Acute Coronary Syndromes Flashcards
acute coronary syndrome (ACS)
an umbrella term covering a number of acute presentations of ischaemic heart disease
STEMI (ST-elevation myocardial infarction):
- ST-segment elevation
- elevated biomarkers of myocardial damage
NSTEMI (non ST-elevation myocardial infarction)
- ECG changes but no ST-segment elevation
- elevated biomarkers of myocardial damage
unstable angina
Ischaemic heart disease is a term synonymous with coronary heart disease and coronary artery disease.
True
acute coronary syndrome pathophysiology
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.
What are Unmodifiable risk factors?
Increasing age
Male gender
Family history
What are modifiable risk factors?
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity
Poor prognostic factors?
age development (or history) of heart failure peripheral vascular disease reduced systolic blood pressure Killip class* initial serum creatinine concentration elevated initial cardiac markers cardiac arrest on admission ST segment deviation
What is Killip Class?
system used to stratify risk post myocardial infarction
Describe Killip Classes
I No clinical signs heart failure, 6% 30 day mortality
II Lung crackles, S3 17% 30 day mortality
III Frank pulmonary oedema 38% 30 day mortality
IV Cardiogenic shock 81% 30 day mortality
initial endothelial dysfunction in IHD is triggered by a number of factors such as
smoking, hypertension and hyperglycaemia
initial endothelial dysfunction results in a number of changes such as?
pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
What type of lipoproteins infiltrate the subendothelial space in IHD?
by low-density lipoprotein (LDL) particles
How do foam cells form?
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.
What are the complications of atherosclerosis?
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
What is the classic and most common feature of ACS?
chest pain.
What are the symptoms of ACS?
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
dyspnoea
sweating
nausea and vomiting
Patients presenting with ACS often have very few physical signs to ellicit
true
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
What are the two most important investigations when assessing a patient with chest pain?
ECG
cardiac markers e.g. troponin
Which cardiac marker is first to rise?
myoglobin is the first to rise
Which marker is useful to look at for re-infarctation?
CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days
How long does troponin T remain elevated?
10 days
What are the cardiac enzymes and protein markers?
Myoglobin CK-MB CK Trop T AST LDH
Interpretation of the various cardiac enzymes has now largely been superceded by the introduction of troponin T and I. Questions still however commonly appear in exams.
true
Describe the orrelation between ECG changes and coronary territories
Anterior V1-V4 usually Left anterior descending artery
Inferior II, III, aVF usually Right coronary artery
Lateral I, V5-6 usually Left circumflex artery
What are the aims of ACS 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 intial treatment of ACS is MONA, what does it stand for?
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
oxygen should only be given if the patient has oxygen saturations < 94%
nitrates
can be given either sublingually or intravenously
useful if the patient has ongoing chest or hypertension
should be used in caution if patient hypotensive
aspirin 300mg
After pharmacological treatment (MONA) what is the next step?
determine whether they meet the ECG criteria for STEMI
What is 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)
In management of a STEMI all patients should be given?
aspirin
a second antiplatelet drug should be given in addition to aspirin. P2Y12-receptor antagonist (ticagrelor is often favoured or prasugrel if the patient is going to have a PCI)
unfractionated heparin is usually given for patients who’re are going to have a PCI
In STEMI management what should you do in terms of oxygen therapy?
do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to:
people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98%
people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.
What is gold standard treatment for STEMI?
Primary 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
radial access is preferred to femoral access in PCI
