Cardiac Flashcards
Use for Primary HTN
thiazides
Ace inhibitors
Angiotensin receptor blockers
HTN with HF
diuretic, ace inhibitor, and arb (only use beta blockers in compensated HF)
HTN with DM
ace inhibitors and angiotensin receptor blockers
HTN in pregnancy
hydrazine, nifedipine, methyldopa, labetalol
Dihydropyridine calcium channel blockers work on?
vascular smooth muscle
Amlodipine, clevidipine, nifedipine, nimodipine
dihydropyridine calcium channel blockers
nondihydropyridine calcium channel blockers
work on the heart
dilitazem, verapamil
nondihydropyridine calcium channel blockers
-“dipine”=
Dihydropyridine calcium channel blockers
MOA of calcium channel blockers
block voltage gated L type calcium channels of cardiac and smooth muscle
(Class 4 will decrease conduction velocity and increase EP and increase PR interval)
Use all Dihydropyridines except nimodipine for:
HTN, angina, raynaud phenomenon
nimodipine used for
subarachnoid hemorrhage
nondihydropyridines used for
HTN, angina, a fib/flutter, and to prevent SVT
SE of dihydropyridines
cardiac depolarization, av block, hyperprolactinemia, constipation
SE of nondihydropyridines
peripheral edema, flushing, dizziness, gingival hyperplasia
Hydralazine works by:
increased cGMP; which works to vasodilator arterioles > veins ; decreases afterload
Hydralazine is used for HF when given with?
nitrate
Hydralazine avoids reflex tachycardia with?
beta blockers
SE: of hydralazine
SLE like symptoms, increase HR, and fluid retention
1 drug for HTN emergency =
nitroprusside
NItroprusside works by:
increase cGMP–> by releasing NO and can cause Cyanide toxicity
Nitrates examples:
nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
MOA of nitrates:
dilate veins> arterioles; which decreases preload
**Will also see a decrease in EDV, BP, ejection time, and MVO2
Nitrates work on EDV and BP by:
decreases MVO2
Beta blockers work on contractility and BP by:
MVO2
Inhibits late phase of sodium current –> decreases diastolic wall tension and oxygen consumption
ranolazine
use for angina due to other therapies; that doesn’t affect the HR or contractility?
ranolazine
Inhibit NA/K ATPase; which indirectly inhibits the Na/Ca exchanger which increases calcium
digoxin
increases calcium means increasing contractility; also + ionotrophy ; which stimulates vagus nerve and decreases the HR
digoxin
digoxin SE:
blurry yellow vision
HMG COA reductase inhibitors MOA:
prevent mevalonate synthesis
Which lipid lowering agents decrease LDL?
HMG COA reductase inhibitors; bile acid resins, ezetimibe
Which lipid lowering agents increase HDL?
niacin
Which lipid lowering agents decrease triglycerides?
fibrates, omega 3 FA
Which lipid lowering agent increases LFTs?
ezetimibe
Statins cause increased or decreased mortality in CAD patients?
decreased
SE of statins:
statin induced myopathy ; esp with vibrates or niacin
examples of bile acid resins:
cholestyramine, colestipol, colesevelam
Bile acid resins MOA:
prevent intestinal reabsorption of bile acids
SE of bile acid resins
decrease absorption of other drugs and fat soluble vitamins
*** cholestyramine can bind C. difficle
MOA: prevent cholesterol absorption at the small intestine brush border
ezetimibe
can be used when a patient cannot handle statins?
ezetimibe
MOA of fibrates:
upregulate LPL which increase TG clearance;
use PPAR gamma to decrease hepatic LDL and increase LPL activity which will ultimately decrease TG and increase HDL
Fibrates SE:
myopathy and cholesterol gallstones
Inhibit lipolysis in adipose tissue:
Niacin
SE of Niacin:
red flushed, face
- can be decreased with NSAIDS
Class 3 K+ channel blockers drugs:
amiodarone, ibutilide, dofetilide, sotalol (AIDS)
Increase AP, increase ERP Increase QT interval
Class 3 K+ channel blockers drugs:
Use for A-fib/flutter, V-tach
Class 3 K+ channel blockers drugs:
For Vtach ( use amiodarone or sotalol)
Sotalol has more risk of _________ and amiodarone has a less risk of _________.
Torsades
You must check what with amiodarone?
PFTS, LFTS, TFTS
Adenosine MOA:
increases K+ out of cells which hyper-polarizes and then decreases intercellular calcium
Adenosine indications:
diagnose and terminate SVT
** effect is blunted by theophylline and caffeine
Magnesium use:
torsades and digoxin toxicity
Class 2 Anti arrhythmic: Beta blockers
metoprolol, propanolol, esmolou, atenolol, timolol, carvedilol
decrease SA / AV node activity by decreases cAMP and decreasing calcium current which also decreases slope of phase 4
Class 2 Anti arrhythmic: Beta blockers
SE of Class 2 Anti arrhythmic: Beta blockers
impotence, COPD exacerbation, can masks signs of hypoglycemia
** beta blockers can cause unopposed alpha 1 agonism if given alone for pheochromocytoma or cocaine toxicity
Class 1 (Sodium channel blockers) action of what phase?
Phase 0; by decreasing slope
Class 1A: drugs?
quinidine, procainamide, disopyramide
Class 1B: drugs?
lidocaine and mexiletine
Class 1C: drugs?
flecainide, propafenone
Class 1A MOA:
prolong the AP, prolong the QT (causes torsades de pointes) , increases effective refractory period
Class 1A SE:
reversible SLE like symptoms ( esp. procainamide) , cinchonism ( esp. quinidine) and heart failure (disopyramide)
Class 1A used for?
atrial and ventricular arrhythmias
Class 1B MOA
decerase AP duration
Class 1B used for?
best for: ventricular arrhythmias that are post MI
Class 1C MOA
prolong ERP in AV node and accessory bypass tracts
Class 1C used for?
use for SVTS ; CONTRAINDICATED POST MI ;
Mneumonic for Class 1 anti-arrhythmics (Sodium) channel blockers
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