Anasarca-mediated attenuation of the amplitude of ... · Anasarca-Mediated Attenuation of the...

Anasarca-Mediated Attenuation of theAmplitude of Electrocardiogram Complexes:A Description of a Heretofore Unrecognized PhenomenonJohn E. Madias, MD, FACC, Raveen Bazaz, MD, Himanshu Agarwal, MD, Moethu Win, MD,Lalitha Medepalli, MDNew York, New York

OBJECTIVES The relationship between the changes of weight (WT) and electrocardiogram (ECG) QRSamplitude in patients with anasarca (AN) was evaluated.

BACKGROUND Attenuation of the ECG voltage occurs as the electrical current spreads from the epicardiumto the body surface. The voltage registered is a function of the cardiac potentials, the electricalresistivities of the intervening tissues and the orientation of the ECG leads with respect to thedirection of propagation of excitation. Lung congestion and pericardial and pleural effusionscan cause attenuation in the ECG potentials; additionally, a similar change was recentlyobserved in patients with AN.

METHODS A prospective study of this phenomenon in 28 patients with a critical illness was carried out.Electrocardiograms and patients’ WTs were recorded daily. Pericardial effusions wereexcluded by serial echocardiograms. The sums of the amplitude of QRS complexes from the12 ECG leads (SQRS) were correlated with the corresponding WTs. Intracardiac ECGs,done in three patients, were correlated with surface ECGs.

RESULTS Admission WT was 148.9 6 37.8 lbs, and it peaked to 197.8 6 52.3 lbs (p 5 0.0005).Admission SQRS was 120.2 6 41.6 mm and dropped to 54.8 6 26.9 mm at time of peakWT (p 5 0.0005). Regression of SQRS on WT revealed an r 5 0.61 and a p 5 0.0005.Subsequent WT loss in 13 patients (from 219.0 6 40.7 lbs to 179.5 6 41.7 lbs, p 5 0.001)led to an increase of SQRS from 53.5 6 24.5 mm to 86.8 6 38.2 mm (p 5 0.001).Intracardiac ECGs remained stable, while surface ECGs changed with perturbations of WT.

CONCLUSIONS Attenuation of ECG voltage in patients with AN correlates with WT gain, and it can beattributed to a shunting of the cardiac potentials due to the low resistance of the AN fluid.(J Am Coll Cardiol 2001;38:756–64) © 2001 by the American College of Cardiology

A low-voltage electrocardiogram (ECG) (LVE) (QRScomplexes of ,5 mm in the limb and ,10 mm in theprecordial leads) has been linked to obesity, pericardial andpleural effusions, constrictive pericardial disease, infiltrativeheart disease, diffuse myocardial necrosis or fibrosis, emphy-sema, pulmonary infiltration or congestion and hypothy-roidism; occasionally it represents a normal variant (1–4).Abrupt emergence of LVE occurs with pneumothorax(5–9), with resolution after its correction. Additionally,aspiration or gradual natural resorption of pericardial effu-sion restores ECG potentials.

Spurred by a patient with anasarca (AN) and a LVE, weprospectively investigated this phenomenon in a case-control study since ECG texts (1,2,10,11) and the literaturedid not refer to any etiologic link between LVE and AN.

METHODS

Study population. Of the 493 patients admitted to ourcoronary care unit (CCU) in 1999, 28 (6.7%) patients withAN were studied.

Study variables. Data on demographics, past and presentillnesses, hemodynamics, clinical laboratory tests, chestradiographs, echocardiograms, respiratory parameters, du-ration of observation, management, complications and out-come were considered.Weight variables. The patients’ weight (WT) on admis-sion, at half WT gain (HF-WG), at peak value and, for thepatients who subsequently lost WT, at the lowest point andthe corresponding percentage of WT change were employedas variables.ECG measurements and variables. Standard ECGs wererecorded daily. Calibration was 1 mV 5 10 mm. Measure-ments of the amplitude (highest positive 1 lowest negativedeflections) of the QRS complexes were made by one of theauthors (J.E.M.) to the nearest 0.5 mm using calipers and amagnifying glass. For ECGs with atrial fibrillation, the averageof measurements of three consecutive beats was used.

