The electrocardiogram in chronic obstructive pulmonary disease

The electrocardiogram in chronic obstructive pulmonary disease

Printed in the USA. Copyright 0 1990 Pergamon Press plc The Journal of Emergency Medicine. Vol. 8. pp. 607-615, 1990 EC6 Commentary THE ELECTROCARD...

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Printed in the USA. Copyright 0 1990 Pergamon Press plc

The Journal of Emergency Medicine. Vol. 8. pp. 607-615, 1990

EC6 Commentary

THE ELECTROCARDIOGRAM David M. Rodman, rqt

IN CHRONIC

OBSTRUCTIVE

Steven R. Lower-stein,

MD, MPH,*

PULMONARY

and Theodore Rodman,

DISEASE MD*

*Emergency

Medicine Research Center and TDepartments of Medicine and Surgery, University of Colorado Health Sciences Center, Denver, Colorado; and the *Temple University School of Medicine, Philadelphia, Pennsylvania Reprint address: David M. Rodman, MD, The Division of Pulmonary Sciences (Box C-272), University of Colorado Health Sciences Center, 4200 E. Ninth Avenue, Denver, CO 80262

0 Abstract - The electrocardiogram is often abnormal in patients who have chronic obstructive pulmonary disease. The most frequent abnormalities are a rightward P-wave axis (2 70’) and a rightward QRS axis (2 90’). In addition, low voltage in the limb leads, an S,S,S, pattern, poor R-wave progression, a posterior-superior termhud QRS vector or other changes may be present. Transient atrial and ventricular dysrhythmias are common. Knowledge of the usual electrocardiographic manifestations of chronic obstructive pulmonary disease enables the clinician to recognize uncharacteristic abnormalities, which often represent the effects of superimposed illnesses or drug toxicity. 0 Keywords - car puhnonale; diagnosis; emphysema; pulmonary hypertension

retrosternal air space; 2) dilatation or hypertrophy of the right heart chambers; and 3) abnormal electrical conduction in the right ventricle (RV) (5-8). In addition, drugs (for example, methylxanthines, beta-sympathomimetics, and digitalis), hypoxia, hypercapnia, electrolyte abnormalities, pulmonary thromboemboli, and ischemic heart disease may contribute to the abnormal ECG pattern. This article has three purposes: first, to review the ECG patterns that suggest the presence of underlying COPD; second,to describe the special ECG abnormalities that suggest acute superimposed illness (these have prognostic or therapeutic significance); and third, to review the abnormalities of cardiac rhythm that occur most often in patients with stable and destabilized

dysrhythmia;

COPD . INTRODUCTION ANATOMIC

The electrocardiographic (ECG) manifestations of chronic obstructive pulmonary disease (COPD) have been the subject of many investigations and reviews over the past 40 years (l-4). Abnormalities of rhythm, axis, and electrical conduction have been described. While the mechanisms responsible for the changes in the ECG in patients with COPD are still controversial, they probably include one or more of the following: 1) changes in the anatomic position of the heart in the thorax due to flattening of the diaphragm and an increase in the

The ECG abnormalities of COPD are the result of a combination of two factors: pulmonary hypertension and anatomic changes. Pulmonary hypertension develops first and causes hypertrophy and altered electrical conduction in the right ventricle. Later, hyperinflation causes a shift of the position of the heart in the thorax. Conduction abnormalities occur late in COPD, after the RV has hypertrophied to such an extent that its electrical forces overcome those of the left ventricle. When this occurs, the QRS-axis shifts rightward in association with a vertical descent and clockwise rotation of the heart. Delay in right ventricular activation is accompanied by

This activity was supported in part by the American Heart Association Clinician Scientist Award #880441.

RECEIVED:

2 May 1990;

ACCEPTED: 4

AND PHYSIOLOGICAL

CONSIDERATIONS

May 1990

0736-4679/90 $3.00 + .OO 607

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Table 1. ECG Criteria for the Diagnosis of Chronic Obstructive Luna Disease 1.

