Differential diagnosis of rSr' pattern in leads V1 -V2. Comprehensive review and proposed algorithm

Abstract

One of the more frequent dilemmas in ECG interpretation is the differential diagnosis of an rSr' pattern in leads V1 -V2 . We often face this finding in asymptomatic and otherwise healthy individuals and the causes may vary from benign nonpathological variants to severe or life-threatening heart diseases, such as Brugada syndrome or arrhythmogenic right ventricular dysplasia. In other cases, a normal variant of rSr' pattern can be misinterpreted as pathological after the occurrence of certain clinical events such as cardiac arrest or syncope of unknown cause. In this review we analyze in detail all the possible conditions, both benign and pathological that may explain the presence of this electrocardiographic pattern. We also propose a simple electrocardiographic algorithm for differential diagnosis.

Keywords: ARVD; Brugada ECG pattern; algorithm; rSr’ pattern.

Figure 1

Leads V₁ to V₃ of a very lean 15‐year‐old man without heart disease. The rSr’ morphology is due to a misplaced V₁ electrode in the second right intercostal space (see negative P wave) and disappears when the electrode is properly positioned (fourth right intercostal space).

Figure 2

Two cases of rSr’ in lead V₁ without associated heart disease. In panel A, note r’ = r and P wave with a ± morphology in lead V₁. In panel B, the morphology of the P wave is also ± in lead V₁ but r < r’. In an isolated tracing it is not possible to distinguish between the proximal origin in partial RBBB or peripheral RV delay (see text).

Figure 3

Progressive RBBB. (A) Lead V₁ with a notch in the upstroke of the S wave; (B) Lead V₁ with r’ and QRS ≥ 120 ms; and (C) Typical rSR’ pattern of RBBB with QRS ≥ 120 ms. In all cases the electrodes are properly placed (note P wave with morphology ± in lead V₁).

Figure 4

Leads V₁ and V₂ in four athletes without heart disease.

Figure 5

Different examples from patients with pectus excavatum. Note the negative P wave in lead V₁.

Figure 6

Typical ECG patterns of Type‐1 (coved) Brugada pattern (A) and Type‐2 (saddle‐back) (B).

Figure 7

(A) Mitral stenosis with moderate pulmonary hypertension and functional tricuspid regurgitation, (B) A 9‐year‐old girl with mild pulmonary stenosis, (C) Chronic cor pulmonale secondary to chronic obstructive pulmonary disease (COPD) in elderly, (D) Ostium secundum‐type atrial septal defect, (E) ECG pattern after regression of RVE in postsurgery of tetralogy of Fallot, (F) epsilon wave (arrow) in lead V₁ in a patient with ARVD, (G) Ebstein disease (note massive atrial enlargement), and (H) Biventricular enlargement in a 8‐year‐old patient with ventricular septal defect and hyperkinetic pulmonary hypertension (Katz‐Watchell pattern)

Figure 8

Wolf‐Parkinson‐White with an RSr’ in lead V₁ and delta wave suggesting a left lateral accessory pathway.

Figure 9

A 20‐year‐old male with chronic renal failure on hemodialysis during the past 2 years. Severe systemic hypertension (210/130 mmHg). Serum potassium levels of 6.4 mEq/1. Note the high and peaked T wave, as well as the ST‐segment elevation in leads V₂ and V₃. The QT interval duration is relatively long in leads I, II, and III at the expense of the ST‐segment due to the associated hypocalcemia.

Figure 10

This figure shows (first red vertical line) the difference in the duration of QRS in lead V₁ compared to lead V₃ in Brugada patterns 1 and 2, ARVD and hyperkalemia (low row). However, in 4 variants of normality (upper row), the duration of QRS in leads V₁‐V₃ is the same. The second vertical line measured 80 ms later, shows that in the two Brugada patterns, the ST‐segment is downsloping (ratio ST at J point/ST 80 ms later > 1; Corrado index), but it is upsloping (in at least lead V₂) in normal variants (upper row) (ratio < 1).

Figure 11

Proposed diagnostic algorithm in patients with r’ in leads V₁‐V₂.

Figure 12

How to measure the ß angle (A) and the base of triangle of the r’ wave (B).