Acute right atrial strain: regression in normal as well as abnormal P-wave amplitudes with treatment of obstructive pulmonary disease.
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 > or = 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 degrees (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.
Asad
Navaid
N
Cardiology Services of Roger Williams Medical Center, Boston University School of Medicine, Providence, RI, USA.
Johnson
Vanessa M P
VM
Spodick
David H
DH
D016001:Confidence Intervals; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D029424:Pulmonary Disease, Chronic Obstructive / Q000145:classification / Q000503:physiopathology* / Q000628:therapy; D012720:Severity of Illness Index