A 47 year-old man was previously being managed for hypertension but stopped taking his medications in favor of a “homeopathic” regimen. There was periodic exertional dyspnea but no chest pain, lightheadedness, orthopenea, or peripheral edema. While driving one day he became acutely short of breath. Paramedics found him severely dyspnic with tachycardia, basilar rails, and a blood pressure of 250/155mmHg. He denied chest pain, heaviness, neck, back, or arm discomfort. An EKG was acquired. ST elevation was noted in contiguous precordial leads accompanied by a late anterior transition zone. There was also ST depression in the inferior and lateral leads. The appearance of LVH was severe but the S/ST proportions were difficult to assess due to the paper size. On arrival at the hospital another two EKGs were captured. This appeared slightly more benign, however a positive troponin assay was returned at 2.24ng/mL.
Physical exam at this time was notable for positive hepatojugular reflux, a pronounced S4 gallop, and crackles throughout the lung fields. There was no JVD or peripheral edema. The BUN was 40, Creatinine 2.2, ALT and AST of 51 and 57. The LDL was >200. No BNP was recorded. Detailed history revealed one prior episode of hypertensive crisis but no established CAD or CHF. He had quit smoking but continued to drink somewhat heavily as per his wife. His father suffered from both HTN and CHF and was no longer living.
The patient was admitted to ICU with hypertensive crisis and heart failure. Ejection fraction by echo was estimated at 30% with LVH and global systolic dysfunction. Cardiac catheterization on the third hospital day revealed a right dominant coronary system with severe triple vessel disease constituted by multiple complex lesions and several well-formed collaterals. Recommendation was for CABG evaluation.
The troponin peaked slightly above 4.0.
Elevation of cardiac troponins in the absence of acute coronary occlusion is not uncommon. This is particularly true of the severely ill. In the absence of a diagnostic electrocardiogram, low and even moderate level elevations should not overly persuade the clinician of an acute thrombotic coronary etiology.
On the molecular scale, muscle contraction results from a ratchet like interaction between actin and myosin microfilaments. The myosin “thick” filaments repeatedly attach, pull, and release from the actin “thin” filaments. As the two filaments slide along one another this telescoping is transmitted to the boundaries of the cell to produce a unified cellular contraction.
Retrieved from: http://www.pathologyoutlines.com/topic/stainsactin.html
In order to regulate and coordinate the contraction of filaments, an inhibitory protein, tropomyosin, lies along the length of each actin strand and occludes the actin-myosin attachment sites. When membrane depolarization occurs, calcium ions are released from the sarcoplasmic reticulum and bind to tropomyosin, shifting it out of the way and disinhibiting the contractile interaction of myosin and actin.
Tropomyosin effects its inhibitory activity at the active site through the troponin regulatory complex. This complex is a trimer consisting of troponin I (cTnI), troponin C (cTnC), and troponin T (cTnT). The cross-bridge active sites are occluded by the inhibitory “I” tropoin subunit. When the myocyte depolarizes, calcium ions are released from the sarcoplasmic reticulum and bind to the troponin C subunit. This produces a conformational change in the complex which retracts troponin I and unblocks the binding site for cross-bridge between actin and myosin.
Serum immunoassays for the proteins troponin I and troponin T have shown high sensitivity for cardiac myocyte injury and necrosis. The aggregate of these proteins is structurally bound to tropomyosin, however some free cytosolic troponin I and T is known to exist. The mechanisms where by these proteins are liberated into the blood serum remain incompletely characterized.
Retrieved from: http://acb.rsmjournals.com/content/45/4/349.abstract
Significant elevations of serum troponins regularly occur in the absence of acute thrombotic coronary occlusion. Thygesen and collegues have described three categories of non-ACS related troponin elevation:
Mechanisms potentially responsible for troponin elevation in this case include:
- Heart Failure
- Malignant Hypertension
- Ischemic Cardiomyopathy
- Alcoholic Cardiomyopathy
- Renal Failure
- Tachycardia with demand ischemia due to stable coronary leisions
- Unlikely but possible PE or significant Pulmonary Hypertension
The literature addressing non-ACS related troponin elevation is extensive; below are excerpts touching on some of the most common etiologies.
