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Clinical Investigations: CARDIOLOGY |

Acute Right Atrial Strain*: Regression in Normal as Well as Abnormal P-Wave Amplitudes With Treatment of Obstructive Pulmonary Disease

Navaid Asad; Vanessa M. P. Johnson; David H. Spodick
Author and Funding Information

*From the Cardiology Services of Roger Williams Medical Center (Dr. Asad), Boston University School of Medicine, Providence, RI; The Centers for Behavioral and Preventative Medicine (Dr. Johnson), Brown University Medical School), Providence, RI; and Saint Vincent Hospital (Dr. Spodick), Worcester Medical Center, University of Massachusetts Medical School, Worcester, MA.

Correspondence to: David H. Spodick, MD, DSc, FCCP, Cardiovascular Division, Worcester Medical Center, 20 Worcester Center Blvd, Worcester, MA 01608; e-mail: david.spodick@tenethealth.com



Chest. 2003;124(2):560-564. doi:10.1378/chest.124.2.560
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Objective: To evaluate right atrial (RA) “strain” as reflected by changes in P-wave amplitude and vector in patients with COPD immediately before and immediately after beginning treatment of exacerbations.

Background: P-pulmonale (frequently temporary, reflecting acute RA strain) occurs under a variety of circumstances, including COPD. Emergency room (ED) ECGs in patients with acute exacerbations of COPD have suggested that P-pulmonale (P waves ≥ 2.5 in leads II, III, and aVF) tends to resolve subsequent to acute treatment. RA strain is defined as a response to RA stress (probably transient pressure rise and/or acute RA enlargement) in patients with COPD. Since P-pulmonale occurs in a small minority of patients with COPD, we investigated dynamic changes in size and mean vector (axis) of all frontal plane P waves in the ED vs the immediate subsequent ward ECG in patients with acute exacerbations of COPD.

Methods: We prospectively compared P-wave amplitude in the ED with the first in-patient ECG in 50 consecutive patients with acute exacerbations of COPD and in 20 consecutive nonpulmonary control patients, analyzing only ECGs showing sinus rhythm and in which P waves were clearly recorded. Despite using a calibrated magnifying graticule, it was difficult to interpret a dynamic change if the initial ED ECG had P-wave amplitude < 1.5 mm in leads II and aVF. We selected lead II because it usually has the largest frontal plane P waves and also aVF to reflect the relative verticality of the mean P vector (axis). We performed a matched-pair analysis to compare the equality of means.

Results: Of the patients with COPD, only seven patients (14%) had classical P-pulmonale on the ED ECG. Forty-eight of 50 consecutive patients (96%) demonstrated a decrease in P-wave amplitude between ED and subsequent ward ECGs. Two patients showed no change. The mean differences of P-wave amplitude between ED and ward ECGs in lead II was 0.78 mm, and that in lead aVF was 0.8 mm. The difference of the mean P-axis between ED and ward ECGs was − 5.24° (p < 0.0001 for all three measurements). There was no P-wave amplitude change in the control group between ED and ward ECGs.

Conclusions: P-wave amplitude in patients with COPD decreases once an acute exacerbation subsides. Thus, P-wave amplitude and vector are dynamic and could reflect reduced RA strain. We question the traditional (1935) absolute cutoff of 2.5 mm for P-pulmonale as of limited value due to insensitivity, hence inappropriate for what this investigation demonstrates to be a continuous variable.

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