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Physiology 208 > Cardiac Muscle > Flashcards

Cardiac Muscle Flashcards

1
Q

Cardiac Muscle

A
  • made up of cardiac myocytes
  • interconnected by intercalated disks
  • has striations
  • less abundant, but larger T-tubules than skeletal muscle and runs perpendicular and parallel to muscle fibres
  • smaller amounts of SR bc cardiac muscle requires entry of extracellular Ca2+
  • abundance of mitochondria
  • oxidative metabolism
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2
Q

Intercalated Disks

A
  1. Desmosomes: link mechanically

2. Gap Junctions: link them electrically

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3
Q

Autorhythmic Cells

A
  • pacemakers
  • generate action potentials spontaneously
  • the depolarization begins in the Sinoatrial node
  • non-contracting myocardial cells
  • smaller and contain few contractile fibres
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4
Q

Electrical Conduction in Myocardial Cells

A
  • autorhythmic cells spontaneously fire AP’s

- depolarization of autorhythmic cells spread rapidly to adjacent contractile cells through gap junctions

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5
Q

Cardiac Conduction Process

A
  1. SA Node
  2. Internodal Pathways
  3. AV Node
  4. Av Bundle
  5. Bundle Branches
  6. Purkinje Fibres
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6
Q

HCN Channels

A
  • only in auto rhythmic cells
  • Hyperpolarization-activated cyclic nucleotide-gated channels
  • responsible for funny current)
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7
Q

AP’s in Autorhythmic Myocardial Cells

A
  1. HCN channels open (start at -60mV to -40mV)
  2. some Ca2+ channels (T-type) open, HCN channels close
  3. lots of Ca2+ channels (L-type) open
  4. Ca2+ channels close, K+ channels open
  5. K+ channels close
  6. repeat
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8
Q

AP’s in Contractile Myocardial Cells

A
  • ions entered from AP are transferred to adj. cells through gap junctions
    1. Resting Potential
    2. Na+ channels open (causing Na+ action potential spike)
    3. Na+ channels close
    4. Ca2+ channels open (L-type channels); fast K+ channels close leads to sustained depolarization
    5. Ca2+ channels close; slow k+ channels open (hyperpolarization)
    6. Resting potential
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9
Q

Why have a Long Action Potential in Cardiac Muscle

A
  • prevents summation of contraction
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10
Q

Excitation-Contraction Coupling in Cardiac Muscle

A
  • DHP receptors are NOT mechanically coupled to RyR

- Ca2+ entry is necessary for contraction

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11
Q

Excitation-Contraction Coupling Process in Cardiac Muscle

A
  1. action potential enters from adjacent cell
  2. voltage-gated Ca2+ channels open. Ca2+ enters cell
  3. Ca2+ induces Ca2+ release through RyR
  4. local release causes Ca2+ spark
  5. summed Ca2+ sparks create a Ca2+ signal
  6. Ca2+ ions bind to troponin to initiate contraction
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12
Q

Cross Bridge Cycling

A
  • increase in [Ca2+]I triggers contraction by removing the inhibition of cross bridge cycling
  • tropomyosin shifts
  • Ca2+ binds to troponin
  • release of Pi strengthens bond btwn actin and myosin
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13
Q

Relaxation of Cardiac Muscle

A
  • reuptake into the SR is primary mechanism

- removal of Ca2+ to extracellular space is more important in cardiac muscle

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14
Q

Relaxation Process of Cardiac Muscle

A
  1. current spreads through gap junctions to contractile cell
  2. AP travel along plasma membrane and T-tubules
  3. Ca2+ channels open in plasma membrane and SR
  4. Ca2+ induces Ca2+ release from SR
  5. Ca2+ binds to troponin, exposing myosin-binding sites
  6. cross bridge cycle begins
  7. Ca2+ is actively transported back into the SR and ECF
  8. Tropomyosin blocks myosin-binding sites (muscle fibre relaxes)
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15
Q

Phospholamban

A
  • regulates the SERCA pump in cardiac muscle
  • crucial regulator of cardiac contractility
  • dephosphorylated state PLN inhibits SERCA
  • phosphorylated: Ca2+-pump inhibition removed, enhancing relaxation rates and contractility
  • rate and amount of Ca2+ uptake is increased, causing quicker relaxation and a larger store of Ca2+ for subsequent contractions
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16
Q

Enhancing Contractile Force in Cardiac Muscle

A
  1. Increase in intracellular Ca2+ in cardiac myocytes enhances contractile force
  2. Length tension relationship
    • cardiac muscle generates a greater force when slightly stretched
17
Q

Increase in Intracellular Ca2+ in Cardiac Myocytes

A
  • cardiac muscle is capable of graded single twitch contractions
  • if cytosolic Ca2+ is low some actin remains covered by tropomyosin
  • increased: additional troponin complexes activated and increased cross bridge formation leading to increased force of contraction
18
Q

Neuronal Inputs in the Heart

A
  • innervated by the autonomic nervous system
  • sympathetic increases heart rate/conduction (auto rhythmic and contractile)
  • parasympathetic decreases heart rate/conduction (autorhythmic)
19
Q

Sympathetic Modulation of Contraction

A
  1. Phosphorylation of Ca2+ channels causes the calcium channels to remain open longer during action potentials
  2. Phosphorylation of RyR enhances sensitivity to Ca2+, increasing release of Ca2+ from SR
  3. increases rate of myosin ATPase
  4. Phosphorylation of SERCA (PLN) increases the speed of Ca2+ re-uptake which increase Ca2+ storage
20
Q

Sympathetic Activity of Heart

A
  • results in a more rapid and forceful contraction

- increase tension in shorter amount of time

21
Q

Cardiac Length Tension Relationship

A
  1. a slightly stretch sarcomere increases the Ca2+ sensitivity of the myofilaments
    • a stretched sarcomere has a decreased diameter which may reduce the distance that Ca2+ needs to diffuse increasing probability of cross-bridge cycling
  2. as slightly stretched sarcomere puts additional tension on stress-activated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release
22
Q

Heart Rate is under Tonic Control

A
  • auto rhythmic cells can be modulated by sympathetic and parasympathetic neurons
  • sympathetic: increases
  • parasympathetic: decreases
  • resting heart rate: 70-72 bpm when parasympathetic is dominant
23
Q

Parasympathetic Modulating Pacemaker Activity

A
  • Parasympathetic neurons containing ACh mainly innervate the SA and AV node influencing autorhythmic myocardial cells, decreasing frequency of heart rate/AP’s
  • ACh acts on muscarinic cholinergic receptors opening K+ channels and closing T-type Ca2+ channels and HCN channels
  • these mechanisms act at the AV node to decrease conduction velocity
24
Q

Decrease Conduction Velocity

A
  1. block HCN channels: slower depolarization requires more time to reach threshold
  2. K+ (GIRK) channels: starting at a more negative value, requires more time
  3. T-type Ca2+ channels: slow channels, so takes more time
25
Q

Sympathetic Modulation of Pacemaker Activity

A
  • Beta1 adrenergic receptors can be activated by NE released from sympathetic neurons or Epinephrine from the adrenal medulla
  • increased Na+ conductance through HCN channels and Ca2+ through T-type causes: cell to reach threshold more rapidly and a decreased level of repolarization

Physiology 208 (11 decks)

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