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Cardiology I > Cardiovascular Disease Part I > Flashcards

Cardiovascular Disease Part I Flashcards

1
Q

What is the primary pacemaker of the heart?

A

SA node

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2
Q

What does automaticity mean?

A

Cells are able to spontaneously generate action potentials

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3
Q

Is the concentration of NA higher intracellularly or extracellularly? K?

A

Na is higher extracellularly (140)

K is higher intracellularly (120)

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4
Q

What structure permits the development of membrane potentials?

A

Cell membranes

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5
Q

What 2 factors contribute to a membrane potential?

A
  • difference in concentration of ions

- permeability of membrane

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6
Q

Intra and extracellular fluids are electrolyte solutions that are _________.

A

Neutral (have equal positive and negative charges)

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7
Q

The voltage generated by ions that diffuse across the cell membrane, is referred to as?

A

The diffusion potential

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8
Q

True or False: The equilibrium potential is defined by the net movement of ions across the membrane; the electrical forces generated by the movement of ions are unbalanced.

A

False. The equilibrium potential is defined by no net movement of ions across the membrane; the electrical forces generated by the movement of ions are exactly balanced by the concentration forces.

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9
Q

How do you calculate the membrane potential?

A

Nernst Equation

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10
Q

The greater the ratio of ions intra and extracellularly, the ______ the tendency for ions to diffuse in one direction. Therefore, a ______ electrical force is required to prevent further diffusion.

A

Greater, greater

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11
Q

What is the function of the NA/K ATPase pump?

A

Removes three NA from inside cell; adds two K into cell; net loss of 1 positive ion=cell is negatively charged

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12
Q

What section of the cell does the membrane potential affect?

A

Membrane

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13
Q

What sets up the membrane potential?

A

Potassium

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14
Q

What is potassiums’s equilibrium potential?

A

-85mV

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15
Q

What ion is the membrane always permeable to?

A

Potassium

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16
Q

How is the cell depolarized?

A

positive charges/ions enter the cell

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17
Q

How is the cell hyperpolarized/repolarized?

A

positive ions leave the cell

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18
Q

What ion is responsible for the upstroke in the myocardium and perkinji fibers?

A

Sodium

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19
Q

What ion is responsible for the initial/short segment of repolarization after the upstroke (phase 1)?

A

Potassium

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20
Q

What ions are responsible for the plateau phase (phase 2) of myocardium/perkinji fibers?

A

Calcium flow into cell balances potassium flow out of cell

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21
Q

What ions are responsible for phase 3/repolarization during the AP of myocardium/perkinji fibers?

A

potassium flow out of cell is greater than calcium flow into cell

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22
Q

what occurs during the plateau phase off an AP of myocardial cells/perkinji fibers?

A

muscle contraction

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23
Q

What ions are responsible for the resting membrane potential of AP in myocardial/perkinji fiber cells?

A

Potassium flow out of cell matches calcium and sodium entry into cell; potassiums equilibrium potential and the cell membrane permeability to potassium drives the membrane potential towards -90mV

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24
Q

What is the mechanism behind phase 0 of AP produced by myocardial cells/perkiji fibers?

A

An electrical stimulus triggers the opening of Na channel’s activation gates. Na+ floods into the cell causing rapid cellular depolarization. The increase of intracellular positivity triggers the inactivation gates of Na+ channels to snap shut: this ends the upstroke of the AP.

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25
Q

T/F: the concentration gradient changes appreciably during the upstroke of myocardial AP?

A

False. The concentration gradient does NOT change appreciably; the electrical gradient DOES change appreciably at the membrane.

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26
Q

What mechanism is responsible for the refractory period of AP?

A

The amount of time for the inactivation gates of Na voltage gated channels to reopen; the number of reopened inactivation gates of Na voltage gated channels.

As membrane begins to repolarize, additional inactivation Na gates are reopened.

In order for a second AP to be fired, a majority of the inactivation gates must be reopened allowing enough positive charges to flood into cell for an upstroke.

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27
Q

What is the significance of the absolute refractory period?

