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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, 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.

Wednesday, April 1, 2020

An 82-year-old woman with a history of GERD and congestive heart failure presented to the ED with two days of generalized weakness. She had no syncope, palpitations, chest pain, shortness of breath, fever, cough, or other symptoms.

She said she felt similar to when she had low potassium and low magnesium in the past. Her doctors had never been able to figure out why she kept having this problem. They stopped her Lasix, but it persisted.

Her vital signs were normal except for a pulse of about 100 bpm. Her exam was otherwise normal.

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

bradycardia-ECG-P wave-pacer strike-QRS-hypomagnesemia.jpg

The computer read the ECG as abnormal and as an atrial-sensed ventricular-paced rhythm. Do you agree? What should you do next?

ECG Analysis: The computer read was correct. There is a P-wave followed by a pacer spike (atrial-sensed) and then the QRS (ventricular-paced). There were no other significant findings, although the QT interval appears to be close to the upper limit of normal.

It is important to be aware that a paced rhythm can hide ischemia and sometimes even complete coronary occlusion, so this ECG does not rule out ACS as a cause of her painless weakness. The Sgarbossa or Smith-modified Sgarbossa criteria can be used to diagnose a STEMI equivalent in a paced rhythm, but the sensitivity is not great. There is no evidence of ischemia on this ECG.

The patient's magnesium level was 0.4 mEq/L, and she was admitted. The astute emergency physician noted that she was on omeprazole, which is a known but frequently unrecognized cause of low magnesium. No one had previously made this connection. The PPI was stopped, and she was switched to an H2 blocker. Her magnesium normalized and remained normal at follow-up two weeks later.

Case Lessons

  • Consider checking the magnesium level in patients with long QT or generalized weakness, especially if they are on a diuretic or PPI.
  • PPIs can cause severe hypomagnesemia. See the highlighted area below, especially the causes of hypomagnesemia. Read more about this at BMJ. 2008;337[7662]:173; http://bit.ly/2PdYfQq.

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

bradycardia-diagnosis-handout-hypomagnesemia.jpg

Monday, March 2, 2020

A 42-year-old man with no past medical history but a family history of early coronary disease was brought by ambulance to the ED as a code STEMI for shortness of breath and syncope. He said he had no chest pain or pressure, and was feeling fine when he suddenly became weak and dyspneic while lifting weights at the gym. He fainted while supine and still felt light-headed at presentation. He had no recent illness, but did injure his left pectoral muscle about two weeks earlier, also while lifting.

He was tachycardic with a pulse of around 150 bpm, and he was hypotensive and diaphoretic.

The initial differential diagnosis was atrial flutter, pulmonary embolism, acute coronary syndrome, and aortic dissection.

This ECG was taken in the field.

The computer read the ECG as STEMI, sinus tachycardia with occasional PVC, inferoapical ST elevation, anterior infarct (age undetermined), and moderate right axis deviation. Do you agree with the computer?

brady-shortnessofbreath-syncope-intraventricular conduction delay-posterior fascicular block-ECG.jpg

The computer read was partially correct. This patient also had an intraventricular conduction delay and a posterior fascicular block. STEMI was possible but unlikely due to the inverted T waves in the inferior leads. No baseline ECG was available.

The patient was unstable, and an immediate bedside ultrasound confirmed tamponade. An immediate pericardiocentesis was done with 200 mL of frank blood removed, and the patient stabilized immediately. A pigtail catheter was left in place, and a CT was ordered, which showed no dissection but a small residual pericardial effusion, catheter in the pericardial space.

The hospital ECG was not done until after the procedure and is shown below. The patient was eventually diagnosed with a left ventricular free wall rupture causing tamponade following a transmural MI two weeks earlier (the injured left pec muscle). He survived.

brady-left ventricular free wall rupture-tamponade-transmural MI-ECG.jpg

Case Lessons

  • Always consider tamponade from acute aortic dissection when there is sudden shortness of breath, sweating, and hypotension even if there is no pain. Tachycardia will also usually be present. A stat bedside echo and pericardiocentesis can save lives.
  • Other causes of acute tamponade include trauma, ruptured ascending aortic aneurysm, ruptured LV free wall, and coronary artery dissection with rupture.

