(Chest. 2003;124:560-564.)
© 2003
American College of Chest Physicians
Acute Right Atrial Strain*
Regression in Normal as Well as Abnormal P-Wave Amplitudes With Treatment of Obstructive Pulmonary Disease
Navaid Asad, MD;
Vanessa M. P. Johnson, MD, MPH and
David H. Spodick, MD, DSc, FCCP
* 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{at}tenethealth.com
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Abstract
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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.
Key Words: COPD • P wave • right atrial strain
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Introduction
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COPD is characterized by verticality of the P-wave axis with peaked P waves (gothic or pulmonale) in leads II, III, and aVF.1
Each is more prevalent with worsening pulmonary function test results.2
Traditional ECG criteria for right atrial (RA) enlargement such as P-pulmonale (P waves 2.5 mm in leads II, III, and/or aVF)3
4
5
have been criticized as nonspecific and insensitive.6
7
Different criteria have been proposed for RA enlargement and "strain" (transient enlargement). Direct and indirect predictors of RA enlargement such as a P wave > 1.5 mm in lead V2, QRS axis > 90°, and an R/S ratio > 1 in lead V1 in the absence of complete right bundle branch block have also been proposed.8
Based on our repeated observations that P-pulmonale (P wave 2.5 mm) was most often found when patients presented to the emergency department (ED) with COPD exacerbations, and such P waves often no longer qualified for "P-pulmonale" (ie, rapidly lost amplitude) when patients were admitted to the ward, our preliminary investigation evaluated the validity of that observation. We found that the amplitude of the P waves was smaller in almost all of the ECGs done on the wards of both our hospitals, as compared to their amplitude in the ED ECGs; therefore, we expanded our study to include ECGs on the wards of all such patients, whose ED ECG showed P waves with an amplitude 1.5 mm in leads II and aVF. The 1.5-mm cutoff was chosen because it was difficult to measure a dynamic reduction if the initial ED ECG had P-wave amplitudes smaller than that.
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Materials and Methods
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The investigation was conducted simultaneously in two medical centers in New England between January and May. We investigated all patients who received consecutive diagnoses in the EDs. Patients in sinus rhythm whose ED admitting diagnosis was COPD exacerbation received further ECGs on the ward. Second (ward) ECGs were done with the same type of equipment, between 6 h and 24 h after the patient’s arrival from the ED, when the episode of acute exacerbation clinically improved. P-wave amplitudes were determined in leads II and aVF using a calibrated magnifying graticule. Mean frontal plane P vectors (axes) were determined in the usual manner.1
2
We performed a matched-pair analysis to compare the equality of means. The null hypothesis is that there is no difference between the mean of the P-wave amplitude or axis before and after treatment. The alternative hypothesis is that a significant difference exists between means before and after treatment. The 95% confidence interval reports the expected upper and lower bounds of the mean under the assumption that the experiment of 50 observations was repeated 100 times. All statistical analyses were carried out using the STATA 6 statistical software package (Stata; College Station, TX). As control, we took sinus rhythm ECGs of patients with nonpulmonary conditions, such as patients whose chief complaint in the ED was chest pain and patients who came to the ED with GI bleed. Their ward ECGs were similarly studied.
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Results
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All patients with COPD were > 55 years old (37 women and 28 men). Of a total of 65 patients, 57 patients were found to be in sinus rhythm, 6 patients were in atrial fibrillation, and 2 patients had a pacemaker. Seven of 57 ED ECGs had P waves < 1.5 mm in amplitude and were therefore excluded. Seven patients (14%) had classical P-pulmonale on the ED ECG. Forty-eight of 50 patients (96%) whose initial ED ECG showed P waves 1.5 mm in leads II and aVF, including those with P-pulmonale, showed decreased P-wave amplitude on the subsequent ward ECG. P waves on the ECGs of two patients did not show any change in amplitude between the ED and the ward. One of the 48 patients, whose condition worsened with another acute exacerbation of COPD on the ward, showed an increase in the P-wave amplitude. Nineteen patients had no significant change in heart rate (increase or decrease by more than five beats in heart rate was considered significant). Six patients had an increase in heart rate on the ward ECG. Fifteen patients had a decrease by > 20 beats in heart rate on the ward ECG. The difference of the means 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 means of axes between ED and ward ECGs was - 5.24° (Figs 1
2
3
), with p < 0.0001 for all three categories (Table 1
). Interobserver variability in measuring P-wave amplitudes in the first eight patients is shown in Table 2
. In the control group, there were no P-wave amplitude changes noted between ED and ward ECGs.
