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S2B3: Physiology > Cardiac Electrophysiology- I Cardiac Muscle > Flashcards

Cardiac Electrophysiology- I Cardiac Muscle Flashcards

1
Q

What are cardiac myocytes & what are their specialized functions?

A
  • Cardiac myocytes
    • all electrically active with specialized function
  • Specialized function
    • Contraction: force generation (working myocytes)
    • Conduction: conduction pathways and working myocytes
    • Automaticity: pacemaker function & conduction pathways in pathology
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2
Q

Expression of what traits that produce myocyte-specific & tissue-specific characteristics & what are those characteristics?

How are they expressed?

A
  • Traits
    • cardiac ion channels
    • gap junctions
    • contractile proteins
  • Characteristics
    • Distribution of channels
    • Distribution of gap junctions
    • Distribution of force-generating capacity
    • Current density
    • Action potential morphology
  • They are expressed in a heterogeneous continuum across the heart
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3
Q

What are the factors affecting conduction?

What are the characterisic of each of these factors in Rapid & Slow conduction areas of the heart?

A
  • Factors
    • Internal resistance
    • Cell-to-cell resistance
    • Rate of rise of AP
    • AP amplitude
  • Rapid Conduction
    • Large cells
    • many gap junction
    • AP - fast rate-of-rise
    • AP - greater amplitude
    • carried by Na+ channels
  • Slow Conduction
    • small cells
    • fewer gap junctions
    • AP - slow rate-of-rise
    • AP - lesser amplitude
    • carried by Ca2+ channels
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4
Q

Describe the progression of electrical syncytium in the heart

Describe the progression of the runctional syncytium in the heart

A
  • Electrical Syncytium (conduction system)
    • Atria –> AV Node –> His bundle-Purkinje cells –> Ventircle
  • Functional Syncytium (force generation– working cells)
    • atrial contraction –> ventricular contraction
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5
Q

What are features of ventricular myocytes?

Shape?

Prominant organelles?

A
  • Ventricular myocytes
    • single central nucleus
    • broad sheets of branching cells
    • lots of mitochondria (20%)
    • Striated muscle
      • Z-lines
      • myofibrils in parallel
    • Sarcoplasmic reticulum
      • well developed t-tubule system
      • triads and diads (circles)
    • Inset
      • t-tubule, triad, lateral sacs
    • Intercalated disc: end to end transmission
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6
Q

What is the function of intercalated discs?

Identify the features of intercalated discs shown in the provided image & describe their functions

A
  • Intercalated cell-to-cell electro-mechanical function : functional syncytium
    • Fascia Adherens
      • cell-cell connection transmits force
    • Desmosomes
      • “press studs” cytoskeleton attachment
    • Gap junctions
      • electrical connection
      • normal heart rhythm depends on coupling cardiac myocytes via gap junctions– dependent on:
        • type & amount connexin expressed
        • size & distribution of GJ plaques
        • proportionof of connexin subtypes assembled
          • distribution related to chamber & how chamber conducts
        • gating and connexin type
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7
Q

Describe the specific features of atrial working myocytes

Shape?

prominent organelles?

A

Rapid, impulse transmission end-to-end and side-to-side

  • bundles of 2-3 cells
  • elliptical shape
  • generally, no branching
  • Intercalated discs
    • horizontally oriented intercalated discs
    • occassional end-end intercalated discs
    • can get side-to-side & end-to-end transmission and this particular structure sets up arrhythmias
  • series of desmosome & gap junctions
  • SR, but abscence of t-tubules
    • part of what makes conduction slow
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8
Q

What is myocardial connective tissue composed of?

What functions does it provide?

A
  • Composition
    • collagen-elastin matrix
    • connects myocytes nerve and capillary networks embedded in meshwork
  • Provides
    • structure
      • collagen struts
    • support
      • passive elastic component
      • prevents overstretching of the heart
    • force transmission
    • may “hold” vessels open during contraction to counter surround pressure
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9
Q

How is the cardiac action potential different from skeletal action potential?

A
  • Skeletal muscle
    • force of contraction is much longer and happens after the action potential
    • important for force production through spatial & temporal summation of action potentials
  • Cardiac muscle
    • Cardiac has a different shape and is longer
    • contraction begins with the action potential, & the duration of the contraction and the action potential are similar
    • prevents temporal summation & can not have tympany
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10
Q
A
  • a. large cells
  • c. many gap junctions
  • f. Na+ channels
  • g. large action potential amplitude
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11
Q
A

longer

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12
Q
A

b. the duration of contraction is roughly the same as the duration of the AP

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13
Q

Cardiac action potentials consist of which membrane boltage-gated, time-dependent currents?

