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.
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)
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.
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.
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
A 63 year-old white female with multiple medical problems presents to EMS via direct call from her nursing facility with complaints of worsening respiratory distress since awakening this AM. The patient’s history includes IDDM, hyperlipidemia, morbid obesity, HTN, and supplemental oxygen dependent COPD. The patient has had several previous MIs, suffers from CHF, and has refused consultation for bypass grafting after a catheterization six months ago revealed advanced CAD.
The patient is found sitting on the edge of her bed in tripod position, diaphoretic, globally cyanotic, audibly wheezing, tachypneic at 32 breaths per minute with “one-word” dyspnea, and markedly agitated. Lung sounds reveal minimal tidal exchange, diffuse high-pitched wheezes, and faint rales at the mid-thorax where her breath sounds disappear. The heart rate is 130, the SpO2 86%, and the BP is 190/90. She denies chest discomfort, nausea, or recent illness.
I remember explicitly thinking to myself that the diagnosis not to miss here was exacerbation of CHF due to new MI. The patient was hypoxic, agitated, and becoming combative. I glanced at the first 12-lead and I thought, “this is non-diagnostic, not a cath-lab activation,” and STEMI disappeared from my mind. The patient was treated with nitrates, broncho-dilators, aspirin, and furosemide; on arrival in the ED, she could speak in complete sentences and her respiratory function was significantly improved.
EKG obtained on arrival in the ED. Subtle ST elevation and deepened Q-waves are present in III and aVF. These findings are new by comparison to the 2007 tracing below, as is the additional ST depression present in aVL and I; new T-wave inversions are also seen in V2 and V3, as well as deepening of the inversions in I and aVL. The patient’s 2007 EKG showing an old inferior infarct, consistent with the previous cath report.
When the ED physician confronted me about missing the STEMI I was incredulous. Even the higher-quality hospital 12-lead seemed to me ambiguous for acute MI. If “you can’t make the diagnosis if you don’t think it,” how could I have missed this STEMI? The quality of the tracings was poor: the baseline wanders; there is substantial movement artifact. Yet the question of STEMI is there: consider the ST depression and T-wave inversion in aVL, I, V5, andV6—there are even hints of ST depression in V1 and V2. Minimal but significant ST elevation can be discriminated in III and aVF. Interestingly, the rhythm strip reveals the elevations in II and III most dramatically.
So what happened?
Medical error is responsible for substantial morbidity and mortality even in today’s climate of patient safety awareness. I want to use this case, in which I missed a critical diagnosis, to discuss cognitive error in clininical decision making with respect to electrocardiographic diagnosis.
Numerous taxonomies of cognitive error have been described; I will highlight several categories which I believe are of particular relevance in electrocardiography.
Premature Closure. This occurs when a clinician makes a rapid, confident diagnosis, often based on prior personal experience, and subsequently ceases to collect additional data or re-evaluate the initial diagnosis in light of new findings. Once I had satisfied myself that the EKG was non-diagnostic, I closed my mind to the possibility of revising this assessment; I made no attempts to improve the quality of the tracings or reconsider the presence of subtle indicators of AMI. The value of serial EKGs even when the initial 12-lead is normal is uncontested; simply because a patient is showing no signs of STE at one juncture does not mean that the EKG will again be negative later on—this is particularly relevant if there is a change in clinical presentation or symptomology. Tom Bouthillet has several superior case presentations highlighting this phenomenon.
Diagnostic Anchoring. This takes place when a clinician clings prejudicially to an initial diagnosis even when new, conflicting data surfaces. I made a decision that my patient was not having a STEMI; even in light of the more obviously pathological and less artifactual hospital 12-lead, it was difficult to unmoor myself from my misguided diagnosis.
Conformation Bias. This occurs when once a diagnosis has been formed the clinician proceeds to only attend to data which support or reaffirm the initial impression; conflicting evidence is often trivialized or explained away. Once I had anchored myself to the diagnosis of a “non-diagnostic EKG,” all abnormalities of subsequent 12-leads were taken as further non-specific evidence rather than viewed as potential revisions of the initial impression.
