In this ECG Cases blog we look at 8 patients who presented with tall R wave in V1

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman, November 2020

Eight patients presented with ECGs that had a tall R wave in V1

Case 1: 70yo with recurring syncope at rest

Case 2: 50yo with palpitations and presyncope

Case 3: 40yo with three hours of chest pain

Case 4: 55yo prior CABG with one hour of chest pain and diaphoresis, HR 40s, BP 70s

Case 5: 60yo with one hour of chest pain and SOB. Serial ECG

Case 6: 80yo with chest pain

Case 7: 60yo history breast cancer with SOBOE

Case 8: 70yo with two days of constant chest pain

Tall R wave in V1-2

As a review article by Dr. Mattu explained,

“In the normal heart, the general direction of ventricular depolarization is in a right-to-left, downward direction because of the larger mass of the left ventricle compared with the right ventricle. This results in a characteristic appearance of the QRS complex in lead V1 of the ECG, the rS configuration. The initial small R wave (symbolized as ‘r’ to denote its small size) occurs because of septal depolarization from left to right. The subsequent larger S wave (symbolized as ‘S’ to denote its larger size) occurs because of the dominant effect of the left ventricle. Tall R waves in lead V1 (tall RV1), defined as an R/S ratio equal to or greater than 1, is not an infrequent occurrence the emergency department patients. However, this ECG finding exists as a normal variant in only 1% of patients. Physicians should therefore be familiar with the differential diagnosis for this important QRS configuration.”[1]

Tall R waves in V1 can be caused by abnormal electrical conduction (RBBB or left-sided VT, which slowly spreads across the right ventricle, or a left-sided accessory pathway), loss of posterior myocardium (old or acute posterior MI) or chronic anterior hypertrophy (HCM), chronic or acute RV strain (RVH, PE), congenital anomalies (dextrocardia or dystrophy), misplaced leads, or a normal variant (persisting juvenile pattern). This differential can be remembered by the mnemonic R-WAVED

  • RBBB (RsR’, QRS>120, wide S in V6, secondary repolarization abnormalities in anterior leads) or left-sided VT/ventricular ectopy
  • WPW left sided pathway: PR<120, QRS>110, delta wave, tall R in V1-2 with discordant ST/T wave changes
  • Acute MI – posterior: tall R wave V1 or V2 and ST depression +/- inferior or lateral ST elevation +/- posterior ST elevation
  • Ventricular hypertrophy: RVH (R/S >1 in V1 and <1 in V6, right axis deviation, secondary repolarization changes) or HCM
  • Embolism: +/- sinus tach, RBBB, S1Q3T3, anterior/inferior TWI
  • Dextrocardia (negative P wave, reversed R wave progression), dystrophy, or displaced leads (eg V1 and V3 switched)

These causes are not mutually exclusive but can co-exist, which can be challenging. Because many causes of tall R waves in V1 are caused by abnormal depolarization (eg RBBB, RVH, WPW, HCM), they produce abnormal repolarization changes that can mask or mimic acute ischemia. Knowing that RBBB causes discordant anterior ST depression and T wave inversion can help identify occlusion MI in the presence of RBBB by either concordant ST elevation (anterior MI) or disproportionate ST depression (posterior MI). In terms of WPW, “some pathways may only carry impulses in the retrograde manner and thus are ‘concealed’ conduction pathways; these pathways are ‘silent’ – normal PR interval and QRS complex and the absence of the Delta wave – on the resting 12 lead ECG. In other cases, the bypass tracts conduct intermittently, depending upon other factors such as cardioactive medication use, physiological stressors with catecholamine release, the development of coronary ischemia, and normal aging.”[2]

Back to the cases

Case 1: syncope from bifascicular block and borderline first degree heart block

  • Heart rate/rhythm: sinus bradycardia
  • Electrical conduction: RBBB + LAFB, borderline first degree heart block
  • Axis: left axis from LAFB
  • R wave: tall R in V1 from RBBB, poor R wave progression from LAFB
  • Tension: no hypertrophy
  • ST/T changes: nonspecific

Impression: recurring syncope at rest with bifascicular block and borderline first degree heart block. Labs normal, admitted for pacemaker.