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Table 1.. Comparison of Means for P-wave Amplitudes (Millimeters) in Leads II, aVF, and Axes Means (Degrees) Before and After Treatment of COPD Exacerbation
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Discussion
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Our investigation demonstrates that P-wave amplitude in patients with COPD is not constant. It decreases following treatment (Fig 4
). This may reflect a decrease in RA strain (size and/or pressure) once COPD exacerbation has subsided, presumably due to the relief of some degree of right ventricular failure, pulmonary hypertension, or both. It is hard to say that a decrease in heart rate alone could be responsible for a decrease in amplitude of P waves in the 15 patients, who had a significant decrease in heart rate following clinical improvement. While we cannot exclude a rate effect as a potential confounding factor, the clinical improvement after treatment is consistent with the change in P-wave amplitude; however, more than one explanation can be offered for the change in P-wave amplitude. Regardless of the mechanism, the results indicate the lability of even normal-size P waves in patients with COPD. The small but consistent and significant (p < 0.0001) leftward P-axis shift (- 5.24°) indicates less P verticality, verticality being a hallmark of COPD.1
2
4
This also tends to increase the P in lead II and decrease it in aVF, but, like amplitude reduction, this significant, though small, left-axis shift is consistent with reduced RA strain. The absence of change in the control group suggests this response is characteristic of COPD.
It is possible that the two patients whose P waves on the ward ECG did not show a decrease in amplitude had already benefited from treatment given by the rescue team on their way to the ED. Their ED ECG could have reflected an already settling COPD exacerbation. It is difficult to speculate that these two patients already had a nondistensible, fixed RA size.
The specific result is not surprising when we consider P-wave size as a potentially labile, continuous variable. The 2.5-mm cutoff for "P-pulmonale"3
4
5
was established in 1935 and has not been revalidated since. It is probably quite specific at the cost of sensitivity (only rare patients with COPD have a permanent P-pulmonale).1
2
It would be interesting to correlate the changes in P waves with echocardiographic measurements or with indwelling catheter-based measurements of right-heart pressures. We believe that the decrease in the amplitude of P waves (in leads II, aVF, and consequently also in lead III) in the subsequent ward ECG after treatment of COPD exacerbation could be explored in an appropriately designed investigation as a convenient indicator of the reduction of RA strain. Further studies are warranted in other pulmonary conditions such as congestive heart failure, pulmonary embolism, and pneumonia to see if such a dynamic P-wave correlation exists before and after treatment of these conditions.
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Footnotes
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Abbreviations: ED = emergency department; RA = right atrial
Received for publication August 28, 2002.
Accepted for publication December 18, 2002.
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References
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- Spodick, DH (1959) Electrocardiographic studies in pulmonary disease: I. Electrocardiographic abnormalities in diffuse lung disease, II. Establishment of criteria for electrocardiographic interference of diffuse lung disease Circulation 20,1067-1074[Abstract/Free Full Text]
- Spodick, DH, Hauger-Klevene, JH, Tyler, JM, et al The electrocardiogram in pulmonary emphysema: relationship ofcharacteristic electrocardiographic findings to severity of disease as measured by the degree of airway obstruction. Am Rev Respir Dis 1963;88,14-19
- Winternitz, M Zur Pathologie des menschlichen Vorhofelektrokardiogramms. Med Klin 1935;31,1575-1581
- Friedman, H Diagnostic electrocardiography and vector cardiography. 3rd ed. 1995,129-131 W. B. Saunders. Philadelphia, PA:
- Chou, TC Electrocardiography in clinical practice. 3rd ed. 1991,29-31 W. B. Saunders Company. Philadelphia, PA:
- Reeves, WC ECG criteria for right atrial enlargement. Arch Intern Med 1983;143,2155-2156[CrossRef][ISI][Medline]
- Surawicz, B Electrocardiographic diagnosis of chamber enlargement. J Am Coll Cardiol 1986;8,711-724[Abstract]
- Kaplan, JD, Evans, GT, Foster, E, et al Evaluation of electrocardiographic criteria for right atrial enlargement by quantitative two-dimensional echocardiography. J Am Coll Cardiol 1994;23,747-752[Abstract]
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Abstract
Introduction
