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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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Friday, February 1, 2019

A 72-year-old man with end-stage COPD presented to the ED with dyspnea on exertion and pleuritic, nonexertional chest pain. He stated that he always had shortness of breath, but it had been getting worse over the past three days. He said he had no fever, cough, leg swelling, or other complaints. He also had no history of pulmonary embolism or coronary artery disease, and said whenever his shortness of breath worsened, it had always been because of his COPD. He stated that this time it felt different from anything he had ever experienced before, primarily because of the pain.

His vital signs were normal, except for a blood pressure of 78/55 mm Hg. Of note, the patient was very thin. His physical exam was also normal, except for moderate labored breathing and wheezing. Our initial differential diagnosis included acute coronary syndrome, pulmonary embolism, pericarditis, COPD, and pneumonia.

The patient's initial ECG showed a normal sinus rhythm with premature atrial contractions and nonspecific ST and T-wave changes.


The ECG also showed diffuse ST segment elevation and mild PR segment depression. It also revealed a premature atrial contraction, which were non-specific changes. They could represent acute coronary syndrome, but they were more consistent with pericarditis.

Cardiology saw the patient and felt he had pericarditis. His blood pressure rapidly improved with fluids (and the use of an appropriately smaller blood pressure cuff helped). Lactic acid and serial troponins were normal, but his D-dimer was elevated. Chest CT and echocardiogram showed a small pleural effusion but no pericardial effusion or PE. He was treated for COPD and pericarditis and did well.


Source: The Emergency Medicine 1-Minute Consult: Quick Essentials Pocketbook, 5th Edition

Monday, December 31, 2018

A 77-year-old man presented to the ED for sudden onset of painless dyspnea 20 minutes earlier. He did not report chest discomfort, nausea, palpitations, lightheadedness, or any other complaints.

His vital signs are normal except for a pulse of 131 bpm. You astutely notice that his blood pressure is soft at 101/83 mm Hg. His exam is otherwise normal except for bilateral mottling of the skin in the legs more than the arms.

His initial differential diagnosis included tachydysrhythmia, pulmonary embolism, and acute coronary syndrome.

His ECG is shown. What does it demonstrate?

bradycardia-submassive PE1.jpg

The ECG shows sinus tachycardia with nonspecific T and ST changes. ACS is possible, but given the lack of pain and tachycardia, submassive PE should top your differential. See the highlighted area below for a one-minute consult.

Major take-home points for PE are that large PEs are frequently painless (because they do not cause lung infarcts), tachycardia is rarely present except in large PEs, and ECG changes can be nonspecific.

bradycardia-submassive PE2.jpg

Source: The Emergency Medicine 1-Minute Consult Pocketbook.

Monday, December 3, 2018

A 37-year-old man with no significant past medical history drove himself to the ED and presented with 25 minutes of ongoing, slightly pleuritic, nonradiating chest tightness that started during the uphill part of a jog. He said the pain did not radiate, but that his arms were tingling and he still felt sweaty and out of breath even though he had stopped exercising 25 minutes earlier. He did not smoke or use drugs, but he had a family history of coronary disease.

His vital signs were normal except for a pulse of 98 bpm (some physicians define 55-95 bpm as normal). His skin was diaphoretic, his head and neck exam was normal, his lungs were clear, and his heart sounds were normal with no peripheral edema.

Our initial concerns included acute coronary syndrome, pulmonary embolism, aortic dissection, and anxiety attack.

His chest x-ray was normal, and his triage ECG is shown below.

bradycardia serial ecgs.jpg

Serial ECGs are never a bad idea in a patient with chest pain, but they can be essential in patients with ongoing chest pain that started an hour or two before presentation or in those with intermittent chest pain that recently returned. Guidelines from the American College of Cardiology recommend serial ECGs every 15-30 minutes for the first hour when there is ongoing pain because 10-15 percent of STEMIs are not apparent on the initial ECG and are only diagnosed on repeat tracings. This ST-segment evolution usually occurs within the first hour but occasionally may occur later, even after more than a 90-minute delay.

The initial ECG in this case shows tall, peaked T-waves, which can be an early sign of ischemia. This T-wave finding is often dubbed "hyperacute T-waves." Other T-wave findings that qualify as hyperacute can include a T-wave that is taller than the QRS complex, a straight or convex T-wave upslope, or a V1 T-wave that is taller than the V6 T-wave. One shouldn't need to see hyperacute T-waves to be prompted to repeat the ECG when the clinical context suggests it, but noticing them can certainly help your patient. A true expert would likely activate the cath lab with this first ECG, which is diagnostic of an LAD occlusion due to the q-wave in V2, which should never be present in early repolarization, and the V1 hyperacute T-wave that is massive in comparison with the QRS in the same lead.  A repeat ECG was done and is shown below.  Fortunately, it was done 12 minutes later rather than two hours later.

Here is the repeat ECG done 12 minutes later.
bradycardia serial ecgs 2.jpg

The patient was taken to the cath lab where a 100 percent occlusion of the left main coronary artery was diagnosed and treated.

bradycardia serial ecgs handout.jpg

Source: The Tarascon Emergency Department Quick Reference Guide

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.


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:


Source: The Tarascon Emergency Department Quick Reference Guide