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circulation and breathing > cardiac action potentials and contraction excitation coupling > Flashcards

cardiac action potentials and contraction excitation coupling Flashcards

1
Q

what are the three pacemakers of the heart and its corresponding frequencies

A
  • primary pacemaker SAN (100/min)
  • secondary pacemaker AVN (40-60/min)
  • tertiary pacemaker purkinje fibres (20-30/min)
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2
Q

what is the structure of the action potential in the SAN

A
  • phase 4- resting phase slight increase in membrane potential
  • phase 0 depolarisation phase
  • phase 3 repolarisation phase
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3
Q

what are the main ionic currents in each phase of the action potential in the SAN

A
  • phase 4 includes I_funny (slow na channel), I_CaL and I_CaT and acetylcholine sensitive potassium channels
  • phase 0- I_CaL
  • phase 3- I_Ks and I_Kr (delayed rectifier potassium channels)
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4
Q

what is the structure of an action potential in the ventricular myocardium

A
  • phase 4 (resting phase is stable)
  • phase 0- depolarisation
  • phase 1- slight depolarisation
  • phase 2- plateau phase
  • phase 3- repolarisation
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5
Q

what is the different ionic currents involved in each phase of the ventricular myocardium action potential

A
  • phase 4- I_Ki (inward rectifier pottasium channels), leaky pottasium channels and Na/K Atpase
  • phase 0- I_Na
  • phase 1- closing of I_Na and I_to (pottasium)
  • phase 2- I_CaL and I_Kr/I_Ks (delayed rectifier pottasium channels)
  • phase 3- I_Kr I_Ks
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6
Q

compare and contrast the two action potentials in the SAN and ventricle

A
  • SAN is spontaneous and slow
  • ventricle is induced and fast
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7
Q

what is the starting membrane potential of a SAN action potential

A

-65/-60

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8
Q

what is the resting membrane potential of a ventricular action potential

A
  • 90
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9
Q

how is the frequency of the action potential in the SAN regulated

A
  • change threshold potential
  • change resting potential
  • change slope of depolarisation (phase 4)
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10
Q

what is the excitation-contraction coupling

A
  • action potential leads to opening of calcium voltage gated channels (I_CaL)
  • this causes the ryanodine receptors in the sarcoplasmic reticulum to open allowing flow of calcium from its store to the sarcoplasmic reticulum
  • this increase in calcium thus leads to contraction
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11
Q

what happens when the calcium ions are re pumped in the sarcoplasmic reticulum and also out of the cell

A
  • muscle relaxation
  • repolarisation
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12
Q

what is the refractory period and what can it be divided into

A
  • absolute refractory period- action potential can not be triggered no matter how strong the stimuli is
  • relative refractory period- action potential most likely would not be triggered, needs a very strong stimuli to trigger one, new action potential would have a low amplitude
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13
Q

what is the characteristic of cardiac muscle

A
  • striated
  • sarcomeres made of actin and myosin making a banding pattern
  • during contraction sarcomere decrease in lengthen
  • nuclei in centre of cell with one per cell
  • interrelated discs are sites of attachments between cells
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14
Q

how does calcium ions cause muscle contraction

A
  • myosin binding site on actin is blocked by troponin
  • troponin has 3 structures a calcium binding site, a site blocking the myosin binding site and a structural domain
  • binding of calcium causes a conformational change in shape resulting in the myosin binding site to be exposed
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15
Q

where are the sources of calcium

A
  • intracellular from sarcoplasmic reticulum
  • extracellular sarcolemma
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16
Q

how does an action potential cause muscle contraction

A
  • action potential goes along the t tubule of the muscle
  • causes calcium voltage gated L channels to open
  • causes calcium influx into myocyte
  • causes the ryanodine receptors to open which allows influx of calcium into sarcoplasm from the sarcoplasmic reticulum
  • this causes binding of calcium to troponin which results in muscle contraction
17
Q

what happens during muscle relaxation

A
  • Ca ATPase found in membrane of sarcolema which pump out calcium ions from the cell
  • Ca/Na exchanger- 3 sodium ions into cell, one calcium ion out of cell
  • Ca2+ pump in membrane of sarcoplasmic reticulum to pump calcium back into its store
18
Q

how does parasympathetic nervous system decrease heart rate

A
  • parasympathetic NS releases Ach which binds to M2 muscarinic (Gi receptors)
  • inhibition of adenylate cyclase and decreased levels of cAMP
  • reduced protein kinase activity less activation of I_funny and I_Ca currents
  • activation of M2 receptors also directly activate acetylcholine sensitive pottasium channels
  • this results in hyperpolarisation making it longer to reach the action potential threshold thus reducing heart rate
19
Q

how does sympathetic activation lead to increased heart rate

A
  • release of noradrenaline from sympathetic fibres derived from paravertebral of sympathetic trunk
  • binds to B1 adrenergic receptors in SAN- increased adenylate cyclase activity- increased cAMP
  • activation of phosphokinase A, phosphorylates I_funny and I_Ca channels
  • more influx of sodium and calcium into cells during phase 4 and action potential threshold met quicker
20
Q

how does sympathetic innervation cause increased contractility of the heart

A
  • noradrenaline binds to B1 receptors in myocardium
  • activation of adenylate cyclase= increased cAMP+activation of phosphokinase A
  • phosphorylates calcium L channels and ryanodine receptors causing more calcium to enter sarcoplasm of cell
  • increased contractility
  • calcium influx also results extended plateau phase of phase 2 meaning contraction happens longer
  • PKA deinhibtis phospholamban meaning more calcium is uptake by Ca pump into their store during relaxation
21
Q

what is channelopathies

A
  • mutations in ion channels (mostly K and Na) responsible for AP generation
  • usually no apparent problem but is responsible for 85% of sudden death syndrome (unexpected cardiac arrest in seemingly healthy individuals due to underlying cardiac arrhythmias)
22
Q

what is long QT syndrome

A
  • due to channelopathies
  • mutation in sodium channel
23
Q

what is idiopathic ventricular fibrillation

A
  • ventricular fibrillation in patients with no underlying heart condition or genetic condition
24
Q

what is the effect of calcium channel inhibition on hear Tate and contractility

A
  • decreased frequency
  • reduced contraction
25
Q

what are the three effect of antihypertensive and antiarrhythmic drugs

A
  1. inhibit spontaneous AP generation- reduced frequency
  2. inhibit ventricular contraction- reduced cardiac output and cardiac work
  3. vasodilation- decrease in bp
26
Q

action potentials arising from the relative refractory period can cause what type of condition

A

arrhythmias

27
Q

how does an ECG work

A
  • galvanometer
  • measures potential changes on surface of heart which is measured by electrolytes
28
Q
A

circulation and breathing (26 decks)

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