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CardioRenal I > electrophysiology and contraction of muscles > Flashcards

electrophysiology and contraction of muscles Flashcards

1
Q

Main differences between Cardiac and Skeletal Muscles -

A

All cardiac cells function in conduction, some function to produce force (working Myocytes), Automaticity, smaller and shorter than skeletal mucle, GAP JUCNTIONS, contained within a connective tissue matrix that supports its function of a pump

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2
Q

Automaticity

A

spontaneously depolarizing and contracting

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3
Q

Importance of gap junctions in cardiac cells

A

permit the rapid conduction of electrical signal - potential generated anywhere in the atria can spread throughout the atria

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4
Q

The heart is made up of two electrical ____ connected by ______

A

the heart is made up of two electrical syncitium connected by unidirectional conduction through the AV node

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5
Q

Whatare the two electrical syncitia of the heart

A

Atrial syncitia and ventricular syncitia

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6
Q

Heart block

A

varying degrees of impairment though the AV bundle leading to varying degrees of functional dissociation of the atrial and ventricular syncitia

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7
Q

Ventricular Myocytes

A

Broad sheet of branching cells, stiated appearance, well developed t-tubule system located near the z line , 2x more mitochondria than skeletal muscle (high oxygen demand)

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8
Q

myocte triad

A

T-tuble and lateral sacs of sarcoplasmic reticulum

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9
Q

Ventricular intercalated discs

A

end to end connection, integrates electormechanical function between cells

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10
Q

desmosome

A

attachment site for cytoskeleton

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11
Q

Components of gap junctions

A

connexion proteins that form a low resistance conduction pathway

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12
Q

Relationship between gap junctions and conduction

A

more gap junctions = more rapid conduction

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13
Q

Atrial Myocites

A

NO branching, intercalated discs

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14
Q

Atrial intercalated discks

A

horizontally organized with occassional end to end connection (transmission of rappid impulse from end to end and side to side)

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15
Q

how many directions do atrial myocytes conduct in?

A

two- end to end and side to side due to the organization of their intercalated discs a

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16
Q

importance of the myocardial connective tissue matrix

A

interconnects myoctes and blood vessels, structural support of the heart, prevents damage by limiting stretching during diastole (due to overfilling), major pathway for force transmission across the heart, determines resting tension (ventricular diastolic pressure), “Holds” vessels open during contraction to limit the impact of surround pressure

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17
Q

importance of the long duration of cardiac action potential

A

assures complete activation of all cardiac cells (ensures synchronozed contraction with each impulse), assres a sustained contraction to empy the chambers of the heart, accounts for the long refractory period

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18
Q

importance of long refractory perior od cardiac action potential compared to skeletal action potential

A

Prevents tetany of the heart (assures relaxation and filling between beats)

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19
Q

timing of action potential and refractory period

A

duration of action potential = duration of refractory period - this is important to prevent tetany of the heart (makes sure it is relaxed before it can respond to a new stimuli)

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20
Q

Major role of sodium channels (Ina) in cardiac myocytes

A

rapid depolarization of atrial and ventricular muscles and purkinje fibers

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21
Q

Major role of calcium channels (Ica) in cardiac myocytes

A

Contributes to atrial and ventricular depolarization and contraction (L-type and T-type)

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22
Q

Major role fo potassium channels (Ik) in cardiac myocytes

A

repolarization pahse in all cardiac myocytes (determined by a series of K channels that open and close at various times)

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23
Q

What type of exhcanger is Na-Ca (INCX) exchanger

A

3:1 electrogenic exchanger (3 Na out, 1 Ca in)

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24
Q

What type of exchanger is Na-ATPase

A

3:2 electrogenic exchanger

25
Q

Describe Phase 4 of cardiac myocyte action potential

A

Flat stable baseline (resting membrane potential -90mV)

26
Q

how is the baseline maintained in cardiac myocytes?

