Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Pharmacology > Cardiovascular pharmacology II > Flashcards

Cardiovascular pharmacology II Flashcards

1
Q

what are the four ways to decrease spontaneous activity in the heart?

A
  1. decrease phase 4 slope
  2. increase threshold
  3. increase maximum diastolic potential
  4. increase AP duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the two ways to increase refractoriness? how do they work?

A
  1. sodium channel blockers - increases ERP by decreasing the % of sodium channels recovered from inactivation
  2. AP prolonging drugs (potassium channel blocker) - increase phases 2 and 3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the class Ia antiarrhythmic drugs?

A
  1. quinidine
  2. procainamide
  3. disopyramide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the class Ib antiarrhythmic drugs?

A

lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the class Ic antiarrhythmic drugs?

A
  1. propafenone

2. flecainide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the class II antiarrhythmic drugs?

A

beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the class III antiarrhythmic drugs?

A

amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the class IV antiarrhythmic drugs?

A
  1. verapamil

2. dilitiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the main function of the class I antiarrhythmics?

A
  1. block fast sodium channels in conductive tissues
  2. decrease max depolarization rate
  3. reduce automaticity, delay conduction
  4. prolong ERP - increased ERP/APD ratio
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

class I antiarryhtmics are good for what condition?

A

MI induced arryhthmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is unique about class Ia antiarrhythmics?

A
  1. block potassium channels - delay phase 3 - prolonged QRS and QT
  2. moderate sodium blocking
  3. calcium blocking at high doses - depressed phase 2 and nodal phase 0
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is unique about class Ib antiarrhythmics?

A

widened QRS complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the clinical uses for quinidine?

A
  1. refractory patients
  2. convert Af or flutter
  3. prevent AF recurrence
  4. life threatening ventricular arrhtyhmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the other effects of quinidine?

A
  1. block potassium channels - prolong APD
  2. block alpha receptors - lower BP
  3. block M receptors - increase HR in intact subjects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are the adverse effects of quinidine?

A
  1. cinchonism - tinnitus, hearing loss, blurred vision
  2. diarrhea
  3. hypotension
  4. proarrythmic - torsades de pointes (prolongs AP due to sodium blocking - early afterdepolarizations)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does procainamide differ from quinidine?

A
  1. very little vagolytic activity
  2. no hypotensive effect
  3. does not prolong QT interval as much
17
Q

what are the clinical applications for procainamide?

A
  1. life threatening ventricular arrhythmias
  2. reentry based SVT
  3. Af
  4. AF associated with wolff-parkinson-white syndrome
18
Q

what are the adverse effects of procainamide?

A
  1. cardiac - arryhthmia aggravation, TdP,

2. extracardiac - SLE like syndrome, GI, nausea and vomiting

19
Q

what are the effects of lidocaine?

A
  1. weak sodium channel binding (blocks slow AND fast)
  2. accelerated phase 3 repolarization - shortened APD and QT because it blocks late sodium channels - good use in digitalis and MI induced arrhythmia
  3. lowers phase 4 slope
20
Q

why is lidocaine more effective in ischemic tissues?

A

shortens AP and decreases ability of changes in calcium leading to arrhythmias in that way

21
Q

which class of antiarrhythmics binds strongest to sodium channels?

22
Q

what are the effects of propafenone?

A
  1. strong inhibitor of sodium channels

2. moderate beta blocker

23
Q

what are the clinical applications of propafenone?

A
  1. atrial arrhythmias

2. heart function must be intact

24
Q

what are the effects of flecainide?

A
  1. potent sodium channel blockade

2. markedly slows interventricular conduction

25
Q

what are the clinical applications for flecainide?

A

refractory life threatening ectopic ventricular arrhythmias

26
Q

what are the effects of the beta blockers on antiarrythmias?

A
  1. SA node automaticity
  2. AV nodal conduction
  3. ventricular contractility
27
Q

what are the clinical applications of beta blockers?

A
  1. supraventricular arryhtmias due to excessive sympathetic activity
  2. prevention of sudden cardiac death in patients with prior MI
28
Q

what are the effects of the class III antiarrythmia drugs?

A
  1. main effect - prolong phase 3 repolarization - increased QT
  2. blocks potassium channels - prolongs refractoriness and APD
  3. blocks sodium channels in inactivated state
  4. blocks calcium channels - slows AV node phase 4
  5. noncompetitive blockade of a, B, M receptors
29
Q

what are the clinical applications of amiodarone?

A
  1. acute termination of VT or VF
  2. conversion and slowing of AF
  3. AV nodal reentry tachycardia
  4. WPW syndrome tachycardias
30
Q

what are the major adverse effects of amiodarone?

A
  1. lethal interstitial pneumonitis - most serious
  2. decrease contractility and PVR - hypotension
  3. hyper or hypothyroidism blocks conversion of T4 to T3 and destroys thyroid tissue

Year 2 Pharmacology (70 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions