Posts tagged “AMI

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

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 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

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. 13: The Devil is in the Details

A 63 year-old white female with multiple medical problems presents to EMS via direct call from her nursing facility with complaints of worsening respiratory distress since awakening this AM. The patient’s history includes IDDM, hyperlipidemia, morbid obesity, HTN, and supplemental oxygen dependent COPD. The patient has had several previous MIs, suffers from CHF, and has refused consultation for bypass grafting after a catheterization six months ago revealed advanced CAD.

The patient is found sitting on the edge of her bed in tripod position, diaphoretic, globally cyanotic, audibly wheezing, tachypneic at 32 breaths per minute with “one-word” dyspnea, and markedly agitated. Lung sounds reveal minimal tidal exchange, diffuse high-pitched wheezes, and faint rales at the mid-thorax where her breath sounds disappear. The heart rate is 130, the SpO2 86%, and the BP is 190/90. She denies chest discomfort, nausea, or recent illness.

Prehospital rhythm strip and 12-lead EKGs

I remember explicitly thinking to myself that the diagnosis not to miss here was exacerbation of CHF due to new MI. The patient was hypoxic, agitated, and becoming combative. I glanced at the first 12-lead and I thought, “this is non-diagnostic, not a cath-lab activation,” and STEMI disappeared from my mind. The patient was treated with nitrates, broncho-dilators, aspirin, and furosemide; on arrival in the ED, she could speak in complete sentences and her respiratory function was significantly improved.

EKG obtained on arrival in the ED. Subtle ST elevation and deepened Q-waves are present in III and aVF. These findings are new by comparison to the 2007 tracing below, as is the additional ST depression present in aVL and I; new T-wave inversions are also seen in V2 and V3, as well as deepening of the inversions in I and aVL. The patient’s 2007 EKG showing an old inferior infarct, consistent with the previous cath report.

When the ED physician confronted me about missing the STEMI I was incredulous. Even the higher-quality hospital 12-lead seemed to me ambiguous for acute MI. If “you can’t make the diagnosis if you don’t think it,” how could I have missed this STEMI? The quality of the tracings was poor: the baseline wanders; there is substantial movement artifact. Yet the question of STEMI is there: consider the ST depression and T-wave inversion in aVL, I, V5, andV6—there are even hints of ST depression in V1 and V2. Minimal but significant ST elevation can be discriminated in III and aVF. Interestingly, the rhythm strip reveals the elevations in II and III most dramatically.

So what happened?

Medical error is responsible for substantial morbidity and mortality even in today’s climate of patient safety awareness. I want to use this case, in which I missed a critical diagnosis, to discuss cognitive error in clininical decision making with respect to electrocardiographic diagnosis.

Numerous taxonomies of cognitive error have been described; I will highlight several categories which I believe are of particular relevance in electrocardiography.

Premature Closure. This occurs when a clinician makes a rapid, confident diagnosis, often based on prior personal experience, and subsequently ceases to collect additional data or re-evaluate the initial diagnosis in light of new findings. Once I had satisfied myself that the EKG was non-diagnostic, I closed my mind to the possibility of revising this assessment; I made no attempts to improve the quality of the tracings or reconsider the presence of subtle indicators of AMI. The value of serial EKGs even when the initial 12-lead is normal is uncontested; simply because a patient is showing no signs of STE at one juncture does not mean that the EKG will again be negative later on—this is particularly relevant if there is a change in clinical presentation or symptomology. Tom Bouthillet has several superior case presentations highlighting this phenomenon.

Diagnostic Anchoring. This takes place when a clinician clings prejudicially to an initial diagnosis even when new, conflicting data surfaces. I made a decision that my patient was not having a STEMI; even in light of the more obviously pathological and less artifactual hospital 12-lead, it was difficult to unmoor myself from my misguided diagnosis.

Conformation Bias. This occurs when once a diagnosis has been formed the clinician proceeds to only attend to data which support or reaffirm the initial impression; conflicting evidence is often trivialized or explained away. Once I had anchored myself to the diagnosis of a “non-diagnostic EKG,” all abnormalities of subsequent 12-leads were taken as further non-specific evidence rather than viewed as potential revisions of the initial impression.

