There are 4 classes of anti-hypertensive, including _____, ______, _____, & _____. 

The class which acts as Ca2+ channel blockers are called = _______.

The class which includes centrally-acting drugs = _______.  What other kinds of drugs are in this class?

90% of HTN is (secondary/ essential) ______.

How high must systolic/ diastolic pressure be to be considered HTN?

Which class of drug should you use first in treating HTN?

β-blockers and α-blockers are ______ drugs in the _____ drug class. 

A non-selective β-blocker is _______; selective β1-blockers include______ & ______; and an α-blocker is _______.  A mixed β-blockers and α-blockers is _______. 

Sympatholytics, Renin-Angiotensin Inhibitors, Vasodilators, & Diuretics.

Vasodilators

Sympatholytics

(centrally acting drugs & peripheral adrenergic receptor blockers)

Essential (primary)

Sustained systolic BP>/= 140, or diastolic >/= 90 mmHg

Diuretic

peripheral adrenergic receptor blockers, symatholytic drug class

propanolol

metoprolol, atenolol

prazosin

carvedilol

Peripheral adrenergic receptor blocker selectivity is relative to ______.

What do β-blockers decrease (CO or TPR) and how?

What do α-blockers decrease (CO or TPR) and how?

Where are β2 receptors located, and what happens when stimulated?

Where are α1 receptors located, and what do they do?

If you wanted to tx a hypertensive patient who also is hyperlipidemic or diabetic, would you Rx a β-blocker or an α-blocker?

What are the main SE for Prazosin?

What are the centrally acting sympatholytic drugs?

The former drug works as a ______, and is used for severe ______.  SE's include: _____, _____, & _____ (upon withdrawal after chronic use).

The latter drug works as a ______, and is used for ______.  Which receptor types does it stimulate?

Dosing!  Start low, go slow.

Decrease HR and contractility, which decreases cardiac output, which decreases blood pressure - by blocking β1 in the heart.

Decrease total peripheral resistance, which decreases mean arterial pressure, by acting as antagonist on vasculature (α1) (remember that α2's are centrally located)

lungs - bronchodilation

vasculature - vasodilation

sk. mm and liver - increase blood glucose

vasculature - vasoconstriction

Selective α1-blocker - Prazosin

Reflex tachycardia (if too high of dose), orthostatic hypotension, and fluid retention

Clonidine and α-Methyldopa

Clonidine = α2-agonist, for severe refractory HTN

SE's= dry mouth, sedation, and rebound HTN upon withdrawal after chronic use (b/c NE receptors were upreg'd)

α-Methyldopa = false neurotransmitter for chronic use

Replaces NE, but less effective for stimulating α-1. (more effective for α-2 receptors)

Clonidine =

α-Methyldopa =

Carvedilol =

Metoprolol =

Atenolol =

Prazosin =

Propanolol =

α2 agonist, centrally acting

α receptor agonist (false Nt)... α2>>α1, centrally acting

Mixed β1-, β2-, and α1-blocker

Selective β1 blocker

Selective β1 blocker

α1-blocker

non-selective β blocker

Renin-angiotensin system inhibitors include 3 main types of drugs, including _____, _____, & _____. 

The "-PRILs" stand for this class =

The "-SARTANs" stand for this class =

Aliskiren =

ACE (-)'rs include _____, _____ and _____. This class works by blocking conversion of ____ to ____, and thus blocking ______, _____ & ____ release.  It also blocks the breakdown of ______.  Why is this important?

What happens when AngII is decreased?

ARB's include ______ & ______.  This class works by blocking release of _____, ____, and blocking ______.

Why is it advantageous to block renin directly with this drug: _____?

These drugs are all used for _______ HTN, ____, and ______.

ACE inhibitors (Angiotensin Converting Enzyme (-)'rs, ARB's (Angiotensin II receptor Blockers), Direct Renin inhibitor.

ACE (-)'rs

ARBs

Renin inhibitor

Captopril, Enalapril, Lisinopril

blocks conversion of Angiotensin I -> II; blocks vasoconstriction and release of ADH (H20 retention) & Aldosterone (Na+ retention). 

