Cardiovascular Final Drugs

Front 1

When do you treat cardiac arrythmias

Back 1

Round the clock

Front 2

What do you use to treat atrial arrhytmias?

Back 2

Verapimil or Dilitiazem (Ca+ channel blockers- Class IV) or digoxin

Front 3

Class I drugs

Back 3

Lidocaine, Mexiletine, Procainamide, Quinidine

Front 4

Class I drugs mechanism

Back 4

Na channel blockers, reduce upstroke of action potential, increase time of phase 0

Front 5

Nipedipine is a calcium channel blocker that is not considered a useful Class IV agent because:

Back 5

Peripheral vasodilation leads to increased sympathetic discharge

Front 6

What is the re-entry phenomenon?

Back 6

Normally, impulses from pacemaker cells travel down the ventricular musculature. If one of the pathways is blocked, a process called reetnry occurs: re-excitation of ventricular muscle causing premature contraction or sustained ventricular arrythmia.

Front 7

What is the most common arrythmia?

Back 7

RE-ENTRY arrythmia, sustained ventricular contraction

Front 8

The most important causes for the generation of arrythmias are:

Back 8

1. impaired impulsse generation (anomalous automaticity) and 2. A problem with impusle propagation or conduction

Front 9

Proven advantages of antiarrythmic drugs

Back 9

1. Adenosine or verapamil for SVT
2.Lidocaine for termination of VT

Front 10

Which two antiarrythmics are actually proven to be proarrythmic when used long term, though they can prevent ventricular ectopic beats? What is the outcome for this?

Back 10

Ecainamide and Flecainamide (Class IC). Myocardial ischemia.

Front 11

Class IA drugs

Back 11

Quinidine, Procainamide, Dysopyramide

Front 12

What are the major side effects of Quinidine (Class IA)

Back 12

Cinchochism (blurred vision, tinnitus, headache, disorientation, psychosis), and lupus like syndrome

Front 13

What is the major adverse effect of procainamide?

Back 13

Lupus like syndrome

Front 14

All Class IA drugs can precipitate arrythmias called

Back 14

torsades des pointes (long QT interval VT)

Front 15

Lidocaine (Class IB) mechanism

Back 15

Shortens phase III repolarization and decreases the duration of the action potential

Front 16

Uses of lidocaine (class IB)

Back 16

Lidocaine suppresses arrythmias caused by abnormal automaticity, stops ventricular reenty, and can control secondary arrhytmias caused by drugs like dogixin

Front 17

Short acting class II drug that is an extrememly short acting B1 selective blocker

Back 17

Esmolol

Front 18

Use of esmolol

Back 18

IV infusion for acute control of HTN or supraventricular arrythmias in a perioperative, postoperative emergency setting

Front 19

What are the Class III drugs?

Back 19

Amiodaropne, Ibutilide, Dofetilide, Breatylium, Sotalol
They are potassium channel blockers

Front 20

True or false, Class III agents are considered interchangeable

Back 20

FALSE

Front 21

Rapid conversion of Afib or Aflutter to normal sinus rhythm

Back 21

Ibutilide (class III)

Front 22

non pharmacologic rapid conversion of afib or aflutter to normal

Back 22

AED electrical cardioversion

Front 23

mechanism of ibutilide

Back 23

promotes influx of NA thru slow inward NA channels, slowing repolarization and prolonging AP

Front 24

when do you use sotalol

Back 24

only in life threatening atrial or ventricular arrythmias

Front 25

true or false: betapace (sotalol) can be substituted for betapace AF

Back 25

FALSE

Front 26

Hypo or hyperthyroidism, pulmonary fibrosis, blue discoloration of skin due to iodine accumulation, photosensitivity

Back 26

amiodarone adverse effects

Front 27

what are the uses of amiodarone?

Back 27

antianginal and antiarrythmic

Front 28

Amiodarone has drug action in which class of drugs?

Back 28

I,II,III,IV

Front 29

Which is more effective in controlling ventricular rate in patients with Afib: Digoxin or Verapamil?

Back 29

Verapamil

Front 30

Drugs effective in arrhythmias that transverse the AV node

Back 30

Verapamil and diltiazem

Front 31

labeled for chronic stable angina

Back 31

Bepridil

Front 32

For acute SVT, life threatening hypotension, Wolff Parkinson White syndrome, and paroxysmal reentrant SVTs

Back 32

adenosine

Front 33

this drug is a diagnostic aid

Back 33

adenosine

Front 34

not effective in managing aflutter, afib or atrial ectopy

Back 34

adenosine

Front 35

mechanism of adenosine

Back 35

stimulates adenosine sensitive K channgels in SA and AV node, causing outward flow of K from myocyte, inducing sinus bradycardia

Front 36

difference betweel calcium channel blockers and adenosine

Back 36

adenosine does not affect the upstroje of action potential of sinus node cells

Front 37

can cause ectopic ventricular beats and toxing levels that can result in Vtach and Vfib

Back 37

digoxin

Front 38

antidote to digoxin

Back 38

lidocaine