Regarding troponin elevation in heart failure:
“Release of TnI from cytosolic pool as a result of myocardial cell membrane injury without damage of structurally bound TnI has been reported. However, cytosolic TnI has been estimated to account for < 2% of total intracellular TnI. It is perhaps more likely that detectable troponin in HF reflects ongoing degradation of contractile protein and cellular injury. An increased level of neurohormonal factors, oxidative stress, and a number of cytokines are universal in HF. Each of these factors is known to promote cardiac cell death; therefore, they may be responsible for the elevation of troponin in HF.” (3)
“…Elevation of troponin in acute pericarditis is believed to represent injury of the epicardial layer of myocardium adjacent to visceral pericardium where the active inflammation occurs…” (3)
“Bonnefoy et al reported that approximately one half of their 69 consecutive patients (49%) with acute idiopathic pericarditis had troponin I (TnI) levels > 0.5 ng/mL. Twenty-two percent had TnI levels > 1.5 ng/mL, their cut-off level for acute MI. The average TnI level was 8 ± 12 ng/mL (range, 0 to 48 ng/mL). The median level was, however, only 1 ng/mL.” (3)
Regarding troponin elevation in sepsis:
“…there are several potential mechanisms, other than acute MI, for troponin release in septic patients. First, it is well known that a number of local and circulating mediators (eg, cytokines or reactive oxygen species) possess direct cardiac myocytoxic properties. Secondly, myocardial injury from the effect of bacterial endotoxins has been demonstrated. Finally, dysfunction of the microcirculation has been described in sepsis. This microvascular dysfunction can lead to ischemia and reperfusion injury of the myocardial cell.” (3)
Regarding troponin elevation in PE:
“Right ventricular dilation and strain from sudden increase in pulmonary arterial resistance is believed to be the cause of troponin release in acute PE.” (3)
“Giannitis et al, reported the incidence and prognostic significance of troponin T (TnT) elevation in patients with confirmed acute PE. Of the 56 patients, 32% had elevated TnT levels (≥ 0.1 ng/mL). In contrast, only 7% had CK levels above twice the upper limit of normal. Using a clinical grading system adapted from Goldhaber, 23%, 46%, and 30% of the patients were classified as having small PE, moderate-to-large PE, and massive PE, respectively. Elevated TnT was only observed in patients with either moderate-to-large PE or massive PE. None of those with small PE had increased TnT. TnT-positive patients were more likely to have right ventricular dysfunction, severe hypoxemia, prolonged hypotension, or cardiogenic shock. They also more often required inotropic therapy or mechanical ventilation than those with negative TnT. Complete or incomplete right bundle-branch block or ST-T changes on ECG were also more prevalent in TnT-positive subgroup. More importantly, TnT positivity was associated with approximately 30-fold increased risk of in-hospital mortality. In addition, TnT level was found to be an independent predictor of the 30-day outcome. Survival rates at 30 days were 60% and 95%, respectively, for those with and without TnT elevation.” (3)
Regarding troponin elevation in renal disease:
“In patients with severe renal dysfunction troponin T as well as troponin I, elevations are found that cannot be linked to myocardial injury. The reasons for these elevations are not yet convincingly explained. Reexpression of cardiac isoforms in skeletal muscles has been excluded by different analyses and investigators.13,14 Loss of membrane integrity and constant outflow from the free cytosolic troponin pool as well as amplified elevation of normal low levels because of impaired renal excretion are more likely. The higher unbound cytosolic pool and higher molecular weight may explain why troponin T is more frequently found elevated than troponin I.” (2)
As a final note, in 2011 Afonso et al retrospectively reviewed 567 patients admitted with a diagnosis of “hypertensive emergency.” Of these, 186 (32%) had cTnI elevation with the mean peak level at 4.06. They conclude, “Predictors of cTnI were age, history of hypercholesterolemia, blood urea nitrogen level, pulmonary edema, and requirement for mechanical ventilation. … Neither the presence nor the extent of cTnI elevation was associated with mortality, while age, history of coronary artery disease, and blood urea nitrogen level were predictive of mortality.” (1)
- Afonso L, et al. Prevalence, determinants, and clinical significance of cardiac troponin-I elevation in individuals admitted for a hypertensive emergency. J Clin Hypertens (Greenwich). 2011 Aug;13(8):551-6. doi: 10.1111/j.1751-7176.2011.00476.x. Epub 2011 Jun 27.
- Hamm, CW, Giannitsis, E, Katus, HA Cardiac troponin elevations in patients without acute coronary syndrome. Circulation 2002; 106, 2871-2872
- Roongsritong C, Warraich I, Bradley C. Common Causes Of Troponin Elevations In The Absence Of Acute Myocardial Infarction: Incidence And Clinical Significance. CHEST. 2004;125(5):1877-1884.
