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CardioPulm > 11.29 B > Flashcards

11.29 B Flashcards

1
Q

Normal extracellular potassium concentration is roughly what?

A

3.5 - 5 mEq/liter

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2
Q

Hypokalemia is characterized by depressed (intracellular/extracellular) potassium levels.

A

extracellular

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3
Q

Hypokalemia and hyperkalemia both have what effect on resting membrane potential in cardiac muscle?

A

they depolarize resting membrane potential

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4
Q

Although both hyperkalemia and hypokalemia depolarize resting membrane potential they have differing effects on what?

A

potassium current

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5
Q

Hypokalemia and hyperkalemia promote what state, one of hyper or hypoexcitability?

A

hypoexcitability due to the diminished sodium current they are responsible for

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6
Q

What happens to the QRS complex when the sodium current is diminished?

A

it has a smaller magnitude and becomes widened

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7
Q

What happens to stroke volume when the QRS complex is widened?

A

it decreases and there is a corresponding drop in MAP

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8
Q

What happens to the nernst potential and conductance of potassium in a hyperkalemic state?

A
  • increased potassium conductance

- more positive nernst potential

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9
Q

What happens to the nernst potential and conductance of potassium in a hypokalemic state?

A
  • decreased potassium conductance

- more negative nernst potential

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10
Q

What happens to the duration of the ventricular action potential in a hypokalemic state?

A

it is prolonged due to reduced potassium current

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11
Q

What happens to the duration of the ventricular action potential in a hyperkalemic state?

A

it is shortened due to increased potassium current

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12
Q

Why does potassium current decrease in a hypokalemic state?

A

because the decreased potassium conductance outweighs the more negative potassium nernst potential

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13
Q

Why does potassium current increase in a hyperkalemic state?

A

because the increased potassium conductance outweighs the more positive potassium nernst potential

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14
Q

Describe the series of changes that happen in hypokalemia?

A
  • diminished extracellular potassium levels
  • decreased potassium conductance and more negative potassium nernst potential
  • conductance change is more significant
  • decreased potassium current
  • longer ventricular action potential duration
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15
Q

What happens to heart rate in a hypokalemic state?

A

it increases to a tachycardic state

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16
Q

Why does hypokalemia lead to tachycardia?

A

due to a decrease in potassium current, MDP is more positive and phase 4 is steeper in the SA node, leading to more frequent depolarization

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17
Q

Why is hyperkalemia not always associated with bradychardia despite an increase in potassium current?

A

the baroreflex kicks in, increasing sympathetic firing and the heart rate

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18
Q

What are the effects of hyperkalemia and hypokalemia on heart rate?

A
  • hypokalemia always leads to tachycardia

- hyperkalemia should lead to bradycardia but is sometimes controlled by the baroreflex

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19
Q

Hypokalemia and hyperkalemia have the same effects on ___ current and different effects on ____.

A
  • same on sodium

- different on potassium

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20
Q

A U wave is characteristic of what medical problem?

A

hypokalemia

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21
Q

Flaccid paralysis is a good indicator of what?

A

a potassium disturbance

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22
Q

What happens to the T wave in hyperkalemia?

A

it is increased, spiked

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23
Q

A spiked T wave is indicative of what potrassium disturbance?

A

hyperkalemia

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24
Q

How is hypokalemia treated?

A

a slow infusion of IV potassium based on a calculation of total body water

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25
Q

What are the four ways in which hyperkalemia is treated?

A
  • calcium gluconate
  • sodium bicarbonate
  • glucose/insulin
  • lasix
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26
Q

How does calcium gluconate help treat hyperkalemia?

A

it recovers resting sodium channels by shifting the sodium channel inactivation curve such that more inactivation gates will reopen during repolarization

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27
Q

Why is calcium gluconate only a temporary treatment for hyperkalemia?

A

because it restores excitability without resetting the resting depolarization

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28
Q

How does sodium bicarbonate help treat hyperkalemia?

A

by indirectly enhancing the Na-K pump

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29
Q

How does sodium bicarbonate indirectly enhance the Na-K pump?

A

by increasing sodium influx via the Na-H exchanger

30
Q

How does insulin help treat hyperkalemia?

A

by directly stimulating the Na-K pump to move extracellular potassium into the cell

31
Q

Which directly stimulates the Na-K pump, insulin or sodium bicarb?

A

insulin

32
Q

How does lasix help treat hyperkalemia?

A

it enhances potassium excretion by the kidney

33
Q

Which is a later onset, longer duration treatment for hyperkalemia, sodium bicarb or insulin?

A

insulin has a later onset and longer duration

34
Q

How does high extracellular calcium alter the sodium inactivation and activate gate curves?

A

it shifts both to the right

35
Q

High extracellular calcium normally does what to excitability?

A

it diminishes excitability

36
Q

If high extracellular calcium normally diminishes excitability, why is it used to treat hyperkalemia?

