Artifactual activity on 12-lead EKG presents a significant impediment to electrocardiographic diagnosis. A case is presented here in which underlying STEMI could not be appreciated due to artifactual interference from frayed electrode leads. Clinicians should to be aware of the causes and presentations of EKG artifact in order to avoid similar pitfalls.
An “all fields” PubMed search was conducted using the term “artifact” in conjunction with each of the terms “STEMI”, “myocardial infarction”, “EKG”, “ECG”, and “ST segment.” Results yielded 0, 76, 19, 317, and 22 references respectively. These 434 citations were then screened for relevance according to title. The scope of the search spanned from 1973 to June 2012.
Numerous sources and types of artifactual interference on EKG have been identified. Artifact may be defined as any electrical activity present on EKG recording which does not directly and appropriately reflect cardiac activity. Artifactual interference may be classified as either of primary, non-cardiac etiology, or of secondary etiology when authentic cardiac signals are deranged due to incompetent acquisition, processing, or presentation. In the former category, a multitude of electrical and mechanical devices have been implicated (1-12, 46). Movement artifacts such as patient tremor, respiration, coughing, and hiccups have also been described (13-21, 43, 44). Artifact resulting from bed or stretcher movement should also be included in this subgroup.
Regarding the derangement of authentic cardiac signals rather than non-cardiac interference, investigators have noted an extensive variety of effects due to electrode misplacement (25-28, 32, 37). Acquisition filters have also been found to deceptively alter the appearance of the electrocardiogram (30, 33). Inconsistent electrode contacts as well as flawed or inverted lead connections can be problematic (45). Printers, monitors, and electronic transmission software have all been implicated in significant distortion or augmentation of the EKG (29, 41).
Too numerous to count case reports involving both primary non-cardiac interference as well as secondary artifact effects have illustrated a diversity of arrhythmic, ischemic, and other electrocardiographic mimics. Typically low frequency primary artifact resulting from tremors or rhythmic movement of physiologic cycle length has been associated with the mimicry of dysrhymias, often wide complex dysrhthmias (13-21, 23). Derangements of authentic cardiac activity resulting from lead reversals, filtering effects, and post-acquisition processing have frequently been associated with the mimicry of ischemic EKG patterns. The appearance of pathologic Q-waves, dramatic changes in cardiac axis, T-wave deflection, and alterations of R-wave amplitude and progression have been documented (25-27). False ST elevation and depression have also been described (30, 31). Both the masking of intrinsic pathology and the pathologic representation of healthy cardiac signals have been noted (30-34, 40, 45). The consequences of unrecognized artifactual interference can include inappropriate pharmacological and electrical therapies; significant morbidity and mortality has resulted (15, 18, 19, 28).
In some cases, the clinician can exploit artifactual activity. Shivering artifact in the presence of electrocardiographic evidence of hypothermia is such a case (42). The utility of respiratory artifact has also been explored (24). More recently, the exploitation of systematic computer algorithm interpretation error has been discussed relative to “double counting” of heart rate in the setting of hyperkalemia (41).
In this case report, an anterior ST-elevation myocardial infarction was masked by opaque artifactual activity resulting from frayed electrode leads. To date, this would appear to be the first documented case of such an occurrence.
An 85 year-old Caucasian man with a history of atrial fibrillation and anxiety awoke at 2:30 AM with chest pressure and shortness of breath. He alerted his daughter and she administered his Xanex, believing his symptoms to be psychosomatic. When this had little effect, an ambulance was called. On their arrival at 3:40 AM, paramedics administered oxygen and 162mg of aspirin. Vital signs at this time were within normal limits. A rhythm strip was acquired which demonstrated heavy artifact obscuring all but one lead. Additional leads were not visualized and no intelligible 12-lead could be obtained.
The patient was transported to a non-PCI capable community hospital. There, a 12-lead EKG was recorded which showed explicit anterior wall STEMI.
The troponin was 0.65. Tenectaplase was administered at 4:30AM; a repeat EKG 90 minutes later was unchanged. At this time, he was transferred to an outside hospital for cardiac catheterization.
