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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

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2
Q

What is M2’s role?

A

parasympathetic control; slows SA/AV node

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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

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4
Q

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

A

Atropine

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5
Q

propanolol

A

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

Anti-arrhythmic (decreases Phase 4 slope)

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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)

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7
Q

What role do M3 and B2 play in the uterus?

A

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

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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)

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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

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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

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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)

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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

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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)

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14
Q

Dronedaron

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

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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

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16
Q

dobutamine

A

B1 agonist, increases cardiac output

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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

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18
Q

B1 agonist, name and function

A

dobutamine, increases cardiac output

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19
Q

B1 antagonists

A

metoprolol, atenolol, carvedilol, propandolol (B blockers)

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

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20
Q

Name the drugs that decrease conduction velocity

A

IA, IC, Class II, Class IV, adenosine

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21
Q

What is B1’s primary role?

A

stimulates SA/AV nodes

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22
Q

epinephrine

A

a1/2, B 1/2 - selective agonist

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23
Q

metropolol

A

B1 antagonist, B blocker (decreases cardiac output)

Anti-arrhythmic (decreases Phase 4 slope)

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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

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25
Q

Isoproterenol

A

B1 and B2 agonist synthetic drug similar to dobutamine (discussed in ANS and cardio lecture)

26
Q

Dofelitide

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

27
Q

what receptors are used by GI and what are their effects?

A

M3 and B2; M3 = contraction, B2 = relaxation for GI

28
Q

a 1, 2, B 1, 2 - selective agonist

A

epinephrine (broncodilation, SM relaxation, among other impacts)

29
Q

Amiodarone

A

Class III K+ blocker

Increases APD

Prolongs QT but not associated w/ Torsades

Hyper/hypothyroidism, blue skin/tongue tint

30
Q

Lidocaine

A

Weak Na+ block with unclear mechanism (beyond increasing threshold potential)

Decreases automaticity, increases RP w/ no increase in APD

31
Q

Diltiazem

A

Class IV Ca++ channel blocker (non-DHP)

Slows nodal depolarization (decreases automaticity), decreases conduction velocity

Also used for HTN

32
Q

Verapamil

A

Class IV Ca++ channel blocker (non-DHP)

Slows nodal depolarization (decreases automaticity), decreases conduction velocity

Also used for HTN

33
Q

carvedilol

A

a1, B1/2/3 (nonselective) antagonist (B blocker), decreases cardiac output

Anti-arrhythmic (decreases Phase 4 slope)

Also used for HTN and HF

34
Q

What mechanisms should you try to use for structural defects/reeentry

A

Increase the refractory period, decrease conduction velocity

35
Q

Solatol

A

Class III K+ blocker

Increases APD

Prolongs QT and is associated w/ Torsades

36
Q

Name the Class IV drugs and describe their mechanism

A

Diltiazem and verapamil (non-DHPs)

Slow AV/SA depolarization (similar to class I except nodally focused)

37
Q

What are M3’s primary roles?

A

SM contraction, secretion (parasympathetic)

38
Q

Rank the relative strength of Na channel blockers

A

IC (flecainide and propafenone) = strongest

IA (procainamide) = middle

IB (lidocaine) = weakest

39
Q

Name the 3 broad mechanisms/goals of antiarrhythmics

A
  1. decrease automaticity
  2. increase refractory period (can increase APD or have no impact on APD)
  3. can slow conduction velocity
40
Q

what role do the following play in urinary control? a1, M3, and B2

A

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
Q

Propafenone

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

42
Q

Ivabradine (didn’t really discuss this in class but it’s on the drug chart)

A

If (HCN) channel inhibitor

43
Q

prazosin

A

a1 antagonist - counters SM contraction and leads to vasodilation, decreasing BP

can cause orthostatic hypotension

44
Q

Name the class II anti-arrhythmic drugs and describe their mechanism

A

B-blockers (B1 antagonists)

Block epi and NE, decrease sympathetic reseponse, DECREASE PHASE 4 SLOPE

Atenolol, metoprolol, carvediol, propanolol

45
Q

atenolol

A

B1 antagonist, B blocker (decreases cardiac output)

Anti-arrhythmic (decreases Phase 4 slope)

Also used for HTN

46
Q

Atropine

A

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
Q

Procainamide

A

Class IA, Na+ K+ blocker

Associated w/ Torsades

Reduces automaticity (Increases threshold potential), increases refractory period, and decreases conduction velocity

Moderate Na+ block

48
Q

name an a1 antagonist and describe how it works

A

prazosin counters SM contraction by blocking a1 and leads to vasodilation, thus decreasing BP

49
Q

What is the main difference between epi and NE sensitivity’s to receptors?

A

NE has low affinity for B2 (this was emphasized in the ANS and cardio lecture)

50
Q

Name Class III side effects

A

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
Q

Describe the differences between direct and indirect acting parasympathetic drugs; give an example of an indirect drug

A

Direct - target the receptor (mAchR) - Ach mimics indirect - target acetylcholinesterase (AchE) in the synapse, AchE inhibitors atropine = indirect

52
Q

describe how phenylephrine works

A

a1 agonist; increases BP by increasing vascular constriction

53
Q

describe mediators of urinary control

A

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
Q

name an a2 agonist and describe how it works + a cardio application

A

clonidine - a2 agonist so it inhibits NE from presynaptic neuron and counterintuitively blocks sympathetic signals - use for HTN

55
Q

B1-selective only drugs

A

metropolol and atenolol (also called selective B blockers) - both used for HTN, metoprolol used for HF

56
Q

What is B2’s primary role?

A

SM relaxation (sympathetic) for GI, lungs, salivary glands, etc.

In eye and bladder, used in conjunction w/ a1

57
Q

what is the role of a2?

A

inhibits NE from presynaptic neuron and postsynaptically induces smooth muscle contraction like a1 COUNTERINTUITIVELY: blocks sympathetic signals

58
Q

what makes vasculature different than other structures in the body? What receptors does it have? What dominates?

A

No parasympathetic receptors; mediated by a1 and B2 a1 dominates so constriction typically wins

59
Q

How should you try to modify abnormal impulse formation

A

decrease automaticity (can target nodal rate or myocytes with premature beats)

60
Q

Which drugs should you avoid using w/ patients who have structural abnormalities?

A

Class IC drugs because they bind tightly to Na+ and are proarrhythmic

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