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

brady-coronary disease-aortic dissection-handout.jpg

Source: The Emergency Medicine 1-Minute Consult Pocketbook.

Friday, January 31, 2020

A 62-year-old man with a history of atrial fibrillation who was on metoprolol and Eliquis was sent from his doctor's office to the ED for tachycardia noted on a routine follow-up visit. He had no palpitations, chest pain, shortness of breath, near-syncope, fever, cough, or other complaints.

His vital signs were normal except for a pulse of 142 bpm, and his exam was normal except for the tachycardia.

The initial differential diagnosis included tachydysrhythmia, electrolyte abnormality, pulmonary embolism, and acute coronary syndrome. The initial ECG is shown below. The patient had a known pre-existing left bundle branch block. The computer read was a wide QRS tachycardia, rightward axis, left bundle branch block, and an abnormal ECG.

bradycardia-ECG-atrial flutter-wide QRS tachycardia-ventricular tachycardia.jpg

The computer read was correct, but it did not suggest the cause of the wide complex tachycardia. The differential diagnosis of regular wide QRS tachycardia includes ventricular tachycardia, PSVT or atrial flutter with a bundle branch block or another intraventricular conduction delay (aberrancy), sinus tachycardia with aberrancy, hyperkalemia, and drug toxicity.

Atrial flutter with left bundle branch block was suspected based on the rate and what looked like flutter waves in the inferior leads and lead V5. Adenosine was given, which confirmed the diagnosis. Following this, additional metoprolol was given, and the rate improved.

Case Lessons

  • Suspect atrial flutter with 2:1 block when the rate is close to 150 bpm and regular. The computer will often miss or misread atrial flutter.
  • When confronted with a wide QRS tachycardia, it is safest to assume ventricular tachycardia until proven otherwise. Avoid AV nodal blockers except for adenosine unless you can confirm it's not ventricular tachycardia. 

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

bradycardia-ECG-atrial flutter-wide QRS tachycardia-ventricular tachycardia handout.jpg

Source: The Emergency Medicine 1-Minute Consult Pocketbook.

Thursday, January 2, 2020

A 52-year-old man with a history of hypertension and high cholesterol presented to the ED with a week and a half of shortness of breath and a dry cough. He did not have syncope, chest pain, fever, sore throat, congestion, or other complaints. He said he had never been this short of breath from a cold and that he was worse on the day of his presentation.

His vital signs were normal except for a pulse of 112 bpm. His exam was otherwise normal. The initial ECG is shown below. The computer read was sinus tachycardia and an anterior and inferior myocardial infarction, possibly acute.

brady-ECG-acute coronary syndrome-pulmonary embolism.jpg

The computer read was incomplete. There was also an S1Q3T3. A D-dimer was negative by the YEARS criteria, but a CT was done because his symptoms had persisted for more than a week. It showed multiple large bilateral pulmonary emboli. He was started on heparin, admitted, and did well.

Case Lessons

  • The ECG showing PE can mimic that demonstrating acute coronary syndrome. T-wave inversion and mild ST changes in the anterior and inferior leads should make you think not only of ACS but also PE as possible diagnoses.
  • This ECG is highly suspicious for PE not because of the S1Q3T3, but because there is precordial T-wave inversion plus T-wave inversion in lead III. The deep T morphology of the T-wave inversion in V1-V4 is also not typical of ACS but very typical of PE.
  • It is important to be aware that in PE cases like this, there will always be some troponin elevation, and physicians may be fooled into thinking that the T-wave inversions and elevated troponin are due to ACS, not PE.
  • T-wave inversion in V1-V4 associated with a positive troponin has a primary differential diagnosis of ACS v. PE.
  • In cases with these findings in V1-V4, the presence of an inverted rather than upright T-wave in lead III is very specific for PE, while the presence of an upright T in lead III is very specific for ACS. In addition, with ACS, the patient will be asymptomatic at the time of this type of abnormal ECG, while with PE, he often won't be. (This ECG was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog.)

brady-ECG-acute coronary syndrome-pulmonary embolism-d-dimer-handout.jpg

Source: The Emergency Medicine 1-Minute Consult Pocketbook