Thanks for visiting!

EmergencyPedia is part of a growing family of critical care blogs based on the values of Free Open Access Medical Education (FOAM). We hope that our website will be useful to medical studentsnursesparamedics, allied health and doctors.

In 2015 we will continue to add more content on topics relevant to Emergency Medicine (EM) with our goal being to provide a high quality medical education resource.  We believe in online medical education and that the sharing of our crisis management experiences is the best way to improve our future practice.

The EmergencyPedia team are always interested in your feedback and comments and we are active on various social media platforms:

images    Unknown    RSS-logo  CC

Why become a Resuscitationist?

 Why become an Emergency Physician

Why Learn Resuscitation

Why Learn CPR


Our ‘FOAM’ Favourites

Screen shot 2015-03-31 at 6.19.39 PM



9 thoughts on “Thanks for visiting!

  1. Hey Andy,
    I am a paramedic student and I have some questions about the pathophysiology of ACS. Also what is the difference between ACS and AMI?
    Lorrie :)

    P.s. Chicago is UNREAL!

    • Hi Lorraine – thanks for the comments!
      I think that your question about Acute Coronary Syndrome (ACS) is a common one.

      To answer with brevity – any patient with significant Cardiac Chest Pain (chest pain from narrowing of the coronary arteries) has ACS.

      ACS is sub-divided into 3 further ‘syndromes’ that have overlap in terms of their pathophysiology and presenting symptoms.

      These 3 ACS sub groups are treated historically differently. The first two of the three sub-groups are types of Myocardial Infarction (Acute MI) known as Non ST Elevation MI or ST Elevation MI. ST Elevation is detected and diagnosed on the Electrocardiogram (ECG).

      The 3rd sub type of ACS is known as Unstable Angina. Unstable Angina has the same underlying pathology as NSTEMI but without detectable death of cardiac cells (we determine this in the ED by measuring various cardiac enzymes such as Troponin).

      So to answer your question directly – MI is cardiac cell death due to coronary occlusion and ACS is coronary occlusion causing symptoms such as chest pain with or without permanent damage to the heart muscle cells.

      What is the reason why a distinction has been made between NSTEMI and STEMI? Well, this has been seen as important because active re-perfusion therapy has improved survival in patients with ST elevation on the 12 lead ECG. ST elevation is suggestive of coronary artery occlusion due to ‘plaque rupture’. This is (in theory) is readily amenable to treatment with re=perfusion therapies. Re-perfusion can be achieved either Thrombolysis drugs or an Invasive Cardiac Intervention known as Angioplasty. Despite the separation of NSTEMI and STEMI many patients with NSTEMI have complete blockages that would normally be associated with a STEMI when the cardiology doctors do an angioplasty/angiogram so the two conditions are not truly separate entities – they have the same underlying cause.

      • Wow! Great response. I understand what you mean. In regards to q wave elevation, with NSTEMI, there is no q wave elevation, so what are the typical ECG signs of a NSTEMI ?


      • Hi Lorrie,

        I think you are getting confused between Q waves and ST segments.
        Q waves can develop on an ECG several hours after an AMI and may become a permanent fixture of that person’s ECG. Q waves do not show elevation.

        STEMI = ST Elevation Myocardial Infarction

        NSTEMI = Non-ST Elevation Myocardial Infarction

        So NSTEMIs will have no ST elevation on their ECG. They may have ST depression, T wave inversion or no changes. They will however have a positive troponin result indicating due to ischaemia to the cardiac cells.


  2. Hi Dr Coggins,

    I’m Raz, the medical student who attended the Emergency Management Airway Workshop yesterday and asked about oxygenation during a cricothyrotomy. I’ve been taught by an anaesthetist to oxygenate for 4 seconds initially and release, and re-oxygenating if the saturation drops for 2 secs consecutively.

    This is a different approach when comparing to oxygenating for 1 sec and releasing for 4 secs, and was wondering if this is also accepted widely and if there will be any significant impact/difference?


    p.s – This blog is superb will definitely recommend it and spread the word

Leave a Reply

Fill in your details below or click an icon to log in: Logo

You are commenting using your account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s