Cardiovascular Drugs

Front 1

Anti-hypertensive Therapies: Drugs used in treatment of Essential hypertension

Back 1

Diuretics
ACE inhibitors
Angiotensin II Receptor Blockers (aka ARBs)
Calcium Channel Blockers

Front 2

Anti-hypertensive Therapies:
1) Congestive Heart Failure (CHF)
2) Contraindications

Back 2

1) *Diuretics
*ACE inhibitors
*Angiotension II Receptor Blockers (ARBs)
*Beta-blockers (only in compensated CHF)
*Potassium sparing diuretics (ex: Aldosterone antagonist)
2) Beta-blockers contraindicated in decompensated Congestive Heart Failure.

Front 3

Anti-hypertensive
1) Therapies: Diabetes mellitus
2) Cautions:

Back 3

1) *ACE inhibitors (protective against diabetic nephropathy)
*Angiotensin II Receptor Blockers (ARBs)
*Calcium Channel Blockers
*Diuretics
*Beta-Blockers
*alpha-blockers (alpha 1 blocker stops vasoconstriction, alpha 2 blocker stops decrease insulin release )
2) Caution: Beta-blocker and Diuretics mask signs of hypoglycemia

Front 4

Hydralazine
1) Mechanism
2) Clinical Use
3) Toxicity
4) Contraindication

Back 4

1) Increase cGMP (increase cyclic GMP) --> smooth muscle relaxation (arteries more than veins) = afterload reduction
2) Severe hypertension, Congestive Heart Failure, Hypertension during pregnancy (also alpha-methyldopa). Co-administered with beta-blocker to prevent reflex tachycardia
3) Reflex Tachycardia, fluid retention, angina, Lupus-like syndrome
4) Contraindicated: Angina/CAD (Coronary Artery Disease)

Front 5

Minoxidil
1) Brand Name
2) Mechanism
3) Clinical Use
4) Toxicity

Back 5

1) Rogaine
2) Potassium Channel Opener - hyperpolarizes and relaxes vascular smooth muscle
3) Clinical use: Severe Hypertension
4) Hypertrichosis (excessive hair growth), pericardial effusion (fluid around heart), Reflex tachycardia, angina, salt retention.

Front 6

Calcium Channel Blockers
1) Examples (Very Nice Drugs)
2) Mechanism
3) Clinical Use
4) Toxicity

Back 6

1) Verapamil, Nifedipine, diltiazem
2) Reduces contractility of cardiac and smooth muscles
Vascular Smooth Muscle: Nifidipine > diltiazem>Verapamil
Heart: Verapamil>diltiazem>nifedipine
3) Hypertension, angina, arrhythmias (not nifideipine), Prinzmetal's angina, Raynaud's Phenomenon, Esophageal spasam.
4) Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

Front 7

Nitroglycerin, Isosorbide dinitrate
1) Function
2) Mechanism
3) Clinical Use
4) Toxicity

Back 7

1) Function: Dilates veins (more than arteries) to decrease preload. (only preload)
2) Mechanism: Releases nitric oxide in smooth muscles increase cyclic-GMP and smooth muscle relaxation.
3) Clinical Use: Angina, Pulmonary Edema, aphrodisiac/ erection enhancer
4) Toxicity: Reflex tachycardia, hypotension. Monday's Disease (workers in Nitroglycerin factory develop tolerance due to exposure and lose tolerance over weekend: drastic vasodilation = tachycardia, dizziness, headache.

Front 8

Malignant Hypertension Treatment: Key Drugs and function

Back 8

1) Nitroprusside: Short actiing, increases cyclic-GMP via release of NO (nitric oxide). Can also cause cyanide toxicity. Effects Preload and Afterload
2) Fenoldopam: Dopamine D1 receptor agonist: relaxes renal vascular smooth muscle.
3) Diazoxide: Potassium (K+) channel opener: hyperpolarizes and relaxes smooth muscle. Can cause hyperglycemia as it reduces insulin release.

