Right ventricular dilatation: an often neglected component in the electrocardiographic assessment of patients with heart failure

When assessing patients with heart failure (HF) using the electrocardiogram (ECG), the primary focus is on the left ventricle and left atrium. Clinicians look for left ventricular hypertrophy, evidence of previous or current myocardial infarction, ST/T changes suggestive of left ventricular strain, or myocardial injury or ischaemia, perturbations of the QRS complex amplitude, depending on the patients' oedematous state,1 and left atrial hypertrophy, dilatation, or hypertension, since the last three cannot be differentiated by the ECG. However, major changes in the size and function of the right ventricle and right atrium take place in patients with HF, depending on the degree of compensation consequent to the natural course and the impact of co-morbidities, and therapeutic modalities. Such changes are reflected in the ECG as additional to the changes signifying left ventricular/atrial involvement, or cause partial or complete cancellation of the features attributed to the left ventricular/atrial pathology. Although right ventricular hypertension (consequent to pulmonary hypertension) leads to right ventricular hypertrophy and eventually right ventricular dilatation (RVD) with associated right atrial hypertension, or hypertrophy or dilatation, the eventual outcome is a picture of biventricular and biatrial enlargement in patients with ischaemic or non-ischaemic cardiomyopathy. As RVD develops, the right ventricle moves more to the left and ‘wraps around’ and pushes posteriorly an already dilated left ventricle. The ECG counterparts of the above chamber changes and their repositioning in the thorax, aided by the systemic fluid engorged tissues, leads to low voltage in the limb leads, increased voltage in some pre-cordial leads, and counter-clockwise rotation in the V1–V6 leads with a ratio of R-wave to S-wave (R/S) <1 in lead V4, described in the mid-1980s by Goldberger,2,3 in a form of an ECG triad seen in patient with HF. Often patients with HF develop left bundle branch block (LBBB), necessitating implementation of cardiac resynchronization therapy in those patients with a low left ventricular ejection fraction and poor response to medical therapy. But even with this obscuring effect of LBBB emergence, not all is lost ECG wise. Childers et al.4 have described the occasional association of LBBB with right frontal QRS axis deviation as indicative of dilated cardiomyopathy with biventricular enlargement, and one could look for this ECG dyad in patients with HF. Recently, Van Bommel et al.5 reported on their finding of detecting RVD in 173 patients with HF and LBBB, implementing a triad of ECG features of late R-wave in lead aVR, QRS amplitude of <0.6 mV in limb leads, and R/S ratio <1 in lead V5. The article is an example of the accelerating pace of contributions being made by the employment of aVR, in its traditional orientation.6 Although the threshold for low-QRS voltage for limb leads is ≤0.5 mV, the earlier-mentioned authors have used <0.8 mV 2,3 and <0.6 mV.5 Also, the criterion of an R/S ratio of <1 in the pre-cordial leads has been considered with reference to V5 by Goldberger,2 and V4 by Van Bommel et al.5 This author has used for sometime in his practice and teaching all the above (except the aVR finding), and in addition, the emergence of P-pulmonale in limb leads, or a significant positive component of the P-wave in V1, or a marked positive/negative P-wave in V1, or an unexpected ‘normal’ P-wave in V1, due to cancellation of P-mitrale by the superposition of P-pulmonale due to right atrial abnormality consequent to an RVD. The earlier-mentioned ECG alterations can be appreciated by analysing two or more ECGs taken at different time points in the course of observation of a patient with HF. Although print outs of the ECG recordings may suffice, the wide-spread employment of computer digital recording and analysis of ECGs renders this task all too easy. Indeed by toggling between two different ECGs, one could appreciate changes in the different components of the ECGs that had taken place between the corresponding time points of the clinical course of a patient. With repeated back and forth rapid , one also appreciates a movie-like effect imparted on the ECG changes. Finally, one does not need to resort to measurements of amplitudes or durations of the ECG complexes, waves or intervals, or even areas, since all of these are provided for all two ECG leads, by most automated ECG management systems, upon recording of the ECG. Conflict of interest: none declared.