Ca Channel Blockers Flashcards
Angina
Clinical manifestation of ischemia
Stable Angina (what it is, cause, treatment)
Exertional angina from increase in chronotropy and ionotropy. Usually from >70% blockage. Can stent for symptomatic, won’t reduce M&M
Unstable Angina (what it is, cause, and treatment)
Rest pain/increase in freq w/ minimal activity. Usually 30-40% block, but very irregular w/ clumps and fat outgrowths. Treat w/ statins
Accelerating Angina
Worsening pattern but still exertional from big block
Printzmals Angina
Spasm of a coronary, often genetic
Angina of HTN
Increased afterload and LVH increases demand so much that normal supply just can’t keep up
Angina of Aortic Stenosis
Increased demand/afterload/LVH, but also maybe decreased supply to coronaries
Nitrates
Huge venodilators, so systemic return to the heart decreases so POTENT PRELOAD REDUCERS. May also reduce afterload and increase coronary supply
2 Effects of Ca Blockers
Vasodilate and decrease ionotropy
Preactivated State
More effective to block conduction than reducing Ca influx is to block Ca channels from reverting to preactivated state
Nondihydropyridine (effect, mech, 2 examples)
Delay preactivated state so they slow node conduction and decrease ionotropy, causing decreased HR, contractility, and causing vasodilation
Verapamil and Diltiazem (Cardiazem)
Dihydropyridines (point about mech, and effects, 5 points total)
Don’t block preactivated state, so little to no effect on conduction or contractility, but VERY POTENT VASODILATORS D IS FOR DILATE. But also increase CATs!
4 Dihydropyridines
Nifedipine - very strong
Nicardipine - similar but IV
Amlodipine, Felodipine are long acting
Main Summary of Nons and Dis
Nons relax heart and dilate
Dis dilate and either nothing on heart or increase via CATs
Huge Drug-Drug Interaction w/ Nons
DO NOT USE VERAPAMIL AND BETA BLOCKERS. Heart block and severe bradycardia from the multiple sources slowing conduction and heart activity (can use diltiazem cautiously)