ECG Leads I and II to Evaluate Diuresis of Patients with Congestive Heart Failure Admitted to the Hospital via the

Emergency Department
SUTHAPORN LUMLERTGUL, M.D.,* BORIBOON CHENTHANAKIJ, M.D.,* and JOHN E. MADIAS, M.D.
From the *Faculty of Medicine of Chiang Mai University, the Emergency Unit of Maharat Nakorn Chiangmai Hospital, Chiang Mai, Thailand, and The Mount Sinai School of Medicine, New York University, New York, New York, and the Division of Cardiology, Elmhurst Hospital Center, Elmhurst, New York

Background: Attenuation of electrocardiogram (ECG) QRS complexes is observed in patients with a variety of illnesses and peripheral edema (PERED), and augmentation with alleviation of PERED. Serial ECGs in stable individuals display variation in the amplitude of QRS complexes in leads V1V6, stemming from careless placement of recording electrodes on the chestwall. Electrocardiographs record only leads I and II, and mathematically derive the other four limb leads in real time. This study evaluated the sum of the amplitudes of ECG leads I and II, along with other sets of ECG leads in the monitoring of diuresis in patients with congestive heart failure (CHF). Methods: Twenty patients with CHF had ECGs and weights recorded on admission and at discharge. The amplitude of the QRS complexes in all ECG leads were measured and sums of I and II, all limb leads, V1V6, and all 12 leads were calculated. Results: There was a good correlation between the weight loss and the increase in the sums of the amplitudes of the QRS complexes from leads I and II (r = 0.55, P = 0.012), and the six limb leads (r = 0.68, P = 0.001), but a poor correlation with the V1V6 leads (r = 0.04, P = 0.85) and all 12 leads (r = 0.1, P = 0.40). Conclusions: Sums of the amplitudes of the ECG QRS complexes from leads I and II constitute a reliable, easily obtainable, ubiquitously available, bedside clinical index, which can be employed in the diagnosis, monitoring of management, and follow-up of patients with CHF. (PACE 2009; 32:6471) congestive heart failure, echocardiography , electrocardiogram, electrophysiologyclinical, biomedical engineering Introduction The standard 12-lead electrocardiogram (ECG) has been used in the diagnosis, management, and prognosis of patients with congestive heart failure (CHF) for many decades. However, its employment by the medical community is not in the form of a useful index for the evaluation and day-to-day monitoring of patients under therapy, with the immediacy of response found in a sensitive test, as the patients lose weight with diuresis. However, such a function is inherently available in serial ECGs, and here is why. A number of reports have shown that the ECG is useful in the diagnosis, monitoring of therapy, and follow-up of patients with various edematous states, including perioperative uid administration, hemodialysis, sepsis, chronic obstructive lung disease with chronic cor pulmonale, CHF, and many others.117 What has been shown in all these conditions is a significant inverse correlation of decrease/increase of the amplitudes of the QRS complexes with an increase/decrease in weight (WT) or uid loss.117 Changes in serial ECGs in patients with edematous states are rampant in the hospital, the clinic, and critical care areas, but are rarely appreciated because many physicians do no know about this ECG/peripheral edema (PERED) interaction. Moreover, physicians are in the habit of reviewing ECGs as isolated tracings rather than by displaying them next to each other in chronological sequence. When the latter approach is taken, physicians are in disbelief, wondering how such a gross change in the ECGs of their patients could have taken place without being detected. Nevertheless, some physicians familiar with the ECG voltage/PERED association are not motivated to use this diagnostic/monitoring feature of the ECG, discouraged by what is viewed as a cumbersome measurement of data from 12 leads with subsequent summation of the measured values, to generate the ECG indices employed in studies.117 Finally, another impediment to use ECGs quantitatively in this setting is

Address for reprints: John E. Madias, M.D., Professor of Medicine (Cardiology), Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373. Fax: 718334-5990; e-mail: madiasj@nychhc.org Received June 3, 2008; revised July 29, 2008; accepted August 29, 2008.

