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BradyCardia by Brady Pregerson, MD
​​​This 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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Monday, November 2, 2020

A 42-year-old man with a history of hypertension, prior tobacco use (as recently as two weeks ago), prior polysubstance abuse, and currently in rehab presented to the ED with three months of intermittent central and left-sided chest pressure that was exertional and associated with shortness of breath.

The episodes lasted about five minutes and occurred after he walked a couple blocks and resolved after resting for a couple minutes. These episodes were happening over the past week with shorter distances and a little more intensity.

The triage ECG (not shown) and the troponin were normal. The hospitalist was called to admit the patient and documented: “Patient is currently in a drug and alcohol treatment center ordered by the law. He has a negative troponin and normal ECG. He is pain-free and reports symptoms consistent with reflux disease. He also seems anxious. I recommend repeating his troponin and discharging him home with a PPI if it is negative.”

This type of advice, bias, and dismissiveness sometimes occurs. A clinical presentation like this is ACS until proven otherwise. It is dangerous to assume a benign cause such as GERD or anxiety until provocative testing is completed and normal. Fortunately, the EP did not feel this was safe and did a poor-man's stress test. Shown is the repeat ECG after the patient did jumping jacks until developing pain.

The computer read the ECG as atrial flutter with RVR and minimal ST depression. Do you agree with the computer? What should you do next?
bradycardia-substance abuse-ACS-GERD-anxiety.jpg

Case Lessons The computer read is incorrect. This is sinus tachycardia. The rate is close to 150 bpm, and the P waves are not that obvious, which is why the computer is calling it atrial flutter. There is also more than minimal ST depression, especially in leads V4 and V5.

The troponin I was <0.01, as was the repeat troponin. A different hospitalist was called, and the patient was admitted and had a positive stress test followed by an angiogram and a stent.

We must avoid bias caused by substance abuse, and avoid choosing an alternate explanation such as anxiety or GERD until ACS is ruled out. Chest pain that lasts five minutes is typical of ACS, so always start with this at the top of your differential for intermittent chest pain. When it is exertional, it is classic for ACS.

Normal ECGs and troponins can rule out NSTEMI, but they still cannot rule out unstable angina. The typical presentation of unstable angina is episodic chest discomfort lasting a few minutes, especially when triggered by tachycardia often caused by physical or emotional stress. Other common triggers include blood shunting after meals or any other cause of tachycardia.

Expect the ECG to be normal in ACS if the pain has resolved. Expect the troponin to be normal when episodes last fewer than 30 minutes. You are less likely to be falsely reassured by normal results if you expect these findings before you order the test.

This post was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog (https://bit.ly/306xAeq​).

Thursday, October 1, 2020

A woman in her 90s with a pacer for heart block but no history of coronary artery disease presented to the ED for 45 minutes of nonradiating, nonpleuritic chest pain that woke her from an afternoon nap. She had no syncope, palpitations, shortness of breath, fever, cough, or other symptoms. Nitroglycerin was given by the paramedics, and may have helped slightly.

Her vital signs were within normal limits, and her exam was otherwise normal. The initial differential diagnosis included GERD, acute coronary syndrome, and gallstones. The computer read the ECG as the patient having an electronic AV pacemaker and an abnormal rhythm. Do you agree with the computer? What should you do next?

bradycardia-ECG-chest pain-right bundle branch block.jpg

The computer read was incomplete. This ECG was diagnostic of a proximal left anterior descending artery occlusion by two of three of the Smith-modified Sgarbossa criteria. This was a potentially deadly occlusion MI. There was concordant ST elevation >1 mm in multiple leads: I, aVL, and V2, and there was discordant ST elevation >25% of the QRS height in leads V5 and V6 and perhaps also V4.

There was also concordant ST depression >1 mm in leads III and aVF and perhaps lead II, which was concerning but not the third criterion, which for a right bundle branch block (RBBB) pattern paced rhythm is concordant ST depression in one of the leads, V1-V6. It is V1-V3 for left bundle branch block (LBBB).

The cardiologist declined to take the patient to the cath lab based on age, and could or would not come to the ED to see the patient. He did call a second cardiologist to see the patient. That cardiologist did a bedside echo and recommended heparin but not tPA. The patient's troponin I was <0.01, drawn about one hour after pain onset (99% URL <0.030: troponin I immunoassay, Abbott). The second troponin drawn two hours after pain onset was 0.07 and five hours later was 2.1. The peak troponin was >77.0.

The patient survived the hospitalization, but was left with severe congestive heart failure.

Case Lessons

  • Know the criteria identifying STEMI in LBBB and RBBB. For most pacers, there will be an LBBB-like pattern. This one had more of a RBBB pattern, however.
  • The traditional Sgarbossa criteria using >5 mm of appropriately discordant ST elevation as criteria C is about 56% sensitive and 97% specific. The Smith-modified Sgarbossa criteria using appropriately discordant ST elevation >25% of the height of the preceding QRS as criteria C is better, with about 86% sensitivity and 97% specificity.
  • It is not appropriate to withhold PCI based on age. Even thrombolytics should not be withheld based on age.

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

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