On arrival at 7:05AM, the patient was hypotensive with a systolic blood pressure of 70mmHg.
An aortic balloon pump was placed and dopamine initiated. A complete occlusion of the mid-LAD was identified; thrombectomy was performed and the vessel stented with TIMI3 result. Hypotension persisted and the patient developed increasing lethargy and dyspnea. He vomited and became apenic while in cath lab. At 8:15AM he was intubated and placed on levophed; his ejection fraction was less than <15%. Hypotension remained refractory despite the addition of vasopressin and dobutamine. At 10:25AM, the troponin was 92. At this time he was unresponsive on exam with central cyanosis and mottling to all four extremities. There was pulmonary edema with an arterial line indicating a systolic BP of 50mmHg. Blood gas analysis indicated a pH of 7.10. He was described as not likely to survive and made DNR at 10:50AM. At 11:58 AM no carotid pulse could be appreciated and he was pronounced dead.
Retrospective analysis of the prehospital EKG artifact was undertaken. The system was traced from the electrode-lead junctions back to the monitor. In this case, a Physio-Control Life Pack 12 device was being utilized and revealed cable-junction fraying. Experienced operators of this device are often familiar with this type of artifact, and the cable-junction is a known weak point.
Cable fraying or, more broadly, lead-connection artifact, has a distinct electrocardiographic signature. Fequentlely there is an erraticly wandering baseline with sharp, irregular voltage spikes showing inconsistantly varrying amplitudes. As usualy only one connection is effected, the artifact should localize to a particular lead. Thus there should also be leads present which are free of artifact.
Note that in the initial EKG from this case there are voltage spikes of varying amplitudes, a chaotically wandering baseline, and a lead-specific artifact distribution. Other etiologies may mimic lead-connection artifact, but are readily distinguishable once they become familiar to the clinician.
60Hz AC interference should demonstrate almost exactly 60 deflections per second; the baseline typically will not wander and the amplitude will be constant or demonstrate orderly undulation. (Image retrieved from “Doktorekg.com,” http://www.metealpaslan.com/ecg/artef3en.htm)
Shivering artifact may or may not be accompanied by hypothermic ECG stigmata such as bradycardia or Osborne waves; note that the artifact is not confined to any single lead distribution. (Image retrieved from “LifeInTheFastLane.com,” http://lifeinthefastlane.com/ecg-library/basics/hypothermia/)
Artifact from resting tremor is typically of lower (physiologic) frequency and thus can mimic VT or a-flutter; relative to lead-connection artifact, tremor interference is pervasive, consistent, and of much longer cycle length.
The distinguishing hallmarks of lead-connection artifact are,
- It is confined to a specific lead distribution– the lead with inconsistent connectivity.
- There is a chaotically wandering baseline.
- The cycle lengths are short (30-70Hz ?) and grossly irregular.
- The amplitude is widely variable and randomly distributed.
When lead-connection artifact is recognized, operators can trouble-shoot the system for correctable problems. Often a “positional” solution can be temporarily utilized to acquire an acceptable tracing before the cables can be replaced. As in this case, when the origin of the artifact is unknown to the practitioner, it is not possible to investigate such a solution. The tragic coincidence presented here, where in the detection of STEMI was obscured by lead-connection artifact, illustrates that the potential significance of this issue.
While newer lead hardware has been made available, many operators continue to utilize the monitoring cables described in this case.
In this case, an anterior wall STEMI could not be appreciated due to artifactual interference. The patient was therefore transported to a non-PCI capable facility; subsequently, he did not receive definitive reperfusion until nearly five hours after his initial encounter with ACLS providers. The result was a catastrophic infarction from which he could not recover.
Operators should be familiar with the appearance of lead-connection artifact and maintain a high index of suspicion when checking and trouble-shooting this hardware.
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In 2007, Littmann and colleagues presented a novel EKG indicator of hyperkalemia based on the computerized “double counting” of heart rate. Over a 13-year period they identified 33 cases in which the GE-Marquette computerized 12SL EKG interpretation algorithm “double counted” or “near double counted” the actual heart rate seen on electrocardiogram. All 33 patients had hyperkalemia (between 5.3-8.8 mEq/L K+) as confirmed by serology taken within two hours of the double-counted EKG recording.