Blocks breakdown of bradykinin -> more robust vasodilatory effect!

Decreased PVR, decreased afterload

Losartan & Valsartan.  Blocks release of ADH, Aldosterone, and blocks vasoconstriction.

drug: Aliskiren ? --> b/c ACE (-)'rs and ARBs both increase Renin levels.

essential HTN, early stages of HF, Diabetic nephropathy

Captopril is a ______.  It has a (high/ low) ____ bioavailability, and has the (shortest/ longest) ____ T1/2.

What else are ACE (-)'rs indicated for?

What is it the DOC for?

What are the main SE of this class of drug?

What is a bonus of using these drugs, and what co-morbidity might it be useful in?

What population is this class less effective in?

Does this class have effects on lipid profiles or glycemic control?

Which drug in combo might interfere with PGI2-mediated vasodilation?

Losartan is a ______. 

How does it work, specifically?

SE's?

What happens with diabetic patients?

When is this drug used? 

Any special concerns with different populations?

ACE inhibitor

the HIGHEST bioavailability, with the SHORTEST T1/2.  (This means compliance will decrease b/c need to take more frequently!!)

HTN, HF, Renal protection in diabetics, LV dysfunction

HTN in diabetics

Non-productive cough, angioedema (b/c bradykinin is a vasodilator), Hyperkalemia (b/c aldosterone (-)'d), Fetotoxic, Renal failure

1. anti-inflammatory effect; reduces vascular complications assoc'd w/ DM type 1

2. cardioprotective; especially for CAD patients.

African Americans

No.

NSAIDs

Angiotensin II receptor Blocker (ARB) (1st generation)

Blocks AT1 receptors, thus AT2 receptors are more stimulated.

Well tolerated, Less cough than ACE1, still Fetotoxic

slows progression of nephropathy

when ACE-1 is not tolerated

less effective as anti-hypertensive in blacks.

An example of a Direct Renin Inhibitor, or DRI, is _____

How does it work?

Why is this important?

Vasodilators work by this general MOA: ______.

There are three main drug classes involved, including _____, and these prototypic drugs: _____, _____.

There are also 2 others less frequently used for chronic tx:_____ & ______.

How do the first 3 vasodilators decrease blood pressure?

What 3 things happen if they are not doses properly?

Do they have effects on serum lipids?

Aliskiren

Binds Renin and prevents formation --> Angiotensin I, lowering plasma renin, AngI, AngII, and Aldosterone.

Renin has mitogenic effect, and is increased with ARB's and ACE(-)'rs.

Block L-Type Ca2+ channels

DHP's (dihydropyridines) - DIPINEs

Diltiazem, Verapamil

Hydralazine, Minoxidil

promote vascular smooth muscle relaxation, decrease TPR

↑ Contractility, HR

↑ Myocardial O2 consumption

↑ RAAS system

No

Amlodipine and Nifedipine are both examples of _____.

What category does this class belong to?

In terms of selectivity, where do these drugs work: cardiac or vasc:

DHP -

Verapamil -

Diltiazem -

How do Ca2+ channel blockers (CCBs) affect conduction in the heart, and what effect do they have on coronary blood flow?

Which drug is most likely used for antihypertensive tx?

What if HR and BP is high?

Which drug is most likely to cause reflex tachycardia?

Which drug increases cGMP similar to NO?

Which drug opens K+-ATP channels (what does this do)?

When are these 2 drugs used/ when are they C/I'd?

DIPINEs = DHPs

Vasodilators

DHP = vasculature

Verapamil = cardiac

Diltiazem = both

Slow AV conduction and SA rate

improve coronary blood flow

DHPs

Ditiazem

DHP if given too fast, b/c heart thinks it needs to pump more to increase TPR.

Hydralazine

Minoxidil (oral) - hyperpolarizes the cell and makes it harder for Ca2+ channels to open.

