initiation of heartbeat Flashcards

1
Q

difference between speed for neuronal and cardiac action potential

A

neuronal - short <1mesc

cardac - longer 250msec

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2
Q

what maintains the plateau phase of a cardiac action potential

A

Ca channels opening and entering

K channels opening and slowly leaving

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3
Q

describe cardiac action potential

A

1) Na enters rapidly
2) K out
3) plateau - a enters
4) drops: Na and Ca transported out by Na/k ATPase and Na/Ca exchanger protein (respectively)

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4
Q

Explain the difference between the lengths of action potentials for cardiac and skeletal muscle

A
  • skeletal muschas short refractory periods to allow discrete contraction which are v close together. Contract with temporal summation, unfused tetanus or fused tetanic contractions
  • cardiac: cannot tetanise cardiac muscle due to long refractory
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5
Q

list the cardiac pacemakers from fastest to slowest

A

sinus node, AV node, His bundle, Purkinje fibres

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6
Q

describe SA node

A
  • highest intrinsic rate (drives the prevailing rate and overdrives the tissues downstream from it.)
  • designed to generate action potential, not cause contraction
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7
Q

describe the 2 pacemaker theories

A

1) membrane clock: cyclical changes in ion currents, mainly Na and K. stimulated by adrenaline, inhibited by acetylcholine and blocked by ivabradine
2) calcium clock: release of Ca from intracellular stores. Regulates pacemaker, drives membrane potential up and down diastole

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8
Q

why is there slow conduction from SA to AV nodes

A
  • allow ventricular filling

- filter out high frequencies so ventricles don’t beat too fast

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9
Q

describe the layout of cells in ventricular muscle

A

conduction ALONG the length of cells.

intercalated disks give good strength and good conduction.

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10
Q

what are at the gap junctions of intercalated disks

A

connexons (protein channels) formed by connexins

  • allow small molecules and electrical currnts to pass
  • at ends of cells as conduction occurs mostly along cell. Anisotropic conduction?
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11
Q

describe Eithoven’s triangle and the different ways of taking measurements

A
  • formed by 2 shoulder and groin - pick any 2 corners
  • limb lead I: L arm to R arm
  • limb lead II:L foot to R arm: classic ECG shape
  • Limb lead III: L foot to L arm
  • bipolar (recording and reference electrode) and augmented leads (recording and virtual)
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12
Q

what could go wrong with PQ interval and whats the pathology

A

atrial conduction and AV node delay

AV block

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13
Q

what could go wrong with QRS duration and whats the pathology

A

ventricular contraction velocity.

bundle branch block

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14
Q

what could go wrong with ST interval and whats the pathology

A

heterogeneity of ventricular polarisation - all of ventricle depolarised.
myocardial infarction

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15
Q

what could go wrong with QT interval and whats the pathology

A

ventricular action potential duration

Long QT syndrome

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16
Q

where does Ca entering the myocyte accumilate

A

dyadic cleft - gap between SR and T-tubule

17
Q

key difference between cardiac and skeletal muscle Ca release

A

cardiac: CALCIUM-induced Ca release
skeletal: VOLATAGE-induced

18
Q

describe the relaxation of the action potential in the myocyte

A

1) Ca removed from cytosol by active transport - Sarcoendoplasmic Calcium ATPase (SERCA)
2) small amount entered through L channels is removed by Na/Ca exchangers

19
Q

what regulated the activity of SERCA

A

phospholamban

20
Q

what’s resting intracellular Ca

21
Q

explain chronotropy and give examples

A

Heart rate.

  • positive chronotropy = increase HR, e.g.adrenaline, nor-adrenaline: increase funny current = faster rate of diastolic depolarisation
  • Negative chronotropy, e.g. acetylcholine. decrease If, opens K (ACh) channels, slower HR
22
Q

what is intropy

A

strength/force of contraction.

23
Q

explain lusitropy and give clinical examples

A

rate of relaxation of cardiac muscle.

  • heart failure = unable to take up ca.
  • diastolic dysfunction - heart doesnt relax between pumps. HFpEF: heart failure with a preserved ejection fraction. diastolic.
24
Q

examples of positive intropy and lusitropy

A
  • positive: Beta-1 receptor stimulation - adrenaline and NA.

- isoprenaline - B1 agonist. B1 stimulation acts via Gs and PKA

25
what are the PKA targets and explain the effects
1) pacemaker 2) L-type Ca channels: 3) RYR2 4) ATPase subunits 5) myofilaments
26
what are the both of the pacemaker theories inhibited/stimulated by
-both stimulated and inhibited by neurotransmitters (NA and ACh)
27
what does PKA do to pacemaker cells
cAMP and PKA increase pacemaker currents = positive chronotropy
28
what does PKA do to L-type channels
PKA phosphorylates L- type Ca channels and increases channel opening. more Ca enters positive chonotropy and intropy
29
what does PKA do to ATPase subunits (on SR)
PKA phosphorylates phospholamban (PLB) and phospholemman (PLM) - increases SR Ca uptake and cellular Na extrusion – positive lusitropy
30
what does PKA do to myofilaments
phosphorylates troponin I and myosin binding protein C and increases rate of cross bridge cycling – faster contraction (inotropy) - faster relaxation (lusitropy)
31
what does PKA do to RYR2
phosphorylates RyR2 and increases SR Ca release | – positive inotropy
32
what is membrane clock stimulated, inhibited and blocked by
adrenaline ACh ivabradine
33
what is a role of the calcium clock model
regulate pacemaker