A 47 year-old man was previously being managed for hypertension but stopped taking his medications in favor of a “homeopathic” regimen. There was periodic exertional dyspnea but no chest pain, lightheadedness, orthopenea, or peripheral edema. While driving one day he became acutely short of breath. Paramedics found him severely dyspnic with tachycardia, basilar rails, and a blood pressure of 250/155mmHg. He denied chest pain, heaviness, neck, back, or arm discomfort. An EKG was acquired. ST elevation was noted in contiguous precordial leads accompanied by a late anterior transition zone. There was also ST depression in the inferior and lateral leads. The appearance of LVH was severe but the S/ST proportions were difficult to assess due to the paper size. On arrival at the hospital another two EKGs were captured. This appeared slightly more benign, however a positive troponin assay was returned at 2.24ng/mL.
Physical exam at this time was notable for positive hepatojugular reflux, a pronounced S4 gallop, and crackles throughout the lung fields. There was no JVD or peripheral edema. The BUN was 40, Creatinine 2.2, ALT and AST of 51 and 57. The LDL was >200. No BNP was recorded. Detailed history revealed one prior episode of hypertensive crisis but no established CAD or CHF. He had quit smoking but continued to drink somewhat heavily as per his wife. His father suffered from both HTN and CHF and was no longer living.
The patient was admitted to ICU with hypertensive crisis and heart failure. Ejection fraction by echo was estimated at 30% with LVH and global systolic dysfunction. Cardiac catheterization on the third hospital day revealed a right dominant coronary system with severe triple vessel disease constituted by multiple complex lesions and several well-formed collaterals. Recommendation was for CABG evaluation.
The troponin peaked slightly above 4.0.
Elevation of cardiac troponins in the absence of acute coronary occlusion is not uncommon. This is particularly true of the severely ill. In the absence of a diagnostic electrocardiogram, low and even moderate level elevations should not overly persuade the clinician of an acute thrombotic coronary etiology.
On the molecular scale, muscle contraction results from a ratchet like interaction between actin and myosin microfilaments. The myosin “thick” filaments repeatedly attach, pull, and release from the actin “thin” filaments. As the two filaments slide along one another this telescoping is transmitted to the boundaries of the cell to produce a unified cellular contraction.
Retrieved from: http://www.pathologyoutlines.com/topic/stainsactin.html
In order to regulate and coordinate the contraction of filaments, an inhibitory protein, tropomyosin, lies along the length of each actin strand and occludes the actin-myosin attachment sites. When membrane depolarization occurs, calcium ions are released from the sarcoplasmic reticulum and bind to tropomyosin, shifting it out of the way and disinhibiting the contractile interaction of myosin and actin.
Tropomyosin effects its inhibitory activity at the active site through the troponin regulatory complex. This complex is a trimer consisting of troponin I (cTnI), troponin C (cTnC), and troponin T (cTnT). The cross-bridge active sites are occluded by the inhibitory “I” tropoin subunit. When the myocyte depolarizes, calcium ions are released from the sarcoplasmic reticulum and bind to the troponin C subunit. This produces a conformational change in the complex which retracts troponin I and unblocks the binding site for cross-bridge between actin and myosin.
Serum immunoassays for the proteins troponin I and troponin T have shown high sensitivity for cardiac myocyte injury and necrosis. The aggregate of these proteins is structurally bound to tropomyosin, however some free cytosolic troponin I and T is known to exist. The mechanisms where by these proteins are liberated into the blood serum remain incompletely characterized.
Retrieved from: http://acb.rsmjournals.com/content/45/4/349.abstract
Significant elevations of serum troponins regularly occur in the absence of acute thrombotic coronary occlusion. Thygesen and collegues have described three categories of non-ACS related troponin elevation:
Mechanisms potentially responsible for troponin elevation in this case include:
- Heart Failure
- Malignant Hypertension
- Ischemic Cardiomyopathy
- Alcoholic Cardiomyopathy
- Renal Failure
- Tachycardia with demand ischemia due to stable coronary leisions
- Unlikely but possible PE or significant Pulmonary Hypertension
The literature addressing non-ACS related troponin elevation is extensive; below are excerpts touching on some of the most common etiologies.
Regarding troponin elevation in heart failure:
“Release of TnI from cytosolic pool as a result of myocardial cell membrane injury without damage of structurally bound TnI has been reported. However, cytosolic TnI has been estimated to account for < 2% of total intracellular TnI. It is perhaps more likely that detectable troponin in HF reflects ongoing degradation of contractile protein and cellular injury. An increased level of neurohormonal factors, oxidative stress, and a number of cytokines are universal in HF. Each of these factors is known to promote cardiac cell death; therefore, they may be responsible for the elevation of troponin in HF.” (3)
“…Elevation of troponin in acute pericarditis is believed to represent injury of the epicardial layer of myocardium adjacent to visceral pericardium where the active inflammation occurs…” (3)
“Bonnefoy et al reported that approximately one half of their 69 consecutive patients (49%) with acute idiopathic pericarditis had troponin I (TnI) levels > 0.5 ng/mL. Twenty-two percent had TnI levels > 1.5 ng/mL, their cut-off level for acute MI. The average TnI level was 8 ± 12 ng/mL (range, 0 to 48 ng/mL). The median level was, however, only 1 ng/mL.” (3)
Regarding troponin elevation in sepsis:
“…there are several potential mechanisms, other than acute MI, for troponin release in septic patients. First, it is well known that a number of local and circulating mediators (eg, cytokines or reactive oxygen species) possess direct cardiac myocytoxic properties. Secondly, myocardial injury from the effect of bacterial endotoxins has been demonstrated. Finally, dysfunction of the microcirculation has been described in sepsis. This microvascular dysfunction can lead to ischemia and reperfusion injury of the myocardial cell.” (3)
Regarding troponin elevation in PE:
“Right ventricular dilation and strain from sudden increase in pulmonary arterial resistance is believed to be the cause of troponin release in acute PE.” (3)
“Giannitis et al, reported the incidence and prognostic significance of troponin T (TnT) elevation in patients with confirmed acute PE. Of the 56 patients, 32% had elevated TnT levels (≥ 0.1 ng/mL). In contrast, only 7% had CK levels above twice the upper limit of normal. Using a clinical grading system adapted from Goldhaber, 23%, 46%, and 30% of the patients were classified as having small PE, moderate-to-large PE, and massive PE, respectively. Elevated TnT was only observed in patients with either moderate-to-large PE or massive PE. None of those with small PE had increased TnT. TnT-positive patients were more likely to have right ventricular dysfunction, severe hypoxemia, prolonged hypotension, or cardiogenic shock. They also more often required inotropic therapy or mechanical ventilation than those with negative TnT. Complete or incomplete right bundle-branch block or ST-T changes on ECG were also more prevalent in TnT-positive subgroup. More importantly, TnT positivity was associated with approximately 30-fold increased risk of in-hospital mortality. In addition, TnT level was found to be an independent predictor of the 30-day outcome. Survival rates at 30 days were 60% and 95%, respectively, for those with and without TnT elevation.” (3)
Regarding troponin elevation in renal disease:
“In patients with severe renal dysfunction troponin T as well as troponin I, elevations are found that cannot be linked to myocardial injury. The reasons for these elevations are not yet convincingly explained. Reexpression of cardiac isoforms in skeletal muscles has been excluded by different analyses and investigators.13,14 Loss of membrane integrity and constant outflow from the free cytosolic troponin pool as well as amplified elevation of normal low levels because of impaired renal excretion are more likely. The higher unbound cytosolic pool and higher molecular weight may explain why troponin T is more frequently found elevated than troponin I.” (2)
As a final note, in 2011 Afonso et al retrospectively reviewed 567 patients admitted with a diagnosis of “hypertensive emergency.” Of these, 186 (32%) had cTnI elevation with the mean peak level at 4.06. They conclude, “Predictors of cTnI were age, history of hypercholesterolemia, blood urea nitrogen level, pulmonary edema, and requirement for mechanical ventilation. … Neither the presence nor the extent of cTnI elevation was associated with mortality, while age, history of coronary artery disease, and blood urea nitrogen level were predictive of mortality.” (1)
- Afonso L, et al. Prevalence, determinants, and clinical significance of cardiac troponin-I elevation in individuals admitted for a hypertensive emergency. J Clin Hypertens (Greenwich). 2011 Aug;13(8):551-6. doi: 10.1111/j.1751-7176.2011.00476.x. Epub 2011 Jun 27.
