- Email: [email protected]
Significance of shortening of the mean QRS duration of the standard electrocardiogram in patients developing peripheral edema
Significance of Shortening of the Mean QRS Duration of the Standard Electrocardiogram in Patients Developing Peripheral Edema John E. Madias,
MD
n electrocardiographic syndrome was reported recently linking a gradual decrease in the QRS poA tentials of the standard electrocardiogram (ECG) with a parallel development of peripheral edema in patients with a critical illness of varying etiology.1 In that study, a decrease in the sums of QRS amplitude of 12-lead ECGs (⌺QRS) correlated well with weight gain (r ⫽ 0.61, p ⫽ 0.0005). Perusal of the daily ECGs from that study revealed gradual shortening of the mean QRS duration. To investigate this matter further, a documentation of the decrease in the mean QRS duration and an analysis of its relation with weight and ⌺QRS was carried out. The objectives of this study were: (1) to define whether mean QRS duration correlates with weight gain; (2) to determine whether it has any advantages when compared with ⌺QRS in predicting weight gain; and (3) to determine whether it provides a better indicator of weight gain when combined with ⌺QRS in a form of a product. Speculation as to the mechanism of decrease in the mean QRS duration consequent to weight gain is also included in this study. •••
The study population and the methods employed have been previously described.1 For the purposes of this study, data from the consecutive series of 28 patients with peripheral edema admitted to our Coronary Care Unit in 1999 with a critical illness were reevaluated. The patients had daily weights and electrocardiographic tracings recorded. Information on percent change of weight from admission to the point of peak weight value, and half-weight gain were used as study parameters. The ⌺QRS and mean QRS duration and the percent change of ⌺QRS and mean QRS duration from admission to the peak weight and half-weight points were also considered. In addition, a composite variable consisting of the product of ⌺QRS and mean QRS duration of the corresponding ECG was included. ⌺QRS was calculated as the sum of the QRS complex amplitudes (highest positive ⫹ lowest negative deflection) of all electrocardiographic leads, measured to the nearest 0.5 mm, using a magnifying glass and calipers (Figure 1). The average of measurements of 3 consecutive beats was used for ECGs of patients with atrial fibrillation. The Hewlett-Packard (now acquired by Royal From the Division of Cardiology, Elmhurst Hospital Center, Elmhurst; and the Mount Sinai School of Medicine/New York University, New York, New York. Dr. Madias’ address is: Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, New York 11373. E-mail: [email protected]. Manuscript received December 12, 2001; revised manuscript received and accepted February 15, 2002.
1444
©2002 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 89 June 15, 2002
FIGURE 1. ECGs from patient 1 obtained on admission (A), at peak weight (B), and at subsequent lowest weight (C). QRS durations were 83, 58, and 75 ms at (A), (B), and (C), respectively. ⌺QRS ⴝ sums of amplitudes of QRS complexes of all 12 electrocardiographic leads. (Reprinted with permission from the American College of Cardiology [J Am Coll Cardiol 2001;38:756–764].)
