The Resting Electrocardiogram in the Management of Patients with Congestive Heart Failure: Established Applications and New Insights

JOHN E. MADIAS, M.D., FACC, FAHA

From the Mount Sinai School of Medicine of the New York University and the Division of Cardiology, Elmhurst Hospital Center, New York

The resting electrocardiogram (ECG) furnishes essential information for the diagnosis, management, and prognostic evaluation of patients with congestive heart failure (CHF). Almost any ECG diagnostic entity may turn out to be useful in the care of patients with CHF, revealing the non-specicity of the ECG in CHF. Nevertheless a number of CHF/ECG correlates have been proposed and found to be indispensable in clinical practice; they include, among others, the ECG diagnoses of myocardial ischemia and infarction, atrial brillation, left ventricular hypertrophy/dilatation, left bundle branch block and intraventricular conduction delays, left atrial abnormality, and QT-interval prolongation. In addition to the above wellknown applications of the ECG for patients with CHF, a recently described association of peripheral edema (PERED), sometimes even imperceptible by physical examination, with attenuated ECG potentials, could extend further the diagnostic range of the clinician. These ECG voltage attenuations are of extracardiac mechanism, and impact the amplitude of QRS complexes, P-waves, and T-waves, occasionally resulting also in shortening of the QRS complex and QT interval duration. PERED alleviation, in response to therapy of CHF, reverses all above alterations. These fresh diagnostic insights have potential application in the follow-up of patients with CHF, and in their selection for implantation of cardioverter/debrillator and/or cardiac resynchronization systems. If sought, PERED-induced ECG changes are abundantly present in the hospital and clinic environments; if their detection and monitoring are incorporated in the clinicians routine, considerable improvements in the care of patients with CHF may be realized. (PACE 2007; 30: 123128) electrocardiography, congestive heart failure, peripheral edema, body volume conductor, electrical impedance, diuresis, ICDs, cardiac resynchronization therapy, QRS duration, QT interval Introduction Patients with dilated cardiomyopathy (DCM) and diastolic dysfunction are admitted to the hospital or seen in outpatient clinics with manifestations (symptoms and signs) of congestive heart failure (CHF). The resting 12-lead electrocardiogram (ECG) constitutes a sine qua non component of laboratory testing in such encounters, and it is relied upon in speculating about the cause of DCM or CHF, and the plausible mechanisms that led to the clinical deterioration. Undoubtedly, there is other information deriving from history of past or present illnesses, physical examination, and other laboratory testing that is useful in guring out or reasoning the case. Nevertheless, it is contributory to the management of the patient and the continuous scientic betterment of the cardiologist to interpret initially the ECG, disregarding information from any other source, including previAddress for reprints: Dr. John E. Madias, Professor of Medicine (Cardiology), Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373. Fax:(718) 334-5990; e-mail: madiasj@nychhc.org Received August 29, 2006; revised September 27, 2006; accepted October 6, 2006.

ous ECGs. In this respect, a feeling about the independent or incremental value of the ECG in the management of patients with CHF can be quickly acquired.1 Looking at the ECG at hand de novo, and not in the context of the details of the clinical presentation, one should establish at a glance whether there is evidence of previous or acute myocardial infarction, current ischemia, atrioventricular or intraventricular blocks, electronically paced rhythms, or supraventricular and ventricular arrhythmias. Following this, a comparison of the current ECG with previous tracings is in order, and could provide an insight about previous illnesses, progression of disease, and plausible reasons for the patients deterioration. This task is nowadays facilitated by the availability, in hospitals or even in physicians private ofces, of electronic ECG les containing all the patients ECGs recorded at a specic medical facility. The nal step in employing the ECG in the patients management is to nalize the tracings interpretation in the context of all other information. The above exposition may lead to the notion that there is nothing specic about the ECG, in terms of making it essential for the diagnosis and management of patients with CHF, since ECG patterns seen in