- Hamm, CW, Giannitsis, E, Katus, HA Cardiac troponin elevations in patients without acute coronary syndrome. Circulation 2002; 106, 2871-2872
- Roongsritong C, Warraich I, Bradley C. Common Causes Of Troponin Elevations In The Absence Of Acute Myocardial Infarction: Incidence And Clinical Significance. CHEST. 2004;125(5):1877-1884.
- Thygesen K, Mair J, Katus H, et al. Recommendations for the use of cardiac troponin measurement in acute cardiac care. Eur Heart J 2010; 31:2197
- Gibson, M. et al. Elevated cardiac troponin concentration in the absence of an acute coronary syndrome. UpToDate. July 11, 2012.
Although the previous case study was written for formalistic reasons and is admittedly neither very interesting nor particularly original, there is one interesting feature here worthy of note:
The arrows indicate complexes resulting from intermittant LBBB or PVCs with LBBB morphology. The latter is more likely given that their differing frontal plane axes (-60 vs +60) implicate two separate foci.
Despite aberrant conduction, the current of injury resulting from the anterior infarct remains explicit and is diagnostic of coronary occlusion.
In the first EKG (04:15) the complexes in V2 and V3 show appropriately discordant STE, but the ST/S ratio is groselly excessive. In 2010, Dodd and colegues demonstrated that an ST/S ratio >0.2 carries high specificity for LAD occlusion (1). Note the ratios in this case:
V2: ST/S = 6mm/7mm = ~0.86
V3: ST/S = 5.5mm/11mm = 0.5
In the second EKG (07:10) there is >1mm concordant STE in V4 and V6. In LBBB, the ST segments should always be discordant, and, when the terminal R wave is positive, they should show an appropriate proportion of ST depression. Thus, even in V6 where the J-point is isoelectric, there is a conspicuous absence of ST depression. This is a STEMI equivalent (2). Even if this patient had a baseline LBBB and the entire EKG showed wide-complex aberrancy, the MI would not be hidden.
These features as illustrated here closely reflect the more thorough and authoratative work of Dr. Smith in his May 21, 2011 blog post, “LBBB: Is There STEMI?“
Reproduced from his text:
Smith modified Sgarbossa rule:
- At least one lead with concordant STE (Sgarbossa criterion 1) or
- At least one lead of V1-V3 with concordant ST depression (Sgarbossa criterion 2) or
- Proportionally excessively discordant ST elevation in V1-V4, as defined by an ST/S ratio of equal to or more than 0.20 and at least 2 mm of STE. (this replaces Sgarbossa criterion 3 which uses an absolute of 5mm)
- Dodd KW. Aramburo L. Broberg E. Smith SW. For Diagnosis of Acute Anterior Myocardial Infarction Due to Left Anterior Descending Artery Occlusion in Left Bundle Branch Block, High ST/S Ratio Is More Accurate than Convex ST Segment Morphology (Abstract 583). Academic Emergency Medicine 17(s1):S196; May 2010.
- Dodd KW. Aramburo L. Henry TD. Smith SW. Ratio of Discordant ST Segment Elevation or Depression to QRS Complex Amplitude is an Accurate Diagnostic Criterion of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block (Abstract 551). Circulation October 2008;118 (18 Supplement):S578.
- Dr. Stephan Smith. “LBBB: Is There STEMI?” Dr. Smith’s ECG Blog. http://hqmeded-ecg.blogspot.com/2011/05/lbbb-is-there-stemi.html
Artifactual activity on 12-lead EKG presents a significant impediment to electrocardiographic diagnosis. A case is presented here in which underlying STEMI could not be appreciated due to artifactual interference from frayed electrode leads. Clinicians should to be aware of the causes and presentations of EKG artifact in order to avoid similar pitfalls.
An “all fields” PubMed search was conducted using the term “artifact” in conjunction with each of the terms “STEMI”, “myocardial infarction”, “EKG”, “ECG”, and “ST segment.” Results yielded 0, 76, 19, 317, and 22 references respectively. These 434 citations were then screened for relevance according to title. The scope of the search spanned from 1973 to June 2012.
Numerous sources and types of artifactual interference on EKG have been identified. Artifact may be defined as any electrical activity present on EKG recording which does not directly and appropriately reflect cardiac activity. Artifactual interference may be classified as either of primary, non-cardiac etiology, or of secondary etiology when authentic cardiac signals are deranged due to incompetent acquisition, processing, or presentation. In the former category, a multitude of electrical and mechanical devices have been implicated (1-12, 46). Movement artifacts such as patient tremor, respiration, coughing, and hiccups have also been described (13-21, 43, 44). Artifact resulting from bed or stretcher movement should also be included in this subgroup.
Regarding the derangement of authentic cardiac signals rather than non-cardiac interference, investigators have noted an extensive variety of effects due to electrode misplacement (25-28, 32, 37). Acquisition filters have also been found to deceptively alter the appearance of the electrocardiogram (30, 33). Inconsistent electrode contacts as well as flawed or inverted lead connections can be problematic (45). Printers, monitors, and electronic transmission software have all been implicated in significant distortion or augmentation of the EKG (29, 41).
Too numerous to count case reports involving both primary non-cardiac interference as well as secondary artifact effects have illustrated a diversity of arrhythmic, ischemic, and other electrocardiographic mimics. Typically low frequency primary artifact resulting from tremors or rhythmic movement of physiologic cycle length has been associated with the mimicry of dysrhymias, often wide complex dysrhthmias (13-21, 23). Derangements of authentic cardiac activity resulting from lead reversals, filtering effects, and post-acquisition processing have frequently been associated with the mimicry of ischemic EKG patterns. The appearance of pathologic Q-waves, dramatic changes in cardiac axis, T-wave deflection, and alterations of R-wave amplitude and progression have been documented (25-27). False ST elevation and depression have also been described (30, 31). Both the masking of intrinsic pathology and the pathologic representation of healthy cardiac signals have been noted (30-34, 40, 45). The consequences of unrecognized artifactual interference can include inappropriate pharmacological and electrical therapies; significant morbidity and mortality has resulted (15, 18, 19, 28).
In some cases, the clinician can exploit artifactual activity. Shivering artifact in the presence of electrocardiographic evidence of hypothermia is such a case (42). The utility of respiratory artifact has also been explored (24). More recently, the exploitation of systematic computer algorithm interpretation error has been discussed relative to “double counting” of heart rate in the setting of hyperkalemia (41).
In this case report, an anterior ST-elevation myocardial infarction was masked by opaque artifactual activity resulting from frayed electrode leads. To date, this would appear to be the first documented case of such an occurrence.
An 85 year-old Caucasian man with a history of atrial fibrillation and anxiety awoke at 2:30 AM with chest pressure and shortness of breath. He alerted his daughter and she administered his Xanex, believing his symptoms to be psychosomatic. When this had little effect, an ambulance was called. On their arrival at 3:40 AM, paramedics administered oxygen and 162mg of aspirin. Vital signs at this time were within normal limits. A rhythm strip was acquired which demonstrated heavy artifact obscuring all but one lead. Additional leads were not visualized and no intelligible 12-lead could be obtained.
The patient was transported to a non-PCI capable community hospital. There, a 12-lead EKG was recorded which showed explicit anterior wall STEMI.
The troponin was 0.65. Tenectaplase was administered at 4:30AM; a repeat EKG 90 minutes later was unchanged. At this time, he was transferred to an outside hospital for cardiac catheterization.
On arrival at 7:05AM, the patient was hypotensive with a systolic blood pressure of 70mmHg.
An aortic balloon pump was placed and dopamine initiated. A complete occlusion of the mid-LAD was identified; thrombectomy was performed and the vessel stented with TIMI3 result. Hypotension persisted and the patient developed increasing lethargy and dyspnea. He vomited and became apenic while in cath lab. At 8:15AM he was intubated and placed on levophed; his ejection fraction was less than <15%. Hypotension remained refractory despite the addition of vasopressin and dobutamine. At 10:25AM, the troponin was 92. At this time he was unresponsive on exam with central cyanosis and mottling to all four extremities. There was pulmonary edema with an arterial line indicating a systolic BP of 50mmHg. Blood gas analysis indicated a pH of 7.10. He was described as not likely to survive and made DNR at 10:50AM. At 11:58 AM no carotid pulse could be appreciated and he was pronounced dead.
Retrospective analysis of the prehospital EKG artifact was undertaken. The system was traced from the electrode-lead junctions back to the monitor. In this case, a Physio-Control Life Pack 12 device was being utilized and revealed cable-junction fraying. Experienced operators of this device are often familiar with this type of artifact, and the cable-junction is a known weak point.
Cable fraying or, more broadly, lead-connection artifact, has a distinct electrocardiographic signature. Fequentlely there is an erraticly wandering baseline with sharp, irregular voltage spikes showing inconsistantly varrying amplitudes. As usualy only one connection is effected, the artifact should localize to a particular lead. Thus there should also be leads present which are free of artifact.