Philips Electronics, Eindhoven, The Netherlands) PageWriter XLi electrocardiograph, model M1700A was used for recording the ECGs. Measurements of mean QRS duration, representative of the entire ECG, were automatically provided by the Hewlett-Packard electrocardiographic analysis program.2 Calibration was 1.0 mV ⫽ 1.0 cm. The intraobserver variability of ⌺QRS was found previously in 10 random ECGs to be 0.41 ⫾ 3.34%.1 All data were continuous and are reported as mean ⫾ 1 SD. Mean QRS duration from admission and time point of peak weight and half-weight gain were compared with Student’s t test for paired data. The relation of mean QRS duration and ⌺QRS was evaluated by Pearson’s correlation. Bivariate regression analysis was used considering the percent change of mean 0002-9149/02/$–see front matter PII S0002-9149(02)02367-6
TABLE 1 Correlations and/or Regressions of Electrocardiographic Data and Weights from Patients With Peripheral Edema Variables A B A B A B
%⌬QRSd (⫺11.4⫾19.3%) %⌬QRSd (⫺13.5⫾12.3%) %⌬QRSd (⫺11.4⫾19.3%) %⌬QRSd (⫺13.5⫾12.3%) %⌬⌺QRS ⫻ QRSd (⫺50.5⫾21.6%) %⌬⌺QRS ⫻ QRSd (⫺59.6⫾16.6%)
vs vs vs vs vs vs
%⌬⌺QRS (⫺41.2⫾14.7%) %⌬⌺QRS (⫺54.2⫾15.4%) %⌬WT (16.9⫾10.7%) %⌬WT (48.9⫾28.1%) %⌬WT (16.9⫾10.7%) %⌬WT (48.9⫾28.1%)
r
p Value
0.18 0.62 0.12 0.29 0.36 0.59
0.35 0.0005 0.54 0.13 0.06 0.001
A ⫽ data at half-weight gain; B ⫽ data at peak weight gain; %⌬ ⫽ percent change; ⌺QRS ⫽ sums of the amplitudes of all ECG leads; QRSd ⫽ QRS duration; ⌺QRS ⫻ QRSd ⫽ product of ⌺QRS and QRSd; WT ⫽ weight.
QRS duration and percent change of the product of ⌺QRS and mean QRS duration at peak weight and half-weight gain as the dependent and the corresponding percent change in weight as the independent variables.3 The SPSS/PC⫹ 4.0.1 (SPSS Inc., Chicago, Illinois) statistical package was employed.4 A p value of ⬍0.05 was considered statistically significant. Mean QRS duration on admission and at halfweight gain points were 104.1 ⫾ 30.6 ms and 91.4 ⫾ 26.7 ms, respectively (p ⫽ 0.01). Mean QRS duration at peak weight gain point was 89.5 ⫾ 27.9 ms, and comparison with the mean QRS duration on admission revealed a p ⫽ 0.0005. The products of ⌺QRS and mean QRS duration on admission and at half-weight gain point were 12,625.1 ⫾ 5,720.8 and 6,698.1 ⫾ 3,870.5 mm 䡠 ms, respectively (p ⫽ 0.0005). The product of ⌺QRS and mean QRS duration at peak weight was 5,229.9 ⫾ 3,526.7 mm 䡠 ms, and comparison with the product of ⌺QRS and mean QRS duration on admission revealed a p ⫽ 0.0005. Correlations and/or regressions of electrocardiographic data and weights are listed in Table 1. A close relation of the percent change in mean QRS duration with percent change in ⌺QRS and percent change in the product of ⌺QRS and mean QRS duration percent change in weight between admission and peak weight gain point was found. •••
The findings derived from this investigation are that: (1) significant shortening of the mean QRS duration of the standard ECG takes place over time when patients develop peripheral edema; (2) mean QRS duration shortening correlates strongly with attenuation of ⌺QRS at peak weight gain, but not at halfweight gain; (3) mean QRS duration shortening does not correlate with changes in weight, in contrast to change in ⌺QRS, which correlates strongly with weight gain; and (4) change of the composite parameter of the product of ⌺QRS and mean QRS duration correlates well with peak weight (Table 1). The electrical potentials recorded in the surface ECG reflect activity of the cardiac generator (both action potentials and the spread of excitation in the heart) and the influence of the intervening inhomogeneous conducting medium between the heart and the recording electrodes.5,6 Alterations in the attributes or the geometry of the volume conductor influence the