Front 9

Lipid-Lowering Agents
1) List drugs

Back 9

1) HMG-CoA reductase inhibitors "statins"
2) Niacin
3) Bile Acid Resins
4) Cholesterol Absorption Blockers
5) "Fibrates"

Front 10

HMG-CoA Reductase Inhibitors
1) Drug list
2) Major Effect on Lipids
3) Mechanism
4) Side Effects
5) Contraindication

Back 10

1) Lovastatin, Pravastatin, Simvastatin, Atorvastatin, rosuvastatin
2) Big effect on lowering LDL
3) Inhibits production of Mevalonic acid by inhibiting HMG-CoA Reductase.
4) Hepatotoxicity, Rhabdomyolysis
5) Never give Statins with Fibrates: Similar side effect = compounded effects

Front 11

Niacin
1) Major Effect on Lipids
2) Mechanism
3) Side Effects

Back 11

1) Increases HDL and Decreases LDL equally (HDL more important)
2) Inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation
3) Red, flushed face (decreased by aspirin), Hyperglycemia (acanthosis nigricans), Hyperuricemia (exacerbates gout)

Front 12

Bile Acid Resins
1) Examples
2) Major Effect on Lipids
3) Mechanism
4) Side Effects/problems

Back 12

1) Cholestyramine, Colestipol, Colesevelam
2) Decreases LDL
3) Prevents intestinal reaborption of bile acids so that the liver must use up already present cholesterol to make more (needed normally)
4) Tastes bad, GI discomfort, decreased absorption of fat-soluble vitamins, Cholesterol gallstones. Not commonly used.

Front 13

Cholesterol Absorption Blockers
1) Example
2) Major Effect on Lipids
3) Mechanism
4) Side Effects

Back 13

1) Ezetimibe (Zetia)
2) Decreases LDL, no effect on HDL or Triglycerides
3) Prevents cholesterol reabsorption at small intestine brush border.
4) RARE: Increased Liver Function Tests (always said as: LFTs). Increases plaque thickeness. Not commonly used.

Front 14

Fibrartes
1) Examples
2) Major Effect on Lipids
3) Mechanism
4) Side Effects
5) Contraindication

Back 14

1) Gemfibrozol, Clofibrate, Bezafibrate, Fenofibrate
2) Decreases Triglycerides
3) Upregulates LPL (Lipoprotein Lipase - enzyme hydrolyzes triglycerides in lipoproteins ex: chylomicrons and VLDL (very low-density lipoproteins) thereby increases triglyceride clearance.
4) Myositis, hepatotoxicity, cholesterol gallstones.
5) Never give Fibrates with Statins: Similar side effects = compounded effects.

Front 15

Omega 4 Fatty Acids
1) Source
2) Effect

Back 15

1) Fish Oil, Salmon, Cold Water Fish and Flax Seed
2) Decrease arrhythmia, triglycerides and severity of Rheumatoid arthritis.

Front 16

List of Drugs that Treat Congestive Heart Failure
1) List with function

Back 16

1) Digoxin = Increases contractility and cardiac output
2) ACE Inhibitors/ARBs = remove Renin/Angiotensin System
3) Loop Diuretics = Remove effects of Aldosterone, drug example is Furosemide)
4) Beta-Blockers = Decrease Sympathetic Activity

Front 17

Treatment for Exacerbation of Congestive Heart Failure:
LMNOPs (Ps as in PP)

Back 17

L = Loop Diuretic
M = Morphine (peripheral dilatory vascular effect and relaxor)
N = Nitrates (Dilates vasculature)
O = Oxygen
P = Position (Edge of bed so blood pools at feet
P = Pressors (Beta Blocker and dobutamine)

Front 18

Cardiac Glycosides
1) Drug
2) Bioavailability
3 Protein Binding
4) Half Life
5) Mechanism of Excretion

Back 18

1) Digoxin
2) 75% Bioavilability
3) 20-40% Protein Bound
4) Half Life = 40 hours
5) Urinary Excretion

Front 19

Digoxin:
1) Mechanism
2) Clinical Use

Back 19

1) Direct inhibition of Sodium/Potassium ATPase leading to indirect inhibition of Sodium/Calcium Exchanger/Antiport = increase Calcium = positive contractility (aka inotropy). Stimulates Vagus Nerve
2) Long Term Congestive Heart Failure for Contractility, Atrial Fibrillation for Decrease conduction at AV node and depression of SA node.

Front 20

Digoxin
1) Toxicity
2) Disease/Drugs that worsen Toxicity
3) Antidote

Back 20

1a) Cholinergic: Nausea, vomiting, diarrhea, blurry vision.
1b) EKG: Increase PR, Decrease QT, scooping, T-wave inversion. Arrhythmia, hyperkalemia, bradycardia.
2) Renal Failure (Digoxin excreted via urine), Hypokalemia, Quinidine (decreases clearance by displacing digoxin from tissue-binding sites)
3) Stop Dig, Normalize Potassium, Lidocaine, Magnesium, Anti-dig Fab Fragments, Pacemaker

Front 21

Definitions:
Depolarization:
Repolarization (and Hyperpolarization):
Refractory Period: Absolute/Effective vs Relative Refractory Period

Back 21

Depolarization: Cell becoming more positive (less negative) and when it becomes positive enough, an action potential will occur. Ions: Influx of Sodium+, Calcium ++ to cell.
Repolarization (and Hyperpolarization): Cell becomes more negative (less positive) and inhibits the rise of an action potential = REST. Efflux of Potassium+ from cell and influx of Cloride- to cell.
Refractory Period: time cells take before it can go from one action potential to another. Absolute refractory period (aka Effective Refractory Period): no matter the stimulus, no action potential can be initiated. Relative Refractory Period: Time between action potentials is inhibited but no impossible.

