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Cardiology I > Cardiovascular Disease Part I > Flashcards

Cardiovascular Disease Part I Flashcards

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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
T/F: the concentration gradient changes appreciably during the upstroke of myocardial AP?
False. The concentration gradient does NOT change appreciably; the electrical gradient DOES change appreciably at the membrane.
26
What mechanism is responsible for the refractory period of AP?
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.
27
What is the significance of the absolute refractory period?
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.
28
what is the significance of the relative refractory period?
Random Na inactivation gates have reopened, possibly enough to support upstroke; enough Na must be provided for the second AP to be initiated.
29
What is the mechanism responsible for phase 1 (initial repolarization) of AP in myocardial cells/perkinji fibers?
Increased electrical gradient of potassium ions, created by Na influx, supplements drive of potassium out of cell down its concentration gradient.
30
What is the mechanism behind the plateau phase/ phase 2 of an AP triggered by myocardial/perkinji fibers?
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.
31
Why is additional Ca release from SR during phase 2, the plateau of the AP?
The calcium coming in from L-type Ca channels is not enough to allow muscle contraction.
32
What is the physical process occurs during the plateau phase?
muscle contraction
33
During what phase does ca-induced-ca-release occur?
Phase 2, plateau of AP
34
What is the mechanism behind phase 3 of the AP?
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
Potassium is constantly moving out of cells through leaky channels in the cell membrane; how is it replenished?
Na/K ATPase
36
What mechanism is responsible for phase four of AP?
K conductance (permeability through cell)... K moving down its concentration gradient driving the cell more negatively towards its equilibrium potential.
37
From high to low, what cell types have the longest plateau phases?
midmyocardial> purkinji fibers> endocardial> epicardial>atrial>SA&AV node=0
38
From high to low, rate length of AP: ventricles, atrium, SA node.
SA
39
How do AP of the SA and AV node differ from muscle cell action potentials?
1. Automaticity 2. unstable RMP 3. no plateau (no phase 1 or 2) 4. Ca drives AP
40
How do calcium channel blocker affect the heart?
decrease HR
41
How does the SA node function?
By concentration gradients, Na leaks through funny channels slowly depolarizing cell until threshold is met that triggers Ca upstroke.
42
What ions are involved in phase 0 (upstroke) of AV and SA node APs? What is the mechanism of upstroke?
Upstroke driven by Ca influx through L-type calcium channels.
43
What ions are involved in phase 3/repolarization of the AV/SA node AP? What is the mechanism.
Potassium; it's concentration gradient and high conductance. Efflux of potassium drives membrane potential more negative.
44
What ions are responsible for phase 4/spontaneous depolarization of AV/SA node depolarization? What is the mechanism?
Na; funny channels leak Na into cells; funny channels are opened by repolarization from previous AP.
45
What phase of AV/SA node AP is responsible for the automaticity of nodal cells?
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
What event signifies the end of phase 4 (spontaneous depolarization) and initiation of phase 0 (upstroke) in AV/SA node APs?
Threshold. Once depolarization (caused by Na influx) becomes positive enough, Ca channels open and the Ca driven upstroke occurs.
47
What are chronotrophic effects?
Effects that change the heart rate through altering the SNS/PSNS or changing SA node firing rate.
48
What are inotropic effects?
Effects that change the contractility of the heart.
49
What are dromotropic effects?
Effects that change the conduction velocity of the heart.
50
What phase of AP conduction is altered by chronotropic effects?
Phase 4; steeper=faster HR; shallower=slower HR
51
What receptor on the SA node does the SNS stimulate to increase HR?
B1
52
In what 2 ways does the the SNS chronotropically effect phase 4 of SA node AP?
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
What two medications can be given to decrease HR?
Beta-blockers or Ca-Channel blockers
54
What are the 3 ways that the PSNS chronotropicly effect phase 4 of SA node AP?
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
If there is a heart block that results in a damaged AV node, what needs to be done?
Pacemaker
56
What is the gate keeper of the ventricles?
AV node
57
what does conduction velocity correlate with?
magnitude of influx of positive ions during upstroke
58
is conduction velocity higher in ventricles or SA node?
ventricles, all cells with vertical upstrokes have greatest conduction velocities
59
change in voltage/time=
velocity of upstroke
60
In what 3 ways does the SNS inotropicly affect AV node?
1. increase Ca 2. increased influx (increased conduction velocity) 3. increases efflux of K+ (decreases NET influx of Ca)
61
Describe excitation-contraction coupling.
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
What does contractility correlate with?
Ca concentration in cells
63
How is intracellular Ca concentration increased?
increased influx=increased storage=greater contractility when released
64
When does cross-bridge formation between actin and myosin stop?
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
What is the magnitude of the tension developed by myocardial cells proportional to?
intracellular Ca concentration
66
How does the SNS dromotropically affect heart cells?
increases Ca availability=increases magnitude of tension/contraction
67
how does the PSNS dromotropically affect heart cells?
decreases Ca availability AND increases potassium efflux= decreased magnitude of tension/contraction
68
The SNS affects what receptors of the heart?
B1
69
Activation of B1 by SNS increases HR how? (2)
1. increased funny channels (Na influx) | 2. increased ca influx
70
Activation of B1 by SNS increases conduction velocity how? (1)
increased ca influx
71
Activation of B1 by SNS increases contractility how? (2)
increased ca influx and phosphorylation of phospholamban
72
Activation of M receptor by PSNS decreases HR how?
1. decreases funny channels (and NA influx) 2. decreases Ca influx 3. increases K efflux thru K/ACH channel
73
Activation of M receptor by PSNS decreases conduction velocity how?
1. decreases ca influx | 2. increases K efflux thru K/ACH channel
74
Activation of M receptor by PSNS decreases contractility how? (Atria only)
1. decreases ca influx | 2. increases K efflux thru K/ACH channel
75
what segments of the EKG represent ventricular systole?
QRS complex and ST segment
76
What segments of EKG represent ventricular diastole?
T wave, p wave

Cardiology I (2 decks)

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