Case 2: left-sided WPW

  • H: NSR
  • E: short PR and delta seen in V3-4
  • A: normal
  • R: tall R in V1-2
  • T: none
  • S: mild discordant ST depression in V3-4

Impression: WPW. Normal labs, referred to cardiology clinic

Case 3: infero-posterior occlusion MI

  • H: sinus tach
  • E: normal conduction
  • Axis: normal
  • R: tall R wave in V1
  • T: no hypertrophy
  • S: subtle inferior ST elevation with reciprocal ST depression in aVL (which confirms inferior MI) and inferior Q waves, and anterior tall R wave and ST depression from posterior MI)

Impression: infero-posterior occlusion MI. Cath lab activated: 100% distal RCA occlusion, Trop I rise from 70 to 38,000.

Discharge ECG: resolved ST changes, normalization of R wave progression, inferior and posterior reperfusion T wave inversion (the latter appear as hyperacute T waves V1-2)

Case 4: RBBB + posterior occlusion MI

  • H: alternating sinus and junctional bradycardia
  • E: RBBB
  • A: right axis
  • R: tall R wave in V1 from RBBB
  • T: no hypertrophy
  • S: profound ST depression and T waver inversion in anterior leads, hyperdynamic T wave in V6

Impression: RBBB with unstable bradycardia from posterior MI. Posterior leads not needed and not helpful, as they were equivocal (below). Patient given vasopressors, aspirin, plavix and heparin, and cath lab activated: 100% occlusion to circumflex graft. Peak Trop I of 50,000.

Case 5: WPW + infero-posterior occlusion MI

  • H: NSR
  • E: first has WPW, repeat has normal conduction; both have small U waves in V2-3
  • A: normal axis
  • R: first has tall R in V1 from WPW, repeat has early R wave progression (R=S in V2)
  • T: no hypertrophy
  • S: first has secondary anterior ST depression from WPW, repeat has primary anterior ST depression, inferior ST elevation and reciprocal change in aVL

Impression: left-sided WPW intermittently conducted and masking infero-posterior occlusion MI. Cath lab activated. ECG recorded before cath has intermittent WPW masking the MI, with beats 2-3 normally conducted and revealing inferior elevation:

Discharge ECG has concealed conduction, resolution of primary ST changes, and inferior reperfusion TWI.

Case 6: HCM

  • H: sinus bradycardia
  • E: RBBB
  • A: left axis from LVH
  • R: reverse R wave progression
  • T: LVH
  • S: secondary repolarization changes

Impression: BBB + severe LVH with repolarization changes. Cath lab was activated but coronaries were clean, and HCM was diagnosed on echo.

Case 7: PE

  • H: NSR
  • E: normal conduction (RsR’ in V2 likely from high lead placement)
  • A: normal axis
  • R: almost R=S in V1
  • T: no hypertrophy
  • S: S1Q3T3 and antero-inferior T wave inversion

Impression: multiple findings concerning for PE with RV strain. CT: saddle embolism.

Case 7: dextrocardia

  • H: NSR with inverted P wave in I – lead reversal vs dextrocardia
  • E: normal conduction
  • A: extreme axis deviation
  • R: reverse R wave progression
  • T: no hypertrophy
  • S: diffuse T wave inversions concordant to inverted P waves and QRS complex

Impression: dextrocardia. Negative trops and Dimer. ECG normalized by reversing the leads:

Take home points for ECG Cases 15: Tall R Wave in V1

  1. Remember the “R-WAVED” differential for tall R wave in V1: RBBB or left sided VT, WPW left sided, AMI posterior, Ventricular hypertrophy, Embolism, or Dextrocardia/dystrophy/displaced leads
  2. Tall R waves in V1 from abnormal depolarization (RBBB, WPW, RVH, HCM) produce secondary repolarization ST/T changes that can mask or mimic ischemia

References for ECG Cases 15: Tall R Wave in V1

  1. Mattu A, Brady WJ, Perron AD, et al. Prominent R wave in lead V1: electrocardiographic differential diagnosis. Am J of Emerg Med 2001 Oct;19(6):504-13
  2. Rosner MH, Brady WJ, Kefer MP, et al. Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and therapeutic issues. Am J Emerg Med 1999 Nov;17(7):705-14
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