2009, The Authors. Journal compilation

2009, Blackwell Publishing, Inc.

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the variation in the ECG complexes in leads V1 V6 from serial ECGs recorded in clinically stable patients, due to the widespread laxity in placing the chest electrodes at the recommended sites.18,19 A way to deal with the last two problems has been conceived, by rst concentrating only on the changes observed in the six limb ECG leads, and second by taking advantage of the fact that all modern digital electrocardiographs record only leads I and II, and mathematically derive in real time the voltages of the other four limb leads.19,20 Thus, the objective of this study was to determine which lead sets, deriving from the standard ECG correlated best with a prospectively demonstrated diuresis in a small group of selected patients with decompensated CHF admitted to the hospital. Methods Study Population Of the 1,409 adult patients with medical illnesses who presented (not admitted) to the Emergency Department (ED) of the Maharat Nakorn Chiangmai Hospital during a 5-month period starting in June 2007, 49 (3.5%), with acute decompensated CHF, who were admitted and received diuresis were considered. Enrollment criteria on admission consisted of dyspnea at rest, pulmonary crackles on chest auscultation, PERED on inspection and deep palpation of the lower extremities (in some patients), and lung congestion on chest radiography. Eventually, the study was directed at a selected group of 19 CHF patients (20 admissions) who underwent diuresis in hospital with WT measurements at the time of admission (ADM) and discharge (DSC); the remaining 30 patients were excluded, since they were diagnosed as having other comorbidities (myocardial infarction [ve patients], sepsis and anemia [three patients, who did not receive diuresis], and marked right pleural effusion diagnosed by radiography on admission [one patient]), which would have confounded the ECG/WT correlations, or because they were not weighed on ADM, since they could not be transferred to a bedscale due to their profound dyspnea. Study Variables Data on demographics; past and present illnesses; systolic and diastolic blood pressures; heart and respiratory rates; clinical laboratory tests; admission chest radiographs for evidence of pulmonary congestion and/or inltrates; acute respiratory distress syndrome; pleural effusions; pneumothorax; pneumomediastinum; and pericardial effusions; echocardiograms done 1.43 0.53 (range 13) days after ADM, for assessment of cardiac structure and function; and duration

of observation, management, complications, and outcome were considered. WT of the patients on ADM at the ED and prior to DSC and the corresponding percentage WT change were employed as variables. ADM and prior to DSC WTs of the patients were measured and recorded in kilograms, employing a standard hospital WT scale, and under the supervision of a member of the research team. Patients were weighed wearing a hospital gown, both on admission to the ED and prior to DSC. Hospital WT scales were calibrated daily for the purpose of this study. Intravenous furosemide was started in all patients on ADM at a dose of 0.5 1 mg/kg, and was substituted with oral furosemide 4.9 1.52 days later. Three patients received one dose of 50 mg of intravenous nitroglycerin for acute pulmonary edema. Seven patients received oral digoxin and 14 patients an angiotensin converting enzyme inhibitor on days 1 to 3 of hospitalization. Aspirin was given to 14 patients starting on day 1, and 14 patients received a -blocker in days 3 to 5 of hospitalization; 17 patients received an isosorbide dinitrate tablet for chest tightness as needed. ECG Measurements and Variables ECGs were recorded on ADM to the ED, and prior to DSC, at paper speed of 25 mm/s and calibration of 1.0 mV = 10 mm. As expected in some of the patients on ADM the inclination of the upper body during the ECG recording was higher than upon DSG, when clinical improvement permits ECG recordings in a more supine position. Although there is concern about the comparability of ECGs done at different degrees of upper body inclination, prior work from our laboratory showed that comparisons of ECGs done at the extreme positions of supine and standing led only to minor quantitative QRS changes, and thus such ECGs were comparable.21 Measurements of the amplitude (highest positive + lowest negative) deections of the QRS complexes in all ECG leads to the nearest 0.5 mm were made by one of the authors (SL), using calipers and a magnifying glass. For ECGs with atrial brillation (four patients, two of who were in sinus rhythm at DSC), the average of measurements of three consecutive beats was used. The sums of the QRS amplitudes from all ECG leads ( QRS) on ADM and prior to DSC were calculated for each patient. The following four sets of ECG leads were employed as variables: (a) QRS12 = the sums of the QRS voltages in all 12 leads; (b) QRSp = the sums of the QRS voltages of leads V1V6; (c) QR6 = the sums of the QRS voltages of the six limb leads; and (d) the QRS2 = the sums of the QRS voltages of leads I and II. The intraobserver variability of QRS12 in 10 random ECGs evaluated twice was 0.384 0.15% and