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this condition can also be encountered in many other cardiological syndromes. Perhaps it can be stated that almost any of the gamut of ECG appearances described in the standard textbooks24 can also be found in patients with CHF. Although this is true, the absence of specicity of the ECG for patients with CHF does not mitigate this modalitys contribution. In reference to sensitivity, almost all patients with CHF show some abnormality in the ECG, although rarely a patient may present with a completely normal or almost normal ECG, showing merely subtle nonspecic ST and T abnormalities, either transient or persisting. The ECG can also be viewed from another vantage point, i.e., that of a body of ECG/CHF associations which have been proposed, with some of whom, having withstood the test of time becoming quasi-established, as reliable ECG correlates of CHF. Again this does not imply that these ECG patterns are specic for CHF. These include: (1) sinus tachycardia, particularly if it is of new onset and/or dissipates after the management of CHF, (2) pathological (deep and wide) Q waves involving many ECG leads indicative of previous myocardial infarction(s), (3) persisting ST elevation, associated with Q waves, suggestive of ventricular aneurysm, (4) deep S waves and tall R waves in specic ECG leads suggestive of left ventricular hypertrophy (LVH),5 and/or ventricular dilatation (the ECG cannot differentiate LVH from ventricular dilatation,6 or systolic from diastolic CHF), (5) atrial brillation indicative of atrial structural and/or functional derangement,7 (6) left bundle branch block (LBBB), particularly with right axis deviation suggestive of DCM, and which often has led to right ventricular decompensation (biventricular involvement),8 (7) intraventricular conduction delays, particularly of LBBB, or of nonspecic, but not of right bundle branch block (RBBB) types,5 suggestive of extensive myocardial necrosis, scarring, or brosis, and predictive of a good response to cardiac resynchronization therapy (CRT).9 The incidence of the frequent combination of RBBB and left anterior fascicular block per se in patients with CHF, or the rate of CHF in patients with this ECG pattern, is difcult to discern, because most of the studies refer to such data in patients with prior infarctions, or other comorbidities. Left axis deviation >30 in patients with LBBB is a marker of signicant left ventricular systolic dysfunction, although it does not correlate well with ejection fraction,10. (8) persistent ST elevation in association with predominantly positive QRS complexes (usually V5 and V6) in the presence of LBBB suggestive of ventricular aneurysm and DCM,11 (9) persistent ST elevation in association with predominantly positive QRS complexes (usually V1-

V3) in the presence of RBBB suggestive of ventricular aneurysm and DCM,12 (10) low amplitude QRS complexes suggestive of mutual electrical cancellation of large myocardial zones of infarction opposite each other,13,14 although this feature is also found in some patients with chronic nonischemic DCM,15,16 and acute myocarditis, with transient cardiac dilatation and CHF17 (it is a misconception that low amplitude QRS complexes is a specic feature of restrictive or inltrative cardiomyopathy without cardiac dilatation), (11) low amplitude of the limb leads, with high voltage of the precordial leads, and an R/S ratio <1.0 in lead V4, which has been described to be associated with CHF,18 (12) the strain pattern in hypertensive patients with ECG LVH, receiving aggressive blood pressure lowering, which was found to be predictive of new onset of, and dying from, CHF,19 although it was not independently predictive of those patients with more severe diastolic dysfunction.20 The ECG, in general, has not been implemented prospectively as a predictor for the development of CHF; this will require studies with long follow-up and serial ECGs, in patients at risk, (13) an LBBB-like ECG pattern, found in patients with CHF and pacemakers or implantable cardioverter/debrillators (ICD), (14) an intraventricular conduction delay ECG pattern, seen in patients with CHF and implanted CRT systems, (15) a widened P wave in limb and precordial leads, an increase in P-wave dispersion, and an accentuated negative component of the P wave in lead V1, found in patients with CHF, and which indicate intra-atrial block,21 left atrial hypertrophy, hypertension, or dilatation (not specic for any of the four), which predict emergence of atrial brillation in patients with CHF, and show dynamic changes with therapy.22,23 Studies on short-term and long-term changes of the accentuated negative component of the P wave in V1 in response to therapy of CHF are needed, similar to the ones carried out in the follow-up of patients with mitral stenosis, post balloon commissurotomy, (16) increase in the QRS duration, which reects the severity of CHF, and which shows lengthening or shortening when patients with CHF decompensate, or improve.24,25 The QRS duration at baseline is not predictive of response to CRT, and although signicant reduction in QRS duration after such therapy is noted in responders, the individual response varies highly, not allowing the decrease of the QRS postimplantation to be employed as a predictor of eventual response,9 (17) prolongation of the QTc interval, noted in patients with CHF,26,27 (18) a wide frontal QRS/T angle, ST-segment depression in lead V5, and high T-wave amplitude in V1, which are prognostic of incident CHF in

