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Dr. Littmann's Monthly ECG Lessons

9/27/2020 0 Comments

September 2020 ECG Lesson: Wellens Syndrome

By: Quinton Nannet, MD and Dominic Nicacio, MD
​Editors: Drs. Littmann and Gibbs 
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Quinton Nannet, MD
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Dominic Nicacio, MD
Case:
A 56-year-old man with a medical history of schizophrenia, tobacco abuse, and coronary artery disease presented to our emergency department for chest pain. The patient had drug-eluting stents placed to the mid-circumflex and right coronary arteries 13 months before the current presentation. He reports that he has not been taking aspirin or clopidogrel due to financial limitations. He also continues tobacco use of ½ pack a day. The patient describes 3 weeks of severe left-sided, exertional chest pain and associated dyspnea. The pain is normally relieved with rest and ibuprofen, but over the past two days he has had similar pain at rest with only intermittent relief. 
 
The following electrocardiogram was obtained:
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ECG Interpretation:
  • Rate: 48/min
  • Rhythm: Sinus bradycardia
  • Axis: Normal QRS axis
  • QRS: <120 msec; no abnormal Q waves
  • ST segments: No ST elevation or ST depression
  • T waves: Inverted T waves in I, aVL, V2-V6 with biphasic (positive-negative) T waves in V2 and V3 classified as Wellens syndrome type A
Diagnosis:
Wellens syndrome
Significance of Findings:
  • Wellens syndrome is a pattern of electrocardiographic T-wave changes associated with usually severe or critical proximal left anterior descending (LAD) coronary artery stenosis. The syndrome is also referred to as LAD coronary T-wave syndrome.
  • The T-wave abnormalities are seen in the anterior chest leads, usually from V1-V4
  • The T-wave changes are persistent and may remain in place for hours to weeks; making it likely that the clinician will encounter these changes when the patient is chest pain-free.
  • Pathophysiology: not clearly established. According to one theory, the LAD experiences an occlusion that would result in a STEMI if captured on the ECG. This occlusion is reperfused either from spontaneous lysis, from aspirin, or resolution of vasospasm leading to pain relief and progressing to biphasic T waves and then deeply inverted T waves. Since the artery is highly unstable, a recurrent occlusion may progress to tall “hyperacute” T waves or frank ST elevation myocardial infarction (STEMI).
  • Wellens type A ECG pattern
    • T wave morphology: biphasic, initially positive and terminally negative
    • Prevalence: ~ 25% of Wellens syndrome patients
    • Significance: represents an early phase of Wellens syndrome with T wave morphology then progressing toward type B T waves
  • Wellens type B ECG pattern
    • T wave morphology: symmetric and deeply inverted
    • Prevalence: ~ 75% of Wellens syndrome patients
    • Significance: represents a later phase of Wellens syndrome
  • The same ECG may show both type A and type B patterns in different chest leads
  • The ECG findings may persist for weeks:
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Image Source: https://www.ncbi.nlm.nih.gov/books/NBK482490/
 
Diagnostic criteria of Wellens syndrome:
  • Presentation with acute, subacute, recent or stuttering chest pain (probable acute coronary syndrome)
  • Biphasic (positive-negative) or deeply inverted, usually symmetrical T waves in leads V1-V4
  • Isoelectric or minimally elevated (<1 mm) ST segments
  • Preservation of precordial R-wave progression and no abnormal Q waves
  • ECG pattern may be present in a pain-free state
  • Normal or slightly elevated cardiac biomarkers
Management:
  • Immediate cardiac consultation is warranted
  • Patients should be treated with aspirin and heparin
  • Definitive management is heart catheterization with LAD stent placement
  • In Wellens syndrome, early revascularization is far superior to medical management
  • Without appropriate intervention, patients are at high risk for STEMI with significant morbidity and mortality
Patient Disposition:
The patient was admitted to the interventional cardiology service. Cardiac catheterization revealed 99% stenosis of the left main coronary artery, 50% stenosis of the left anterior descending coronary artery and 100% occlusion of the previously stented left circumflex. The previously stented right coronary artery was patent.

Results of cardiac catheterization are shown below:

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Interventions:
Due to the extent of stenoses, the patient had an intra-aortic balloon pump placed to reduce myocardial oxygen demand. The next day, he underwent multivessel coronary artery bypass grafting.
 
