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Troponin Bump

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.

Discussion

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.

Retrieved from: http://www.nature.com/scitable/content/troponin-and-tropomyosin-regulate-contraction-via-calcium-14723328

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.

Retrieved from: 
http://cardiovascres.oxfordjournals.org/content/77/4/649/F1.expansion

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:

Modified from Thygesen et al. (4)

Mechanisms potentially responsible for troponin elevation in this case include:

  1. Heart Failure
  2. Malignant Hypertension
  3. Ischemic Cardiomyopathy
  4. Alcoholic Cardiomyopathy
  5. Renal Failure
  6. Tachycardia with demand ischemia due to stable coronary leisions
  7. 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)

Regarding pericarditis:

“…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)

References

  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.
  2. Hamm, CW, Giannitsis, E, Katus, HA Cardiac troponin elevations in patients without acute coronary syndrome. Circulation 2002; 106, 2871-2872
  3. 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.
  4. 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
  5. Gibson, M. et al. Elevated cardiac troponin concentration in the absence of an acute coronary syndrome. UpToDate. July 11, 2012.

Posted by  |  July 31, 2012 | Categories: ECGs | Tags: , , , , , , , , | Leave A Comment »

STEMI seen in PVC

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:

  1. At least one lead with concordant STE (Sgarbossa criterion 1) or
  2. At least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
  3. 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)

References

  1. 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.
  2. 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.
  3. Dr. Stephan Smith. “LBBB: Is There STEMI?” Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2011/05/lbbb-is-there-stemi.html

Posted by  |  July 26, 2012 | Categories: Anterior Wall MI, ECGs, Uncategorized | Tags: , , , , , , , , , , , , | Leave A Comment »

Artifact from Frayed Leads Obscures STEMI

Introduction:

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.

Methods:

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.

Review:

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.

Case Presentation:

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.

Discussion:

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)

Artifact from nerve or muscle stimulators should also be of fixed amplitude and hold to a stable baseline. (1)

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,

  1. It is confined to a specific lead distribution– the lead with inconsistent connectivity.
  2. There is a chaotically wandering baseline.
  3. The cycle lengths are short (30-70Hz ?) and grossly irregular.
  4. 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.

Conclusion:

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.