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0.44 0.21%, respectively, with a mean value of 0.41 0.04%. The QT interval, QTc interval (QT interval divided by the R R interval in sec), QRS duration, and PR interval were employed as variables. Statistical Analysis All data were entered into a digital spreadsheet at the end of the data collection period. Continuous variables were presented as means SD, and percentage changes (% ) were evaluated with paired t-testing. Percentage change of WT between ADM and DSC was correlated with the corresponding % in the QRS12, QRp, QRS6, and QRS2, using linear regression analysis with the WT as the independent, and the above four ECG variables as the dependent variables. The SPSS/PC 16.0 software for statistical analysis was used (SPSS Inc., Chicago, IL, USA), and a P < 0.05 was taken as statistically signicant.

Results Typical ECG changes before and after diuresis are shown on Figure 1. The patients WT in the ED was 58.29 12.06 kg; all lost WT, with the prior to DSC WT decreasing to 55.74 11.35 kg (P = 0.00002) (Table V). Loss of WT after diuresis led to statistically signicant increase in the sums of ECG QRS voltage for all four sets of ECG leads (Table V and Fig. 2). Correlation of % in QRS12, QRSp, QRS6, and QRS2 with % of WT revealed an r = 0.192, 0.036, 0.679, and 0.552, and P = 0.404, 0.845, 0.001, and 0.012, correspondingly. Demographic and clinical characteristics of the patients are presented in Table II, vital signs and conventional ECG parameters from the ECG at ED are shown in Table III, echocardiographic data are presented in Table IV, and other routine laboratory data from ED and prior to DSC are shown in Table V. Nineteen patients were included in this study, with one admitted

Figure 1. ECG of patient 18 on admission (A) and prior to discharge (B). Some change in the morphology in leads I and aVR between the two ECGs is due to a change in the frontal QRS axis from 77 degrees (A) to 56 degrees (B).

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Figure 2. Absolute mean QRS amplitude changes by the sums of the four ECG sets (white columns represent ED data and black columns represent data prior to DSC) Abbreviations: As in the text).

to the hospital on two separate occasions (20 sets of data). Seventeen patients (18 sets of data) had pulmonary congestion on chest radiography. Patient 8 did not have lung congestion or PERED but had cardiomegaly with decrease in heart size on a repeat chest radiogram, and he had a 3-kg (4%) loss of weight. The other patient (17) without lung congestion on chest radiography had cardiomegaly, did not have a repeat chest radiogram, or PERED, but lost 2 kg (3.64%) of his WT. Thirteen patients had PERED. From the seven patients without PERED, ve had lung congestion by chest radiography, but two (patients 8 and 17, vide supra) did not. No pleural effusion, pneumothorax, or chronic lung disease was detected. Sixteen patients had PERED in their legs on physical examination. Patient 3 died of pulmonary embolism, but prior to his demise he had lost WT and showed improvement in CHF; the other 18 patients were discharged from the hospital alive. Seven patients (2, 5, 9, 10, 13, 15, and 19) had preserved systolic function, but had diastolic dysfunction (Table IV). Discussion More than a half a century ago the German literature2224 suggested that patients with CHF revealed lower QRS voltage in their ECGs during poor clinical compensation associated with heart dilatation, and higher QRS voltage during periods of improvement, and alleviation of cardiomegaly. In 1971, Ishikawa et al.25 showed in 12 patients with CHF that clinical improvement led to an increase in the voltage of the ECG QRS complexes, while poor response resulted in a decrease in the

