What effect do BB's and nitrates have on ejection time?
nitrates decrease ejection time and BB's increase injection time
Name 5 drugs commonly used to Tx malignant HTN
nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam
Which aspect of the heart is most sensitive to the effects of Class II antiarrhythmics?
Which lipid-lowering agents act by upregulating LPL?
2 clinical indications of cardiac glycosides
CHF to increase contractility; Atrial Fibrillation to depress SA node and decrease AV conduction
What are 4 AE of bile acid resins
CHOLESTEROL GALLSTONES, decreased fat soluble vitamin absorption (ADEK), GI discomfort, tastes bad
Why does renal failure predispose to digoxin toxicity?
Althought most beta blockers fit into class ____ antiarryhthmics, sotalol is actually a class _________
How does the effect of class IC antiarrhythmics on AP duration differ from Ia and Ib
IC does NOT affect AP duration, Ia increases, Ib decreases
What are 5 determinants of myocardial oxygen demand?
End Diastolic Volume (preload), Blood Pressure (afterload), heart rate, contractility, and ejection time
What are 2 partial beta agonists that are contraindicated in angina?
pindolol and acebutolol
What autoantibodies might you expect in the blood of a patient who is on hydralazine having an AE?
anti-histone, these are the autoantibodies present in drug induced lupus, which hydralazine can cause
Which lipid lowering agents do patients not like because they taste bad?
bile acid resins
What are 6 EKG findings with digoxin toxicity?
increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block
What class is quinidine when used to tx the heart? What is its major AE?
Class Ia; cinchonism = headache and tinnitus
Name 2 class IC antiarrhythmics
Which class Ia anti-arrhythmic is associated with lupus-like syndrome? What antibodies?
Which 3 organ systems should you regularly monitor when a person is on amiodarone?
LFT's (hepatoxicity), PFT's (pulmonary fibrosis), and TFT's (hypo/hyperthryoidism)
Which CCB's are most effective on the heart (as opposed to vessels)?
Verapamil and diltiazem
What are 4 side effects of hydralazine?
Compensatory Tachycardia, Fluid Retention, Nausea, Headache, and LUPUS-LIKE SYNDROME
What are the 3 AE of fibrates?
Myositis, hepatoxicity, cholesterol gallstones
What are the 3 AE of Class Ib antiarrhythmics?
CNS stimulation or depression and CV depression, also can be a local anesthetic
What are 3 class I anti-arrhythmics
quinidine, disopyramide, procainamide
Compare and contrast the effect of BB's and nitrates on the End Diastolic Volume
BB's increase EDV because they decrease HR and increase filling time; Nitrates decrease EDV by decreasing preload
What is blocked by Class I, II, III, and IV antiarrhythmics?
Class I = Na channels, Class II = beta blockers, Class III = K channels, Class IV = Ca channels
What 3 factors predispose to digitalis toxicity?
Hypokalemia, renal failure, co-administration of quinidine
What toxicities do ALL class Ia anti-arryhthmics cause?
thrombocytopenia and torsades due to QT prolongation
Name 3 bile acid resins
Cholestyramine, Colestipol, Colesevelam
What drug is DOC for diagnosing and abolishing SVT?
Which drugs are first line for increasing HDL?
3 AE of niacin
Flushing, Acanthosis nigricans (hyperglycemia), Hyperuricemia (precipitating gout)
Which drug ONLY decreases LDL and does not affect HDL or TG's?
ezetimibe = decrease in LDL uptake by intestines
What is the treatment for beta blocker OD?
Why does quinidine predispose to digoxin toxicity?
it displaces digoxin from tissue binding sites and decreases its clearance
Why is it that class II antiarrhythmics act so heavily on SA and AV nodes?
Because, being beta blockers they decrease Ca currents which are necessary for upstroke in nodal tissue
What is the MOA of hydralazine? What drugs are often co-prescribed and why?
It increases cGMP in the ARTERIOLES thereby reducing afterload. It is co-administered with beta-blockers to prevent reflex tachycardia
The effect of adenosine is blocked by what 2 drugs?
theophylline and caffeine
What class is procainamide in? Major AE?
Class Ia antiarrhythmic; SLE like syndrome with anti-histone abs
Name 4 Class III antiarrhythmics. What is the mnemonic?
Amiodarone, Ibutilide, Dofetilide, and Sotalol (AIDS)
Why do DM pts get ACE inhibitors?
They are protective against diabetic nephropathy
Which drug prevents cholesterol reabsorption at the small intestine brush border?
Why would a CCB cause constipation?
Because Ca is needed for smooth muscle contraction in the gut
In whom (2) is hydralazine contraindicated? Why?
Coronary Artery Disease and Angina patients because it causes a reflex tachycardia due to its effect on reducing afterload
Which CCB's are most effective on vascular smooth muscle?
Amlodipine and nifedipine
How do cardiac glycosides increase contractility AND decrease HR?
CONTRACTILITY = inhibition of Na/K pump inhbits the Na/Ca antiport leading to greater Ca in cytoplasm = more contractility? HR is mediated by increasing vagal tone to heart
Name 3 class Ib antiarrhythmics
Lidocaine, tocainide, mexilitine
Which calcium channel is blocked by diltiazem? What about ethosuximide?
L type; T type
What is the major AE of ibutilide?
