Acute Coronary Syndrome (ACS) - General

Question 1

What is Acute Coronary Syndrome?

Answer 1

Acute Presentations of Ischaemic heart Disease including STEMI, NSTEMI and Unstable Angina.

Question 2

Non-Modifiable Risk Factors of ACS (4).

Answer 2

1. Age.
2. Male.
3. Family History.
4. South Asian Ethnicity.

Question 3

Modifiable Risk Factors of ACS (6).

Answer 3

1. Smoking.
2. Diabetes.
3. Hypertension.
4. Hypercholesterolaemia & Hyperlipidaemia
5. Obesity & High-Fat Diet.
6. Stress & Physical Inactivity.

Question 4

Pathophysiology of Atherosclerosis (7).

Answer 4

1. Initial Endothelial Dysfunction : Smoking, HTN, Hyperglycaemia.
2. Endothelial Changes : Pro-Inflammatory, Pro-Oxidant, Proliferative, Reduced NO Bioavailability.
3. Fatty Infiltration of Subendothelial Space by LDLs.
4. Monocytes migrate from blood and differentiate into macrophages.
5. Macrophages phagocytose oxidised LDL to become large foam cells.
6. Foam cells die to propagate the inflammatory process.
7. Smooth Muscle Proliferation and Migration from Tunica Media forms fibrous capsule to cover fatty plaque.

Question 5

Aetiology of Acute Coronary Syndrome.

Answer 5

Sudden Rupture of a Vulnerable Atherosclerotic Plaque with Superimposed Thrombosis in the Lumen at the Site of Rupture, resulting in partial/complete occlusion.

Question 6

Clinical Presentation of Acute Coronary Syndrome (6).

Answer 6

*Lasting more than 20 minutes = Or Angina.
1. Central/Left-Sided Constricting/Heavy Chest Pain.
2. Sweating and Clamminess.
3. N&V.
4. SOB.
5. Palpitations.
6. Pain Radiating to Jaw/Arms.

Question 7

What is a Silent MI?

Answer 7

No typical chest pain e.g. Diabetes, Elderly.

Question 8

Acute Management of ACS (5).

Answer 8

MONAC :
1. Morphine - Severe Pain.
2. Oxygen : If SpO2 < 94%).
3. Nitrates - GTN (Sublingual/IV) - Caution : Hypotension.
4. Aspirin.
5. Clopidogrel.

Question 9

Secondary Prevention of ACS - Medical Management (6).

Answer 9

6As :
1. Aspirin 75mg Once Daily.
2. Another Antiplatelet : Clopidogrel 75mg or Ticagrelor 90mg (up to 12 months).
3. Atorvastatin 80mg Once Daily.
4. ACE Inhibitors (up to 10mg Once Daily).
5. Atenolol (or another B-Blocker).
6. Aldosterone Antagonist (if Clinical Heart Failure).

Question 10

Secondary Prevention of ACS - Lifestyle (5).

Answer 10

1. Smoking Cessation.
2. Reduce Alcohol.
3. Mediterranean Diet.
4. Cardiac Rehabilitation.
5. Optimise Co-Morbidities.

Question 11

What system is used to stratify risk post-MI?

Answer 11

Killip Class:
I - No Clinical Signs of Heart Failure (6%).
II - Lung Crackles/S3 (17%).
III - Frank Pulmonary Oedema (38%).
IV - Cardiogenic Shock (81%).

Question 12

Complications of an MI (5).

Answer 12

DREAD :
1. Death.
2. Rupture of the Heart Septum/Papillary Muscles.
3. Edema (Heart Failure).
4. Arrhythmia (Ventricular) /Aneurysm.
5. Dressler’s syndrome.

Question 13

What is Dressler’s Syndrome?

Answer 13

Post-MI Syndrome occurring 2-3 weeks after an MI causing a localised immune response and pericarditis.

Question 14

Clinical Presentation of Dressler Syndrome (4).

Answer 14

1. Pleuritic Chest Pain.
2. Low Grade Fever.
3. Pericardial Rub on Auscultation.
4. Can cause Pericardial Effusion (and Pericardial Tamponade).

Question 15

Investigations of Dressler’s syndrome (3).

Answer 15

1. ECG : Global ST Elevation and T Wave Inversion.
2. Echo : Pericardial Effusion.
3. Raised Inflammatory Markers.

Question 16

Management of Dressler’s Syndrome (3).

Answer 16

1. NSAIDs e.g. Aspirin, Ibuprofen.
2. Severe : Steroids e.g. Prednisolone.
3. Pericardial Effusion : Pericardiocentesis.

Question 17

What does Rupture of Papillary Muscles cause?

Answer 17

Acute MR - pan systolic murmur at apex and severe sudden acute LV heart failure - poor prognosis.

Question 18

What is the cause and result of Ventricular Fibrillation?

Answer 18

Cause : K+ released from necrotic myocytes induces arrhythmias in the hyper-excitable tissues around the infarct.
Complication : Sudden Death.

Question 19

What does Rupture of the Free Wall of the Ventricle cause?

Answer 19

Haemopericardium and Cardiac Tamponade.

Question 20

What is the body’s response to an MI?

Answer 20

Host Acute Inflammatory Response - the myocardium is unable to regenerate so the infarcted myocardium undergoes a process of repair, resulting in the formation of scar (fibrous) tissue.