Dr musab abdalrahman family medicine specialist

24/12/2025

Acute coronary syndrome: initial management
Acute coronary syndrome (ACS) is a very common and important presentation in medicine. The
management of ACS has evolved over recent years, with the development of new drugs and
procedures such as percutaneous coronary intervention (PCI).
Emergency departments often have their own protocols based on local factors such as the
availability of PCI and hospital drug formularies. The following is based on the 2020 update to the
NICE ACS guidelines.
Acute coronary syndrome can be classified as follows:
ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of
myocardial damage
non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation
+ elevated biomarkers of myocardial damage
unstable angina
The management of ACS depends on the particular subtype. NICE management guidance groups
the patients into two groups:
1. STEMI
2. NSTEM/unstable angina
Common management of all patients with ACS
Initial drug therapy
aspirin 300mg
oxygen should only be given if the patient has oxygen saturations < 94% in keeping with
British Thoracic Society oxygen therapy guidelines
morphine should only be given for patients with severe pain
previously IV morphine was given routinely
evidence, however, suggests that this may be associated with adverse outcomes
nitrates
can be given either sublingually or intravenously
useful if the patient has ongoing chest pain or hypertension
should be used in caution if patient hypotensive
The next step in managing a patient with suspected ACS is to determine whether they meet the
ECG criteria for STEMI. It is, of course, important to recognise that these criteria should be
interpreted in the context of the clinical history.
STEMI criteria
clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (>
20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥
2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)

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Management
Once a diagnosis of ACS has been made there are a number of elements to treatment:
prevent worsening of presentation (i.e. further occlusion of coronary vessel)
revascularise (i.e. 'unblock') the vessel if occluded (patients presenting with a STEMI)
treat pain
A commonly taught mnemonic for the treatment of ACS is MONA:
Morphine
Oxygen
Nitrates
Aspirin
Whilst useful it should be remember that not all patients require oxygen therapy. British Thoracic
Society guidelines are now widely adopted and oxygen should only be given if the oxygen
saturations are < 94%.
For patients who've had a STEMI (i.e. one of the coronary arteries has become occluded) the
priority of management is to reopen, or revascularise, the blocked vessel.
a second antiplatelet drug should be given in addition to aspirin. Options include
clopidogrel, prasugrel and ticagrelor
for many years the treatment of choice was thrombolysis. This involved the intravenous
administration of a thrombolytic or 'clot-busting' drug to breakdown the thrombus blocking
the coronary artery
since the early 2000's thrombolysis has been superseded by percutaneous coronary
intervention (PCI). In this procedure the blocked arteries are opened up using a balloon
(angioplasty) following which a stent may be deployed to prevent the artery occluding again
in the future. This is done via a catheter inserted into either the radial or femoral artery.
If a patient presents with an NSTEMI then a risk stratification too (such as GRACE) is used to
decide upon further management. If a patient is considered high-risk or is clinically unstable then
coronary angiography will be performed during the admission. Lower risk patients may have a
coronary angiogram at a later date.
Secondary prevention
Patients who've had an ACS require lifelong drug therapy to help reduce the risk of a further
event. Standard therapy comprises the following as a minimum:
aspirin
a second antiplatelet if appropriate (e.g. clopidogrel)
a beta-blocker
an ACE inhibitor
a statin
Further images
The following images show the progress of coronary artery atherosclerosis:

22/12/2025

Symptoms and signs
The classic and most common feature of ACS is chest pain.
typically central/left-sided
may radiate to the jaw or the left arm
often described as 'heavy' or constricting, 'like an elephant on my chest'
it should be noted however in real clinical practice patients present with a wide variety of
types of chest pain and patients/doctors may confuse ischaemic pain for other causes such
as dyspepsia
certain patients e.g. diabetics/elderly may not experience any chest pain
Other symptoms in ACS include
dyspnoea
sweating
nausea and vomiting
Patients presenting with ACS often have very few physical signs to ellicit:
pulse, blood pressure, temperature and oxygen saturations are often normal or only mildly
altered e.g. tachycardia
if complications of the ACS have developed e.g. cardiac failure then clearly there may a
number of findings
the patient may appear pale and clammy
Investigations
The two most important investigations when assessing a patient with chest pain are:
ECG
cardiac markers e.g. troponin

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Once a plaque has formed a number of complications can develop:
the plaque forms a physical blockage in the lumen of the coronary artery. This may cause
reduced blood flow and hence oxygen to the myocardium, particularly at times of increased
demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This
may result in a myocardial infarction

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Pathophysiology
Ischaemic heart disease is a complex process which develops over a number of years. A number
of changes can be seen:
initial endothelial dysfunction is triggered by a number of factors such as smoking,
hypertension and hyperglycaemia
this results in a number of changes to the endothelium including pro-inflammatory, pro-
oxidant, proliferative and reduced nitric oxide bioavailability
fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
monocytes migrate from the blood and differentiate into macrophages. These macrophages
then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages
die the result can further propagate the inflammatory process.
smooth muscle proliferation and migration from the tunica media into the intima results in
formation of a fibrous capsule covering the fatty plaque.

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Unmodifiable risk factors
Increasing age
Male gender
Family history

Modifiable risk factors
Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

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Acute coronary syndrome: a very basic introduction
Acute coronary syndrome (ACS) is an umbrella term covering a number of acute presentations of
ischaemic heart disease.
It covers a number of presentations, including
ST elevation myocardial infarction (STEMI)
non-ST elevation myocardial infarction (NSTEMI)
unstable angina
considered to be present in patients with ischaemic symptoms suggestive of an ACS and
no elevation in troponins, with or without electrocardiogram changes indicative of
ischaemia
however, as a rise in troponins may take some hours it may be indistinguishable for
NSTEMI initially and is therefore treated the same until the troponin result is known
Before we go into more detail into these presentations it's useful to take a step back and consider
how such conditions develop.
ACS generally develops in patients who have ischaemic heart disease, either known or previously
undetected. Ischaemic heart disease is a term synonymous with coronary heart disease and
coronary artery disease. It describes the gradually build up of fatty plaques within the walls of the
coronary arteries. This leads to two main problems:
1. Gradual narrowing, resulting in less blood and therefore oxygen reaching the myocardium
at times of increased demand. This results in angina, i.e. chest pain due to insufficient oxygen
reaching the myocardium during exertion
2. The risk of sudden plaque rupture. The fatty plaques which have built up in the
endothelium may rupture leading to sudden occlusion of the artery. This can result in no
blood/oxygen reaching the area of myocardium.
Remember that there are a large number of factors which can increase the chance of a patient
developing ischaemic heart disease:

17/11/2025

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