QRS voltage. These authors observed a decrease in cardiomegaly, as assessed by chest radiography, in the patients who responded to therapy; however, they were at a loss in reference to the mechanism of the ECG phenomenon since they knew that a decrease in the heart volumes due to therapy is expected to be associated with a decrease in the amplitude of the QRS complexes (instead of the increase that they found), as per the Brody effect.26 Thus, they admitted that they could not offer any plausible explanation for their observations.25 In a number of case reports of patients with CHF treated in the hospital and/or observed in the clinic an association of a decrease in the QRS amplitude with WT gain, and of increase in the QRS amplitude with WT and uid loss have been described.4,5,9,12,13 Also in two series of patients treated in the hospital, one with intravenous diuretics over the course of 48 hours7 and one employing a mechanical ultraltration pump,17 the same conclusions were reached. However, both of these studies were retrospective in design. In contrast, this study is the rst to report on a series of consecutive patients with CHF admitted to the hospital via the ED, with employment of the ECG from ADM and DSC paired to the ECGs WTs done prospectively. In all this recent experience, the QRS voltage change with WT gain or loss has been attributed to the extracardiac effect of the passive volume conductor surrounding the heart, by virtue of the changes in the electrical conductivity imparted by changes in the uid content.27,28 Thus, congestion of the tissues and organs embedded in the body volume conductor increases its

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Table I. Admission and Discharge Weights, and Corresponding ECG Variables of Patients Variables Weight (kg) QRS12 (mm) QRSp (mm) QRS6 (mm) QRS2 (mm) ED 58.29 12.06 136.50 45.85 105.52 43.26 31.55 9.63 11.30 4.17 Discharge 56.13 11.21 151.83 41.43 118.17 39.11 36.00 10.01 13.06 4.10 P Value 0.00002 0.003 0.006 0.0002 0.001

Abbreviations: As in the text.

conductivity (due to the reciprocal decrease in the electrical resistance), which in turn leads to decrease in the amplitude of the recorded ECG potentials at the body surface. In contrast, alleviation of the tissue congestion via diuresis leads to a decrease in conductivity (due to the reciprocal increase in the electrical resistance), which leads to an increase in the amplitude of the recorded ECG

potentials at the body surface.1 Limited experience in a single patient with CHF and one patient who underwent multiple sessions of hemodialysis showed a relationship of changes in WT, amplitudes of the QRS complexes, and electrical resistance measured at the body surface.2,5 What is new in this study is that the decrease in the WT in these patients with CHF between ED and DSC, resulting from diuresis, correlated well with the increase in the sum of the QRS amplitudes from ECG leads I and II. The original 49 patients were representative of what one encounters in the ED the world over, regarding demographics, underlying pathology, clinical characteristics, ECG measurements, WT loss resulting from diuresis during hospitalization, and length of observation (Tables IV); certainly by including only 39% of these patients the studied subgroup was transformed to a selective one, and it should be considered as such. Of course the objective of this study was to evaluate the contribution of the ECG in reecting diuresis in patients with CHF, and in this respect, patients with confounding comorbidities (see Methods) had to be excluded. Also a large number of patients could not be weighed

Table II. Demographic Data and Clinical Characteristics of the Patients Age (Years) 54 76 46 74 51 35 73 59 68 80 60 53 49 80 52 28 45 70 73 Gender (M/F) M F M F F F M M F F M M F M M M F M F Observation (days) 9 11 10 6 28 19 7 4 5 4 5 6 3 6 10 6 11 11 6 Present Illnesses CHF HypoCa, ARF, CHF CHF CHF CHF CHF CHF CHF CHF CHF CHF CHF, PNEU CHF CHF, ARF CHF CHF CHF CHF CHF

