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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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Tuesday, September 1, 2020

A 52-year-old man with no past medical history presented to the ED with six days of chest pain. He had been seen in the ED two days earlier and sent home because his serial troponins were negative with four days of pain, which "ruled out coronary disease," according to the account of his first visit.

A more detailed history revealed that he actually had had intermittent pain with two to three episodes per day, each lasting two to five minutes, but that night, it had been happening for more than an hour. He reported no syncope, shortness of breath, nausea, sweating, or other complaints.

His vital signs were normal except for a pulse of 110 bpm, and his exam was otherwise normal.

The initial differential diagnosis was tachydysrhythmia, electrolyte abnormality, pulmonary embolism, and acute coronary syndrome.

This was his initial ECG.

bradycardia-ECG-angina-acute myocardial infarction.jpg

The computer read this as sinus tachycardia, an inferior infarct, possibly acute, with a lateral injury pattern. Do you agree with the computer? What should you do next?

The computer read was correct but incomplete. There was some ST elevation in lead II, V6, and possibly a bit in I and aVL. There was also evidence of a posterior MI with ST depression and relatively tall R waves in V1-V4. These findings were most likely due to a posterolateral STEMI. The ECGs from his visit two days earlier were checked and deemed to be normal, but they were done while the patient was free of pain.

The patient's troponin I was elevated at 2.7 (99% URL <0.030: troponin I immunoassay, Abbott Laboratories). He went to the cath lab, and had a 100% proximal left circumflex artery occlusion. This case was a classic example of new-onset angina with a normal ECG and troponin followed by an acute MI a few days later. A good history is the key to picking up unstable angina before the MI because the ECG and troponin rarely will. A repeat troponin was 365.

Case Lessons

The ECG is much less sensitive when the patient is free of pain, as in unstable angina. Troponins should be expected to stay normal with episodic chest pain lasting less than 15-30 minutes, as in unstable angina. It is really the history alone that makes the diagnosis of unstable angina, so take a good one!

Untreated unstable angina often leads to MI (or death) in the following week or two.

Posterior MI is considered a STEMI equivalent. Other STEMI equivalents include de Winter's pattern, ROSC, shark fin pattern, and Smith-Modified Sgarbossa criteria in left bundle branch block, or paced rhythms. De Winter's and posterior MI share some features, but de Winter's, which is anterior ischemia, has briefer ST depression and taller T-waves than posterior MI.

This post was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog.

bradycardia-coronary disease-angina-acute myocardial infarction-handout 1.jpg

Source: Emergency Medicine 1-Minute Consult Pocketbook

Monday, August 3, 2020

A 72-year-old man with a pacemaker, hypertension, and diabetes mellitus presented to the ED with nonpleuritic, nonexertional, nonradiating chest pain lasting 20-30 minutes. It improved after 10 minutes, and resolved after paramedics gave him nitroglycerin.

The patient reported no syncope, palpitations, shortness of breath, fever, cough, or other complaints. His vital signs were normal except for a pulse of 101 bpm. His exam was otherwise normal.

The differential diagnosis included accelerated idioventricular rhythm (AIVR), slow ventricular tachycardia (VT), bundle branch block, electrolyte abnormality, and acute coronary syndrome. This was the initial ECG.

bradycardia-ECG-accelerated idioventricular rhythm.jpg

The computer read the ECG as sinus tachycardia with first-degree AV block, right atrial enlargement, and intraventricular conduction delay. Do you agree with the computer? What should you do next?

The computer read was incorrect. This is most likely AIVR because it is wide and regular with a rate between 40-120 and no P waves. Another possibility is slow VT. The computer was likely misreading the prior T wave as a P wave and calling it right atrial enlargement. The QRS is regular with precordial concordance and a QRS duration of approximately four boxes, or 160 ms, and the initial part of the QRS is the widest, all of which support this rhythm being ventricular in origin.

The initial troponin I was 0.03 (99% URL <0.030: troponin I immunoassay, Abbott Laboratories). The hospitalist saw the patient and believed he was in a paced rhythm. The EP saw no pacer spikes, and called the patient's cardiologist and sent him the ECG.