Note that in the initial EKG from this case there are voltage spikes of varying amplitudes, a chaotically wandering baseline, and a lead-specific artifact distribution. Other etiologies may mimic lead-connection artifact, but are readily distinguishable once they become familiar to the clinician.
60Hz AC interference should demonstrate almost exactly 60 deflections per second; the baseline typically will not wander and the amplitude will be constant or demonstrate orderly undulation. (Image retrieved from “Doktorekg.com,” http://www.metealpaslan.com/ecg/artef3en.htm)
Shivering artifact may or may not be accompanied by hypothermic ECG stigmata such as bradycardia or Osborne waves; note that the artifact is not confined to any single lead distribution. (Image retrieved from “LifeInTheFastLane.com,” http://lifeinthefastlane.com/ecg-library/basics/hypothermia/)
Artifact from resting tremor is typically of lower (physiologic) frequency and thus can mimic VT or a-flutter; relative to lead-connection artifact, tremor interference is pervasive, consistent, and of much longer cycle length.
The distinguishing hallmarks of lead-connection artifact are,
- It is confined to a specific lead distribution– the lead with inconsistent connectivity.
- There is a chaotically wandering baseline.
- The cycle lengths are short (30-70Hz ?) and grossly irregular.
- The amplitude is widely variable and randomly distributed.
When lead-connection artifact is recognized, operators can trouble-shoot the system for correctable problems. Often a “positional” solution can be temporarily utilized to acquire an acceptable tracing before the cables can be replaced. As in this case, when the origin of the artifact is unknown to the practitioner, it is not possible to investigate such a solution. The tragic coincidence presented here, where in the detection of STEMI was obscured by lead-connection artifact, illustrates that the potential significance of this issue.
While newer lead hardware has been made available, many operators continue to utilize the monitoring cables described in this case.
In this case, an anterior wall STEMI could not be appreciated due to artifactual interference. The patient was therefore transported to a non-PCI capable facility; subsequently, he did not receive definitive reperfusion until nearly five hours after his initial encounter with ACLS providers. The result was a catastrophic infarction from which he could not recover.
Operators should be familiar with the appearance of lead-connection artifact and maintain a high index of suspicion when checking and trouble-shooting this hardware.
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- Pseudo-atrial flutter/fibrillation in Parkinson’s disease. Prabhavathi B, Ravindranath KS, Moorthy N, Manjunath CN. Indian Heart J. 2009 May-Jun;61(3):296-7.
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- “Unusual EKG/ECG Pattern: You don’t see this everyday”. The Happy Hospitalist. 04-15-2011. Retrieved from: http://thehappyhospitalist.blogspot.com/2011/04/unusual-ekgecg-pattern-you-dont-see.html
The following was recorded from a 90 year-old Caucasian man with shortness of breath.
This is very suspicious for second degree block; bigeminal PACs or PJCs with compensatory pauses are also possibilities. There is poor visualization of atrial activity due to background noise and intrinsic low voltage. The 12-lead is referenced for the best lead to visualize:
V1 seems promising; a V1 rhythm strip is acquired:
Worse still. Next, the Lewis lead:
Now the diagnosis is transparent. Before resorting to the placement of Lewis electrodes, the voltage gain can be doubled and noise reduction strategies applied. These were not utilized here.
12-lead under Lewis electrode placement:
There is diminished QRS voltage, new inferior Q-waves and ST-segment abnormalities. This could easily be misinterpreted, but it is an artifact of the lead system.
Switching back to standard placement. Different electrodes were used at this time and the voltage is altered; the background noise has faded but the atria remain quiet:
This patient was ultimately found to be pancytopenic (WBCs 3.1, RBCs 1.17, Hem 4.8, Crit 13.0, Platelets 96, Neu 23, Lym 60, Monos 16) and was worked up for myelodysplastic syndrome. The electrocardiographic findings may be associated with the anemia; they may also be incidental.
Christopher Watford brought the Lewis lead to my attention; he has described its physiology and advantages extensively in his blog post, Highlighting Atrial Activity on an ECG: The S5 Lead, as well as via audio on the EMCrit Podcast with Scott Wiengart.
There are numerous alternative lead systems: Brughada leads, high and low precordial placements for visualizing poorly represented territories, systems designed to emphasize pacemaker activity, etc. Body surface mapping technologies (e.g. The 80-Lead Prime ECG) have also shown promise. Some of these lead systems are described on this site under EKG Resources.
Bakker, A., et al. (2009). The lewis lead: Making recognition of P waves easy during wide QRS tachycardia. Circulation, (2009), 119; e592-e593. [Free Full Text] doi: 10.1161/CIRCULATIONAHA.109.852053
Lewis T. (1931). Auricular fibrillation. Clinical Electrocardiography. 5th ed. London, UK: Shaw and Sons; 1931: 87–100.
For background regarding EKG double counting and Littmann’s sign of hyperkalemia, see March, 2012.
The following was recorded from an 82 year-old female with lethargy and malaise; electrolyte status is unknown, as is any further clinical data.
This is a 10 second strip with 9 QRS complexes; the true heart rate is thus 54bpm. The GE-Marquette 12SL interpretation algorithm has counted 163bpm, (3 x 54 = 162). Assuming that this is a result of systematic error and not coincidence, both the mechanism and significance of triple counting remain unclear.
New EKGs and new insights on a 2010 cold case. To recap:
While vacationing in Saigon a 57 year-old Caucasian female presented to the local emergency center with complaints of nausea and light-headedness. She experienced cardiac arrest, was resuscitated, and was found to have a persistent idioventricular rhythm coupled with significant acidosis and hypotension. She required multiple pressors and ultimately recovered despite a syndrome of multi-system organ failure. She was stabilized and transferred back to the states to a medical rehab facility. Infectious disease work up revealed only Candida Pelliculosa.
After several weeks in rehab, she again presented to the ED with complaints of nausea and light-headedness. Her past medical history included an aortic valve replacement (secondary to aortic stenosis), paroxysmal a-fib, diabetes, and depression. She was taking coumadin, flecainide, lexapro, januvia, and lopressor. Her BP on arrival was 81/44; the following EKG was recorded:
She had no complaints of chest discomfort or shortness of breath. At this time the potassium was 4.1, sodium 133, chloride 104, creatinine 3.1, BUN 31, glucose 114, and lactic acid 1.4. The white blood count was elevated at 15.6k. Amylase, lipase, AST and ALT were all mildly above normal. The pH was 7.01.
Her mental status deteriorated; she was intubated in the ED and transferred to the ICU. That night she suffered a PEA arrest and was resuscitated; multiple pressors were added sequentially for homodynamic support and a dialysis catheter and arterial line were placed. Peri-arrest bradyarrythmias were frequent and a transvenous pacemaker was inserted.
On the second hospital day the following EKG was recorded:
The potassium was 4.9, the sodium 135, chloride 101, creatinine 3.9, BUN 41, glucose 187, and lactic acid 13.
The cardiology consultant believed this to be an idioventricular rhythm of likely metabolic origin, secondary to electrolyte disturbance, possible flecainide or lexapro toxicity, or sepsis. Despite a widened QRS, the echocardiogram revealed a normal EF. Lexapro and flecainide were discontinued at this time.
On the third hospital day this EKG was recorded:
Labs from this date show a potassium of 3.5, sodium 143, chloride 97, creatinine 4.1, BUN 30, glucose 256, and lactic acid 23.
The blood pressure and electrocardiogram gradually stabilized; all cardiac enzyme assays were negative. By the seventh day she was extubated and transferred back to the hospital at which she had been originally treated returning from Vietnam. No bacteria, fungus, or parasites were isolated during this admission, however, she did have a positive hep-c antibody. Prior to discharge this EKG was recorded:
Labs from this date indicate a potassium of 3.4, sodium of 142, chloride 110, creatinine 2.4, BUN 40, glucose 303, and lactic acid 2.4.
She was subsequently lost to follow up.
The differential diagnosis for a sinusoidal, wide complex rhythm between 80-120bpm with QRST fusion includes hyperkalemia, sodium channel blocker toxicity, aberrant QRS AIVR, and tachycardia with aberrant conduction and massive ST elevation. In 2010, when I first presented these EKGs, I believed that this case (in the acute phase) represented AIVR.
The dominant pacemaker may in fact be idioventricular. The presence of AV dissociation would confirm this, but I do not see P waves. The third EKG (hospital day 3) is equivocal. This could also be a-fib with AIVR and dissociation.
Even if the rhythm is AIVR, there is still a more important diagnosis at stake.