- Thygesen K, Mair J, Katus H, et al. Recommendations for the use of cardiac troponin measurement in acute cardiac care. Eur Heart J 2010; 31:2197
- Gibson, M. et al. Elevated cardiac troponin concentration in the absence of an acute coronary syndrome. UpToDate. July 11, 2012.
Although the previous case study was written for formalistic reasons and is admittedly neither very interesting nor particularly original, there is one interesting feature here worthy of note:
The arrows indicate complexes resulting from intermittant LBBB or PVCs with LBBB morphology. The latter is more likely given that their differing frontal plane axes (-60 vs +60) implicate two separate foci.
Despite aberrant conduction, the current of injury resulting from the anterior infarct remains explicit and is diagnostic of coronary occlusion.
In the first EKG (04:15) the complexes in V2 and V3 show appropriately discordant STE, but the ST/S ratio is groselly excessive. In 2010, Dodd and colegues demonstrated that an ST/S ratio >0.2 carries high specificity for LAD occlusion (1). Note the ratios in this case:
V2: ST/S = 6mm/7mm = ~0.86
V3: ST/S = 5.5mm/11mm = 0.5
In the second EKG (07:10) there is >1mm concordant STE in V4 and V6. In LBBB, the ST segments should always be discordant, and, when the terminal R wave is positive, they should show an appropriate proportion of ST depression. Thus, even in V6 where the J-point is isoelectric, there is a conspicuous absence of ST depression. This is a STEMI equivalent (2). Even if this patient had a baseline LBBB and the entire EKG showed wide-complex aberrancy, the MI would not be hidden.
These features as illustrated here closely reflect the more thorough and authoratative work of Dr. Smith in his May 21, 2011 blog post, “LBBB: Is There STEMI?“
Reproduced from his text:
Smith modified Sgarbossa rule:
- At least one lead with concordant STE (Sgarbossa criterion 1) or
- At least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
- Proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S ratio of equal to or more than 0.20 and at least 2 mm of STE. (this replaces Sgarbossa criterion 3 which uses an absolute of 5mm)
- Dodd KW. Aramburo L. Broberg E. Smith SW. For Diagnosis of Acute Anterior Myocardial Infarction Due to Left Anterior Descending Artery Occlusion in Left Bundle Branch Block, High ST/S Ratio Is More Accurate than Convex ST Segment Morphology (Abstract 583). Academic Emergency Medicine 17(s1):S196; May 2010.
- Dodd KW. Aramburo L. Henry TD. Smith SW. Ratio of Discordant ST Segment Elevation or Depression to QRS Complex Amplitude is an Accurate Diagnostic Criterion of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block (Abstract 551). Circulation October 2008;118 (18 Supplement):S578.
- Dr. Stephan Smith. “LBBB: Is There STEMI?” Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2011/05/lbbb-is-there-stemi.html
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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- Pseudo-atrial flutter/fibrillation in Parkinson’s disease. Prabhavathi B, Ravindranath KS, Moorthy N, Manjunath CN. Indian Heart J. 2009 May-Jun;61(3):296-7.
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- “Unusual EKG/ECG Pattern: You don’t see this everyday”. The Happy Hospitalist. 04-15-2011. Retrieved from: http://thehappyhospitalist.blogspot.com/2011/04/unusual-ekgecg-pattern-you-dont-see.html
The following was recorded from a 90 year-old Caucasian man with shortness of breath.
This is very suspicious for second degree block; bigeminal PACs or PJCs with compensatory pauses are also possibilities. There is poor visualization of atrial activity due to background noise and intrinsic low voltage. The 12-lead is referenced for the best lead to visualize:
V1 seems promising; a V1 rhythm strip is acquired:
Worse still. Next, the Lewis lead:
Now the diagnosis is transparent. Before resorting to the placement of Lewis electrodes, the voltage gain can be doubled and noise reduction strategies applied. These were not utilized here.
12-lead under Lewis electrode placement:
There is diminished QRS voltage, new inferior Q-waves and ST-segment abnormalities. This could easily be misinterpreted, but it is an artifact of the lead system.
Switching back to standard placement. Different electrodes were used at this time and the voltage is altered; the background noise has faded but the atria remain quiet:
This patient was ultimately found to be pancytopenic (WBCs 3.1, RBCs 1.17, Hem 4.8, Crit 13.0, Platelets 96, Neu 23, Lym 60, Monos 16) and was worked up for myelodysplastic syndrome. The electrocardiographic findings may be associated with the anemia; they may also be incidental.
