2.2.2 Abnormal Cardiac Electrophysiology Flashcards

1
Q

What is the mechanism by which hypoxia will affect an action potential in the tissue?

A

Insufficient O2 will decrease ATP formation. L-type Ca++ must be phosphorylated during each action potential to allow Ca++ through. Decreased ATP will impair the Ca++ current which will decrease the duration of the action potential.

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2
Q

Long QT syndrome can be cause by?

A

Decreased Na or K current

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3
Q

Why is V (membrane potential) being pushed towards ENa during hypokalemia?

A

The decreased gK is increasing the fgNa. Increasing the conductance to an ion moves the membrane potential to the Nernest potential of that ion.

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4
Q

How does the conductance of potassium relate to the concentration of potassium outside the cell?

A

It is directly related. As potassium concentration increases outside the cell so does the conductance

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5
Q

Why are M cells more susceptible to problems with action potentials?

A

Action potential prolongs disproportionately relative to the action potential of other ventricular myocardial cells in response to slowing of rate and or in response to action potential prolonging agents.

Less potassium current - less repolarizing current that prolongs phase 2

Larger Na-Ca exchange current - provides inward current to prolong phase 2

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6
Q

What is the Nernst potential formula?

A
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7
Q

What is the mechanism by which calcium corrects hyperkalemia?

A

Increased calcium produces a positive shift in the Na channel inactivation curve. Calcium also produces a positive shift in the Na channel inactivation curve. This shift can be utilized to recover some excitability by converting inactive sodium channels back to the resting state and increasing the current of sodium.

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8
Q

How will insulin act as a regulator of potassium?

A

Direct stimulation of the Na-K pump by insulin will also act to move potassium into the cell.

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9
Q
A

C

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10
Q
A

E

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11
Q

In regards to a reentrant loop, what will cause a reduce in duration of the AP?

A

Increase of IK or decrease in ICaL

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12
Q

What is a normal extracellular potassium concentration?

A

3.5 to 5 mEq/liter

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13
Q

What are the terms for increased and decreased extracellular potassium levels?

A

Hypokalemia - decreased

Hyperkalemia - increased

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14
Q

What causes the resting depolarization associated with hyperkalemia?

A

A less negative EK than normal

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15
Q

What is the mechanism by which hypokalemia will produce a depolarizing resting membrane potential?

A

Hypokalemia reduces K conductance. Apparently, the effect on membrane potential produced by the reduction of K conductance more than offsets the effect of the more negative Nernst potential produced by hypokalemia. The depolarized resting potential in hypokalemia depresses membrane excitability similar to that occurring in hyperkalemia. The decreased K conductance slows phase 3 repolarization causing the T-wave to flatten and a U wave may appear.

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16
Q

What is the mechanism by which EADs can occur?

A

EAD production occurs via conversion of inactive L-type calcium channels back to the active state during phase 2 or early phase 3 of the action potential. This reactivation can occur because there is a potential region where the Ca-channel activation and inactivation curves overlap. Decreased rate of repolarization (low IK) markedly increases the chances of these because there is more time in the “calcium window”. This can allow Ca++ to move into the cell through those channels and create a depolarizing current and move V more positive.

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17
Q

What effect will hypokalemia have on gK, IK, and action potential? What will hyperkalemia do?

A
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18
Q

What two conditions make reentrant loops more likely?

A

Conduction velocity in decreased and duration of the AP is decreased.

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19
Q

As potassium outside the cell increases what happens to EK? What happens to EK when potassium outside the cell decreases?

A

As K outside the cell increases, EK becomes less negative and moves toward zero.

As K outside the cell decreases, EK becomes more negative.

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20
Q

What effect will hyper and hypokalemia have on the T wave of an ECG?

A

The T wave is the repolarization of the ventricles. This is largely dependent on potassium. Hypokalemia will have a reduced current thus causing the T wave to look flat and prolonged. Hyperkalemia will have the opposite effect and the T wave will appear shorter and spiked.

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21
Q
A

C

22
Q

How will ischemia affect action potential generation?

A

Ischemia (insufficient blood flow) will lower O2 levels in the heart and decrease ATP formation. The mechanism is similar to hypoxia, but the decreased blood flow will allow K+ to accumulate which will result in local hyperkalemia. This will cause a depolarization of resting membrane potential, phase 4 of resting membrane potential will be more positive.

23
Q

What would be the effect of hyperkalemia on EK in a cell?

A

There would be a reduced chemical force driving K+ out of the cell as compared to normal. The electrical force needed to balance the reduced chemical force will be less than under normal conditions. Therefore, the Nernst potential will be less negative or more positive than under normal conditions

24
Q

Increasing the membrane potential would have what effect on the number of sodium activation gate needed to open to hit the threshold value?

A

There would need to be and increased number of activation gates open in order to achieve the threshold value. This is due to the threshold value being more positive.

25
Q

What is the formula for changes in potassium current?

A
26
Q

What can occur due to a suppression of K+ current?