For comparison, and to illustrate this, here are some exemplars:
This is typical AIVR:
Image courtesy of Life In The Fast Lane
This is RBBB with LAFB and massive STE:
Image courtesy of Dr. Smith’s ECG Blog
Hear are three cases of sodium channel blockade with TCA cardio-toxicity:
Unknown TCA toxicity. Image courtesy of EB Medicine.
This is purported cocaine cardiotoxicity with features of sodium channel blockade:
Image courtesy of ECGpedia.
Two cases of flecainide toxicity:
Image courtesy of Bond et. al., Heart 2010.
Image courtesy of EB Medicine.
Sodium channel blocker and specifically flecainide toxicity has been covered extensively in the literature; the following excerpts are particularly relevant in light of this case.
“Flecainide is an increasingly used class 1C antiarrhythmic drug used for the management of both supra-ventricular and ventricular arrhythmias. It causes rate-dependent slowing of the rapid sodium channel slowing phase 0 of depolarization and in high doses inhibits the slow calcium channel.” (Timperley, 2005)
“Cardiac voltage-gated sodium channels reside in the cell membrane and open in response to depolarization of the cell. The sodium channel blockers bind to the transmembrane sodium channels and decrease the number available for depolarization. This creates a delay of sodium entry into the cardiac myocyte during phase 0 of depolarization. As a result, the upslope of depolarization is slowed and the QRS complex widens.” (Hollowell, p.880– graphic and text.)
“Bradydysrhythmias are rare in sodium channel blocking agents because many of these also possess anticholinergic or sympathomimetic properties. These agents can, however, affect the pacemaker cells that are dependent on sodium entry, thus causing bradycardia. In severe poisoning, the combination of a wide QRS complex and bradycardia is a sign of overwhelming sodium channel blockade of all channels, including the pacemaker cells.” (Delk, p.683)
“Due to its significant effect on sodium channels, flecainide prolongs depolarization and can slow conduction in the AV node, the His-Purkinje system, and below. These changes can lead to prolongation of the PR interval, increased QRS duration, and first- and second-degree heart block. ….In contrast, flecainide does not affect repolarization and therefore has little effect on the QT interval.” (Giardina, G. 2010)
“Impending cardiovascular toxicity in adult patients [with TCA poisoning] is usually preceded by specific ECG abnormalities: the majority of pateints at significant risk will have a QRS duration >100ms or a rightward shift (130-270) of the terminal 40ms of the frontal plane QRS vector. The later finding is characterized by a negative deflection of the terminal portion of the QRS complex in lead I and a positive deflection of the same portion in lead avR.” (Van Mieghem, p.1569)
“In severe cases [of sodium channel blocker toxicity], the QRS prolongation becomes so profound that it is difficult to distinguish between ventricular and supraventricular rhythms. Continued prolongation of the QRS complex may result in a sine wave pattern and eventual asystole.” (Holstege, p166.)
There are multiple mechanisms for flecainide toxicity in this case.
- Reduced metabolism and elimination due to impairment of liver and renal function.
- Significant acidosis resulting in a decrease in protein bound flecainide and an increase in the free (active) agent in the blood stream.
- Borderline hyponatremia as a potential predisposing condition for over-therapeutic sodium channel blockade.
Bond, R., et al. (2010). Iatrogenic flecainide toxicity. Heart (2010), 96:2048-2049 doi:10.1136/hrt.2010.202101
Delk, C., et al. (2007). Electrocardiographic abnormalities associated with poisoning. American Journal of Emergency Medicine, (2007), 25, 672-687.
Giardina, G. (2010). Major side effects of flecainide. UpToDate.
Harrigan, R., et al. (1999). ECG abnormalities in tricyclic antidepressant ingestion. American Journal of Emergency Medicine, (1999), July 17(4), 387 – 393.
Hollowell, H. et al. (2005) Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with aberrant conduction. American Journal of Emergency Medicine, (2005), 23, 876 – 889.
Holstege, C., et al. (2006). ECG manifestations: The poisoned patient. Emerg Med Clin N Am, 24 (2006) 159–177. Free full text.
Timperley, J., et al. (2005). Flecainide overdose– support using an intra-aortic balloon pump. BMC Emergency Medicine, (2005), 5: 10. doi: 10.1186/1471-227X-5-10
Van Mieghem, C., et al. (2004). The clinical value of the ECG in noncardiac conditions. Chest (2004), 125, 1561-1576.
Williamson, K., et al. (2006). Electrocardiographic applications of lead aVR. American Journal of Emergency Medicine (2006), 24, 864-874.
In April of 2011 I presented a case of subtle hyperkalemia. A reader, Dr. George Nikolic, author of Practical Cardiology 2nd Ed., responded with the following commentary,
“The QT is unusually long for hyperkalemia; the lady may have additional pathology (e.g., myxoedema) or be on some QT prolonging medication. The commonest cause of low voltage is large or multiple infarcts in the past. What were her other medical problems?”
I was unable to follow up on this case until recently. Here is what I uncovered:
The patient was an 81 year-old caucasian female nursing home resident of unknown social background with a past history of hypertension, dyslipidemia, diabetes, colon cancer (s/p diverting ileostomy), depression and dementia. Despite numerous cardiac risk factors, she had no explicit history of myocardial infarction, coronary disease, or CHF. There was no history of thyroid disease or obesity.
Her medications consisted of Lexapro 10mg, Aricept 5mg q.h.s, Lopressor 12.5mg b.i.d., folic acid, and Imdur 30mg daily.
She had visited the Emergency Department 12 days prior to this episode with complains of weakness and bradycardia. At that time her BUN was 22, Creatinine 0.8, Sodium 136, Potassium 3.7, and Calcium 9.1. The following EKG was recorded:
Cardiology was consulted and a differential of sick-sinus syndrome vs. beta-blocker toxicity was considered. The Lopressor was reduced, and, following a 48-hour admission, she was discharged back to the nursing home with a slightly increased heart rate.
Two weeks later, on the date in question, she again presented to the ED with complaints of syncope and generalized weakness. This EKG was recorded on arrival:
The hospitalist’s admission note described a provisional diagnosis of acute renal failure secondary to dehydration and possible UTI. Obstructive failure was also considered in light of the cancer history. Most revealing, a thorough chart review revealed two prior admissions for acute renal failure secondary to dehydration from high-output ileostomy syndrome.
Echocardiography on the second hospital day reported no chamber enlargement, no increased wall thickness, no wall motion abnormalities, no valvular disease, no pericardial or pleural effusion, and a normal systolic function with an EF > 55%.
On the third hospital day she was discharged back to her nursing facility with the following EKG:
The differential diagnosis for low voltage is broad; neoplastic, metabolic, autoimmune, infectious, genetic, and acquired disease states are all represented.
When bradycardia is added, the field narrows: thyroid disease, acute or chronic ischemia, and hypothermia are among the most common etiologies.
In hyperkalemia, it is traditionally understood that when the QRS is normal, the QTc should be either shortened or unremarkable. (Smith, Jan 12, 2010; Lipman-Massie, p.579) In this case, the QTc at 6.4mEq K+ (394) is practically identical to the QTc at 4.0 mEq K+ (394). I do not know if the GE-Marquette algorithm uses the Bazett formula for QTc, but this formula is known to under-correct at abnormally low heart rates. (Wikipedia, 2012) Therefore, although the QTc here may be longer than the computer estimates, in an adult female, a QTc of 395 remains if anything on the short side of normal. Regarding medications, however, Lexapro is known to cause QT prolongation.
There was no effusion, as I had originally hypothesized in 2011. We do not have a solid culprit for the low voltage. The QT looks relatively normal. I am grateful for Dr. Nikolic’s attention and comments regarding this case. Fortunately for the patient, the clinical correlations do not seem to support either of our theories.
Dunn, B. and Lipman, B. (1989) Lipman-Massie Clinical Electrocardiography, 8th Ed. Yearbook Medical Publisher Inc.
Smith, S. (2010) Hyperkalemia with cardiac arrest. Peaked T waves: hyperacute (STEMI) vs. early repolarization vs. hyperkalemia. http://hqmeded-ecg.blogspot.com/2010/01/peaked-t-waves-hyperacute-stemi-vs.html
Wikipedia. (2012) QT interval. http://en.wikipedia.org/wiki/QT_interval
In 2007, Littmann and colleagues presented a novel EKG indicator of hyperkalemia based on the computerized “double counting” of heart rate. Over a 13-year period they identified 33 cases in which the GE-Marquette computerized 12SL EKG interpretation algorithm “double counted” or “near double counted” the actual heart rate seen on electrocardiogram. All 33 patients had hyperkalemia (between 5.3-8.8 mEq/L K+) as confirmed by serology taken within two hours of the double-counted EKG recording.
