cardio drugs Flashcards
primary essential HTN treatment
diuretics, ACE inh, ARBs, Ca2+ channel blockers
HTN with CHF treatment
diuretics, ACE inh, ARBs, beta-blockers (compensated CHF, not decompensated or cardiogenic shock), aldosterone antagonists
HTN with DM treatment
ACE inhibitors/ARBs, Ca2+ channel blockers, diuretics, beta-blockers, alpha-blockers
MOA of calcium channel blockers
block the V-dep L-type Ca++ channels of cardiac and smooth muscle –> reduce muscle contractility
which ca++ channel blockers work on the vascular smooth muscle?
amlodipine = nifedipine > diltiazem > verapamil
which ca++ channel blockers work on the heart?
verapamil > diltiazem > amlodipine = nifedipine
clinical use of ca++ channel blockers
dihydropyridine (except nimodipine): HTN, angina, raynauds
non-dihydropyridine: HTN, angina, atrial fibrillation/flutter
nimodipine: subarachnoid hemorrhage
toxicity of ca++ channel blockers
cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation
amlodipine
dihydropine ca++ channel blocker
nimodipine
dihydropine ca++ channel blocker
nifedipine
dihydropine ca++ channel blocker
diltiazem
non-dihydropine ca++ channel blocker
verapamil
non-dihydropine ca++ channel blocker
hydralazine MOA
inc cGMP –> smooth muscle relaxation, vasodilates arterioles > veins; afterload reductino
clinical use of hydralazine
severe HTN, CHF, first line for HTN in pregnancy, methyldopa, with beta blockers to prevent reflex tach
toxicity of hydralazine
compensatory tach, fluid retention, nausea, headache, angina, lupus like syndrome
hypertensive emergency drugs
nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam
nitroprusside
SA
increase cGMP via NO
may cause CN tox beause it releases CN
fenoldopam
D1R agaonist - oronary, peripheral, renal and splanchnic vasodilation, decrease BP and natriuresis
MOA of nitroglycerin and isosorbide dinitrate
vasodilate via increase NO in vascular smooth muscles –> increased cGMP and smooth muscle relaxation
dilates veins more than arteries
decreased preload
clinical use of nitroglycerin and isosorbide dinitrate
angina, ACS, PE
nitroglycerine and isosorbide dinitrate toxicity
reflex tach, hypoTN, flushing, headache
MOA of HMG - CoA reductase inhibitors
inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor
Side effects of statins
hepatotoxicity
rhabdomyolysis
MOA of niacin
inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis
Side effects of niacin
red flushed face which is decreased with aspirin or long term use
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)
what are the bile acid resins?
cholestyramine, colestipol, colesevelam
MOA of bile acid resins
prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more
side effects of bile acid resins
tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, cholesterol gallstones
MOA of fibrates
upregulates LPL leading to TG clearance
activates PPAR-a to induce HDL synthesis
side effects of fibrates
myositis (increased risk of concurrent statins)
hepatotoxicity
cholesterol gallstones
cardiac glycoside drug
digoxin
moa of cardiac glycoside
direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca++ exchanger/antiport –> increased intracellular calcium –> positive inotropy –> vagus nerve stimulation –> decreased HR
clinical use of cardiac glycosides
CHF, atrial fib
toxicity of cardiac glycosides
cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, hyperkalemia
what does ECG show with cardiac glycoside use?
increased PR decreased QT ST scooping T wave inversion arrhythmia AV block
what factors predispose to toxicity
renal failure, hypokalemia, verapamil, amiodarone, quinidine
antidote to cardiac glycoside use
slowly normalize k+, cardiac pacer, anti-digoxin Fab fragments, Mg2+
quinidine
class 1a
procainamide
class 1a
disopyramide
class 1a
lidocaine
class 1b
mexiletine
class 1b
flecainide
class 1c
propafenone
class 1c
metoprolol
class 2
propranolol
class 2
esmolol
class 2
atenolol
class 2
timolol
class 2
carvedilol
class 2
amiodarone
class 3
ibutilide
class 3
dofetilide
class 3
sotalol
class 3
verapamil
class 4
diltiazem
class 4
class 1 antiarrhythmics moa
Na+ channel blockers, slow or block conduction
decrease slope of phase 0 depolarization and increased threshold for firing in abnormal pacemaker cells
state dependent
hyperkalemia causes increased toxicity
moa of class 1a
increased AP duration, increased effective refractory period, increased QT
clinical use of class 1a
both atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT
toxicity of class 1a
cinchonism, reversible SLE like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de points due to increased QT
MOA of class 1b
Myositis (increased risk of concurrent statins)
hepatotoxicity
cholesterol gallstones
clinical use of class 1b
acute ventricular arrhythmias, digitalis induced arrhythmias. Best post-MI
toxicity
CNS stimulation/depression, cardiovascular depression
MOA of class 1c
prolongs refractory period in AV node
minimal effect on AP duration
clinical use of class 1c
SVTs, including atrial fib last resort in refractory VT
toxicity of class 1c
proarrhythmic, especially post-MI contraindicated in structural and ischemic heart disease
MOA of class 2
decrease SA and AV nodal activity by decreasing cAMP and ca++ currents
suppresses abnormal pacemaker by decreasing slope of phase 4
clinical use of class 2
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
toxicity of class 2
impotence COPD, asthma exacerbation cardiovascular effects, CNS effects metoprolol: dyslipidemia propanolol: exacerbates vasospasm in Prinzmetal angina contraindiated in cocaine users
how do you treat class 2 overdose?
glucagon
class 3 moa
K+ channel blocker
AP duration increase with increased ERP
increase QT
clinical use of class 3
atrial fibrillation, atrial flutter, ventricular tach (amiodarone, sotalol)
toxicity of sotalol
torsades de points, excessive beta blockade
toxicity of ibutilide
torsades de points
toxicity of amiodarone
pulmonary fibrosis, hepatotoxicity, hypothyroidism, hyperthyroidism, corneal deposits, skin deposits, photodermatitis, neurological effects, constipation, cardiovascular effects
moa of class 4
ca++ channel blocker, decreased conduction velocity, increased ERP, PR interval increase
clinical use of class 4
prevention of nodal arrhythmias, rate control in atrial fibrillation
toxicity of class 4
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
what are the other antiarrhythmics
adenosine, Mg++
adenosine
increased K+ out of cells –> hyperpolarizing the cell and decreasing calcium current
used for diagnosing and abolishing supraventricular tachycardia
very short acting (15 seconds)
adverse effects: flushing, hypotension, chest pain
effects blocked by theophylline and caffeine
mg2+
effective in torsades de points and digoxin
