YouTube Transcript:
Acute Coronary Syndrome (Heart Attack) - Unstable Angina vs NSTEMI vs STEMI | With ECGs

acute coronary syndrome is a spectrum of
conditions resulting from the formation
of a thrombus in the coronary arteries
following rupture of an atherosclerotic
plaque
they include unstable angina
non-st elevation myocardial infarction
and st elevation myocardial infarction
the heart is supplied with blood via the
coronary arteries which are connected to
the aorta near the aortic valve
when the heart is in diastole the
backflow of blood to the aortic valve
leads to the coronary arteries being
perfused
there are two main coronary arteries the
left and the right
the left coronary artery divides into
the left anterior descending artery
which supplies the left ventricle and
interventricular septum as well as some
of the right ventricle
then there is the left marginal artery
that supplies the left ventricle and the
circumflex artery that supplies the left
atrium and part of the left ventricle
the right coronary artery supplies the
right atrium including the sa and av
nodes and the right ventricle
over time these arteries can become
atherosclerotic
which is the formation of fatty plaques
on the walls
atherosclerotic plaques have a fibrous
cap that contains cell debris lipids and
inflammatory cells that all together
make up a thrombogenic substance
in some cases these plaques develop over
years and extend far enough into the
lumen of the vessel to narrow it which
can lead to ischemia if the demand
increases such as during exercise
this is what happens in stable angina a
slow change over time
however in acute coronary syndrome these
plaques rupture then the thrombogenic
material is exposed to blood leading to
formation of a clot which causes a very
sudden reduction in blood flow to the
cardiac cells and therefore ischemia
depending on the severity of the
reduction of flow we can see the
different spectrums of acute coronary
syndrome
in unstable angina the myocytes are
ischemic but are not yet necrosed and no
cell death has occurred
in non-st elevation myocardial
infarction and st elevation myocardial
infarction there is death of some of the
myocytes
the non-st and st portion of the name
refers to the elevation of the st
segment in the ecg the reason this
occurs is because in stemi there is
typically a complete occlusion of the
coronary artery and therefore transmural
necrosis meaning the death of the
cardiac myocytes extends across the
entire thickness of the wall whereas in
n-stemi this only extends through a
portion of the wall typically
risk factors are divided into modifiable
and non-modifiable
modifiable ones include smoking
hypertension diabetes and hyperlipidemia
obesity and drug use including cocaine
non-modifiable ones include age male sex
family history and ethnicity
clinically each one can present
similarly
symptoms include chest pain or
discomfort often described as heavy or
dull with radiation to the jaw arm or
shoulder that comes on at rest
upper back pain and epigastric pain or
indigestion-like symptoms are also
possible symptoms of acute coronary
syndrome these were previously termed
atypical symptoms
patients can also complain of
lightheadedness nausea or vomiting
sudden heavy sweating known as
diaphoresis palpitations and dyspnea or
shortness of breath however bear in mind
that people may present without chest
pain this happens more commonly in women
than in males and therefore the
presentation may be more subtle and is
more commonly missed this is also true
for older patients and patients with
diabetes
an ecg is a key part of the diagnosis
as the name suggests for diagnosis of
stemi there must be elevations in the st
segment specifically in two contiguous
leads of at least one millimeter in
height
except in leads v2 and v3 where it must
be 1.5 millimeters in women or two
millimeters in men a new left bundle
branch block is also included in
criteria for stemi
each lead corresponds to different parts
of the hat and can suggest the location
of the event
leads v1 to v4 are known as the anterior
or septal leads and roughly represent
the left anterior descending artery
leads 1 avl v5 and v6 are known as
lateral leads which represent the left
circumflex artery and part of the left
anterior descending artery leads 2 3 and
avf are the inferior leads
showing part of the right coronary
artery or the left circumflex
leads of v7 v8 and v9 are required to
see the posterior aspect of the heart
there are typically reciprocal st
depressions in opposite leads to the
occlusion which may be the only findings
in posterior stemi pathological key
waves may also develop in large
infarctions
in non-st elevation acute coronary
syndrome which includes both n-stemi and
unstable angina the hallmark is st
depressions and t-wave inversions
in contrast to stemi these changes do
not necessarily represent the affected
vessels
q-waves are typically not present and
this also coincides with the fact that n
stemies are smaller in factions than
stemis generally
t wave inversions alongside st segment
changes indicate ongoing ischemia
however isolated t-wave inversions are
post-ischemic meaning they occur after
the ischemic episode
also remember that the st segment is
especially challenging in paste or known
left bundle branch blocks which is where
criteria such as the scabosa criteria
are used
in rare cases the ecgs can be normal
the primary lab investigation is use of
cardiac troponin eye assays a protein
released from the cardiac myocytes upon
cell death
exact values vary by lab but generally
values above the 99th percentile are
considered abnormal
levels generally rise from 2 hours after
the onset of chest pain and peak at
around 12 to 48 hours they can remain
elevated for between 4 and 15 days
coronary angiography is the definitive
investigation and provides visualization
of the affected coronaries especially
prior to primary percutaneous coronary
intervention a chest x-ray is not
directly involved in the workup but it
can reveal pomona edema or cardiomegaly
but may also reveal other causes of
chest pain
echocardiography isn't done routinely
acutely but can be done to evaluate
secondary complications such as
disruption to valves or a tamponade
general management involves analgesia
which is often morphine oxygen therapy
as required to maintain saturations
above 94
provided there is not another
appropriate range such as in chronic
obstructive pulmonary disease the use of
nitrates most commonly glycerol
trinitrate sublingually or via
intravenous infusion
aspirin is also used in most cases this
is remembered with the pneumonic mona
antiometics such as metaclopramide may
also be added
patients with stemi undergo reperfusion
therapy as early as possible if the
onset of chest pain was within 12 hours
high risk non-st elevation acute
coronary syndrome patients should also
be considered
primary percutaneous coronary
intervention which involves inserting a
balloon and stent into the clogged
coronary artery to reintroduce blood
flow is preferred if it can be performed
within 90 minutes of medical contact
while fibrinolytic therapy is preferred
if this is not feasible
this involves the use of tissue
plasminogen activators like altiplays to
tenecta plays or retiplase
further medical therapy for confirmed
stemi and non-st elevation acute
coronary syndrome includes additional
anti-platelets like the p2 y12
inhibitors ticagrelor or clopidogrel and
anticoagulation such as unfractionated
heparin intravenously or low molecular
weight heparin subcutaneously
secondary prevention medications include
statins as not only do they help prevent
dyslipidemia but they also provide
plaque stabilization
an ace inhibitor or angiotensin receptor
blocker are also included and beta
blockers are used if there is evidence
of left ventricular systolic dysfunction