Physiology and Pharmacology 22: (Davies) Coronary blood flow and angina Flashcards
What is angina?
Angina is chest pain or pressure usually due to not enough blood flow to the heart muscle
Angina usually due to obstruction or spasm of the coronary arteries
When does most coronary blood flow occur?
Ventricular Diastole (~ 80%)
What is coronary circulation regulated by?
Local vasodilator signals
- increase in extracellular K+
- reduction in pH
- reduction in partial pressure of O2 (PO2)
-> increase blood flow
3 types of angina?
Stable angina - pain with exercise, fixed coronary narrowing
Unstable angina - pain with increasingly less exercise, then at rest - formation of thrombus (blood clot)
(high risk of myocardial infarction aka heart attack)
Variant angina - much rarer, spasm in coronary arteries
What is ischaemia?
Inadequate blood flow (to heart)
- usually caused by coronary artery narrowing via atherosclerosis
Treatments of angina? Types of anti anginal drugs - how do they work?C
Act to
- decrease cardiac workload and therefor O2 demand
- improve O2 delivery by dilating coronary arteries
Beta blockers
- decrease force of contraction, increase efficiency
- > reduces strain on heart
Agents that cause relaxation of arterial smooth muscle
- organic nitrates
- Ca2+ channel blockers
- K+ channel blockers
Coronary angioplasty (surgery) -> opening of narrow coronary arteries
Mechanism of nitrate vasodilators?
Nitrates enter cell
Nitric oxide from nitrates stimulates action of gyanylyl cyclase
- increases convertion of GTP to cGMP
stimulates PKG which inhibits IP3 induced calcium release from ER/SR,
- also phosphorylates K+ channels, activating + inducing hyperpolarisation
- > inhibits contraction, leads to relaxation
Mechanism and effect of Calcium channel blockers? e.g.?
Most block L-type Calcium channels -> act on both smooth muscle and cardiac muscle
Cardiac muscle: reduces force of contraction so decreases O2 consumption
Smooth muscle: reduces force of contraction so results in vasodilation
e.g. diltiazem (intermediate), dihydropyridines (smooth muscle) verapamil (cardiac)
Mechanism of K+ channel openers?
Act by hyperpolarising arterial smooth muscle
-> closes Ca2+ channels, reducing Ca2+ entry and so causes vasodilation
e.g. nicorandil
What events lead to myocardial infarction (heart attack) and what events proceed it?
Plaque rupture followed by blood platelet aggregation/adhesion causes formation of thrombus (clot)
Thrombus becomes reinforced by fibrin and blocks coronary artery
Leads to severe myocardial ischaemia -> ATP depletion
-pain -> sympathetic activity
Contribute to cell death -> further complications
Treatments for myocardial infarction?
Electrical defibrillation (if cardiac arrest)
Nitrovasodilator or adrenaline
Fibrinolytic agent to break down blood clots#
Aspirin (inhibits platelet aggregation)
B- adrenoceptor antagonist (reduces sympathetic drive on B-adrenoceptors) -> less O2 and ATP usage