Littmann’s sign can be seen in the following EKG, initially presented here as a study in hyperkalemia in September of 2010.
A 65 year-old Caucasian man with sepsis and HHNKC; the potassium was 7.7mEq/L. The heart rate is 72 bpm; the computer counts 137 bpm.
Although the GE algorithm is proprietary and unavailable for analysis, they argue that, “The QRS width and axis measurement by the interpretation software suggested that, on many occasions, the computer recognized the T waves as being the QRS complexes….” (p.586)
Littmann et al. conclude stating, “Although interpretation software double counting of heart rate appears to be quite specific for hyperkalemia, its sensitivity is almost certainly very low.” (p.586)
While this research represents an intriguing new insight, it leaves many open questions. How were these 33 EKG cases identified? Were certain populations screened for this anomaly? How many total EKGs were reviewed in the course of this investigation?
Littmann claims that double counting “appears to be quite specific” presumably because all 33 EKGs were associated with underlying hyperkalemia. Yet without insight into the methods used to assemble this case series, I remain skeptical that these investigators did not succumb to confirmation bias in the process of collecting their EKGs. The existence of non-hyperkalemic double counting is not discussed in this publication and no differential diagnosis is presented regarding alternative etiologies.
In fact, concerning alternative etiologies and the specificity of double QRS counting, it turns out that this phenomenon has been extensively described in the pacemaker literature for over a decade. A Pubmed search using the combined terms “double counting QRS” produces numerous references. (Al-Ahmad A, Barold SS, Boriani G)
I reviewed 22 pacemaker EKGs collected over a 10 month period, recorded pre-hospitaly using the same GE-Marquette algorithm. This is what I found:
Looking further through ~50 EKGs collected over the same 10 months I found this as well:
In the first pair of EKGs, the computer appears to be confusing the pacemaker spike for a QRS complex; this is clearly “double counting of the QRS.”
The second pair is more complicated. This is not technically “double counting” of the QRS; there is not a 1:1 relationship between each QRS and a particular artifactual deflection. This is over-counting with a coincidental but not precise 2:1 relationship between the total count made by the computer and the total number of true QRS complexes. The interpretation of “Atrial Fibrillation” supports this in that it suggests that numerous complexes are counted during the first 5 seconds and then much fewer in the last 5. Although Littmann’s sign is not technically present here, the 12-lead EKG must be scrutinized to reach this conclusion. This seems problematic given Littmann’s stated goal of elucidating an “objective”, and “easily identifiable” indicator. (p.586)
No clinical data is available on these EKGs and it cannot be proven that these patients did not in fact have elevated potassium.
While producing these two hypothetical “false positives” hardly constitutes significant evidence, it is interesting that such counterpoints to Littmann’s specificity claims were so easily identified. Of further concern is the distinction between perfect double counting as seen in the pacemaker case and “near double counting” as seen in both the hyperkalemia case from Sept. 2010 and artifact case. What bearing this has on Littmann’s argument remains unclear.
Although a novel indicator, I am not sure that there is as yet persuasive evidence for what exactly Littmann’s sign indicates or how often this indication is specific for any one underlying clinical etiology.
Littmann L, Brearley WD, Taylor L, Monroe MH. Double counting of heart rate by interpretation software: a new electrocardiographic sign of severe hyperkalemia. Am J Emerg Med 2007;25:584-90.
Tomcsányi J, Wágner V, Bózsik B. Littmann sign in hyperkalemia: double counting of heart rate. Am J Emerg Med. 2007 Nov;25(9):1077-8.
Al-Ahmad A, Wang PJ, Homoud MK, Estes NA 3rd, Link MS. Frequent ICD shocks due to double sensing in patients with bi-ventricular implantable cardioverter defibrillators. J Interv Card Electrophysiol. 2003 Dec;9(3):377-81.
Barold SS, Herweg B, Gallardo I. Double counting of the ventricular electrogram in biventricular pacemakers and ICDs. Pacing Clin Electrophysiol. 2003 Aug;26(8):1645-8.
Boriani G, Biffi M, Frabetti L, Parlapiano M, Galli R, Branzi A, Magnani B. Cardioverter-defibrillator oversensing due to double counting of ventricular tachycardia electrograms. Int J Cardiol. 1998 Sep 1;66(1):91-5.
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 37 year-old Caucasian male presents to the emergency department with palpitations of two hours duration. A 12-lead EKG is recorded.
This 12-lead demonstrates an irregularly irregular, polymorphic wide complex tachycardia; this can only be atrial fibrillation with frequent conduction through a Wolf-Parkinson-White accessory pathway system.
The differential diagnosis for this presentation principally consists of polymorphic VT, RVR a-fib with ventricular conduction aberrancy, and a-fib with underlying WPW. The presence of multiple wide complex QRS morphologies excludes the diagnoses of a-fib with BBB, and, as Mattu and Brady have pointed out, polymorphic VT will typically hold a constant rate while this EKG shows significant variance between R-R intervals– from >450ms to <240ms. (Mattu, 2003, p.138)
RVR a-fib with aberrant conduction and gross ST-segment abnormalities but uniform QRS morphology. (EMS 12-Lead: http://ems12lead.com/2011/09/68-year-old-male-cc-chest-pain/)
Polymorphic VT of Torsades de Points in the setting of hypokalemia and prolonged QT; multiple QRS morphologies but uniform rate. (LITFL: http://lifeinthefastlane.com/ecg-library/tdp/)
Note that due to the fixed duration of the AV nodal refractory period, synchronized atrio-ventricular conduction is typically limited to below 200 impulses per minute. It is for this reason that RVR a-fib very rarely exceeds 180-200bpm. The bypass tract in WPW, however, has a dangerously short refractory period and thus can support re-entrant tachycardias well above this limit. As Chou has stated, “…the presence of the WPW syndrome can be suspected from the rhythm strip alone if the atrial fibrillation is accompanied by a ventricular rate greater than 200bpm. Such a rapid ventricular response would be highly unusual if the conduction is by way of the normal AV conduction system.” (Chou, 1996, p.480)
Antiarrhythmic agents which slow or block AV nodal conduction are contraindicated in this setting as they can enhance conduction through the accessory pathway and accelerate ventricular response. Procainamide and related sodium channel antagonists have therefore been used with favorable results.
Regarding amiodarone, although numerous case reports have tracked poor outcomes, it remains a popular treatment modality for this syndrome and may statistically be a safe alternative. In 2005, for example, Tijunellis and Herbert demonstrated a case-series of 10 patients in which amiodarone was malignantly proarhythmic; in half of these, the initial arrhythmia was v-fib. Nonetheless, case-series can be misleading and I do not know of definitive research in this area.
In light of this, judicious use of electrical therapy is often considered the safest and most reliable approach.
Mortality associated with the Wolf-Parkinson-White syndrome remains at <1% and is thought to result from rapid response a-fib degenerating into v-fib arrest (Ellis, 2011). This outcome can be fostered through inappropriate pharmacological management if the initial presentation is misunderstood. Fortunately, once this dramatic EKG signature has been appreciated, it is unlikely to go unrecognized.
Dr. Stephen Smith has discussed this syndrome and the treatment risks, and his insights can be found here. Among other remarks, he states, “Atrial fib with WPW is very recognizable: there are bizarre QRS with multiple morphologies, and very fast rhythms with short R-R intervals. If you can find any R-R interval shorter than 240 ms, then AV nodal blockers are definitely dangerous.” (Smith, 2011)
I wish also to excerpt Dr. Johnson Francis of Cardiophile MD who has addressed this topic directly. Dr. Francis states, “The shortest RR interval gives an estimate of the ventricular refractory period. If it is below 250 msec, it is ominous as the ventricular rates can go very high and it can degenerate into ventricular fibrillation.” (Francis, 2008) Note that in this particular case, the overall ventricular rate is not excessively fast and perhaps speaks to the relative clinical stability of the patient.
Additional case studies of WPW a-fib can be found in the Case Library.
Chou, T. and Knilans, T. (1996). Electrocardiography in Clinical Practice: Adult and Paediatric, 4th Ed. W.B. Saunders Co.
Ellis, C., et al. (2011). Wolff-Parkinson-White Syndrome. Medscape eMedicine. Retrieved from: http://emedicine.medscape.com/article/159222-overview
Mattu, A. and Brady, W. (2003). ECGs for the emergency physician, V.1. BMJ Publishing Group.