Sums of the QRS amplitudes of all ECG leads (SQRS)from the day of admission, HF-WG, peak and lowest WTswere calculated for each patient. Since V5 and V6 revealedbigger changes than V1 and V2 with AN, the sums of theamplitudes from these two sets of leads (SV5V6 and SV1V2)were used as variables. Changes in the SQRS, SV5V6 andSV1V2 were expressed as the percentage of the admissionand peak WT values. The intraobserver variability of SQRSin 10 random ECGs was 0.41 6 3.34%.

From the Zena and Michael Wiener Cardiovascular Institute, Mount Sinai/ NewYork University Medical Center Health System, New York, New York; and theDivision of Cardiology, Elmhurst Hospital Center, Mount Sinai School of Medicine,New York, New York.

Manuscript received August 28, 2000; revised manuscript received May 4, 2001,accepted May 21, 2001.

Journal of the American College of Cardiology Vol. 38, No. 3, 2001© 2001 by the American College of Cardiology ISSN 0735-1097/01/$20.00Published by Elsevier Science Inc. PII S0735-1097(01)01429-2

Controls. Controls were: 1) 28 patients (16 men) admittedto the CCU concurrently with the study patients for avariety of cardiovascular and other illnesses. Data includedwhether they had undergone endotracheal intubation, WTchange, the duration of observation and the ECG variablessimilar to the study patients. 2) Of these 28 patients, 10 whowere intubated, 17 who had pneumonia and 4 who hadacute pulmonary edema were also separately analyzed to

evaluate the above conditions as determinants of change inthe SQRS by comparing the ECGs before and afterextubation or recovery from their illness. 3) All 10 CCUpatients who underwent hemodialysis (13 sessions) in 1999had ECGs and WT recorded before and after this proce-dure.Intracardiac ECG (IC-ECGs) recordings. IntracardiacECGs were obtained in three patients, (nine sessions),recording via the Wilson central electrode, a needle and asaline-filled central venous catheter connection; IC-ECGsand surface ECGs were correlated.Other variables. The effects of changes in temperature andhematocrit, which are thought to minimally impact theamplitude of ECG complexes (12), were explored.

The influence of inspiration, expiration, endotrachealintubation and extubation and the application/change ofpositive end-expiratory, end-inspiratory and continuouspositive airway pressures were studied in all patients inmeasurements on ECGs or by viewing the bedside ECGmonitors before and after such actions.

Daily chest radiographs and frequent echocardiograms

Table 1. Demographic and Clinical Characteristics of the Cohort

PatientAge(yrs)

Gender(M/F)

Obs(days) Present Illness Past History

1 80 F 49 Hip Fx, GI bld, RF, SEP HYP2* 47 M 59 INF MI, VF, ANO ENCE DM3* 78 F 42 IP MI, VF, PNEU, SEP HYP4 65 F 27 PNEU, ARDS, SEP HYP, DM, asthma5 74 F 15 PNEU, RF, SEP COPD6 68 F 36 ?MI, GI bld, PNEU, SEP, CHF AF7 79 F 17 PNEU, SEP CHF8 83 F 19 Non-Q-MI, VF, SEP, MulOrgFl HYP, DM, COPD, ANG9 71 M 189 PNEU, VT, SEP HYP, COPD

10 73 M 9 Duodenal ulcer repair, SEP HYP, DM, AF, TB, RF11 43 F 59 PNEU, CS, SEP 3-vessel CAD12 83 F 14 MI, VF, PNEU, CS, SEP HYP13 89 M 13 non–Q-MI, ASYS, PNEU, SEP HYP14 82 M 19 PNEU, bradycardia DM, ANG, MI, PTCA15 61 F 4 SEP, DIC, MulOrgFl HYP, AF, MI, CVA16 97 F 60 MI, CHB, SEP HYP, ANG17 76 F 15 PNEU, SEP, CHF HYP, ANG, COPD18 53 M 17 PNEU, ARDS, ASYS Cardiomyopathy19* 80 F 70 PNEU, SEP HYP, AF, CHF20 72 F 17 MI, ANO ENCE, SEP HYP, AF, Asthma21 82 F 17 ANO ENCE, CHF HYP, CAD, MI22 85 M 9 SEP HYP, DM23 58 F 12 ANO ENCE, CVA HYP, DM, CVA24 77 M 51 GI bld, PNEU HYP25 55 M 18 PNEU, SEP, CHF Cirrhosis26 31 M 58 GI bld, TB, SEP, DIC Cirrhosis27* 61 F 30 PNEU, SEP, VF AF, VSD repair28 68 F 16 PNEU, SEP HYP