Severe HTN, C/I's for angina or ischemic heart disease

Diuretics used for HTN include the following classes: _____, _____, & _____.

Furosemide if from _____

Amiloride f/ ______

Hydrochlorothiazide f/ ______

Spironolactone f/ _______

What are the clinical considerations of diuretics in tx'ing HTN as compared with DHP's or ACE(-)'rs?

What are the advantages to fixed drug combos, and what are the disadvantages?

What are some of the combos out there?

Thiazides, Loop diuretics, & Potassium-Sparing diuretics

Loop = furosemide

K+ sparing = amiloride, spironolactone

Thiazide = hydrochlorothiazide

Most effective tx, especially considering ethnicity differences; least SE's; Frequency of dosing is less; cost is reasonable.

+: Compliance

-: Impossible to adjust dose of 1 and not the other

β-blocker, ACE (-)'r, or ARB & Diuretic;

Ca2+ channel blocker & ACE (-)'r

How does the presence of co-morbidities affect the following in?

Thiazide diuretic + β-blocker:

ACE (-)'rs:

ACE (-)'r + diuretic:

β-blocker or CCB:

Diuretics + CCB:

Both adversly affect lipid profiles and insulin sensitivity (exacerbate CAD, atherosclerosis, DMII)

Beneficial for diabetic nephropathies

Useful for ventricular dysfunction

Useful for angina

Blacks respond better to each, vs β-blocker or ACE (-)'r

Thiazide diuretics are most appropriate for treating (HTN or HF) ______, and include this drug: _____.

Loop diuretics are most appropriate for treating (HTN or HF) ______, and include these drugs: ____, ____.

Potassium sparing diuretics are used as ______ , and include these drugs: ____, ____, & ____.

What is the rationale for using diuretics in HTN?

in HF?

Diuretics promote _____.

List the relative potencies of diuretics f/ most to least:

Where is Renin produced?

What determines perfusion and filtration of the kidney?

Where is the most predominant site of Na+ reabsorption?  2nd most?

Thiazides for HTN: hydrochlorothiazide.

Loops for HF: Furosemide, ethacrynic acid

K+ sparing as adjuncts to maintain K+: spirinolactone, amiloride, eplerinone

↓ blood V and TPR → ↓'s preload → ↓'s CO → ↓'s BP

↓ blood V → ↓'s preload (cardiac work), ↓'s congestion (edema)

Natriuresis (Na+ excretion), and since water follows Na+, diuresis.

Loops>> Thiazides >>>>> K+ Sparing

Macula Densa in kidney

Afferent and Efferent renal arterioles

Ascending loop of Henle (40%)

2nd most = distal convuluted tubule (10-15%)

Hydrochlorothiazide is indicated for ______.  Short term effects = _____, whereas LT effects = _______.  In combination, it can be used for ______ with other _______ drugs.

Its dose response curve shows: ______.  This means??

Where do thiazides work?

How do they work, specifically?

What condition are they ineffective in and why?

What other drug can interfere with function, and why?

SE's of thiazides include ____, _____, and it increases ____, ____, & _____.

What 2 conditions does it have a positive SE for, and what are they?

mild HTN.. 1st line Rx of HTN in non-diabetics!!

ST = ↓'s blood V

LT = ↓'s TPR (loses diuretic effect, but controls intracellular Na+ in vasc, which reduces IC Ca2+)

In combo w/ anti-hypertensives => moderate HTN

Flat dose response curve = increasing dose doesn't increase effectiveness!!

DCT (modest effect)

Inhibits Na+/Cl- co-transport

Renal insufficiency b/c requires filtration/ secretion to work!

NSAIDs -> require renal prostaglandins to work

hypokalemia, metabolic alkalosis (more Na+ in CD so the potential is there to lose K+ and H+) increases: blood Glc, lipids, & uric acid

Osteoporosis & kidney stones (increases blood Ca2+, and decreases urine Ca2+)

Furosimide and ethacrynic acid are considered "_______", because they work in a dose-(independent/ dependent) _______ manner.  They are in this class: ____.

When is ethacrynic acid used?