Socio-economic considerations:
This case highlights the importance of dual antiplatelet therapy and smoking cessation in patients with stent placement. It also demonstrates the challenges mental health and socioeconomic factors play in the patients’ ability to adhere to treatment plans.
Dr. Littmann’s comments:
There are 4 major types of high-risk acute coronary syndrome (ACS) where the ECG does not show diagnostic ST-segment elevation. These include:
  • Posterolateral MI (old nomenclature: true posterior or high posterior MI). This diagnosis should be suspected in patients who present with typical ACS and the ECG shows ST depression in the anterior chest leads. The diagnosis can be confirmed by placing ECG leads to the back. This condition is a STEMI equivalent that warrants emergent cardiac catheterization and reperfusion.
  • De Winter sign. This diagnosis should be suspected in patients who present with typical ACS and the ECG shows depression of the ST segment at the J point followed by tall, symmetrical upright T waves (“hyperacute T waves”). It usually signifies total or subtotal acute occlusion of the LAD. In my view, this too should be considered a STEMI equivalent and patients should undergo emergent cardiac catheterization and reperfusion. See the August 2020 ECG blog for details.
  • aVR sign. This is characterized by acute chest pain, diffuse ST-segment elevation and ST elevation in aVR of ³ 1 mm. The aVR sign is strongly suggestive of severe and diffuse ischemia due to tight left main or multivessel coronary artery disease. However, it is not a STEMI equivalent. If other important causes such as proximal aortic dissection and hemorrhagic shock have been ruled out, the patients should undergo relatively urgent cardiac catheterization.
  • Wellens syndrome. This is characterized by acute, subacute or stuttering chest pain, biphasic (positive-negative) and/or deep symmetrical T waves in the anterior chest leads and normal or slightly elevated troponins. The patients may be chest pain free on presentation.
    • Of the above listed 4 conditions, the Wellens syndrome is the “oldest” first described in 1982 and therefore, it is the best known among emergency medicine providers.
    • In my view, however, of the above listed conditions it is the least worrisome that usually does not require emergent intervention. In the original description of the Wellens syndrome, those patients who presented with ACS with the Wellens sign in the ECG and did not undergo bypass surgery (there was no PCI available at that time), had a significant likelihood of progressing to STEMI in the weeks or months after presentation. Also, medical management in the 1970s-1980s only included beta blocker and nitrates; we did not even use aspirin, heparin or statin.
    • In general, patients with ACS, ongoing chest pain and/or elevated troponin routinely undergo cardiac catheterization regardless of Wellens or not Wellens.
    • Those patients, however, who are pain free and have negative troponin and no Wellens sign usually first undergo noninvasive evaluation and then cardiac catheterization if the noninvasive test shows high-risk abnormalities.
    • In patients with ACS and the Wellens-type T-wave abnormalities, however, noninvasive testing should usually be avoided. Most patients should undergo cardiac catheterization even if they are pain free and have negative troponins.
    • Wellens-type T-wave changes are not completely specific for tight proximal LAD stenosis. They can be present in patients with massive pulmonary embolism, hypertensive urgency, acute or acute-on-chronic renal failure and severe hypertension. In questionable cases, adenosine Myoview, Lexiscan Myoview or CT coronary angiogram can be safely performed. Frank exercise testing and dobutamine studies, however, should not be done because they can provoke acute MI.​
References:
  • doi: 10.1053/ajem.2002.34800
  • Miner B, Grigg WS, Hart EH. Wellens Syndrome. [Updated 2020 May 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482490/
  • doi: 10.1161/CIRCULATIONAHA.119.043780
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8/27/2020 0 Comments

August 2020 ECG Lesson: "That is an Interesting Sign"

BY: ERIC SABATINI-REGUEIRA, MD and COURTNEY FLEMING, MD
EDITORS: DRS. LITTMANN and GIBBS
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Eric Sabatini-Regueira, MD
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Courtney Fleming, MD
Case:
A 36-yo obese female with no other known past medical condition presented to the emergency department with a 30-minute history of chest pain. The pain was described as being a retrosternal pressure-like discomfort that was non-radiating, and 10/10 in severity. The patient denied having similar episodes in the past. There were no alleviating or worsening factors. During the physical examination, the patient was noted to have the Levine’s sign (clenched fist held over her chest).
 
The following electrocardiogram was obtained:
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ECG Interpretation
Rate: 78/min
Rhythm: Normal sinus rhythm
Axis: Normal QRS axis
QRS: <120 msec; no abnormal Q waves
ST-T: ST depression at the J point (at the junction between the QRS complexes and ST segments) in the anterior/lateral leads, mostly upsloping ST segments and then, very tall peaked T waves (de Winter T waves). ST segment elevation in aVR.
Significance of ECG Finding