Framing. This occurs when demographic or prejudicial stereotypes cause the clinician to dismiss or trivialize certain diagnoses based on a-priori judgment rather than clinical assessment. In electrocardiography this is sometimes encountered in the context of relatively positive stereotypes: the patient is too young, too healthy, or too asymptomatic for their ST-segment abnormalities to be due to coronary occlusion. In these cases, the “healthy person” frame results in the exclusion of an important differential. Alternatively, a “sick person” frame can result in inappropriately minimizing acute results: “Given this patient’s complex medical history, this grossly pathological EKG is probably normal for them.” Most frequently, however, framing errors likely result in failure to perform a 12-lead in the first place rather than misinterpretation of an EKG result. Protocols can help with this: some systems have policies which mandate a 12-lead EKG for all patients complaining of certain symptoms or presenting with certain histories. While the sentiment is not unwise in certain respects, it is sometimes said that one should “treat the patient, not the monitor.” Framing a patient by their symptoms alone can be a grave oversimplification. Rather, a responsible assessment will address all components of a clinical scenario in appropriate proportions.
Finally, I believe the issue of distraction has some application here. “Distracting injuries” are dramatic, attention grabbing foci which can divert either the clinician or the patient from observing an often more serious but more subtle finding. In this case, I was distracted by the patient’s clinical acuity. Yet even in non-bedside electrocardiography a profoundly obvious finding such as dramatic ST-elevation can distract from more subtle diagnostic features such as chamber enlargement or conduction abnormalities. In the previous case as well as the case series of October 2010, there are significant derangements of rhythm together with ST-elevation. It can be difficult to adhere to an unwaveringly systematic approach to EKG diagnosis when a finding such as STEMI is jumping out at you. In radiology, there is a cognitive forcing strategy used to address this phenomenon: “If you see a fracture, look for another one!” There may be a role for a similar forcing strategy in electrocardiography.
This is a subtle case, yet it illustrates how one diagnostic oversight can lead to a cascade of cognitive errors. Although the ED physician activated the cath-lab after viewing these EKGs, the patient ultimately made an informed refusal of PCI and again restated her wishes to not be evaluated for bypass grafting. Due to the absence of chest pain, she ruled out for lytic therapies and was subsequently transferred to the ICU for continued observation and conservative management. A positive troponin was returned 4 hours after ED arrival. Laboratory assays were notable for elevated BNP, Glucose, BUN and creatinine. A review of the prior catheterization in 2007 indicated severe ostial RCA disease with a total distal occlusion combined with a totally occluded LCx and moderate, diffuse LAD disease becoming more severe in the distal portions.
This case involved a critical error on my part which resulted in failure to activate time-sensitive resources. Under other circumstances this oversight could have cost the patient her life. I carry the memory of my errors forward.
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.
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). 
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. 
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. 
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.
As always, comments and additional observations are welcome. I am indebted to both Tom Bouthillet and Dr. Steven Smith for consultation on this case.
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 et. al.
 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
A 68yr long-term care inmate presented to nursing with an altered level of consciousness, chest pain, and bradycardia. Paramedic services were called to the scene for transport and found the nursing staff encouraging the pt to walk back and forth across the exam room to, “help bring his pulse up.” The following EKG was recorded. Note that voltage enhancement has been maximized in the rhythm strip to 2cm/mv, while the 12-lead is displayed with the standard gain of 10mm/mv.
As this is a third party case, little direct clinical or situational information is available to contextualize this EKG or the surrounding events. Objectively speaking, a markedly bradycardic junctional rhythm can be appreciated with retrograde conduction of p-waves, seen inverted, buried 160ms into the QRS complex. Net positive QRS deflections in I-III, avL and avF, and negative in avR indicate an axis in the lower left quadrant. Close examination reveals a 0.1mv electrical alternans, perhaps most evident in the limb leads, but also apparent (~0.05mv) in V5 and V6. Explicitly pathological features include subtle precordial T-wave inversions in V1-3 and conspicuous low voltage QRS amplitude in all leads.
Regarding this latter subject, numerous criteria have been suggested as to what constitutes abnormally low voltage; a consensus approach would consider either the sum of the QRS voltages in all 12 leads as necessarily less than 12mv, or a combined judgment requiring the average of QRS voltages in the limb leads as less than 5mm and that in the precordial leads less than 10mm.