A

“inward rectifying K+ current” IK1 - pumps- pumps K out of the cell at or near resting potential to maintain stability

27
Q

what channel opens at phase 0 of cardiac myocyte action potential

A

Sodium channels - causes rapid influx

28
Q

Describe phase 2 of the cardiac myocyte action potential

A

IT01 closes at the end of phase 1 but other potassium channels remain open (k out) and offset the influx of Ca - results in the plateau stage

29
Q

sodium channel gates in the relative refractory period

A

Phase 3 - m gates closed and h-gates are beginning to open

30
Q

sodium channel gates in the absolute refractory period

A

Phase 1 and 2 - m gates open and h-gates closed

31
Q

define refractory period

A

deminsished capacity to respond to a stimulus

32
Q

when the ___ gate is closed the cell cannot respond to a stimulus no matter how great the intensity

A

h gate

33
Q

Supranormal or Dangerous period

A

breif period of tue at the end of relative refractory when ANY stimulus (even subthreshold) can generate an action potential resulting in abnormal activation or arrythmias

34
Q

Calcium induced calcium release

A

Ca enters the cell from extracellular space through voltage gated L-type Ca channels on sarcolema and into t-tubules = “Trigger Ca” - these Ca stimulate the release of Ca from SR via ryanodine receptors in the SR membrane

35
Q

“Trigger” Ca

A

the calcium that enters the cell through t-tubules in order to bind ryanodine and cause more calcium release from the SR

36
Q

phospholambam

A

phospholambam inhibits SERCA resulting in slowing calcium reuptake

37
Q

phosphorylated phospholambam

A

“Inhibits the inhibitor” - accelerated aclium uptake

38
Q

Preload

A

passive tension prior to muscle contraction - determined by the state of stretch (volume of blood in the ventricle just prior to contraction= end diastolic volume EDV)

39
Q

EDV

A

volume of blood in the ventricle just prior to contraction - related to ventricular stiffness

40
Q

Afterload

A

load that a muscle has to contract against - resistance to ejection of blood (diastolic blood pressure) Pressure in the aorta when it tries to open the valve

41
Q

Isovolumic contraction

A

tension is developed in the myocardium by there is no change in ventricular volume

42
Q

Starlings law (the quick and dirty)

A

The more you stretch the heart ( increase preload/amout of blood entering) the stronger the force contraction (to a certain point) Ex: faster pitch in baseball - you can hit it further

43
Q

Active force generation in muscle is determined by what two mechanisms?

A

1.) Number of cross bridges; myofilament overlap (determined by stretch - represents preload) 2.) Activation state of the mucle - timing and concentration of Ca in sytosol

44
Q

which principle (law) represents the ventricles ability to increase stroke volumbe with increased preload in the heart

A

Frank-Starling Law of the Heart

45
Q

contractility referes to what state of the heart

A

ionotropic state

46
Q

Contractility

A

how fast the myocardium is capable of shortening (maximal shortening - Vmax)

47
Q

Ionotropic state of the heart is under the control of what

A

Sympathetic nervous system

48
Q

Effect of increasing preload on contractility

A

NONE!! Increasing preload will increase force generation (frank starling) but with NOT change the contractility (remember: contractility is the ionotropic state of the heart)

49
Q

Sympathetic stimulation of the heart

A

increased calcium, catecholamines bind and cause activation of CAMP which causes an increase in the phosphorylation state of the cell- phosphorylation of phospholambam results in faster reuptake of calcium (faster relaxation)

50
Q

which channel is responsible for the change seen in phase 1 of cardiac myocyte action potential

A

IT01 opens and is responsible for the early repolarization

51
Q

IK1

A

open in the resting state (to maintain the balanced resting membrane potential) Reopens at the end of phase 2 disrupting the balance (plateua) and K wins resulting in depolarization (phase 3)

52
Q

Phase 3 of cardiac myocyte action potential

A

IK1 overcomes the K Ca balance in phase 2 resulting in potassium leaving the cell and depolarization

53
Q

Role of Na K ATPase in cardiac myocyte action potential

A

after the action potential the cell has gained small amount of Na and lost a small amount of K (not a significant amount but can build up over time) continual operation of NA K ATPase is required in order to prevent disruption of the Na and K gradients

54
Q

during the depolarization stage of cardiac myocyte action potential which channels open (and when)

A

Rapid sodium influx results in the sharp rise. L-type (slow) calcium channels open at -40 and start to cause a slow and steady influx of calcium (L-type remain open) . T-type calcium channels open at -50 and then close quickly. The Na channels then close as the voltage approaches membrane potential and we move to phase 1

55
Q

what is the general role of calcium channels in phase 0 of cardiac myocyte action potentials

A

working to contribite to depolarization. L-type remain open and contribute to the plateu phase (phase 2)

56
Q

which phases of the cardiac myocyte action potential are absolute refractory

A

Phase 1 and Phase 2

57
Q

which phase(s) of the cardiac myocyte action potential is relative refractory

A

Phase 3 - m gates closed and h-gates are beginning to open

58
Q

when do h-gates on sodium channels begin to reopen

A

begin to reopen in phase 3 (relative refractory) and are all open and reset by phase 4

CardioRenal I (13 decks)

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