The cardiologist felt this was slow VT and recommended trying amiodarone, which did not work. The cardiologist knew the patient had an automatic implantable cardioverter defibrillator (AICD) and a history of prior ablations. He said the VT rate was too slow to trigger the AICD, so he came in and converted the rhythm with anti-tachycardic pacing (overdrive pacing). He said the patient likely had slower-than-normal VT from his multiple prior ablations.

Case Lessons

VT is almost always faster than 120 bpm. Some exceptions include prior ablations and medications that cause bradycardia. Assume regular wide complex tachycardia is VT until proven otherwise and consult cardiology. It is usually safe to give a trial of adenosine if you think there is supraventricular tachycardia with aberrancy but not if you think it could be WPW.

Avoid giving nitroglycerin when the pain is already improving. You have no way of knowing if it helped in such a case. It's usually better to wait and see if the pain resolves on its own.

This post was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog.

bradycardia-tachycardia-accelerated idioventricular rhythm-handout.jpg

Source: Emergency Medicine 1-Minute Consult Pocketbook

Wednesday, July 1, 2020

A 40-ish-year-old man with a history of asthma presented to the ED with months of gradually worsening leg edema and dyspnea on exertion that he said had become really annoying over the previous five days, each day worse than the last. He had no syncope, palpitations, chest pain, fever, cough, or other complaints.

His vital signs were normal, but his exam was notable for no wheezing or rales but bilateral symmetric leg edema. Four to five small scabs were seen on his neck and forearms; a few looked relatively fresh.

The initial differential diagnosis included congestive heart failure, pulmonary embolism, acute coronary syndrome, and cor pulmonale.

bradycardia-ECG-leg edema-dyspnea-right ventricular hypertrophy-pulmonary hypertension.jpg

The computer read the ECG as normal sinus rhythm, possible left atrial enlargement, incomplete right bundle branch block, not able to rule out inferior infarct, age undetermined, and T wave abnormality concerning for anterolateral ischemia. Do you agree with the computer?

The computer read was correct but incomplete. The rhythm was normal sinus, but it was almost tachycardic. I am actually in the camp that believes that a normal heart rate is 50-90 bpm rather than 60-100 bpm. The P wave in lead II was a bit wide, which is consistent with left atrial enlargement. There was an RSR in V1-V2 with a QRS of <120 ms consistent with an incomplete right bundle branch block. There were insignificant Q waves in two inferior leads. There was also T wave inversion across the precordial leads. This is the finding that is most likely to be acute. It is consistent with ischemia, but has other potential etiologies, including PE and pulmonary hypertension.

What was not in the computer read was that this ECG highly suggested right ventricular hypertrophy and pulmonary hypertension for several reasons: There was a large deep S wave in lead I, signifying rightward axis, as well as deep wide S waves in the lateral precordial leads. It also showed precordial T inversion and suggestion of right atrial enlargement (a borderline tall P wave in lead II). See more right ventricular hypertrophy examples in Dr. Smith's ECG Blog: https://bit.ly/306xAeq.

The patient's troponin I was 0.05, but did not change on repeat (99% URL <0.030: troponin I immunoassay, Abbott Laboratories). D-dimer was negative. Given the overall picture with the scabs, pulmonary hypertension from methamphetamine was suspected and confirmed.

Case Lessons

Pulmonary hypertension is one of the important causes of dyspnea on exertion or shortness of breath, leg edema, and clear lungs. ECG and echo can have findings similar to PE. There are many causes, but methamphetamine abuse is a common one.

Bonus Pearl: Try to avoid intubation in critical patients with pulmonary hypertension because it can worsen the situation.

This post was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog.

bradycardia-right ventricular hypertrophy-pulmonary hypertension-handout.jpg

Source: The Emergency Medicine 1-Minute Consult Pocketbook  

Monday, June 1, 2020

A 72-year-old man with a history of lung cancer in remission, congestive heart failure, and paroxysmal atrial fibrillation on Eliquis and metoprolol presented to the ED for dyspnea on exertion and palpitations for the past three days. He had no syncope, chest pain, fever, cough, or other symptoms.

