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Cardiovascular & Respiratory Pharmacology (Karen) > Drugs affecting heart rate and arrhythmias/dysrhythmias > Flashcards

Drugs affecting heart rate and arrhythmias/dysrhythmias Flashcards

1
Q

Arrhythmia

A

Absence of rhythm

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2
Q

Dysrhythmia

A

Abnormal rhythm

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3
Q

What are the PSNS targets of the heart to control rate?

A

SA & AV nodes

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4
Q

What is the chemical transmitter for PSNS control of heart rate?

What is the pathway?

What is the target tissue receptor?

A

Acetylcholine

  1. Preganglionic (SC)
  2. ACh onto postganglionic nicitonic receptors
  3. ACh onto muscarinc receptors (M2, GPCR)
  4. decreased HR

Muscarinic receptor (SA)

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5
Q

What does PSNS ACh stimulation do to heart rate?

A

Slows/bradycardia

ACh acts on M2R to decrease cAMP, opening K+ channels

K+ efflux slows Na+ and Ca2+ in, delays repolarization, tf takes longer for SA to reach threshold

**M2R is GPCR**

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6
Q

What does SNS NA(+Adr) stimulation do to heart rate?

A

Increases/tachycardia, +contractility

NA acts on B1-aR to increase cAMP, opens Ca2+ channels, Ca2+ influx

Ca2+ influx in Phase 4 depolarization increases slope @ SA & AV - tf reach threshold faster, +firing rate, +conduction (rate and rhythm)

*can trigger dysrhythmias*

**B1-aR is GPCR(stimulatory)**

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7
Q

Atropine

A
  • Muscarinic antagonist
  • PSNS: blocks muscR, +HR (~60bpm)
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8
Q

At rest, in normal healthy individuals, neural drive comes significantly from the

A

PSNS

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9
Q

What are the SNS targets of the control of heart rate?

A

innervates SA node

conducting tussue

myocardial cells

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10
Q

What is the chemical transmitter for SNS control of heart rate?

What’s the ganglionic pathway?

What is the target tissue receptor?

A

Noreadrenaline (+ circulating adrenaline)

  1. Preganglionic neurons release ACh onto NicR
  2. Postganglionic neurons release NA onto B-aR (B1, GPCR) and myocardial cells
  3. +HR, +contractility
  • +circulating adrenaline also activates alpha and B-aRs, w/ different selectivity to

Beta-adrenoceptors

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11
Q

What are the primary ativations by the SNS and PSNS at the heart?

A

PSNS - rate

SNS - rate and contractility

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12
Q

Noreadrenaline

A
  • SNS: at B-aR, +HR, +contractility
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13
Q

alpha-1 adrenergic receptors

A

In smooth muscle (skin, sphincters, kidney, brain, bladder/uterus)

mediate contraction

activation = vasoconstriction

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14
Q

alpha-2 adrenergic receptors

A

In brain and spinal cord

Vascular smooth muscle cells of certain blood vessels (skin arterioles, veins)

Binds NA from SNS postganglion and adrenaline from adrenal medulla

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15
Q

beta-1 adrenoceptors

A

Cardiac tissue, cerebral cortex, kidney

Increase CO (+HR at SA, +contractility)

+renin from juxtaglomerular cells

Lipolysis in adipose tissue

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16
Q

beta-2 adrenoceptors

A

Smooth muscle (bronchi, GIT, uterus)

blood vessels (vasodilation)

Heart (+contraction, +CO, +HR @SA +contractility)

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17
Q

Proranalol

A
  • Beta blocker/antagonist
  • SNS: -HR (~10bpm)
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18
Q

What is unique about the resting potential the SA node?

A

It’s unstable due to a unique leaky Na+ channel which causes an I-funny current and spontaneous depolarization (Phase 4)

~60mV - +20mV

19
Q

Ivabradine

A
  • Targets SA leaky Na+ channels
  • Trialled for angina - primary effect on rate
  • Potential use for some dysrhythmias
20
Q

Phase 0 of the SA action potential is

A

Ca2+ influx causing depolarization

(this is in contrast to ventricular APs where its Na+)

21
Q

Phase 3 of the SA AP is

A

repolarization

K+ out

Same as ventricular AP

22
Q

What is the resting membrane potential of the ventricular myocyte AP?

A

-90mV

Stable

Phase 4

23
Q

What is Phase 0 of the ventricular AP?

A

Depolarization by Na+ influx

(remember: pacemaker cells use Ca2+ here)

24
Q

What is Phase 1 of the ventricular AP?

