Drugs Influencing Heart Rate and Arrythmias

Question 1

What are the targets of parasympathetic control of the heart?

Answer 1

SA node and AV node

Question 2

What is the neurotransmitter used in parasympathetic control of the heart?

Answer 2

Acetylcholine

Question 3

What is the receptor used in parasympathetic control of the heart?

Answer 3

muscarinic receptors

Question 4

What is the response of parasympathetic control of the heart?

Answer 4

slower heart rate

Question 5

Which has more influence over the heart at rest - the parasympathetic or sympathetic nervous system?

Answer 5

The parasympathetic

Question 6

What are the targets of sympathetic control of the heart?

Answer 6

SA node, conducting tissue and myocardial cells

Question 7

What are the neurotransmitters used in sympathetic control of the heart?

Answer 7

noradrenaline and circulating adrenaline

Question 8

What are the receptors in sympathetic control of the heart?

Answer 8

beta-adrenoceptors

Question 9

What is the response of sympathetic control of the heart?

Answer 9

increased heart rate and increased contractility

Question 10

What are the phases of the SA node action potential?

Answer 10

• phase 0: upstroke - depolarisation caused by calcium coming in
  
  • phase 3: downstroke - repolarisation caused by potassium going out
  • phase 4: spontaneous depolarisation caused by leaky sodium channels

Question 11

What is the resting membrane potential of the SA node?

Answer 11

unstable -60mV to +20mV

Question 12

How does parasympathetic activity influence SA node cells?

Answer 12

acetylcholine acts on M2 muscarinic receptors to decrease the levels of cAMP and open potassium channels - this leads to a longer repolarisation phase so it slows sodium and calcium channels so it takes longer to reach potential at the SA node and slows conduction at the AV node

Question 13

How does sympathetic activity influence SA node cells?

Answer 13

noradrenaline acts on beta1 adrenoceptors to increase levels of cAMP and open calcium channels - this leads to a quicker upstroke (phase 4), increased rate of firing at the SA node and increased conduction at the AV node

Question 14

What are the phases of the ventricular action potential?

Answer 14

phase 0: depolarisation due to sodium entry, phase 1: rapid repolarisation because potassium floods out, phase 2: plateau due to calcium going in and potassium going out, phase 3: repolarisation due to potassium going out, phase 4: stable membrane potential (no leaky sodium channels)

Question 15

What is the resting membrane potential of ventricular cells?

Answer 15

-90mV

Question 16

What are the 3 different mechanisms underlying dysrhythmias?

Answer 16

altered impulse formation, altered impuslse conduction (block or re-entry) or triggered entry (early or late after depolarisations)

Question 17

What is altered impulse formation?

Answer 17

Where there is an abnormal generation of action potentials at a site other than the SA node

Question 18

What is a conduction block?

Answer 18

Where the action potential can’t be conducted through the AV node so the ventricles adopt their own slowed rate

Question 19

What is re-entry?

Answer 19

Where a loop of conduction fibres causes extra beats to be generated and the rate increases

Question 20

Liv- I accidently lost this question. Can you re-do it?

Answer 20

An abnormal action potential before normal repolarisation is completed - due either to increased calcium channel activity or by NA activity

Question 21

What is late after depolarisation?

Answer 21

An abnormal action potential after repolarisation is completed but before another action potential would normally occur

Question 22

What are the four major classes of antidysrhythmics?

Answer 22

sodium channel blockers, beta-adrenoceptor antagonists, potassium channel blockers, calcium channel blockers

Question 23

What is the action of sodium channel blockers?

Answer 23

To reduce the phase 0 slope of ventricular action potentials

Question 24

What are the 3 different types of sodium channel blockers?

Answer 24

Type 1a - moderate block, type 1b - weak block, type 1c - strong block

Question 25

What is quinidine?

Answer 25

A type 1a moderate sodium channel blocker that also prolongs repolarisation

Question 26

What is lignocaine?

Answer 26

A type 1b mild sodium channel blocker that also shortens repolarisation

Question 27

What is flecainide?

Answer 27

A type 1c strong sodium channel blocker that has no effect on repolarisation

Question 28

What are the side effects of sodium channel blockers?

Answer 28

Initially causes lip and tongue numbness - shows that the drug is at an effective concentration but then quickly progresses to respiratory arrest and cardiovascular depression - narrow range of concentrations it can be used over

Question 29

What is the action of beta-adrenoceptor antagonists?

Answer 29

Inhibits sympathetic influence on SA nodes and AV nodes - but also has membrane stabilising effects in purkinje fibres

Question 30

What are the adverse effects of beta-adrenoceptor antagonists?

Answer 30

bradycardia, hypotension, AV conduction block, bronchoconstriction, hypoglycaemia

Question 31

What is the action of potassium channel inhibitors?

Answer 31

slows phase 3 repolarisation to prolong cardiac action potentials

Question 32

When are potassium channel inhibitors used?

Answer 32

for re-entry type arrythmias

Question 33

What is amiodarone?

Answer 33

a potassium channel inhibitor that also blocks sodium and calcium channels and beta-adrenoceptors

Question 34

What is the action of calcium channel inhibitors?

Answer 34

slows conduction velocity and increases refractory period - acts preferentially on SA and AV nodal tissue