What are they indicated for?

Where and how do they work?

How are they different from Thiazides in regards to renal insufficiency?

Do they have any similarities with Thiazides?

SE's include ______, _____, _____, & ______.

high-ceiling diuretics, dose-dependent manner

Loop diuretics

ethacrynic acid is used for sulfonamide allergy

severe edema, ie HF (not HTN)

block Na+/K+/Cl- transport in ascending loop of Henle

effective for renal insufficiency b/c they directly increase renal blood flow, whereas thiazides require filtration/ secretion and are not effective.

Yes -> NSAIDs interfere b/c require renal prostaglandins to work

Hypokalemic metabolic alkalosis, hyperuricemia, hypovolemia, ototoxicity

Decreases Mg2+ and Ca2+!!

GREATER RISK THAN THIAZIDES!!

Epelerone is an example of a ______, as are these two: _____, _____.

How do they work as a class?

They are useful in combo with loop diuretics and thiazides. Why?

What must you be cautious of, especially if CHF patient is on ACE (-)'r?

Spirinolactone's MOA is slow because: _____. (How does it work?)

SE's include _____ & ____ in men, and _____ & ____ in women.

What condition is this also indicated for?

Anything else about spirinolactone?

K+ sparing diuretic

spirinolactone, amiloride

antagonize aldosterone effects

prevents hypokalemia

be cautious of hypERkalemia

has a hormone-related effect: inhibits aldosterone-induced synthesis of pumps, and competitively binds to aldosterone receptors nonselectively (mineralcorticoid, androgenic, and progesterone receptors), but has no effect on pumps already processing.

Men: gynecomastia, ED

Women: menstrual irregularities, hirsutism

hyperaldosteronemia (surprise, surprise!)

YES! -- improves morbidity and mortality in pts with end-stage HF independent of K+ sparing effects! WOW!

The drug that is more specific for aldosterone receptors in the kidney than spirinolactone is _____, and therefore SE are reduced.

This drug is approved for _____ and _____.

What can increase blood levels of this drug and why?

Does this drug have anything in common with spirinolactone??

How does the last of the K+ sparing diuretic drugs, ____, work?

How does its onset of action compare with spirinolactone?

SE?

eplerenone

HTN and post-MI LV dysfunction

grapefruit juice, veparamil, erythromycin --> anything that inhibits CYP450 3A4 !

YES, it is cardioprotective because decreases aldosterone... aldosterone is associated with increased endothelial dysfunction and fibrotic effects in HTN, HF, atherosclerosis.

Amiloride works by directly inhibiting pumps in distal tubules and CD's, therefore INDEPENDENT of aldosterone.

onset of action is FASTER b/c no gene expression needed

hyperkalemia

Drugs for heart failure include these classes: _____, _____, _____, _____, _____, & _____.

What is important to have balanced before you begin treating CHF patients?

What is the main problems in CHF, and what two things does it trigger?

The hallmarks of HF include a reduced ____ and ____ for a given fiber length, or ______.

Systolic dysfunction (dilated ventricle, myocardial ischemia) = ↓'d _____.

Diastolic dysfunction (decreased compliance, decompensated hypertrophy)= ↓'d _____.

LV failure leads to ____ and RV failure leads to ____.

Does stroke V improve with SNS stimulation?

Diuretics (furosemide), Aldosterone Antagonists (K+ sparing diuretics to reduce cardiac remodeling), B-blockers, Vasodilators (CCB and direct acting), Angiotensin inhibitors, Positive Inotropic Agents (for later stages).

Must be hemodynamically balanced!! Preload = afterload.

↓'d CO & perfusion -> ↓'d carotid sinus firing (+'s SNS to increase CO by TPR) & ↓'d renal blood flow (increases RAAS to increase flow, leads to retention of Na+ and vasoconstriction -> makes heart work harder!)

stroke volume & CO

for a given end-diastolic volume

systolic = decreased contractility

diastolic = decreased filling (relaxation is slower)

hypoxemia

peripheral edema (and eventual LV failure)

Yes, short term is good, long term = remodeling.

