Cardiology Drugs- Firstaid

Front 1

Class I - Sodium channel blockers

Back 1

Local anesthetics, slow or block conductance (esp in depolarized cells), slow the slope of phase 0 depolarization (increase ERP) and increase the threshold for firing in abnormal pacemaker cells.
-Hyperkalemia causes increased toxicity for all drugs

Front 2

Class IA

Back 2

Quinidine, Procainamide, Disopyramide
Mechanism- Increase the AP duration, Increase ERP, increase QT interval
Use- Atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VTs
Toxicity- Quinidine causes cinchonism; torsades de pointes (increased QT); procainamide causes SLE-like syndrome

Front 3

Class IB

Back 3

Lidocaine, Mexiletine, Tocainide
Mechanism- Decrease AP duration, preferentially affect ischemic or depolarized Purkinje and ventricular tissue
Use- Acute VT (esp post-MI) and in digitalis-induced arrhythmias
Toxicity- Local anesthetic, CNS stimulation/depression, CV depression

Front 4

Class IC

Back 4

Flecainide, Encainide, Propafenone
Mechanism- NO effect on AP duration
Use- VT that progress to VF and intractable SVT. Usually used as a last resort. FOR PATIENTS WITHOUT STRUCTURAL ABNORMALITIES.
Toxicity- Proarrhythmic, especially post-MI (CX); Significantly prolongs refractory period in AV node

Front 5

Class II

Back 5

Beta-blockers: Propanolol, esmolol, metoprolol, atenolol, timolol
Mechanism- Decrease cAMP, decrease Ca currents, decrease slope of phase 4; AV node is most sensitive (increased PR interval). Esomol is very short acting
Use- VT, SVT, slowing ventricular rate during a-fib and a-flutter
Toxicity- impotence, exacerbation of asthma, bradycardia, AV block, CHF, sedation, sleep alteration, mask signs of hypoglycemia. Metoprolol can cause dyslipidemia. Treat overdose with glucagon!

Front 6

Class III

Back 6

Sotalol, ibutilide, bretylium, dofetilide, amiodarone
Mechanism- Increase AP duration, increase ERP. Increase QT interval
Use- Used when other antiarrhythmics fail. Rhythm control in a-fib; Amiodarone in WPW.
Toxicity- Sotalol causes torsades de pointes, excessive beta block; ibutilide causes torsades; bretylium causes new arrhythmias and hypotension; amiodarone causes pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits (blue/grey), photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF (has I, II, III, IV effects because it alters the lipid membrane). Amiodarone does NOT cause torsades.

Front 7

Class IV

Back 7

Verapamil, diltiazem
Mechanism- Decrease conduction velocity (slope phase 0), increase ERP, increase PR interval.
Use- Prevention of nodal arrhythmias (SVT).
Toxicity- Constipation, flushing, edema, CHF, AV block, sinus node depression. Use with beta-blockers can give significant sinus bradycardia and heart block

Front 8

Adenosine

Back 8

Mechanism- Increases K out of cells, causing hyperpolarization and decreased calcium current.
Use- Abolishing SVT and seeing if its a-fib. Very short acting (15 s),
Toxicity- Flushing, hypertension, chest pain. Effects blocked by theophylline

Front 9

K, Mg

Back 9

Mechanism- Depresses ectopic pacemakers in hypokalemia (digoxin toxicity)
Use- Torsades de pointes and digoxin toxicity

Front 10

What antihypertensives are used in CHF patients?

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1. Diuretics
2. ACEI/ARB
3. B-blocker- but contraindicated in decompensated CHF
4. K-sparing diruetics

Front 11

What antihypertensives are used in diabetic patients?

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1. ACEI/ARBs- protective against nephropathy
2. CCBs
3. Diuretics
4. Beta-blockers
5. Alpha-blockers

Front 12

Hydralazine

Back 12

Mechanism- Increase cGMP to cause smooth muscle relaxation; arterioles > veins; afterload decreases
Use- Severe HTN, CHF. First line for HTN in pregnancy. Coadminister B-blocker to prevent reflex tachycardia
Toxicity- Reflex tachycardia (CX in angina/CAD), fluid retention, nausea, headache, angina, SLE-like syndrome