amplitude of QRS complexes, as has been previously described,5 and also been shown recently in patients who developed peripheral edema.1 Intuitively, it should not be expected that changes of the volume conductor properties will have any influence on the duration of the ventricular conduction, as perceived at the body surface. Certainly there must be some delay in its detection (both the onset and offset), depending on the characteristics of the conducting medium, but the total duration of conduction is not expected to change. More specifically, if we assume that patients who developed peripheral edema had not experienced any cardiac electrophysiologic alterations, then changes in the surface ECG should be totally attributed to alterations in the extracardiac conducting medium. This contention can be supported in the case of peripheral edema where marked augmentation of the surface ECG occurred, as a result of large fluid removal with veno-venous hemofiltration, whereas the intracardiac electrograms remained unchanged.1 In an idealized surface electrocardiographic recording system, the QRS duration would be expected to be similar to the time interval from the onset to the completion of cardiac excitation. However, as the electrocardiographic potentials were acquired with our standard electrocardiographic recording devices, at a finite resolution (5, in the case of our equipment),2 certain portions of the onset and offset of the QRS complex (after its overall attenuation from peripheral edema) reached the recording electrodes at subthreshold microvolt amplitudes, and therefore, were not detected. This resulted in a measured shortened mean QRS duration.2 Therefore, the gradual shortening of mean QRS duration, as a result of peripheral edema, is more apparent than real. An analogy thus emerges that as the attenuation of ⌺QRS in patients with peripheral edema does not imply a reduction in the cardiac potentials as they will be recorded on the surface of the heart, so is the shortened mean QRS duration an artifact of the recording apparatus rather than an indication of an abbreviated ventricular depolarization. Differences in the correlations between mean QRS duration and ⌺QRS with the change in weight in patients with peripheral edema must be related to methodologic reasons. In principle both these 2 electrocardiographic parameters are expected to be strong correlates of weight gain in patients with peripheral edema. However, ⌺QRS is the sum of peak-to-peak BRIEF REPORTS
1445
amplitudes of all of the 12 electrocardiographic leads that were manually calculated, whereas mean QRS duration is an electronically derived index of the entire electrocardiographic tracing, as calculated by the electrocardiographic analysis program.2 As to the product of ⌺QRS and mean QRS duration, there is some artificiality about its adoption, intended to combine the attributes of the 2 terms of the product. Perhaps instead of using the peak-to-peak amplitude or the duration of QRS complexes, the QRS area may be more electrophysiologically appealing. Calculation of the QRS area in Ashman units (1 such unit ⫽ 40 ms ⫻ 0.1 mV) in all of the 12 electrocardiographic leads is provided by the “extended measurements report” of the Hewlett-Packard analysis program,2 and can be used to calculate a sum of areas for the entire 12-lead ECG. It would be of interest to evaluate such a parameter for its correlation with weight gain or subsequent loss in patients who develop peripheral edema. In conclusion, a close relation of percent change in mean QRS duration (QRSd) with percent change in the sum of the amplitudes of QRS com-
1446 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 89
plexes (⌺QRS), and percent change in ⌺QRS ⴛ QRSd with percent change in weight between admission and time of peak weight gain was found in 28 patients who developed anasarca as a result of a critical illness of varying etiology. No such correlations as the above were noted at the time point of half peak weight gain. The shortening of the mean QRSd was considered to be more apparent than real, and was attributed to failure to detect parts of the onset and offset of QRS complexes stemming from their subthreshold (for detection) amplitudes. 1. Madias JE, Bazaz R, Agarwal H, Win M, Medepalli L. Anasarca-mediated
attenuation of the amplitude of ECG complexes: a description of a heretofore unrecognized phenomenon. J Am Coll Cardiol 2001;38:756 –764. 2. Hewlett-Packard Interpretive Cardiograph. Physician’s Guide HP Part No. M1700 –92908, Edition 4, Printed in USA September 1994:3–3, 4 –3, 4 – 4, C-1-C9. 3. Colton T. Statistics in Medicine. 1st Edition. Boston, MA: Little, Brown and Company, 1974:17, 33, 120. 4. Norusis MJ. The SPSS Guide to Data Analysis for PDD/PC⫹. 2nd ed. Chicago, IL: 1991:244,362,374,390. 5. Rudy Y, Liebman J. The effects of variations in conductivity and geometrical parameters on the electrocardiogram, using an eccentric spheres model. Circ Res 1979;44:104 –111. 6. Surawicz B. Electrophysiologic Basis of ECG and Cardiac Arrhythmias. Baltimore, MD: Williams & Wilkins, 1995:493–496, 498.
