Cardiac Flashcards
A 45-year-old man presents to the ED with blurry vision and headache. His blood pressure is 190/130 mmHg. How could you treat?
Nitroprusside, nicardipine, clevidipine, fenoldopam, or labetalol
What are the three indications for NO
Angina, pulmonary edema, and acute coronary syndrome
What are the calcium blockers?
dihydropyridines: amlodipine, clevidipine, nicardipine, nifedipine, nimodipine –> vascular SM
nondihydropyridines: verapamil, diltiazem
Fenoldapam MOA? use?
D1 agonist - severely vasodilates - dec BP
-used in hypertensive emergency
What are the clinical indications for the use of dihydropyridine calcium channel blockers?
For all but nimodipine = hypertension, angina (including Prinzmetal), Raynaud phenomenon;
for nimodipine = subarachnoid hemorrhages
When cant you use hydralazine?
CAD and angina- compensatory tachy
A 40-year-old woman with chronic hypertension has a positive pregnancy test. What is the first-line hypertensive therapy for her?
Hydralazine with methyldopa
How can the reflex tachycardia that is associated with hydralazine be prevented?
By administering hydralazine with a β-blocker
Which two β-blockers are contraindicated in angina and why?
Pindolol and acebutolol, as they are partial β-agonists and can increase myocardial oxygen consumption
What drugs are proven to improve survival in CHF?
ACEIS/ARBS, carvedilol, spironolactone
What are the s/e of the CCBs?
all: cardiac depression, peripheral edema, flushing, gingival hyperplasia
nondihydros: AV block, verapamil - constipation, hyperprolactinemia
MOA hydralazine?
vasodilates arterioles > veins - dec afterload
inc cGMP
What is a s/e you worry about with hydralazine?
lupus like syndrome - dec acetylation
MOA of nitrates
inc cGMP - vasodilate veins» arteries - dec preload
What is monday disease?
some people develop a tolerance for the vasodilating action of NO
What are the main meds used in angina?
Beta blockers - exertional - reduce contractility, dec HR
nitrates - dec preload and ejection time, inc HR - reflex
combined of both: dec BP, MVO2
nefedipine - vasospasm
nitrates
Which drugs dec LDL
statins> bile acid resins =ezetimibe= niacin > fibrates
which drugs inc HDL
all but ezetimibe - niacin does the most
which drug decreases TGs the most - why?
fibrates
Which drug inc TGs?
bile acid resins
Which cholesterol lowering agents can cause myopathy?
statins when combined with fibrates or niacin
Which drugs prevent cholsterol reabsorption at small intestine brush border?
ezetimibe
which drug upregulates LPL - inc TG clearance and activates PPAR-a to induce HDL synthesis?
fibrates
gemfibrozil, clofibrate, bezafibrate, fenofibrate
How does niacin work?
inhibits lipolysis
reduces hepatic VLDL synthesis
What are the s/e of niacin
red flushed face - use NSAIDs or just wait it out
hyperglycemia
hyperuricemia
What are the indications for digoxin?
CHF - inc contractility
atrial fib - dec conduction at AV node, depresses SA
MOA of digoxin
inhibition of Na/k ATPase
inc ca2+ - positive inotropy
stimulates vagus nerve - dec HR
(cholinergic s/e)
What vision complaint can occur with digoxin use?
Blurry yellow vision (also from cholinergic effects of stimulating the vagus nerve)—think van Gogh
Which lipid-lowering agent causes the greatest increase in high-density lipoprotein (HDL) levels? Which agents cause a more modest increase?
Niacin causes the greatest increase in HDL; statins and fibrates have a moderate effect on HDL, & bile acid resins increase it slightly
What medications dec digoxin clearance by displacing it from tissue binding sites? what can happen?
verapamil, amiodarone, quinidine
Long PR, short QT, ST scooping, T-wave inversions, arrhythmias;
What indicates poor prognosis with digoxin?
hyperkalemia
What should you measure before treating someone with digoxin?
creatinine levels
K+ levels - hypokalemia allows more digoxin to bind
what are the first line drugs for hypertriglyceridemia
fibrates
what drugs inc TGs
bile acid resins
which agents inc hepatic cholesterol synthesis
bile acid resins
fibrates
What is the order of sodium blocking in class I antiarrythmics? why does this occur
1c> 1a>1B
class IC displays the most use dependence - cause a delay in conduction speed that is out of proportion to prolongation of refractory period
sodium blocking effects intensify as the HR inc due to less time btwn APs for the medication for dissociate from the receptor
which drugs have an affinity for ischemic myocardium
IB - lidocaine, mexiletine, tocainide
what do class 3 antiarrythmics do
block potassium channels and prolong repolarization
which class exhibits reverse use dependence and what does this mean
class III - activate K + channels - the slower the heart rate the more QTC is prolonged