Front 22

Cardiac Action Potential: Non Nodal Cells
1) Type of cells
2) Phases
Phase 0: Action, Ion Conductance
Phase 1: Action, Ion Conductance
Phase 2: Action, Ion Conductance
Phase 3: Action, Ion Conductance
Phase 4: Action, Ion Conductance

Back 22

1) Atrial and Ventricular Myocotes and Purkinje System in Ventricles
Phase 0: Rapid Depolarization, Increase Sodium, Decrease Potassium
Phase 1: Initial repolarization, Decrease Sodium, Increase Potassium
Phase 2: Plateau Phase, Increase Calcium
Phase 3: Repolarization: Increase Potassium, Decrease Calcium
Phase 4: Resting Potential: Increase Potassium, Decrease Calcium

Front 23

Nodal Cell Action Potential
1) Type of Cells
2) Phases: Action, Ion Conductance
3) Major Differences between Nodal and Non-Nodal Action potentials

Back 23

1) Sinoatrial Node (SA node) and Atrioventricular Node (AV node)
2)
Phase 0: Depolarization: Increase Calcium, Decrease Potassium
Phase 3: Repolarization: Increase Potassium, Decrease Calcium
Phase 4: Spontaneous Depolarization: Increase Calcium, Decrease Potassium (Sinoatrial Node and AtrioVentricular Node))
3) No Phase 1 or Phase 2, No Sodium ions

Front 24

Anti-arrhythmics
1) List Classes
Mneumonic: No Bad Boy Keeps Clean

Back 24

Class I: Sodium (Na+) Channel Blockers (Na = No)
Class II: Beta Blockers (Beta = Bad)
Class III: Potassium (K+) Channel Blockers (K+=Keeps)
Class IV: Calcium (Ca++) Channel Blockers (Ca++ = Clean)

Front 25

Sodium Channel Blockers
1) Use
2) Mechanism To Treat Arrhythmias
3) Phase
4) Best used in what condition
5) Condition that increases toxicity

Back 25

1) Local Anesthetic
2) Reduces Phase 0 Slope and Peak Action Potential
3) Sodium Channels are Phase 0
4) Selectively depress tissue that frequently depolarizes - fast tachycardia)
5) Hyperkalemia

Front 26

Sodium Channel Blocker Mneumonic in order of Class subtypes: Police Department Questioned The Little Mexican For Pushing Ecstasy
1) List Drug from Class I in their subtypes

Back 26

1) Class IA
*Police: Procainamide (treats Wolf Parkinson White along with Amiodarone)
*Department: Disopyramide
*Questioned: Quinidine
2) Class IB
*The: Tocainide
*Little: Lidocaine
*Mexican: Mexiletine
3) Class IB
For: Flecainide
Pushing: Propafenone
Ecstasy: Encainide

Front 27

Sodium Channel Blockers Class Ia:
1) List The Drugs
2) Mechanism To Treat Arrhythmias
3) Toxicity

Back 27

1) Procainamide, Disopyramide, Quinidine (Police Department Questioned)
2) Moderate Reduction in Phase 0 Slope, Increased Action Potential Duration, Increased Effective Refractory Period
3) Quinidine: Cinchonism: Headache, Tinnitus, Thrombocytopenia; torsades de pointes from increase QT. Procainamide: Reversible Systemic Lupus Erythematosus (aka lupus): anti-histone bodies

Front 28

Sodium Channel Blockers Class Ib:
1) List the drugs
2) Non-cardiac drug that can also be part of this class
3) Mechanism To Treat Arrhythmias
4) Useful for
5) Toxicity

Back 28

1) Tocainide, Lidocaine, Mexiletine
2) Phenytoin (Seizure medication)
3) Weak Reduction of Phase 0 Slope, Reduces Action Potential Duration, Decrease Effective Refractory Period
4) Acute ventricular arrhythmia (especially post MI) and digitalis-induced arrhythmia.
5) Local anesthetic, CNS stimulant/depressive, Cardiovascular Depression.