A

Early after depolarizations

27
Q
A

C

28
Q

The negative shift in MDP acts to do what on the heart?

A

This negative shift in MDP acts to slow heart rate by increasing the potential difference between MDP and the threshold for activation of the L-type calcium current

29
Q

What are the mechanisms by which decreased potassium current will speed up the heart?

A

The decreased conductance causes MDP to become more positive even though EK becomes more negative. In addition, the decreased K conductance allows the funny sodium current to be more effective at driving phase 4 depolarization which results in a faster phase 4 depolarization.

30
Q

How do treat hypokalemia? While treating hypokalemia what will you notice on a patients ECG?

A

Slow infusion of potassium in order to not overshoot the needed K level. While correcting the hypokalemia you would notice the T wave become shorter and the U wave would disappear.

31
Q

Why do normal people tend to not have problems with EADs?

A

Normally the ventricle repolarizes quickly enough through the calcium window that activation gates close before there is enough time for inactivation gates to open.

32
Q

What are the three things required for a reentrant loop?

A
33
Q

Is a U wave characteristic of hyper of hypokalemia?

A

Hypokalemia

34
Q
A

D

35
Q

How can cocaine increase a person’s chances for an EAD?

A

Cocaine blocks delayed rectifier K channels, slowing the rate of repolarization, and impairs the reuptake of norepinephrine by SYM nerves (increases Ca++ window)

36
Q

What are four important outcomes when INa is decreased?

A

Threshold potential becomes more positive - decreased excitability

Rate of rise in an action potential would be decreased

Amplitude of action potential will be decreased (diminished height of QRS complex on ECG)

Decreased conduction velocity (Resulting in wide P wave and wide QRS complex on ECG)

37
Q

Hyper and hypokalemia both cause depolarization of resting membrane potential. What would this effect be on the number of resting Na+ channels and the INa?

A

This would decrease the number of resting Na channels thus decreasing the INa during the upstroke of the action potential

38
Q

In regards to a reentrant loop what will cause a decrease in conduction velocity?

A

Decrease INa

39
Q

How can Beta-adrenergic blockers treat Torsades de Pointes?

A

Potassium current would be decreased throughout the ventricles action potential would be prolonged and that could affect the reentrant loop.

40
Q

Why in this graph might the line for EK be trending upwards?

A

Because as KO increases EK becomes less negative and moves towards zero.

41
Q

How does resting depolariztion of cardiac muscle during hyperkalemia affect resting calcium channels?

A
42
Q

What will the effect of hypo and hyperkalemia be on MDP (maxiumum diastolic potential)?

A

Hyper - decrease make more negative; phase 4 will be less steep; decreased rate of firing of the SA node

Hypo - increase make more positive; phase 4 more steep; Tachycardia

Phase 4 is in reference to an action potential

43
Q

What is flaccid paralysis and what is it a result of?

A

Potassium disturbances will reduce voltage-gated sodium current in nerve and skeletal muscle. This will result in a person experiencing difficulty contracting their limbs.

44
Q

How does sodium bicarbonate affect potassium regulation?

A

An increase in extracellular pH (as produced by infusing sodium bicarbonate) will enhance the movement of Na into the cell by the Na-H exchanger. This is an indirect effect.

45
Q

In hypokalemia, what is the major cause of resting depolarization?

A

Decreased gK. This will lead to an increase fgNa

46
Q
A

A

47
Q

Short QT syndrome can be caused by?

A

Increased potassium current

48
Q

What is the mechanism by which DADs can occur?

A

Elevated heart rates can cause an accumulation of calcium within the myocytes (because there is insufficient time to pump all Ca++ out of cell). sarcoplasmic reticulum. Normally these calcium sparks are of no consequence. However, when the sarcoplasmic reticulum becomes overloaded with calcium the intracellular calcium (most likely in microenvironments) can increase to the level that activates a non-selective cation channel in the cell membrane. At negative membrane potentials, sodium ions will enter the cell providing an inward ionic current that can depolarize the cell. Also, the increased calcium level will favor the movement of calcium out of the cell via the Na-Ca exchanger. Since the movement of a calcium ion out of the cell via the exchange also moves 3 sodium ions into the cell, a net inward current is produced by the exchanger. The inward current carried by the Na-Ca exchanger also contributes to DAD production.

49
Q

What will an increase in extracellular Ca levels do to excitability of nerve, skeletal muscle, and cardiac muscle in a person with normal extracellular K+ level?

A

This would shift Na inactivation and activation curves more positive. Since the person has normal K+ levels the positive shift in Na inactivation channels would have little effect on the number of resting Na+ channels. The positive shift in the Na+ activation curve would shift the threshold to a more positive value and thus would cause reduced excitability in the person.

50
Q

If enough myocytes are generating EADs or DADs, the depolarizing current could be sufficient enough to trigger what?

A

Reentrant loop

51
Q

How does succinyl choline affect potassium regulation?

A

The increased intracellular sodium will stimulate the Na-K pump and move potassium into the cell