Patient 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19

Past History HYP ANM AF, MS, MR HYP, ANM Interstitial lung disease, Hashimoto thyroiditis DM, Thalassemia, cirrhosis HYP, CAD HYP, CAD DysL, CAD, UTI COPD DCM, DM, HYP, DysL PNEU HYP, DM, CAD, ANM ANM HIV HYP HYP, CKD COPD, CAD

Abbreviations: AF = atrial brillation; ANM = anemia; ARF = acute renal failure; CAD = coronary artery disease; CHF = congestive heart failure; CKD = chronic kidney disease; COPD = chronic obstructive pulmonary disease; DCM = dilated cardiomyopathy; DM = diabetes mellitus; DYSL = dyslipidemia; HIV = human immunodeciency virus infection; HYP = hypertension; hypoCa = hypocalcemia; MR = mitral valve regurgitation; MS = mitral valve stenosis; PNEU = pneumonia; UT I = urinary tract infection.

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Table III. Vital Signs and Other ECG Parameters Parameters Systolic BP Diastolic BP Heart Rate PR interval QT interval QTc interval QRS width QRS axis ED 117.2 13.77 79.00 25.41 88.00 21.00 180.00 68.83 364.33 84.24 457.25 57.30 102.75 29.31 45.75 62.50 Discharge 108.8 20.68 82.6 19.11 88.3 10.37 183.43 48.47 406.67 61.37 470.83 47.63 105.58 28.33 21.25 54.96 % Change 17.02 15.19 33.84 26.16 18.57 14.78 8.38 0.08 16.6 12.87 10.05 9.89 5.38 3.70 18.30 11.33 P value 0.35 0.737 0.951 0.003 0.02 0.464 0.185 0.61

Table IV. Echocardiographic Findings Patient 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 Echocardiographic Findings DCM, MS, AR, S/P MVR AVR, TVR, LVSD Inferior HK, no LVSD DCM, severe LVSD Inferior HK, LVSD RVF, severe PHT, TR, chronic IE, no LVSD Restrictive cardiomyopathy, hemochromatosis DCM, severe LVSD Mild TR, PR, MR, dilated RV, no RVF, PHT, severe LVSD Severe MR, CAD mod PHT, no LVSD, no RVF DD, HOCM Dilated LV and LA, no RVF, LVSD LVSD, anteroseptal wall HK, LVSD DD, mild LA dilate, mild anterolateral HK Severe MR, moderate TR, AF No LVSD DCM, severe TR, LVSD Severe AR, moderate MS, severe TR, severe LVSD Ischemic DCM S/P CABG, dilate LV chamber, severe LVSD DD, no chamber dilatation

on admission due to the gravity of their clinical presentation; this underscores the importance of potentially employing an alternative to the WT index of body uid status in patients who cannot be weighed on ADM. WT and sums of amplitudes of QRS complexes in all four ECG sets analyzed showed statistically signicant alterations between ED and DSC (Table I). However, correlations of % of WT and ECG QRS complexes were statistically signicant only for the QRS6 and QRS2, conrming our hypothesis that information from leads V1V6 exclusively, or inclusion of these leads as part of the 12-lead ECG, renders the ECG unreliable and unt for WT/ECG correlations. Moreover, the success of the QRS2, suggests that mere eye-balling of leads I and II, and mentally summing up their QRS amplitudes, in serial ECGs recorded in the same patient at different time points during the clinical course may be useful in providing instant information regarding the degree of clinical compensation of the patient with CHF. In this study only ECGs from the ED and prior to DSC were employed; however, an index ECG

Table V. Routine Laboratory Parameters Parameter ED DC P Value 0.13 0.19 0.31 0.24 0.77 0.05