A

because the shift in the inactivation gate curve is more significant and has a greater effect than does the simulatenous shift of the activation gate curve, which normally accounts for the diminished excitability it elicits

37
Q

How does sodium bicarb indirectly treat hyperkalemia?

A

it increases pH, thus changing the proton gradient that drives the Na-H exchanger, thus changing the sodium graident that controls the K-Na exchanger

38
Q

What is the key difference between the action potential changes associated with hypoxia and those associated with ischemia?

A

there is no change in phase 4 resting membrane potential in hypoxia

39
Q

How does hypoxia affect the cardiac action potential?

A
  • limited ATP production
  • less calcium channel phosphorylation
  • less calcium current
  • decrease duration of the action potential
40
Q

Hypoxia decreases what about the cardiac action potential?

A

the duration

41
Q

Why does ischemia increase the resting potential of the cardiac cells while hypoxia does not?

A

because ischemia prevents blood flow and allows extracellular potassium to accumulate, causing local hyperkalemia

42
Q

Ischemia induces local ____.

A

hyperkalemia

43
Q

Ischemia has what effects on cardiac action potential?

A

it diminishes excitability by increasing resting membrane potential and it shortens the duration of the AP

44
Q

Potassium disturbances have what effects on sodium and calcium channels?

A

it decreases the number of resting sodium channels and does not affect the number of resting calcium channels

45
Q

Arrhythmias are the result of what?

A

abnormal impulse generation

46
Q

Abnormal impulse generation can lead to arrhythmias via what two mechanisms?

A
  • increased automaticity

- EADs/DADs

47
Q

Arrhythmias can be induced by increased automaticity which can arise from what changes?

A
  • enhanced beta-adrenergic agonists
  • decreased potassium conductance (hypokalemia)
  • depolarizing current that flows from an ischemic region into adjacent normally polarized tissue
48
Q

EADs and DADs are limited in their roles for re-entry loops in that they are only…

A

triggers, they do not sustain the loop

49
Q

EAD and DAD stand for what?

A

early after depolarization and delayed after depolarization

50
Q

EADs are associated with what two ionic changes?

A
  • decreased rate of repolarization from decreased potassium current
  • calcium window current due to opening of inactivation gates before activation gates have all closed
51
Q

If ____ current is suppressed, EADs can occur in late ____ or early ____ due to the _____.

A
  • potassium
  • late phase 2
  • early phase 3
  • calcium window
52
Q

EAD production is favored by conditions that do what?

A

increase the calcium window overlap or prolong action potential repolarization

53
Q

Cocaine is related to re-entry loops how?

A
  • it blocks potassium rectifier channels and impairs reuptake of NE by sympathetic nerves, increasing the calcium window
  • it leaves one susceptible to EADs
54
Q

Delayed after depolarizations occur when during an action potential?

A

phase 4

55
Q

Delayed after depolarizations occur in what cell population?

A

ventricular myocytes

56
Q

EADs occur when during an action potential?

A

late phase 2 or early phase 3

57
Q

DADs are associated with what two factors?

A
  • tachycardia

- increased cytosolci calcium levels

58
Q

Why is tachycardia associated with DADs?

A

because it causes accumulation of calcium within myocytes, which aren’t able to pump it out fast enough

59
Q

Why is increased cytosolic calcium associated with DADs?

A

the calcium activates a Na/Ca exchanger and a non-specific cation channel, which both allow extracellular ions into the cell, creating a depolarizing current

60
Q

M cells are unique ventricular cells in that they….

A

have a longer action potential duration

61
Q

Ventricular fibrillation results from the development of what?

A

multiple re-entry loops

62
Q

What three things are required for reentrant conduction?

A
  • a closed conduction loop
  • unidirectional conduction
  • an action potential length shorter than the loop length
63
Q

How does hypertrophy make reentrant conduction more likely?

A

by increasing the mass of the heart, it makes the conduction loop length longer, making it more likely that an action potential length will be shorter than the loop length

64
Q

Reentrant loops are more likely when what is true about the cardiac action potential?

A

conduction velocity is decreased and/or the duration of the AP is decreased

65
Q

Torsades de Pointes is treated with what?

A

a beta-aderenergic blocker which decreases potassium current, increasing the AP duration and hopefully interrupting the loop

66
Q

Long QT syndromes are the result of abnormal ___ channels.

A

sodium and potassium channels

67
Q

Short QT syndrome is the result of increased ____.

A

potassium current

68
Q

Brugada syndrome is an inherited arrhythmogenic syndrome caused by what abnormality?

A

reduced inward sodium current

69
Q

Catecholaminergic polymorphic ventricular tachycardia is an inherited arrhythmogenic syndrome caused by what abnormality?

A

decreased ability of SR to control calcium

70
Q

Atrial fibrillation is an inherited arrhythmogenic syndrome caused by what abnormality?

A

increased potassium current and impaired gap junctions

71
Q

Sinus node dysfunction is an inherited arrhythmogenic syndrome caused by what abnormality?

A

decreased funny sodium current

CardioPulm (31 decks)

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