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postmenopausal women,28 (19) a QTc 487 ms, a QRS dispersion 42.7 ms, voltage criteria for LVH, two ambulatory ECGs, and three non-ECG parameters, which stratied outpatients with CHF into subgroups with high and low mortality risk.29 There is large variation in the reported sensitivity and specicity of the different ECG abnormalities in patients with CHF, since such data derive from small or large cohorts, include patients with different degrees of CHF, emanate from subjects admitted to the hospital or followed in clinics, or patients considered for transplantation, ICD, or CRT, or patients with a variation of comorbidities. The above associations or correlates may not be specic for patients with CHF, but their value has been shown in the literature, and their continuing testing in clinical practice and research could rmly establish whether or not they possess incremental utility in the diagnosis, follow-up, and prognosis of CHF. To accomplish this, one needs to implement the above ECG/CHF associations in conjunction with other non-ECG parameters, like cardiac imaging-based information on volumes of heart chambers, ventricular ejection fraction, hemodynamic proles, humoral (e.g., brain natriuretic peptide [BNP]),30,31 and neurohumoral (e.g., catecholamines)31 parameters, purported to have independent diagnostic and prognostic utility for patients with CHF. In reference to the BNP, there has been some utilization in patients with CHF in conjunction with some ECG indices (QTc interval27 and QRS duration30 ); however, there has not been as yet a systematic exploration as to what other BNP/ECG indices combinations could accomplish in diagnosing CHF, or assessing its prognosis, or monitoring its management. Also correlations of the BNP and ECG parameters in patients with CHF have not as yet been attempted. The resting ECGs of diabetic and nondiabetic patients with CHF are not different, however, some evidence is forthcoming that in diabetic patients with CHF the QTc is significantly longer than in nondiabetic patients with CHF.32 The bulk of the work in diabetes and the ECG has been focused on the ST segment in acute coronary syndromes. More than the above enumerated ECG/CHF associations have been described in the literature, and thus no claim for an allinclusive treatment of the topic can be made in this communication. However, the issue herein is not to compile a comprehensive listing of all that has been described in the literature, but to concentrate on evaluating a group of the most promising ECG parameters, in order to establish unambiguously that some of them have independent value. An example of such an ECG parameter, which could justiably become the focus of attention, is the QRS duration as a marker of severity of pathology and

its perturbations, or as an index to be used in the selection of patients for implantation of ICD or CRT. Some literature supports such a claim,24,25,33 but other work does not.34,35 Indeed, the Center for Medicare & Medicaid Services announced on January 27, 2005, an expansion of ICD implantation coverage for patients with ischemic and nonischemic DCM that is based on a left ventricular ejection fraction 35%, without binding considerations of the QRS duration.36 Nevertheless, current literature indicates that this issue is far from having been conclusively decided37 (also, vide infra). Many of the ECG patterns described above are correlates of existing CHF, although they can also be employed as predictors of new CHF. There is a need to identify new ECG indices, or employ quantitatively the above described ECG patterns, for prediction of new CHF. In addition, there is a need for studies, again relying on quantitative analysis of serial ECGs, to evaluate the contribution of the ECG in prognosis of patients who already have CHF, and effectiveness (or the lack thereof) of various therapies administered. In closing this section, it is important to note that this report focuses on the resting ECG per se, thus excluding reference to ECG in the exercise or pharmacological stress testing, signal-averaged ECG, heart rate variability, T-wave alternans, and other resting ECG, and ambulatory ECG recording-based indices, useful for patients with CHF, but dependent on special data acquisition and analysis technologies. Recent reports on the association of peripheral edema (PERED) of varying pathophysiology and attenuation of the ECG voltage in general (P waves, QRS complexes, and T waves)3842 offer fresh opportunities for the employment of the ECG in CHF. The European literature of the 1950s referred to the association of clinical deterioration of patients with CHF and attenuated QRS potentials.4345 The issue was revisited only once more in 1971, with a report that patients with CHF and radiographically derived cardiomegaly who responded to digitalization and diuresis showed an increase in the QRS potentials of their ECG along with decrease in heart volume.46 More recently, a relationship of attenuated amplitude of the QRS complexes with clinical decompensation, and subsequent augmentation of potentials with attainment of clinical compensation, has been repeatedly shown in patients with CHF, both admitted to the hospital or followed in the outpatient clinic.4751 These perturbations of the amplitude of QRS complexes correlated inversely with changes in the patients weight.4751 In a futile attempt to explain the phenomenon of changing QRS potential amplitudes with changing degrees of CHF compensation previous workers39 invoked the Brody effect,52 which theorizes that increase in intracardiac blood mass leads