Abbreviations: DCM = dilated cardiomyopathy; MS = mitral stenosis; AR = aortic regurgitation; AVR = aortic valve replacement; S/P = post operative; MVR = mitral valve replacement; TVR = tricuspid valve replacement; HK = hypokinesis; LVSD = left ventricle systolic dysfunction; RVF = right ventricle failure; PHT = pulmonary hypertension; TR = tricuspid regurgitation; IE = infectious endocarditis; PR = pulmonary regurgitation; MR = mitral valve regurgitation; CAD = coronary artery disease; LA = left atrium; DD = diastolic dysfunction; HOCM = hypertrophic cardiomyopathy; AF = atrial brillation; CABG = coronary artery bypass; LV = left ventricle; RV = right ventricle.

BUN (mg/dL) 16.40 15.5 13.5 10.04 Creatinine (mg/dL) 1.59 0.83 1.47 0.47 Hb (g/dL) 8.65 4.37 9.65 3.51 Hct (%) 26.68 0.90 29.78 8.37 K+ (mEq/L) 3.71 0.54 3.76 0.49 HCO3 (mg/dL) 22.17 4.17 26.33 2.07
Abbreviations: As in the text.

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can be compared with previous tracings, or subsequent ECGs in the clinic or the hospital. Also, instead of using only two ECGs, one could evaluate serial ECGs in the monitoring of patients undergoing therapy in the hospital (day-to-day) or clinic (clinic appointment-to-clinic-appointment), emphasizing only the limb leads (or leads I and II), since the precordial leads are subject to large variations in serial ECGs, and thus are unreliable for comparisons. Of course the above is speculative, and it should be tested in a properly designed prospective study. This clinical insight can be found useful also when serial weighing of the patient has not been done, was done erratically or inappropriately, or recording of WT values was not done or was done improperly (this applies to both weights obtained in the hospital or clinic, or in the patients home or other residence). Too frequently, there is ambivalence whether a patient has responded to diuresis when records of uid intake/output are poorly maintained, and patients WTs cannot be relied upon (e.g., use of bedscales in the hospital with a variety of articles on the patients bed at different times, or different clothes being worn by a patient at different clinic appointments, depending on the season). Only 30% and 46% of the changes in the QRS amplitude in leads I and II and all six limb leads can be explained by changes in WT; probably the small number of patients and a host of other parameters (e.g., cardiac volumes, lung congestion) could have been also exerting a confounding effect, thus decreasing the degree of correlation between changes in WT and amplitudes of QRS complexes. Weighing the patients daily is an inexpensive, noninvasive procedure, and thus we do not advocate replacing it with a more complicated method that shows only modest correlation. However, many times when discrepancies in the WT records occur the ECG may be of clinical value. Other potential inuences on the surface ECG in patients undergoing diuresis is the resultant increase in hemoglobin (Hb)/hematocrit (Ht) due to hemoconcentration. An increase in Hb/Ht is expected to be associated with a decrease in the amplitude of QRS complexes as shown in previous theoretical, animal and clinical studies,2732 the opposite of what was documented in this study. Also, K+ changes are thought to have a number of References
1. Madias JE, Bazaz R, Agarwal H, Win M, Medepalli L. Anasarcamediated attenuation of the amplitude of electrocardiogram complexes: A description of a heretofore unrecognized phenomenon. J Am Coll Cardiol 2001; 38:756764. 2. Madias JE, Narayan V. Augmentation of the amplitude of electrocardiographic QRS complexes immediately after hemodialysis: A study of 26 hemodialysis sessions of a single patient, aided by measurements of resistance, reactance, and impedance. J Electrocardiol 2003; 36:263267.

