Ischaemic heart disease

Ischaemia

Insufficient blood supply (o2 and nutrients)

Angina

Partial reduction in blood flow

Stable or unstable

Mycocardisl infarction

Prolonged or complete blockage of blood flow

Necrosis of cardiac muscle cells and scar formation

Stable angina

Atheroma in coronary artery reduces blood flow

Plaque with fibrous cap can prevent rupture

No ECG change

Intense chest pain

Symptoms relieved by rest

Unstable angina

Rupture of surface of atheroma leads to plug and thrombus formation

Unpredictable, fast progression

Normal ECG or subtle changes

Intense chest pain

Symtopms not relieved by rest

Avoid progression to MI

STEMI and NSTEMI

Rupture of surface of an atheroma leading to platelet plug and thrombus formation

Cardiac muscle die (MI)

Stemi- total occlusion of coronary artery, elevation of ST leads to death of cells (transmural ischaemia)

NSTEMI- partial occlusion, non-ST elevation

Acute myocardial ischaemia mechanism

Reduced o2 and nutrients

Cellular metabolism changes from mitochondrial oxidative phosphorylation to glycolysis which reduces ATP and increases lactase and H+

Leads to increase ca levels in mitochondria, but reduced in muscles - less contraction

Cell death- apoptosis or necrosis

Cardiac cells start dying…

Plasma membrane becomes leaky, releases components to bloodstream

Troponin increases

ECG

Waves and why they are at level they are

Stable angina pharmacology

Symptom relief (pain)- short-acting nitate

Symptom control- beta-blocker or calcium channel blocker, beta-blocker and calcium channel blocker, long active nitrates, nicorandil, ranolazine, ivabradine, beta blocker or calcium channel blocker and alternative

Cor-morbidity treatment- hypertension, diabetes, hyperlipidaemia

Preventative treatment: aspirin

Nitrates

Short acting: GTN spray

Rapid onset

Long acting: isosorbide mononitrate

Slower onset

Vasodilators: NO reducing cardiac work, preload

Beta blockers

Decrease cardiac output

Receptors found in heart

Their activation increases rate and strength of cardiac contraction so we inactivate

Decrease HR, decrease stroke volume and CO

Calcium channel blockers

Decrease entry of ca 2+ into muscle cells

Dihydropyridines: decrease contraction, increase vasodilation, decrease peripheral resistance, decrease Afterload, decrease cardiac work

Non-dihydropyridines: decrease contraction, decrease HR, decrease o2 demand

Nicrorandil

Nitrate like action

Potassium channel activator

Vasodilation- increase coronary flow and decrease preload

K+ATP channel activator

Ranolozine

Sodium levels, reduces Ca, reduced contraction force

Ivabradine

Reduces HR, ion channels in sinoatrial node effected

Aspirin

Secondary prevention

Antiplatelet

Irreversibly inhibits COX-1 enzyme, blocks TA2 from arachidonic acid, inhibits formation if blood clots

Dual antiplatalet therapy

Aspirin + clopidogrel/ prasugrel/ ticagrelor