  • Thought to be first described by Dr. Robbert Jan de Winter in 2008 in his letter to the editor to the New England Journal of Medicine, the pattern of peaked T-waves as a sign of myocardial ischemia was actually first noted by Dr. William Dressler in 1947 in a case series of over 27 patients. What de Winter defined was “1- to 3-mm upsloping ST-segment depression at the J point in leads V1 to V6 that continued into tall, positive symmetrical T waves” that are often accompanied by a “1- to 2-mm ST-elevation in lead aVR”.
  • The de Winter pattern is significant because it is associated with occlusion of the proximal left anterior descending coronary artery (LAD) if found in the ECG of patients with chest pain or a history suspicious for acute coronary syndrome. In fact, this patytern is found in 2% of patients diagnosed with proximal occlusion of the LAD, with an associated positive predictive value of 95-100%. The other 98% of patients with acute LAD occlusion had frank STEMI in the ECG. As such, it is critical not to overlook the de Winter pattern which is not common, but is associated with important clinical outcomes.
  • The pattern has been found to be more common in young males (mean age 52 compared with mean age of 61 in patients with STEMI on ECG) and in ptients with history of hypercholesterolemia, smoking and family history of coronary artery disease.
  • The exact pathophysiologic mechanism of why the de Winter pattern occurs in patients with occlusion of the proximal LAD is largely unknown. It has been speculated that it may be due to endocardial conduction delay due to anatomical variations in the Purkinje fibers. Other theories attribute the pattern to variations in coronary anatomy and collateral recruitment.
  • There has been much debate in the medical literature in regard to whether the de Winter pattern should be considered a STEMI equivalent. Many studies have defined the de Winter pattern as being a static sign that occurs very early after symptom onset and persists until reperfusion therapy. However, recent studies have identified the de Winter pattern as a more dynamic entity that can either evolve into classic ST-elevation or occur after the resolution of ST-elevation on the ECG. The theory behind this is that the de Winter pattern represents subtotal occlusion of the LAD, and progression to frank STEMI occurs with continued thrombus formation towards total arterial occlusion. Conversely, resolution from STEMI to a de Winter pattern could represent autolysis of a totally occlusive thrombus back to subtotal occlusion. Regardless if the pattern is static or dynamic, it does remain highly suggestive of a high degree of arterial occlusion.
  • There are few definitive guidelines for management of patients who present with symptoms suggestive of ACS and the de Winter pattern on the ECG. Most recent guidelines by the American Heart Association do not explicitly recommend percutaneous intervention or outline thrombolysis management for patients presenting with the de Winter sign as a singular indication for acute coronary intervention. Though rare, specific guidelines for management of patients with de Winter pattern is warranted as studies show this important ECG sign is often missed by clinicians, and delay in diagnosis can lead to higher total ischemic time and possible higher mortality. In the emergency department, this should include immediate cardiology consultation and when available, immediate bedside echocardiography to assess for the presence of left ventricular wall motion abnormalities.
Disposition
The patient underwent emergent cardiac catheterization which found a 99% occlusion of the ostial LAD. The initial troponin-T was 4.78ng/mL and peaked at >50ng/mL (detection limit) later that day. It is important to remember that a positive troponin is not needed to make the diagnosis of STEMI or a STEMI equivalent.

Results of cardiac catheterization and stenting of the proximal LAD are shown below
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Dr. Littmann’s comments:
Drs. Sabatini-Regueria and Fleming have beautifully summarized our current understanding of the de Winter sign, its prevalence, clinical significance, possible mechanism and the somewhat controversial guideline recommendations how to proceed when it is manifest. I have a few comments about the de Winter sign:
  • The original description of the de Winter sign requires depression of the ST segment at the J point followed by very tall T waves. In my view, the ST depression part is not mandatory; very tall (“hyperacute”) T waves alone are equally diagnostic of proximal LAD occlusion (see example below).
  • Unfortunately, there are no absolute diagnostic criteria what constitute hyperacute T waves, how tall the T waves need be. The clinical scenario is most important: if a patient has acute chest pain suggestive of acute MI, very tall T waves in the chest leads should warrant emergent catheterization and reperfusion.
  • How can one distinguish tall T waves of hyperkalemia from tall T waves of de Winter? The clinical scenario is usually completely different. In a patient with sepsis, shock and renal failure, tall T waves almost certainly indicate hyperkalemia. In a patient who presents with acute chest pain, it is most likely the de Winter sign. Also, tall T waves of hyperkalemia are usually narrow based whereas the de Winter T waves are usually not.
  • Although it is uncertain why 98% of patients with acute occlusion of the proximal LAD present with frank STEMI and 2% with the de Winter sign, the most compelling evidence suggests that the de Winter sign signifies subtotal occlusion of the proximal LAD, and STEMI signifies total occlusion. That is probably why most de Winter presentations are very early after the onset of chest pain and why, if not reperfused, the de Winter sign usually progresses to frank STEMI.
  • In my view with a clinical presentation of acute chest pain, the de Winter sign should unequivocally be considered a STEMI equivalent mandating emergent cath and reperfusion. A lot is at stake!
  • What is now known as the de Winter sign was originally described in 1947 by Dr. Dressler, the same cardiologist who described the Dressler syndrome. Although the de Winter group deserves huge credit for presenting more details about the de Winter sign and for popularizing it, in my view it should be renamed the Dressler – de Winter sign.
  • Dr. de Winter is from the cardiology group in the Netherlands which used to be headed by Dr. Wellens. Both on the de Winter article and on the Wellens sign article, Dr. Wellens is the last author. They not only described these two syndromes, but also were one of the first to study the aVR sign. Dr. Wellens was a giant in electrocardiology and cardiac electrophysiology. He passed away a few months ago at age 85. The cardiology world is mourning his loss.
​
Below are the three types of de Winter ECGs. Note that in the third type, there is no ST depression, just hyperacute T waves.
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Below is an edited version of the de Winter sign as described by Dr. Dressler in 1947
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​References (all represented by DOI numbers):
10.1056/NEJMc0804737
10.1016/0002-8703(47)90343-8
10.1016/j.jacc.2018.08.1038
10.1016/j.ajem.2013.09.037
10.12998/wjcc.v7.i20.3296
10.4103/HEARTVIEWS.HEARTVIEWS_90_19
10.1155/2018/6868204
10.21037/atm.2019.07.19
10.1016/j.jelectrocard.2017.08.024
10.1016/j.jacc.2020.07.015
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7/4/2020 0 Comments

June 2020 ECG Lesson: "Is It Right?"

