#KYJ - knowing your jargon.
Cardiac terminology.
For some time the terms NSTEACS and STEMI have been used to describe acute cardiac conditions that frequently manifest as chest pain.
In fact the term myocardial infarction (MI) is without doubt, the alpha predator in the mortality stakes. Our synonymous use of the term MI with the more colloquial “heart attack” has permeated medical drama and pop culture for many years. There is sound reason too; MI and it’s gang head quarters(cardiovascular disease), have risen to be the #1 killer of adults in all 1st world countries.
But what if our understanding of heart attack was changed, and as clinicians, we had to review not just the condition “MI“, but it’s diagnostic criteria?
Well this occurred in August 2018. The premise that MI was caused from an ischaemic blockage in a coronary artery has been scrutinised and left falling short of the whole truth.
Myocardial infarctions have long been divided into two categories: STEMI and Non STEMI with the focus on the ECG as the Rex of diagnosis.
Now,there is a lot to support that when the ECG shows ischaemic changes, a diagnosis of MI can be made. Especially in the context of ST elevation ,new Q waves or a new left bundle branch block; but now, it seems that the Troponin Blood test it the king of the diagnostic castle.
MI has been recategorised into 5 different categories or three main types.
So what is the common feature???
Troponin . That cardiac Troponin (cTn) is inside cardiac cells, locked up like a prisoner inside a ...um Cell.
If there was cell damage (injury) or death (infarction), that cTn leaks out and is detected as it is picked up by lymphatic vessels, and distributed into the blood stream.
So cTn rise on the background of a cardiac event is always sensitive for MI... but what type?
Type 1 MI
These are the traditional STEMIs. A brittle atheroma inside a coronary vessel ruptures, and in attempt to stop bleeding from an arterial rupture, vasoconstriction, a clot and fibrin reinforcing mesh forms a solid thrombus that occludes the blood flow. No flow, no O- oh no!! Ischaemic heart cells soon die (necrosis) - infarction.
These blockages are often extensive, and the scar that results from a large area of muscle death, slows and alters the electrical pathway- thus, ST segment elevation and the development of a big Q wave.
Type 2 MI
These infarcts are cardiac cell death from ischaemia, but instead of a blockage in a specific vessel, there exists a vessel network spasm- construction and shutting down of a section of myocardial perfusion.
No flow- oh No, no O.!!!
Infarction!
We previously called these NSTEMI. The damage area is not full thickness of the muscle wall, so no Q wave, and rarely an ST segment elevation. Little cell death but extensive ischaemia in the penumbra around the dead stuff.
Types 3-5
These MIs are complex and caused from things like toxins, drugs, and physical injury like surgery, or trauma. The injury to the heart muscle causes it to inflame (like all injuries) and some injured tissue will die (infarct). The difference here is that they are not directly ischaemic.
So these groups of MI are called #MINOCAs - MIs with non obstructed Coronary Arteries.
The heart may be directly injured, or indirectly die off. Think of extreme shock, or hypovolaemia/sepsis/anaemia; in these cases there is greater cardiac demand for Oxygen than the shocked or anaemic patient’s ability to supply. Too little too late- muscle dies but not from coronary blockage... MINOCA
Big topic- best addressed in our #ARRR , #Acute Deterioration and #Cardiac seminars.
All our seminars in one place here . Www.Ect4Health.Com.Au/whats
All our seminars in one place here . Www.Ect4Health.Com.Au/whats
~Rob Timmings
