Cardio Drugs - CLASSES/MECHANISMS Flashcards
Hydralazine
Increases cGMP → smooth muscle relaxation
(arterioles > veins)
Nitroprusside
Short acting
Increases cGMP via direct release of NO
Fenoldopam
D1 receptor agonist → coronary, peripheral, renal, and splanchnic vasodilation
Decreases BP
Increases natriuresis
Ranolazine
Inhibits the late phase of sodium current → reducing diastolic wall tension and oxygen consumption
Does NOT affect HR or contractility
Milrinone
Selective PDE-3 inhibitor
Cardiomyocytes: Increases cAMP → Inccreases calcium influx → increases inotropy/chronotropy
Vascular smooth muscle: Increases cAMP → inhibition of MLCK → general vasodilation
Cholestyramine
- *Bile acid resin:** Prevent intestinal reabsorption of
- *bile acids** → liver must use CH to make more
Colestipol
- *Bile acid resin:** Prevent intestinal reabsorption of
- *bile acids** → liver must use CH to make more
Colesevelam
- *Bile acid resin:** Prevent intestinal reabsorption of
- *bile acids** → liver must use CH to make more
Ezetimibe
Prevent cholesterol absorption at
small intestine brush border
Gemfibrozil
Upregulate LPL → increases TG clearance
Activates PPAR-alpha → HDL synthesis
Bezafibrate
Upregulate LPL → increases TG clearance
Activates PPAR-alpha → HDL synthesis
Fenofibrate
Upregulate LPL → increases TG clearance
Activates PPAR-alpha → HDL synthesis
Niacin
Inhibits lipolysis (hormone sensitive lipase) in adipose tissue → reduces hepatic VLDL synthesis
Alirocumab
Inactivation of LDL-receptor degradation → increases amount of LDL removed from bloodstream
Evolocumab
Inactivation of LDL-receptor degradation → increases amount of LDL removed from bloodstream
Quinidine
Class IA antiarrhythmic
Increase AP duration
Increase ERP
Increase QT interval
Some K+ channel blocking effects
Procainamide
Class IA antiarrhythmic
Increase AP duration
Increase ERP
Increase QT interval
Some K+ channel blocking effects
Disopyramide
Class IA antiarrhythmic
Increase AP duration
Increase ERP
Increase QT interval
Some K+ channel blocking effects
Lidocaine
Class IB antiarrhythmic
Decrease AP duration
Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue
Mexiletine
Class IB antiarrhythmic
Decrease AP duration
Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue
(Phenytoin)
Class IB antiarrhythmic
Decrease AP duration
Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue
Flecainide
Class IC antiarrhythmic
Significantly prolongs ERP in AV node
and accessory bypass tracts
No effect on ERP in Purkinje and ventricular tissue
Propafenone
Class IC antiarrhythmic
Significantly prolongs ERP in AV node
and accessory bypass tracts
No effect on ERP in Purkinje and ventricular tissue
Beta-blockers
Class II antiarrhythmic
Decrease SA and AV nodal activity by
decreasing cAMP and calcium currents
Suppress abnormal pacemakers by
decreasing slope of phase 4
AV node particularly sensitive → increases PR interval
Amiodarone
Class III antiarrhythmic: K+ channel blocker
Increase AP duration
Increase ERP
Increase QT interval
Ibutilide
Class III antiarrhythmic: K+ channel blocker
Increase AP duration
Increase ERP
Increase QT interval
Dofetilide
Class III antiarrhythmic: K+ channel blocker
Increase AP duration
Increase ERP
Increase QT interval
Sotalol
Class III antiarrhythmic: K+ channel blocker
Increase AP duration
Increase ERP
Increase QT interval
(also a beta-blocker)
Verapamil, Diltiazem
Class IV antiarrhythmics: CCBs
Decrease conduction velocity
Increase ERP
Increase PR interval
Adenosine
Increase K+ efflux from cells → hyperpolarizing cell and decrease calcium influx (inhibits L-type calcium channels) → decreasing AV node conduction
Mg2+
Effective in torsades and digoxin toxicity
Ivabradine
Selective inhibition of funny sodium channels → prolonging slow depolarization phase (phase 4)
Decreases SA node firing
Negative chronotropic effect without inotropy
Reduces cardiac O2 requirement