A

Na inactivation gates closed; Na can’t enter cell to effectively trigger upstroke of AP. It is a period of time after an initial AP that another AP cannot be produced in.

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28
Q

what is the significance of the relative refractory period?

A

Random Na inactivation gates have reopened, possibly enough to support upstroke; enough Na must be provided for the second AP to be initiated.

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29
Q

What is the mechanism responsible for phase 1 (initial repolarization) of AP in myocardial cells/perkinji fibers?

A

Increased electrical gradient of potassium ions, created by Na influx, supplements drive of potassium out of cell down its concentration gradient.

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30
Q

What is the mechanism behind the plateau phase/ phase 2 of an AP triggered by myocardial/perkinji fibers?

A

Net current of ions=0. L-type Ca channels are opened due to depolarization of cell caused by influx of Na during upstroke. Ca enters cells at a similar rate that potassium leaves cells through leaky channels on cell membrane. Ca entering the cell triggers the release of additional Ca from SR.

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31
Q

Why is additional Ca release from SR during phase 2, the plateau of the AP?

A

The calcium coming in from L-type Ca channels is not enough to allow muscle contraction.

32
Q

What is the physical process occurs during the plateau phase?

A

muscle contraction

33
Q

During what phase does ca-induced-ca-release occur?

A

Phase 2, plateau of AP

34
Q

What is the mechanism behind phase 3 of the AP?

A

efflux of potassium ions>influx of Ca ions; membrane potential becomes more negative. As the membrane potential becomes more negative more Ca channels close decreasing influx of Ca.

35
Q

Potassium is constantly moving out of cells through leaky channels in the cell membrane; how is it replenished?

A

Na/K ATPase

36
Q

What mechanism is responsible for phase four of AP?

A

K conductance (permeability through cell)… K moving down its concentration gradient driving the cell more negatively towards its equilibrium potential.

37
Q

From high to low, what cell types have the longest plateau phases?

A

midmyocardial> purkinji fibers> endocardial> epicardial>atrial>SA&AV node=0

38
Q

From high to low, rate length of AP: ventricles, atrium, SA node.

A

SA

39
Q

How do AP of the SA and AV node differ from muscle cell action potentials?

A
  1. Automaticity
  2. unstable RMP
  3. no plateau (no phase 1 or 2)
  4. Ca drives AP
40
Q

How do calcium channel blocker affect the heart?

A

decrease HR

41
Q

How does the SA node function?

A

By concentration gradients, Na leaks through funny channels slowly depolarizing cell until threshold is met that triggers Ca upstroke.

42
Q

What ions are involved in phase 0 (upstroke) of AV and SA node APs? What is the mechanism of upstroke?

A

Upstroke driven by Ca influx through L-type calcium channels.

43
Q

What ions are involved in phase 3/repolarization of the AV/SA node AP? What is the mechanism.

A

Potassium; it’s concentration gradient and high conductance. Efflux of potassium drives membrane potential more negative.

44
Q

What ions are responsible for phase 4/spontaneous depolarization of AV/SA node depolarization? What is the mechanism?

A

Na; funny channels leak Na into cells; funny channels are opened by repolarization from previous AP.

45
Q

What phase of AV/SA node AP is responsible for the automaticity of nodal cells?

A

Phase 4/spontaneous depolarization; Na leakage through funny channels opened by repolarization of initial AP induces spontaneous depolarization (no outside neural input required to generate AP).

46
Q

What event signifies the end of phase 4 (spontaneous depolarization) and initiation of phase 0 (upstroke) in AV/SA node APs?

A

Threshold.

Once depolarization (caused by Na influx) becomes positive enough, Ca channels open and the Ca driven upstroke occurs.

47
Q

What are chronotrophic effects?

A

Effects that change the heart rate through altering the SNS/PSNS or changing SA node firing rate.

48
Q

What are inotropic effects?

A

Effects that change the contractility of the heart.

49
Q

What are dromotropic effects?

A

Effects that change the conduction velocity of the heart.

