Acute coronary syndrome (CVS) Flashcards

CVS

1
Q

What is acute coronary syndrome? Define it

A

It is an umbrella term for unstable angina, STEMI, and NSTEMI. It refers to a set of symptoms and signs that occur due to sudden, acute, reduced blood flow to heart at rest. It is an emergency situation.

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2
Q

What is the leading cause of death in the UK?

A

Coronary artery disease remains the largest cause of death in the UK. There are over 80,000 hospital admissions due to ACS every year.

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3
Q

Describe the anatomy of coronary arteries (which supply which areas of the heart)

A

Look at anatomy + https://zerotofinals.com/medicine/cardiology/acs/

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4
Q

Give a basic summary of the pathology of CAD

A

Coronary artery disease refers to the gradual narrowing of coronary arteries by atherosclerosis and plaque formation. This results in stable angina where chest pain occurs due to myocardial ischemia tf insufficient o2 during exertion. It also causes the risk of plaque rupture (-> thrombus -> ACS)

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5
Q

Give a summary of the pathophysiology of ACS

A

ACS usually occurs in patients with CAD. Unlike stable angina, the symptoms occur at rest - this is due to sudden plaque rupture and thrombus formation in the narrowed coronary arteries. Partial occlusion results in ischemia and chest pain at rest = unstable angina. More occluded or fully occluded this leads to significant ischemia of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI).

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6
Q

Describe the aetiology of CAD/IHD

A

Ischaemic heart disease is a complex process, develops over a number of years. 1. Multiple risk factors cause initial endothelial damage leading to activation + dysfunction and expressing adhesive molecules -> LDL chol accumulates in intima and monocytes migrate in 2. Tissue macrophages engulf oxidised LDL and become big foam cells. 3. VSMCs also migrate and proliferate into the intima from media -> this results in the formation of fibrous capsule covering the fatty plaque.

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7
Q

What are the risk factors for coronary heart disease? Which are modifiable and which are non-modifiable?

A

Modifiable - smoking, hypertension, Hypercholesterolaemia, hyperlipidemia diabetes, obesity, physical inactivity (no exercise).
Non-modifiable - age, male, family history, ethnicity (particularly south asians)

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8
Q

Describe the classification of acute coronary syndrome?

A

3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction, ST elevation myocardial infarction

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9
Q

List the typical symptoms and signs of ACS

A

Chest pain - central/left, sudden, crushing or heavy feeling, radiates to left arm, neck and jaw, associated symptoms (nausea, sweating, clamminess, shortness of breath, sometimes vomiting/syncope/palpitation), timing is constant, worsened by exertion and may be improved by GTN, very severe.

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10
Q

Describe atypical presentation of ACS

A

Epigastric pain.
No pain - known as silent heart attack (more common in elderly and people with diabetes, being female also makes it more likely)

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11
Q

What is the difference between angina and myocardial infarction in terms of damage?

A

Angina is myocardial ischemia that results in damage but does not cause myocardial tissue cell death. In MI, the ischemia is so profound that it leads to death - the death of the myocardial tissue results in troponin release into bloodstream (so MI shows troponin rise in blood test while angina does not)

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12
Q

What are the differential diagnoses of ACS?

A

The chest pain can be due to non-ACS causes as well as ACS.
Myocard/pericard/pancreat/oesophag/cholecyst/costochondritis, cardiomyopathy, valvular disease, cardiac trauma, PE, Pneumonia, pneumothorax, aortic dissection, oesophageal spasm, peptic ulcer, rib fracture, muscle injury, herpes zoster

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13
Q

How do we differentiate between unstable angina, NSTEMI and STEMI in investigation (since their symptoms are very similar/same)?

A

Unstable angina is troponin negative and ECG may be normal or abnormal. NSTEMI’s troponin level is raised and ECG does not ST elevation. So if T+ then it is

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14
Q

List the investigations done for suspected ACS

A

ECG, blood tests (troponin, renal function, HbA1c and lipid profile, FBC and CRP, D-dimer for some), CXR imaging. ECG most important, then troponin

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15
Q

What are we looking for in the ECG when suspecting ACS (simple)?

A

Looking for ST-elevation (new left bundle branch block can indicate STEMI as well but this is complicated) ECG should not be delayed for other investigations. If shows STEMI, patient requires immediate treatment. If ST segment depression/ T wave inversion suggests NSTEMI (as long as troponin pos)

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16
Q

Describe how troponin is investigated and interpreted when suspecting ACS

A

Performed baseline, then at least 3 hrs after, then repeated more to see if troponin is rising - this is because serum troponin levels start to rise 3 hours after MI/chest pain starts. If low - no myocardial death so no MI. If mildly raised it may be due to either MI or non-MI - to figure this out, repeat troponin increasing = MI likely, repeats are stable or falling = unlikely to be MI. If raised hugely and is sequential rises in repeats = MI confirmed.

17
Q

Describe each 4 extra blood tests for sus ACS investigation

A

Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast.
HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease.
FBC and CRP - rule out infectious causes of chest pain
D-dimer - may be used in appropriate patients to rule out PE. Be very careful about who you do a D-dimer on!

18
Q

Why is 12 lead ECG used specifically (for STEMII)?

A

Allows us to see which territory and tf which vessel has been affected. this is bc we can see which lead has the ST elevation and each lead relates to diff areas of myocardium.

19
Q

List the leads and which areas of myocardium and coronary artery it refers to.

A

Leads II, III and aVF = inferior myocardium = RCA
Leads V1-2 = Septal = proximal LAD
Leads V3-4 = Anterior = LAD
Leads V5-6 = Apex = Lcx/ distal LAD/ RCA
Leads I, aVL = lateral = Lcx

20
Q

Describe initial management for ACS and what is the mnemonic?

A

300mg loading dose of aspirin and continue unless contraindicated. Oxygen. IV Morphine if in severe pain (+antiemetic i.e. metoclopramide) . Sublingual GTN or IV nitrates for pain (caution if pt is hypotensive)

MONA - Morphine, oxygen, nitrates (GTN), aspirin (not in order)
However, not all pts need oxygen therapy - only if less than 94%

21
Q

Describe the management of STEMI (basic)

A

300mg loading dose at initial management.
Offer reperfusion therapy if presentation is within 12 hours of onset. Two types: Primary percutaneous coronary intervention - this is given if it can be given within 120 mins of presenting/fmc to the hosp. If not, give fibrinolysis (+ an anti thrombin agent as well)

22
Q

Describe the procedure of PCI for Myocardial Infarction

A

Percutaneous coronary intervention involves putting a catheter into the patient’s radial or femoral artery (radial is preferred), feeding it up to the coronary arteries under x-ray guidance and injecting contrast to identify the area of blockage (angiography). Blockages can be treated using balloons to widen the lumen (angioplasty) or devices to remove or aspirate the blockage. Usually, a stent is inserted to keep the artery open.

23
Q

Describe what fibrinolysis is for myocardial infarction

A
24
Q
A