Drugs Influencing Heart Rate and Arrythmias Flashcards
What are the targets of parasympathetic control of the heart?
SA node and AV node
What is the neurotransmitter used in parasympathetic control of the heart?
Acetylcholine
What is the receptor used in parasympathetic control of the heart?
muscarinic receptors
What is the response of parasympathetic control of the heart?
slower heart rate
Which has more influence over the heart at rest - the parasympathetic or sympathetic nervous system?
The parasympathetic
What are the targets of sympathetic control of the heart?
SA node, conducting tissue and myocardial cells
What are the neurotransmitters used in sympathetic control of the heart?
noradrenaline and circulating adrenaline
What are the receptors in sympathetic control of the heart?
beta-adrenoceptors
What is the response of sympathetic control of the heart?
increased heart rate and increased contractility
What are the phases of the SA node action potential?
- 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
What is the resting membrane potential of the SA node?
unstable -60mV to +20mV
How does parasympathetic activity influence SA node cells?
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
How does sympathetic activity influence SA node cells?
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
What are the phases of the ventricular action potential?
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)
What is the resting membrane potential of ventricular cells?
-90mV
What are the 3 different mechanisms underlying dysrhythmias?
altered impulse formation, altered impuslse conduction (block or re-entry) or triggered entry (early or late after depolarisations)
What is altered impulse formation?
Where there is an abnormal generation of action potentials at a site other than the SA node
What is a conduction block?
Where the action potential can’t be conducted through the AV node so the ventricles adopt their own slowed rate
What is re-entry?
Where a loop of conduction fibres causes extra beats to be generated and the rate increases
Liv- I accidently lost this question. Can you re-do it?
An abnormal action potential before normal repolarisation is completed - due either to increased calcium channel activity or by NA activity
What is late after depolarisation?
An abnormal action potential after repolarisation is completed but before another action potential would normally occur
What are the four major classes of antidysrhythmics?
sodium channel blockers, beta-adrenoceptor antagonists, potassium channel blockers, calcium channel blockers
What is the action of sodium channel blockers?
To reduce the phase 0 slope of ventricular action potentials
What are the 3 different types of sodium channel blockers?
Type 1a - moderate block, type 1b - weak block, type 1c - strong block
What is quinidine?
A type 1a moderate sodium channel blocker that also prolongs repolarisation
What is lignocaine?
A type 1b mild sodium channel blocker that also shortens repolarisation
What is flecainide?
A type 1c strong sodium channel blocker that has no effect on repolarisation
What are the side effects of sodium channel blockers?
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
What is the action of beta-adrenoceptor antagonists?
Inhibits sympathetic influence on SA nodes and AV nodes - but also has membrane stabilising effects in purkinje fibres
What are the adverse effects of beta-adrenoceptor antagonists?
bradycardia, hypotension, AV conduction block, bronchoconstriction, hypoglycaemia
What is the action of potassium channel inhibitors?
slows phase 3 repolarisation to prolong cardiac action potentials
When are potassium channel inhibitors used?
for re-entry type arrythmias
What is amiodarone?
a potassium channel inhibitor that also blocks sodium and calcium channels and beta-adrenoceptors
What is the action of calcium channel inhibitors?
slows conduction velocity and increases refractory period - acts preferentially on SA and AV nodal tissue
