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BradyCardia by Brady Pregerson, MD
​​​NEW BRADIA PHOTO FOR BLOG.JPGThis blog covers a new ECG topic every month with emphasis on interesting tracings and lessons that will change or improve your practice of emergency medicine.​

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Thursday, November 1, 2018

A 32-year-old woman presented to the ED with shortness of breath and a dry cough. She had recently had a cold, but all of her symptoms, including fever, sore throat, and runny nose, had since resolved. She denied any chest pain, leg swelling, or other complaints.

Vital signs were normal except for a respiratory rate of 22 bpm. Her physical exam was normal except for some mild jugular vein distention with no rales, wheezes, or leg edema.

The initial differential diagnosis included pneumonia, congestive heart failure, myocarditis, and pulmonary embolism.

Her CBC, HCG, and BMP were normal. A chest x-ray showed borderline cardiomegaly. Her ECG is shown.

bradycardia-pericardial effusion.jpg

Pericardial effusions are usually painless, and can present with dyspnea and generalized weakness. Additional symptoms may include palpitations, sweating, syncope, near-syncope, and, of course, chest discomfort. The most common findings on physical exam are pulsus paradoxus, tachycardia, and JVD. Other findings tend to be quite insensitive.

The diagnostic test of choice for a significant pericardial effusion is an echocardiogram, but chest x-ray and ECG will also suggest it. A large cardiac silhouette, especially if it is boot-shaped, is suggestive of a pericardial effusion. On the ECG, low voltage is the most sensitive finding. If the effusion is new (as was the case for our patient), start with an echocardiogram to rule out a large pericardial effusion as the cause of low voltage. The echocardiogram of our patient showed one. (See echo image below.) An effusion is even more likely if it is or could be new or if the patient has otherwise unexplained tachycardia. Electrical alternans may also be present but is not sensitive.

bradycardia-pericardial effusion 2.jpg

Tamponade is suggested by tachycardia, diastolic right ventricular collapse, systolic right atrial collapse, or systolic left ventricular wall "kissing." See sample page below for the differences between subacute tamponade, which is more common, and acute tamponade, which is rarer but deadlier and is usually caused by trauma or aortic dissection. Treatment of pericardial effusions depends on the cause and the severity.

The patient was diagnosed with idiopathic pericarditis with a large effusion. She was admitted for observation and remained stable. She was started on colchicine and aspirin and did well.

bradycardia-pericardial effusion 3.jpg

Source: The Tarascon Emergency Department Quick Reference Guide

Saturday, September 29, 2018

A 32-year-old man presents with palpitations that had started suddenly while he was playing and running after his son. He said he had Wolff-Parkinson-White syndrome with an ablation about four years before. He said he had no chest pain, trouble breathing, syncope or near-syncope, or other complaints except that he was hungry.

His vital signs were normal except for a pulse of 128 bpm, as was his physical exam except for a regularly irregular tachycardia. There are no rales and no peripheral edema.

The initial differential diagnosis was atrial fibrillation, atrial flutter, and sinus tachycardia with premature beats.

His CBC, troponin, magnesium, and BMP were all normal, and his ECG is shown.

bradycardia-wolff.jpg

The ECG shows atrial fibrillation with a rapid ventricular response. The next step should be to call cardiology and keep him NPO for now. You want to consider cardioversion, and start with procainamide if you use drugs.

Wolff-Parkinson-White syndrome is caused by an abnormal myoelectrical tract in the heart that bypasses the AV node and its built-in delay. It typically presents clinically as recurrent episodes of tachycardia, most commonly with a narrow complex, but may also be picked up incidentally on ECGs performed for other indications. WPW rarely presents as a wide complex tachycardia, which can be deadly, especially if improperly treated with any agents that block the AV node.

The baseline ECG in an asymptomatic patient will show a short PR in all leads and a delta wave in at least one lead. The delta wave is a slurred beginning to the R-wave. A symptomatic patient may have one of a variety of findings, usually causing a tachycardia. Orthodromic conduction of atrial dysrhythmias occurs in 70 percent of cases, and manifests as other narrow complex tachycardias, such as SVT, atrial flutter, and atrial fibrillation, and is indistinguishable from their non-WPW counterparts. They should be treated the same as patients with and without WPW.

Antidromic conduction occurs in 30 percent of cases and results in wide-complex tachycardias that can look bizarre because some beats use the bypass tract and others the AV node. They can be fast enough that they appear regular and therefore can be mistaken for ventricular tachycardia or torsades de pointes. These tachydysrhythmias are best treated with cardioversion because any medications that can block the AV node can lead to all of the beats going down the bypass tract, which can sustain rates approaching 300 bpm, which can prove fatal. If medication is tried, one should use procainamide, which does not block the AV node.

Definitive treatment of WPW is with cardiac electro-ablation performed by an electrophysiologist in the cath lab.

The patient was successfully cardioverted at 120 joules using etomidate for sedation.  A post-cardioversion ECG showed a computer read of a short PR interval at 100 milliseconds but without a delta wave. The measured PR interval was closer to 120 milliseconds, which is actually normal.

Excerpt on Wolff-Parkinson-White from The Emergency Medicine 1-Minute Consult Pocketbook:

bradycardia-wolff2.jpg

Source: The Tarascon Emergency Department Quick Reference Guide

Friday, August 31, 2018

A 22-year-old woman with no prior medical history was brought to the ED from her workplace by ambulance for acute altered mental status and syncope. Coworkers called 911 after she fainted. Unfortunately, they were not available for an interview.

