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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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

Friday, June 1, 2018

A 99-year-old woman with a history of dementia, CAD, and COPD (but not A-fib) presented for cough, congestion, tachycardia, and a low pulse ox. The patient cannot give a useful history. She admits to shortness of breath, but denies any pain, fever, palpitations, or other complaints. 

Her vital signs were normal except for a pulse in the 120s, and her heart rate seemed irregular. Her physical exam was normal except for tachycardia and mild wheezing. The thyroid gland was normal to palpation, and no hepatosplenomegaly, rales, or peripheral edema was seen.

Our initial concerns were COPD exacerbation, pneumonia, pulmonary embolism, and tachydysrhythmia. A chest x-ray came back normal, as did her CBC and metabolic panel. Her ECG is shown, and the computer read was "Atrial fibrillation with rapid ventricular response (rate 124), nonspecific ST and T-wave changes."

bradycardia ECG.jpg 

What other findings do you note on the ECG? What is the most appropriate initial treatment?

The ECG was read by the computer as showing atrial fibrillation, but it actually shows multifocal atrial tachycardia (MAT) at a rate of 124. Treatment of MAT is supportive for the most part.

MAT is usually asymptomatic, or any symptoms it produces are overshadowed by the clinical condition that causes it. By definition, the heart rate in MAT is higher than 100, typically in the 110-130 range, and three or more morphologies of P-waves are seen. Causes of MAT include COPD exacerbations, other causes of hypoxia, sepsis, drug toxicity, and electrolyte abnormalities. (More details below.)

Treatment of MAT is usually supportive, with special attention to treating any potential underlying causes. A calcium channel blocker or amiodarone may be tried if these methods are not adequate. This patient's MAT resolved with treatment of COPD, including magnesium and IV fluids. She was admitted for observation and did well.

bradycardia guide.png

Source: The Tarascon Emergency Department Quick Reference Guide.

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Monday, April 30, 2018

A 40-year-old man presented to the emergency department with two hours of rapid regular palpitations and dizziness. He denied vertigo, chest pain, shortness of breath, and syncope, and he said he had never had palpitations like this. His symptoms started suddenly and are continuous. He denied any significant prior medical history and tobacco, alcohol, and drug use, and he takes no prescription medications.



His vital signs were normal except for a softish blood pressure of 101/84 mm Hg and a pulse rate of 196 bpm. His head and neck exam was normal with no thyromegaly or jugular vein distention. His lungs were clear, and his heart was regular but tachycardic. The abdomen was benign, and the legs had no chords, tenderness, or edema.



The precordial leads of an ECG:



  • What is the rhythm?
  • What is initial treatment of choice?
  • What is the second-line treatment?
  • What medication is overused for this condition?



The patient's rhythm is supraventricular tachycardia (SVT), and the initial treatment should be a modified Valsalva maneuver. The second-line treatment is diltiazem. Adenosine is overused for this condition.


SVT: Rate 125-250 and regular. If the rate is under 200, consider Wolff-Parkinson-White syndrome.


Causes: Usually idiopathic, but consider these causes with the acronym TWAM: TCA, WPW, Autism spectrum disorder, MI/mitral valve prolapse.


Tests: K, MG, post-conversion ECG, troponin only needed if clinical concern for ischemia.


Treatment: Modified Valsalva first, then diltiazem. Both are better than adenosine.



Treatment                Rate         Method/Dosing

Modified Valsalva    ~40%           Hold for 15 sec., then supine with

45° leg raise for 15 sec.

Regular Valsalva     ~15%           Not recommended, but if used, hold

for > 15 sec.

Diltiazem IVPB*      ~98%           10-20 mg. Cheaper, safer, and easier to

                                                  use than adenosine,

Adenosine IVP*       ~87%           Not recommended, but if used, start

with 6 mg; repeat 12 mg.**


* If rate >200, consider WPW and avoid all AV nodal blockers.

** 3 mg dose if on Tegretol, Persantine, or Aggrenox. Avoid if WPW or heart transplant.


Prevention: Replete K and Mg; metoprolol, diltiazem, or verapamil; ablation



SVT is a regular tachycardia that usually has a paroxysmal onset and a regular rate between 125 and 250 with no P waves and a narrow QRS. Symptoms are primarily palpitations and lightheadedness. Chest pain, dyspnea on exertion, and syncope or near-syncope may also occur. Most cases are idiopathic, but SVT can be triggered by a variety of cardiac conditions as well as certain antidepressants. Low potassium and magnesium may also contribute.


Treatment of SVT has been primarily with adenosine in the recent past. A Valsalva maneuver may be tried first, but success rates are only about 15 percent. Recent studies have shown there is a better medication and a better Valsalva maneuver. The modified Valsalva, which consists of a Valsalva for at least 15 seconds followed by a passive leg raise, has been shown to terminate SVT in about 40 percent of patients. Diltiazem, with an initial dose of 15 mg, has been shown to be about 10 percent more effective than adenosine, with the additional benefits of a better safety profile, decreased cost, and patient preference.


Patients diagnosed with SVT can usually be discharged home with cardiology follow-up. Prevention for frequent or severe episodes may include beta or calcium channel blockers and ablation by an electrophysiologist.