70.4 6 14.9 34.5 6 36.7

*Survival.AF 5 atrial fibrillation; ANG 5 angina; ANO ENCE 5 anoxic encephalopathy; ARDS 5 adult respiratory distress

syndrome; ASYS 5 asystole; CHB 5 complete heart block; CHF 5 congestive heart failure; COPD 5 chronic obstructive lungdisease; CRF 5 chronic renal failure; CS 5 cardiogenic shock; CVA 5 cerebrovascular accident; DIC 5 disseminatedintravascular coagulation; DM 5 diabetes mellitus; Fx 5 fracture; GI bld 5 gastrointestinal bleeding; HYP 5 hypertension;INF 5 inferior; IP 5 inferoposterior; MI 5 myocardial infarction; MulOrgFl 5 multiorgan failure; Obs 5 observation;PNEU 5 pneumonia; PTCA 5 percutaneous transluminal coronary angioplasty; RF 5 respiratory failure; SEP 5 sepsis; TB 5tuberculosis; VF 5 ventricular fibrillation; VSD 5 ventricular septal defect.

Abbreviations and AcronymsAN 5 anasarcaCCU 5 coronary care unitECG 5 electrocardiogramHF-WG 5 half weight gainHF-WT 5 weight, at the point of half weight gainIC-ECG 5 intracardiac ECGLVE 5 low-voltage ECGSQRS 5 sum of the amplitudes of QRS complexesSV1V2 5 sum of the amplitudes of QRS in V1 and V2

SV5V6 5 sum of the amplitudes of QRS in V5 and V6

WT 5 weight

757JACC Vol. 38, No. 3, 2001 Madias et al.September 2001:756–64 Anasarca and Low ECG Voltage

were obtained in all study patients to evaluate for evidenceof pulmonary infiltrates, acute respiratory distress syndrome,pulmonary congestion, pleural effusions, pneumothorax,pneumomediastinum and pericardial effusions and to assessthe cardiac structure and function.Statistical analysis. Continuous data are reported as mean 6SD. Weights and SQRSs from admission, times of peak WT,of half weight gain (HF-WT) and subsequent lowest WT andSQRSs from control patients were analyzed by two-tailedpaired t tests. The relationship between percentage of changefrom admission of peak WT gain or HF-WG and correspond-

ing reduction of the SQRS, SV5V6 and SV1V2 were evaluatedby regression analysis, considering the WT as the independentand the ECG as the dependent variables (13). Analyses of theHF-WG evaluated for a dose-response relationship betweenWTs and SQRS. The relationship between maximal loss ofWT (expressed as the percentage of change from peak WT)and corresponding increase of the SQRS, SV5V6 and SV1V2

(expressed as a percentage change from the time of peak WT)was evaluated by regression analysis. The SPSS/PC1 4.0.1statistical package (14) was employed, and a p ,0.05 was takenas statistically significant.

Figure 1. Electrocardiograms on the designated days of hospitalization revealing the decrease (A and B) and subsequent increase (B and C) in the amplitudeof QRS complexes. SQRS 5 sum of the amplitudes of QRS complexes.

758 Madias et al. JACC Vol. 38, No. 3, 2001Anasarca and Low ECG Voltage September 2001:756–64

RESULTS

Demographic and clinical data are shown in Table 1. Allpatients underwent endotracheal intubation and receivedintravenous fluids and vasopressors or inotropic agents forhypotension or sepsis. Typical ECG changes are shown inFigures 1 to 3. Electrocardiograms changed gradually (Fig.3), as could be shown by daily comparisons. Loss of thegained WT led to regeneration of the ECG potentials (Figs.1 and 4).

Weights at various time points are depicted in Table 2.

