Erin McDonald (Prehospital Class FB page)
Understanding ST elevation and depression on the ECG
This is something that I think many paramedics struggle with
comprehending - certainly we get that ST elevation in the right context
is considered injury and ST depression ischaemia, but what is the
underlying physiological process?
To get a grasp on this we need to go back to the basic electrophysiology
of the cardiac myocyte (muscle cell)…
We know that the cardiac action potential is a graphic representation of
the resting (diastole), depolarisation (systole), and repolarisation of
the myocyte when stimulated sufficiently to produce an action potential
(AP). We also know that this AP graph coincides with the tracing that we
see on our standard ECG - therefore it stands to reason that any change
to the action potential will correspond to changes on the ECG.
The AP of the myocyte (non-pacemaker cell) is divided into 4 phases.
# Phase 4 - This is the resting or diastolic period of the AP. It
corresponds to the T-P segment of the ECG and is considered the
isoelectric line or baseline from which electrical activity is recorded.
During this phase the cellular membrane is maintaining a steady
electrical state due to the exchange of electrolytes across its membrane
and the work of the ATP dependent Na+ and K+ pumps (ATP refers to the
fact that these pumps are not passive and require energy to continue
working correctly). The healthy myocyte will 'rest' at around -90mV
(this is actually a resting potential energy as opposed to an exact
electrical charge). In other terms the electrolyte pumps will excrete
enough Na+ and pump in sufficient K+ so that the electrical difference
between the outside of the cell and the inside of the cell is around
90mV. Because the inside of the cell is has LESS overall positive ions
than outside the electrical difference is said to be -90mV this is
sometimes referred to as a resting potential energy or potential
difference. Anything that impacts on the ability of the Na+ K+ pumps to
exchange ions will change the resting voltage of the cell membrane and
therefore impact the ECG.
# Phase 0 - This is the rapid upstroke seen on the AP graph and occurs
when the myocyte has been depolarised (most commonly) by an adjacent
myocyte or pacemaker cell (de-polarised refers to the mV being taken
closer to 0mV hence the cell is no longer polarised). During this period
fast Na+ on the cell membrane open and large amounts of Na+ flood the
cell pushing the cellular membrane to around +35mV. We known that there
is a greater amount of Na+ present in the body when compared to K+ and
this increased addition of positive electrolytes (cations) drives the
membrane resting potential towards and beyond 0mV. This rapid upstroke
or depolarisation in Phase 0 normally corresponds to the ventricular
depolarisation seen on the ECG as a QRS complex.
# Phase 1 - The cell has depolarised due to the propagation of an AP and
now works to restore to membrane back to its resting state. K+ starts to
leave the cell, at the same time Ca+ is entering through slow channels
on the membrane wall. This exchange of ions means that there is not a
rapid decline in electrical change as is seen in neurons and skeletal
muscle cells but rather the membrane potential leads into a flattened
section or plateau.
# Phase 2 - During the plateau portion of the AP Ca+ continues to enter
the cell until the resting potential reaches around -40mV when Ca+
channels are closed off. During this phase the cell is slowly
repolarising (RE-polarising - moving away from 0mV and becoming
polarised) through the leakage and active pumping of electrolytes across
the membrane.
# Phase 3 - Ca+ channels close and K+ rapidly exits the cell causing the
membrane to repolarise further back to its original resting state of
-90mV. The cell is now fully repolarised and ready to propagate another
AP should sufficient stimulus be applied.
Phases 1, 2 and 3 (primarily) are represented on the ECG as the
repolarisation of the ventricles which, we understand, corresponds to
the ST segment of the ECG.
Ok I get all that but what does ischaemia and injury have to do with ST
changes in the ECG?
I mentioned that anything that interferes with the Na+ K+ pumps on the
cellular membrane will change the efficiency of the cell in maintaining
its repolarised state and achieving a normal depolarised state. I also
mentioned that these pumps are ATP dependent, ATP is short for adenosine
triphosphate.
These molecules have 3 high energy phosphorous bonds that the cells of
the body cleave to utilise energy from which to fuel their processes.