His vital signs were normal except for a pulse of 120 bpm. His blood pressure was soft at 103/66 mm Hg, and his exam was otherwise normal.

The initial differential diagnosis included tachydysrhythmia, tamponade, pulmonary embolism, and acute coronary syndrome. This was the initial ECG.

bradycardia-ECG-dyspnea-palpitations-tamponade-tachycardia-low voltage.jpg

The computer read the ECG as atrial fibrillation with RVR and nonspecific ST and T wave abnormality. Do you agree with the computer?

The computer read was correct. The voltages looked very low but were actually normal. When I first saw this triage ECG, I thought this was tamponade (tachycardia and low voltage), and had them bring the patient stat to a room where I did an echo and noted only a very small pericardial effusion.

I then went back to the ECG and noticed that the voltage standard had accidentally been reset. If you look at the voltage standard, the tabletop part of the tracing to the left of the first QRS complex, you will notice it was set at 2.5 mm in height. It should be 10 mm in height unless someone intentionally adjusted it for a patient with excessively tall QRS complexes. The EMT who did the ECG wasn't sure how this happened or how to reset it. He probably did it accidentally while he was inputting the patient's name and ID number.

The ECG was repeated with the voltage standard properly set after the patient was treated with diltiazem for rate control. It showed a rate-controlled atrial fibrillation. The troponin I was <0.03 ng/ml (99% URL <0.030: troponin-I immunoassay, Abbott Laboratories), and electrolytes were normal, as was the chest x-ray. The patient's symptoms resolved, and at the request of his cardiologist, he was sent home with close follow-up.

Case Lessons

  • Always consider tamponade when there are tachycardia and low voltage, especially if new or if there is a history of malignancy.
  • If the QRS amplitude seems incorrect, check the reference tabletop at the far left of the 12-lead. The usual ECG machine setting has that box at 10 mm or two large boxes high.
This post was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog.

bradycardia-tamponade-tachycardia-low voltage-causes.jpg

Friday, May 1, 2020

A 72-year-old woman with a history of SVT and taking prophylactic metoprolol but no other cardiac history was brought to the ED by ambulance for chest palpitations. The paramedics stated that she had gone in and out of atrial fibrillation four or so times since they picked her up, and the rate averaged around 120 bpm. The patient had no shortness of breath, dizziness, chest pain, or other complaints. She said she felt a little pressure but no pain when asked if she felt any chest discomfort.

Her vital signs were normal except for a pulse of 105 bpm. Her exam was otherwise normal.

The initial differential diagnosis included tachydysrhythmia, electrolyte abnormality, pulmonary embolism, and ACS. This was the initial ECG.

bradycardia-ECG-atrial flutter-flecainide-metoprolol-NSTEMI.jpg

The computer read the ECG as abnormal and as sinus tachycardia and an undetermined inferior infarct age. Do you agree with the computer?

The computer read was incorrect. The 12-lead shows atrial flutter with a ventricular rate of about 100 bpm, which would usually signify a 3:1 block because the typical atrial rate in flutter is about 300 bpm. This ECG, however, is actually a 2:1 block with slow flutter waves at an atrial rate of only 200 bpm. Flutter waves this slow are usually found in patients on certain medications, especially flecainide. In this case, it may have been due to the metoprolol she was taking. The patient was admitted for observation and ruled in for an NSTEMI.

Case Lessons

  • The computer not infrequently gets the rhythm wrong and may say that atrial flutter is sinus tachycardia, and vice versa. Whenever you see a heart rate of about 150 bpm, look carefully for flutter waves because this is the classic rate for flutter with a 2:1 block. Other ventricular rates may occur with a 3:1 block or a variable block. The rate may be slower if the patient is on AV nodal blockers.
  • Palpitations alone are rarely a sign of cardiac ischemia, but it could be considered equivalent to failing a stress test if the patient feels pressure or there are significant ST changes with a rapid heart rate. Be sure to ask if there is chest discomfort if patients report no pain. 

This post was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog.

bradycardia-tachycardia-atrial flutter-NSTEMI.jpg

Source: The Emergency Medicine 1-Minute Consult Pocketbook.