Pharmacology Exam 3

Front 1

Normal heart rhythm

Back 1

SA node -> atrial muscle -> AV node -> ventricles

Front 2

Tachyarrhythmia

Back 2

If firing is too rapid

Front 3

Arrhythmia

Back 3

- An altered impulse pathway
=> altered pacemaker or ectopic focus
=> alteration in normal pathway

Front 4

What is the major cause of sudden cardiac death?

Back 4

Ventricular arrhythmias

Front 5

Normal resting heart cells contain more __, __, and __ on the outside of the cell and more __ on the inside

Back 5

Na+, Ca2+, Cl-; K+

Front 6

Calcium influx relates to __ and potassium efflux relates to ___.

Back 6

Contraction; relaxation

Front 7

Tx of arrhythmias

Back 7

- No Tx is often the best course of action, especially when it's not life threatening
- Any anti-arrhythmia drug can cause an arrhythmia

Front 8

Non-drug Tx options to arrhythmias

Back 8

Cardiac pacemakers, cardioversia, surgical removal of damaged heart muscles

Front 9

Antiarrhythmia drugs affect what?

Back 9

Abnormal foci

Front 10

Class I drugs- Local Anesthetics

Back 10

Inhibit Na+ influx into cell
Ia- Quinidine, Procainamide, Dispyramide
Ib- Lidocaine, Mexitilene

Front 11

Procainamide
(Class Ia)

Back 11

- Lupus-like symptoms in slow acetylators
- Doesn't enter the CNS
- Given orally
- Inhibits Na+ influx

Front 12

Quinidine
(Class Ia)

Back 12

- Given orally
- All arrhythmias
- Depresses all muscle function
- Anticholinergic effects=> inc HR
- Inhibits Na+ influx
- S.E: nausea, vomiting, anorexia, gets into CNS, tinnitus and altered color vision

Front 13

Dispyraminde
(Class Ia)

Back 13

- Strong anti-vagal effects
- For ventricular arrhythmias
- Opposite of DUMBBEL effects
- Inhibits Na+ influx

Front 14

Lidocaine
(Class Ib)

Back 14

- DOC in emergency situations for ventricular arrhythmias
- Given IV
- Low toxicity
- Gets into CNS (tremors, slurred speech, seizures)
- Inhibits Na+ influx

Front 15

Mexitilene
(Class Ib)

Back 15

- Lidocaine analog
- Can be given orally
- Inhibits Na+ influx

Front 16

Class II Drugs (overview)

Back 16

- Beta blockers
- Prevents Epi and NE from reaching the heart
- Tx of arrhythmias due to excess sympathetic stimulation
- DOC for atrial fibrillation

Front 17

Class II Drugs (3)

Back 17

1) Propranolol: decreases pacemaker firing rate, dec HT; contraindicated in patients w/ lung problems
2) Metoprolol: more specific for beta 1
3) Esmolol: even more specific and faster onset

Front 18

Class III Drugs (3)
K+ Channel Blockers

Back 18

- For atrial fibrillation
1) Sotalol: blocks beta receptors too
2) Amiodarone: works on all four pathways; fatal pulmonary fibrosis, liver damage, corneal and skin deposits, optic neuritis, blue-gray skin coloring, alters thyroxine production
3) Dronedarone: Like the above but no iodine

Front 19

Class IV Drugs

Back 19

- Ca2+ channel blockers
- Vasodilators- dec BP
- Useful for atrial tachycardia but not ventricular arrhythmias

Front 20

Adenosine

Back 20

- DOC for paroxysmal ventricular tachycardia
- Given by IV
- T.5 is 10 seconds

Front 21

Angina

Back 21

- Not enough blood flow to heart muscle
- Chest pains: may be atherosclerotic plaques in coronary artery; pain upon exercise or pain at rest (unstable angina)

Front 22

Prinzmetal Angina

Back 22

Spasms of coronaries

Front 23

Drugs that Tx angina act to do what?

Back 23

Increase blood flow to the heart

Front 24

The Nitrates

Back 24

Nitroglycerin (GTN)
- Will dec pain in 2 min
- Cause rapid dilation in all BVs
- Given sublingually- due to first pass effect
Mechanism of action: release of NO => inc cGMP=> dilation

Front 25

Isosorbide dinitrate

Back 25

- Longer lasting nitrate
- Can be given orally

Front 26

Side effects of nitrates (3)

Back 26

Orthostatic hypotension, flushing, headache

Front 27

T/F Tolerance doesn't develop with nitrate use

Back 27

False, tolerance develops rapidly (tachyphylaxis)

Front 28

Other drugs that can Tx angina

Back 28

Anything that can decrease heart work (beta 1 blockers, calcium channel blockers)

Front 29

Congestive heart failure

Back 29

- Heart can't pump enough blood to the body
- Blood gets to heart but isn't pumped rapidly enough so heart becomes enlarged => blood backs up into the lungs (pulmonary congestion) => edema of lungs => can't breathe => kidney under perfused => retains sodium and water => full body edema

Front 30

Causes of CHF

Back 30

MI, heart valve problems

Front 31

How the heart adapts to failure

Back 31

Early stages => dec CO, dec effective blood volume
1- Inc release of Epi, NE, angiotensin II => inc BP, in HR
2- Kidney in blood vol => angiotensin II => inc Na+ and H20 retention
3- Enlargement of the heart => inc force of contraction
Finally... heart failure

Front 32

Tx of cardiac insufficiency

Back 32

Ionotropic agents
- Increase force of heart contraction
- Increase calcium in heart muscle
- The cardiac glycosides: Digoxin

Front 33

Mechanism of action of ionotropic agents

Back 33

- Inc force and rate of contraction
- Enzyme inhibitors (Na+/K+ ATPase pump): Na+ stays in cell, inhibits Ca2+ pumps => inc contractility
- Increases vagal tone and anti-arrhythmic effects

Front 34

Toxic effects and drug interactions of ionotropic agents

Back 34

- Cardio: arrhythmias
- CNS: vision (inc yellow/green tinting), hallucinations, inc nausea and vomiting
- Effects of digoxin greatly increase when K+ is low because digoxin binds to K+ site of Na+K+ ATPase

Front 35

Other Ionotrops

Back 35

Beta agonists: dobutamine, DA

Front 36

Best Tx for cardiac insufficiency

Back 36

Prevent the body from accommodating the failing heart which increase the life span of patients

Front 37

Agents that increase blood flow to selected organs (3)

Back 37

1- Sildenafil
2- Vardenafil
3- Tadalafil
- These are Enzyme inhibitors: inhibit cGMP phosphodiesterase=> dilates arteries of the corpus cavernosum
S.E: slight dec in BP, don't use w/ other vasodilators, visual disturbances, direct retinal damage
Other uses: pulmonary hypertension