After peaking to a WT of 219.0 6 40.7 lbs, 13 patients lostWT (179.5 6 41.7 lbs; p 5 0.001), reaching a WT notdifferent from admission WT (161.1 6 23.2 lbs, p 50.143). Two patients gained/lost WT, repeatedly. SQRSsat various time points are shown in Table 2. AdmissionSV5V6 was 23.0 6 13.2 mm and dropped to 11.2 66.07 mm at HF-WG (p 5 0.0005) and 8.2 6 6.0 mm atpeak WT gain (p 5 0.0005) (Figs. 1 to 3 and 5). AdmissionSV1V2 was 24.0 6 13.2 mm and dropped to 18.0 6 9.9 mmat HF-WG (p 5 0.0005) and 14.7 6 8.1 mm at peak WTgain (p 5 0.0005) (Figs. 1 to 3 and 5). SQRSs of thepatients with subsequent WT loss are shown in Table 2.SQRS at the time of their lowest WT (86.8 6 38.2 mm)was lower than the admission value (118.0 6 38.1 mm, p 50.041). Two patients who gained/lost WT repeatedly,showed reproducible SQRS and WT perturbations.

Regression of changes of SQRS, SV5V6 and SV1V2 onWTs revealed an r 5 0.61, 0.65 and 0.22 and p 5 0.0005,0.0002 and 0.26, correspondingly; similarly, changes inSQRS, SV5V6 and SV1V2 and HF-WG revealed an r 50.41, 0.27 and 0.20 and a p 5 0.03, 0.16 and 0.30,correspondingly. Regression analysis of 21 pairs of WT andSQRS of one patient revealed an r 5 20.68 and a p 50.0007 (Fig. 3).

Regression of changes in SQRS, SV5V6 and SV1V2 onloss of WT showed an r 5 0.56, 0.59 and 0.65 and a p 50.0579, 0.04 and 0.02, correspondingly. The relationshipbetween SQRS and WT in nine patients who gained andlost WT is depicted in Figure 4.

Controls aged 65.2 6 19.0 years (20 to 99 years) had twoECGs recorded 9.1 6 6.5 days (2 to 30 days) apart, had a

Figure 2. Gradual reduction in the QRS potentials was observed in thispatient (Pt) with left bundle branch block. 1⁄2 wt. 5 weight in betweenadmission and peak weights; wt. 5 weight.

Table 2. Admission, HF-WG, Peak and Subsequent WTs andCorresponding ECG Variables of Patients (n 5 28)

Admission WT (lbs) 148.9 6 37.8WT at HF-WG (lbs) 172.8 6 42.8†HF-WG (lbs) 23.9 6 14.8HF-WG (%) 16.9 6 10.7Peak WT (lbs) 197.8 6 52.3†Peak WT gain (lbs) 48.9 6 28.1Peak WT gain (%) 33.5 6 19.5Time to HF-WG (days) 9.4 6 6.9Time to peak WT (days) 17.1 6 11.4Subsequent lowest WT (lbs)* 179.5 6 41.7‡§WT loss (lbs)* 39.4 6 31.4WT loss (%)* 217.6 6 12.8Time from peak to lowest WT (days)* 20.2 6 22.1SQRS on admission (mm) 120.2 6 41.6SQRS at HF-WG (mm) 70.2 6 29.8†Change of SQRS from admission to half WT (%) 241.2 6 14.7SQRS at peak WT (mm) 54.8 6 26.9†Change of SQRS from admission to peak WT (%) 254.2 6 15.4SQRS at peak WT of patients who lost WT (mm)* 53.5 6 24.5SQRS at subsequent lowest WT (mm)* 86.8 6 38.2\

Change of SQRS from peak to lowest WT (%)* 69.9 6 56.1

Numbers are X 6 SD. *Data on 13 patients who lost weight after gaining weight;†p 5 0.0005 from admission data; ‡p 5 0.001 from peak weight; §p 5 0.143 fromadmission weight; \p 5 0.001 from SQRS at peak weight.

