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Physiology > Cardiac Lecture 1 > Flashcards

Cardiac Lecture 1 Flashcards

1
Q

which type of cells have gap junctions

A

cardiac muscle cells

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2
Q

where are gap junctions located

A

within the intercalated discs

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3
Q

what do gap junctions do?

A

help carry the action potential through the cell

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4
Q

draw the action potential of a contractile cell

A

n

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5
Q

Phase 0 of a contractile cell

A

voltage-gated Na+ channels open
Na+ floods into the cell
start of depolarization

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6
Q

Phase1 of contractile cell

A

initial depolarization due to closure of the voltage gated Na+ inactivation gate

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7
Q

phase 2 of contractile cell

A
  • plateau phase
  • voltage gated Ca++ channels open and Ca++ rushes into the cell
  • maintains depolarization (positive charge entering the cell)
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8
Q

phase 3 of contractile cell

A
  • repolarization
  • K+ leaves the cell and inside of cell becomes more negative- down to resting membrane potential
  • resembles skeletal muscle
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9
Q

phase 4 of contractile cell

A
  • leak K+ channels help keep cell at resting membrane potential
  • 90mV
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10
Q

type of voltage-gated Ca++ channels in contractile cell

A

L-type

-slow to open, slow to close

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11
Q

what is the time of the absolute refractory period in

cardiac muscle cells

A

.2-.25 seconds

  • good to have long absolute refractory period that lasts as long as cardiac muscle contraction
  • allows muscle to relax for adequate filling of blood before next contraction
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12
Q

what is the time of the relative refractory period in cardiac muscle cells

A

.05 seconds

  • will require a bigger stimulus to initiate contraction
  • weaker contraction
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13
Q

how long does the action potential last in a cardiac muscle cell

A

almost as long as the entire contraction

-good because you do not want tetanus in cardiac muscle

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14
Q

how is cardiac muscle contraction different from skeletal muscle contraction

A

some of the Ca++ came from outside the cell

  • 25% is from the outside
  • 75% is from SR
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15
Q

how is cardiac muscle contraction different from skeletal muscle contraction

A

some of the Ca++ came from outside the cell

  • 25% is from the outside
  • 75% is from SR
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16
Q

three ways Ca++ can be excreted from the cell to get ride of contraction

A
  1. SERCA pump
  2. Ca++ ATP-ase pump on the membrane
  3. Na+/ Ca++ exchanger- uses the natural gradient of Na= to pump Ca++ against its gradient
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17
Q

what does the enzyme phospholambin do?

A

puts the brakes on the SERCA pump to slow it from pumping Ca++ back into the SR

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18
Q

what are the mutations involved with genetic Hypertrophic cardiomyopathy

A
  1. myosin heavy chain involved w/ contraction
  2. mutations in sarcomere proteins in the heart
    - troponin, tropomyosin, titin, actin, myosin
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19
Q

what are the effects of genetic hypertrophic cardiomyopathy?

A
  1. obstructs outflow of blood through the aorta
  2. reduces filling volume of the ventricle
  3. prone to arrhythmia
    - takes longer for the action potential to spread throughout the heart because of increased muscle
    - changing the refractory period
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20
Q

what are 2 ways to augment (increase) the force of contraction of contractile cells

A
  1. beta agonists
    - epi and NE on b1 receptors on heart
    - increases the amount of Ca++ in the cell by phosphorylation of voltage gated Ca++ channels( cAMP to pKA)
  2. phosphorylate actin and myosin to get stronger contractions
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21
Q

one way to decrease the force of contraction of contractile cells

A
  1. decrease Ca++
    - beta-blockers
    - verapamil, nifedipine-block the voltage gated- Ca++ channels
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22
Q

difference of pacemaker cells than muscle cells

A
  1. few contractile cells- does not contribute to contraction
    2 faster conduction rate
  2. no sarcomeres (t-tubules)
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23
Q

what leads to automatic depolarization in pacemaker cells

A

funny current- leaky Na+ channels

-Na+ moves into cell slowly and depolarizes it

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24
Q

in cardiac muscle cell, action potential is led by _____ while in pacemaker cells, the action potential is carried by ____

A

Na+ , Ca++

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25
Q

what happens when pacemaker hits threshold by funny current

A

voltage gated Ca++ channels open

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26
Q

what type of voltage gated Ca++ channels do pacemaker cells have

A

T-type: fast to open and fast to close

27
Q

in pacemaker cells what happens after opening of voltage gated Ca++ channels

A

voltage gated K+ channels open and K+ leaves the cell and repolarizes the cell membrane

28
Q

what is the resting membrane potential of a pacemaker cell

A

-60 mV

29
Q

drug that reduces the funny current without changing contractility

A

ivabradine

30
Q

what had the fastest depolarization rate from the funny current

A

SA node- 60-80/min
AV node- 40-60/ min
perkinjie fibers- 15-30 bpm

31
Q

3 ways to alter the heart rate by the sympathetic (adrenergic) nervous system ( increase HR)