Front 29

Sodium Channel Blockers Class Ic:
1) List of Drugs
2) Mechanism To Treat Arrhythmias
3) Used for:
4) Contraindication
5) Toxicity

Back 29

1) Flecainide, Propafenone, Encainide
2) Strong reduction in phase 0 slope, no effect on Action Potential Duration or Effective Refractory Period
3) Ventricular tachycardia that progresses to Ventricular Fibrillation and intractable Superventricular Tachycardia. Last resort for refractory tachyarrhythmias. For patients with no structural abnormalities.
4) Contraindicated in Post MI (proarrhythmic), Prolongs refractory period in Atrioventricular Node.
5) Proarrhythmic.

Front 30

Beta Blockers
1) Class
2) Drug Examples
3) Mechanism To Treat Arrhythmias
4) Clinical Use
5) Toxicity
6) Toxicity Antidote (main)

Back 30

1) Antiarrhythmic Class II
2) Propranolol, esmolol, metoprolol, atenolol, timolol
3) Blocks Sympathetic Activity, Reduce Rate and Conduction
4) Ventricular tachycardia, Superventricular tachycardia, slowing ventricular rate during atrial fibrillation and flutter.
5) Impotence, exacerbation of asthma, bradycardia, AV block, Congestive Heart Failure, Sleep alteration, sedation. Masks signs of hypoglycemia. Metoprolol: Dyslipidemia.
6) Glucagon

Front 31

Potassium Channel Blockers
1) Class
2) Drug Examples (A Big Dog Is Scary)
3) Mechanism To Treat Arrhythmias
4) Toxicity
5) Amiodarone treats, effect and tests

Back 31

1) Class III
2) Amidarone, Bretylium, Ibutilide, Sotalol (A Big Dog Is Scary)
3) Delay Repolarization (Phase 3) causing increase Action Potential Duration and Effective Refractory Period
4)
*Sotalol: Torsades de pointes, Excessive Beta Block. *Ibutilide: Torasades de points.
*Bretylium: New arrhythmias, hypotension
*Amiodarone: Pulmonary Fibrosis, Hepatotoxicity, Hypo/Hyperthyroidism, Corneal and skin deposits (photodermatitis), neurologic effects, constipation, Bradycardia, heart block, CHF.
5) Amiodarone treats Wolf Parkinson White (also Procainamide - Class IA Sodium Channel Blocker), has Class I, II, III and IV effects because it alters the lipid membrane. Must test Pulmonary, Liver and Thyroid Function tests.

Front 32

Calcium Channel Blockers - Anti-Arrhythmics Only
1) Class
2) Examples
3) Mechanism To Treat Arrhythmias
4) Use
5) Toxicity

Back 32

1) Class IV
2) Verapamil, Diltiazem
3) Block L-Type Channels. Most Effective at SinoAtrial Nodes and Atrioventricular Nodes. Reduces rate and Conduction
4) Prevention of Nodal Arrhythmias (Super Ventricular Tachycardia)
5) Constipation, Flushing, Edema, Congestive Heart Failure, AV block, Sinus Node Depression.

Front 33

Non-Classed Antiarrhythmics
1) Examples (3 of them), use (Toxicity if any)

Back 33

1) Adenosine: Increase Potassium of cell= hyperpolarizing plus decreasing permeability of Calcium. Drug of choice diagnosing and abolishing supraventricular tachycardia. Short acting (15 seconds). Toxicity: Flushing, hypotension, chest pain. Blocked by Theophylline (Treats COPD)

2) Potassium: Depresses ectopic pacemakers in hypokalemia (like indigoxin toxicity)
3) Magnesium: Effective in Torsades de Pointes and digoxin toxicity.

Front 34

Summary Affects of Anti-arrhythmics
Class I
Class Ia
Class Ib
Class Ic
Class II
Class III
Class IV
*ADP = Action Potential Duration
*ERP = Effective Refractory Period

Back 34

Class I: Reduce Phase 0 Slope and Peak Action Potential
Class Ia : Moderate Reduction in phase 0 Slope, Increased APD and ERP
Class Ib: Weak reduction in Phase 0 Slope, Reduced APD and ERP
Class Ic: Strong reduction in Phase 0 slope: no effect on APD and ERP
Class II: Block Sympathetic Activity, reduce rate and conduction
Class III: Delay repolarization (Phase 3) = increases APD and ERP
Class IV: Block L-Type Calcium Channel; Effective for Sino Atrial Nodes and AtrioVentricular Nodes. Reduces rate and conduction

*ADP =Action Potential Duration
*ERP = Effective Refractory Period