Ischaemic Heart Disease Flashcards
Risk Factors
Non-modifiable: age, sex, family history (first degree relatives <50yrs)
Modifiable: dyslipidaemia, smoking, HTN, DM, high fat/salt diet, obesity, lack of exercise, stress/depression
Atherosclerosis Pathophysiology
Initial endothelial injury causes macrophages to accumulate and lipoproteins to form foam cells, resulting in fatty streaks. Smooth muscle cells proliferate, creating a fibrous cap. Increasing amounts of collagen are produced, resulting in a plaque, which grows and slowly encroaches on the lumen. Breaching of the fibrous cap due to injury or rupture results in the aggregation and adhesion of platelets, local thrombosis, vasoconstriction and the potential for distal thromboembolus
Complications
CCF MI Stroke Valvular heart disease Arrhythmias
Clinical Presentation - Signs
Anaemia Thyroid disease Hyperlipidaemia Diaphoresis Hypoxia Tachycardia MR murmur Cyanosis Diminished pulses Carotid bruits S3
Clinical Presentation - Symptoms
Chest pressure provoked by exercise or stress, relieved by rest or GTN; radiating to the jaw/arm Epigastric discomfort Dyspnoea on exertion N&V Fatigue
ECG - STEMI
ST elevation in leads II, III, aVF
Peaked T waves
Deep Q waves
T wave inversion
ECG - NSTEMI
ST depression in I, II, III, aVF, V5, V6
T wave inversion
Investigations
Bloods - FBE, UEC, cardiac enzymes (Troponin, CK-MB), BGL and HbA1c, lipids, TFT
Imaging - ECG, CXR, echocardiogram, coronary angiogram
Troponins
Appears after 2 hours and resolves after 7 days
CK-MB
Appears after 3 hours and resolves after 3 days
Management - Lifestyle
Smoking cessation Regular exercise Healthy diet Limited alcohol intake Treat/prevent T2DM
Acute Management
MONASH Morphine Oxygen Nitrates Aspirin Statins Heparin
Long-term Management
SAAB-C Statins ACE inhibitor Aspirin Beta-blockers Clopidogrel
Management - Revascularisation
Angioplasty/PCI (in STEMI/significant angina)
CABG
