-
For Beta Blockers: What is the MOA on myocardial O2 demand?
Decreases all 3 determinants of myocardial oxygen demand (heart rate, contractility, intramyocardial wall tension during systole)
-
What are the common adverse reactions for Beta blockers?
decompensated heart failure, heart block, depression, bradycardia, bronchospasm, fatigue
-
For NDHP CCB what is the MOA and the effects on myocardial oxygen?
Inhibits calcium ion influx into vascular smooth muscle and myocardium. Decreases all 3 determinants of myocardial oxygen demand and increases oxygen supply.
-
What are the adverse effects of NDHP CCB?
bradycardia, AV block, arrhythmia, hypotension, heart failure, edema, constipation
-
For DHP CCB:
What is the MOA and effects on myocardial oxygen?
Inhibits calcium ion influx into vascular smooth muscle and myocardium. Decreases myocardial demand (reduced contractility and systolic wall tension) AND increases oxygen supply
-
What are the adverse effects of DHP CCB?
edema, fatigue, dizziness
-
For Nitrates:
What is the MOA and effects on myocardial oxygen?
Increases supply of nitric oxide causing relazation of smooth muscle in veins (decreases preload) and arteries (decreases SVR); vasodilates cornary arteries. Decreases myocardial oxygen deman (by decreasing systolic wall tension) and increases supply
-
What are the adverse effects for nitrates?
headache, flushing, tolerance
-
For ranolazine:
What is the MOA and effects on myocardial oxygen?
Reduces calcium overload through inhibition of late sodium channels. Leads to more efficient use of oxygen by reducing ischemia induced mechanical dysfunction.
-
What are the adverse effects for Ranolazine?
dizziness, headache, constipation, nausea; QT prolongation concentration dependent
-
What is the MOA for aspirin?
inhibits cyclooxygenase and synthesis of platelet thromboxane A2
-
What is the MOA for clopidogrel?
it inhibits platelet aggregation by preventing adenosine diphosphate (ADP)-mediated activation of platelets by selectively and irreversibly inhibiting the binding of adenosine diphosphate to its platelet receptors and thereby blocking adenosine diphosphate-dependent activation of the GP IIb/IIIA complex
|
|