Christopher Watford brought the Lewis lead to my attention; he has described its physiology and advantages extensively in his blog post, Highlighting Atrial Activity on an ECG: The S5 Lead, as well as via audio on the EMCrit Podcast with Scott Wiengart.
There are numerous alternative lead systems: Brughada leads, high and low precordial placements for visualizing poorly represented territories, systems designed to emphasize pacemaker activity, etc. Body surface mapping technologies (e.g. The 80-Lead Prime ECG) have also shown promise. Some of these lead systems are described on this site under EKG Resources.
Bakker, A., et al. (2009). The lewis lead: Making recognition of P waves easy during wide QRS tachycardia. Circulation, (2009), 119; e592-e593. [Free Full Text] doi: 10.1161/CIRCULATIONAHA.109.852053
Lewis T. (1931). Auricular fibrillation. Clinical Electrocardiography. 5th ed. London, UK: Shaw and Sons; 1931: 87–100.
For background regarding EKG double counting and Littmann’s sign of hyperkalemia, see March, 2012.
The following was recorded from an 82 year-old female with lethargy and malaise; electrolyte status is unknown, as is any further clinical data.
This is a 10 second strip with 9 QRS complexes; the true heart rate is thus 54bpm. The GE-Marquette 12SL interpretation algorithm has counted 163bpm, (3 x 54 = 162). Assuming that this is a result of systematic error and not coincidence, both the mechanism and significance of triple counting remain unclear.
New EKGs and new insights on a 2010 cold case. To recap:
While vacationing in Saigon a 57 year-old Caucasian female presented to the local emergency center with complaints of nausea and light-headedness. She experienced cardiac arrest, was resuscitated, and was found to have a persistent idioventricular rhythm coupled with significant acidosis and hypotension. She required multiple pressors and ultimately recovered despite a syndrome of multi-system organ failure. She was stabilized and transferred back to the states to a medical rehab facility. Infectious disease work up revealed only Candida Pelliculosa.
After several weeks in rehab, she again presented to the ED with complaints of nausea and light-headedness. Her past medical history included an aortic valve replacement (secondary to aortic stenosis), paroxysmal a-fib, diabetes, and depression. She was taking coumadin, flecainide, lexapro, januvia, and lopressor. Her BP on arrival was 81/44; the following EKG was recorded:
She had no complaints of chest discomfort or shortness of breath. At this time the potassium was 4.1, sodium 133, chloride 104, creatinine 3.1, BUN 31, glucose 114, and lactic acid 1.4. The white blood count was elevated at 15.6k. Amylase, lipase, AST and ALT were all mildly above normal. The pH was 7.01.
Her mental status deteriorated; she was intubated in the ED and transferred to the ICU. That night she suffered a PEA arrest and was resuscitated; multiple pressors were added sequentially for homodynamic support and a dialysis catheter and arterial line were placed. Peri-arrest bradyarrythmias were frequent and a transvenous pacemaker was inserted.
On the second hospital day the following EKG was recorded:
The potassium was 4.9, the sodium 135, chloride 101, creatinine 3.9, BUN 41, glucose 187, and lactic acid 13.
The cardiology consultant believed this to be an idioventricular rhythm of likely metabolic origin, secondary to electrolyte disturbance, possible flecainide or lexapro toxicity, or sepsis. Despite a widened QRS, the echocardiogram revealed a normal EF. Lexapro and flecainide were discontinued at this time.
On the third hospital day this EKG was recorded:
Labs from this date show a potassium of 3.5, sodium 143, chloride 97, creatinine 4.1, BUN 30, glucose 256, and lactic acid 23.
The blood pressure and electrocardiogram gradually stabilized; all cardiac enzyme assays were negative. By the seventh day she was extubated and transferred back to the hospital at which she had been originally treated returning from Vietnam. No bacteria, fungus, or parasites were isolated during this admission, however, she did have a positive hep-c antibody. Prior to discharge this EKG was recorded:
Labs from this date indicate a potassium of 3.4, sodium of 142, chloride 110, creatinine 2.4, BUN 40, glucose 303, and lactic acid 2.4.
She was subsequently lost to follow up.