Framing. This occurs when demographic or prejudicial stereotypes cause the clinician to dismiss or trivialize certain diagnoses based on a-priori judgment rather than clinical assessment. In electrocardiography this is sometimes encountered in the context of relatively positive stereotypes: the patient is too young, too healthy, or too asymptomatic for their ST-segment abnormalities to be due to coronary occlusion. In these cases, the “healthy person” frame results in the exclusion of an important differential. Alternatively, a “sick person” frame can result in inappropriately minimizing acute results: “Given this patient’s complex medical history, this grossly pathological EKG is probably normal for them.” Most frequently, however, framing errors likely result in failure to perform a 12-lead in the first place rather than misinterpretation of an EKG result. Protocols can help with this: some systems have policies which mandate a 12-lead EKG for all patients complaining of certain symptoms or presenting with certain histories. While the sentiment is not unwise in certain respects, it is sometimes said that one should “treat the patient, not the monitor.” Framing a patient by their symptoms alone can be a grave oversimplification. Rather, a responsible assessment will address all components of a clinical scenario in appropriate proportions.

Finally, I believe the issue of distraction has some application here. “Distracting injuries” are dramatic, attention grabbing foci which can divert either the clinician or the patient from observing an often more serious but more subtle finding. In this case, I was distracted by the patient’s clinical acuity. Yet even in non-bedside electrocardiography a profoundly obvious finding such as dramatic ST-elevation can distract from more subtle diagnostic features such as chamber enlargement or conduction abnormalities. In the previous case as well as the case series of October 2010, there are significant derangements of rhythm together with ST-elevation. It can be difficult to adhere to an unwaveringly systematic approach to EKG diagnosis when a finding such as STEMI is jumping out at you. In radiology, there is a cognitive forcing strategy used to address this phenomenon: “If you see a fracture, look for another one!” There may be a role for a similar forcing strategy in electrocardiography.

This is a subtle case, yet it illustrates how one diagnostic oversight can lead to a cascade of cognitive errors. Although the ED physician activated the cath-lab after viewing these EKGs, the patient ultimately made an informed refusal of PCI and again restated her wishes to not be evaluated for bypass grafting. Due to the absence of chest pain, she ruled out for lytic therapies and was subsequently transferred to the ICU for continued observation and conservative management. A positive troponin was returned 4 hours after ED arrival. Laboratory assays were notable for elevated BNP, Glucose, BUN and creatinine. A review of the prior catheterization in 2007 indicated severe ostial RCA disease with a total distal occlusion combined with a totally occluded LCx and moderate, diffuse LAD disease becoming more severe in the distal portions.

This case involved a critical error on my part which resulted in failure to activate time-sensitive resources. Under other circumstances this oversight could have cost the patient her life. I carry the memory of my errors forward.


Case No. 12: Eerily Calm

A 35 yr old white male presents to EMS with 20 minutes of 8/10 burning epigastric discomfort and left arm numbness. He denies nausea and shortness of breath; he is non-diaphoretic. He appears fit, healthy, and eerily calm.The pt. relates that this is not his “typical heartburn.” The only thing it reminds him of is when, 10 years ago, “a truck I was working on fell on my chest.” His BP is 180/110; his glucose is 399mg/Dl.  He states that he has no medical history and has not seen a doctor in years. His father had an MI at 45, and died of another at 56; his mother died of an MI when she was 53. Social history reveals 16 pack-years of smoking.

The following EKG was recorded on arrival at the ED:The initial prehospital 12-lead in this case demonstrates a junctional tachycardia with ST elevation in V2-5, I, and avL; reciprocal depressions are suggested in V6, III, and avF sealing the diagnosis acute anterolateral MI. Evidence of an inverted P-wave buried within the QRS complex may be appreciated in the first deflection of the depolarizations in lead I. Sinus tachycardia supervenes in the second and third prehospital 12-leads, as well as the tracing obtained on arrival in the ED. Note the dramatic Q waves and loss of R-wave progression seen across the precordium, often a valuable tool for differentiating STEMI from benign early repolarization. Also of interest in this case is the 7th complex seen in the third prehospital tracing. The QRS morphology here reflects that of the initial junctional rhythm, while the p-wave preceding the complex remains normative, perhaps indicating an event of junctional fusion.

Contiguous precordial ST elevations are typically associated with lesions of the LAD and circumflex. Although the majority of coronary systems are right-dominant with the AV nodal branch arising from the distal RCA, in a left-dominant system the AV node is perfused by a distal branch of the left circumflex. Thus, while the specific anatomy remains unknown here, the presence of junctional tachycardia may reflect an irritable AV nodal focus resulting from circumflex disease in the setting of left-dominance. The graphics below illustrate these coronary variants.