JUNE 15, 2002
MD
n electrocardiographic syndrome was reported recently linking a gradual decrease in the QRS poA tentials of the standard electrocardiogram (ECG) with a parallel development of peripheral edema in patients with a critical illness of varying etiology.1 In that study, a decrease in the sums of QRS amplitude of 12-lead ECGs (⌺QRS) correlated well with weight gain (r ⫽ 0.61, p ⫽ 0.0005). Perusal of the daily ECGs from that study revealed gradual shortening of the mean QRS duration. To investigate this matter further, a documentation of the decrease in the mean QRS duration and an analysis of its relation with weight and ⌺QRS was carried out. The objectives of this study were: (1) to define whether mean QRS duration correlates with weight gain; (2) to determine whether it has any advantages when compared with ⌺QRS in predicting weight gain; and (3) to determine whether it provides a better indicator of weight gain when combined with ⌺QRS in a form of a product. Speculation as to the mechanism of decrease in the mean QRS duration consequent to weight gain is also included in this study. •••
The study population and the methods employed have been previously described.1 For the purposes of this study, data from the consecutive series of 28 patients with peripheral edema admitted to our Coronary Care Unit in 1999 with a critical illness were reevaluated. The patients had daily weights and electrocardiographic tracings recorded. Information on percent change of weight from admission to the point of peak weight value, and half-weight gain were used as study parameters. The ⌺QRS and mean QRS duration and the percent change of ⌺QRS and mean QRS duration from admission to the peak weight and half-weight points were also considered. In addition, a composite variable consisting of the product of ⌺QRS and mean QRS duration of the corresponding ECG was included. ⌺QRS was calculated as the sum of the QRS complex amplitudes (highest positive ⫹ lowest negative deflection) of all electrocardiographic leads, measured to the nearest 0.5 mm, using a magnifying glass and calipers (Figure 1). The average of measurements of 3 consecutive beats was used for ECGs of patients with atrial fibrillation. The Hewlett-Packard (now acquired by Royal From the Division of Cardiology, Elmhurst Hospital Center, Elmhurst; and the Mount Sinai School of Medicine/New York University, New York, New York. Dr. Madias’ address is: Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, New York 11373. E-mail: [email protected]. Manuscript received December 12, 2001; revised manuscript received and accepted February 15, 2002.
1444
©2002 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 89 June 15, 2002
FIGURE 1. ECGs from patient 1 obtained on admission (A), at peak weight (B), and at subsequent lowest weight (C). QRS durations were 83, 58, and 75 ms at (A), (B), and (C), respectively. ⌺QRS ⴝ sums of amplitudes of QRS complexes of all 12 electrocardiographic leads. (Reprinted with permission from the American College of Cardiology [J Am Coll Cardiol 2001;38:756–764].)
Philips Electronics, Eindhoven, The Netherlands) PageWriter XLi electrocardiograph, model M1700A was used for recording the ECGs. Measurements of mean QRS duration, representative of the entire ECG, were automatically provided by the Hewlett-Packard electrocardiographic analysis program.2 Calibration was 1.0 mV ⫽ 1.0 cm. The intraobserver variability of ⌺QRS was found previously in 10 random ECGs to be 0.41 ⫾ 3.34%.1 All data were continuous and are reported as mean ⫾ 1 SD. Mean QRS duration from admission and time point of peak weight and half-weight gain were compared with Student’s t test for paired data. The relation of mean QRS duration and ⌺QRS was evaluated by Pearson’s correlation. Bivariate regression analysis was used considering the percent change of mean 0002-9149/02/$–see front matter PII S0002-9149(02)02367-6
TABLE 1 Correlations and/or Regressions of Electrocardiographic Data and Weights from Patients With Peripheral Edema Variables A B A B A B
%⌬QRSd (⫺11.4⫾19.3%) %⌬QRSd (⫺13.5⫾12.3%) %⌬QRSd (⫺11.4⫾19.3%) %⌬QRSd (⫺13.5⫾12.3%) %⌬⌺QRS ⫻ QRSd (⫺50.5⫾21.6%) %⌬⌺QRS ⫻ QRSd (⫺59.6⫾16.6%)
vs vs vs vs vs vs
%⌬⌺QRS (⫺41.2⫾14.7%) %⌬⌺QRS (⫺54.2⫾15.4%) %⌬WT (16.9⫾10.7%) %⌬WT (48.9⫾28.1%) %⌬WT (16.9⫾10.7%) %⌬WT (48.9⫾28.1%)
r
p Value
0.18 0.62 0.12 0.29 0.36 0.59
0.35 0.0005 0.54 0.13 0.06 0.001
A ⫽ data at half-weight gain; B ⫽ data at peak weight gain; %⌬ ⫽ percent change; ⌺QRS ⫽ sums of the amplitudes of all ECG leads; QRSd ⫽ QRS duration; ⌺QRS ⫻ QRSd ⫽ product of ⌺QRS and QRSd; WT ⫽ weight.