The differential diagnosis for a sinusoidal, wide complex rhythm between 80-120bpm with QRST fusion includes hyperkalemia, sodium channel blocker toxicity, aberrant QRS AIVR, and tachycardia with aberrant conduction and massive ST elevation. In 2010, when I first presented these EKGs, I believed that this case (in the acute phase) represented AIVR.
The dominant pacemaker may in fact be idioventricular. The presence of AV dissociation would confirm this, but I do not see P waves. The third EKG (hospital day 3) is equivocal. This could also be a-fib with AIVR and dissociation.
Even if the rhythm is AIVR, there is still a more important diagnosis at stake.
For comparison, and to illustrate this, here are some exemplars:
This is typical AIVR:
Image courtesy of Life In The Fast Lane
This is RBBB with LAFB and massive STE:
Image courtesy of Dr. Smith’s ECG Blog
Hear are three cases of sodium channel blockade with TCA cardio-toxicity:
Unknown TCA toxicity. Image courtesy of EB Medicine.
This is purported cocaine cardiotoxicity with features of sodium channel blockade:
Image courtesy of ECGpedia.
Two cases of flecainide toxicity:
Image courtesy of Bond et. al., Heart 2010.
Image courtesy of EB Medicine.
Sodium channel blocker and specifically flecainide toxicity has been covered extensively in the literature; the following excerpts are particularly relevant in light of this case.
“Flecainide is an increasingly used class 1C antiarrhythmic drug used for the management of both supra-ventricular and ventricular arrhythmias. It causes rate-dependent slowing of the rapid sodium channel slowing phase 0 of depolarization and in high doses inhibits the slow calcium channel.” (Timperley, 2005)
“Cardiac voltage-gated sodium channels reside in the cell membrane and open in response to depolarization of the cell. The sodium channel blockers bind to the transmembrane sodium channels and decrease the number available for depolarization. This creates a delay of sodium entry into the cardiac myocyte during phase 0 of depolarization. As a result, the upslope of depolarization is slowed and the QRS complex widens.” (Hollowell, p.880– graphic and text.)
“Bradydysrhythmias are rare in sodium channel blocking agents because many of these also possess anticholinergic or sympathomimetic properties. These agents can, however, affect the pacemaker cells that are dependent on sodium entry, thus causing bradycardia. In severe poisoning, the combination of a wide QRS complex and bradycardia is a sign of overwhelming sodium channel blockade of all channels, including the pacemaker cells.” (Delk, p.683)
“Due to its significant effect on sodium channels, flecainide prolongs depolarization and can slow conduction in the AV node, the His-Purkinje system, and below. These changes can lead to prolongation of the PR interval, increased QRS duration, and first- and second-degree heart block. ….In contrast, flecainide does not affect repolarization and therefore has little effect on the QT interval.” (Giardina, G. 2010)
“Impending cardiovascular toxicity in adult patients [with TCA poisoning] is usually preceded by specific ECG abnormalities: the majority of pateints at significant risk will have a QRS duration >100ms or a rightward shift (130-270) of the terminal 40ms of the frontal plane QRS vector. The later finding is characterized by a negative deflection of the terminal portion of the QRS complex in lead I and a positive deflection of the same portion in lead avR.” (Van Mieghem, p.1569)
“In severe cases [of sodium channel blocker toxicity], the QRS prolongation becomes so profound that it is difficult to distinguish between ventricular and supraventricular rhythms. Continued prolongation of the QRS complex may result in a sine wave pattern and eventual asystole.” (Holstege, p166.)
There are multiple mechanisms for flecainide toxicity in this case.
- Reduced metabolism and elimination due to impairment of liver and renal function.
- Significant acidosis resulting in a decrease in protein bound flecainide and an increase in the free (active) agent in the blood stream.
- Borderline hyponatremia as a potential predisposing condition for over-therapeutic sodium channel blockade.
Bond, R., et al. (2010). Iatrogenic flecainide toxicity. Heart (2010), 96:2048-2049 doi:10.1136/hrt.2010.202101
Delk, C., et al. (2007). Electrocardiographic abnormalities associated with poisoning. American Journal of Emergency Medicine, (2007), 25, 672-687.
Giardina, G. (2010). Major side effects of flecainide. UpToDate.
Harrigan, R., et al. (1999). ECG abnormalities in tricyclic antidepressant ingestion. American Journal of Emergency Medicine, (1999), July 17(4), 387 – 393.
Hollowell, H. et al. (2005) Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with aberrant conduction. American Journal of Emergency Medicine, (2005), 23, 876 – 889.