Anterior views of the coronary arterial system, with the principal variations. The right coronary arterial tree is shown in magenta, the left in full red. In both cases posterior distribution is shown in a paler shade. A, The most common arrangement. B, A common variation in the origin of the sinuatrial nodal artery. C, An example of left ‘dominance’ by the left coronary artery, showing also an uncommon origin of the sinuatrial artery. (Text and images retrieved from: http://pgmcqs.com/2011/05/17/anatomy-thorax/)

Coronary angiography in this case revealed an 85% proximal occlusion of the left circumflex, a 60% proximal occlusion of the first diagonal branch and a 40% diffuse occlusion of the second diagonal branch. Stents were deployed across the two more serious lesions, reducing their stenosis to 0% post procedure. A 22-minute DTB time was recorded. Documentation of cardiac enzymes was not available at the time of follow up, however this pt made a good recovery and was discharged several days post PCI.


Case No. 10: An occlusion, an aneurysm, or a trap for an octopus…

Two EKGs from an outside source, apparently found on the counter in the ED…

The differential diagnosis for this patient’s EKGs includes acute MI, historical MI with left ventricular aneurysm, reperfusion effects, and acute neurological catastrophe with catecholaminergic stress pattern.

AMI must be ruled out. Frank concave downward ST elevation in V2-6 with subtle findings (~0.5-1.0mm STE) in the inferior distribution raises immediate concern for the inferolateral territory via a lesion of the circumflex in a left-dominant system. This apprehension is tempered by the absence of ST depression in the anterior leads. In left-dominant systems (15% of the population), the PDA originates from the LCx; thus, although a proximal occlusion can present with STE in the inferior and lateral leads, it should also demonstrate reciprocal depression opposite the posterior wall in the anterior leads.

On the left is a normal (80%) Right-Dominant coronary system showing the PDA branching from the RCA. On the right is a volume rendered CT image demonstrating a Left-Dominant system with the PDA (arrowhead) and a posterolateral branch (white arrow) arising from the circumflex (black arrow). [1]

Inferolateral STEMI secondary to Left-Dominant LCx occlusion showing reciprocal depressions across the anterior leads.

A proximal occlusion of a wraparound LAD resulting in an “inferoanterior” STE pattern could also be hypothesized, perhaps with greater similarity to the case study EKGs, and a good case report of this phenomenon with angiographic evidence can be found in Akdemir et al. (2005). The graphic bellow illustrates the interpretive advantages of such a theory.

Note that the inferior elevations in both this case from Akdemir et al. and in the title EKGs are most apparent in aVF. Given that aVF views the inferior apical region, elevation seen here might be considered contiguous and consistent with elevations in V2-5 looking at the anterior wall. The territory of infarction can then be seen as a continuous band, reaching down the path of the wraparound LAD, down the anterior wall, and curling under the heart to the inferior wall.

Ultimately the diagnosis of STEMI would command greater credence here were there clearly pronounced reciprocal changes in corresponding leads. While in the first EKG one can imagine a fraction of a millimeter of ST depression in aVL, there are no explicit reciprocal depressions and the global T-wave inversions cannot be accorded any significance in this regard. Rather, if committed to the diagnosis of STEMI, the T-wave inversions might be considered a Wellenoid feature, perhaps suggesting a prodrome of isolated T inversions which has subsequently evolved into acute STE. Lastly, the case for AMI is supported by the prolonged QT interval, although this remains a non-specific factor.

On consultation with Tom Bouthillet of EMS 12-Lead, it was suggested that a reperfusion T-wave pattern might help to explain some of what is seen here. This view is attractive from a morphological standpoint and can perhaps be best explicated via comparison with an exemplar case as seen below.

This EKG represents post-reperfusion of a 100% occluded wraparound LAD; Dr Smith (2011) states, “There are “reperfusion” T-waves in V1-V6 and I, aVL.  There is a QS-wave in V2, and QR-wave in aVL, and poor R-wave progression in V3 and V4, all diagnostic of anterolateral MI, subacute.”

As in this EKG from Dr. Smith, the QS complexes and obliteration of R-wave progression from the case study tracings raises suspicion of a subacute or chronic pathology. In conjunction with the concave downward ST segment morphology, an extinction of anterior electrical forces with deep pathologic Q-waves suggests the possibility of persistent ST elevation due to prior MI and LV aneurism. Dr. Smith (2005) has proposed a formula for the differentiation of anterior STEMI from persistent STE secondary to historical MI premised on the ratio of the T-wave to the QRS amplitude; qualitatively, AMI should present with large T-wave amplitude relative to the QRS, while LV aneurysm should demonstrate a comparatively lower T/QRS ratio. Smith states, “the T/QRS ratio in any one of leads V1-V4 was almost always higher than 0.36 in acute MI, and almost always lower in LV aneurysm. Better was a T amplitude (V1+V2+V3+V4) / QRS amplitude (V1+V2+V3+V4) <> 0.22.”

