Heart 1 Flashcards

1
Q

Working myocardium

A

Atrial and ventricular muscle

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2
Q

Specialized conduction system

A

SA node, internodal pathways, AV node, bundle of His, bundle branches, Purkinje fibers

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3
Q

P wave

A

Atrial activation

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4
Q

QRS complex

A

Ventricular activation

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5
Q

T wave

A

Ventricular recovery

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6
Q

Difference between Nernst and Goldman-Katz equations

A

Nernst gives the theoretical equilibrium potential with only taking into account the ions in question; Goldman-Katz gives the actual resting membrane potential considering ALL ions in the solution

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7
Q

What pharmaceutical inhibits the Na-K pump?

A

Digitalis - has been in use in medicine for the last 200 years, but the mechanism of action has only been known for the last 30

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8
Q

Na-Ca exchange

A

Exchanges 3 sodium ions in for one calcium ion out to produce an electrogenic net inward current

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9
Q

How is the sodium-calcium exchange indirectly affected?

A

Since sodium is also being used to exchange potassium, the concentrations of sodium will flux within the cell and indirectly affect calcium exchange

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10
Q

Anomalous rectification

A

A decrease in potassium permeability that occurs when either the electrical or chemical driving force on potassium is increased

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11
Q

What are the two reasons for the deviation between the predicted Ek by Nernst and the actual Vm?

A

Small amount of sodium influx and a decrease in potassium permeability when the concentration is within normal limits and lower

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12
Q

Which is better for the heart: hyperkalemia or hypokalemia?

A

Hypokalemia, due to anomalous rectification

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13
Q

What happens with K current during the action potential plateau?

A

K permeability decreases, which then delays repolarization

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14
Q

Normal physiological concentration of potassium

A

3-5 meq/L

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15
Q

Describe the consequences of hyperkalemia

A

It increases membrane potassium permeability, which decreases K+ concentration gradient across the membrane. This creates a more positive membrane potential

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16
Q

Describe the consequences of hypokalemia

A

Decreases membrane potassium permeability due to inward rectification. It then increases the potassium gradient across the membrane, but there is no measurable effect due to the anomalous rectification.

17
Q

Waveform in the SA node

A

Continuous rise and fall; no true “resting” phase

18
Q

Phase 0

A

Upstroke of AP due to influx of sodium

19
Q

Phase 1

A

Peak and fall due to closing of sodium channels and opening of the potassium channels

20
Q

Phase 2

A

Plateau phase: continuation of efflux of potassium (inward rectification), net influx of calcium

21
Q

Phase 3

A

Fall of plateau due to closing of calcium channels. Potassium channels remain open

22
Q

Phase 4

A

Resting phase; only potassium channels remain open. Sodium channels are available, but non-active

23
Q

Effect of TTX on phase 0

A

Fast sodium channels are blocked so fast upstroke is now the responsibility of slow Ca2+ channels

24
Q

Effect of TTX on phases 2-4

A

None

25
Q

Fast response action potentials activate what?

A

Both fast sodium AND slow calcium channels during initial upstroke

26
Q

What happens with local damage to heart tissue?

A

Fast responses can become slow responses from infarct, so the damaged region can slow dramatically and cause arrhythmias due to reentry of excitation

27
Q

Where do slow responses happen in the heart?

A

The SA node and AV node

28
Q

What phases do slow response waves lack?

A

1 and 2

29
Q

Membrane potential for slow response tissue and its threshold

A

-40 to -60 with threshold of -40 mV

30
Q

In what tissues do fast responses happen?

A

Atrial, His-Purkinje, ventricular

31
Q

Membrane potential and threshold for fast response cells

A

-90 to -80 with a threshold of -65 mV