Functional production of ATP requires a steady supply of oxygen to the
cells to be utilised within the electron transport system (don't stress
about this at the moment) this process is known as aerobic (in the
presence of oxygen) metabolism. If there is no oxygen available the
cells will switch the much less efficient form of ATP production this is
known as anaerobic (in the absence of oxygen) metabolism. In the case of
a myocyte whose blood supply has been reduced or cut off completely
oxygen cannot be delivered to the cells and they switch to an anaerobic
method of generating energy to fuel their pumps. If this oxygen debt is
not repaid within minutes the cells are no longer able to keep up with
the required level of ATP production and the pumps begin to fail usually
within 5 to 15 minutes [1]…
This leads us to the most widely accepted explanation for ST elevation
and ST depression: the CURRENT of INJURY THEORY.
This theory states that differences in resting potentials during Phase 4
of injured or ischaemic myocyte and during Phases 1,2 and 3 cause
disruptions in the normal flow of energy throughout the myocardium.
Depending on the degree, location and size of injured myocardium energy
will either flow towards or away from the site of ischaemia / injury.
# The current of injury theory is broken down further into the DIASTOLIC
current of injury and the SYSTOLIC current of injury.
As previously mentioned Phase 4 of the AP of the myocyte is when the
heart is fully repolarised and 'resting' this correlated with the T-P
segment of the ECG and is said to be the DIASTOLIC current. Phases 0, 1
,2 are representative of the depolarisation of the cell and the
beginning of repolarization - This corresponds with the S-T segment of
the ECG and is termed the SYSTOLIC current.
Now lets look at what happens to the resting and depolarized AP of a
myocyte that is injured…
# When the cell is injured K+ begins to leak from the intracellular
space into the extrastitial space creating a short-lived environment of
localised hyperkalaemia. This is thought to be responsible for the
peaked T waves seen during early cardiac ischemia and some studies have
suggested contribute to the increased the risk of arrhythmias [2].
# The outflow of K+ ions from the cell causes the cellular membrane to
become less polar i.e. moves closer towards 0mV. During this time Na+
and Ca+ also being to accumulate on the inside of the cell which moves
the cell resting potential closer towards 0mV. The resting potential of
the cell now sits around -70mV. The cells surrounding the ischaemic area
are still being perfused adequately and thus their membrane is
maintaining its normal resting potential at -90mV. This means that there
is an electrical difference between the two resting potentials of the
healthy and injured cells. We know that electrical current is primarily
K+ driven and numerous studies have shown that electrical current will
flow from an area of greater +ve charge TOWARDS an area of lesser +ve
charge.
With this in mind the ischaemic cells which are sitting at -70mV will
produce a current which flows TOWARDS the surrounding healthy cells at
-90mV. Because this current is flowing in a –ve direction (from -70mV to
-90mV) the result will be a lowering of the T-P segment on the ECG. This
is the period of the ECG in which the myocytes are resting thus this
explanation is referred to as the DIASTOLIC CURRENT of injury.
# We now know an injured myocyte has a resting potential which is more
+ve than that of a healthy cell. It is also important to note however
that the cells do not depolarize correctly or to the same degree as
their healthy counterparts. Where as a health myocyte will depolarize to
a voltage around +35mV the injured cell may only produce a +ve
depolarisation of around +20mV. Thus if you compare the two voltages the
healthy cells are more +ve at 35mV and the injured cells less +ve at
25mV. Remember that current flows from more +ve areas to less +ve areas
thus the current will travel from the healthy cells TOWARDS the injured
cells. Remembering that the depolarisation portion of the myocyte AP
represents the ST segment of the ECG this is the explanation given as to
why ST elevation occurs and is termed the SYSTOLIC CURRENT of injury.
To summarise:
# Current flows towards areas that are LESS +ve
# During diastole the injured cells resting potential is more +ve than
that of the healthy cells. The current flows away from the injured areas
towards healthy cells which is seen as depression of the TP segment of
the ECG
# During systole the injured cells do not depolarise correctly and their
charge is less +ve than surrounding healthy cells. Energy now flows from
the healthy cells towards the injured area during this phase creating
elevation of the ST segment of the ECG.
Hopefully that makes some sense
[1]http://cardiovascres.oxfordjournals.org/content/57/4/1044.full
[2]http://cardiovascres.oxfordjournals.org/content/62/1/9.full
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I wrote it, and you may copy it in full given it was properly attributed.