inuences on the ECG curve, mainly affecting the ST segments and the T waves; however, no specic effects have been noted in association with the usual range of K+ values encountered in patients with CHF. There were no signicant changes in Hb/Ht, or serum K+ values in the present study, and only mild increase in the serum bicarbonate was noted between the ED and DSC in our patients (Table IV). This corroborates our previous work in patients with CHF, where Hb/Ht, serum Na+ , K+ , Mg++ , BUN, and creatinine did not show changes with diuresis in patients with CHF.7,17 Also previous workers found no signicant changes in Hb/Ht and electrolytes before and after diuresis of patients with CHF.25 It is interesting that both increase in HB/Ht and alleviation of cardiomegaly after diuresis are expected to produce decrease in the amplitude of the ECG QRS complexes, the opposite observed in our study. Consequently, if any inuence could be considered of these two parameters in addition to loss of WT after diuresis in patients with CHF, that would be of a mitigation of the augmentation of the increase in the amplitude of the QRS complexes. Thus it appears that the main demonstrable determinant of QRS increase with diuresis in patients with CHF is the loss of interstitial uid and resultant WT loss. The nding of the reciprocal change of body weight/ECG QRS voltage with diuresis awaits routine application in the diagnosis and monitoring of therapy in patients with CHF. This study should be considered a pilot work, and has some limitations, particularly due to its small sample size, and the large number of patients excluded on ADM. Also the excluded patients were not weighed and had not ECGs prior to DSC, preventing us from performing an intention-to-treat. In addition to the on treatment analysis, thus, these results may apply only to a minority of the patients admitted with a possible acute CHF failure and only after exclusion of the above mentioned exclusion conditions. A much larger prospective study of patients with CHF is needed to corroborate our ndings, before recommendations for implementation of an ECG index, employing the limb leads or leads I and II, can be made. Also, such a study should probably include serial WT and ECG assessments, and echocariographic volume measurements on ADM and prior to DSC.

3. Madias JE. A comparison of 2-lead, 6-lead, and 12-lead ECGs in patients with changing edematous states: Implications for the employment of quantitative electrocardiography in research and clinical applications. Chest 2003; 124:20572063. 4. Madias JE, Agarwal H, Win M, Medepalli L. Effect of weight loss in congestive heart failure from idiopathic dilated cardiomyopathy on electrocardiographic QRS voltage. Am J Cardiol 2002; 89:8688. 5. Madias JE, Attanti S, Narayan V. Relationship among electrocardiographic potential amplitude, weight, and resistance/