2. 3. 4. 5. 6. 7. 6.

S,S2S3syndromewith R/S ratio -c 1 in limb leads I, II, and III. “P pulmonale,” with P waves 2 2.5 mm in limb leads II, Ill, or AVF. Mean P wave axis 2 60” in the frontal plane. “Lead I sign” with an isoelectric P wave, QRS amplitude < 1.5 mm, and T wave amplitude < 0.5 mm. Mean QRS axis 2 90” in the frontal plane. Low voltage: QRS amplitude in limb leads 5 5 mm. QRS amplitude 5 5 mm in leads V, and/or V,, or an R-wave 5 7 mm in lead V,, or 5 5 mm in lead V,. R/S ratio < 1 in leads V, and/or V,.

Adapted from Kamper et al (reference

10).

abnormalities of repolarization as well, with repola.rization progressing from endocardium to epicardium. This may result in S-T segment and T-wave abnormalities in leads overlying the RV.

ECG CRITERIA FOR DIAGNOSING COPD While it is unusual for the diagnosis of COPD to be made on electrocardiographic criteria alone, the ECG is often an integral part of the initial diagnostic evaluation. The most salient electrocardibgraphic features of COPD are listed in Table 1. Of course, none of the individual criteria is specific for COPD; similar abnormalities of voltage, P-wave axis and QRS axis are found in congenital heart disease, other forms of pulmonary hypertension, and in some normal individuals (9). Kamper et al determined that for a single ECG criterion the sensitivity for detecting COPD was 89%) while the specificity was 32%. If a patient’s ECG contained two or more abnormalities the specificity for COPD was 68% and the sensitivity was 52% (10). As the number of ECG abnormalities increased - especially if both P-wave and QRS axis changes were present - the predictive value for lung disease increased (as did the severity of the airflow obstruction). Kamper et al discovered some variability in the ECG over a 24-hour period in these patients, primarily a normalization of false-positive ECGs. Shmock et al studied a set of ECG criteria similar to those of Table 1 and made clinical-electrocardiographicnecropsy correlations. They found that the presence of two or more criteria predicted right ventricular hypertrophy at autopsy (11). They also observed that low voltage in the limb leads was related to emphysema alone, while the other abnormalities were the result of right ventricular hypertrophy . In 1959 Spodick studied 100 consecutive patients with COPD admitted to a university hospital (12). He identified abnormalities of the P-wave axis and morphol-

ogy that, in concert with abnormalities of the QRS axis, appeared to be sensitive and specific indicators of COPD. In Spodick’s study the most common ECG finding was a “vertical” P-wave axis (rightward of +80”). Whereas in the normal heart the P-wave is upright in lead I and has an axis of - 50” to +60”, in patients with COPD the axis of the P-waves shifts away from the left arm and inferiorly. The P-waves become tall and peaked (“gothic”) in leads II, III, and AVF; when the height of the P-waves exceeds 2.5 mm the pattern is called “P-pulmonale.” The P-wave may become inverted in AVL and flat or low voltage in lead I. As COPD progresses the QRS axis also is directed vertically, and there is a similar diminution in the voltage of the QRS in lead I. When both the P-wave and the QRS are flat in lead I - the “isoelectric lead I sign” underlying COPD is virtually certain (Figure 1). In patients above age 40, a rightward P-wave axis alone is almost always abnormal and pexmits the inference of diffuse lung disease. In summary, in stable COPD the most frequent abnormalities are low voltage and vertical P-wave and QRS axes. Other helpful features, such as delayed precordial transition (“poor R-wave progression”), the S,S,S, pattern, and tall R-waves in V,, are described below.