The patient was alert but bizarre, and asked more questions than she answered. The only useful history was provided by the medics, who said she was acting odd and fainted once. They saw no evidence of trauma. The patient's vital signs were normal except for a regular pulse rate of 130 bpm. Her blood pressure and temperature were normal as was her physical exam except for tachycardia and her bizarre responses to questions.

Specifically, she had no evidence of head trauma, her neck was not tender and had no thyromegaly, and her lungs were clear. Neurologically, she was oriented and followed commands, but she was also slightly tremulous and appeared to be responding to external stimuli.

Initial Concerns:

  • Drug abuse
  • Syncope
  • New onset schizophrenia
The patient's tox screen was negative. Her labs showed a WBC count of 12 and a possible UTI. CT of the brain and a lumbar puncture were normal. An ECG was eventually done for the persistent tachycardia.​

bradycardia-AET.jpg

The ECG shows ectopic atrial tachycardia (AET). The next thing to do was to admit the patient to telemetry.

Atrial ectopic tachycardia (AET) is an uncommon dysrhythmia that presents as a regular narrow rhythm with a heart rate typically between 125 and 250 bpm, often but not always with a short PR interval. The patient often feels palpitations but may be asymptomatic as well. The differential diagnosis includes any other regular narrow rhythm. The most common causes of AET other than idiopathic are COPD, digoxin toxicity, and other triggers of increased automaticity.

Treatment of AET is usually supportive, with an emphasis on stabilizing or treating any underlying causes. Medications are typically not effective.

bradycardia-AET2.jpg

Source: The Tarascon Emergency Department Quick Reference Guide​

This patient's medical workup was otherwise negative. The atrial ectopic tachycardia resolved on its own, and the patient was sent to the psych ward. She was eventually diagnosed with new onset paranoid schizophrenia.

Excerpt on Ectopic Atrial Tachycardia from The Emergency Medicine 1-Minute Consult Pocketbook.

Wednesday, August 1, 2018

A 64-year-old woman presented to the emergency department for chest pain radiating to her arms that started at rest and was slightly pleuritic. She also complained of associated dyspnea but no nausea, vomiting, or sweating. She denied any syncope, near-syncope, cough, fever, calf pain, or other symptoms. Her past medical history was notable for hypothyroidism and high cholesterol, for which she took thyroid replacement and a statin. She drank socially, but had never smoked.

Her vital signs were normal except for mild tachycardia, with a pulse rate of 95-105 bpm. The patient's head and neck were normal to inspection with no arcus senilis or xanthelasma. Her lungs were clear without splinting, and the cardiac exam was normal other than the elevated pulse. Her abdomen was benign, and no peripheral edema or calf tenderness was detected.

Initial Concerns

  • Acute coronary syndrome
  • Pulmonary embolism
  • Aortic dissection
  • Pericarditis
This was her ECG.
bradycardia-lead avt.jpg

The image shows ST elevation in lead aVR with reciprocal ST depression in leads V4-V6. We called cardiology to take the patient to the cath lab. She had severe triple vessel disease requiring four stents.

Lead aVR is often called the forgotten lead because many medical school professors were taught that it is useless, and they pass this on to their students. That's what I was taught in medical school. I was taught in residency that lead aVR was useful for tricyclic overdoses. It wasn't until perhaps 10 years ago that I started to hear how ST elevation in lead aVR could signal a variety of life-threatening conditions.

Lead aVR should not be forgotten. It's fine if you want to make it the last stop on your trip around the 12-lead as long as you visit it at least once before you hand the ECG back to the tech to place in the chart. ST elevation in lead aVR can often mean serious ischemic pathology, especially with reciprocal ST depressions in other leads. Occlusion of the left main or left anterior descending coronaries or triple vessel disease can all cause ST elevation in aVR. Other conditions known to cause aVR ST elevation include massive PE, Brugada syndrome, and right ventricular MI.​

Give lead aVR the respect it deserves, which may be quite different from what you have been taught in the past. Your patients will benefit, and so will you.

Monday, July 2, 2018

A 74-year-old man with a history of dementia, hypertension, and GERD was found at a street corner confused and incontinent of stool. He was brought to the emergency department by ambulance after a passerby called 911.

The patient didn't remember what happened or how he felt, but said he felt fine at the time of presentation. He denied any weakness, pain, fever, nausea, or trouble breathing. We were unable to contact any witnesses, but got in touch with the family, who said their father seemed to be at his baseline.

Vital signs were normal except for a pulse of 110 bpm. His physical exam was normal except for his incontinence, being oriented x2 only (baseline per family), and a slow gait, which his family said seemed a little worse than baseline.

No evidence of trauma or bony tenderness was seen. The heart and lung exams were normal except for the tachycardia, and no abdominal tenderness, peripheral edema, and focal neurologic findings were detected. Our initial concerns were syncope, near-syncope, stroke, TIA, and seizure. His ECG showed junctional tachycardia.​

brady ECG Junctional tachycardia.jpg

What should you do next? Junctional tachycardia is an uncommon rhythm characterized by a regular, narrow QRS complex at a rate between 100 and 130, and absent, retrograde, or very narrow P-waves. Other junctional rhythms are named based on whether the rate is <60 or 60-100. The most common mimic of junctional tachycardia is sinus tachycardia with a type 1 AV block so long that the P-wave is hidden in the prior T-wave.

Treatment of junctional tachycardia is basically by determining and treating the primary cause, which may include hyperkalemia, myocardial ischemia or inflammation, uncontrolled congestive heart failure, and toxicity with digoxin, theophylline, or a beta agonist. Overdrive pacing can be tried if none of the treatments is effective and the rhythm dose not resolve on its own or the patient is unstable.

Our patient was ruled in for an MI, so the cause was thought to be an episode of painless ischemia.

 

Source: The Tarascon Emergency Department Quick Reference Guide