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to augmentation of QRS voltage, and, according to which, improved clinical compensation should have resulted in reduced cardiac volumes, and decreased QRS potentials, the opposite of what they found.46 Drawing on the experience from patients with a diversity of edematous states3842,4751 it now appears that the underlying common mechanism of this phenomenon is extracardiac, mediated by the decrease in the electrical impedance of the body volume conductor enveloping the heart and resulting from the uid engorged interstitium (interstitial uid has the lowest possible special resistance in the body).53 The lowering of electrical impedance of the body volume conductor is translated in turn into attenuated body surface ECG potentials. As expected, amelioration of the PERED results in augmentation of the QRS complexes,38 P waves,39 and T waves.42 An illustrative case is that of an 82-year old woman with history of hypertension and CHF, an S3 gallop, rales 1 the way up on auscultation of 2 her chest, marked pitting PERED of her legs on physical examination, and weight of 169.0 lbs, on admission to the hospital. Her CHF responded to management, she was discharged, and was followed at the clinic at frequent time intervals. At her latest clinic evaluation she was asymptomatic, had clear lungs, trace of PERED around her ankles, and weighed 135.0 lbs. ECGs corresponding to her hospital admission (Fig. 1A) and her latest clinic assessment (Fig. 1B) showed complete LBBB and an interim augmentation in the QRS potentials of the limb leads and attenuation of precordial QRS potentials. Quantitative evaluation of the ECGs is

Figure 1. ECGs of a patient with CHF, on her admission to the hospital (A), and at her latest clinic follow-up 18 months later (B); between these two time-points the patient lost 34.0 lbs, and the ECGs showed augmentation of the QRS complexes in the limb leads, and attenuation of the QRS voltage in leads V2-V5.

based on sums of the QRS complexes from nadir to zenith to the nearest 0.5 mm and involves the sets of all 12 leads, the 6 limb leads, the 6 precordial leads, and leads I + II, as done previously.31,47,54 Justication for using sums of leads I and II is based on the fact that most ECG machines measure only leads I and II, and calculate online the remaining four limb leads, based on the known mathematical relations among leads.4 This patient lost 20.1% of her admission weight, and showed a 21.7% increase in the sums of the six limb leads, and 24.3% in the sums of leads I and II; in contrast, a counterintuitive 37.9% decrease in the sums of the six precordial leads, and 23.5% of the 12 ECG leads was found (Fig. 1A and B). This discrepancy in response between the limb leads and precordial leads does not occur always, but it is a frequent encounter, and its mechanism is the known poor reproducibility in recording the precordial leads via the same appropriate thoracic landmarks.4 Erratic precordial recordings affect in turn the 12lead ECG, as noted in this case. Attenuation/augmentation of the ECG voltage results in shortening/lengthening of the QRS duration55 and QT intervals,56 respectively; these changes are apparent, i.e., not electrophysiologically induced, but due to partial failure of the manual or automated measurement of the QRS and QT durations, involving the early portion of onset and late portion of offset of the QRS complexes and QT intervals. These portions are sensitive to changes in the ECG potentials because they are close in amplitude to the noise signal. This concept was recently corroborated in a study of articial attenuation of the amplitude of the ECG voltage, which resulted in shortening of the QRS complexes.57 Such perturbations of the QRS duration and QTc depending on attenuated/augmented ECG voltage due to poorly/well compensated CHF, with development/amelioration of PERED, probably compromise their diagnostic value. Of course, since the duration of QRS complexes and QTc intervals is also mediated by the continuously changing underlying electrophysiology, extracardiac inuences due to PERED create a problem for physiologically meaningful evaluation of these ECG parameters. Accordingly, one wonders about the degree to which the data on the QRS duration and the QTc interval in previous studies of patients with CHF and PERED might have been confounded.58 Another outcome of the PERED-based shortening of the QRS duration is the apparent reversible conversion of complete bundle branch blocks and intraventricular conduction delays, to incomplete ones.59 ECG voltage perturbations due to PERED should be expected to exert a similar modulating effect on the P-wave duration, leading to its apparent shortening; however, the issue here may

