Angina and drugs
- Created by: milliehubbard1
- Created on: 19-04-17 11:37
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- Stable angina and drugs
- Myocardium is only perfused with oxygenated blood during diastole
- Oxygen demand is a function of heart rate and ventricular wall tension (pressure, volume, thickness)
- Coronary blood flow: 225ml/min - Exercise: 800+ml/min
- Arterial stiffness: normal blood flow relies on vessels elasticity expanding after pulsatile ejections
- Age and risk factors make walls less elastic, increasing cardiac inotropy to compensate
- Leading to ventricular hypertrophy and increased myocardial oxygen demand
- Heart has to work harder against increased load due to stiffened vessel: increase muscle: needs more oxygen
- Leading to ventricular hypertrophy and increased myocardial oxygen demand
- Atherosclerosis: growth of LDL-cholesterol plaque in sub-endothelium
- Leads to tissue ischaemia: oxygenated blood can't meet myocardial demand
- Large quantities of lactate are generated from pyruvate formed by myocardial anaerobic glycolysis
- Lactate can trigger pain > angina is due to large quantities / ischaemia
- Large quantities of lactate are generated from pyruvate formed by myocardial anaerobic glycolysis
- Leads to tissue ischaemia: oxygenated blood can't meet myocardial demand
- Age and risk factors make walls less elastic, increasing cardiac inotropy to compensate
- Stable angina: chest pain (crushing, burning, tight) (down left arm) with SOB, nausea, sweating
- Symptoms precipitated by exertion and stress
- ST depression on 12-lead ECG during exercise stress test (asymptomatic) : ischaemia
- Coronary angiography: identify narrowing / occlusion > dye injected via catheter in femoral artery
- Acute coronary syndrome
- Symptoms appear at rest, indicate unstable plaque rupture with thrombus fragments narrowing vessels
- Drugs
- Reduce symptoms during episode: GTN
- Organic nitrates reduced in body to NO
- NO activates guanylyl cyclase in SM cells > cGMP activates PKG > PKG prevents Ca entry into cells > dilation of vessels > reduces symptoms
- Organic nitrates reduced in body to NO
- Prophylactic: bisoprolol
- B1-adrenoceptor antagonist: reduce onset of episodes
- Block B1AR's in cardiac tissue, adrenaline cannot bind
- Negative chronotropy and inotropy: reduce cardiac output / oxygen demand
- Block B1AR's in cardiac tissue, adrenaline cannot bind
- B1-adrenoceptor antagonist: reduce onset of episodes
- Reduce symptoms during episode: GTN
- Myocardium is only perfused with oxygenated blood during diastole
- Other drugs
- CCBs: impede Ca traffic through L-type VGIC's
- Intracellular face of calcium channel blocked > prevent contraction > vasodilation
- Also reduce force of contraction and rate limit heart: decrease CO
- E.g Verapamil
- Nicorandil
- Vasodilator: increases cGMP reducing Ca entry
- Activates K/ATP channel, cells hyperpolarise > prevent calcium channel activity
- Ivabradine
- Rate limiter: inhibits Na/K current in SAN, reducing pacemaker automacity
- Statins (not used in angina treatment)
- Inhibit HMG CoA reductase (required for cholesterol synthesis)
- Reduces CAD risk
- Inhibit HMG CoA reductase (required for cholesterol synthesis)
- CCBs: impede Ca traffic through L-type VGIC's
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