Posts tagged “cardiac arrest

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

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  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
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  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
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  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 SEmerg 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 PPlast 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
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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.


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.


Case No. 14: Rear View Mirror

A 59 year-old white female presents to EMS with two hours of 9/10 substernal chest pressure radiating into her left arm. Her history is significant for HTN, hyperlipidemia, and 30 pack-years smoking. The blood pressure is 90/50; she is diaphoretic and pale.

1st degree AV block can be seen complicating this inferolateral MI. Note that the STE in lead III is greater than that in II and caution should therefore be observed regarding right ventricular involvement. Of additional note is the unexpectedly tall R-wave in V2, a remarkable finding when met with right sided ST-depression.

In light of the ST elevations in V5 and 6, II, III, avF, and right precordial depressions suggestive of posterior wall infarction, it might seem reasonable to assume that a proximal culprit lesion is placing a large territory of myocardium at risk. In the past, however, there has been a lack of consensus among investigators with regard to whether either the number of leads demonstrating STE or the net magnitude of STE can be reliably correlated with the extent of myocardial injury. (Birnbaum and Drew, 2003, 492-493)

Without engaging the question of how myocardial injury can or should be quantified, it is clear that the 12-lead EKG does not equitably represent all myocardial territories. Not only are some regions better visualized than others, but electrical vectors can augment and dampen one another. This phenomenon is of particular interest when we consider that ST elevation in V4R, V1, and V2 due to right ventricular involvement may be canceled from view by the opposing vectors of a concomitant posterior wall infarction. Posterior forces may be likewise mitigated, even as they already demonstrate proportionally lower voltage due to the greater distance of the surface electrodes from the depolarizing myocardium.

Case reports of “normalization” resulting from the opposition of two independent currents of injury have been described. Wang and colleagues present a case in which the electrocardiographic evidence of acute anteroseptal infarction suddenly disappeared from view, they contend, as a direct result of a new, electrically oppositional, infarction of the posterior wall. Their abstract is as follows:

In a 76-year-old man an electrocardiographic pattern of acute anteroseptal myocardial infarction disappeared suddenly. At necropsy, a more recent posterior myocardial infarct was found, in addition to an acute anteroseptal infarct. “Normalization” of the electrocardiogram from the pattern of anteroseptal myocardial infarction in this case resulted from the loss of opposing electromotive forces in the posterior wall because of posterior infarction. (Wang, K., et al., 1976)

Thus, when considering the “rear view” leads, there is a real sense in which things “may be larger than they appear.” Therefore, regardless of ones skepticism as to the proportionality between ST elevation and actual myocardial tissue necrosis (Birnbaum), a high index of suspicion should be maintained when a pattern of acute changes implicates an arterial lesion likely placing two ischemic myocardial territories opposite one another (Wang).

Although this 15-lead EKG shows only non-specific T-wave inversion in V4R, the posterior leads V7 and V8 demonstrate subtle ST elevation, thus confirming what can be suspected from the initial tracing. The 1st degree block has resolved, and the magnitude of ST elevation has diminished.

Despite what appeared to be an initially positive response to medical management, the final pre-hospital tracing recorded from this patient shows unifocal PVCs in the pattern of bigeminy.

This was to prove an ominous sign in this case, as shortly after arrival in the ED the patient became unconscious and was noted to be in ventricular tachycardia. Pulses were initially present and cardioversion was performed. Sinus rhythm resumed briefly but again gave way to VT, this time without pulses. Despite aggressive efforts, refractory VF persisted for over 30 minutes and the patient could not be resuscitated.

Dr. Stephen Smith has discussed the issue of posterior wall STEMI through a series of case presentations and his insights on this topic can be found here.

Tom Bouthillet also has a superior set of case studies addressing the issue of posterior STEMI; the category “Acute Posterior STEMI” can be found here, in his site index.

Of additional note, AV block is a frequent finding in inferior wall MI and further case studies illustrating this and discussing the mechanism involved can be found on this site in the case series of September, 2010.

References

Birnbaum, Y. and Drew, B. 2003. The electrocardiogram in ST elevation acute myocardial infarction: correlation with coronary anatomy and prognosis. Postgrad. Med. J. 2003;79;490-504. doi:10.1136/pmj.79.935.490

Wang, K., et al. 1976. Sudden disappearance of electrocardiographic pattern of anteroseptal myocardial infarction. Result of superimposed acute posterior myocardial infarction. Chest. 1976;70;402-404. doi: 10.1378/chest.70.3.402 


Case No. 5: Coded in a Vietnamese ICU, now Lethargic in a US Rehab

While vacationing in Vietnam two months ago, this 57 yr old white female presented to an urgent care center with complaints of nausea and weakness. Within twenty-four hours she had coded and was on life support in a Vietnamese ICU.

Now she is home, in a rehab center, recuperating as mysteriously as she had fallen ill. Her medical team believes that perhaps she had been given a paralytic agent in the Vietnamese ED; theoretically, this may have resulted in elevated potassium and a state of recurrent iatrogenic cardiac arrest. She has been feeling progressively better, she states, until this morning, when she began experiencing an unusual nausea and sense of weakness.

