Poor R wave progression (2024)

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Poor R wave progression is a common EKG pattern in which the expected increase of Rwave amplitude in precordial leads does not occur1.

In a normal EKG, the Rwave progressively increases in amplitude from leadV1 toward leadsV5 andV6, and the Swave decreases from the right toward the left precordial leads2.

At some point, generally around theV3 orV4 position, the QRScomplex changes from predominately negative to predominately positive.

It is important to note that poor Rwave progression is a non-specific finding on anEKG and requires clinical correlation to determine the underlying cause.A detailed medical history, physical examination, and further diagnostic testing may be required to establish a diagnosis.

The situations in which poor Rwave progression may be seen are as follows:

Causes of Poor RWave Progression

  • Normal variation
  • Lead misplacement
  • V1 and V3 leads reversal
  • Anterior wall myocardial infarction
  • Left ventricular hypertrophy
  • Right ventricular hypertrophy
  • Pneumothorax
  • Pericardial Effusion
  • Emphysema
  • Dilated cardiomyopathy
  • Congenital heart disease
  • Left bundle branch block, Wolff-Parkinson-White syndrome

Normal Variation

Poor Rwave progression may be found in approximately 7% of in asymptomatic subjects with no disease and proper electrode application, and was unrelated to patient morphology34.

However, poor R wave progression may be a marker of unrecognized structural or electrical abnormalities and should prompt further evaluation3.

Poor Rwave progression in newborn and infant

Term newborn infants usually demonstrate right ventricular preponderance with prominent Rwaves in the right precordial leads and deep Swaves in the left lateral precordial leads25.

The amplitude of R waves in the right precordial leads of normal children decreases with age while the amplitude increases in the left precordial leads6.

Similar but inverse changes occur in respect of the S wave amplitude. There is substantial individual variation in the rate at which these changes occur6.

Lead misplacement

The absence of Rwaves in leadsV1, V2, and even V3 or V4 in persons without heart disease is often caused by relatively high placement of electrodes in relation to the heart2.

This means that when the diaphragm position is low, even the correctly placed precordial electrodes may face not the ventricles but the atria or the great vessels2.

V1 and V3 Leads Reversal

This is one of the more common errors involving lead placement. This erroneous switching produces an EKG pattern in which the normal Rand Swave progressions in the precordial leads V1 to V3 is lost.

It may be recognized by the presence of biphasic Pwaves in leadV3, while Rwaves in leadsV1 andV2 are upright2.

Anterior Wall Myocardial Infarction

A significant portion of patients with previous anterior wall myocardial infarction will masquerade merely having as poor Rwave progression on surface EKG4.

On the other hand, only 20% of patients with poor Rwave progression have anterior myocardial infarction1.

R waves are significantly lower in all precordial leads in patients with prior anterior myocardial infarction than those without7.

In patients with prior anterior myocardial infarction, poor Rwave progression usually reflects large myocardial infarct size and severely impaired left ventricular systolic function7.

Left ventricular hypertrophy

Related article: Left ventricular hypertrophy.

Poor progression of the Rwave in precordial leads occurs commonly with left ventricular hypertrophy and is associated with a leftward shift of the transitional zone in the precordial leads2.

In left ventricular hypertrophy, the electrical activity is redirected due to the thickening of the left ventricular wall, which can lead to a lack of normal progression of the Rwave from the right precordial leads to the left precordial leads.

Occasionally, Rwaves are absent in leads V1, V2, and even V3, resulting in a QS deflection in these leads that mimics anteroseptal myocardial infarction2.

More information: Left ventricular hypertrophy.

Right ventricular hypertrophy

Related article: Right ventricular hypertrophy.

In right ventricular hypertrophy, there is an increase in the size and thickness of the right ventricle, which can lead to a shift in the electrical axis of the heart towards the right side. This can result in a lack of normal progression of the Rwave from the right precordial leads to the left precordial leads.

Electrocardiographic manifestations of right ventricular hypertrophy includes right axis deviation, tall Rwaves in the right precordial leads (V1 and V2), deep Swaves in the left precordial leads (V5 and V6), and a slight increase in QRScomplex duration2.

More information: Right ventricular hypertrophy.

Pneumothorax

A left-sided pneumothorax may cause poor Rwave progression in precordial leads due to rotation of the heart by intrathoracic air. This situation may mimic an anterior wall myocardial infarction8.

The electrocardiographic abnormalities described in left pneumothorax include poor Rwave progression, Twave inversion in precordial leas, phasic QRS voltage variation. QRS voltage ratio (aVF/DI) greater than2 has high sensitivity and specificity9.

Electrocardiographic changes are secondary to several factors including clockwise rotation axis of the heart, dilated right ventricle, posterior displacement of the mediastinum, hypoxemia, and decreased coronary blood flow9.

