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Case 2 – Atrial Fibrillation notes
Therapeutics 3 (University of Brighton)
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Case 2 – Atrial Fibrillation
Case 2 – Atrial Fibrillation
Page 1 of 31
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Case 2 – Atrial Fibrillation
Dysrhythmias and Anti-dysrhythmic agents
Atrial fibrillation = a heart condition that causes an irregular and often abnormally fast
heart rate.
Dysrhythmia = abnormal rhythm
Arrhythmia = no rhythm
Dysrhythmias = any group of conditions in which the electrical activity of the heart is
irregular or consistently faster (more than 100bpm) or slower (less than 60bpm) than
normal
Causes:
a) Changes in the rate or site of impulse formation (SAN)
b) Changes in the route of impulse conduction
The most excitable heart in the cell is the SAN (Sino-atrial node)
The SAN is the pacemaker of the heart because it has:
The least negative membrane potential
Largest if current
Lowest threshold for action potential generation
Cells have a refractory period – after a period of which they have just been excited, they
can’t be excited again
Most excitable - SAN Different shapes – different ions are
responsible for depolarisation and
repolarisation
Bundle branch
Potassium leaving the
cell and calcium going
in resulting in a
plateau
Straight-voltage gated channel
– different to iF in terms of
structure and pharmacology
Na ions flow through as the cell
hyperpolarises
i = current, flow of ions across the membrane
Page 2 of 31
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Case 2 – Atrial Fibrillation
The cell depolarises further to reach threshold
iK = potassium channels open and potassium ions rush out and the cell repolarises
In order to target the ventricular rate, you have to target the ion channels
Mechanisms of altering impulse formation
Tachydysrhythmias – faster than normal
Most drugs focus on tachydysrhythmias
SAN increases its rate (sinus tachycardia)
Due to sick sinus syndrome (the older you get, the more likely you are to get sick
sinus syndrome – tissue around the whole of your body including the SAN goes
through fibrosis; lining down of connective tissue), infection (infections release
toxins in the blood which can affect the way your heart works), anaemia
(anaemia can make your heart beat faster – the blood doesn’t carry enough
oxygen to the tissues so the heart has to work harder to pump more blood to
carry enough oxygen), thyrotoxicosis (hyperthyroidism), drug therapy
(salbutamol and adrenaline)
Damage to the heart cells can change its properties – make it become more
excitable e.g. heart attack (cells become leakier as there is a lot more positive
ions that can start action potentials)
Latent pacemaker starts firing faster than the SAN (ectopic beat – heartbeat
outside the normal rhythm) due to MI, alcohol, hyperthyroidism
Bradysdysrhythmias – slower than normal
SAN is much slower, so the other cells (e.g. AVN) take over – SAN can slow down
so much that the other cells that are repressed by the SAN, can take over
If the SAN is slower, the next cell can take over but at a lower rate so it pumps the
heart or the heart rate is much lower and you become more out of breath trying
to get some oxygen in the system
Due to acute MI, sick sinus syndrome, drug therapy (e.g. ivabradine, beta
blockers, CCBs, Ach antagonists)
Pathological Mechanisms for Changing Impulse Formation
Ischaemia can lead to tissue injury which will cause the cells to become leaky and
increase sympathetic activity – if a cell is ischaemic (lack of oxygen), it may express
other channels to allow positive ions to flow in at rest.
This will cause the cells to have a pacemaker current that it didn’t have before – the
cells will become more excitable and the changed channels can lead to arrhythmias.
Triggered activity (abnormal action potentials)
Early
Late
Due to alterations in Na+/Ca2+ exchange or Ca2+ opening non-specific cation
channels in membrane
Cells may be more permeable to potassium at rest – gives it its negative membrane
potential
If someone has a heart attack, the heart won’t work as well as it should do – might
breath more to get more oxygen and the sympathetic system will try to make the
heart beat faster as the organs aren’t getting enough oxygen (blood vessels will dilate
and blood pressure will decrease)
Page 3 of 31
Downloaded by Neha Kanri ()
Case 2 – Atrial Fibrillation notes
Therapeutics 3 (University of Brighton)
Studocu is not sponsored or endorsed by any college or university
Downloaded by Neha Kanri ()
, lOMoARcPSD|25541772
Case 2 – Atrial Fibrillation
Case 2 – Atrial Fibrillation
Page 1 of 31
Downloaded by Neha Kanri ()
, lOMoARcPSD|25541772
Case 2 – Atrial Fibrillation
Dysrhythmias and Anti-dysrhythmic agents
Atrial fibrillation = a heart condition that causes an irregular and often abnormally fast
heart rate.
