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Cardio Drugs

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Drug

M.O.A.

Therapeutic Uses

Pharmacokinetics

Adverse Effects

Drug Interactions

Nuggets

Anti-lipoproteinemics

Lovastatin

[       HMG CoA  reductase inhibitor

[        à ñ synthesis of LDL receptors in liver à less LDL in system

 

[       òLDL,  òTGs

[       Slight ñ HDL

[       1st line therapy for ñLDL

[       Give po

[       Taken at night

[       Met by liver

[       GI

[       ñ Liver enzymes

[       Myopathy (rhabdomyolysis?)

[       Contraindicated in:

[       Preganancy

[       Hepatic insufficiency

 

[       CYP3A4 substrates

[       Possibly induces change in LDL composition

[       ò heart disease M&M separate from cholesterol ò effects

[       òinflamma-tion (?)

Gemfimbrozil

[       Fibric acid

[       ñ activity of LPL

[       Ligand for PPARa

[       ñVLDL clearance

 

[       ò VLDL à òTGs

[       ñHDL

 

[       Used for ñTGs

[       Types III, IV & V hyperlipoproteinemias

[       Well absorbed orally

[       GI

[       Skin rash

 

[       With statin à ñ risk of myopathy

[       May ò incorp. of long chain FAs into new TGs à òVLDL synthesis

[       Arrhythmias in older drugs

 

Cholestyramine

 

 

 

 

 

 

 

 

  

[       Bile Acid Binding Resin

[       Prevent bile acid reabsorption

[       ñchol. à bile acid à ñ brkdown

 

[       ò LDL

[       small ñ HDL

[       Used with HMG CoA inhibitors

[       Type Iia hypercholesterolemia (LDL receptor defect)

[       Not absorbed orally

 

[       Consipation

[       Mild steatorrhea

[       Can bind other drugs concurrently

[       Newer drug – Colesevelam à òadverse effects & drug interactions

Nicotinic Acid

[       ò synthesis of VLDL

[       inhibits lipolysis in adipose tissue

[       ò esterification of TGs in liver

[       ñ LPL

 

[       òVLDL (rapid)

[       ñHDL

[       òLDL

[       all types of hyperlipid disorders except LPL def.

[       Not 1st line

[       Well absorbed from all parts of intestinal tract

[       Cutaneous flush and pruritus

[       GI

[       Hepatic toxicity

[       Peptic ulcer

[       Hyperglycemia

[       ò glucose tolerance

[       hyperuricemia

[       Contraindicated in:

[       Pregnancy

[       Hepatic disease

[       Peptic ulcer

[       Gouty arthritis

 

[       ??

[       Because of toxicities not 1st line

[       Sustained release ñ risk of hepatic tox

[       Start with low dose and give with meals

Antiarrhythmic Drugs

Quinidine

[       Class 1a

[       Na+ channel blocker

[       Antimuscarinic & a blocker

 

 

 

 

 

 

 

 

 

 

  

[       SVTs

[       Ventricular arrhythmias

 

[       Give po

[       90% plasma bound

[       met in liver

[       T 1/2 - 6 hours

Cardiac

[       SA block

[       TPD

[       Paradoxical ñ on Ventricular rate when given for A flutter

[       Asystole or arrhtymias with QRS > 30% wider

 

Noncardiac

[       Cinchonism – tinnitus, dizziness, HA

[       GI

[       Hypotension

[       ò K+

[       ñ digoxin levels

[       may also block K+ channels à with GI effects beware of hypokalemia

[       Liver and Kidney insufficiency is problem

[       IM is painful

[       òK+ à ñ arrhythmias caused by drug (TDP, etc.)

Procainamide

[       Class 1a

[       SVT

[       Ventricular arrhythmias

[       Given po or IV

[       Met and excreted (L&K)

[       Met by acetylation – fast vs. slow

Cardiac

[       Similar to quinidine

[       NAPA is proarrhthmic à K+ blocker à TPD

Misc.

[       Hypotension

[       Lupus like syndrome

[       Antinuclear Abs

[       Rash and arthralgias

 

??

[       Metabolite – NAPA à proarrhythmic

[       òK+ à ñ arrhythmias caused by drug (TDP, etc.)

Disopyramide

[       Class 1a

[       Antimuscarinic

[       Ca++ channel blocker à negative ionotropic activity

 

[       SVT

[       Ventricular arrhythmias

 

[       Not specified

 Cardiac

[       See quinidine

[       Antimuscarinic effects (SA block) ñ

[       ò contractility

 

[       òK+ à ñ arrhythmias caused by drug (TDP, etc.)