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By: Andrew Yde, MD
Editors: Drs. Littmann and Gibbs


Case:
A 61-year old woman with coronary artery disease and interstitial lung disease, on home O2 therapy, presented with a 3-day history of constant right-sided chest pain radiating to the right neck. She also complained of worsening dyspnea and exertional lightheadedness. On physical examination, the patient was afebrile, had a heart rate in the 60s, was mildly hypertensive at 147/71 mmHg, and was maintaining normal oxygen saturations on 2L supplemental O2. The examiner did not note abnormalities on cardiopulmonary exam. Chest CT angiogram was negative for pulmonary embolism and high sensitivity troponin was <6. She was given morphine and Toradol with some relief in her chest pain.

The following electrocardiogram was obtained:

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Physician interpretation of the ECG was as follows:
Normal sinus rhythm with a rate of 67, right axis deviation, otherwise normal intervals. ST depression in the septal and lateral leads. No ST elevation. When compared to an ECG obtained two months before, the complex morphology is generally unchanged. The ST depression is a bit more pronounced.
What is your interpretation of this initial ECG? Do you agree with the physician interpretation?
Do not agree.
The ECG shows sinus rhythm with dextrocardia. The ST-T morphology cannot be reliably assessed. Repeat ECG with limb leads reversed, and place right-sided chest leads.
Summary of key ECG findings:
  • Negative QRS complexes and inverted P and T waves in lead I (everything negative in lead I).
  • Negative QRS in lead II.
  • Reversal of direction of the P, QRS and T in aVR and aVL, largely positive in aVR and largely negative in aVL.
  • Reversal of typical QRS progression (R wave progression) in the chest leads. The tallest R waves are in V1. This is followed by R-wave regression and a decrease in the amplitudes of the QRS complexes rather than R-wave progression and an increase in the amplitudes of the QRS complexes.
  • In patients with dextrocardia, reversal of the arm leads will “normalize” the directionality of the QRS and P waves. On the same note, placement of the precordial leads in a right sided fashion (V1R-V6R) will result in “normalized” R wave progression and septal depolarization.
In this patient with dextrocardia, the chest leads were reversed but the limb leads were not. See ECG below:
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Note that the limb leads remained unchanged, but the QRS progression in the chest leads has normalized. One can now diagnose probable left ventricular hypertrophy (LVH) with secondary repolarization abnormality vs. anterolateral ischemia. As the repolarization abnormality was identical to that seen two years before, LVH was the more likely diagnosis. Possible abnormalities in the limb leads may have remained obscure.
Proof of situs inversus totalis:
(1) ECG showing dextrocardia – see above.
(2) Chest X-ray demonstrating a right-sided heart with the ventricular apex pointing to the right – below left.
(3) Abdominal CT showing the liver on the left and the spleen on the right – below right. The abdominal CT was recorded during a prior admission.

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Hospital Course:

Two sets of high-sensitivity troponin measurements remained within normal limits. An echocardiogram showed new moderate biventricular dysfunction with left ventricular ejection fraction (LVEF) calculated at 35%, changed from echocardiogram three years prior in which biventricular function was normal and LVEF was 55%. Given a history that was concerning for ischemia and new biventricular dysfunction, the Cardiology service recommended cardiac catheterization which revealed calcification and minor luminal irregularities of all coronary vessels and a 50% stenosis of the mid left main coronary artery. No stents were placed, and medical management was recommended. The patient experienced several bouts of right sided chest pain reliably relieved by oral Tylenol. Her chest pain was felt to be musculoskeletal in nature. She was discharged in stable condition with follow-up appointments with both her primary care physician and Cardiology.

What is situs inversus, and what does it mean for our patient?
Situs solitus refers to the normal orientation/location of the thoracic and abdominal viscera. In situs solitus, we find a tri-lobed right lung, a bi-lobed left lung, and a heart on the left side with the apex facing left. The liver and gallbladder are on the right, the spleen is present on the left, the descending colon is on the right, the ascending colon on the left, and the inferior vena cava (IVC) runs to the right of the aorta in the abdomen, etc.

In 1 out of 10,000 people, the orientation of the thoracic and abdominal viscera is reversed - a heterotaxy syndrome called situs inversus. Of these patients, the vast majority have situs inversus totalis, in which the heart is in the right chest with the apex oriented toward the right (dextrocardia). The remainder of the thoracic and abdominal viscera are in positions exactly mirroring situs solitus. For example, the right lung is bi-lobed, the left lung is tri-lobed, the liver and gallbladder are on the left side, the spleen is on the right side, the ascending colon is on the left, the descending colon is on the right, the IVC runs to the left of aorta in the abdomen, etc. Approximately 2-5% of these patients will have congenital cardiac anomalies, but the vast majority will be asymptomatic with normal quality of life and life expectancy.