Dysrhythmia = abnormal rhythm
Arrhythmia = no rhythm
Dysrhythmias = any group of conditions in which the electrical activity of the heart is
irregular or consistently faster (more than 100bpm) or slower (less than 60bpm) than
normal
Causes:
a) Changes in the rate or site of impulse formation (SAN)
b) Changes in the route of impulse conduction
The most excitable heart in the cell is the SAN (Sino-atrial node)
The SAN is the pacemaker of the heart because it has:
The least negative membrane potential
Largest if current
Lowest threshold for action potential generation
Cells have a refractory period – after a period of which they have just been excited, they
can’t be excited again
Most excitable - SAN Different shapes – different ions are
responsible for depolarisation and
repolarisation
Bundle branch
Potassium leaving the
cell and calcium going
in resulting in a
plateau
Straight-voltage gated channel
– different to iF in terms of
structure and pharmacology
Na ions flow through as the cell
hyperpolarises
i = current, flow of ions across the membrane
Page 2 of 31
Downloaded by Neha Kanri ()
, lOMoARcPSD|25541772
Case 2 – Atrial Fibrillation
The cell depolarises further to reach threshold
iK = potassium channels open and potassium ions rush out and the cell repolarises
In order to target the ventricular rate, you have to target the ion channels
Mechanisms of altering impulse formation
Tachydysrhythmias – faster than normal
Most drugs focus on tachydysrhythmias
SAN increases its rate (sinus tachycardia)
Due to sick sinus syndrome (the older you get, the more likely you are to get sick
sinus syndrome – tissue around the whole of your body including the SAN goes
through fibrosis; lining down of connective tissue), infection (infections release
toxins in the blood which can affect the way your heart works), anaemia
(anaemia can make your heart beat faster – the blood doesn’t carry enough
oxygen to the tissues so the heart has to work harder to pump more blood to
carry enough oxygen), thyrotoxicosis (hyperthyroidism), drug therapy
(salbutamol and adrenaline)
Damage to the heart cells can change its properties – make it become more
excitable e.g. heart attack (cells become leakier as there is a lot more positive
ions that can start action potentials)
Latent pacemaker starts firing faster than the SAN (ectopic beat – heartbeat
outside the normal rhythm) due to MI, alcohol, hyperthyroidism
Bradysdysrhythmias – slower than normal
SAN is much slower, so the other cells (e.g. AVN) take over – SAN can slow down
so much that the other cells that are repressed by the SAN, can take over
If the SAN is slower, the next cell can take over but at a lower rate so it pumps the
heart or the heart rate is much lower and you become more out of breath trying
to get some oxygen in the system
Due to acute MI, sick sinus syndrome, drug therapy (e.g. ivabradine, beta
blockers, CCBs, Ach antagonists)
Pathological Mechanisms for Changing Impulse Formation
Ischaemia can lead to tissue injury which will cause the cells to become leaky and
increase sympathetic activity – if a cell is ischaemic (lack of oxygen), it may express
other channels to allow positive ions to flow in at rest.
This will cause the cells to have a pacemaker current that it didn’t have before – the
cells will become more excitable and the changed channels can lead to arrhythmias.
Triggered activity (abnormal action potentials)
Early
Late
Due to alterations in Na+/Ca2+ exchange or Ca2+ opening non-specific cation
channels in membrane
Cells may be more permeable to potassium at rest – gives it its negative membrane
potential
If someone has a heart attack, the heart won’t work as well as it should do – might
breath more to get more oxygen and the sympathetic system will try to make the
heart beat faster as the organs aren’t getting enough oxygen (blood vessels will dilate
and blood pressure will decrease)
Page 3 of 31
Downloaded by Neha Kanri ()
