Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardio > ANS and anti-arrhythmic drugs > Flashcards

ANS and anti-arrhythmic drugs Flashcards

1
Q

Name the classes that decrease automaticity for antiarrhythmics

A

All classes

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

What is M2’s role?

A

parasympathetic control; slows SA/AV node

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

Adenosine

A

Antiarrhythmic

Makes cell more depolarized at baseline (increases max diastolic potential)

Slows Ca++ influx, opens K+ channels

Works through all 3 paths

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

non-selective parasympathetic antagonist used to increase cardiac output or to dilate eyes

A

Atropine

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

propanolol

A

B1/2/3 - selective antagonist (B blocker), decreases cardiac output

Anti-arrhythmic (decreases Phase 4 slope)

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

What is a1’s primary role? Where are these located/how do the receptors work?

A

SM contraction (sympathetic) eye and bladder contraction - in conjunction w/ B2

Also very important for vascular constriction and dilation (a1 dominates so constriction typically wins dominates)

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

What role do M3 and B2 play in the uterus?

A

M3 - contractions, B2, relaxation (L+D plus menstrual applications)

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

name an a1 agonist and describe how it works

A

phenylephrine; increases BP by increasing vascular constriction Activates voltage-gated Ca++ channels, increases SR release (increases contraction)

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

Describe how adenosine works

A

Increases max diastolic potential (cell is more negative between action potentials)

Opens K+ channels, slows CA influx, is a nodal agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name the Class III antiarrhythmics and describe their mechanism

A

K+ blockers

Increase AP duration (increase refractory period and slow repol)

Amiodarone, dronedaron, dofelitide, solatol

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

What type of muscle does not fire action potentials?

A

Vascular smooth muscle (under involuntary control - hormones, ANS neurotransmitters like adrenergic receptors, local stimuli)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name the Class I anti-arrhythmic drugs + subclasses, and describe their mechanism

A

Na+ channel blockers - increase threshold potential and make it harder to depolarize

Slow resetting of NA+ channels

IA - Procainamide

IB lidocaine

IC flecainide, propafenone

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

how is a2 different from other receptors?

A

effects of a2 work on presynaptic neuron (inhibits the release of NE from presynaptic neuron, but postsynaptically, a2 induces smooth muscle contraction like a1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dronedaron

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name the classes that increase refractory period (including those that increase APD and those that do not)

A

APD increased: IA (because of K+), III

No change in APD: IB, IC, adenosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

dobutamine

A

B1 agonist, increases cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Flecainide

A

IC Na+ blocker (strong)

Don’t use in pts w/ structural abnormalities

Increases threshold potential (decreases automaticity), increases RP (no increase in APD), and decreases conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

B1 agonist, name and function

A

dobutamine, increases cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

B1 antagonists

A

metoprolol, atenolol, carvedilol, propandolol (B blockers)

Primarily works by decreasing the slope of Phase 4 depolarization and decreasing HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name the drugs that decrease conduction velocity

A

IA, IC, Class II, Class IV, adenosine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is B1’s primary role?

A

stimulates SA/AV nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

epinephrine

A

a1/2, B 1/2 - selective agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

metropolol

A

B1 antagonist, B blocker (decreases cardiac output)

Anti-arrhythmic (decreases Phase 4 slope)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What receptors are used by salivary glands and what are their effects? **what do you need to remember about the sympathetic receptor in this case?