References

  1. Equipment-related electrocardiographic artifacts: causes, characteristics, consequences, and correction. Patel SI, Souter MJ. Anesthesiology. 2008 Jan;108(1):138-48.
  2. Electrocardiographic artifacts during electroconvulsive therapy. Patel SI. J Electrocardiol. 2009 Jul-Aug;42(4):307-9. Epub 2009 Apr 2.
  3. Differential electrocardiographic artifact from implanted thalamic stimulator. Khan IA. Int J Cardiol. 2004 Aug;96(2):285-6. PMID: 15262047
  4. Electrocardiographic artifact caused by extracorporeal roller pump. Kleinman B, Shah K, Belusko R, Blakeman B. J Clin Monit. 1990 Jul;6(3):258-9. PMID: 2380757
  5. Electrocardiogram artifacts caused by deep brain stimulation. Constantoyannis C, Heilbron B, Honey CR. Can J Neurol Sci. 2004 Aug;31(3):343-6.
  6. ECG artifact produced by crystalloid administration through blood/fluid warming sets. Paulsen AW, Pritchard DG. Anesthesiology. 1988 Nov;69(5):803-4. PMID: 3189938 Free full text
  7. Life-threatening ECG artifact during extracorporeal shock wave lithotripsy. Schiller EC, Heerdt P, Roberts J. Anesthesiology. 1988 Mar;68(3):477-8. PMID: 3345012 Free full text
  8. ECG artifact due to deep brain stimulation. Martin WA, Camenzind E, Burkhard PR. Lancet. 2003 Apr 26;361(9367):1431. PMID: 12727397
  9. Electrocardiographic artifact induced by an electrical stimulator implanted for management of neurogenic bladder. Madias JE. J Electrocardiol. 2008 Sep-Oct;41(5):401-3. Epub 2008 Apr 28.
  10. An unusual electrocardiogram artifact: what is its source? [Gastric PM]  J Reddy NK, Merla R, Pehlivanov ND, Pasricha PJ, Ware DL, Birnbaum Y. Electrocardiol. 2005 Oct;38(4):337-9. PMID: 16216608
  11. Unusual ECG artifact. [Infusion Pump] Graham MM. J Nucl Med. 1981 Jul;22(7):660. PMID: 7252570 Free full text
  12. Electromechanical association: a subtle electrocardiogram artifact.[Radial arterial impulse] Aslanger E, Yalin K. J Electrocardiol. 2012 Jan-Feb;45(1):15-7. Epub 2011 Feb 24.
  13. Tremor-induced ECG artifact mimicking ventricular tachycardia. Srikureja W, Darbar D, Reeder GS. Circulation. 2000 Sep 12;102(11):1337-8.
  14. Tremor-related artefact mimicking ventricular tachycardia. Ortega-Carnicer J. Resuscitation. 2005 Jun;65(3):243-4. PMID: 15919558
  15. Parkinson’s tremor mimicking ventricular tachycardia. Bhatia L, Turner DR. Age Ageing. 2005 Jul;34(4):410-1. PMID: 15955765 [Free full text]
  16. Pseudo-ventricular tachycardia: electrocardiographic artefact mimicking non-sustained polymorphic ventricular tachycardia in a patient evaluated for syncope. A Vereckei. Heart. 2004 January; 90(1): 81. PMCID: PMC1768000. [Free Full Text]
  17. Ventricular pseudo-bigeminy due to sustained myoclonus. Chung DK, Reed JR, Chung EK. Heart Lung. 1976 Nov-Dec;5(6):961-3. PMID: 1049219
  18. An unusual case of misdiagnosed ventricular tachycardia. Boos CJ, Khan MY, Thorne S. Emerg Med J. 2008 Mar;25(3):173-4.
  19. Pseudo ventricular tachycardia: a case report. Riaz A, Gardezi SK, O’Reilly M. Ir J Med Sci. 2010 Jun;179(2):295-6. Epub 2009 Aug 7. PMID: 19662493
  20. Tremor-induced ECG artifact mimicking ventricular tachycardia. Srikureja W, Darbar D, Reeder GS. Circulation. 2000 Sep 12;102(11):1337-8. PMID: 10982552 Free full text
  21. Tremor-induced ECG artifact mimicking ventricular tachycardia. Freedman B. Circulation. 2001 May 29;103(21):E112-2. PMID: 11382744 Free full text
  22. ECG artifact simulating supraventricular tachycardia during automated percutaneous lumbar discectomy. Lampert BA, Sundstrom FD. Anesth Analg. 1988 Nov;67(11):1096-8. PMID: 3189899
  23. 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.
  24. The diagnostic use of respiratory artifact. Littmann L. J Electrocardiol. 2010 May-Jun;43(3):264-9. Epub 2009 Dec 2. PMID: 20399349
  25. Capsular contracture simulating myocardial infarction on ECG. Peters W, McEwan P. Plast Reconstr Surg. 1993 Mar;91(3):529-32. PMID: 8438025
  26. Influence of electrode misplacement on the electrocardiographic signs of inferior myocardial ischemia. Rudiger A, Schöb L, Follath F. Am J Emerg Med. 2003 Nov;21(7):574-7.
  27. [False diagnosis of myocardial infarction due to inversion of the electrocardiographic leads in the right limbs (author's transl)]. [Article in Spanish] Guijarro Morales A, Martos Ferrés F, Pagola Vilardebó C, Martín Jiménez V, Martí García JL, Peláez Redondo J. Med Clin (Barc). 1980 May 25;74(10):395-8.
  28. Delayed defibrillation caused by unexpected ECG artifact.[Bad lead selection and artifact] Stewart JA. Ann Emerg Med. 2008 Nov;52(5):515-8. Epub 2008 Apr 3. PMID: 18387704
  29. An unusual ECG artifact–results of a faulty recorder. Agarwal SK. JAMA. 1979 Aug 17;242(7):617-8. PMID: 448997
  30. Electrocardiographic ST-segment depression: confirm, deny, or artifact? [Filters] Wong DH. Anesthesiology. 2008 Aug;109(2):352; author reply 352. PMID: 18648245 Free full text
  31. False ST elevation in a modified 12-lead surface electrocardiogram. Toosi MS, Sochanski MT. J Electrocardiol. 2008 May-Jun;41(3):197-201. Epub 2008 Mar 14. PMID: 18342880
  32. Myocardial infarction or technical artifact? [Electrode misplacement] MacKenzie R. J Insur Med. 2006;38(4):289-92. PMID: 17323759
  33. Simulation of anteroseptal myocardial infarction by electrocardiographic filters. Burri H, Sunthorn H, Shah D. J Electrocardiol. 2006 Jul;39(3):253-8. Epub 2006 Feb 28. PMID: 16777511
  34. Electrocardiographic artifact mimicking acute myocardial infarction. Siddiqui MA, Munugoti S, Khan IA. Int J Cardiol. 2003 Jan;87(1):99-101. PMID: 12468060
  35. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Chase C, Brady WJ. Am J Emerg Med. 2000 May;18(3):312-6. PMID: 10830688
  36. An unusual electrocardiogram artifact in a patient with near syncope. Aslanger E. J Electrocardiol. 2010 Nov-Dec;43(6):686-8. Epub 2010 Jun 2. PMID: 20553822
  37. [Brugada or not-Brugada: misdiagnosis of recorder-induced artifact]. [Article in German] Z Kardiol. 2002 Dec;91(12):1061-3. Martius P, Krämer H.
  38. ECG artifacts and heart period variability: don’t miss a beat! Berntson GG, Stowell JR. Psychophysiology. 1998 Jan;35(1):127-32. PMID: 9499713
  39. Pacemaker malfunction: fact or artifact? Murdock DK, Moran JF, Stafford M, King L, Loeb HS, Scanlon PJ. Heart Lung. 1986 Mar;15(2):150-4.  PMID: 3633245
  40. An example of apparently normal electrocardiogram originating from incorrect electrocardiographic acquisition in a patient with ST-segment elevation myocardial infarction. J Electrocardiol. 2010 May-Jun;43(3):222-3. Epub 2010 Mar 23. Aslanger E, Yalin K, Golcuk E, Oncul A.
  41. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med. 2007 Jun;25(5):584-6. Littmann L, Brearley WD Jr, Taylor L 3rd, Monroe MH. PMID: 17543665
  42. Classic EKG changes of hypothermia. Mareedu RK, Grandhe NP, Gangineni S, Quinn DL. Clin Med Res. 2008 Dec;6(3-4):107-8. PMID: 19325173
  43. Common electrocardiographic artifacts mimicking arrhythmias in ambulatory monitoring. Márquez MF, Colín L, Guevara M, Iturralde P, Hermosillo AG. Am Heart J. 2002 Aug;144(2):187-97. PMID: 12177632
  44. Hiccup as an electrocardiographic artifact simulating arrhythmias. Am Heart J. 2003 Oct;146(4):E15; author reply E16. Cheng TO. PMID: 14564338
  45. “The Bait and Switch”. [Limb lead reversal due to inverted lead coupling conceals STEMI] Tom Bouthillet. EMS 12-Lead. 01-22-2011. Retrieved from: http://ems12lead.com/2011/01/the-bait-and-switch/
  46. “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

Posted by  |  July 16, 2012 | Categories: Anterior Wall MI, ECGs | Tags: , , , , , , , , , , | 9 Comments »

Lewis Lead Parallax

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.

 Discussion

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.

References 

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.

Posted by  |  June 11, 2012 | Categories: Dysrhythmia, ECGs | Tags: , , , , , , , | 4 Comments »

In re Littmann et al. (2007)…

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.

Posted by  |  June 5, 2012 | Categories: Dysrhythmia, ECGs, Electrolyte Imbalance | Tags: , , , , , , , , , , , | Leave A Comment »

The study of history teaches us that we do not learn from the study of history.

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.

Discussion

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:

Nortriptyline toxicity. Image courtesy of ECGpedia.

Dothiepin toxicity. Image courtesy of Life In The Fast Lane.

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.
The root cause of all of this remains unclear.

References

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.

Posted by  |  May 31, 2012 | Categories: Dysrhythmia, ECGs, Electrolyte Imbalance, s/p Arrest | Tags: , , , , , , , , | Leave A Comment »

The past is not dead, it is not even past.

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:

There is subtle evidence of hyperkalemia. Serology returned a BUN of 63, a Creatinine of 2.4, Sodium of 128, Potassium of 6.4, and Calcium of 10.0.

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:

AM lab results from this date indicated a BUN of 44, Creatinine of 1.4, Sodium of 136, and potassium of 4.0.

Discussion

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.

References

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

Posted by  |  March 26, 2012 | Categories: ECGs, Electrolyte Imbalance | Tags: , , , , , , , , | 1 Comment »

Littmann’s Sign

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.

References

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.

Posted by  |  March 15, 2012 | Categories: ECGs, Electrolyte Imbalance | Tags: , , , , , , , , , , | 4 Comments »

The Persistence of Memory: A return to “Atypical symptoms with a critical lesion.”

In 2010, as part of a case series exploring the presentation of AV block in the setting of inferior wall STEMI, I discussed the following EKGs:

It was hypothesized from these tracings that a proximal RCA lesion was responsible for the manifest inferior wall and right ventricular involvement, likely in the setting of a right dominant coronary system owing to the AV nodal dysfunction.

Recently I was able to follow up on this case.

This was a 64 year-old Caucasian female complaining of nausea, vomiting, and a syncopal episode while attempting to ambulate. Her history was significant for HTN, hyperlipidemia, breast cancer, and a mechanical aortic valve replacement in 2005. At that time a presurgical cath had identified a 70% ostial RCA stenosis. This baseline EKG was recorded on admission:

In 2008, on the date the case study EKGs were recorded, she became progressively hypotensive while in the emergency department and required intubation and vasopressor circulatory support. During emergent catheterization stents were placed across a 99% diffuse ostial RCA lesion and a further stenosis of the distal RCA. The interventionalist described a right dominant coronary system with a small LAD and circumflex. On arrival in the ED, a troponin of 0.14ng/mL was recorded. At noon on the following day the value had climbed to 55.20 and peaked at over 90 later that evening.

Due to cardiogenic shock, both an IABP and temporary pacemaker were placed. A long ICU course ensued during which numerous abnormalities were identified and addressed including but not limited to severe sepsis, a ruptured breast implant, gall bladder disease, elevated LFTs, and a renal mass suspicious for carcinoma. The following EKGs were recorded on ICU days 2, 3, and 4.

In June of 2009 she was again admitted to the hospital, at this time with a primary diagnosis of aspirational pneumonia complicated by renal insufficiency.

A tracheotomy was placed. Respiratory failure and sepsis were treated in the ICU and ventilator weaning was begun only to rebound with recurrent episodes of septic shock. This was repeated four times over a two-month period. Renal function progressively declined, as did her baseline mental status. This is the last EGK on file for this patient:

She experienced asystolic arrest and died the next day.

Discussion

Persistent ST-segment elevation following PCI has been shown to closely reflect the presence of microvascular reperfusion injury as demonstrated by impairment of microcirculatory flow on PET imaging and intracoronary contrast echocardiography. Mechanisms of reperfusion injury include neutrophil infiltration, tissue edema, and direct mivrovascular damage following tissue hypoxia. Impaired microcirculatory reperfusion resulting from these mechanisms has been correlated with more extensive infarction and a worse clinical outcome. Roughly 30%-40% of patients undergoing PCI demonstrate persistent STE on hospital discharge.

In their 1999 publication, Claeys et al. utilized persistent ST-segment elevation following PCI to identify patients at risk for reperfusion injury. They report, “Patients >55 years of age with systolic pressures <120mmHg were at high risk for development of impaired reperfusion compared with patients not meeting these criteria (72% versus 14%, P<0.001).” (Claeys et al., 1999, p.1972)

Also in 1999, Matetzky et al. demonstrated similar findings comparing clinical outcomes in patients with comparable angiographic results following PCI but contrasting presentations on ECG regarding the persistence of ST-segment elevation. Results of this research indicated that, “…ST segment elevation resolution was associated with better predischarge left ventricular ejection fraction…. Group B patients [those with persistent STE], as compared with those of Group A [those with early resolution of STE], had a higher incidence of in-hospital mortality (11% vs. 2%, p 0.088), congestive heart failure (CHF) (28% vs. 19%, odds ratio (OR) 4, 95% confidence interval (CI) 1 to 15, p 0.04), higher long-term mortality (OR 7.3, 95% CI 1.9 to 28, p 0.004 with Cox proportional hazard regression analysis) and long-term CHF rate (OR 6.5, 95% CI 1.3 to 33, p 0.016 with logistic regression).” (Matetzky et al., 1999, p.1932)

In 2007, Galiuto et al. investigated the clinical correlates found in patients demonstrating persistent STE following primary or rescue PCI. They report, “Such an ECG sign at hospital discharge may be considered associated with a large infarct size, and, in 30% of cases, with LV aneurysm formation and with continuing LV remodeling.” (Galiuto et al., 2007, p.1380)

These three studies reviewed between 100-150 patients each.

In 2010, however, Verouden et al. reviewed over 2100 patients undergoing PCI with the intent of further characterizing the clinical and demographic determinants of persistent ST-elevation after coronary intervention. They report that, “Incomplete ST-segment recovery was a strong predictor of long-term mortality…,” and, “…incomplete ST-segment recovery at the end of PCI occurred significantly more often in the presence of an age >60 years, nonsmoking, diabetes mellitus, left anterior descending coronary artery–related STEMI, multivessel disease, and preprocedural Thrombolysis In Myocardial Infarction grade 3 flow.” (Verouden et al., 2010, p.1692)

References

Claeys, M., et al. (1999). Determinants and prognostic implications of persistent ST-segment elevation after primary angioplasty for acute myocardial infarction: importance of microvascular reperfusion injury on clinical outcome. Circulation. 1999;99:1972-1977, doi: 10.1161/01.CIR.99.15.1972

Galiuto, L., et al. (2007). Functional and structural correlates of persistent ST elevation after acute myocardial infarction successfully treated by percutaneous coronary intervention. Heart. 2007; 93: 1376-1380, doi: 10.1136/hrt.2006.105320

Matetzky, S., et al. (1999). The significance of persistent ST elevation versus early resolution of ST segment elevation after primary PTCA. Journal of the American College of Cardiology. Vol. 34, No. 7, 1999.

Verouden, N., et al. (2010). Clinical and angiographic predictors of ST-segment recovery after primary percutaneous coronary intervention. American Journal of Cardiology. 2010;105:1692-1697.

Posted by  |  February 27, 2012 | Categories: Dysrhythmia, ECGs, Inferior Wall MI | Tags: , , , , , , , , , , , , | 2 Comments »

Case No. 16: Morbid Signature

A 37 year-old Caucasian male presents to the emergency department with palpitations of two hours duration. A 12-lead EKG is recorded.

The man is sedated and cardioversion is performed.

This 12-lead demonstrates an irregularly irregular, polymorphic wide complex tachycardia; this can only be atrial fibrillation with frequent conduction through a Wolf-Parkinson-White accessory pathway system.

