Normal Cardiac Electrophysiology Flashcards Preview

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Flashcards in Normal Cardiac Electrophysiology Deck (45):

How does hypercalcemia decreases muscle weakness

Muscles get less excitable


What happens when there are more Ca ions outside the cell

There are more divalent cations outside in the cell that changes the preception of resting potential as seen by the Na channels. Ca ions do not affect the resting potential, they only increase the threshold potential to more positive - the field effect


Path of wave of excitation in the heart

1. Starts at SA Node

2. Travels along the atrial myocytes

3. Goes to the AV Node

4. Bundle of his (above the median septum)

5. Purkinje fibers

6. Ventricular myocytes



Velocities are high in bundle of his and the purkinje node, very slow in the AV node


What are the different kinds of action potential that drive the rythm of the heart

In the SA and AV node it is calcium dependent action potential (maybe thats why they look different)

In the atrial myocytes, bundle of His, Purkinje fibers and ventricular myocytes it is Na drived action potential (maybe thats why they all are so rapid and look the same)


What kind of channels are in the SA and AV nodes

Calcium L channel


Define the different segments of EKG

1. P Wave: atrial depolarization

2. PR interval: P wave plus PR segment, AV node depolarization

3. QRS segment: ventricular depolarization

4. ST segment: phase 2 of ventricular action, action potential doesnt change

5. T wave: ventricular repolarization, K current

QT interval = QRS + ST + T wave


 What determines each of these segments

Voltage gated Na channel and Ca channel determines the PR segment

ST segment depends on a balance between Ca current and K current

T wave is by K current

QT segment is the entire time of ventricular depolarization and then complete repolarization


What are the different phases of the action potential in a cardiomyocyte that he kept talking about


Why are the Na channels on SA node called funny

They open at a membrane potential of -50mV and close when the potential is more positive to -50 mV. So they are on during phase 4 and turn off during phase 0 


Explain what is happening in each of these phases

In phase 4 funny Na channels open at -50mV which causes the phase 4 depolarization trend. Na channels are open during phase 4 and closes during phase 3.

Phase 0 marks the opening of T type Ca channels which open initially and causes the opening of the L type Ca channels. Both of these channels drive the phase 0 depolarization current and as a result Ca flows into the SA node cell.

Phase 3 is marked by the opening of delayed rectifier K channels that open and causes repolarization of the cells. The membrane potential moves to -50 mV and the Na channels open again.

Important to note that towards the end of phase 3 Na funny channels start to open but their current is opposed by the K current which allows the potential to drop down to -50mV


What is the same and different about SA node and AV node

SA and AV node has the same ionic current and they dont have any resting membrane potential but the AV node has a lower intrinsic firing rate than the SA node. This means that if the SA node is damaged due to hypoxia or injury the AV node takes over the beating frequency of the heart.


Why does the AV node have a lower firing rate than the SA node

The slope of the phase 4 is less steep than the one in SA node


  What is unique about funny Na channels and what is the significance of it

Funny Na channels have only one gate which is called the activation gate. What makes them "funny" is that they open during repolarization (slowly) which causes the I-Na to increase. During phase 3 I-Na increase steadily and I-K decreases steadily giving us the shape of the graph of the SA node


What is the definition of threshold

The balance between I-depolarizing and I repolarizing, when depolarizing is more there is a generation of action potential as the threshold is reached


What causes the depolarization of the SA node cells? Is it Na or Ca

Na does not cause the depolarization, it is Ca involved in phase 4 which causes depolarization of the SA node cells. So the threshold in this case depends on the balance between I-Ca and I-K, but how quickly the threshold is reached depends on the funny Na current



Define the structure of the Ca L channel

It is very similar to the Na channel, it has 2 gates one activation and the other inactivation gate. The activation gate opens and closes quickly whereas the Inactivation gate opens and closes slowly


What is different between the Ca channel and the Na channel

There is Calcium window that is present in the Ca channel as it is the area of overlap in the probability of gate open curve


What is determined the by the magnitude of Ca current in the SA and AV node

1. Threshold potential

2. Amplitude of action potential

3. Conduction velocity

4. Rate of rise of the action potential


What happens to the PR segment when there is a larger Ca current generated

The PR segment is the flat space where the AV node is depolarizing. Due to higher Ca current the conductance velocity will be higher and the PR segment will decrease


Phases of ventricular potential

Phase 0: resting membrane potential at about -70 mV. This is more positive than E-K so there has to be leakage of K out of the cell and some Na into the cell. K moves out through the inward rectified K channel and Na moves in through leak channels

Phase 0: upstoke due to Na current

Phase 1: transient repolarization due to K current into the cell

Phase 2: This is the platuea phase due to the balance between Ca moving out of the cell and K moving in

Phase 3: Eventually Ca current ends and there is repolarization only due to K current


Inward rectifier K channel and Delayed rectifier K channel

These 2 are completely different K channels, only the inward rectifier K channel is open during resting membrane potential


What will happen if the Na current is reduced in a cardiomyocyte

There will be less positive membrane potential and as a result fewer Ca gates will open, the function of Na current is to open the Ca volatage gated channels so that Ca can move out of the cell


How does phase 2 end in a cardiomyocyte

There is finally time for the Ca inactivation gate to close that will stop Ca current, driving repolarization


What is the purpose of this slide

There are several K currents, the delayed rectifier is all that is important for our purposes


What are the effects of autonomic nervous system on the AV and SA node that regulate the rythym of the heart