OTHER CHARACTERISTIC

ECG PATTERNS

Poor R-wave Progression and Tall Right-Precordial RWaves One of the most diagnostic patterns of COPD is the presence of tall, prominent R-waves in V, (or a qR pattern) (Figure 2); these suggest pulmonary hypertension and full-blown right ventricular hypertrophy. However, in most COPD patients pulmonary artery pressures are only mildly elevated and strict criteria for RVH are not met (13,14). Instead, most patients with COPD have only mild right ventricular hypertrophy and demonstrate an intermediate pattern on the ECG: S-waves persist across the precordium, and delayed precordial transition - or “poor R-wave progression.” Indeed, one of the most common ECG abnormalities in patients with COPD is the pattern of poor R-wave progression in the precordial leads (Figure 3). This pattern is characterized by low amplitude of the R-waves in the‘right-sided leads: V, is zz 1.5 mm or V, 5 3 mm. Poor R-wave progression is also present if the voltage in V, is less than that in V, or the voltage in V, is less than that in V,; this condition is often termed “reverse R-wave progression” (15). In COPD poor R-wave progression is probably caused

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I

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Figure 1. ECG of a 44-year-old man with precocious emphysema illustrating the “lead I sign.” Note the lsoelectrlc P-wave and the low amplltude of both the QRS complex and the l-wave.

by several conspiring anatomic factors. First, the heart lies low in the thorax, and the precordial leads are in a high position relative to the heart’s electrical center,

aVR

resulting in electronegativity (16). Second, in COPD the heart rotates clockwise along its longitudinal axis; the right ventricle and atrium move anteriorly, drawing

v4

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Figure 2. ECG of a 24year-old man wlth cystic flbrosls. Note tall precordlal R-waves Indicative of right ventricular hypertrophy. In addltlon the QRS axis In the frontal plane Is rlghtward and the P-pulmonale Is present.

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Flgure 3. ECG of a W-year-old woman wlth emphysema. Poor R-wave progresston lo evidenced by V,11.5 mm and V&3 mm. In addition, there Is a strlklng lead I sign, P-pulmonale, and right axls devlatlon.

closer to the first three recording electrodes (Vi_,), while the mass of the left ventricle moves posteriorly. Third, there is some evidence that in COPD, the right ventricle undergoes hypertrophy in a distinct pattern: the earliest (and sometimes the only) area of hypertrophy is often the posterior-lying base of the right ventricle with less hypertrophy of the anterior and apical portions. Finally, when the lungs are emphysematous, the electrical currents generated by the heart are dampened, contributing to low voltage in the limb and precordial leads. Poor R-wave progression is common among hospitalized adult patients; an estimated 10% of admission ECGs show this abnormality (15). In addition to right ventricular hypertrophy, three other common conditions may cause poor R-wave progression: anterior wall myocardial infarction, left ventricular hypertrophy, and a variant of normal (15). Less often, poor R-wave progression may be caused by idiopathic hypertrophic subaortic stenosis (IHSS), left anterior fascicular block, left bundle-branch block (LBBB), mitral valve prolapse, or dextroversion (15,17). In patients with COPD, tall right precordial R-waves probably represent a further progression of RVH (15). While poor R-wave progression may be observed in COPD in the absence of RVH (due to the abovementioned changes in the anatomic position and electrical vectors of the heart), prominent R-waves (or R’waves or a qR pattern) in lead V 1(extreme counterclockwise

rotation) develop late in COPD and are a telling sign of pulmonary hypertension, especially if accompanied by T-wave inversions in these same leads (18). The same patterns may be seen in the Wolff-Parkinson White syndrome, posterior myocardial infarction, atria1 septal defect, and other conditions. The S,S,S, Syndrome The S,S,S,

syndrome is characterized by: negative (S) deflections in limb leads 1, 2, and 3 (in each lead the S is of near to or greater magnitude than the R); often, an R’ in lead Vi; and a normal QRS duration (Figure 4). It occurs if the terminal QRS forces are directed superiorly and to the right (19). S,S,S, is often a normal finding in young individuals, where it is associated with enlargement of the right ventricular outflow tract. It is also frequently seen in patients with RVH due to other acquired and congenital lesions, such as ventricular septal defect. In adults the most common cause is emphysema, where the S iS,S, pattern may exist with or without other electrocardiographic manifestations of car pulmonale ( 19).