Which electrogenic transporters carry current?

Who are the important players in action potentials?

A
  • Membrane coltage-gated, time-dependent currents
    • sodium current (INa)
    • funny current (If)
    • Calcium current (ICa)
    • Potassium current (IK)
      • IK1
      • It01
  • electrogenic transporters carry current
    • Na+ - Ca2+ exchanger (INCX)
    • Na+ - K+ ATPase (INa-K)
  • Sarcoplasmic Reticulum
    • SERCA (uptake Calcium)
      • inhibited by phospholambam
        • when phosphorylated, it is inhibited itself
    • RYR (release Calcium)
  • Adenylate Cyclase
    • converts ATP to cAMP which activates PKA, which phosphorylates
      • phospholambam
      • RYR
      • L type Calcium channels
      • Potassium Channels
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14
Q

What stage in indicated by the provided photo?

What is the determinig factor of this stage?

A
  • Phase 4: Resting Potential
    • flat line
    • determined by stable potassium conductance
      • IK1 - inward rectifying K+ (maintains the membrane potential at -90 mV)
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15
Q

Describe what occurs in phase 0-3 of a cardiac action potential

A
  • Phase 0: Sodium - Rapid Depolarizaion
    • INa - Na+ channels
    • gNa (sodium conductance)- rapid increase
    • CaL - L type calcium channels are open
    • INCX - Na-Ca Exchanger (bring some sodium into the cell)
  • Phase 2: CaL closing
  • Phase 3: INCX reverses - Calcium removal
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16
Q

Describe the state of the sodium channel during each of the 4 phases of a cardiac action potential

A
  • In Phase 4, the sodium channel is activatable
  • As we enter Phase 0, and membrane potential approaches 0, the sodium gates will be deactivated, so sodium can no longer be conducted at the end of Phas 0
  • Phase 1 & 2 the sodium gate & the channel is inactivated & inactivatable
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17
Q

What are the important repolarizing currents & in what phases do they occur?

A

​

  • Repolarizing currents
    • transient outward (It0)
      • Rapid repolarization of Phase 1
    • other potassium channels begin to open as It0 closed
    • Plateau phase (2) is due to the fact that the calcium that is entering the cell is roughly proportional to the charge caused by the potassium leaving the cell
    • End of phase 2, beginning phase 3, calcium channels close & potassium channels open, and we repolarize the cell and go back to phase 4
18
Q

What is an imporant characteristic about IK1 at resting membrane potential

A
  • Around resting membrane potential, IK1 can bring potassium into the cell
  • As a rectifier, it may go negative (inward) or positive (outward), but in the end you have a very stable baseline
19
Q
A

c. opening of Na+ channels

20
Q
A

d. movement of K+ in and Ca2+ out

21
Q
A

b. Ca2+ close

22
Q
A

d. IK1 channels

23
Q

What is the clinical importance of the cardiac refractory period?

A

any change in heart rate is due to a change in refractory period

and most if not all arrhythmias are due to a change in refractory period

24
Q

What is a refractory period & during which cardiac phases is the absolute refractory period?

Relative Refractory period?

Super normal period?

A
  • Period of:
    • abolished excitability
    • reduced ability to resopnd to a stimulus
  • absolute refractory (phase 1 to end of phase 2)
    • sodium channels are closed & cannot be activated
  • Relative refractory (phase 3)
    • sodium channels are able to be activated
    • with a strong enough impulse, you can get an action potential, but not a very good one – it will have a slower rate of rise & lower amplitude
      • can be disturbing, enough to excite other cells
  • Super normal period (phase 4)
    • membrane is back at rest and any impulse can generate an action potential
25
Q
A

b. tetany

26
Q
A

d. inactivation of Na channels

27
Q
A

a. Ca channels close and some Na channels become activatable

28
Q

Similarities between Cardiac vs. skeletal muscle contractions.

What components are important for excitation-contraction coupling?

A
  • Similarities
    • force generation - sliding filament theory
      • actin-regulated – myosin interaction
    • excitation- contraction coupling; Ca2+
    • dependence on Ca2+
      • however, heart is reliant on extracellular calicium for contraction
    • ATP
  • Excitation-Contraction coupling
    • Sarcoplasmic reticulum
      • well developed & similar to skeletal muscle
      • Ca2+ source
        • sarcoplasmic reticulum
        • extrecellular
      • T-tubules (centricular muscle only)
        • critica source of calcium
        • 5x wider & 25x volume of skeletal muscles
29
Q

Describe the mechanism of excitation-contraction coupling in the heart

A
  • CAM: Excitation-contraction coupling
  • wave of excitation (depolarization)
    • gap junctions- sarcolemma
    • interior of cell - t-tubules
  1. When there is an action potential on a sarcolemmal, Ca2+ channel open & allow entry of extracellular Ca2+
    • this “triggers”:
  2. SR calcium release RYR channels
    • Ca2+ induced Ca2+ release
  3. Ca2+ - TnC Complex
  4. Actin-Myosin cycle
30
Q

How do we stop the muscle contraction in the heart?