ECG 5 electrocardiogram; HF-WG 5 half weight gain; SQRS 5 sum of theamplitudes of QRS complexes; WT 5 weight.


change of 22.5 6 5.3% (217% to 13.6%) in their WT inthe intervening time, and their SQRS for the two ECGswere 136.8 6 46.6 mm and 134.0 6 44.1 mm (p 5 0.44).SQRSs of the controls before and after intubation, treat-ment of pneumonia and pulmonary edema were 150.5 659 mm and 135.4 6 53 mm (p 5 0.1), 136.2 6 62.6 mmand 141.1 6 45.1 mm (p 5 0.58) and 120.3 6 26.4 mm and117.9 6 32.0 mm (p 5 0.6), correspondingly. SQRSsbefore and after hemodialysis were 143.7 6 20.2 mm and144.9 6 18.2 mm (4.9 6 4.7%; p 5 0.83), with a WT lossof 4.9 6 4.7 lbs (0.9 to 12.1) (23.2 6 0.6%).

Temperature and hematocrit perturbations, alterations ofrespiratory parameters or the status of being intubated orextubated did not influence SQRSs. SQRS before and afterthoracostomy in one patient with left-sided pneumothoraxwas 30.5 mm and 55 mm, respectively.

Anasarca of the torso and extremities was documented bydaily inspection and palpation, and was found to be greaterin the dorsal than in the ventral regions of the body,presumably due to the gravity effect in patients mostlymaintained in a supine position.

Echocardiograms did not reveal pericardial effusions (Fig.5). Only Patient 26 had a pericardial effusion early in hisillness, but antituberculosis therapy led to its clearing (Fig.6). This was one of three patients whose IC-ECGs re-mained stable, while the corresponding surface ECGsshowed marked changes as WT changed (Fig. 6).

DISCUSSION

Study findings. What is novel about our study is thelinkage of LVE to AN. This is supported by: 1) therelationship between peak SQRS drop and peak WT rise;

2) the lower attenuation effect of the HF-WT than the peakWT on the SQRS; 3) the gradual decrease in SQRS whileWT rose; 4) the reciprocal relationship of the absolutevalues of these two variables (Fig. 3); 5) the rise of SQRS inpatients who lost WT; 6) the reproducible relationshipbetween SQRS and WT in two patients who gained/lostWT more than once; 7) the marked effect that AN had onSV5V6, reflecting the region with major fluid accumulation;and 8) the attenuated influence of AN on SV1V2, corre-sponding to the area with less fluid accumulation.Electrophysiology of current conduction. Body ECGpotentials are a function of the currents generated by theheart, the transfer factors of the intervening tissues, organs,or air- and fluid-filled spaces (15–17) and the location andproperties of the surface electrodes with the resulting leadaxes. The conducting medium attenuates the heart’s poten-tials so that about 1/100 of their original value is recorded atthe body’s surface (16). As per Ohm’s law, the potentialdifference between the two ends of a conductor is a functionof current and resistance (11). When the resistance of theconducting medium enveloping the heart increases, surfaceECG potentials are augmented, whereas decreasing resis-tance leads to an attenuation (shunting) of the heart’spotentials (1,2,15–17). Resistance in turn depends on thematerial of a conductor (its resistivity). The operationalresistance is a composite of the different resistances, deter-mined by the geometries and resistivities of the constituents(15–19). Bayley et al. (20) and Rudy et al. (21) haveexplored in theoretical models the effects of such inhomo-geneity on the surface ECG. Voltages are also affected bythe differences in resistivities at the boundary of adjacent

Figure 3. Serial weights and corresponding sum of the amplitudes of QRS complexes (SQRS) revealing the reciprocal relation of these two variables inthis patient (Pt).


tissues and the orientation of the activation front impactingthese interfaces.

Geddes et al. (12) have summarized the work on theresistivity of various tissues, organs and body fluids inhumans and animals. Accordingly, plasma has the lowestresistivity, whereas blood, lung, fat and bone have highresistivities. Additionally, increase in temperature, as infever, decreases the resistivity of biologic tissues and fluids.Relevant literature. Previous work explored the influenceof the transthoracic resistance on the amplitude of ECGpotentials (22–24). Van Der Water et al. (25) used changesin the transthoracic resistance to monitor patients with avariety of heart and lung illnesses, but they did not employECGs. Also, an increase in ECG potentials after removal of700 ml to 3,000 ml of fluid with hemodialysis was previ-ously reported, but the loss of WT was small compared withthe one noted in our study (26,27); the increase in the ECG

