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Stanford, CA
Washington, DC
Palo Alto, CA
Dr. Yue is a Cardiology Fellow, and Dr. Froelicher is Professor of Medicine, Stanford University. Dr. Atwood is affiliated with Walter Reed Army Medical Center.
Correspondence to: Vic F. Froelicher, MD, Palo Alto Veterans Affairs Medical Center, 3801 Miranda Ave, Bldg 100, Room E2-441, Palo Alto, CA 94304-1207; e-mail: vicmd{at}aol.com
COPD is the fourth leading cause of mortality in the United States, accounting for 119,000 deaths in the year 2000 alone.1 Acute exacerbations of COPD are a common complication, resulting in significant morbidity2 and mortality.3
The ECG finding of P pulmonale refers to a pattern in which the P-wave amplitude in leads II, III, and/or aVF is augmented to > 2.5 mm.4 It is thought to reflect the overload of the right atrium (so-called right heart strain) and is accordingly a marker for disease processes that involve stress to the right heart circulation.
Atrial enlargement and the P wave received attention in the first half of the 1900s, and a myriad of criteria were made for both right and left atrial enlargement. Despite the initial enthusiasm about its usefulness, P pulmonale fell out of favor over time due to concerns regarding its clinical validity. Indeed, studies5 6 seeking to correlate P pulmonale with echocardiographic findings were disappointing, demonstrating low sensitivity. Moreover, other ECG patterns, including right axis deviation, S1S2S3, S1Q3, and P-wave axis, have emerged as more sensitive indicators of right heart strain.7 8 However, there has been a renewed interest in the atrium, rekindled by the recent prominence of atrial fibrillation in clinical practice and the literature. With the availability of echocardiography, the ECG terms of enlargement was changed to right and left atrial abnormalities, because of the relative inadequacy of ECG in predicting atrial size.9
Not surprisingly, most of the literature relating to atrial abnormalities is dated. However, a PubMed search came up with some interesting citations. Perkiomaki et al10
studied the independent value of ECG variables in predicting cardiac events after acute myocardial infarction (AMI) in the era of modern therapy. Patients (1,034 patients) underwent standard electrocardiography from 5 to 7 days after experiencing an AMI. During 2 years of follow-up, 42 patients (4%) experienced cardiac death, and 259 patients (25%) experienced cardiac death, a nonfatal AMI, or unstable angina. After adjustment for all risk variables, ST-segment depression and atrial abnormality were the only ECG variables that independently predicted cardiac death. Mehta et al11
used echocardiography to conclude that left atrial abnormality was significantly diagnostic of left ventricular hypertrophy in the presence of left bundle-branch block. Bossone et al12
examined whether ECG features in patients with primary pulmonary hypertension were associated with a decrease in survival to determine the value of the ECG in risk stratification. They analyzed the ECGs of 51 untreated patients with primary pulmonary hypertension. Significant predictors of decreased survival by Cox regression analysis included pulmonary vascular resistance, cardiac index, P-wave amplitude in lead II, p 
0.25 mV in lead II, QR wave in lead V1, and right ventricular hypertrophy. The authors suggested that an ECG might be useful for deciding therapeutic choices including the timing for lung transplantation listing.
In the current issue of CHEST (see page 560), Asad and colleagues revisit the P wave and demonstrate the mechanistic underpinnings of this pattern. They contended that the low sensitivity of P pulmonale in prior studies was due to the inclusion of patients who, at the time of their ECG, were not experiencing acute right heart strain. Based on this reasoning, the authors sought to investigate a population consisting solely of patients whose conditions were of acute onset. In order to examine such a population, they identified 65 consecutive patients who had been admitted to the hospital from an emergency department setting with an acute COPD exacerbation. After the exclusion of 8 patients whose initial ECGs did not show a sinus rhythm, as well as 7 patients with P-wave amplitudes of < 1.5 mm, 50 patients were included for further analysis. To document tracings both before and after the initial phase of treatment, ECGs on each eligible patient were obtained at 0, 6, and 24 h after clinical presentation.
Several findings deserve notice. First, although only 7 of the 50 patients demonstrated classic P pulmonale, each of them had a P-wave amplitude of > 1.5 mm in both leads II and aVF. Second, the P-wave axis, which is a more sensitive indicator of right heart strain, shifted slightly more than 5° to the left over the 24-h period. Finally, and most importantly, Asad and colleagues were able to demonstrate that the P-wave amplitude was significantly diminished at 24 h (presumably when most patients had improved clinically). In fact, all but 2 of the 50 patients (96%) were reported to have decreased P-wave amplitude at 24 h. While confirming that P pulmonale is an indicator of right heart strain, these results also provide indirect evidence that the P-wave amplitude correlates with the degree of right heart strain.
Are these findings surprising? From a mechanistic standpoint, they should not be. Although P pulmonale has traditionally been characterized as an isolated hallmark of pulmonary disease, it should not be considered a static phenomenon. The P wave is dynamic and subject to change, like all other components of the ECG. Similar to the R wave and ST segment, which fluctuate as left ventricular myocytes are stretched in the setting of an acute insult to the left side of the heart, it would appear that the P wave also varies in size as right atrial cardiomyocytes are expanded in overload situations. Ultimately, it seems that P pulmonale merely represents an extreme at one end of a large continuum of P-wave amplitudes. The dynamic nature of the P wave is further documented by the known changes in P-wave amplitude and duration with exercise.13
Despite the well-conceived design of the study, several limitations also should be mentioned. The clinical characteristics and outcomes of the patients were not reported. It is thus not possible to precisely conclude that the observed decrease in P-wave amplitude correlated with clinical improvement or attenuation of right heart strain. That said, the alternative hypothesis that most of the 50 patients did not improve with in-hospital treatment does not seem credible. Additionally, due to technical concerns, the 7 patients with a P-wave amplitude of < 1.5 mm were not included in the analysis. However, the inclusion of these seven patients would not have significantly altered the results. Even if the seven patients had shown no change in P-wave amplitudes for > 24 h, the difference in amplitudes for leads II and aVF (0.78 and 0.80, respectively) would have been 0.69 and 0.70, respectively.
Of course, COPD is not the only cause of acute right heart strain. Multiple other acute cardiopulmonary processes, including pneumonia, congestive heart failure, pulmonary embolism, and asthma, are associated with right atrial overload. In 1979, Gelb et al14 reported a similar finding in 129 patients with status asthmaticus. Interestingly, the likelihood of P pulmonale correlated significantly with the severity of disease, and a significant number of patients with P pulmonale lost this pattern with clinical improvement.
As the authors suggest, after an appropriately designed clinical investigation, the P-wave amplitude could be considered as a convenient indicator of the efficacy of management of COPD exacerbation. A recent study15 has suggested that P-wave width could be used to monitor diuresis therapy in patients with congestive heart failure. Anticipating the day that appropriate clinical studies are accomplished, it is wise for clinicians to pay attention to dynamic changes in P-wave morphology.
References
This article has been cited by other articles:
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  A. D. Carilli, J. Seiden, and D. H. Spodick P Wave in Pulmonary Impairment Chest, July 1, 2004; 126(1): 313 - 314. [Full Text] [PDF]
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