Lidocaine

[       Class 1b

[       Slows conduction in depolarized tissue – little effect on normal tissue

[       Blocks Na+ channels in inactivated state

  

[       Ventricular tachycardias following MI, heart surgery

[       After cardioversion

[       Given IV or IM

[       Blood levels have biphasic decline

[       Protein bound

[       CNS: parathesis, drowsiness

[       Convulsions

[       Hearing disturbances

[       Respiratory arrest

[       Liver disease will ñ levels

[       Blockade rapidly reverses between beats

[       Elderly are more sensitive to side effects

[       Silences diseased tissues à no reentry

Propafenone

[       Class 1c

[       Na+ channel blocker

[       Variable b-blocker activity

[       SVTs

[       Life-threatening ventricular arrhythmias

[       Not specified

[       Proarrhythmic

[       Slow to dissociate from Na+ channels à likes active channels

 

[       BAD DRUG but flecainide/ecainide are worse – CAST study

Propanolol

[       Class 2

[       b-blocker

[       òSA node & AV node activity

[       ñrefractory period of AV node

[       Direct effect on Na/K channels

 

[       Catecholamine induced arrhythmias à emotion/exercise

[       After MI

[       SVTs

 

[       Given po

[       Worsen CHF

[       SA & AV block

[       Sudden withdrawal à worsen angina or arrhythmias

 

[       Not specified

[       Chronic use will ñ b receptors

 

 

Amiodarone

[       Class 3 – K+ channel blocker, ñ APD

[       Na+ channel blocker

[       Ca++ channel blocker

[       b-blocker

[       Prevent V fib & V tach

[       SVTs

[       Extensively tissue bound

[       Met by liver

[       1-2 month half life

[       Mets are active

[       Pulmonary toxicity

[       Thyroid toxicity

[       Hepatic toxicity

[       Photosensitivity

[       Neurologic

[       ñ plasma levels of antiarrhythmics

[       + b-blockers or Ca++ blockers = sinus arrest or complete heart block  & worsen CHF

[       Blocks T­4 à T­3 conversion

[       Very effective but not used because of toxicities

Bretylium

[       Class 3 – K+channel blocker, ñ APD

[       Specific for ventricle

[       Transient NE release followed by ò NE release

 

[       Drug-resistant V fib

[       Sustained V tach

[       IV use

[       Hypotension (due to ò NE)

[       None specified

 

Solatol

[       Class 3

[       b-blocker

[       SVTs

[       Ventricular arrhythmias

 

 

[       Not specified

[       TDP

[       Not specified

 

Verapamil

[       Class 4 – Ca++ channel blockade (think slow)

[       ò AV node conduction (ñ PR)

[       SVT due to AV nodal reentry

[       òventricular rate in A flutter

[       Not specified

[       Contraindicated in:

[       Severe heart failure

[       Hypotension

[       SSS

[       AV block

[       V tach

[       WPW syndrome

 

[       Used with b-blockers or digitalis à bradycardia or AV block

[       ò contractility

 

Adenosine

[       No classificaton

[       Opens K+  channels

[       Hyperpolarizes AV nodal tissue à ñ refractory time

[       ñ K+ activity in SA & AV

[       ò cAMP à Ca++ (opp NE)

 

 

[       Paroxysmal SVT

 

[       Very short duration of action

[       Not specified

[       Not specified

[       Considered safer than verapamil

 

Cardiac Glycosides

Digoxin

(Digitalis)

[       Inhibits Na/K ATPase à ñ Na+  à òNa/Ca exchanger activity à ñ Ca++  è ñ contractility

[       ñ Parasympathetic activity à ñ refractory period of AV node

[       CHF

[       òventricular rate in A flutter/fib prior to quindine to block arrhythmia

[        

[       Given po or IV (no IM!)

[       T1/2 = 6 days

[       Excreted by kidneys

[       Very common

[       High doses à ñ sympathetic activity

 

Cardiac

[       Ventricular extrasystoles (DAD)

[       SA block & AV block

[       AV junctional rhythm

 

Misc.

[       GI – anorexia, nausea, diarrhea

[       CNS – HA, aphasia, confusion, delirium, altered color perception

[       K+ depleting diuretics

[       Quinidine, verapamil & amiodarone à ñ digoxin concentration

[       Drugs that induce hepatic enzymes

[       Toxicity due to òK+ (from diuretics, etc.)