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Bradycardia: shortness of breath and wheezing: PE or MI? : Emergency medicine news

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cardiology, pulmonary embolism, myocardial infarction

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A woman in her 70s with asthma, diabetes mellitus, hypertension and a pacemaker came to hospital with shortness of breath and chest tightness lasting two hours. She had had a similar episode the day before which was milder and resolved with albuterol.

She had a cough but no fever, runny nose or known exposure to COVID-19. She had no syncope, palpitations or other complaints. She tried albuterol at home, but got worse and called 911.

His blood pressure was 182/86 mm Hg, pulse 81 bpm, respiratory rate 26 bpm, and pulse 55% on room air and 95% at 10L.

Examination revealed wheezing, decreased basal breath sounds, and mild to moderate respiratory distress, but no leg edema. An ECG was done (shown).

The computer read it as normal sinus rhythm at age 82 and septal infarction, age indeterminate. A chest X-ray showed perihilar and lower lobar infiltrates. What is the most likely cause of the ECG findings in this patient? Hypokalemia due to albuterol, pulmonary embolism, MI type I or MI type II?

ECG analysis

The ECG showed sinus rhythm and some concerning ST depression in V5, V6, I and II. V2 has a slight ST elevation.

Hypokalemia due to albuterol is possible, but usually causes ST-segment depression rather than the flat ST-segment depression seen here. Pulmonary embolism is unlikely to cause this degree of wheezing and hypoxia, and if it did, the patient would likely have low blood pressure rather than high blood pressure.

A type II MI was possible. This would be likely if the ECG changes and the symptoms resolve with medical management. The patient would likely still require catheterization to confirm that no acute coronary syndrome was present. Type I MI is the correct answer, but the ECG should be repeated once blood pressure, wheezing, and oxygenation have been addressed and improved.

To Cath or not to Cath?

This patient had wheezing, but asthma is extremely unlikely to cause severe hypoxia, and almost never so severe. The etiology of hypoxia is most likely pulmonary edema. Acute coronary syndrome with acute “flash” pulmonary edema and ST-segment depression should be strongly suspected and also an acute type I MI should be assumed until proven otherwise because troponin is elevated. Type II MI and ischemia are caused by a mismatch between supply and demand. Low oxygen supply can produce low blood pressure, severe anemia, or low oxygenation (which can also include abnormal hemoglobin or hemoglobin toxins). High oxygen demand leads to high heart rate, high blood pressure, or high LV end diastolic dimensions.

If this patient turns out to have ACS, these ECG results could be caused by supply issues (because the oxygen supply is very low), but not blood pressure because it does not. was not high enough to cause demand ischemia. Given the overall presentation, it is more likely that ACS caused acute heart failure with flash pulmonary edema and hypoxia, and ACS ischemia was further exacerbated by hypoxia. The patient could be catheterized the next day if she stabilized with medical management, but she would need emergency catheterization otherwise.

Case outcome

Her symptoms and ECG improved and then resolved once her blood pressure, pulmonary edema, wheezing and hypoxia were adequately treated. An initial high-sensitivity troponin-i was approximately 700 ng/L (99% URL

Flash pulmonary edema is often caused by ACS, but is also sometimes the result of severe high blood pressure, usually much higher than in this patient. Severe hypertension can also be triggered by pulmonary edema (ACS causing pulmonary edema in turn producing severe hypertension, which triggers worsening ischemia and a vicious cycle).

Type II myocardial infarction is to be considered when blood pressure and heart rate are significantly abnormal, whether high or low, or when the patient is suffering from hypoxia or other severe stress on the body. heart and symptoms and ECG changes resolve with medical attention. ST segment elevation or depression can be seen in both type I and type II MIs.

Try to stabilize the patient’s hemodynamics and respiratory status, then repeat the ECG whenever a patient has an ischemic ECG and is also critically ill. Peak troponins are usually significantly higher in type I MI than in type II, but there is no reliable threshold. (Tell of the coronary artery. 2018;29[1]:46; https://bit.ly/3gtc9v8; Acute Cardiovascular Care Eur Heart J. 2014;3[4]:317; https://bit.ly/3370NKf.) Only type I MI with acute congestive heart failure usually requires cardiac catheterization, but it may be delayed if the patient is stabilized. Type II MI only requires angiography when in doubt about type I versus type II.

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Dr Pregersonis an emergency physician with Palomar Health in San Diego. He is the author of 1 Minute Emergency Medicine Consultation, The 8 in 1 Quick Reference Guide for Emergency Services, A to Z Emergency Pharmacopoeia and Antibiotics Guide, Don’t Try This at Home, and Think twice: no more lessons from urgency. Follow him on Twitter@EM1MinuteGuru, and visit his website athttps://em1minuteconsult.com. Read his past columns onhttp://bit.ly/BradyCardiaEMN. Dr. Smithis Professor of Emergency Medicine at Hennepin Healthcare, Professor of Emergency Medicine at the University of Minnesota Medical School, and Editor of Dr. Smith’s ECG Blog. (https://bit.ly/306xAeq). Follow him on Twitter@smithecgblog.