A
  • To stop the contraction, we need to get Calcium out of the cell– where does it go?
    • Slow: Sarcolemma Ca-ATPase and Mitochondria
    • NCX
    • SR will take up most of it via CERCA
      • removes Ca2+ from sarcoplasm; SR- calesquestrin Ca2+ dissociates from Troponin-C
      • phosphorylated phospholamban - facilitates relaxation (+lusitropic)
  • once calcium is out, ATP can break the actin-myosin bond
  • repolarize membrane; K+ efflux
31
Q

Fill out the provided table

A
32
Q

What are the two major control mechanisms that accound for force generation in the heart?

A
  1. number of cross bridges
    1. myofilament overlap
    2. Ca2+ sensitivity
    3. muscle cross-sectional area
  2. Activation state; timing &/or concentration of Ca2+
33
Q

Describe the force-length relationship of muscles fibers

What is the major difference between cardiac & skeletal muscle

** pretty confused about this

A
  • L0 (Lmax) = greatest active tension
    • optimal sarcomere length
  • Cardiac muscles have a greater stiffness (RT curve)
    • high % connecive tissue
    • titan
  • As you change the lenght of the sarcomere, you change the impact of Calcium (this is unique to heart tissue)
    • shorter fibers are less sensitive to calcium, stretched are more sensitive
  • So, when you are lengthing a muscle, up to L0, the force is going to be greater because it is becoming more sensitive to calcium
34
Q

What is the Frank Starling Law of the Heart

A

Heart - intrinsic control

end diastolic volume - stretch - increased venous return - increased preload (improve force generation & enance stroke volume)

alteration of sarcomere length & calcium sensitivity that changes the force to cause the next stroke volume

35
Q

Describe force generation in the activation state

A
  • Contractility: the inotropic state (calcium & contractility) of the myocardium determiens the force generation
    • functional syncytium
    • all cells depolarize
      • no spatial summation; recruitment as in skeletal muscle
    • dependent on entry of extracellular Ca2+ to “trigger” SR Ca2+ release
    • Force is modulated by the concentration of free Ca2+; [Ca2+]I
    • Changing preload does not alter contractility
    • Starling’s Law of the Heart is not related to changes in contractility
      • due to sarcomere alignment & calcium sentitivity – NOT calcium concentration or ionotropic state
36
Q

What ionic concentration is associated with contractility?

What does inotropic state indicate?

How does contractility apply to skeletal muscle versus cardiac?

A

Contractility is indicative of calcium concentration. Increased calcium concentration results in increased contractility

Inotropic state refers to a change in contractility therefore a change in calcium concentration

Contractility does not apply to skeletal muscle because every skeletal muscle contraction has the same concentration of calcium associated. Contractility is associated with cardiac muscle because different strengths of triggers can result in varying level of calcium release and varying contractility and force

37
Q

What are the two basic components that change the force produced by the heart?

A

Calcium concentration

Length component

38
Q

Describe sympathetic control of force of contraction of the heart.

A

Binds beta1 receptor

Positive Inotropic Effect

adenylyl cyclase

Increase cAMP

Activate PKA

phosphorylate phospholamban (SERCA, ryanidine channels) and calcium channels

phosphorylate calcium channels - more calcium - big trigger

Phosphorylate phospholamban faster uptake (SERCA) and release of calcium meaning more available calcium

more calcium more trigger more force

39
Q

How would you expect this graph of contractility to change given a beta1 agonist?

A

Beta1 agonist induces inotropic state, elevating calcium therefore contractility and force in cardiac muscle

40
Q

What is the relationships between velocity of shortening and preload?

What is the relationship between velocity and sarcomere length?

A

Velocity of shortening is inversely related to load
low load leads to high velocity
infinite load leads to isometric contraction

Velocity of shortening is independent of sarcomere length

41
Q

How does shortening velocity and force of contraction change with positive inotropic state of cardiac muscle?

A

Increase Vmax and increase contractility

so

Faster shortening and greater force

42
Q
A

S2B3: Physiology (6 decks)

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