Pseudo-L.& Axis Deviation

The vast majority of patients with chronic lung disease have right axis deviation of the QRS axis in the frontal

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aVL

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Figure 4. Thls ECG Illustrates the S&S3 pattern which, In persons wlth COPD, Is due to right ventricular enlargement. In younger persons this may be a normal flndlng. Note also the lndetermlnant QRS-axls, bordering on pseudo-left axls devlatlon.

plane. Occasionally, and paradoxically, left axis deviation or an “indeterminant” axis develops (Figure 4). An axis of - 90” (+270”) is not unusual. This pattern is called “pseudo left axis deviation” because left anterior fascicular block and coronary disease are usually not present. When pseudo left axis deviation occurs in COPD, it is due to a general posterior direction of ventricular activation in COPD. In the frontal plane the terminal forces are directed initially leftward (due to the emphysematous lungs), and terminally rightward (due to RVE). The result is a superior and posterior vector. In one series of 158 patients with severe airflow obstruction (but no evidence of coronary or hypertensive heart disease), pseudo left axis deviation was present in 15% of cases, while the S,S,S, pattern occurred in 9% (19).

PROGNOSTIC

VALUE OF AN ABNORMAL ECG

Morbidity in COPD is a function of a diminished ability to exchange gases, an increased susceptibility to respi-

ratory infection, and an association with other diseases such as lung cancer, ischemic heart disease and thromboembolic disease. While other tests, such as arterial blood gas analyses, pulmonary function tests, chest x-ray studies, and exercise tests, provide specific information about these comorbid and complicating conditions, the ECG can also be of prognostic value. Kamper et al found that the presence of three or more electrocardiographic criteria for COPD correlated with increased severity of disease, and that the presence of the S,S,Ss pattern, while uncommon, was also specific for severe disease (10). In Spodick’s review the degree of P-wave “verticalization” was related to increasing airflow obstruction (3). Smit et al studied 128 patients with severe COPD (all had a l-second forced expiratory volume less than 1 liter). He found that an increased P-wave amplitude in limb lead 2 and an increased S-wave amplitude in lead V, were independent predictors of a decreased 5-year survival (20). In Kok-Jensen’s study of 288 patients, the presence of a QRS axis between +90” and + 180” and a P-wave amplitude in limb lead 2 > 2 mm were associated with 4-year survivals of 37% and 42%, respectively (21). Thus, in many series the degree of verticalization of both the QRS axis and the P-wave axis are related significantly to the severity of the airway obstruction. In these studies the presence of right ventricular enlargement is probably the underlying feature that heralds premature death.

ECG MANIFESTATIONS OF ACUTE ILLNESS IN PATIENTS WITH COPD Ischemic Heart Disease in COPD

Ischemic heart disease frequently accompanies COPD, due primarily to the extensive use of cigarettes by many of these patients. Unfortunately, even in uncomplicated COPD the ECG often demonstrates a mixture of findings that suggests infarction or ischemia, and differentiating between COPD and ischemic heart disease is sometimes difficult (Figure 5). For example, poor R-wave progression and anterior Q-waves may be seen in both conditions. Differentiation is facilitated by re-recording the precordial leads one or two interspaces lower than the conventional position. In the case of COPD, a small R-wave will generally appear; in the case of anteroseptal myocardial infarction, Q-waves will persist. Because repolarization abnormalities are often present in COPD (due to RVH), ST-segment and T-wave abnormalities may be seen in the right precordial leads. However, if deep, symmetric T-wave inversions are present in the right precordial leads, anterior myocardial infarction is suggested.

