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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A 63 year-old white female with multiple medical problems presents to EMS via direct call from her nursing facility with complaints of worsening respiratory distress since awakening this AM. The patient’s history includes IDDM, hyperlipidemia, morbid obesity, HTN, and supplemental oxygen dependent COPD. The patient has had several previous MIs, suffers from CHF, and has refused consultation for bypass grafting after a catheterization six months ago revealed advanced CAD.
The patient is found sitting on the edge of her bed in tripod position, diaphoretic, globally cyanotic, audibly wheezing, tachypneic at 32 breaths per minute with “one-word” dyspnea, and markedly agitated. Lung sounds reveal minimal tidal exchange, diffuse high-pitched wheezes, and faint rales at the mid-thorax where her breath sounds disappear. The heart rate is 130, the SpO2 86%, and the BP is 190/90. She denies chest discomfort, nausea, or recent illness.
I remember explicitly thinking to myself that the diagnosis not to miss here was exacerbation of CHF due to new MI. The patient was hypoxic, agitated, and becoming combative. I glanced at the first 12-lead and I thought, “this is non-diagnostic, not a cath-lab activation,” and STEMI disappeared from my mind. The patient was treated with nitrates, broncho-dilators, aspirin, and furosemide; on arrival in the ED, she could speak in complete sentences and her respiratory function was significantly improved.
EKG obtained on arrival in the ED. Subtle ST elevation and deepened Q-waves are present in III and aVF. These findings are new by comparison to the 2007 tracing below, as is the additional ST depression present in aVL and I; new T-wave inversions are also seen in V2 and V3, as well as deepening of the inversions in I and aVL. The patient’s 2007 EKG showing an old inferior infarct, consistent with the previous cath report.
When the ED physician confronted me about missing the STEMI I was incredulous. Even the higher-quality hospital 12-lead seemed to me ambiguous for acute MI. If “you can’t make the diagnosis if you don’t think it,” how could I have missed this STEMI? The quality of the tracings was poor: the baseline wanders; there is substantial movement artifact. Yet the question of STEMI is there: consider the ST depression and T-wave inversion in aVL, I, V5, andV6—there are even hints of ST depression in V1 and V2. Minimal but significant ST elevation can be discriminated in III and aVF. Interestingly, the rhythm strip reveals the elevations in II and III most dramatically.
So what happened?
Medical error is responsible for substantial morbidity and mortality even in today’s climate of patient safety awareness. I want to use this case, in which I missed a critical diagnosis, to discuss cognitive error in clininical decision making with respect to electrocardiographic diagnosis.
Numerous taxonomies of cognitive error have been described; I will highlight several categories which I believe are of particular relevance in electrocardiography.
Premature Closure. This occurs when a clinician makes a rapid, confident diagnosis, often based on prior personal experience, and subsequently ceases to collect additional data or re-evaluate the initial diagnosis in light of new findings. Once I had satisfied myself that the EKG was non-diagnostic, I closed my mind to the possibility of revising this assessment; I made no attempts to improve the quality of the tracings or reconsider the presence of subtle indicators of AMI. The value of serial EKGs even when the initial 12-lead is normal is uncontested; simply because a patient is showing no signs of STE at one juncture does not mean that the EKG will again be negative later on—this is particularly relevant if there is a change in clinical presentation or symptomology. Tom Bouthillet has several superior case presentations highlighting this phenomenon.
Diagnostic Anchoring. This takes place when a clinician clings prejudicially to an initial diagnosis even when new, conflicting data surfaces. I made a decision that my patient was not having a STEMI; even in light of the more obviously pathological and less artifactual hospital 12-lead, it was difficult to unmoor myself from my misguided diagnosis.
Conformation Bias. This occurs when once a diagnosis has been formed the clinician proceeds to only attend to data which support or reaffirm the initial impression; conflicting evidence is often trivialized or explained away. Once I had anchored myself to the diagnosis of a “non-diagnostic EKG,” all abnormalities of subsequent 12-leads were taken as further non-specific evidence rather than viewed as potential revisions of the initial impression.
Framing. This occurs when demographic or prejudicial stereotypes cause the clinician to dismiss or trivialize certain diagnoses based on a-priori judgment rather than clinical assessment. In electrocardiography this is sometimes encountered in the context of relatively positive stereotypes: the patient is too young, too healthy, or too asymptomatic for their ST-segment abnormalities to be due to coronary occlusion. In these cases, the “healthy person” frame results in the exclusion of an important differential. Alternatively, a “sick person” frame can result in inappropriately minimizing acute results: “Given this patient’s complex medical history, this grossly pathological EKG is probably normal for them.” Most frequently, however, framing errors likely result in failure to perform a 12-lead in the first place rather than misinterpretation of an EKG result. Protocols can help with this: some systems have policies which mandate a 12-lead EKG for all patients complaining of certain symptoms or presenting with certain histories. While the sentiment is not unwise in certain respects, it is sometimes said that one should “treat the patient, not the monitor.” Framing a patient by their symptoms alone can be a grave oversimplification. Rather, a responsible assessment will address all components of a clinical scenario in appropriate proportions.
Finally, I believe the issue of distraction has some application here. “Distracting injuries” are dramatic, attention grabbing foci which can divert either the clinician or the patient from observing an often more serious but more subtle finding. In this case, I was distracted by the patient’s clinical acuity. Yet even in non-bedside electrocardiography a profoundly obvious finding such as dramatic ST-elevation can distract from more subtle diagnostic features such as chamber enlargement or conduction abnormalities. In the previous case as well as the case series of October 2010, there are significant derangements of rhythm together with ST-elevation. It can be difficult to adhere to an unwaveringly systematic approach to EKG diagnosis when a finding such as STEMI is jumping out at you. In radiology, there is a cognitive forcing strategy used to address this phenomenon: “If you see a fracture, look for another one!” There may be a role for a similar forcing strategy in electrocardiography.
This is a subtle case, yet it illustrates how one diagnostic oversight can lead to a cascade of cognitive errors. Although the ED physician activated the cath-lab after viewing these EKGs, the patient ultimately made an informed refusal of PCI and again restated her wishes to not be evaluated for bypass grafting. Due to the absence of chest pain, she ruled out for lytic therapies and was subsequently transferred to the ICU for continued observation and conservative management. A positive troponin was returned 4 hours after ED arrival. Laboratory assays were notable for elevated BNP, Glucose, BUN and creatinine. A review of the prior catheterization in 2007 indicated severe ostial RCA disease with a total distal occlusion combined with a totally occluded LCx and moderate, diffuse LAD disease becoming more severe in the distal portions.
This case involved a critical error on my part which resulted in failure to activate time-sensitive resources. Under other circumstances this oversight could have cost the patient her life. I carry the memory of my errors forward.