CAD drugs Flashcards
Oxygen saturation of blood as it returns to the heart
MVO2
SVO2
Myocardial O2 supply determined by these factors:
1) perfusion pressure
2) intrinsic vascular resistance
Myocardial O2 demand determined by:
1) heart rate
2) contractility
3) wall stress
4) MVO2 = HR x SBP
First line drugs in CAD
Nitrates
Primary effect of nitroglycerin and related drugs:
venous dilation (relaxes all types of smooth muscle)
Secondary effects if nitroglycerin
Coronary artery dilation increases supply
Arterial dilation decreases afterload
Disadvantage for chronic use of nitrates?
Drug tolerance
Effect of venous dilation on CO?
Venodilation increases venous capacitance –> decrease venous return –> decreasing preload and thus decreasing CO
How does the consumption of sulfhydryl groups contribute to nitrate tolerance?
Sulfhydryl groups on cell membrane are needed for nitrates to enter cell.
No nitrates will enter the cell if nitrates are constantly given.
How does continuous nitrate use cause receptor down-regulation?
vasodilation –> larger blood volume –> sympathetic receptors downregulated
MoA of nitrates:
Enter cell membrane –> Nitrification process
NO activates guanylyl cyclase –> increase in cGMP –> Ca release is INHIBITED –> smooth muscle relaxation –> venous dilation
venous dilation –> decreased preload –> decreased CO –> decrease O2 demand
Nitrate drug interactions:
Nitrates cannot be taken with other drugs that use cGMP pathway like PDE-5 inhibitors –> severe hypotension
sildenafil, vardenafil, tadalafil
Type of beta blocker for CAD treatment?
beta 1 blocker
Decreases oxygen demand by decreasing heart rate.
How do beta blockers enhance coronary blood flow?
B1 blockage –> Dereased HR –> Increased diastolic perfusion –> increased filling time
Negative effect of increased filling time?
preload inreased –> more force required –> hypertrophy
How do beta blockers reduce MVO2
B1 blockage –> Decreased HR and contractility
Why are B blockers without ISA preferred?
ISA = partial agonist at receptor
Therefore they will show less decrease in HR.
Why are non-selective 3rd gen BBs unwanted in CAD patients?
3rd gen BB (mostly non-selectives) can have alpha antagonistic effect or stimulate NO release –> increase vasodilation –> profound hypotension –> REFLEX TACHYCARDIA –> higher O2 demand for heart
CAD + asthma: what drugs could be used
Cardio-selective 3rd gen with partial B2 agonism
Celiprolol
A patient with CAD is on BBs. What drugs should be avoided?
CCBs (verapamil, diltiazem)
Anti-arrhythmics (amiodarone)
They have cardiosuppressive effects leading to profound decrease in HR and CO.
BB with highest lipid solubility?
propanolol
This is why it can cause lethargy, mental depression, hallucinations
BBs used for early administration after ischemic episodes:
IV esmolol
IV metoprolo or atenolol followed by oral metoprolol/atenolol
BBs used for late administration after ischemic episode:
BBs without ISA
Two mechanisms of CCBs
- Block L-type voltage operated channels (VOCs) and receptor operated channels at membrane
- Bind to calcium channel protein