QRS duration and percent change of the product of ⌺QRS and mean QRS duration at peak weight and half-weight gain as the dependent and the corresponding percent change in weight as the independent variables.3 The SPSS/PC⫹ 4.0.1 (SPSS Inc., Chicago, Illinois) statistical package was employed.4 A p value of ⬍0.05 was considered statistically significant. Mean QRS duration on admission and at halfweight gain points were 104.1 ⫾ 30.6 ms and 91.4 ⫾ 26.7 ms, respectively (p ⫽ 0.01). Mean QRS duration at peak weight gain point was 89.5 ⫾ 27.9 ms, and comparison with the mean QRS duration on admission revealed a p ⫽ 0.0005. The products of ⌺QRS and mean QRS duration on admission and at half-weight gain point were 12,625.1 ⫾ 5,720.8 and 6,698.1 ⫾ 3,870.5 mm 䡠 ms, respectively (p ⫽ 0.0005). The product of ⌺QRS and mean QRS duration at peak weight was 5,229.9 ⫾ 3,526.7 mm 䡠 ms, and comparison with the product of ⌺QRS and mean QRS duration on admission revealed a p ⫽ 0.0005. Correlations and/or regressions of electrocardiographic data and weights are listed in Table 1. A close relation of the percent change in mean QRS duration with percent change in ⌺QRS and percent change in the product of ⌺QRS and mean QRS duration percent change in weight between admission and peak weight gain point was found. •••
The findings derived from this investigation are that: (1) significant shortening of the mean QRS duration of the standard ECG takes place over time when patients develop peripheral edema; (2) mean QRS duration shortening correlates strongly with attenuation of ⌺QRS at peak weight gain, but not at halfweight gain; (3) mean QRS duration shortening does not correlate with changes in weight, in contrast to change in ⌺QRS, which correlates strongly with weight gain; and (4) change of the composite parameter of the product of ⌺QRS and mean QRS duration correlates well with peak weight (Table 1). The electrical potentials recorded in the surface ECG reflect activity of the cardiac generator (both action potentials and the spread of excitation in the heart) and the influence of the intervening inhomogeneous conducting medium between the heart and the recording electrodes.5,6 Alterations in the attributes or the geometry of the volume conductor influence the
amplitude of QRS complexes, as has been previously described,5 and also been shown recently in patients who developed peripheral edema.1 Intuitively, it should not be expected that changes of the volume conductor properties will have any influence on the duration of the ventricular conduction, as perceived at the body surface. Certainly there must be some delay in its detection (both the onset and offset), depending on the characteristics of the conducting medium, but the total duration of conduction is not expected to change. More specifically, if we assume that patients who developed peripheral edema had not experienced any cardiac electrophysiologic alterations, then changes in the surface ECG should be totally attributed to alterations in the extracardiac conducting medium. This contention can be supported in the case of peripheral edema where marked augmentation of the surface ECG occurred, as a result of large fluid removal with veno-venous hemofiltration, whereas the intracardiac electrograms remained unchanged.1 In an idealized surface electrocardiographic recording system, the QRS duration would be expected to be similar to the time interval from the onset to the completion of cardiac excitation. However, as the electrocardiographic potentials were acquired with our standard electrocardiographic recording devices, at a finite resolution (5, in the case of our equipment),2 certain portions of the