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be more complex, since the hemodynamic burden on the atria with CHF may lead to P-wave lengthening, thus canceling the effects due to PERED, and resulting in an unchanged P-wave duration.60 However, this matter requires further study. This new insight about the interrelation among PERED/weight, amplitude of ECG potentials, and durations of P waves, QRS complexes, and QTc intervals in patients with CHF can be immediately implemented in the daily practice. One can either use calculated sums of the amplitudes of QRS complexes of all 12 leads, or the 6 limb leads, or only leads I and II. As noted above, the precordial leads are unreliable, compromising by their inclusion calculations deriving from the set of 12 ECG leads. It appears, therefore, that using sums of data from the six limb leads or leads I and II sufces. Correlations of these two sets have been found to be very strong.47 According to this schema, measuring, or even eye-balling leads I and II at the bedside or the clinic examining table will be found very useful while managing patients with CHF. The issues of accuracy of patient weights and uid intake and output data are vexing and frequently a source of frustration for all physicians. In this context, one can use available serial References
1. Madias JE. How I read, and teach others to read, ECGs. J Electrocardiol 2006; 39:110111. 2. Zipes DP, Libby P, Bonow RO, Braunwald E (eds.): Braunwalds Heart Disease: A Textbook of Cardiovascular Medicine, 7th Ed. St. Louis, W.B. Saunders, 2005, p. 107. 3. Macfarlane PW, Veitch Lawrie TD (eds.): Comprehensive Electrocardiology. Theory and Practice in Health and Disease, 1st Ed. New York, Pergamon Press, 1989. 4. Wagner GS. Marriotts Practical Electrocardiography, 10th Ed. Philadelphia, Lippincott Williams & Wilkins, 2001. 5. Zimetbaum PJ, Buxton AE, Batsford W, Fisher JO, Haey GE, Lee KL, OToole MF, et al. Electrocardiographic predictors of arrhythmic death and total mortality in the multicenter unsustained tachycardia trial. Circulation 2004; 110:766769. 6. Mirvis DM Electrocardiography. A physiological approach. St Louis, Mosby, 1993, p. 259. 7. Sanders P, Morton JB, Davidson NC, Spence SJ, Vohra JK, Sparks PB, Kaiman JM. Electrical remodeling of the atria in congestive heart failure: Electrophysiological and electroanatomic mapping in humans. Circulation 2003; 108:14611468. 8. Childers R, Lupovich S, Sochanski M, Konarzewska H. Left bundle branch block and right axis deviation: a report of 36 cases. J Electrocardiol 2000; 33(Suppl):93102. 9. Molhoek SG, VAN Erven L, Bootsma M, Steendijk P, Van der Wall EE, Schalij MJ. QRS duration and shortening to predict clinical response to cardiac resynchronization therapy in patients with endstage heart failure. Pacing Clin Electrophysiol 2004; 27:308313. 10. Das MK, Cheriparambil K, Bedi A, Kassotis J, D ES, Reddy CV, Makan M, et al. Prolonged QRS duration (QRS >/= 170 ms) and left axis deviation in the presence of left bundle branch block: A marker of poor left ventricular systolic function? Am Heart J 2001; 142:756759. 11. Madias JE, Ashtiani R, Agarwal H, Win M, Narayan VK, Sinha A. Diagnosis of myocardial infarction-induced ventricular aneurysm in the presence of complete left bundle branch block. J Electrocardiol 2001; 34:147154. 12. Madias JE, Ashtiani R, Agarwal H, Narayan VK, Win M, Sinha A. Diagnosis of ventricular aneurysm and other severe segmental left ventricular dysfunction consequent to a myocardial infarction in the presence of right bundle branch block: ECG correlates of a

ECGs to corroborate, or disprove the information derived from charted weight values, or uid intake/output records. When the latter two are not available, the author has found serial ECGs to be a very reliable substitute. In conclusion, the combination of the ECG/CHF associations discussed above can materially facilitate the management of patients with CHF. Implementation of the insights about PERED and ECG voltage, in particular, require comparison of parameters in serial ECGs, with a mindset at some quantication. In this respect, quantitative analysis of the ECG may be needed instead of adherence to established thresholds or criteria; accordingly, it is more informative to refer to increase or decrease in the QRS voltage in a specic patient than to establish whether criteria are met for the diagnoses of LVH or low voltage ECG, respectively. Of course, such an approach requires more than a single ECG tracing. Incorporation of these ideas in ones routine is not cumbersome, necessary information derives from ubiquitously available and cheap technology, and interpretation is instant. Finally, it is hoped that the use of the ECG along these lines in the care of patients with CHF will lead to further progress.

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