2 indications for nitrates
angina and pulmonary edema
What is the MOA of adenosine?
it increases K efflux out of the cell and hyperpolarizes it. It is thus the DOC in diagnosing and abolishing supraventricular tachycardia
What aspect of cardiac depolarization do ALL class I drugs acts on?
all decrease the slope of phase 0 depolarization
What cholinergic side effects occur with cardiac glycosides?
N/V, diarrhea, BLURRY YELLOW VISION
What is "Monday Disease" in industrial exposure?
People working with nitrates can develop tolerance to the vasodilating effects and then loss of tolerance during the weekend causes a reflex tach and hypotension with facial flushing on Monday
What are the 2 MOA's of niacin?
it inhibits lipolysis in adipose tissue and reduces VLDL secretion from the liver
Which drug used in malignant HTN is a D1 agonist?
What class is disopyramide in? Major AE?
Class Ia antiarrhythmic ; heart failure!
What is the antidote to digoxin toxicity?
Slowly normalize K, LIDOCAINE, cardiac pacer, anti-digoxin Fab fragments, Mg
What is the shortest acting class II antiarrhythmic?
Magnesium is useful for what 2 cardiac conditions?
torsades de pointes and digoxin toxicity
What is the MOA of nitroprusside?
Short acting increase in cGMP to decrease afterload by primarily acting on arterioles
Co-administration of what drug predisposes to digoxin toxicity?
Which CCB's are similar to BB's in their effect? Which are more similar to nitrates?
Similar to BB's = verapamil and diltiazem; similar to nitrates = nifedipine and amlodipine
Which drug are first line for decreasing triglycerides?
How is the effect of nitroglycerin and isosorbide dinitrate different from that of hydralazine?
All increase cGMP to dilate vessels; however, hydralazine predominately affects arterioles and the nitrates affect veins so they decrease preload
Which Class I class is best for MI and which is contraindicated?
Class I B = B est; Class I C = C ontraindicated
The formation of which molecule is prevented by statins?
mevalonate (produced from HMG-CoA reductase)
Class IV antiarrhythmics are used to prevent _________ and have this MOA _______
nodal arrhythmias (SVT) and they are CCB's
Which subset of class I drugs is particularly useful in treating digitalis toxicity?
Class Ib (LIDOCAINE, mexilitine, and tocainide)
In which setting of heart failure must you be cautious with the use of beta blockers?
Acute decompensated heart failure--they need all the contractility they can get
What are the AE of class IC antiarrhythmics?
proarrhythmic ESPECIALLY post-MI, and significant prolongation of AV node refractory period
Which cardiac drug can cause cyanide toxicity?
Which anticonvulsant drug can function as a class Ib antiarrythmic?
How do class II antiarrhythmics depress abnormal pacemakers?
decreasing slope of phase IV depol
Which lipid lowering agents can cause cholesterol gallstones and why?
Bile acid resins because the liver needs to use cholesterol to create new bile acids; also, fibrates
Which drugs are first line for decreasing LDL?
What effect to BB's and nitrates have on A) contractility and B) heart rate
BB's decrease contractility and HR but nitrates cause a reflex increase in HR and contractility
Name 6 AE of CCB's
Cardiac Depression, AV block, Peripheral edema, flushing (vasodilation), dizziness, and constipation
What is first line Tx of HTN in pregnancy?
Hydralazine and methyldopa
Which drug decreases VLDL secretion from the liver and inhibits lipolysis in fat tissue?
What are 2 AE of ezetimibe?
diarrhea (probably osmotic), and rarely, increase in LFTs
What is the major AE of sotalol?
torsades and excessive beta blockade
Compare and contrast the effect of Class Ia antiarrhythmics and Class Ib on the action potential duration
Class Ia increases AP duration so is useful for reentrant tachycardias; Class Ib decreases AP duration so is useful for ischemic tissue and POST-MI
What electrolyte imbalance may be present with digoxin toxicity?
hyperkalemia--a poor prognostic indicator
Why does hypokalemia predispose to digoxin toxicity?
it is permissive for digoxin to bind to the Na/K pump and have a more potent effect
2 AE of statins
increased LFT's (hepatotoxicity) and rhabdomyolysis
What is the physiological goal of anti-anginal therapy?
Decrease myocardial oxygen demand
What is the MOA of fenoldopam?
D1 agonist that acts on coronary, peripheral, renal, and splanchnic vessels causing vasodilation to decrease BP and facilitate natriuresis
Why does amiodarone have class I, II, III, and IV effects?
it alters the lipid membrane, thereby affecting all of the channels
Name 2 class IV antiarrhythmics
Verapamil and diltiazem
What cardiac drug can cause yellow vision?
Why wouldn't you give propanolol to a person using cocaine?
it can exacerbate prinzmetal's variant angina
Why is it that amiodarone can cause hypothyroidism?
It is heavily comprised of iodine, this can result in the Wolff-Chaikoff effect in the thyroid whereby there is autoregulation and decreased synthesis of T3/4
What does the statement "Class I anti-arryhthmics are state-dependent" mean
they selectively act on DEPOLARIZED tissue (i.e. their activity depends on the "state" of the tissue)
What is a unique AE of metoprolol? Of propanolol?
Metoprolol = dyslipidemia; propanolol = exacerbates prinzmetal angina vasospasm