onset and offset of the QRS complex (after its overall attenuation from peripheral edema) reached the recording electrodes at subthreshold microvolt amplitudes, and therefore, were not detected. This resulted in a measured shortened mean QRS duration.2 Therefore, the gradual shortening of mean QRS duration, as a result of peripheral edema, is more apparent than real. An analogy thus emerges that as the attenuation of ⌺QRS in patients with peripheral edema does not imply a reduction in the cardiac potentials as they will be recorded on the surface of the heart, so is the shortened mean QRS duration an artifact of the recording apparatus rather than an indication of an abbreviated ventricular depolarization. Differences in the correlations between mean QRS duration and ⌺QRS with the change in weight in patients with peripheral edema must be related to methodologic reasons. In principle both these 2 electrocardiographic parameters are expected to be strong correlates of weight gain in patients with peripheral edema. However, ⌺QRS is the sum of peak-to-peak BRIEF REPORTS
1445
amplitudes of all of the 12 electrocardiographic leads that were manually calculated, whereas mean QRS duration is an electronically derived index of the entire electrocardiographic tracing, as calculated by the electrocardiographic analysis program.2 As to the product of ⌺QRS and mean QRS duration, there is some artificiality about its adoption, intended to combine the attributes of the 2 terms of the product. Perhaps instead of using the peak-to-peak amplitude or the duration of QRS complexes, the QRS area may be more electrophysiologically appealing. Calculation of the QRS area in Ashman units (1 such unit ⫽ 40 ms ⫻ 0.1 mV) in all of the 12 electrocardiographic leads is provided by the “extended measurements report” of the Hewlett-Packard analysis program,2 and can be used to calculate a sum of areas for the entire 12-lead ECG. It would be of interest to evaluate such a parameter for its correlation with weight gain or subsequent loss in patients who develop peripheral edema. In conclusion, a close relation of percent change in mean QRS duration (QRSd) with percent change in the sum of the amplitudes of QRS com-
1446 THE AMERICAN JOURNAL OF CARDIOLOGY姞
VOL. 89
plexes (⌺QRS), and percent change in ⌺QRS ⴛ QRSd with percent change in weight between admission and time of peak weight gain was found in 28 patients who developed anasarca as a result of a critical illness of varying etiology. No such correlations as the above were noted at the time point of half peak weight gain. The shortening of the mean QRSd was considered to be more apparent than real, and was attributed to failure to detect parts of the onset and offset of QRS complexes stemming from their subthreshold (for detection) amplitudes. 1. Madias JE, Bazaz R, Agarwal H, Win M, Medepalli L. Anasarca-mediated
attenuation of the amplitude of ECG complexes: a description of a heretofore unrecognized phenomenon. J Am Coll Cardiol 2001;38:756 –764. 2. Hewlett-Packard Interpretive Cardiograph. Physician’s Guide HP Part No. M1700 –92908, Edition 4, Printed in USA September 1994:3–3, 4 –3, 4 – 4, C-1-C9. 3. Colton T. Statistics in Medicine. 1st Edition. Boston, MA: Little, Brown and Company, 1974:17, 33, 120. 4. Norusis MJ. The SPSS Guide to Data Analysis for PDD/PC⫹. 2nd ed. Chicago, IL: 1991:244,362,374,390. 5. Rudy Y, Liebman J. The effects of variations in conductivity and geometrical parameters on the electrocardiogram, using an eccentric spheres model. Circ Res 1979;44:104 –111. 6. Surawicz B. Electrophysiologic Basis of ECG and Cardiac Arrhythmias. Baltimore, MD: Williams & Wilkins, 1995:493–496, 498.
JUNE 15, 2002