50
Q

What phase of AP conduction is altered by chronotropic effects?

A

Phase 4; steeper=faster HR; shallower=slower HR

51
Q

What receptor on the SA node does the SNS stimulate to increase HR?

A

B1

52
Q

In what 2 ways does the the SNS chronotropically effect phase 4 of SA node AP?

A
  1. Increases number of funny channels= faster influx of Na=increased rate of depolarization
  2. Opens more Ca channels during phase 4= decreased threshold potential= less positives needed in cell to trigger Ca upstroke
53
Q

What two medications can be given to decrease HR?

A

Beta-blockers or Ca-Channel blockers

54
Q

What are the 3 ways that the PSNS chronotropicly effect phase 4 of SA node AP?

A
  1. decrease funny Na channels (slows Na influx)
  2. increases conductance of K-ACH channels=increased efflux of K=hyperpolarization of cell= increased threshold potential
  3. decreases Ca channels that are open: hyper polarizes cell=further away from threshold=increased threshold potential
55
Q

If there is a heart block that results in a damaged AV node, what needs to be done?

A

Pacemaker

56
Q

What is the gate keeper of the ventricles?

A

AV node

57
Q

what does conduction velocity correlate with?

A

magnitude of influx of positive ions during upstroke

58
Q

is conduction velocity higher in ventricles or SA node?

A

ventricles, all cells with vertical upstrokes have greatest conduction velocities

59
Q

change in voltage/time=

A

velocity of upstroke

60
Q

In what 3 ways does the SNS inotropicly affect AV node?

A
  1. increase Ca
  2. increased influx (increased conduction velocity)
  3. increases efflux of K+ (decreases NET influx of Ca)
61
Q

Describe excitation-contraction coupling.

A
  1. AP spread through t-tubules
  2. Ca influx causes SR to release Ca
  3. Ca binds Troponin C
  4. Tropomyosin moves out of way so myosin can bind actin (muscle contraction)
  5. CaATPase in SR reabsorbs Ca causing muscle relaxation
  6. Ca/Na uses energy from NA/K ATPase to remove Ca and NA from cells
62
Q

What does contractility correlate with?

A

Ca concentration in cells

63
Q

How is intracellular Ca concentration increased?

A

increased influx=increased storage=greater contractility when released

64
Q

When does cross-bridge formation between actin and myosin stop?

A

When the concentration is too low to occupy Ca binding sites on troponin. When troponin is not bound, tropomyosin moves back over myosin binding sites on actin, preventing cross-bridge formation (contraction).

65
Q

What is the magnitude of the tension developed by myocardial cells proportional to?

A

intracellular Ca concentration

66
Q

How does the SNS dromotropically affect heart cells?

A

increases Ca availability=increases magnitude of tension/contraction

67
Q

how does the PSNS dromotropically affect heart cells?

A

decreases Ca availability AND increases potassium efflux= decreased magnitude of tension/contraction

68
Q

The SNS affects what receptors of the heart?

A

B1

69
Q

Activation of B1 by SNS increases HR how? (2)

A
  1. increased funny channels (Na influx)

2. increased ca influx

70
Q

Activation of B1 by SNS increases conduction velocity how? (1)

A

increased ca influx

71
Q

Activation of B1 by SNS increases contractility how? (2)

A

increased ca influx and phosphorylation of phospholamban

72
Q

Activation of M receptor by PSNS decreases HR how?

A
  1. decreases funny channels (and NA influx)
  2. decreases Ca influx
  3. increases K efflux thru K/ACH channel
73
Q

Activation of M receptor by PSNS decreases conduction velocity how?

A
  1. decreases ca influx

2. increases K efflux thru K/ACH channel

74
Q

Activation of M receptor by PSNS decreases contractility how? (Atria only)

A
  1. decreases ca influx

2. increases K efflux thru K/ACH channel

75
Q

what segments of the EKG represent ventricular systole?

A

QRS complex and ST segment

76
Q

What segments of EKG represent ventricular diastole?

A

T wave, p wave

Cardiology I (2 decks)

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