Applying this rule to the initial case study EKG, (V1-1.5mm, V2-2mm, V3-3mm, V4-4.5mm) / (10mm, 23mm, 21mm, 12mm) = 0.16. Biphasic or inverted T-waves are unlikely in AMI, yet they are not uncommon in LVA. Observe the ST morphology and T-wave inversions in the EKG below.

In their 2008 case study, Biyik et al. captured this EKG, stating, “Thirty days after myocardial infarction, echocardiography revealed an akinetic apical aneurysm, anterolateral hypokinesia of the left ventricle, and decreased ejection fraction (45%).”

Both the results from the Smith formula and comparison with the EKG above point away from AMI and more toward a historical MI w/ LVA. It has been suggested, however, that a tall R-wave in aVR may be correlated with aneurysm; the absence of this finding here is of unclear significance but perhaps counts against the mounting argument for LVA.

Lastly, global, deep symmetric T-wave inversions transgressing multiple territories of coronary perfusion have long been documented in the setting of acute neurological catastrophe. Inferoanterior ST elevation and prolonged QT have also been described in this context, specifically with regard to Takotsubo syndrome, and can be seen below.

A patient with Takotsubo cardiomyopathy demonstrating ST elevation in anterior and inferior leads. [2]

Top represents a pt’s baseline EKG with QTc of 407; bottom is the same pt., now with echocardiographic evidence of Takotsubo syndrome, showing diffuse T-wave inversions and a prolonged QTc calculated at 519. [3]

The mechanism of these neurogenic EKG manifestations is believed to result from an autonomicaly mediated catecholamine surge leading to transient coronary vasospasm and myocardial ischemia. The case study, “Status post arrest, now with transtentorial herniation,” from September 2010 of The Jarvik 7 discusses this issue at greater length, and it should be noted that the ST deflections in the 2010 case are comparably global in distribution, again showing incongruity with traditional zones of coronary perfusion.

Returning, however, to Biyik’s 2008 case, it is not surprising to find a correlation between LV aneurysm morphology and neurogenic stress cardiomyopathy. An LVA electrocardiographic overlay may reflect the physiological reality that Takotsubo syndrome is partly characterized by a “ballooning” or temporary aneurysm of the apical region of the left ventricle. In this case, Biyik reports of a 35yr male presenting with intense agitation following a narrowly avoided attempt on his life. Future inquiry and systematic literature review may yield confirmation of this relationship and further insight into the mechanisms involved.

In the absence of clinical context or additional test results, these EKGs present a challenging electrocardiographic differential diagnosis. By morphological as well as mathematical criteria, the anterior leads are suggestive of LVA, yet the limb leads betray additional findings which demand a more inclusive pathophysiology. In light of the arguments explored above—principally the suspiciously non-localized ST and T-wave abnormalities coupled with the morphological elements of the T inversions—the case for an ischemic stress pattern may carry the most persuasive weight.

References

As always, comments and additional observations are welcome. I am indebted to both Tom Bouthillet and Dr. Steven Smith for consultation on this case.

Akdemir, R. et al. (2003). Simultaneous anterior and inferior myocardial infarction due to occlusion of the left anterior descending coronary artery. Turkish Journal of Medical Science, 34. 121-126.

Biyik, I., Yagtu, V., & Ergene O. (2008). Acute myocardial infarction triggered by acute intense stress in a patient with panic disorder, Turkish Society of Cardiology, 36(2), 111-115.

Smith, S. (2005). T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. American Journal of Emergency Medicine, 23(3), 279-287.

Smith, S. (2011). Hyperacute T-waves, missed by computer, short DTB, but large myocardial infarction. Dr. Smith’s EKG Blog. Retrieved from http://hqmeded-ecg.blogspot.com/2011/01/hyperacute-t-waves-missed-by-computer.html.

Tomich, E., Merchant, E., & Kang, C. (2011). Takotsubo Cardiomyopathy, eMedicine. Retrieved from http://emedicine.medscape.com/article/1513631-overview.

[1]Lin, E., Bredeweg, R., & Sicuro, P. (2010) Coronary CT Angiography, eMedicine. VRCT image retrieved from http://emedicine.medscape.com/article/1603072-overview.

[2] Tomich et. al.

[3] Wong, A. et al. (2010). Preoperative takotsubo cardiomyopathy identified in the operating room before induction of anesthesia. Anesthesia & Analgesia, 110(3), 712-715. doi: 10.1213/ane.0b013e3181b48594