Approximately 1 in 22,000 people in the general population will have situs inversus with levocardia, meaning that, although the thoracic and abdominal viscera are in mirror/reverse position from situs solitus as in situs inversus totalis, the heart remains in levocardia (its normal orientation), located in the left chest with the apex oriented toward the left. Nearly 100% of these patients have congenital cardiac anomalies, usually of the cyanotic variety (i.e. transposition of the great vessels). These patients have a severely shortened life expectancy. In fact, only about 5-13% of patients with situs inversus with levocardia survive beyond 5 years of age.
Of patients with situs inversus totalis, 17-25% will have Kartagener syndrome characterized by chronic sinusitis, bronchiectasis and situs inversus. This syndrome is a result of dynein protein abnormalities causing impaired mucociliary clearance, known as primary ciliary dyskinesia. Interestingly, only 50% of patients with primary ciliary dyskinesia will have situs inversus, and thus only 50% will meet official criteria for Kartagener syndrome.

Based on radiographic, echocardiographic, and ECG evidence proving dextrocardia, CT angiography of the chest confirming a tri-lobed left lung and bi-lobed right lung, and CT abdomen obtained during previous hospital admission, our patient has situs inversus totalis without associated primary ciliary dyskinesia. She had no evidence of congenital cardiac abnormalities on her echocardiogram or catheterization. She had respiratory bronchiolitis associated interstitial lung disease and chronic obstructive pulmonary disease, both secondary to a greater than 25 pack-year history of cigarette smoking, rather than chronic sinusitis. This patient’s coronary disease did not seem to be related to her underlying situs inversus totalis, but rather due to the significant smoking history, diabetes, and hypertension.

Dr. Littmann’s comments:
If you order an ECG, please spend a couple of minutes to analyze it. The first steps include rate, regularity and rhythm. Then go left-to-right, starting with the P waves. The normal sinus P wave cannot be negative in lead I as the SA node is in the upper right atrium and therefore, atrial activation is right-to-left, going towards lead I. If the P wave is negative in lead I, follow the steps below:
  • The most common cause of a negative P wave in lead I is limb lead reversal. If you suspect limb lead reversal, please order a repeat ECG with special attention to correct electrode placement.
  • If both the P and QRS is negative in lead I, as in the current case, the differential diagnosis includes left-right arm lead reversal and dextrocardia: either the heart is on the wrong side or the arm leads are on the wrong side. It is easy to distinguish the two: in arm lead reversal, the QRS progression in the chest leads is normal (see ECG below) whereas in dextrocardia, it is reversed.
  • The conventional ECG of patients with dextrocardia cannot be read; one needs to reverse both the limb leads (R arm - L arm leads and R foot - L foot leads) and the chest leads (place right-sided chest leads). Once you have done that, all ECG abnormalities become real. Unfortunately, as it happened in this patient, the chest leads are frequently reversed, but the limb leads are not which makes it essentially impossible to recognize abnormalities that only show up in the limb leads such as inferior ischemia or infarct.
  • Once dextrocardia is diagnosed, some type of abdominal imaging is needed to confirm or exclude situs inversus totalis.
  • In patients with situs inversus totalis, explore the possibility of the Kartagener syndrome.
Below is an example of right arm – left arm lead reversal. Note that the limb leads look essentially identical to what was seen in dextrocardia (everything negative in lead I, upright P, QRS and T in aVR and negative P, QRS and T in aVL), but in the chest leads, there is normal R-wave progression.
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References:
  • Abdullah, N., MBBS, FRCR, Quek, S., MBBS, FRCPCH, Seto, K., MBBS, FRCR, & Teo, L., MBBS, FRCR. (2015, April). Clinics in diagnostic imaging (160). Levocardia with abdominal situs inversus. Retrieved June 27, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4415098/
  • Burns, E., MD. (2019, March 16). Right Ventricular Infarction • LITFL • ECG Library Diagnosis. Retrieved June 26, 2020, from https://litfl.com/right-ventricular-infarction-ecg-library/
  • Mozayan, C., MD, & Levis, J., MD, PhD, FACEP, FAAEM. (2019, August 15). ECG Diagnosis: Dextrocardia. Retrieved June 26, 2020, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6730946/
  • Paul J. Shogan, MC USA, Les Folio, USAF MC SFS (Ret.), Situs Inversus Totalis, Military Medicine, Volume 176, Issue 7, July 2011, Pages 840–843, retrieved June 26, 2020 from https://doi.org/10.7205/MILMED-D-11-00039
  • Roongruangchai J, Narongsak W, Plakornkul V, Viravud Y, Sripaoraya K, Roongruangchai K. Situs inversus totalis and ultrastructure of respiratory cilia: report of a cadaveric case. J Med Assoc Thai. 2012;95(1):132-138, retrieved June 26, 2020 from https://pubmed.ncbi.nlm.nih.gov/22379754
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5/11/2020 0 Comments

May 2020 ECG Lesson: “Treated for Atrial Flutter”

By: Mark Kastner, MD and Rachel Plate, MD
Editors: Drs. Littmann and Gibbs
Rachel Plate, MD
Rachel Plate, MD
Mark Kastner, MD
Mark Kastner, MD

Case:
A 69-year old man with ischemic cardiomyopathy (LVEF 30%), and a history of both ventricular tachycardia and recurrent atrial flutter, s/p ICD placement, presented with one day of palpitations and associated lightheadedness. His cardiac medications included amiodarone and apixaban (Eliquis). His heart rate was 131 beats/min and regular, blood pressure was 103/84 mmHg. On exam he was slightly diaphoretic and anxious, but in no acute distress. The ECG interpretation software indicated sinus tachycardia with nonspecific intraventricular conduction delay and acute inferior infarct (LCX). This was over-read by the providers as atypical atrial flutter. He received IV amiodarone bolus and drip.