The differential diagnosis for this presentation principally consists of polymorphic VT, RVR a-fib with ventricular conduction aberrancy, and a-fib with underlying WPW. The presence of multiple wide complex QRS morphologies excludes the diagnoses of a-fib with BBB, and, as Mattu and Brady have pointed out, polymorphic VT will typically hold a constant rate while this EKG shows significant variance between R-R intervals– from >450ms to <240ms. (Mattu, 2003, p.138)

RVR a-fib with aberrant conduction and gross ST-segment abnormalities but uniform QRS morphology. (EMS 12-Lead: 
http://ems12lead.com/2011/09/68-year-old-male-cc-chest-pain/
)

Polymorphic VT of Torsades de Points in the setting of hypokalemia and prolonged QT; multiple QRS morphologies but uniform rate. (LITFL: 
http://lifeinthefastlane.com/ecg-library/tdp/
)

Note that due to the fixed duration of the AV nodal refractory period, synchronized atrio-ventricular conduction is typically limited to below 200 impulses per minute. It is for this reason that RVR a-fib very rarely exceeds 180-200bpm. The bypass tract in WPW, however, has a dangerously short refractory period and thus can support re-entrant tachycardias well above this limit. As Chou has stated, “…the presence of the WPW syndrome can be suspected from the rhythm strip alone if the atrial fibrillation is accompanied by a ventricular rate greater than 200bpm. Such a rapid ventricular response would be highly unusual if the conduction is by way of the normal AV conduction system.” (Chou, 1996, p.480)

Antiarrhythmic agents which slow or block AV nodal conduction are contraindicated in this setting as they can enhance conduction through the accessory pathway and accelerate ventricular response. Procainamide and related sodium channel antagonists have therefore been used with favorable results.

Regarding amiodarone, although numerous case reports have tracked poor outcomes, it remains a popular treatment modality for this syndrome and may statistically be a safe alternative. In 2005, for example, Tijunellis and Herbert demonstrated a case-series of 10 patients in which amiodarone was malignantly proarhythmic; in half of these, the initial arrhythmia was v-fib. Nonetheless, case-series can be misleading and I do not know of definitive research in this area.

In light of this, judicious use of electrical therapy is often considered the safest and most reliable approach.

Mortality associated with the Wolf-Parkinson-White syndrome remains at <1% and is thought to result from rapid response a-fib degenerating into v-fib arrest (Ellis, 2011). This outcome can be fostered through inappropriate pharmacological management if the initial presentation is misunderstood. Fortunately, once this dramatic EKG signature has been appreciated, it is unlikely to go unrecognized.

Dr. Stephen Smith has discussed this syndrome and the treatment risks, and his insights can be found here. Among other remarks, he states, “Atrial fib with WPW is very recognizable: there are bizarre QRS with multiple morphologies, and very fast rhythms with short R-R intervals.  If you can find any R-R interval shorter than 240 ms, then AV nodal blockers are definitely dangerous.” (Smith, 2011)

I wish also to excerpt Dr. Johnson Francis of Cardiophile MD who has addressed this topic directly. Dr. Francis states, “The shortest RR interval gives an estimate of the ventricular refractory period. If it is below 250 msec, it is ominous as the ventricular rates can go very high and it can degenerate into ventricular fibrillation.” (Francis, 2008) Note that in this particular case, the overall ventricular rate is not excessively fast and perhaps speaks to the relative clinical stability of the patient.

Additional case studies of WPW a-fib can be found in the Case Library.

References

Chou, T. and Knilans, T. (1996). Electrocardiography in Clinical Practice: Adult and Paediatric, 4th Ed. W.B. Saunders Co.

Ellis, C., et al. (2011). Wolff-Parkinson-White Syndrome. Medscape eMedicine. Retrieved from: http://emedicine.medscape.com/article/159222-overview

Mattu, A. and Brady, W. (2003). ECGs for the emergency physician, V.1. BMJ Publishing Group.

Tijunelis, M. and Herbert, M. (2005). Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. Canadian Journal of Emergency Medicine. (4): No.4, p262. Retrieved from:
http://www.cjem-online.ca/v7/n4/p262

Posted by  |  January 5, 2012 | Categories: Dysrhythmia, ECGs | Tags: , , , , , , , | Leave A Comment »

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