Heart Flashcards
Where does the electrical activity start and travel
Initiated in the SA node (pacemaker)
Conducted to the atria and AV node.
Then to the atrioventricular ring and through the bundle of his
Then to the purkinje fibres and ventricular muscles.
Desmosomes
Connect the cells in the heart and form electrical synapses
Very fast transfer of electrical activity
Faster than neurons synapses.
What happens if the SA node isn’t working.
The AV node can take over
SA node size and conduction and where it is
Where the pulse spreads.
Conduction from the right to left atrium
15mm x 5 x 2
Conduction 0.05ms (slow)
Found in posterior aspect of the heart
Electrical activity spreads to the Av node and left atrium.
Conduction is 1ms via atrial myocardium or Bachman’s bundle.
It is a lot faster in the myocytes in the atria than it is in the nodes.
AV node size, where it is and conduction.
Zones
Why is there the conduction that is has
AV refractoriness
22mm x 10 x 3
Found in the posterior part of the heart in the interatrial septum.
Slow conduction from AN to N.
The zones are the atrial nodal AN, nodal N and nodal ventricular NV.
The slow conduction is the AV delay which allows atrial contraction to finish before stimulating the ventricles.
AV refractoriness- the AV node has a refractory period after firing to stop the over stimulation of ventricles. To slow down the heart rate you increase the AV refractoriness.
Sub nodal conduction and speed
What does the timing cause
Fast conduction via bundle of his 1ms
Septal activation is where the electrical activity travels down the septum separating the ventricles.
Purkinje fibre speed is 4ms.
Ventricular muscle is 1ms.
The timing of how the ventricular muscles contract causes the heart to undergo a spiral muscle contraction.
Cardiac action potentials
Cardiac vs neuron
There are two types. Nodal or contractile/myocyte.
Both the nodes have nodal action potentials
Atrial muscle, purkinje fibres, ventricular muscle, have contractile action potentials.
Nodal action potentials can fire without other signals coming in. Autorythmicity.
Contractile ones need signals from pacemakers to fire.
Cardiac action potentials are longer than neural ones.
Pacemaker cells
What is the pre potential
How does it repolarise
Both the nodes and the purkinje fibres can be pacemakers.
They don’t have a resting membrane potential because as soon as it reaches the lowest potential of -60 it starts to increase again and slowly depolarise.
Slow Na influx until -40 is reached and then there is fast Ca influx to reach the action potential.
Fast K outflow
Ion channel activity graph
IK and IF
The further the outward and inward current moves from 0 the bigger the function of ion channels.
0 means there is no current
IK is the K leaving the cell.
IF is the funny current which mediates the slow Na influx.
Look at picture
When is the IF current active and inactive
The IF current is an ion cation channel and is activated by hyperpolarisation.
When the membrane potential is positive the IF current is inactive.
Control of pacemaker cells
Para NS- hyperpolarises the cell so the potential is moved further away from the threshold and the action potential takes longer to fire.
The pre potential will take longer and start from a more negative potential. And this will slow heart rate.
Symp NS- they will increase the heart rate by increasing the action potential frequency. The prepotential will happen quicker and easier.
What does noradrenaline and ach do for heart rate
The sympathetic noradrenaline activates beta 1 and 2 receptors which increase CAMP levels.
This activates the IF current and will accelerate depolarisation.
The parasympathetic ach activates M2 receptors which will decrease CAMP levels and inhibit the IF current and slow depolarisation
Action potential in the cardiac muscle fire when
What is a consequence of the long action potential
Absolute refractory period and then what
A signal tells them to and are not automatic.
They can’t do summation which is good because we don’t want to make too much of a large response. We only want one and then it turns off.
Action potentials can’t fire.
Then there is the relative refractory period where it is very hard but possible to fire one.
What’s the process of making an action potential
Depolarisation is initiated by opening of Na channels.
This triggers the opening of more Na channels.
They close when the voltage gets to +30 and an action potential fires.
Ca channels open and Ca enters slower than Na. This will prolong the depolarisation and create a plateau on the graph.
Ca channels then close and K open. And this causes repolarisation.
Picture. Between blue and pink is absolute refractory period.
What are the channels used in making the action potential.
What inhibits them
Na channel is the NaV1.5 channel that is found in cardiac myocytes and is inhibited by TTX and local anaesthetic.
Ca channel is CaV1.2 which is inhibited by nifedipine and verapamil.
K channels are IKS AND IKR. KV11.1 and Kv7.1.
If one of the many types of channel are mutated it’s okay because you have more.