potentials was small (26), and it was attributed to alleviationin lung congestion, correction of undocumented electrolyteabnormalities (27) and speculations about changes in theintracavitary heart volume (26). Our experience with com-parable hemodialysis-induced WT loss did not corroboratethese findings (26,27). Prior literature (21–26) has attrib-uted the changes in resistance to the status of the heart andlungs or presence of air or effusions in body cavities, butnowhere was AN implicated. We feel that hemodialysisdoes not produce changes detectable by the ECG, due tothe small WT change effected. This was corroborated by theabsence of significant changes in the ECGs of our patientsduring the early phase of WT gain or loss. In contrast,hemofiltration with marked WT loss led to an impressivegain in the QRS amplitude (Fig. 6). Transthoracic or otherbody resistance measurements (not carried out in our study)would have provided another correlate of the ECG changes.

Figure 4. Points 1 to 3 of the plot for each patient (Pt) represent the one-half, the peak and the subsequent lowest weights, correspondingly. Variables areadjusted to admission values. SQRS 5 sum of the amplitudes of QRS complexes; wt. 5 weight; %D 5 percent change.


Resistance changes have been previously traced to an in-crease in intrapulmonary water (25); however, our controlswith pulmonary edema did not reveal an increase in theirQRS amplitude after relief of congestion, indicating thatthe ECG changes in our study patients could not haveoccurred as a result of changes in the lung water content.Potential confounding factors. Other factors that couldhave caused LVE in our patients can be easily excluded

because their effect is known to be minor (i.e., anemia, fever)(12); they were present intermittently (lung congestion andinfiltrates), while the QRS potential loss was gradual andconstant, paralleling the WT gain. The influence of chang-ing intracavitary blood mass on the ECG potentials (Brodyeffect) could not be studied; this would have required serialprecise measurements of left ventricular dimensions. Such amechanism in our clinically deteriorating patients would be

Figure 5. Marked attenuation of QRS potentials was noted in this patient (Pt). The echocardiogram (2D-Echo) did not reveal a pericardial effusion. Ao 5aorta; A4-Ch 5 apical four-chamber view; LA 5 left atrium; LV 5 left ventricle; PLAx 5 parasternal long-axis view; RA 5 right atrium; RV 5 rightventricle; T 5 thrombus.


expected to result in augmentation of the QRS amplitudesthan the decrease observed (11,26,28). However, the Brodyeffect could also lead to a decrease in ECG potentialsdepending on activation orientation, and its influence mayhave been overrated (21). Although stability of IC-ECGsimplicated the conducting medium for the LVE than theheart, an effect of AN on the IC-ECGs (not seen in ourstudy) is theoretically possible.

Experimental work. Our findings are in accord with theexperimental work of Green et al. (29) (Taccardi B, personalcommunication, 2000) who showed that low-resistivityTyrode’s solution surrounding the heart results in a LVE,which was only noted over the portion of the heart im-mersed in the solution (29). A corollary of this in our studywas that AN affected SV5V6 (overlying larger fluid accu-mulation) more than SV1V2.

Figure 6. Attenuation of QRS potentials was noted in this patient (Pt) before (day 21) continuous venovenous hemofiltration carried out for seven days,with marked recovery of the potentials, paralleling the loss of weight (day 28). Meanwhile, the intracardiac electrocardiograms (IC-ECGs) did not change.The echocardiogram (2D-Echo) revealed a barely perceptible pericardial effusion (day 20). A4-Ch 5 apical four-chamber view; LA 5 left atrium; LV 5left ventricle; RA 5 right atrium; RV 5 right ventricle.


Clinical implications. This study provides a diagnosticexplanation for the frequently encountered LVE in patientswith a large variety of critical illnesses.

AcknowledgmentWe wish to thank Professor Bruno Taccardi of UtahUniversity for reviewing the paper and for directing us torelevant work from his laboratory.

Reprint requests and correspondence: Dr. John E. Madias,Division of Cardiology, Elmhurst Hospital Center, 79-01 Broad-way, Elmhurst, New York 11373. E-mail: [email protected].

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