Tijunelis, M. and Herbert, M. (2005). Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. Canadian Journal of Emergency Medicine. (4): No.4, p262. Retrieved from: http://www.cjem-online.ca/v7/n4/p262
In 2009 the AHA released recommendations for the standardization and interpretation of the electrocardiogram stating that, “The terms atypical LBBB, bilateral bundle-branch block, bifascicular block, and trifascicular block are not recommended because of the great variation in anatomy and pathology producing such patterns. The committee recommends that each conduction defect be described separately in terms of the structure or structures involved instead of as bifascicular, trifascicular, or multifascicular block.” (Rautaharju, P., et al., 2009)
Despite the ambiguity and referential instability of the term, however, the so-called “trifascicular block” remains at large in many clinical settings. So much so, in fact, that it has its own Wikipedia page: “Trifascicular block… has three features: prolongation of the PR interval (first degree AV block), right bundle branch block, and either left anterior fascicular block or left posterior fascicular block.” Wikipedia makes no mention, however, of the AHA guidelines or ongoing controversy surrounding this set of electrocardiographic features. Wikipedia concludes by stating that, “The treatment for diffuse distal conduction system disease is insertion of a pacemaker.” (Wikipedia, 2011)
The idea of “trifascicular block”, however, is not only problematic due to its potential reference to a multiplicity of histopathological substrates, but even assuming a trifascicular model of the sub-Hisian conduction system, the concept of “trifascicular block” cannot be distinguished from complete heart block. If there are only three fascicles leading into the ventricles and all three are blocked, then there is de facto complete heart block. Rather what seems to be meant by the term “trifascicular block” is a situation in which the traditional three fascicles of the left and right bundle branches all demonstrate some degree of disease or dysfunction. For example, typically a RBBB with a left anterior fascicular block and 1° AV block is considered a trifascicular block. Yet even here the situation is unclear: the 1° AV block may be due to disease in the remaining posterior left fascicle or a pathological process above the bifurcation of the His bundle resulting in an AV conduction delay.
Regardless of this semantic debate, it has been known since the early 1900s that in the predominance of human subjects the left bundle branch splits into three rather than two fascicles. Disease of the left septal fascicle has been extensively characterized electrocardiographically, histologically, and otherwise. (Riera, A., et al., 2008)
In fact, extensive individual variance complicates the branching and interconnection of the fascicles of the LBB. This is further confused by evidence indicating that fascicular blockade can occur in the absence of identifiable histological lesions. When making the diagnosis of acquired advanced distal conduction system disease, therefore, toxicological, infectious, and other reversible etiologies must first be ruled out.
Left, Diagrammatic sketches of the LBB reconstructed from transverse sections of the LBB of human hearts. Right, 4 prototypes of LBB dissected from adult normal human hearts. Note that each of these prototypes has a similar pattern among those obtained histologically. (Rautaharju, P., et al., 2009)
While the polyfascicular nature of the LBB remains largely an academic observation with limited utility in most clinical settings, this anatomical variance certainly speaks to the rationale behind the AHA recommendations. The pragmatic concern remains not whether the term “trifascicular block” is semantically sound or anatomically appropriate, however, but whether the electrocardiographic features of “trifascicular block” are sufficient evidence of advanced distal conduction system disease to warrant pacemaker implantation or prophylactic measures in anticipation of complete heart block (for example application of external pacing pads, observational admission, or specialty consultation).
I will examine three case studies exploring the utility of a “trifascicular block” nomenclature, and some treatment indications when faced with “trifascicular” disease.
Case No. 1: Mr. A, a 79 year-old Caucasian man, presents to EMS with complaints of syncope and superficial facial injuries from the subsequent fall. He reports a similar episode of “passing out” once before, but did not follow up on the incident. His medical history consists of glaucoma and a distant history of smoking.
This EKG, recorded by EMS providers at the scene, demonstrates 3rd degree heart block. An atrial rate of ~90bpm persists discontinuously behind a sub-Hisian ventricular escape rhythm of ~ 25-30bpm with LBBB morphology.
On arrival in the ED this EKG was recorded:
This interpretation aligns well with the known pathophysiology of intermittent 3rd degree block. Lipman and Massie state that, “Clinically, [Mobitz type II] often is associated with RBBB and left axis deviation. Thus, Mobitz type II block with wide QRS complexes is often associated with lesions below the AV node. This has been confirmed by His’ bundle electrocardiograms… Mobitz type II block [is] associated with incomplete trifascicular block, is considered more serious, and is much more likely to produce Stokes-Adams attacks and necessitate pacemaker insertion.” (Lipman-Massie, 1989, p.453.)
Given symptoms suggesting Stokes-Adams syncope and evidence of advanced AV block, this patient was admitted for cardiology consultation. Several days later this EKG was obtained.
As seen here, electrocardiographic proof of intermittent sub-Hisian 3rd degree heart block may be considered evidence of poly-fascicular disease with likely future Stokes-Adams events. Current AHA guidelines regarding acquired AV block in adults state that, “Permanent pacemaker implantation is indicated for third degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block.” (Epstien, A., et al., 2008, e358.) In light of this, a pacemaker was placed and the patient was discharged without complications.
Case No. 2: Mr. B, a 90 year-old Caucasian man with multiple medical problems, was brought in by ambulance with reports of increased lethargy and possible altered mental status as per his nursing home care providers. A routine EKG was recorded.
This EKG demonstrates the classic “trifascicular block” features of RBBB, LAFB, and 1st degree HB. Interestingly, there is inappropriate T-wave concordance in some leads of the inferior and high lateral distribution. A previous EKG was not available for comparison and no follow up EKG was recorded, making the significance of these findings difficult to ascertain.
After sleeping for six hours in the emergency department, Mr. B was found walking to the bathroom, articulate but confused, awake and alert to his surroundings, in no ostensible distress. All laboratory assays returned within normal limits and his relatives at the bedside testified that he was behaving and mentating normally. He was discharged without follow up back to his allied nursing facility.
Case No. 3: Ms. C, a 66 year old Hispanic woman with IDDM and known coronary artery disease, presented to the emergency department with sweats, chills, dysuria, and an oral temperature of 101.4° F.
This EKG demonstrates 1st degree HB in the presence of LBBB, another classic pattern of “trifascicular” disease. Incidentally, the 0.04ms notching of the S-wave upstroke in V3 represents Cabrera’s sign, one of several types of QRS fragmentation seen in LBBB and paced rhythms, known typically to be highly specific (~90%) for prior MI, but lacking in sensitivity (~60%) (Mithilesh K., et al., 2008). This ECG feature was consistent in this case with a prior anterior wall MI in 2005.
Unsurprisingly, urinanalysis in this case confirmed the clinical suspicion of UTI and the patient was discharged on antibiotics with follow up to her primary.
Both the cases of Mr. B and Ms. C involve patients with histories consistent with extensive distal conduction system disease and incidental electrocardiographic findings revealing “textbook” “trifascicular block”. Yet neither of these patients’ symptoms or clinical presentation was in any way correlated with the disease process manifest on EKG, and neither warranted intervention.
The initial case of Mr. A, however, involves a patient with a known pathophysiological disease model (ref. Lipman-Massie) and both electrocardiographic proof of intermittent high degree AV block and Stokes-Adams symptoms circumstantially linked to the arrhythmic disturbance. Both of these features are independent absolute indications for pacemaker therapy.
The term “trifascicular block” does not appear in the ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. Regarding indications for pacing in acquired distal conduction system disease as represented by chronic bifascicular block, the 2008 Guidelines make the following recommendations:
- Permanent pacemaker implantation is indicated for advanced second-degree AV block or intermittent third-degree AV block.
- Permanent pacemaker implantation is indicated for type II second-degree AV block.
- Permanent pacemaker implantation is indicated for alternating bundle-branch block.
- Permanent pacemaker implantation is not indicated for fascicular block without AV block or symptoms.
- Permanent pacemaker implantation is not indicated for fascicular block with first-degree AV block without symptoms. (Epstein A., et al., 2008, e360.)
Although case-specific, well reasoned clinical judgment is the best guiding principle of any treatment, the hope in presenting these three cases is to call into question not simply the histopathological verisimilitude of the “trifascicular block” nomenclature but to examine the case for this term’s pragmatic utility. In all three cases, the concept of “trifascicular block” proves to be a misleading descriptor, failing to capture the therapeutic relevance of the EKGs in question.
The remarks presented here are entirely the opinion of the author and should not represent advice or guidelines for any treatment, diagnosis, or test. My ambition has been to address specifically the issue of a “trifascicular block” nomenclature in device-based therapy for distal conduction system disease. There do exist contexts in which this term can be of significant value; of note is this fascinating case report from Tom Buthillet discussing a WCT, classic “trifascicular block”, and the risks of antiarrhythmic administration.