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Figure 5. ECG of a 57-year-old woman with chronic bronchitis and car pulmonale. Inverted T-waves and ST-segment depresslon are present In the rlght precordlum. The presence of right axis deviation and tall R-waves In the rlght precordlum argues In fayor of rlght ventricular hypertrophy and agalnst Ischemla. These flndlngs were unchanged from prevlous tracings, and right heart catheterization revealed a mean pulmonary_ artery __systolic pressure of 65 torr, suggestlng long-standlng pulmonary hypertenslon.

Lead I provides additional useful clues in distinguishing between anterior ischemia and COPD. In patients with RVH, lead I often shows the classic isoelectric (“lead I”) sign. In addition, the R-wave amplitude is diminished and an S-wave (> 1 mm) is present, indicating right axis deviation. In contrast, in patients with anterior myocardial infarction lead I amplitude is often diminished, but the axis is normal and no S-wave is present (15). In addition, the anterior forces are more markedly diminished in anterior myocardial infarction (MI). Thus, if the R-wave in V, is 1 2 mm, anterior MI is unlikely and RVH or another cause is favored. Conversely, if the R-wave in V, is I 1.5 mm, or if significant reverse R-wave progression is present (the R decreases by at least 1 mm from R, to R,, R, to R,, or R, to RJ, then anterior MI is favored. In addition, the greater the R:S ratio in V, and V, the more likely is anterior infarction (22). The presence of anterior precordial Q-waves is also highly suggestive of infarction, while an isolated qR pattern in lead Vi is, instead, virtually pathognomonic of RVH (16).

Dysrythmias in COPD The frequency of dysthythmias in stable COPD was examined in the Nocturnal Oxygen Therapy Trial study

(NOTT) (23). In 64 of 69 patients the basic rhythm was normal sinus, while 5 had atria1 fibrillation or flutter. Complex ventricular ectopy and nonsustained ventricular tachycardia occurred frequently during 24-hour ambulatory ECG monitoring (Table 2). In the NOTT study, patients with edema (and, by inference, car pulmonale) had an &fold increased risk for repetitive ventricular dysrhythmias, as did patients with an elevated PCO*. Most importantly, the NOTT and other studies demonstrated that persistent, sustained dysrhythmias are uncommon in stable COPD (24).

Table 2. Frequency of Dysrythmlas Occurrlng Durlng 24-hour Ambulatory Electrocardlographlc Monltorlng In the NOTT Study Average heart rate Sinus tachycardia(%) Sinus bradycardia(%) Supraventricularbeats (%) Ventricularpremature beats (%) Any ventricularpremature beats Multiform Bigeminy Pairs Ventriculartachycardia Repetitive Frequent (> 25/h) Adapted from Shih et al (reference 23).

90 f 13 38 4 86 83 78 68 61 22 64 35

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Figure 6. This rhythm strip Illustrates multifocal atrial tachy cardia (MAT) compllcatlng COPD. The sallent features of the dysrythmla are 3 or more P-wave morphologles and a rate > 100 beats/mln. MAT should always be consldered a compllcatlng rhythm, and causes of pulmonary or cardiac decompensatlon should be sought.

When acute respiratory failure supervenes in patients with COPD (acute on chronic respiratory failure), atria1 and ventricular rhythm disturbances occur commonly, due to the separate or synergistic effects of hypoxia, acute and chronic car pulmonale, acidosis, and the adrenergic load imposed by bronchodilators. In addition, it is now recognized that frequent administration of aerosolized beta-adrenergic drugs may cause a rapid shift of potassium and magnesium into cells (25). The resultant hypokalemia and hypomagnesemia may induce tachydysrhythmias, QTC prolongation, and T-wave flattening (26). Multifocal atria1 tachycardia (MAT) (Figure 6) was never seen in the NOTT study; therefore, MAT must be considered a complicating rhythm, indicating exacerbation of underlying lung disease, acute respiratory infection, pulmonary thromboembolism, acute pulmonary edema, or another respiratory emergency. MAT and other chaotic atria1 rhythms may be more frequent if acidosis is present, but rarely result from chronic lung disease along. MAT also occurs in patients with theophylline toxicity; in fact it may be a particularly common dysthymia in this condition (27).

