation in the transverse plane (IF you see indeterminate axis Think RVH - COPD - obesity). RAA Only one condition produces RAA without RVH (= tricuspid stenosis). Thus RAA is an indirect sign that RVH is likely. IRBBB (rSr in V1) The presence of an r (r prime) in lead V1 suggests that terminal electrical activity is directed toward the right (Think possible COPD and RVH with terminal rightward activity). Low Voltage Air is not a good conductor of electricity. The large emphysematous chest dampens (reduces) voltage. Technically low voltage means QRS amplitude 5 mm (ie, 1 large box) in all 6 limb leads (I,II,III,aVR,aVL,aVF) but we use low voltage as a relative term for overall reduced amplitude (Think COPD - hypothyroidism - obesity - pneumothorax - pericardial effusion). Persistent S Waves QRS amplitude normally increases as one moves across the precordial leads ( as electrical activity moves to the left where the larger LV lies ). QRS amplitude usually peaks (is tallest) in V4 or V5 and then drops off (in V5,V6). IF there are still S waves in V5,V6 this implies significant rightward activity in these left-sided leads (Think RVH COPD - large body habitus). 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. PEARL Anterior ST depression is not always ischemia (it may reflect RV strain from RVH or pulmonary embolus!). Tall R in Lead V1 Lead V1 is a right-sided lead. As a result, the QRS is normally negative in V1 (electrical activity moves toward the larger LV and away from V1). IF the R is taller than the S wave in lead V1 this means rightward forces are increased (which is a sign of RVH). Clinically by the time a tall R is seen in V1 in an adult with pulmonary disease the extent of RVH is usually marked (ie, the patient has end-stage COPD and/or pulmonary hypertension).

Pediatric RVH The ECG diagnosis of RVH is much easier to make in infants and young children than it is in adults. This is because at birth the RV is comparable in size to the LV and it remains so for the first few years of life (ergo a much lesser degree of RV enlargement is needed to produce the ECG signs of RVH in infants or young children with congenital heart disease ).

Example of RVH
Most of the ECG criteria for RVH are present in the tracing shown below (RAD, RAA, tall R in V1, deep S waves in V5,V6). Note also that there is "RV strain" (which is typically seen in inferior and/or anterior leads both of which are present here). Clinically by the time a tall R is seen in V1 in an adult with pulmonary disease the extent of RVH is usually marked (end-stage COPD/pulmonary hypertension).

Example of Pulmonary Disease

Pulmonary disease (such as COPD) may sometimes be suggested by ECG IF at least two of the first 5 findings in the RVH Table are seen (Seen below are RAD; RAA; rSr in V1; and persistent precordial S waves up to V5,V6).

Tracing Q-2 This 12-lead ECG was obtained from a patient with new-onset shortness of breath thought to be due to congestive heart failure. What else do you suspect?

Answer to Tracing Q-2: Sinus tachycardia at ~115/minute. The PR and QRS intervals are normal (the fast rate makes it difficult to comment on the QT). There is RAD (predominantly negative QRS in I; positive in aVF). An incomplete RBBB (rsR in V1) is seen. There are nonspecific ST-T wave abnormalities but no acute changes. There is RAA (tall, peaked, uncomfortable-to-sit-on P wave in lead II ). There is also LAA (very deep negative component to the P wave in lead V1). RVH is strongly suggested by RAD, RAA, IRBBB and persistence of precordial S waves in V5,V6. Clinical IMPRESSION: This ECG should make one rethink the premise of CHF as the primary cause of this patients new-onset shortness of breath. Instead longstanding/severe pulmonary disease is likely given the combination of findings (and/or maybe pulmonary embolus?).

Pulmonary Embolus
The ECG is usually not diagnostic of pulmonary embolism (PE). But there are times when ECG will suggest the diagnosis before V/Q scan or chest CT is done. Consider P.E. IF: IF the clinical setting is right (new-onset dyspnea pleuritic chest pain - predisposing risk factors or previous history of PE/DVT). IF the patient has sinus tachycardia (usually seen with large PE, albeit clearly nonspecific for the diagnosis). 2 signs of acute right-heart strain (ie, RAD - RAA RBBB - tall R in V1 - deep S in V5,V6). RV strain (ST-T depression in II,III,aVF or V1,V2,V3). New-onset A Fib (common with PE, but nonspecific). Nonspecific ST-T wave changes (not diagnostic). With an ECG (and history) as shown for Tracing Q-2. Academic P.S. The ECG finding known as S1-Q3-T3 is not accurate for detecting PE ( and it should no longer be used).

PEARL: Clinically What 2 entities should you think of given the symmetric T inversion in V1,V2,V3 (arrows) of this ECG obtained from an adult with new-onset dyspnea?

ANSWER: In addition to ischemia this anterior symmetric T wave inversion may reflect RV strain (which with the RAD and RAA seen here should suggest the possibility of pulmonary embolism as a cause for new-onset dyspnea).

Diagnosis of LVH/RVH with BBB?

Diagnosis of ventricular chamber enlargement is difficult with conduction defects (BBB,IVCD). Criteria for LVH/RVH are based on normal ventricular activation which changes with BBB. Consider the following: Criteria for LAA/RAA are unchanged by BBB/IVCD. Most patients with LBBB have underlying heart disease. IF there is longterm hypertension, cardiomyopathy or heart failure and LBBB the prevalence of LVH is ~80%, even before one looks at the ECG. This goes up to >90% IF with LBBB there are deep S waves (>25-30mm) in V1,V2 or V3 (See Figure below). Suspect LVH (despite RBBB) IF the R in aVL is 12, or the R wave in V5 or V6 is 25. It is probably best not to even bother trying to diagnose RVH when LBBB, RBBB or IVCD is present.

Chamber Enlargement despite LBBB: The Figure above shows sinus rhythm with typical LBBB. LAA is suggested by the deep, negative P in V1 (circle). We diagnose probable LVH despite the LBBB because of the very deep S wave in V2 (>25mm).