initiation of heartbeat Flashcards
difference between speed for neuronal and cardiac action potential
neuronal - short <1mesc
cardac - longer 250msec
what maintains the plateau phase of a cardiac action potential
Ca channels opening and entering
K channels opening and slowly leaving
describe cardiac action potential
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)
Explain the difference between the lengths of action potentials for cardiac and skeletal muscle
- 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
list the cardiac pacemakers from fastest to slowest
sinus node, AV node, His bundle, Purkinje fibres
describe SA node
- highest intrinsic rate (drives the prevailing rate and overdrives the tissues downstream from it.)
- designed to generate action potential, not cause contraction
describe the 2 pacemaker theories
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
why is there slow conduction from SA to AV nodes
- allow ventricular filling
- filter out high frequencies so ventricles don’t beat too fast
describe the layout of cells in ventricular muscle
conduction ALONG the length of cells.
intercalated disks give good strength and good conduction.
what are at the gap junctions of intercalated disks
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?
describe Eithoven’s triangle and the different ways of taking measurements
- 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)
what could go wrong with PQ interval and whats the pathology
atrial conduction and AV node delay
AV block
what could go wrong with QRS duration and whats the pathology
ventricular contraction velocity.
bundle branch block
what could go wrong with ST interval and whats the pathology
heterogeneity of ventricular polarisation - all of ventricle depolarised.
myocardial infarction
what could go wrong with QT interval and whats the pathology
ventricular action potential duration
Long QT syndrome
where does Ca entering the myocyte accumilate
dyadic cleft - gap between SR and T-tubule
key difference between cardiac and skeletal muscle Ca release
cardiac: CALCIUM-induced Ca release
skeletal: VOLATAGE-induced
describe the relaxation of the action potential in the myocyte
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
what regulated the activity of SERCA
phospholamban
what’s resting intracellular Ca
100mM
explain chronotropy and give examples
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
what is intropy
strength/force of contraction.
explain lusitropy and give clinical examples
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.
examples of positive intropy and lusitropy
- positive: Beta-1 receptor stimulation - adrenaline and NA.
- isoprenaline - B1 agonist. B1 stimulation acts via Gs and PKA
what are the PKA targets and explain the effects
1) pacemaker
2) L-type Ca channels:
3) RYR2
4) ATPase subunits
5) myofilaments
what are the both of the pacemaker theories inhibited/stimulated by
-both stimulated and inhibited by neurotransmitters (NA and ACh)
what does PKA do to pacemaker cells
cAMP and PKA increase pacemaker currents = positive chronotropy
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
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
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)
what does PKA do to RYR2
phosphorylates RyR2 and increases SR Ca release
– positive inotropy
what is membrane clock stimulated, inhibited and blocked by
adrenaline
ACh
ivabradine
what is a role of the calcium clock model
regulate pacemaker