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reactance/impedance in a patient with peripheral edema treated for congestive heart failure. J Electrocardiol 2003; 36:167171. Madias JE. Amplitude of the electrocardiographic QRS complexes during and after severe pulmonary edema. Ann Noninvasive Electrocardiol 2004; 9:192197. Madias JE, Song J, White CM, Kalus JS, Kluger J. Response of the ECG to short-term diuresis in patients with heart failure. Ann Noninvasive Electrocardiol 2005; 10:288296. Madias JE, Madias NE. Reversible attenuation of the ECG voltage due to peripheral edema associated with treatment with a COX-2 inhibitor. Congest Heart Fail 2006; 12:4650. Madias JE. Congestive heart failure, peripheral edema, and standard and signal-averaged ECGs. Congest Heart Fail 2006; 12:179180. Madias JE. Reversible attenuation of voltage of QRS complexes and P waves and shortening of QRS duration and QTc interval consequent to large perioperative intravenous uid infusions. J Electrocardiol 2006; 39:415418. Drighil A, Madias JE, Yazidi A, Bennani M, Bennis A, Ramdan B, Tahiri A. P-wave and QRS complex measurements in patients undergoing hemodialysis. J Electrocardiol 2008; 41:60.e160.e7. Madias JE. ECG changes in response to diuresis in an ambulatory patient with congestive heart failure. Congest Heart Fail 2006; 12:277 283. Madias JE. Superiority of the limb leads over the precordial leads on the 12-lead ECG in monitoring uctuating uid overload in a patient with congestive heart failure. J Electrocardiol 2007; 40:395 399. Madias JE. Low voltage ECG in myocarditis: Peripheral edema as a plausible contributing mechanism. Pacing Clin Electrophysiol 2007; 30:448452. Drighil A, Madias JE, Mosalami HE, Badaoui NE, Bennis A, Mouine B, Fadili W, et al. Determinants of augmentation of ECG QRS complexes and R waves in patients after hemodialysis. Ann Noninvasive Electrocardiol 2007; 12:111120. Madias JE. Manual-based versus automation-based measurements of the amplitude of QRS complexes and T waves in patients with changing edematous states: Clinical implications. J Electrocardiol 2008; 41:1518. Madias JE, Guglin ME. Augmentation of ECG QRS complexes after uid removal via a mechanical ultraltration pump in patients with congestive heart failure. Ann Noninvasive Electrocardiol 2007; 12:291297. Herman MV, Ingram DA, Levy JA, Cook JR, Athans RJ. Variability of electrocardiographic precordial lead placement: A method to improve accuracy and reliability. Clin Cardiol 1991; 14:469476. 19. Wagner GS. Marriotts Practical Electrocardiography, 10th Ed. Philadelphia, Lippincott Williams & Wilkins, 2001, pp. 29, 34. 20. Kligeld P, Gettes LS, Bailey JJ, Childers R, Deal BJ, Hancock EW, van Herpen G, et al. Recommendations for the standardization and interpretation of the electrocardiogram: Part I: The electrocardiogram and its technology: A scientic statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2007; 49:11091127. 21. Madias JE. Comparability of the standing and supine standard electrocardiograms and standing sitting and supine stress electrocardiograms. J Electrocardiol 2006; 39:142149. 22. Schaefer H. Das Electrokardiogram, Theorie und Klinik. Berlin, Springer-Verlag, 1951, p. 67. 23. Geppert MP, Schaefer H. Statistiche Undersuchugen uber die Beziehingen zwischen Herzgrosse und Maximalspannung von QRS im EKG. Arch Kreislauf-forsh 1951; 17:104116. 24. Friese G. Klinische Beobachtungen uber die Spannugsabuahme des Elekrokardiogramms bei Dilatation des Herzens Z. Kreislaufforsch 1955; 45:99. 25. Ishikawa K, Berson AS, Pipberger HW. Electrocardiographic changes due to cardiac enlargement. Am Heart J 1971; 81:635643. 26. Brody DA. A theoretical anlysis of intracavitary blood mass inuence on the electrocardiogram. Circ Res 1956; 4:731738. 27. Geddes LA, Baker LE. The specic resistance of biological material a compendium of data for the biomedical engineer and physiologist. Med Biol Eng 1967; 5:271293. 28. Rudy Y, Plonsey R, Liebman J. The effects of variation in conductivity and geometrical parameters on the electrocardiogram, using an eccentric spheres model. Circ Res 1979; 444:104111. 29. Oreto G, Luzza F, Donato A, Satullo G, Calabro ` MP, Consolo A, Arrigo F. Electrocardiographic changes associated with haematocrit variations. Eur Heart J 1992; 13:634637. 30. Rudy Y. The electrocardiogram and its relationship to excitation of the heart. In: Sperelakis N (ed.): Physiology and Pathophysiology of the Heart, 3rd Ed. Amsterdam, Kluwer Academic Publishers, 1995, p. 201. 31. Nelson CV, Rand PW, Angelakos ET, Hugenholtz PG. Effect of intracardiac blood on the spatial vectorcardiogram. I. Results in the dog. Circ Res 1972; 31:95104. 32. Rosenthal A, Restieaux NJ, Feig SA. Inuence of acute variations in hematocrit on the QRS complex of the Frank electrocardiogram. Circulation 1971; 44:456465.

6. 7. 8. 9. 10.

11. 12. 13.

14. 15.

16.

17.

18.

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