When should you put a post-MI patient on a Beta blocker?

If a patient has no sxs but is at risk for HF, what should they be tx'd with?

What if they have some evidence of structural changes, but no sxs?

Sxs and structural changes?

Full blown HF?

ACE (-)'rs decrease AngII, and (-) bradykinin breakdown, which in turn (+)'s _____.

What do ACE (-)'rs, ARB's, and beta blockers have in common for CHF?

What makes them different?

Which beta blockers are good for HF?

How does the mixed blocker help in HF?

as soon as hemodynamically stable

ACE-I, ARB

ACE-I, beta-blocker

Loop diuretic, ACE-I, beta blocker, digoxin

LVAD, transplant, IV inotrope

TPA (fibrinolytic).. vasodilation

slows down remodeling/ progression of HF, improves survival

ACE: Hypotension or acute renal failure (1st dose effect), cough,

Beta-blocker: protects heart by decreasing chronic neurohumoral activation, equally effective in blacks/ whites, can cause AV block

Metoprolol and Carvedilol

decreases TPR via a1 blocker, decreases cardiac work via b1 blocker (decreases HR, afterload, contractility)

Positive inotropic agents include _____, _____, and ____. 

Digoxin belongs to the ______ class, and is used for ______ HF, especially for dilated LV, a (systolic/ diastolic)_____ dysfunction.  It can also be used for ______. 

MOA =

When must dose be adjusted?

Digoxin's SE ?  EKG effects?  What makes SE worse?

If too much digitalis is in the blood, what will SE be?

What must you be cautious of and monitor for?

Cardiac glycosides, β-agonists, and PDE (-)'rs (phosphodiesterase inhibitors)

digoxin = cardiac glycoside

used for symptomatic HF, especially for systolic dysfunction

also used for rate control for atrial fibrillation

- increases IC Ca2+ via inhibition of Na+/K+ ATPase pump -> indirect activation of Na+/ Ca2+ exchanger.

- negative dromotropic (conduction) effects => slows conduction in AV node

Renal failure

Low therapeutic: toxic ratio; GI upset, arrhythmias with increased automaticity and heart block (increased with hypokalemia), "Digitalis effect" on EKG (assymetric ST segment depression with inverted T waves).

PVC's (premature ventricular contraction), VTach, atrial tachycardia with block

Arrhythmia increases with hypokalemia, monitor electrolytes, creatinine

Dobutamine is in the _____ drug class, along with this drug: ______. 

It is used to Tx ________.

The second drug helps to maintain _____ but increases ______ in high doses.

Both are indicated for ___________, and provide a (ST/ LT) ______ benefit.  How are they administered?

SE of both = ?

Milrinone is a _______, and is indicated for _______. 

Its MOA is _______.

What is it typically used in combo with, and how is it used?

β-agonist

dopamine (non-selective β and α-agonist)

doputamine tx's severe decompensated (acute) HF in the ICU

BP, TPR

HF refractory to other measures

short term benefit (days)

continuous IV infusion in the ICU

SE = arrhythmias, tachycardia

Phosphodiesterase inhibitor, for HF refractory to other measures

MOA = inhibit PDE III, increase cAMP, increase myocardial contractility, peripheral vasodilator

Used with vasodilator, for short term only.

The PDE inhibitor drug is called ______.

The B-agonists include: ______, _____.

The cardiac glycoside is called ______.

Vasodilators are used for HF, including ______ and _____, which are used in combination.

The first group includes ______ & ______.  These are indicated for acute HF combined with either: _____ or _____.

Which one improves survival in blacks, but not Caucasians?

Which one is a direct vasodilator via cGMP?

What is the MOA for nitrates?

What is the concern with RV failure patients on nitrates?

Milrinone

dopamine, doputamine

digoxin

Nitrates and Hydralazine

nitroglycerin & sodium nitroprusside

hydralazine or loop diuretic

Hydralazine

Generates NO which (+)'s guanylate cyclase to reduce myosin light chain kinase activation

may decrease preload too much

What is the cornorstone for HF tx?

