| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Guest Access | Sign In via User Name/Password
|
|
|
|||||||
Guest Access | Sign In via User Name/Password |
|||||||||
Elmhurst, NY
Dr. Madias is Professor of Medicine (Cardiology), Division of Cardiology, Elmhurst Hospital Center.
Correspondence to: John E. Madias, MD, Professor of Medicine (Cardiology), Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373; e-mail: madiasj{at}nychhc.org
Browsing of serial ECGs obtained in patients with anasarca peripheral edema (AN) in the coronary care unit, respiratory care unit, surgical ICU, other critical care units, and the general medical wards will convince physicians about the ubiquitous presence of examples of patients showing gradual attenuation of the voltage of QRS complexes. Furthermore, such dynamic reduction of the amplitude of QRS complexes will become apparent in patients who merely have gained weight without revealing overwhelming signs of peripheral fluid sequestration. Also what immediately becomes obvious is the large range of pathologic conditions present in patients with this association of AN and reduced QRS potentials; thus, instead of mainly encountering patients with cardiac illnesses, the patients with this ECG syndrome have chronic or acute renal failure, sepsis, or for whatever reasons have received large amounts of IV fluids. A corollary of this is that the pathophysiology involved is not heart-based, but rather of some uniform extracardiac origin.1
This "ECG curiosity" is rarely recognized by physicians, since its description is only recent,1 and when revealed is met with bewilderment; particularly puzzling is that although individual ECGs have been reviewed daily, this reduction of the amplitude of the QRS complexes has been missed, although it becomes apparent at a glance when serial ECGs are placed side by side and their perusal is invited. Also, when the patient’s values of daily weights and the record of fluid intake and output are considered in concert with the serial ECGs, an association immediately emerges. Alternatively, the attenuation of the QRS complexes is detected, and cardiologic consultation is sought. A plausible and the most commonly considered reason is that a pericardial effusion must be present. If found, further inquiry becomes unnecessary; however, more often than not a pericardial effusion is excluded by echocardiography, and the presence of relentless attenuation of QRS voltage calls for an explanation. Rarely the problem is attributed to a malfunctioning or inconsistently calibrated ECG machine(s), a reason that can be easily ruled out.
A case in point was of an 88-year-old woman we cared for recently, with history of hypertension and long-standing atrial fibrillation, who had sepsis, hypotension, and acute renal tubular necrosis. In the process of her hospitalization, she received large amounts of fluids, was oliguric/anuric, and developed AN and a weight gain of approximately 20 kg. There was evidence of peripheral edema by inspection and palpation in her entire body; however, edema was less conspicuous in the ventral than in the dorsal aspects of her body, something commonly observed in patients with AN, who are intubated and are lying (by necessity) supine on their bed (gravity effect). Her ECG showed gradual decrease in the amplitude of QRS complexes (Fig 1 ), pari passu with the increase of her weight. This process affected all ECG leads, with an eventual decrease in the voltage of approximately 50%. An echocardiogram showed left ventricular hypertrophy, hyperdynamic systolic ventricular function, and left atrial enlargement; no pericardial effusion was detected. Daily chest radiographs revealed a normal cardiac silhouette, no pulmonary congestion, and a right basal lung infiltrate consistent with pneumonia. The patient was treated with antibiotics and fluids, received vasoactive drugs, but had frequent episodes of hypotension, became poorly responsive and then unresponsive; as per relatives’ wishes were supportive measures discontinued. She died on March 23, 2003.
|
ECG changes like the above are not only noted in patients with AN due to sepsis, but occur in patients with chronic or acute renal failure and congestive heart failure (CHF). Our patient had both sepsis and acute renal failure. Milder reductions of the QRS voltage occur in patients with end-stage renal failure prior to hemodialysis, with clear enhancement of the QRS potentials after the procedure.8 9 10 11 12 Many years ago, it was noted that the QRS complexes of patients with decompensated CHF were attenuated, and that effective management of their condition led to increase of the amplitude of QRS complexes, but no convincing explanation for these ECG changes was provided.13 Recently, this old observation was revisited,14 and the enhancement of the QRS voltage with effective management of CHF was associated with an increase in the electrical resistance of the body,15 attesting to the causative role of attenuated body resistance in the genesis of attenuated QRS voltages in the presence of AN. Further confirmation of these associations was provided by the finding of similar increases of the electrical resistance of the body commensurate with loss of weight and increase in the amplitude of QRS complexes immediately after hemodialysis.11 12 In all the recent relevant work linking AN and QRS voltage changes, a quantitative assessment of the ECG data was employed. This consisted of calculation of the sum of the QRS complexes of all 12 ECG leads, measured in millimeters, from the zenith to nadir of each complex in serial ECGs1 12 14 15 ; however, since this may be cumbersome in the context of patient caring, one can employ a quick summing (by "eye-balling") of the amplitudes of leads I and II, which can substitute for the sums of all 12 leads (unpublished data; March 2003). Justification for such substitution is based on Einthoven’s law, according to which these two leads are adequate to reproduce the other four bipolar leads via mathematic formulas. Moreover, most modern ECG machines measure only leads I and II, and calculate online the other four limb leads.16 For example, the sum of leads I and II of Figure 1 from our patient reveals an approximate 50% reduction of the amplitude of these QRS complexes, and appears to be representative of the attenuation noted in the rest of ECG leads.
This communication has focused on the effect of AN on QRS potential amplitudes; however, AN exert its effect proportionally on the entire QRST curve; consequently "dwarfing," or virtual disappearance of the P waves occasionally occurs. When this happens, the clinician is presented with an ECG showing low-voltage QRS complexes and no P waves. When the prevailing heart rates are within the normal range, one can assume that the underlying rhythm is still normal sinus rhythm; however, patients with critical care illnesses are prone to both bradycardia and tachycardia, and when such complications arise, it becomes problematic to diagnose the specific rhythm or conduction disorder using the standard ECG. In such an occasion, even employment of special surface ECG leads (ie, "Lewis lead," which utilizes the right and left arm electrodes placed at the upper and lower part of the sternum, respectively, for enhancement of P-wave amplitude)17 is noncontributory, and resorting to esophageal or intracardiac electrography becomes necessary.18
Why is it important for critical care physicians to be aware of the above? What are the implications for the care of patients with critical illness?
Recognizing this AN/low-voltage ECG association provides the following advantages to the physician managing a critically ill patient: (1) low-voltage ECG is not automatically connected to the presence of a pericardial effusion; (2) when a pericardial effusion is ruled out by echocardiography, the presence of low-voltage ECG can be explainable in the setting of weight gain, positive intake and output records, or visible fluid accumulation or AN; (3) in the presence of discrepancy of data pertaining to fluid status of a patient, based on weights, physical examination, or intake/output balance records, review of serial ECGs may be of great help; this issue is of importance in the bedridden patient with a critical illness where weighing by sling scales and accurate intake/output record keeping becomes problematic; (4) the puzzling disappearance of ECG evidence of left ventricular hypertrophy, in a patient known to carry such a diagnosis prior to the development of AN, finds an explanation; and (5) the absence of P waves in the ECG in a patient with AN does not necessarily imply the presence of an AV junctional rhythm or junctional tachycardia; often the rhythm is merely normal sinus or sinus tachycardia in association with "invisible" P waves. Correct identification of the rhythm can be accomplished by intracardiac or esophageal ECG, or by employing a saline solution-filled central venous catheter ECG lead, as shown recently.18
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