Dunn, M., and Lipman, B. (1989). Lipman-Massie Clinical Electrocardiography, 8th ed. Yearbook Medical Publisher Inc.
Mithilesh, K., et al. (2008). Fragmented wide QRS on a 12-lead ECG: a sign of myocardial scar and poor prognosis. Circulation Arrhythmia and Electrophysiology, 2008, 1:258-268. DOI: 10.1161/CIRCEP.107.763284
Rautaharju, P., et al. (2009). AHA/ACCF/HRS Recommendation for the standardization and interpretation of the electrocardiogram. Circulation, 2009, 119:e241-e250. doi: 10.1161/CIRCULATIONAHA.108.191096
Riera, A., et al. (2008). The history of left septal fascicular block: chronological consideration of a reality yet to be universally accepted. Indian Pacing and Electrophysiology Journal, 2008, 8(2):114-128. Retrieved from http://www.ipej.org/0802/riera2.htm
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.
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.
An 81 yr old white female with multiple medical problems presents to the ED complaining only of syncope and weakness; the routine 12-lead EKG is pictured below.
Yet the most remarkable feature of this case is the disarmingly low voltage. Although the electrocardiographic attributes of hyperkalemia remain well exemplified (peaked, sharply pointed T-waves, bradycardia, and a somewhat elongated PR interval), the attention-grabbing mountainous T-waves are conspicuously absent. This is because the EKG must be seen in the context of its own voltage. When viewed against the background of the low-voltage QRS amplitude, the T-waves are proportionally massive, just as in the classic case. Given the considerable incidence of pericardial effusion in pts with renal disease, it is not unreasonable to imagine both of these pathologies contributing to the appearance of this electrocardiogram.
In this case, laboratory assays returned showing a potassium level of 6.4 mEq/L; the pt was temporized in the ED and ultimately admitted for further evaluation. The presence or absence of pericardial effusion could not be confirmed.
Over the past year a variety of superior resources have been released dealing with the problem of critical hyperkalemia, its electrocardiographic manifestations, and its treatment. As it would be a great challenge to improve on what has been done here, I am simply going to replicate the links below.
Link No. 1: Dr. Stephan Smith of Dr. Smith’s ECG Blog has posted a video covering 4 critical hyperkalemia cases with notable EKG presentations. Be sure to take a look at his first case, second EKG, for a valuable signature morphology which can easily be misinterpreted as STE anterior MI.
Link No. 4: Scott Weingart of the EMCrit Podcast has released an incisive 15-minute Pod-Cast covering cutting edge hyperkalemia treatment paradigms. There may be some practice-changing insights here, so check it out.
Link No. 5: Jeffrey Guy of the Surgery ICU Rounds Podcast has a 30-minute overview and discussion of hyperkalemia, normal potassium physiology, and treatment approaches. This is a hospital/ICU-oriented discussion addressing burn medicine, trauma, rhabdomyolysis, etc. More in-depth, more information.
Please feel free to suggest additional resources; also note that the September 2010 case study published here, “Unconscious with Wide Complex Rhythm,” involves a more comprehensive discussion of hyperkalemic EKG changes.
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 64yr old male in no acute distress. History includes ischemic cardiomyopathy w/ EF~10%, multiple MIs, multiple stents, sustained VT, hypertension, CHF, hyperlipidemia, and past tobacco use.
Anti-tachycardia pacing (ATP) via ICD device can effectively terminate >90% of reentrant VT, avoiding the high energy expenditure and pt. discomfort associated with synchronized cardioversion.
This pt. presented to EMS complaining of left subclavicular tenderness and purulent discharge from the incision site through which he had received a biventricular ICD one month prior. Although there is some possibility of infection-induced myocardial irritability, these ECGs most likely represent incidental findings consistent only with the pt’s ongoing state of arrhythmogenic advanced ischemic heart disease.
Two different electrophysiologic approaches can be used to model the mechanism of reentrant VT. Under the first approach, islands of anatomic or functional conduction block arising due to structural or ischemic disease present electrical “forks in the road” at which a depolarizing wavefront can split into two or more signal pathways. Reentrant tachycardia occurs when one of the pathways around the island is unidirectional and sufficiently longer than the other, allowing the ventricle to depolarize via the short path (1), and then repolarize in time to be reactivated by the delayed signal from the long path (4). By the time the ventricle has finished depolarizing via the long path, the short path has had time to recover excitability, and the cycle repeats itself.
Fig. 1: Propagation of normal action potential (left) and conditions for reentrant excitation (right).
An alternative viewpoint holds that the post-ischemic islands of damaged myocardium do not present obstacles of non-conductive terrain, but instead zones of slow conduction. These slow-conduction zones can entrap or waylay a portion of an electrical wavefront long enough for it to emerge on the other side into already repolarized ventricular tissue. By the time the waylaid electrical signal escapes from the slow conduction zone, the initial wavefront has passed, and the healthy myocardium has had time to repolarize. The newly liberated signal then reactivates the ventricle, circles back around, and reenters the damaged hypoconductive region.
Under both models, the physiologic substrate of reentrant VT is damaged, fibrotic myocardial scar tissue. The arrhymogenic cycle can be terminated by overriding the reentrant circuit; anti-tachycardia pacing supercedes the rate of the pt’s VT, seizing control of the wavefront’s path of depolarization. When pacing is withdrawn, the resulting refractory period enables normative conduction pathways to reestablish dominance.
Anti-tachycardia pacing can be categorized into burst and ramp modalities, as distinguished by the graphic below.
Fig. 2: Burst vs. Ramp ATP.
Examination of the second case study ECG presented above reveals a demand pacemaker rhythm overtaken by RBBB pattern monomorphic VT of 265ms cycle length. Burst-type ATP can be seen interceding for ~7 beats at 240ms CL followed by termination and a compensatory pause before the pt’s normative rhythm resumes in the third ECG.
Interrogation of this pt’s pacemaker indicated 56 incidents of ATP-terminated VT within the past two weeks. On the seventh hospital day, a surgical excision and debridement of the pacemaker pocket was undertaken with the placement of a temporary transvenous device and initiation of temporizing amiodarone therapy. An electrocardiogram from this period is seen below.
Six days later Infections Disease Services cleared the pt. for a replacement ICD which was subsequently implanted in the right chest. The pt. was discharged back into his normal state of health 48hrs later.
Fig. 1: Reentrant VT. S. Sinha: Spatiotemporal Dynamics Of Reentry Termination by Pacing.
Fig. 2: Burst vs. Ramp ATP. Michael O. Sweeney: Antitachycardia Pacing for Ventricular Tachycardia Using Implantable Cardioverter Defibrillators. (Medscape, 2004)
Philip J Podrid: Reentry and the Development of Cardiac Arrhythmias (UpToDate, 2006)
Steven J Compton: Ventricular Tachycardia. (EMedicine, 2010)
A 52yr old white male with history of heart failure presents to the Emergency Dept. complaining of nausea, vomiting, and a decreased level of consciousness.
Although nearly every imaginable cardiac dysrhythmia has been linked to digitalis poisoning, junctional tachycardia remains uniquely suspicious for this toxidrome. In order to understand the cellular mechanisms connecting digoxin with this and other highly suggestive EKG signatures, the enzyme-level pharmacodynamics must be appreciated.
The direct cardiotonic effects of digitalis arise from inhibition of the transmembrane ion exchange protein, Na+/K+ATPase. Through the exchange of two extracellular potassium ions for three intracellular sodium ions, the phosphorylation of this complex creates a disequilibrium of monovalent cations necessary to the maintenance of the cell’s 80-90mv resting membrane potential.
Fig 1. Conformational shifts of Na+/K+ATPase relative to ion and phosphate binding. Note that the net result of this cycle is the establishment of intracellular hyponatremia.
When digitalis binds to the extracellular surface of the Na+/K+ATPase, a local deformation of the protein’s tertiary structure cripples the ion transport function of the complex . Na+ export is halted and the intracellular environment becomes relatively hypernatremic. This, in turn, exerts a critical effect on yet another ion exchange system—the Na+/Ca2+ antiporter. Normally, the steep Na+ ion concentration gradient across the cell membrane provides an osmotic motive for the Na+/Ca2+ antiporter to drive excess Ca2+ out of the cell. With the Na+/K+ATPase inhibited, however, intra and extracellular sodium concentrations equilibrate. Intracellular calcium levels rise and the sarcoplasmic reticulum becomes over-saturated; cellular depolarization thus triggers a heaver tide of Ca2+ ions and the contractile apparatus responds with greater force.