Symapthetic nervous system firing:

1. Increases I-funny Na current

2. Increases Ca current

3. Increases K current

All of this is accomplished through adrenaline acting on the beta 1 receptors. Heart rate is primarily increased by the increasing I-funny. Increase in I-Ca increases the conduction velocity as well and decreases the PR interval

Parasympathetic nerve firing:

1. Decreases I-funny Na current

2. Decreases Ca current

3. Decreases K current

4. Very high firing of parasympathetic activates a different channel called I-KAch which increase K current

All of this is achieved through acetylcholine


What is the mechanism of increase of funny Na current

Sympathetic nerve firing shifts the activation curve for funny Na current to a more positive potential, which will cause the funny Na current gated channels to open sooner and cause depolarization at a faster rate. This is done by increasing the conductance of Na. It is important to know how the curve looks like


What will be the effects on the graph for increasing funny Na current

1. More positive MDP

2. Steeper phase 4


How does the graph look like when there is parasympathetic nerve firing

1. Phase 4 will be less steep than usual

2. At very high rates of parasympathetic nerve firing MDV will become more negative


Relative importance of parasympathetic and sympathetic nerve stimulation to the heart

Parasympathetic (blocking acetylcholine) has a much more profound effect 


What is the effect of sympathetic and parasympathetic on atrial and ventricular myocytes

The Na current in phase 0 is a transient increase so it remains unaffected by stimulaton either through the parasympathetic and sympathetic. Even if it does get effected and the QRS complex is wider (which doesnt normally happen) it will still have an insifignificant effect since the duration of action potential is mainly determined by phase 2 and 3 which is due to Ca and K current

However what does get effected is the Ca current and K current that are increased by parasympathetic nervous stimulation. Phase 2 and 3 are shortened as the rate of repolarization is increased (seen as a spike in the T wave). There is an increased amplitude of the action potential and decreased duration. 

There is no parasympathetic innervation of the atrial or ventricular myocytes


How does the P wave and QRS complex change during rest and excercise 

They look identical as explained by the reasons before, RT and QT interval gets shorter.


How does the force of the heart pumping changes during exercise

It increases due to an increase in Ca current which is termed as an increase in inotropic state


What is required for the Ca L channel to open, what phase will be effected if they dont open

It must be p's which requires ATP, in hypoxia this doesnt happen, pahse 2 gets shorter


How is the Ca current increased by sympathetic nerve simulation

The Ca L gates are made to open at a much lower negative potential which means they will open sooner. This is done (obviosuly) by increasing Ca conductance more than normal. As a result the size of the Ca window increases 


Explain the mechanism of action of Calcium channel

The key point here to know is that the inactivation gate only opens once the activation gate has completely closed, just like in the Na gate we talked about earlier


This huge Ca window that he showed us in the graph, when can that be a problem

In a  healthy heart the Ca window is the time when both the activation and inactivation gate are open, although the inactivation gate is slowly closing. The inactivation gate closes, then the activation gate completely closes and it is only then the inactivation gate opens up at resting membrane potential. 

However in a diseased heart this may be a problem as the Ca window is big and this may lead to defective functioning of the heart if the K current is not large enough to repolarize


Mechanism of action of autonomic nervous system on the heart rate


Why is the PR segment decreased due to sympathetic nerve stimulation

This specifically happens in the AV node that an incraase in L type calcium current causes faster conduction of the action potential causing the PR segment to be shorther


Does changes in heart rate correlate with change in ventricular potential

Longer or shorer duration of the ventricular contraction does not mean the heart rate will be faster or slower. The heart beat rate is only determined by the SA node. He illustrated this concept by explaining the fact that even if the ventricular contraction is faster, we can still have a longer phase 4 which would mean the heart will be beating much slower than normal (illustrated in his diagram)


Explain the mechanism of expanding action potential along the heart

1. Starts at the SA node, they have no resting potential so when these cells excite there is an increased Ca current which causes the upstroke of action potential.

2. Incrased Ca then flows from the SA node cells into the atrial myocytes via gap junctions, in the first atrial myocyte there will be an influx of Ca which will cause an action potential

3. Then the action potential travels to the rest of the myocytes via gap junctions but this time it will be the Na that will be flowing from one cell to another via gap junctions causing upstroke of action potential

4. Then this action potential travels to the AV node where initially Na causes the action potential, then the action potential is caused by the increased Ca current

5. This then flows to the bundle of his where the action potential is first caused by the increased Ca current and then the Na current drives the action potential upstroke 


What determines the conduction velocity in the heart

The rate of phase 0 depolarization, that is why there is different conduction velocities in the heart cells


Factors that affect the conduction velocity

1. Hypoxia and ischemia

2. High Na inside cell

3. High Ca inside cell

4. Intracellular acidosis

5. Decreased intracellular cAMP


Absolute refractory period, relative refractory period and functional refractory period


Reentry loop, what are the 2 factors that can cause this

 An abnormal second event of depolarization caused by the first wave of depolarization is called a reentry loop. It is important to understand how this happens. In the illustrated diagram here when the AV node sets off a wave of depolarization in this circular structure, it will travell all the way round and come back to the same cells at a time when the cell is in absolute refractory period. Hence it does not cause another wave of depolarization.

However, the first wave of depolarization can cause a second wave if it travells slowely (1 factor) or if the phase 2 and phase 3 are shortened as illustrated by his drawing as in those cases the wave will travel all the way around and come back to the cells near the AV node when they are in their relative refracotry period