A

for salivation - M3 = watery, B2 = thick (sympathetic) **note B2’s primary role is SM relaxation, not induction of secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Isoproterenol
B1 and B2 agonist synthetic drug similar to dobutamine (discussed in ANS and cardio lecture)
26
Dofelitide
Class III K+ blocker Increases APD Prolongs QT and is associated w/ Torsades
27
what receptors are used by GI and what are their effects?
M3 and B2; M3 = contraction, B2 = relaxation for GI
28
a 1, 2, B 1, 2 - selective agonist
epinephrine (broncodilation, SM relaxation, among other impacts)
29
Amiodarone
Class III K+ blocker Increases APD Prolongs QT but not associated w/ Torsades Hyper/hypothyroidism, blue skin/tongue tint
30
Lidocaine
Weak Na+ block with unclear mechanism (beyond increasing threshold potential) Decreases automaticity, increases RP w/ no increase in APD
31
Diltiazem
Class IV Ca++ channel blocker (non-DHP) Slows nodal depolarization (decreases automaticity), decreases conduction velocity Also used for HTN
32
Verapamil
Class IV Ca++ channel blocker (non-DHP) Slows nodal depolarization (decreases automaticity), decreases conduction velocity Also used for HTN
33
carvedilol
a1, B1/2/3 (nonselective) antagonist (B blocker), decreases cardiac output Anti-arrhythmic (decreases Phase 4 slope) Also used for HTN and HF
34
What mechanisms should you try to use for structural defects/reeentry
Increase the refractory period, decrease conduction velocity
35
Solatol
Class III K+ blocker Increases APD Prolongs QT and is associated w/ Torsades
36
Name the Class IV drugs and describe their mechanism
Diltiazem and verapamil (non-DHPs) Slow AV/SA depolarization (similar to class I except nodally focused)
37
What are M3's primary roles?
SM contraction, secretion (parasympathetic)
38
Rank the relative strength of Na channel blockers
IC (flecainide and propafenone) = strongest IA (procainamide) = middle IB (lidocaine) = weakest
39
Name the 3 broad mechanisms/goals of antiarrhythmics
1. decrease automaticity 2. increase refractory period (can increase APD or have no impact on APD) 3. can slow conduction velocity
40
what role do the following play in urinary control? a1, M3, and B2
M3 - parasympathetic control (contraction - detrusor) B2 - sympathetic control (relaxation - detrusor) a1 - sympathetic control (contraction - internal urethral sphincter) somatic control - external urethral sphincter (nicotinic receptor)
41
Propafenone
IC Na+ blocker (strong) Don't use in pts w/ structural abnormalities Increases threshold potential (decreases automaticity), increases RP (no increase in APD), and decreases conduction velocity
42
Ivabradine (didn't really discuss this in class but it's on the drug chart)
If (HCN) channel inhibitor
43
prazosin
a1 antagonist - counters SM contraction and leads to vasodilation, decreasing BP can cause orthostatic hypotension
44
Name the class II anti-arrhythmic drugs and describe their mechanism
B-blockers (B1 antagonists) Block epi and NE, decrease sympathetic reseponse, DECREASE PHASE 4 SLOPE Atenolol, metoprolol, carvediol, propanolol
45
atenolol
B1 antagonist, B blocker (decreases cardiac output) Anti-arrhythmic (decreases Phase 4 slope) Also used for HTN
46
Atropine
non-selective parasympathetic antagonist (indirect) used to increase cardiac output (tx bradycarida) or to dilate eyes Decreases Phase 4 slope by blocking ACh receptors (increases threshold)
47
Procainamide
Class IA, Na+ K+ blocker Associated w/ Torsades Reduces automaticity (Increases threshold potential), increases refractory period, and decreases conduction velocity Moderate Na+ block
48
name an a1 antagonist and describe how it works
prazosin counters SM contraction by blocking a1 and leads to vasodilation, thus decreasing BP
49
What is the main difference between epi and NE sensitivity's to receptors?
NE has low affinity for B2 (this was emphasized in the ANS and cardio lecture)
50
Name Class III side effects
All K+ blockers besides for Amiodarone: prolong QT and association w/ Torsades (including Procainamide) Amiodarone - prolongs QT but no Torsades (has multiple mechanisms); hypo/hyperthyroidism or blue skin/tongue tint
51
Describe the differences between direct and indirect acting parasympathetic drugs; give an example of an indirect drug
Direct - target the receptor (mAchR) - Ach mimics indirect - target acetylcholinesterase (AchE) in the synapse, AchE inhibitors atropine = indirect
52
describe how phenylephrine works
a1 agonist; increases BP by increasing vascular constriction
53
describe mediators of urinary control
parasympathetic control - detrusor muscle (M3), contracts to put pressure on bladder during times of rest; sympathetic control - detrusor muscle (B2) - relaxes during times of stress (decreasing urge to urinate) sympathetic control - urethra (a1) - contracts during times of stress (also so you don't pee yourself) but is inhibited when at rest; external sphincter - somatic control
54
name an a2 agonist and describe how it works + a cardio application
clonidine - a2 agonist so it inhibits NE from presynaptic neuron and counterintuitively blocks sympathetic signals - use for HTN
55
B1-selective only drugs
metropolol and atenolol (also called selective B blockers) - both used for HTN, metoprolol used for HF
56
What is B2's primary role?
SM relaxation (sympathetic) for GI, lungs, salivary glands, etc. In eye and bladder, used in conjunction w/ a1
57
what is the role of a2?
inhibits NE from presynaptic neuron and postsynaptically induces smooth muscle contraction like a1 COUNTERINTUITIVELY: blocks sympathetic signals
58
what makes vasculature different than other structures in the body? What receptors does it have? What dominates?
No parasympathetic receptors; mediated by a1 and B2 a1 dominates so constriction typically wins
59
How should you try to modify abnormal impulse formation
decrease automaticity (can target nodal rate or myocytes with premature beats)
60
Which drugs should you avoid using w/ patients who have structural abnormalities?
Class IC drugs because they bind tightly to Na+ and are proarrhythmic

Cardio (3 decks)

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