The following electrocardiogram was obtained:

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Presentation ECG
​Here is the patient’s baseline ECG for comparison:
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What is your interpretation of the ECGs? Do you agree that this was atrial flutter?
Correct interpretation of the ECG:
  • RELATIVELY SLOW AND SLIGHTLY IRREGULAR VENTRICULAR TACHYCARDIA.
 Summary of Key Clinical and ECG Findings (see annotated ECG below):
  • Relatively slow and slightly irregular wide-complex tachycardia (WCT); rate 131 beats/min
  • QRS width is 4.5 mm = 180 ms, very wide (see green arrows and numbers)
  • In a patient with ischemic cardiomyopathy, 90-95% of WCT is ventricular tachycardia (VT) (Ref. 1)
  • WCT with more QRS complexes than P waves (see red arrows): 100% specific for ventricular tachycardia (Ref. 1)
  • QRS complexes are bizarre, do not fit a bundle branch block pattern
  • Northwest QRS axis, QRS predominantly negative in leads I and II (see purple box)
  • Initial R wave in aVR (see black box)
  • Tachycardia with wide, bizarre QRS complexes, NW axis and initially upgoing QRS in aVR: almost certainly VT (Ref. 1,2)
  • Explanation: the ventricles are normally depolarized from right to left and from above to below; if the QRS axis is going towards the right shoulder (NW axis, initial R in aVR), then the impulse is coming from the ventricles rather than going towards the ventricles.
  • R-R intervals alternate between 11 mm and 12 mm (440 ms and 480 ms) (see blue numbers)
  • Cycle length alternans, seen in this case, is uncommon but can be present in ventricular tachycardia
  • If you see a wide complex tachycardia, VT must be high on your differential diagnosis. If you are not certain, give IV adenosine. Adenosine, by creating AV block, should expose atrial flutter. If it did not do anything to the tachycardia, VT remains the most likely diagnosis (Ref. 1). In this case, atrial flutter was “diagnosed” but adenosine was not given to prove it.
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Hospital Course:
​The patient remained in WCT overnight. Next morning, he underwent successful electrical cardioversion and was discharged home with a diagnosis of atrial flutter. Over a follow-up of 3 months, he did not have recurrence of the tachycardia.
Dr. Littmann’s Comments:
​Ventricular tachycardia (VT) is often misdiagnosed as SVT. This phenomenon was first described almost 50 years ago. Despite numerous publications and reviews raising awareness to this problem, the misdiagnosis of WCT, unfortunately, continues to be very common. As described above, there are numerous ECG clues that can help you diagnose VT. The most important factor, however, is the clinical likelihood: of all WCTs, about 80% are VT. In patients with heart disease, 90-95% of WCT is VT. “Probable VT” should always be your default diagnosis. It is OK not to remember any of the ECG clues listed by Drs. Kastner and Plate. If you are not sure, just give IV adenosine.
 
In this case, it is reasonable to raise a few additional legitimate questions:
• Why was the VT relatively slow? The patient was on amiodarone which, by suppressing conduction velocity of the reentry circuit, can markedly slow down the rate of VT.
• Why did the ICD not shock the patient? Probably because of the relatively slow heart rate. ICDs are usually programmed to deliver shocks at faster rates.
• Would it have been important to diagnose, or at least consider, the diagnosis of VT? Yes, because an attempt could have been made to overdrive pace the ventricles with the help of the pacemaker/ICD. Slow VTs are uniquely susceptible to overdrive pacing. If successful, it could have immediately resolved the tachycardia and cardioversion, even hospital admission, may have been avoided. In addition, the ICD could have then been reprogrammed to provide automatic overdrive pacing if a similar tachy-event were to be detected in the future.
References:
​1. Littmann L, Olson EG, Gibbs MA. Initial evaluation and management of wide-complex tachycardia: a simplified and practical approach. Am J Emerg Med 2019;37:1340-5.
 
2. Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. A new algorithm using only lead aVR for the differential diagnosis of wide QRS complex tachycardia. Heart Rhythm 2008;5:89-98.
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3/30/2020 0 Comments

February 2020 ECG Lesson : A Sneaky Rhythm

PictureTravis Barlock, MD
By: Forrest Turner, MD and Travis Barlock, MD
Editors: Drs. Littmann and Gibbs

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Forrest Turner, MD

Case: 
A 63-year-old male with a history of traumatic brain injury and associated seizure disorder presented from a skilled nursing facility after experiencing syncope and recurrent seizures. EMS reported occasional heart rates in the 200s. The patient received 5 mg of midazolam IM and the seizure activity resolved. On evaluation, he appeared to be post-ictal and minimally responsive. He had a normal pupillary exam and was withdrawing all four extremities. He was tachycardic at 136/min, blood pressure 105/75 mmHg, respiratory rate 20/min and oxygen saturation 95% on room air.
 
The following electrocardiogram was obtained:
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Interpretation by ECG software, confirmed by a physician
Sinus tachycardia with frequent premature ventricular complexes​
What is your interpretation of the ECGs?
​Correct interpretation of the ECG
Atrial flutter with 2:1 AV conduction and frequent premature ventricular complexes
Summary of key ECG findings:
  • Narrow-complex tachycardia, regular except for the PVCs, at a rate of 136/min
  • Differential diagnosis includes sinus tachycardia, ectopic atrial tachycardia, reentrant paroxysmal supraventricular tachycardia, and atrial flutter
  • In sick hospitalized patients, regular supraventricular tachycardia frequently turns out to be atrial flutter with 2:1 AV conduction (“2:1 flutter”)
  • 2:1 flutter is frequently misdiagnosed as sinus tachycardia both by the ECG interpretation software and by providers
CLUES:
Clues to recognizing 2:1 flutter include the following simple “tricks”
  • If you see a regular SVT, always entertain the possibility of 2:1 flutter
  • The interpretation software indicates sinus tachycardia but there is something wrong with the P-wave morphology (as in the current case) or with the PR interval (too short or too long)
  • Usually it is simple to prove the presence of 2:1 flutter by using the “halving” method: measure the R-R interval and try to find P waves at one half of this distance
  • In typical atrial flutter, the P waves (flutter waves) are negative in the inferior leads
  • If uncertain, intravenous adenosine, by creating higher-grade AV block, can easily expose the flutter waves.
​
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In this enlargement of the inferior leads, see the negative P waves spaced at exactly half of the R-R intervals.
Significance of finding?
Significance of recognizing 2:1 flutter in cases initially interpreted as sinus tachycardia
  • Sinus tachycardia is not a primary arrhythmia; its treatment includes treating the underlying condition such as hypovolemia, fever, sepsis, thyrotoxicosis and heart failure
  • Atrial flutter, on the other hand, is a primary arrhythmia; initial treatment should focus on rate control with intravenous diltiazem, beta- blocker and/or digoxin
  • Chronic management options include rate control and anticoagulation vs. rhythm control
  • First-line treatment for rhythm control is catheter ablation; its success rate approaches 90%
  • Indications for anticoagulation are identical to those in atrial fibrillation
  • Atrial flutter is frequently the result of right heart pathology such as atrial septal defect, obstructive sleep apnea, tricuspid regurgitation and pulmonary hypertension; recognizing atrial flutter should prompt evaluation for these listed conditions
HOspital Course
Hospital Course
The patient’s pre-hospital report of extreme tachycardia raised the possibility of 1:1 flutter and possibly syncope due to the dysrhythmia rather than seizure. Cardiology evaluated the patient and recognized the atrial flutter. The patient was given IV diltiazem which resulted in excellent rate control. It was felt that because of his brain injury and seizures, the patient was not a candidate for chronic anticoagulation. Catheter ablation was discussed but eventually rejected. Echocardiogram revealed right ventricular dilatation and hypokinesis, moderate tricuspid regurgitation, moderate pulmonary hypertension and marked right atrial dilatation.
Dr. Littmann’s Comments
Atrial flutter with 2:1 AV conduction (“2:1 flutter”) is one of the most commonly missed ECG diagnosis, both by the interpretation software and by providers. 2:1 flutter should always be entertained if the computer diagnoses “sinus tachycardia” but there is either an abnormal P-wave morphology and/or an abnormal PR interval. Consistent misreadings by the interpretation software include sinus tachycardia with first-degree AV block, sinus tachycardia with very short PR intervals, and ectopic atrial tachycardia. The most important factor in recognizing 2:1 flutter is to always consider this diagnosis in sick patients who present with a regular SVT. Once the diagnosis of 2:1 flutter is entertained, it is usually easy to prove it by using the “halving method”: recognizing negative P waves in the inferior leads whose distance is exactly half of the R-R intervals. If uncertain, the use of IV adenosine, by exposing the flutter waves, can be very helpful.
 
From the ED physician’s perspective, the most important job is to recognize the flutter and provide rate control. In patients who present repeatedly with atrial flutter, it is also prudent to suggest to the accepting team that curative treatment with catheter ablation should be entertained and discussed with cardiology.
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1/14/2020 0 Comments

December 2019 ECG Lesson

This month’s EKG is brought to you by Dr. Clayton Long.
​Editors: Drs. Littmann and Gibbs
Clayton Long, MDClayton Long, MD
​Case 
A 67-year-old male with 6-12 month history of recurrent syncope presented to the ED with facial trauma following a syncopal event. The patient experienced multiple prodromal episodes of presyncope in short succession, ultimately culminating in true syncope causing a nasal fracture. He refused additional work-up at the time of injury given his history of extensive previously negative evaluations for syncope. He had received multiple ECGs, nuclear stress testing and echocardiography in the past. The results of his past evaluations were unrevealing, and he was referred to a specialist with no further clarity provided. 
 