Fig 2. Inhibition of the Na+/K+ATPase results in elevated intracellular Na+; this stymies the Na+/ Ca2+ exchanger and causes intracellular Ca2+ to rise. Pro-contractile inotropic effects ultimately result.
Yet inhibition of the Na+/K+ATPase has its detriments. With the suppression of normative ion exchange comes a reduction in the ability of the conduction tissues to maintain their 80-90mv membrane resting potential. The gradual influx of cations due to natural membrane permeability cannot be opposed by active transport, and the resting voltage of the intracellular space becomes increasingly positive. As the voltage difference across the cell membrane approaches the trigger threshold of the action potential, the excitability of the conduction tissues rises proportionally. Graphically this can be appreciated below—the slope of the baseline intracellular voltage (phase 4) is seen to rise as cations “leak” into the cell making it less negative. Ultimately, the trigger threshold is reached and the cell depolarizes automatically.
Fig 3. Unipolar recording of a transmembrane action potential from a Purkinje fiber. Control conditions are traced with a solid line, digitalized tissue with dashed line. Note the morphological similarities between the experimental digitalis-altered ST segment presented here and the ST segments seen in the precordial distribution of the case study EKG above.
Due to this effect, digitalis enhances the automaticity of the conduction tissues, encouraging the independent activity of ectopic pacemakers. Depolarization occurs not only more automatically, but also more readily due to the heightened excitability of the cells. This results in a shorter R-T interval and a net positive chronotropic influence. Often in digitalis toxicity the rate of ectopic pacemaker depolarization is accelerated beyond the typical upper limit of the cellular tissue, as seen in the title EKG. Perhaps not ironically given Paracelsus’ adage, “only the dose,” the adverse effects of digitalis toward increased automaticity and excitability, therefore, stem from the same mechanistic activity by which the drug confers its beneficial inotropic influence.
Having thus looked more closely at the direct enzyme-level mechanistics of the cardiac glycosides, it is not surprising to find that the greater portion of dysrhythmias arising from digitalis toxicity consist in ectopic tachycardias such as multifocal atrial tachycardia, junctional tachycardia, and (often bifocal) ventricular tachycardia– as seen below.
Fig 4. Bidirectional ventricular tachycardia. Note the alternating QRS axes and right bundle-branch block type morphology. This occurred in the setting of a supratherapeutic serum level of digoxin as a consequence of acute renal failure.
Yet the mainstay of digitalis pharmacotherapy in the modern era lies in controlling rather than encouraging tachydysrthymias; the treatment of atrial fibrillation, for example, remains central to the role of this drug in the contemporary pharmacopoeia. To explain this seeming contradiction, we must appreciate the scope of the indirect influence in digitalis therapy.
Although less well understood, the anti-chronotropic power of the cardiac glycosides appears to be largely mediated through vagomimetic mechanisms. Increases in efferent vagal impulses, decreases in sympathetic tone, modifications of nerve fiber excitability, and sensitization of arterial baroreceptors have all been described as contributors towards this effect . In supratherapeutic concentrations, the vagal activity of digitalis becomes pathological, giving rise to the bradycardic dysrhythmias—sinus bradycardia and various forms of AV block.
Ultimately what we encounter in digitalis toxicity is a pharmacodynamic system capable of inciting almost any imaginable dysrhythmia and imitating any electrophysiologic pathology. The prevalence of junctional tachycardia in this context may be understood as a logical result of excessive supraventricular vagotonia coupled with enhanced automaticity and excitability of distal ectopic pacemakers.
In the case presented here, laboratory assays returned a substantially elevated serum Digoxin level securing the diagnosis of cardiac glycoside poisoning. This pt. received conservative treatment and was discharged on the third hospital day without incident.
The title of this post is quoted from Louis N. Katz, widely known for his work in electrocardiography. In addition to many articles, he is author of Introduction to the Interpretation of the Electrocardiogram (1952), and Electrocardiography Including an Atlas of Electrocardiograms (1946).
Fig. 1: Graphic on loan via http://www.angelfire.com/sc3/toxchick/celmolbio/celmolbio12.html
Fig. 2: Graphic on loan via http://www.cvpharmacology.com.
Fig. 3: A. Goodman Gilman. The Pharmacological Basis of Therapeutics. Pergamon Press, NY 1990. p. 819.
Fig. 4 and explanatory subtext. Joseph L. Kummer. Bidirectional Ventricular Tachycardia Caused by Digitalis Toxicity. Circulation. 2006; 113:p156-156.
 In depth discussion of the molecular mechanistics involved with glycoside / ATPase binding can be explored via H. Ogawa et al. Crystal Structure of the Sodium-Potassium Pump with Bound Potassium and Ouabain. Proceedings of the National Academy of Science, Vol. 106, No. 33, 2009, pp.13742-13747. See also, S.M. Keenan et al. Elucidation of the NaKATPase Digitalis Binding Site. Journal of Molecular Graphics and Modeling, Vol. 23, 1995, pp.465-475.
 A. Goodman Gilman, Pp. 814-829.
As a final note, due to the nature of this material the account presented here is necessarily simplified and incomplete in many respects; further inquiry can be well satisfied via A. Goodman Gilman, Lipman-Massie Clinical Electrocardiography, Goldfrank’s Toxicologic Emergencies, as well as other more detailed resources.
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.
In 1899, 4 years prior to the invention of the EKG, Karel Wenckebach utilized arterial kymographs to characterize a clinical presentation of regular irregularity in cardiac systoles. This entity was to become one of most well known eponyms in medicine– what we now know as the Wenckebach phenomenon.
With this case, I want to call attention not to the rhythm itself, but to an unusual feature seen here in conjunction with the Wenckebach: look closely at the 4th QRS complex– how do we know this is a junctional escape and not simply a grossly prolonged PR interval? If such a distinction can be made, what clinical significance should we ascribe to the finding?
In normal cardiac physiology, as the impulse descends from the His bundle, the first portion of myocardium to be activated is the septum; thus the initial deflection of the QRS complex reflects the vector of septal depolarization. Further, given that the septum is predominantly supplied by the posterior fascicle of the LBB, the septal myocardium depolarizes from left to right; it is therefore not pathological to note an initially negative deflection in lead II.
Graphic courtesy of http://www.cvphysiology.com/Arrhythmias/A016.htm
What is noteworthy about the complexes on these tracings, however, is not that there is an initial Q-wave in II, but that the escape complexes in the lead II tracing reveal a conspicuously more pronounced initial Q wave deflection than that present in the normative systoles. Although the QRS morphology and R-wave axis here remain consistent, pointing into the lower left quadrant (~+60°), in the escape complex there is a greater mass of initial electrical activity dissipating away from the lead II electrode (~-120°). This suggests that the ectopic focus responsible for these junctional escape beats is slightly more inferior relative to that authoring the normative QRS signals. In short, due to a more inferior position in the AV nodal tissue, a greater portion of myocardium would depolarize backwards towards the superior and rightward hexaxial quadrant, thus giving rise to the slightly greater Q wave in the escape complexes.
Although these observations on the initial deflection axis suffice to demonstrate a junctional rather than sinus origin to the complexes in question, it should be emphasized that alternative, “markedly slow pathways” through the junctional tissue may mimic this finding. Shinji Kinoshita et al. have recently presented an interesting and more sophisticated analysis of how to approach this issue in their article, Apparent AV Junctional Escape in Wenckebach AV Block: Markedly Slow Conduction Through The Slow AV Pathway, which can be found in the Journal of Cardiovascular Medicine 2009, 10:161–166.
Given that the existence of a junctional focus can be positively or negatively established, however, we might propose a risk stratification dichotomy between Wenckebach pts demonstrating a functional escape pacemaker (as seen above) and those with “escape failure” who must endure QRS dropping without junctional compensation. While systematic study and clinical correlates remain necessary to validate this hypothesis, pts in this latter category would presumably carry greater risk of symptomatic bradycardia than those in the former, and the absence of junctional escape activity might therefore be a positive predictor of greater morbidity in this population.
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:
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.
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.
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.
A 52yr old hispanic male with history of hyperlipidemia, IDDM, hypertension, and 30 pack/yr smoking presents to the ED with c/o nausea and diaphoresis. His mother had an MI at 50, and he has two sisters– one suffered an MI at 52 with subsequent CABG, and the other had an MI at 49. His BP on arrival was 92/48.
Another 3:2 Wenkibach; the second ECG shows the pathology resolving slightly to a 1st degree conduction delay, perhaps reflecting beneficial pharmacotherapy.
This pt. received medical management at an outside facility until he could be transported to the cath lab. His Pro-BNP on admission to CCU was 4668, and his Troponin peaked at 8.36ng/ml. No further is known.