Littmann’s sign can be seen in the following EKG, initially presented here as a study in hyperkalemia in September of 2010.
A 65 year-old Caucasian man with sepsis and HHNKC; the potassium was 7.7mEq/L. The heart rate is 72 bpm; the computer counts 137 bpm.
Although the GE algorithm is proprietary and unavailable for analysis, they argue that, “The QRS width and axis measurement by the interpretation software suggested that, on many occasions, the computer recognized the T waves as being the QRS complexes….” (p.586)
Littmann et al. conclude stating, “Although interpretation software double counting of heart rate appears to be quite specific for hyperkalemia, its sensitivity is almost certainly very low.” (p.586)
While this research represents an intriguing new insight, it leaves many open questions. How were these 33 EKG cases identified? Were certain populations screened for this anomaly? How many total EKGs were reviewed in the course of this investigation?
Littmann claims that double counting “appears to be quite specific” presumably because all 33 EKGs were associated with underlying hyperkalemia. Yet without insight into the methods used to assemble this case series, I remain skeptical that these investigators did not succumb to confirmation bias in the process of collecting their EKGs. The existence of non-hyperkalemic double counting is not discussed in this publication and no differential diagnosis is presented regarding alternative etiologies.
In fact, concerning alternative etiologies and the specificity of double QRS counting, it turns out that this phenomenon has been extensively described in the pacemaker literature for over a decade. A Pubmed search using the combined terms “double counting QRS” produces numerous references. (Al-Ahmad A, Barold SS, Boriani G)
I reviewed 22 pacemaker EKGs collected over a 10 month period, recorded pre-hospitaly using the same GE-Marquette algorithm. This is what I found:
Looking further through ~50 EKGs collected over the same 10 months I found this as well:
In the first pair of EKGs, the computer appears to be confusing the pacemaker spike for a QRS complex; this is clearly “double counting of the QRS.”
The second pair is more complicated. This is not technically “double counting” of the QRS; there is not a 1:1 relationship between each QRS and a particular artifactual deflection. This is over-counting with a coincidental but not precise 2:1 relationship between the total count made by the computer and the total number of true QRS complexes. The interpretation of “Atrial Fibrillation” supports this in that it suggests that numerous complexes are counted during the first 5 seconds and then much fewer in the last 5. Although Littmann’s sign is not technically present here, the 12-lead EKG must be scrutinized to reach this conclusion. This seems problematic given Littmann’s stated goal of elucidating an “objective”, and “easily identifiable” indicator. (p.586)
No clinical data is available on these EKGs and it cannot be proven that these patients did not in fact have elevated potassium.
While producing these two hypothetical “false positives” hardly constitutes significant evidence, it is interesting that such counterpoints to Littmann’s specificity claims were so easily identified. Of further concern is the distinction between perfect double counting as seen in the pacemaker case and “near double counting” as seen in both the hyperkalemia case from Sept. 2010 and artifact case. What bearing this has on Littmann’s argument remains unclear.
Although a novel indicator, I am not sure that there is as yet persuasive evidence for what exactly Littmann’s sign indicates or how often this indication is specific for any one underlying clinical etiology.
Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007;25:584-90.
Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med. 2007 Nov;25(9):1077-8.
Al-Ahmad A, Wang PJ, Homoud MK, Estes NA 3rd, Link MS. Frequent ICD shocks due to double sensing in patients with bi-ventricular implantable cardioverter defibrillators. J Interv Card Electrophysiol. 2003 Dec;9(3):377-81.
Barold SS, Herweg B, Gallardo I. Double counting of the ventricular electrogram in biventricular pacemakers and ICDs. Pacing Clin Electrophysiol. 2003 Aug;26(8):1645-8.
Boriani G, Biffi M, Frabetti L, Parlapiano M, Galli R, Branzi A, Magnani B. Cardioverter-defibrillator oversensing due to double counting of ventricular tachycardia electrograms. Int J Cardiol. 1998 Sep 1;66(1):91-5.