Holstege, C., et al. (2006). ECG manifestations: The poisoned patient. Emerg Med Clin N Am, 24 (2006) 159–177. Free full text.
Timperley, J., et al. (2005). Flecainide overdose– support using an intra-aortic balloon pump. BMC Emergency Medicine, (2005), 5: 10. doi: 10.1186/1471-227X-5-10
Van Mieghem, C., et al. (2004). The clinical value of the ECG in noncardiac conditions. Chest (2004), 125, 1561-1576.
Williamson, K., et al. (2006). Electrocardiographic applications of lead aVR. American Journal of Emergency Medicine (2006), 24, 864-874.
In April of 2011 I presented a case of subtle hyperkalemia. A reader, Dr. George Nikolic, author of Practical Cardiology 2nd Ed., responded with the following commentary,
“The QT is unusually long for hyperkalemia; the lady may have additional pathology (e.g., myxoedema) or be on some QT prolonging medication. The commonest cause of low voltage is large or multiple infarcts in the past. What were her other medical problems?”
I was unable to follow up on this case until recently. Here is what I uncovered:
The patient was an 81 year-old caucasian female nursing home resident of unknown social background with a past history of hypertension, dyslipidemia, diabetes, colon cancer (s/p diverting ileostomy), depression and dementia. Despite numerous cardiac risk factors, she had no explicit history of myocardial infarction, coronary disease, or CHF. There was no history of thyroid disease or obesity.
Her medications consisted of Lexapro 10mg, Aricept 5mg q.h.s, Lopressor 12.5mg b.i.d., folic acid, and Imdur 30mg daily.
She had visited the Emergency Department 12 days prior to this episode with complains of weakness and bradycardia. At that time her BUN was 22, Creatinine 0.8, Sodium 136, Potassium 3.7, and Calcium 9.1. The following EKG was recorded:
Cardiology was consulted and a differential of sick-sinus syndrome vs. beta-blocker toxicity was considered. The Lopressor was reduced, and, following a 48-hour admission, she was discharged back to the nursing home with a slightly increased heart rate.
Two weeks later, on the date in question, she again presented to the ED with complaints of syncope and generalized weakness. This EKG was recorded on arrival:
The hospitalist’s admission note described a provisional diagnosis of acute renal failure secondary to dehydration and possible UTI. Obstructive failure was also considered in light of the cancer history. Most revealing, a thorough chart review revealed two prior admissions for acute renal failure secondary to dehydration from high-output ileostomy syndrome.
Echocardiography on the second hospital day reported no chamber enlargement, no increased wall thickness, no wall motion abnormalities, no valvular disease, no pericardial or pleural effusion, and a normal systolic function with an EF > 55%.
On the third hospital day she was discharged back to her nursing facility with the following EKG:
The differential diagnosis for low voltage is broad; neoplastic, metabolic, autoimmune, infectious, genetic, and acquired disease states are all represented.
When bradycardia is added, the field narrows: thyroid disease, acute or chronic ischemia, and hypothermia are among the most common etiologies.
In hyperkalemia, it is traditionally understood that when the QRS is normal, the QTc should be either shortened or unremarkable. (Smith, Jan 12, 2010; Lipman-Massie, p.579) In this case, the QTc at 6.4mEq K+ (394) is practically identical to the QTc at 4.0 mEq K+ (394). I do not know if the GE-Marquette algorithm uses the Bazett formula for QTc, but this formula is known to under-correct at abnormally low heart rates. (Wikipedia, 2012) Therefore, although the QTc here may be longer than the computer estimates, in an adult female, a QTc of 395 remains if anything on the short side of normal. Regarding medications, however, Lexapro is known to cause QT prolongation.
There was no effusion, as I had originally hypothesized in 2011. We do not have a solid culprit for the low voltage. The QT looks relatively normal. I am grateful for Dr. Nikolic’s attention and comments regarding this case. Fortunately for the patient, the clinical correlations do not seem to support either of our theories.
Dunn, B. and Lipman, B. (1989) Lipman-Massie Clinical Electrocardiography, 8th Ed. Yearbook Medical Publisher Inc.
Smith, S. (2010) Hyperkalemia with cardiac arrest. Peaked T waves: hyperacute (STEMI) vs. early repolarization vs. hyperkalemia. http://hqmeded-ecg.blogspot.com/2010/01/peaked-t-waves-hyperacute-stemi-vs.html
Wikipedia. (2012) QT interval. http://en.wikipedia.org/wiki/QT_interval