She is ill appearing and hypotensive, near syncopal on ambulation. The following ECG is recorded by EMS at the scene:

And in the ED:

The Accelerated Idioventricular Rhythm was first characterized as a distinct pathophyiological entity in 1950 by A.S. Harris following the ligation and reperfusion of coronary vessels in animal models. A reperfusion based etiology has continued to predominate as the leading documented setting for AIVR, particularly in light of the growing population of post-PCI patients receiving telemetry services. Incidence has also been well established, however, in structural heart disease– both congenital as well as acquired forms– and in the setting of presumed pharmacological effects. Digitalis, cocaine, halothane, and desfurane, among others, have all been cited in the literature as culprit agents, believed to accelerate the phase 4 action potential depolarization of His-Purkinje pacemaker sites, leading to the possibility of rate competition between atrial and ventricular foci. Less pathological contexts have also been reported, however, and include highly conditioned athletes, pregnant women, and some pediatric populations. A.R. Perez Riera et al. hypothesize that a hypervagotonic / hyposympathetic mechanism is at work here, facilitating the automaticity of ventricular activity by suppressing sino av-nodal pacemakers; work in animal models seems to support this, and there is case documentation in the literature of AIVR resolving through treatment with vagolytic agents such as atropine.

Electrocardiographically, AIVR may be identified when a monomorphic wide complex ventricular rhythm supervenes over the atrial rate, persisting between 60-100bpm. Fusion beats, capture complexes, and retrograde atrial depolarization may be observed, and it is not unusual to note frank evidence of AV dissociation. These findings, including clinical evidence of cannon A waves, may expedite or cement the diagnosis as it does in VT as well as 3rd degree block. AIRV is often spontaneously initiating and resolving, and it is frequently seen as a transient phenomenon– again, most typically post reperfusion or resuscitation. While some patients predisposed to cardiac insufficiency may experience critical loss of ejection fraction as a result of AV dissociation, AIVR is not typically associated with a declining clinical picture. Treatment of the condition should, as always, reflect respect for the pt’s clinical presentation rather than certainty in the pathology of the rhythm; over-treatment may be a greater clinical risk than under-treatment.

An excellent case of AIVR can be seen here at Dr. Wiki, showing fusion and capture complexes, or here, at Medscape ECG of the week. The Emergency Medicine site, Life In The Fast Lane, has also presented a case of AIVR in the highly conditioned athlete which demonstrates subtle isorhythmic AV dissociation.

In the case presented above, our patient suffered a precipitous cardiovascular collapse shortly after admission to the intensive care service; she was resuscitated from PEA arrest twice on the first hospital day and required ventilatory support and renal replacement therapy for most of her 12-day course. Ultimately, a transfer to a large academic medical center with more extensive capabilities was arranged and the patient was subsequently lost to follow up.

Despite consultation with Cardiology, Infectious Disease, and Critical Care services, no definitive diagnostic position was ever reached in this case. Cardiac enzymes, echo, electrolytes, and cultures were all unrevealing. I developed a close relationship with this patient and even now remain discouraged that we had nothing to say to her and her family when so much was at stake.

References

I am indebted to A.R. Perez Riera et al. for their excellent review and discussion of the literature; many of the following references are via their guidance.

Harris AS. Delayed development of ventricular ectopic rhythms following experimental coronary occlusion. Circulation 1950; 1:1318-1328.

Marret E, Pruszkowski O, Deleuze A, et al. Accelerated idioventricular rhythm associated with desflurane administration. Anesth Analg 2002; 95: 319-321.

Jonsson S, O’Meara M, Young JB. Acute cocaine poisoning. Importance of treating seizures and acidosis. Am J Med. 1983; 75: 1061-1064.

Bonnemeier H, Ortak J, Wiegand UK, et al. Accelerated idioventricular rhythm in the post-thrombolytic era: incidence, prognostic implications, and modulating mechanisms after direct percutaneous coronary intervention. Ann Noninvasive Electrocardiol 2005; 10: 179-187.

Scheinman MM, Thorburn D, Abbott JA. Use of atropine in patients with acute myocardial infarction and sinus bradycardia. Circulation 1975; 52: 627-633.

Basu D, Scheinman M. Sustained accelerated idioventricular rhythm. Am Heart J 1975; 89: 227-231.


Case No. 3: Status Post Cardiac Arrest

An 84yr old white female, s/p VT/PEA arrest.

This ECG demonstrates AV dual sequenced pacing with loss of atrial capture. Note the high left axis in the x-y plane, consistent with typical pacer findings, but an atypical rightward shift of electrical forces across the precordial z-axis (inverse R-wave progression). Traditionally ventricular pacing electrodes are deployed in the right heart and result in a LBBB ECG morphology as the myocardial tissue depolarizes from right to left. Yet in this case we see a dramatic RBBB pattern, raising concerns about displacement or septal perforation, particularly given that the pt. has received CPR. The etiology of RBBB pacer morphology is not exclusively pathological, however, and receives a good discussion on Dr. S. Venkatesan’s Cardiology Blog. Note that the QRS in this case is elongated above 160ms, and necessarily reflects slow and poorly coordinated ventricular contraction, perhaps betraying a newly aberrant interventricular conduction pathway, even for this 100% paced patient.

Another interesting example of a similar RBBB effect can be seen at Dr. M. Rosengarten’s electrocardiography site, and there is a thorough case report and research analysis of the phenomenon in The Journal of Electrocardiography Vol.6 No. 1, 2003.

Shortly after this 12-lead was captured, the pt. again deteriorated into PEA and was lost to resuscitative efforts.