Acute car pulmonale The term “car pulmonale” - a synonym for pulmonary hypertensive heart disease - denotes enlargement of the right ventricle due to hypertrophy, dilatation, or both (18). Many patients with stable COPD have chronic car pulmonale. It is important for emergency and critical care clinicians to recognize the ECG changes of acute car pulmonale, which may be superimposed on the patterns of stable COPD. The electrocardiographic syndrome of acute car pulmonale is often the result of acute

aVL

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Figure 7. Thls ECG demonstrates the classic pattern of acute car pulmonale. Note the deep S-wave In llmb lead I, and the G-waves and Inverted T-waves In leeds Ill and a VF. In practice these changes are often less dramatic than those Illustrated here.

hypoxemia, ventilatory insufficiency, or acute obstruction of the pulmonary vasculature by thromboemboli (8). Acute right heart dilatation occurs in response to abrupt arterial desaturation and elevations of pulmonary artery pressure, and characteristic ECG changes result. The most characteristic electrocardiographic pattern of acute car pulmonale consists of the sudden appearance of a Q-wave in limb leads 3 and AVF; a deep S-wave in lead I, due to an exaggerated rightward axis, and inversion of the T-wave in lead 3 (thus, the acronym S1Q3T3) (Figure 7). Additional electrocardiographic changes of acute car pulmonale, which are common but not specific, include 1) sinus tachycardia; 2) premature atria1 contractions, often aberrantly conducted in a RBBB pattern; 3) ectopic atria1 pacemakers; 4) Q waves, S-T segment elevations, or T-wave inversions in the right precordial leads, indicating right ventricular dilatation and, often, suprasystemic elevations of right ventricular

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04 Figure 8. a. ECG of a 73-year-old man with longstanding emphysema who presented with an acute exacerbation complicated by hypoxemia. Sinus tachycardia and complete right-bundle-branch block are present. The unusually tail R’(> 15 mm) in lead V, suggests the presence of right ventricular enlargement. Figure 8. b. ECG from the same individual 18 hours later, after oxygen and bronchodiiator therapy had been administered. Note the complete resolution of the right-bundle-branch block. Now present are an inferior P-wave axis and a lead I sign as the sole eiectrocardiographic manifestations of COPD.

pressure; 5) an incomplete or complete right bundle branch block pattern in V,, often with an R’ > 15 mm; 6) deepening or slurring of the S-waves in leads VI and

V,; and 7) new right atria1 abnormalities (P-pulmonale) (8). A rightward axis shift alone - usually more than 30” from its previous position - is often the only clue to

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right heart strain. While nonspecific, the most common ECG abnormality that suggests acute car pulmonale is the development of an atrial dysrhythmia. The pattern of acute car pulmonale may develop rapidly even in a matter of minutes or hours. Then, once the stress of hypoxemia is over and the pulmonary hypertension has abated, the car pulmonale pattern often reverts to baseline (Figures 8 a,b).

acute

CONCLUSIONS The ECG is often abnormal in patients with COPD. The ECG signs of stable COPD are variable and depend on the prevailing anatomic and electrical conditions, including hyperaeration of the lungs, a low position of the

heart, right ventricular hypertrophy, and clockwise cardiac rotation. The most common abnormality is a vertical P-wave axis which, in concert with a vertical QRS-axis, is suggestive of COPD. However, the ECG is neither sensitive nor specific for this diagnosis, nor for the presence of underlying RVH. Recognizing the common ECG patterns which present in COPD will heighten the clinician’s awareness of uncharacteristic abnormalities, which should suggest the possibility of superimposed illnesses such as myocardial ischemia, drug toxicity, acute respiratory failure, or pulmonary thromboemboli.

Acknowledgment - Heartfelt thanks to Dr. Ray Pryor for reviewing this manuscript and providing illustrations of unusual ECG patterns.

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