Within weeks he returned for outpatient surgical repair of his nasal fractures. In the perioperative period he was noted to have AV block on telemetry which self-resolved. He was reportedly symptomatic at the time this rhythm was recognized and was referred for subspecialty Cardiology – Electrophysiology (EP) for evaluation where the following ECGs were obtained.

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What is your interpretation of the ECGs?
Correct interpretation of the ECGs
ECG #1
- NSR with normal PR, normal QRS axis and RBBB 
- Sinus rate of 85/min with 1:1 AV conduction
 
ECG #2
- Regular bradycardia, still normal PR intervals and normal QRS axis, unchanged RBBB pattern 
- The sinus rate is now 90/min with 2:1 AV block; hence, the ventricular rate is 45/min
- Blue arrows below demonstrate twice as many sinus P waves as QRS complexes
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Significance of these findings? 
​These ECG findings are consistent with right bundle-branch block and acceleration-dependent second-degree AV block where there is 1:1 AV conduction at slower sinus rates but 2:1 AV block at faster atrial rates. Acceleration- dependent AV block localizes the block to the His-Purkinje system, which is characterized by all-or-none conduction. At a critical sinus rate, only every other sinus impulse is able to conduct through the His-Purkinje system and every other P wave is blocked. On the conducted complexes, there is no change in the PR interval. The blocked P waves are almost never recognized by the interpretation software, which usually reads the rhythm as sinus bradycardia, a clinically trivial dysrhythmia. Therefore, the ECG must be carefully scrutinized in order to identify this ominous rhythm and the correct diagnosis.
 
- In this case, slowing down the sinus rate with carotid massage or IV beta-blocker can paradoxically improve AV conduction.
- Atropine, on the other hand, is contraindicated because it can worsen AV conduction by increasing the sinus rate.
- This finding is concerning for extensive distal conduction disease. Patients with bundle-branch block and acceleration-dependent AV block are at high risk of complete heart block at an anatomically distal level, which may result in asystole and cardiac arrest. 
- This finding requires urgent EP evaluation and is an absolute indication for dual-chamber (AV sequential) pacemaker implantation
Hospital Course
​The patient was admitted directly from the outpatient EP office visit to Cardiology for permanent pacemaker implantation. He received a dual-chamber pacemaker. He continued to experience syncopal symptoms following his initial procedure due to intermittent loss of lead capture requiring revision and a brief admission to the cardiac ICU. The remainder of his hospitalization was uncomplicated, and he was discharged shortly thereafter with no recurrence of symptoms. During his first outpatient EP follow-up he was noted to be asymptomatic with no recurrence of syncope and a fairly low pacing burden. EP noted that they anticipate his pacing burden will increase over time.
Summary 
​This patient had right bundle-branch block and an occult acceleration-dependent 2:1 AV block that was present but unrecognized on the ECGs during multiple prior ED visits for syncope. 
 
Bundle-branch block combined with acceleration dependent 2:1 AV block is indicative of extensive distal conduction system disease and requires urgent EP evaluation for pacemaker implantation to avoid degeneration to complete heart block and potentially, cardiac arrest. 
 
This rhythm is rarely detected by the interpretation software and will be missed on ECG review unless thoughtfully searched for. 
Dr. Littmann’s Comments
It is well known that patients with bifascicular block are at risk of developing complete heart block. This is especially true for patients with bifascicular block who experience syncope. It is less appreciated, but still well documented that patients with simple left or right bundle branch block and syncope too, as in the current case, are frequently found to have paroxysmal AV block and asystole.1 Based on these data it is recommended that patients with unexplained syncope who have any type of intraventricular block should undergo prolonged monitoring with an implanted loop recorder (class I recommendation).2 In this case, the patient had numerous previous workups by cardiologists and underwent a number of minimal value testing such as echocardiography and stress testing, but was never offered cardiac monitoring.
 
A second important lesson of the case is that 2:1 heart block is almost never recognized by interpretation softwares and is rarely recognized by providers. Most cases are interpreted as sinus bradycardia, which is usually a more benign dysrhythmia. Whenever a patient’s ECG appears to demonstrate regular sinus bradycardia, please carefully search for twice as many P waves than meets the eye by halving the interval between the conducted P waves. This “trick” only takes a few seconds to do. It is most important to search for 2:1 heart block in patients who have bundle-branch block and in patients who present with presyncope or syncope.
Key references
  1. Moya A, et al. Bradycardia detection in Bundle Branch Block (B4) study. Eur Heart J 2011;32(12):1535-41.
  2. Kusumoto FM, et al. 2018 ACC/AHA/HRS guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2019;74:e51-156.
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    Author

    This blog represents important ECG lessons that the Emergency Medicine Residents from Carolinas Medical Center (Charlotte, NC) rotating through the Cardiology service encounter.  Test your knowledge with them! The esteemed educators Dr. Laszlo Littmann and Dr. Michael Gibbs serve as the primary content editors and course directors. 

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