A
  1. activate the B1 receptors with epi or NE
    - increase cAMP which activates the funny current
    - more Na+ leaks into the cell and depolarizes it faster and you get a faster HR (chronotropic)
  2. activate PKA which will block the enzyme phospholambin
    - inhibits the SERCA pump and more Ca++ can be pumped into the SR to increase muscle relaxation (lusitropic)
  3. Caffeine allows more cAMP to be around
32
Q

ways to alter the heart rate by parasympathetic (muscarinic) nervous system (decrease HR)

A
  1. ach binds to muscarinic receptors (increases K+)
    - stimulates GI which inhibits AC and decreases cAMP and PKA (decreases funny current and Ca++ influx)
  2. Adenosine stimulates GI
33
Q

what nerve is the parasympathetic nervous system mediated by

A

vagus nerve

34
Q

what is the conduction velocity through the nodal pathways

A

1 m/s

35
Q

function of the SA node

A

automatic depolarization triggers action potential in cardiac muscle cells through gap junctions

36
Q

what is the conduction velocity through the AV node

A

.05 m/s

-has the SLOWEST conduction velocity

37
Q

3 reasons why conduction is slow in the AV node

A
  1. fewer funny current
  2. fewer gap junctions
  3. lots of vagal innervation with Ach
38
Q

why is slow conduction through the AV node a good thing?

A

allows atria to fully contract before ventricles contract

39
Q

where is the only place conduction signal can cross through the conduction system

A

bundle of HIS

- everywhere else is insulated

40
Q

conduction velocity through the perkinjie fibers

A
  1. 5-4 m/s

- has the FASTEST conduction velocity

41
Q

conduction velocity through the muscle fibers

A

0.3-0.5 m/s

42
Q

total time it takes the impulse to travel through the heart

A

1/3 of a second= 0.22

43
Q

common cardiac agents used for short term treatment of heart failure

A

inotropic agents

44
Q

mechanism of digoxin/ digitalis

A
  • cardiac glycoside/ inotropic agent
  • inhibits the Na+/ K+ pump
  • Ca++ builds inside the cell and increases contraction
  • depresses SA node and slows conduction through the AV node
45
Q

effects of digoxin/ digitalis

A
  1. proper dose will increase cardiac contractility
  2. decrease HR and prevents arrythmias
  3. too high of dose can lead to arrythmias from increased Ca++
46
Q

mechanism of dobutamine

A

inotropic agent- increases contractility

  • B1 adrenergic agonist
  • increases Ca++
47
Q

effects of dobutamine

A
  • increases HR

- arrhythmias

48
Q

mechanism of milrinone

A
  • inotropic agent- increases contractility
  • phosphodiesterase 3 inhibitor
  • increases cAMP (prevents breakdown)
  • increases Ca++
49
Q

effects of milrinone

A
  • increases the HR

- arrhythmias

50
Q

mechanism of levosimenden

A
  • inotropic agent- increases cardiac contractility
  • increases calcium sensitization of troponin C
  • does NOT increase HR
51
Q

what does the QT interval represent

A

depolarization and depolarization

52
Q

what is the normal time of the QT interval?

A

0.35-0.42 s

53
Q

what does hypocalcemia do to the QT interval

A

long QT interval

-less Ca++ takes more time for Ca++ to move in to the cell

54
Q

what does hypercalcemia do to the QT interval

A

short QT interval

-increased Ca++ outside the cell increases the drive of Ca++ to want to move into the cell more quickly

55
Q

what do changes to the QT interval do to the contractility of the heart

A

susceptible to arrhythmias because you are changing the absolute refractory period

56
Q

what is the most likely ion channel that is involved in prolonged QT intervals due to genetic mutations

A

K+ channels because you are changing the repolarization rate

57
Q

ST segment depression refers to

A

myocardial ischemia

58
Q

ST segment elevation refers to

A

myocardial infarction ( heart attack)

59
Q

what does the ECG measure as far as membrane potential

A
  • measures the potential outside of the cardiomyocytes with is positive (why the ECG is positive waves)
  • measures the potential difference between 2 leads
60
Q

which directions does the heart repolarize

A

from epicardium to endocardium
-epicardium action potential and absolute refractory period is shorter
“first area to depolarize is the last area to repolarize”

61
Q

in which direction does the heart depolarize

A

from endocardium to epicardium

62
Q

why is the t-wave positive?

A

you are repolarizing the heart in the opposite direction

63
Q

when would you get an inverted t-wave?

A
  1. when the first area to depolarize is the first area to repolarize
    - endocardium repolarizes first
64
Q

3 causes of an inverted t-wave

A
  1. coronary ischemia
  2. hypertrophy- more heart muscle so endocardium action potential will actually be quicker
  3. bundle branch block

Physiology (6 decks)

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