Electrocardiographic findings immediately improved after simple aspiration8.

Pericardial Effusion

The most common EKG finding of pericardial effusion with or without cardiac tamponade is low voltage QRS complexes10. Poor R progression in precordial leads can also be observed.

The presence of low voltage and sinus tachycardia should always raise concern about pericardial effusion with cardiac tamponade10.

Another EKG finding that can occur with pericardial effusion and cardiac tamponade is electrical alternans. Electrical alternans with sinus tachycardia is a highly specific electrocardiographic sign of cardiac tamponade, but its absence does not exclude pericardial tamponade10.

Emphysema

Poor R wave progression in precordial leads caused by emphysema are related to anatomic changes in heart position11.

In emphysema, a significantly higher R/S ratio is observed in leads V1-V4, whereas in anterior myocardial infarction this higher ratio is observed in leads V5-V611.

Dilated cardiomyopathy

Poor Rwave progression with QS complexes in precordial leads V1-V4 (“pseudo-infarction” pattern) is a common finding in patients with dilated cardiomyopathy.

Low QRS voltages in peripheral and precordial leads have also been described, being the electrocardiographic expression loss of vital myocardium and its replacement by fibrotic tissue12.

Congenital heart disease

While the specific mechanisms can vary depending on the type and severity of the defect, congenital heart diseases may sometimes be associated with poor R-wave progression on an EKG.

One possible reason for poor Rwave progression in congenital heart diseases is the abnormal orientation of the electrical activity caused by the structural defects. The altered position and size of the heart chambers can affect the normal progression of the Rwave on the precordial leads.

Furthermore, certain types of congenital heart diseases, such as right ventricular outflow tract obstruction or pulmonary hypertension, may lead to right ventricular hypertrophy. Right ventricular hypertrophy can also contribute to poor Rwave progression.

Other Causes of Poor R Wave Progression

Left bundle branch block and Wolff-Parkinson-White syndrome, are characterized by recognizable intraventricular conduction patterns, in both cases, poor Rwave progression in precordial leads can be observed2.

References

  • 1. Gami SA, Holly TA, Rosenthal JE. Electrocardiographic poor R-wave progression: analysis of multiple criteria reveals little usefulness. Am. Heart J. 2004; 148(1): 0–85. doi:10.1016/j.ahj.2004.02.005.
  • 2. Surawicz B, Knilans TK. Chou’s electrocardiography in clinical practice, 6th ed. Philadelphia: Elservier; 2008.
  • 3. Zema MJ. ECG Poor R-Wave Progression. Arch Intern Med. 1982; 142(6): 1145-1148. doi:10.1001/archinte.1982.00340190101018.
  • 4. Zema MJ. Poor R Wave Progression Revisited. Am. J. Cardiol. 2010; 105(3) 422-3. doi10.1016/j.amjcard.2009.09.023.
  • 5. Schwartz PJ, Garson A, et al. Guidelines for the interpretation of the neonatal electrocardiogram. A Task Force of the European Society of Cardiology. Eur Heart J. 2002; 23(17): 1329–44. doi:10.1053/euhj.2002.3274.
  • 6. Dickinson DF. The normal ECG in childhood and adolescence. Heart. 2005; 91(12): 1626–1630. doi:10.1136/hrt.2004.057307.
  • 7. Kurisu S, Iwasaki T, Watanabe N, et al. Poor R-wave progression and myocardial infarct size after anterior myocardial infarction in the coronary intervention era. Int J Cardiol Heart Vasc. 2015; 7: 106–109. doi:10.1016/j.ijcha.2014.09.002.
  • 8. Mitsuma W, Ito M, et al. Poor R-Wave Progression in the Precordial Leads in Left-Sided Spontaneous Pneumothorax. Circulation. 2009; 120: 2122. doi:10.1161/CIRCULATIONAHA.109.885137.
  • 9. Carrillo-Esper R, Garnica-Escamilla MA, Carrillo-Córdova JR. Electrocardiographic abnormalities in left pneumothorax. Gac Med Mex. 2010; 146(2): 157-9.
  • 10. Badiger S, Akkasaligar PT, et al. Electrocardiography – Pericarditis, Pericardial Effusion and Cardiac Tamponade. Int. J. Intern. Med. 2012; 1(4): 37-41. doi:10.5923/j.ijim.20120104.01.
  • 11. Gupta P, Jain H, Gill M, et al. Electrocardiographic changes in Emphysema. World J Cardiol. 2021; 13(10): 533–545. doi:10.4330/wjc.v13.i10.533.
  • 12. Crescenzi C, Silvetti E, et al. The electrocardiogram in non-ischaemic-dilated cardiomyopathy. Eur Heart J Suppl. 2023; 25: C179–C184. doi:10.1093/eurheartjsupp/suad043.

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