L8 - Angina Flashcards
What is ischaemia? What can it lead to?
- interruption of cardiac blood supply due to blocked in vessels, primarily involving coronary vessels
- lack of nutrients and oxygen leading to tissue death
Why does ischaemia occur?
- as a consequence of atherosclerosis (coronary artery disease)
- plaque build-up in vessels causing blockage
What is the spectrum of ischaemic heart disease?
early stages: angina
later stages: acute MI
What is angina?
pain in chest caused by decreased blood supply to myocardium due to atherosclerosis
- it can be a symptom of coronary artery disease
What is atherosclerosis?
hardening and narrowing of arteries due to plaque formation (deposition of fatty material in arteries)
What are the 4 stages of cardiovascular disease?
- normal
- fatty streak
- fibrous plaque
- advanced plaque
describe the 1st stage of CVD
NORMAL
- normal blood flow and BP
- exposed to risk factors
- initial lesion occurs = macrophage infiltration
What are the risk factors of CVD?
- diet
- inflammation
- poor oral health
- hypertension
- diabetes
- smoking
- weight
describe the 2nd stage of CVD
FATTY STREAK
- accumulation of lipid-filled white blood cells including active WBC and “dead” cells containing cholesterol
- reduce elasticity of artery walls but doesn’t affect blood flow for decades
describe the 3rd stage of CVD
FIBROUS PLAQUE
- hardening of the arteries (calcification of fatty streak)
- plaque continues to progress and expand
describe the 4th stage of CVD
ADVANCED PLAQUE
- lumen so narrow blood can’t flow through anymore
- plaque becomes unstable and breaks off
- initiates clotting cascade
- can turn angina into MI
What are the types of angina?
Stable angina
- chest pain occurs when heart is working hard and needs more oxygen (stress and exercise)
- caused by narrow arteries
Unstable angina
- new chest pain or change in usual pattern of chest pain
- cause by clot formation
What are the 3 things involved in the management of stable angina?
- dilation of coronary arteries (increase blood supply)
- control HR and force of contraction (reduce work load of heart)
- reduce CV risk factors
What is the 1st line treatment for acute attacks?
GTN - dilation of coronary arteries
What drug class is GTN and how does it work?
- nitrate
- mimics endogenous NO and causes non-specific vasodilation
- increases blood supply to the heart (coronary arteries) and reduces cardiac work (venous dilation)
How is GTN administered?
- sublingual spray
- rapid onset + short lived
How does NO cause vasodilation?
- acts on vascular smooth muscle to increase guanylate cyclase activity
- increased cGMP activates kinases
- promotes smooth muscle relaxation
- cGMP terminated by phosphodiesterase (PDE5)
What are the side effects of GTN?
dose related side effects:
- hypotension
- headaches
- flushing
- reflex tachycardia
When is GTN used?
first line treatment for acute angina attacks
What are other treatments for angina? (chronic treatment)
beta blockers or calcium channels blockers- control HR and force of contraction
What are beta blockers? What is a feature of them?
B adrenergic receptor antagonists
- their degree of response is proportional to the level of sympathetic stimulation i.e. increased response in disease state, exercise, stress
selective/non-selective B blockers: where do they act?
non-selective: block B1 and B2 receptors
selective: B1 receptors
What are three B blockers and how are they different?
propranolol: non-selective B blocker, cross BBB
metoprolol: B1 selective, cross BBB
atenolol: B1 selective, cannot cross BBB
What are B blockers used for?
- primarily angina
- tachycardia
- hypertension
not 1st line in combination with diuretic
What are the adverse effects of B blockers?
B1 mediated: - fatigue/ poor exercise tolerance - CNS effects (if cross BBB) B2 mediated: - bronchoconstriction in lungs - worsening lipid profiles - hypoglycaemia - increased toxicity in elderly
How do CCBs work?
they inhibit Ca2+ influx through L-type calcium channels
What effect do CCBs have on different parts of the heart?
- cardiac muscle: reduce force of contraction
- SA nodal tissue: reduce rate of contraction
- AV node: decrease conduction velocity
What are the 2 types of CCBs? What makes them different?
- cardiac specific: require open channel in order to bind and block the pore = able to act in the heart because channels frequently open
- vessel specific: stabilises inactive channel = only able to act in vessels where channels less frequently open
What are the cardiac and vessel selective CCBs?
verapamil and diltiazem
What is the vessel specific CCB?
nifedipine
What are the cardiac specific CCBs used for and why?
- mainly angina
because increase oxygen supply and decrease oxygen demand - hypertension
causes vasodilation and reduces HR and force of contraction - tachycardia
reduces HR and slows contraction of the heart
What are the adverse effects of cardiac specific CCBs?
- generally well tolerated
- most side effects vascular related e.g. flushing
- dose-related effects e.g. hypotension + bradycardia
can cause cardiac depression if used with B blockers
What is the vessel specific CCB used for?
- newer 1st line treatment for hypertension especially in elderly with vessel stiffness
What are the side effects of vessel specific CCBs?
- don’t use alone in angina because causes reflex tachycardia and increased workload on heart
- most are dose dependent e.g. hypotension, flushing, dizziness + headache