What about in black populations?

Which diuretic drug decreases Ca2+ and may be used for hypercalcemia?  When is this drug used in HF?

Which drug is used for class III and class IV heart failure?

Which drugs may cause hyperkalemia, especially if used with potassium supplements?

What is the beta-blocker of choice for HF?

ACE (-)'rs!!!

Blacks:  hydralazine plus isosorbide dinitrate

furosemide (loop).  used for acute and chronic HF (diuretic of choice)

Spirinolactone

K+ sparing drugs (direct acting)

Carvedilol

The nitrates used for HF include ______ & ______.

Organic nitrates are used for _______.  They include _____ & _____. 

Which is short acting and which is long acting?

How are these drugs administered?

Why is the patch form only applied in 10-12 hr intervals?

What occurs in high doses?

SE include ____ and ____.

Why should sildenafil (Viagra) be avoided with this class of drugs?

What is the main MOA of these drugs?

Nitroglycerin & sodium nitroprusside

Angina pectoris, improve exercise capacity, and coronary spasm

Nitroglycerin & isosorbide dinitrate or mononitrate

NTG = short acting, sub lingual/ mucousal spray

Isosorbide dinitrate-NTG = long acting, slow release capsules or patch/ointment

Tolerance can develop with long acting preps

High doses => mild arteriolar dilator

SE = Headaches, hypotension

May cause severe hypotension

VENOdilator, releases endothelial NO, decreases myocardial O2 demand (decreases preload) and coronary spasm.

Isosorbide dinitrate is used to tx ______.

The antiAnginal drugs include _____, _____, _____, ______, & _____.

Which two drugs do you want to avoid use together, and why?

Verapamil is (cardiac/ vasc)____ specific, and can cause negative ______, ______, & ______ effects, which slows conduction.  How does diltiazem compare?

What are some of the cautions with using this drug with HF?

What drugs does it interact with?

What are the SE of Ca2+ channel blockers?

Which drug used for tx of angina is a venodilator?

Which is a vasodilator?

What are the EKG effects of using verapamil or Diltiazem?  How can you prevent this?

angina (and HF when combo'd w/ hydralazine!)

Organic nitrates, CCB's, β-blockers, Ranolazine, & heme drugs (ASA, etc)

AVOID Diltiazem or Verapamil with β-blocker (causes heart block, bradycardia)

cardiac specific

causes negative dromotropic, inotropic, and chronotropic effects that slow conduction and decrease myocardial O2 demand (decreases afterload).

Diltiazem is similar but with LESS negative dromotropic or chronotropic effects.

Can worsen HF!! Can cause sinus node dysfunciton and heart block!

Increases digoxin levels!

Fatigue, HA, edema, constipation (verapamil), sinus and AV node dysfunction with V and D

Veno = Nitroglycerin

Vaso = Ca2+ channel blockers

sinus bradycardia, increased PR interval leading to heart block (esp in patients with underlying conduction dz)

-- Use preps with long T1/2 (amlodipine) or slow release

Which β-blockers are used for angina?

Which β-blockers are lipophilic?

Hydrophillic?

How do these properties affect SE?

What can all β-blockers cause?

When do you want to avoid the use of β-blockers?

Which drug is used for Tx of chronic stable angina in pts who do not respond to conventional regimens?  How is it Rx'd?

What is the MOA?

What can it cause in a dose-related manner?

atenalol, propanalol, metoprolol, timolol (non-selective)

Lipophilic = propanolol, metoprolol

Hydrophilic = atenolol

Lipophilic cross BBB and cause nightmares, fatigue, sexual dysfunction, mask hypoglycemia.

sinus and AV node dysfunction

AVOID w/ acute HF (use in chronic HF)

also, avoid with Diltiazem or Verapamil, and in asthmatics

Ranolazine!

Used in combo with nitrate, BB, or amlodipine

late Na+ channel blocker -> leads to reduced intracellular Ca2+ overload

QT interval prolongation (esp with D or V or with CYP3 blockers)

What is the most effective class of drugs for lowering an elevated LDL-C?