A

Rapid repolarization by initial K+ efflux w/Ca2+ influx fighting K+ to extend AP

25
Q

What is Phase 2 of the ventricular AP?

A

Plateau; Ca+ in and K+ out

26
Q

What is Phase 3 of the ventricular AP?

A

Ca2+ gives up fighting against K+ coming out; tf get replarization by K+ efflux

27
Q

Symptoms of dysrhthmia are

A

Shortness of breath, fainting, fatigue, chest pain

28
Q

How does altered impulse formation cause dysrhythmia?

A
  • abnormal pacemaker cell function
  • abnormal AP generation (at sites other than SA)
  • due to: changes in ionic environment or electrochemical balance; fibrosis (leads to oedmea)
29
Q

How does altered impulse condiction cause dysrhythmia?

A
  • Conduction block: ventricles beat, nothing from SA –> generate their own rhythm, rely on AV; causes slower rate
  • Re-entry: circulation of electrical activity, sometimes localized; extra beats increase rate (Wolf-Parkinson-White: Bundle of Kent, extra pathway, can lead to re-entry)
30
Q

How does triggered activity cause dysrhythmia?

A
  • Early or late adter-depol, excessive SNS activation
  • Stray currents in refractory period cause EADs by some active Ca2+ channels letting Ca2+ in; NA can do this
  • Ca2+ overload can cause LADs in post-refractory relaxation phase (SNS overactivity)
31
Q

What are the 4 major classes of antidysrhythmics?

A
  • Na+ channel blockers
  • B-aR antagonists
  • K+ channel blockers
  • Ca2+ channel blockers
32
Q

What are the three types of Na+ channel blockers?

A
  • 1A: moderate
  • 1B: weak
  • 1C: strong
33
Q

How does a Class 1a Na+ channel blocker affect the ventricular AP?

A

e.g. quinidine

  • moderate/intermediate block
  • prolong repolarization
  • increased effective refractory period (ERP)
  • slows tachydys
34
Q

How does a Class 1b Na+ channel blocker affect ventricular AP?

A

e.g. lignocaine

  • Mild block
  • Shortens repolarization (K+ channel)
  • Decrease ERP
  • Affects contraction quality (smaller APs)
35
Q

Lignocaine

A
  • Class 1b (mild) Na+ block (shortens repolarization and ERP)
  • Local anaesthetic
  • Intravenous antiarrhythmatic (ER)
36
Q

How does a Class 1c Na+ channel blocker affect the ventricular AP?

A

e.g. flecainide

  • Strong block
  • Decreases slope of Phase 0 the most
  • Repolarization stays the same
  • No effect on ERP
37
Q

What is the main action of Na+ channel blockers on the ventricular AP?

A

Reduce the Phase 0 (depolarization) slope and tf the peak

Variably change ERP

38
Q

What is the main action of B-aR antagonists as antidysrhythmics?

A

Decrease rate and conduction

  • inhibit SNS influence
  • prevent B1aR effects on SA & AV
  • decrease sinus rate
  • decrease conduction velocity
  • decrease aberrant pacemaker activity
  • membrane stabilizing in Purkinje fibres (local anaesthetic type activity)
  • can block Na+ channels too
39
Q

What is the main action of K+ channel blockers as antidysrhythmics?

A

Delay Phase 3, prolong duration

  • Stop K+ leaving
  • Prolong AP through delayed Phase 3 repolarization
  • decrease incidence of re-entry
  • increase risk of triggered events (E/LADs) because prolonged Phase 3 allows greater potential Ca2+ interference
40
Q

What is the main action of Ca2+ channel blockers as antidysrhythmics?

A

Reduce rate and conduction at SA and AV nodes

  • Cardioselective: SA & AV tissue, Ca2+ channels
  • Stop initiation of AP
  • limit tachy
  • slow conduction velocity
  • increase refractoriness
41
Q

What are the adverse effects of B-aR antagonist antidysrhythmics?

A
  • bradycardia
  • reduced exercise capacity
  • hypotension
  • AV conduction block
  • bronchoconstriction
  • hypoglycemia
42
Q

Amiodarone

A
  • Blocks K+ (antidysrhythmic), Na+, Ca2+ channels
  • Blocks B-aR

Adverse effects:

  • reversible photosensitization
  • skin discolouration
  • thryroid problems
  • LT: pulmonary fibrosis
43
Q

What are the adverse effects of Ca2+ channel blocker antidysrhythmics?

A
  • facial flushing
  • peropheral oedema
  • dizziness
  • bradycardia
  • headache
  • nausea

Cardiovascular & Respiratory Pharmacology (Karen) (15 decks)

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