IF current is most permeable to Na the channel is called HCN4 and is blocked by Cs.
How many people have sudden cardiac death
What are the causes
70,000 in the UK
60% due to ischeamic heart disease
40% have no detectable cause.
Some can be inherited syndromes.
Like changes in ventricular myocyte action potentials and ion channel mutations.
A normal ECG
P- atrial depolarisation
QRS- ventricular depolarisation
T- ventricular repolarisation
The atrial repolarisation is masked by the QRS wave.
Picture
What is Q - T
What happens if the T wave is too early or late.
The time for ventricle depolarisation and repolarisation.
If the T wave is too early or too late it means that Q-T will be longer or shorter and then ventricle repolarisation will be accelerated or delayed.
Many of the syndromes cause differences in the ECGs. The T wave will be shifted left or right.
Length of a normal QT interval
A long QT interval
A short QT interval
What if there are minimal changes
- 36s
- 45s+
- 34s-
The ECG will not pick up small changes and can only be detected during exercise.
What is triggered activity
What is re entrant excitation
Cells are able to reach threshold at times where it shouldn’t and this can cause extra heart beats.
This will cause ventricular tachycardia (increased ventricle contraction) and ventricular fibrillation (uncontrolled rapid contraction)
Only certain clusters of myocytes have the additional beats and this spreads to surrounding cells and causes the firing at wrong times. This leads to ventricular fibrillation.
Long QT syndrome 4
Prolonged QT interval leading to syncope (fainting) and could cause sudden death.
Symptoms are not seen until teenage years.
Lack of pattern on ECG 1 in 10,000 have it.
12 forms of long QT mutations. Can be gain or loss of function.
What is a self limiting episode and who has it.
But what about other episodes
The irregular beating stops itself and goes back to a normal rate In long QT patients
They can lead to ventricular fibrillation suddenly.
Torsades de pointes
A form of ventricular tachycardia
ECG up and down quickly which means the heart could stop
What are the mutations for long QT syndrome.
LQT1 is a mutation in the Kv7.1 channel and is loss if function. There is a 30-35% frequency. And is associated with the IKS current
LQT3 mutation in NaV1.5 alpha channel and is gain of function. 5-10% frequency.
LQT5 is a Mink loss of function mutation with the IKS current. Mnk regulates the K channel.
LQT1 K channelopathy
Where are most mutations and what does this do to the QT interval
In the Kv7.1 channel many of the mutations lie in the transmembrane spanning domains. This causes loss of function.
The QT interval takes longer because there are less functioning K channels to help repolarise the ventricles.
Some are dominant and some are recessive.
Long QT and the ear
Some forms of long QT syndrome cause deafness.
Mainly those with mutations in the Q1 K channel and it’s regulator E1.
The Q1 channel is needed to supply the endolymph in the ear with K to allow for cochlea function. The lack of endolymph causes kiessners membrane to collapse and cover other ear structures.
Long QT
Ca channel mutations
Na channel mutations
They have a gain of function and are open for too long.
This prolongs the plateau depolarisation phase and delays the start of repolarisation. Which will make the interval longer.
Gain of function that makes the channels open for longer. Causing a longer plateau and delayed repolarisation. Same as above
Treatment for long QT
And who it can’t be used on
Beta blockers are class 2 antidysrhythmic drugs. For example atenolol is a beta 1 antagonist which stops the activation of camp. It will reduce the heart rate to stop ventricular tachycardia and fibrillation.
It can’t be used on people who also have obstructive lung diseases like asthma because of the risk of bronchoconstriction.
Short QT syndrome symptoms
What kinds of mutations
How many are male
When does it start to show
Reduced QT interval
Arrhythmias, palpitations and syncope (fainting). Ventricular tachycardia and fibrillation lead to sudden death.
5 forms of mutations both gain and loss of function.
75% of cases are males.
Late adolescence is when it starts to show.
Short QT on the ECG.
There is a short or absent ST segment on ECGs
A tall T wave
And a fixed QT interval.
The QT interval cannot shorten anymore than it already has.
Short QT mutations
SQT2 a gain of function mutation in Kv7.1 channel associated with the IKS current.
The opposite of in LQT.
There is loss of function mutations in Ca channels. Meaning a shorter depolarisation.
Gain of function mutation in K channels due to more channel being present and this causes early repolarisation and a shorter QT interval.
Short QT treatment
Implant defibrillator and this will correct arrhythmia.
Quinidine is a K channel blocker which will slow repolarisation but it will affect other areas of the body too.