The typical differential diagnosis associated with low voltage QRS includes etiologies of increased impedance (such as obesity, hyperinflative lung disease, and pericardial/pleural effusion), etiologies of infiltrative disease (such as hemochromatosis, amyloidosis, and neoplasm), and metabolic or toxicological causes (such as hypothyroidism and alcoholism). Low voltage has also been associated with both chronic and acute ischemic heart disease. An exhaustive review of the DDx can be found here.
While neither the clinical nor the electrocardiographic features of this case are sufficiently specific to seal any one diagnostic verdict, there are nonetheless some possibilities here worthy of note. Exogenous toxicological etiologies should be ruled out; hypotension with a slow junctional escape could be linked to digitalis, beta and calcium channel blockers, or other readily available pharmaceuticals. Of particular interest, the possibility of RCA associated ischemia must also be entertained. The pt’s clinical picture, low voltage QRS amplitude, and junctional bradycardia are strongly suggestive in this direction. Similar presentations with more explicit pathological substrates can be seen on this site in case nos. 4A- 4D, particularly the slow junctional STEMI of no. 4D.
Lastly, the subtle finding of electrical alternans forces a compelling consideration of pericardial effusion. Were the heart indeed spatially shifting within the pericardium from beat to beat, one would anticipate a greater shift of axis in the frontal, limb-lead plane than the transverse plane of the precordial leads, just as is present on this tracing. Alternating junctional foci or an artifact of physical positioning could produce a similar bigeminal effect, yet when this alternans is seen in the context of low voltage, the finding commands greater attention.
Paramedic services successfully temporized this pt’s status with atropine and supportive care until he reached the emergency department; there, after 20 minutes, he receded into semi-consciousness. No follow-up could be done.
A 64 yr old white female presented to EMS with n/v/d times three days and a recent episode of orthostatic syncope. She had no complaints of chest discomfort or shortness of breath. She was pale in apearance and found to be hypotensive on exam.
Although AV dissociation can be appreciated in the first three tracings, the fourth appears consistent with undifferentiated 2nd degree conduction block and prolonged (>200 ms) PR interval with bigeminal junctional escape. Close examination of II and V4-6 reveal a subtle morphological variation in the complexes, supporting the argument for multiple depolarization foci. A narrow-complex junctional escape rhythm is typical of a culprit RCA lesion resulting in often transient ischemia to the superior portion of the nodal tissue. Wide-complex 3rd degree block more frequently reflects a significant LCA infarction which has resulted in distal, more inferior conduction system damage that is less likely to recover. Note that the ST elevation in III is greater than that in II— a finding that has been correlated with RV involvement, although I know of no EBM trials to support this. It is regrettable that right-sided and posterior leads were not recorded.
AV conduction abnormalities can be appreciated in as much as 30% of inferior wall MIs owing to the ~70% prevalence of the RCA as the dominant vessel supplying the AV nodal branch. Left dominant coronary systems present a variation to the predictability of progressive conduction pathway ischemia but constitute only 10% of the populace. This leaves 20% with co-dominant systems. In the absence of confounding factors, it would be interesting if there has been a study demonstrating a decreased incidence of AV conduction blocks in pts with redundant AV nodal circulation who present with acute coronary syndrome.
Despite what appear to be convalescent ECG changes over the course of these three 12-leads, the pt. deteriorated rapidly in the ED and required pressor support and intubation before she could be transported to the cath lab. The outcome is unknown.
A 68 year old white male presenting to EMS with chest pain and a history of HTN. No further on this case in known at this time.
This ECG demonstrates a 3:2 Wenkibach phenomenon with an initial inconsistency, possibly due to an A:V ratio shift or artifactual event. Note the subtle elevation in V6; again, a 15lead tracing would have been optimal here.
It should not be forgotten that although inferior wall STEMI typically results from RCA occlusion, it may also arise from a lesion in the Circumflex; in the latter case, the right heart is spared and RCA dependent conduction system elements remain unaffected. Dr. Smith has recently presented an example of this phenomenon as well as a review of a risk stratification ECG algorhythm recently proposed to deliniate RCA vs CLX lesions on ECG. While the case above meets several of these criteria (aVR depression and V6 eleveation), the manifest conduction system involvment all but eliminates the possibility of a CLX eitiology. I hope to post a better example of the DeVerna RCA/CLX decision tool in the near future; see Dr. Smith’s ECG site for a superior and more appropriately exemplified discussion of this new research.