Front 13

Calcium channel blockers

Back 13

Mechanism-Block voltage-dependent L-type calcium channels of cardiac and smooth muscle to reduce contractility. In vascular smooth muscle nifedipine>diltiazem>verapamil. In the heart, verapamil>diltazem>nifedipine
Use- HTN, esophageal spasm, angina, arrhythmias (not nifedipine), Prinzmetal's angina (nifedipine), Raynaud's (nifedipine)
Toxicity- Cardiac depression, AV block, peripheral edema, flushing, dizziness, and constipation

Front 14

Nitroglycerin, isosorbide dinitrate

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Mechanism- Release NO in smooth muscle to increase cGMP. Dilates veins >> arteries to reduce preload.
Use- Angina, pulmonary edema, aphrodesiac
Toxicity- Reflex tachycardia, hypotension, flushing, headache, Monday disease

Front 15

Nitroprusside

Back 15

Mechanism- Short acting increases cGMP via direct release of NO. Vasodilates arteries and veins
Use- Malignant HTN
Toxicity- Cyanide toxicity (releases cyanide)

Front 16

Fenoldopam

Back 16

Mechanism- D1 agonist, relaxes renal vascular smooth muscle and naturesis
Use- Malignant HTN

Front 17

Diazoxide

Back 17

Mechanism- K channel opener that hyperpolarizes and relaxes smooth muscle
Use- Malignant HTN
Toxicity- Hyperglycemia (reduces insulin release)

Front 18

What antihypertensive drugs are safe to use in pregnancy?

Back 18

Hydralazine, nifedipine, labetalol, methyldopa

Front 19

What drug is nifedipine similar to?

Back 19

Nitrates

Front 20

What drug is verapamil similar to?

Back 20

Beta-blockers

Front 21

What beta blockers are contraindicated in angina?

Back 21

Acebutolol and pindolol (partial agonists)

Front 22

Statins

Back 22

Mechanism- Block HMG-CoA reductase (RLS in cholesterol synthesis- cannot form mevalonate). Greatly reduces LDL, increases HDL, decreases TGs
Toxicity- Hepatotoxic (increased LFTs), rhabdomyolysis, myalgias, myositis

Front 23

Niacin

Back 23

Mechanism- Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation. Decreased LDL, INCREASED HDL, decrease TGs
Toxicity- Flushing (reduce with aspirin), hyperglycemia (acanthosis nigricans), hyperuricemia (gout)

Front 24

Cholestyramine, colestipol, colesevlam (bile acid resins)

Back 24

Mechanism- Prevents reabosorption of bile acids; liver must use cholesterol to make more instead of recycling. Decreased LDL, slightly increased HDL, slightly INCREASED TGs.Also binds C. diff toxin so can give to patients with pseudomembranous colitis.
Toxicity- tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, cholesterol gallstones

Front 25

Cholesterol absorption blockers (ezetimibe)

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Mechanism- Prevent cholesterol reabsorption in the small intestine brush border. Decrease LDL
Toxicity- Rare increase in LFTs

Front 26

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

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Mechanism- Upregulate LPL to increase TG clearance. decrease LDL, increase HDL, GREATLY decrease TGs
Toxicity- Myositis, hepatotoxicity (increased LFTs), cholesterol gallstones (don't use with statins)

Front 27

How do beta receptors interact with L-type calcium channels in the heart?

Back 27

They use PKA to phosphorylate and inactivate the channel

Front 28

Digoxin

Back 28

Mechanism- Direct inhibition of Na/K ATPase. This leads to less activity of the Na/Ca exchanger and Ca stays inside the cell (positive ionotropy). Also stimulates the vagus nerve
Use- CHF (increased contractility), ATRIAL FIBRILLATION (decreased conduction at the AV node and depression of the SA node)
Toxicity- BLURRY YELLOW VISION, cholinergic toxicity (dumbbelss), Increase PR interval, Decrease QT interval, scooping, T wave inversion, arrhythmia, hyperkalemia, bradycardia.

Front 29

What worsens digoxin toxicity?

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1. Renal failure (decreased excretion)
2. Hypokalemia (permissive for digoxin binding at the K-binding site on Na/K ATPase)
3. Quinidine (decreases digoxin clearance and displaces digoxin from tissue-binding sites)

Front 30

What are the pharmacokinetic properties of digoxin?

Back 30

-75% bioavailability
-20-40% protein bound
-40 hour half life
-Urinary excretion- reduce dose in elderly