How does it work?

What are the main SE for this class?

Which drugs inhibit the metabolism of these agents?

An inhibitor of intestinal absorption of cholesterol is ______.  This drug has SE that make sense with its MOA: ______.  Also, avoid in pts with _____.  It likely has a synergistic effect when used with _____.

The other classes of lipid-regulating drugs include: ______, _____, _____, & _____.

Of these, the 2nd line to statins is _____, the one that activates lipoprotein lipase is _____ (and thus targets VLDL), the one that causes flushing is ______, and the one that inhibits hepatic triglyceride synthesis / enhances clearance is _____.

HMG CoA reductase inhibitors (STATINS)

Inhibits RL step in hepatic cholesterol/ LDL-C synthesis

increased LFT's, myopathy (dose related and enhanced by drugs that inhibit statin metabolism)

FCK M

Fibrates, Cholestyramine, macrolide ATBs, Ketoconazole

Ezetimibe

mild GI sxs

liver disease

synergistic effect with statins

Bile acid binding resins, Fibric acid derivitives (fibrates), Niacin (nicotinic acid), and Omega 3 FA.

Bile acid binding resins = 2nd line

Lipoprotein lipase (+)'r = Fibrates

Flushing = niacin

INhibits hepatic TG synthesis = Omega3 fa

Cholestyramine is a _______ agent, and thus its MOA is: ______.  SE include _____ and ______, and it may interfere with other drugs (___x4). 

The other drug in this class is called ______.

The fibrates include _____ & _____, and are especially good at decreasing ______ by activating this enzyme: ______.  The SE for these drugs is _____.

How do you decrease flushing with niacin use?

What drug may reduce risk of CHD?

bile acid binding resin

binds intestinal bile acids, interupts entero-hepatic recycling

SE = flatulance, constipation

digoxin, warfarin, phenobarbital, thyroxin

Colestipol

Gemfibrozil, fenofibrate

VLDL

lipoprotein lipase

myopathy

Pretreat with ASA

Omacor-3

Antiarrhythmic drugs may have proarrythmic effects, including _____ and _____.  They also have toxic side effects, and thus drug selection must be ______.

They are organized by class as follows.  List what each class blocks, the general MOA, indications, major drugs in the class, and ECG effects if they have them.

Class I =

Class II =

Class III =

Class IV =

"Others" =

Ventricular tachyarrythmias (VTach and Torsades de Pointes)

individualized

I: Na+ channel blockers

(ECG effects = ↑'s QRS duration, prolongs QT interval)

IA: Procainamide. MOA: blocks fast Na+ channels & K+ channels. Ind - maintain sinus rhythm w/ AFib; some V arrythmias. Drugs: Quinidine, disopyramide.

IB: Lidocaine (IV), tocainide (oral lidocaine congener/ derivitive).  MOA: Strong affinity Na+ channels in depol ischemic tissue; spares normal tissue. Ind - Ventricular arrythmias. 

IC: Flexainide, propafenone.  MOA: Blocks fast Na+, slows conduction throughout heart, esp in His-Perkinje system; Proprofenone has mild BB effects. Ind - same as IA, except used for life threatening V arrythmias also.

II: β-blockers

Propanolol, metoprolol (post-MI, HF), esmolol (for emergencies & Sx).

Ind - Supraventricular arrythmias, V arrythmias

MOA: slows conduction thru AV node, (-)'s SNS activation of automaticity

III: K+ channel blockers

MOA: prolong AP and refractory period

Ind - see class IA

ECG: prolonged QT interval

IV: Ca2+ channel blockers

MOA: slow conduction through AV node

Ind- supraventricular arrythmias

Others: Adenosine

MOA: Slows conduction thru AV node, increases refractory period by cell hyperpolarization

Ind - Termination of paroxysmal supraventricular tachycardia (PSVT)

ECG: breif asystole or AV block following cardioversion to sinus rhythm