cardiac physiology 2 Flashcards
what is Bachmann’s bundle
an anatomical structure between the right and left atrium and is considered to be the main route of inter-atrial conduction with specialized conduction properties - preferred route of conduction during atrial depol (R to L)
what is a membrane potential
difference in electrical potential between the inside and outside of a cell - due to an unequal distribution of ions
what is a resting membrane potential
the potential difference in an unexcited cell - inside is always -ve
cardiomyocyte resting membrane potential
-80/-90mV
cardiac pacemaker resting membrane potential
between -50mV and -70mV
what ion is most responsible for maintaining the RMP
K+ (membrane is most permeable, can leave the cell to maintain negative gradient)
what 3 ions do cardiomyocytes primarily express channels for?
Na+; K+; Ca2+
cardiomyocytes electrical properties
not auto-rhythmic - don’t generate their own AP; conduct APs via gap junctions, T tubules and intercalated discs
pacemaker cells electrical properties
auto-rhythmic - rate can be modulated by autonomic inputs; hagiarchy of pacemakers exist (SAN is most frequent so therefore overrides the others)
heart depol steps (4)
- pacemakers cells in SAN initial depol, conducted across atria;
- depol reaches AVN and conduction to ventricles is delayed for 100ms
- depol spreads down the bundle of His and purkinje fibres
- depol of ventricles, delay allows for filling prior to contraction
what do T tubules allows for
quick conduction of APs (they penetrate deep into the cells)
why are gap junctions, intercalated discs, T tubules (and desmosomes) important in conduciton
all allow for fast electrical depol between cells allowing to muscle to contract in one uniform wave
ionic bases for the conduction of an AP in cardiomyocytes + draw out graph (5)
phase 4: RMP - there are not time-dependent currents in this phase, it is the electrical diastolic phase;
phase 0: rapid depol - initiation of AP, influx of Na+ due to opening of fast VG gated Na+ channels, Ca2+ ch subsequently open;
phase 1: rapid repol - almost complete inactivation of Na+ Chs (and fast K+ outward current);
phase 2: plateau phase - elongation of AP due to continued entry of Ca2+ from L-type Ca2+ Chs (and Na+/Ca2+ exchanger NCX1);
phase 3: repolarisation phase - opening of delayed rectifier K+ current leading to outward K+ flow, return to RMP
why is the plateau phase necessary
AP must be drawn out (200-300ms) to allow the muscle to relax before the next contraction (otherwise tetanus); contraction occurs due to Ca2+ influx
what causes difference in AP shape across myocytes
depends on which ions are carrying out the AP and the number of channels used
how do pacemaker cells self-depolarise
due to the funny current - PMCs have an unstable, decaying resting potential which slowly drifts towards the depol threshold (-40mV) and allows for spontaneous depol; funny current causes this drift and is formed from the activation of HCN Chs and Na+ influx (during phase 3)
AP of pacemaker cells + draw out graph
- threshold reached by funny current (Na+ influx);
- rapid depol due to Ca2+ influx (L-type Ca2+ Chs), not as fast as myocytes;
- repol due to VG K+ Chs causing K+ outflux
effect of sympathetic stimulation on pacemaker potential
Sympathetic stimulation (adrenaline or nor-adrenaline via B-adrenergic receptors) instantly increase rate until stimulation is removed
effect of parasymp stimulation on pacemaker potential
Parasympathetic stimulation (vagal stimulation and acetylcholine) instantly decrease rate until stimulation removed
how can the rate of pacemaker depol be altered? (2)
Changing the slope of pacemaker potential’s decay to threshold; Increasing or decreasing the polarisation of the basal pacemaker (resting) potential making either it more or less negative (i.e. how much change in membrane potential is needed to reach the threshold)
what is the (cardiac) cellular response to muscarinic stimulation (6)
Acetylcholine interacts with the Msc receptors and inhibit the attached adenylate cyclase;
causes a reduction in levels of cAMP and in turn protein kinase A;
Reduction in levels of cAMP = reduces pacemaker (funny) inward currents - Takes longer to depolarise to the threshold;
decreased protein kinase A = reduces Ca2+ inward currents and K+ outwards currents;
causes increase in the duration of time for the pacemaker potential to drift to threshold causing AP;
Acetylcholine also has a direct effect on Muscarinic K+ channels that allows potassium efflux and this increased the level of hyperpolarisation of the resting membrane potential
Cellular Response to B-Adrenergic Stimulation in pacemaker cells
Noradrenaline interacts with the B-adrenergic receptors and activates the attached adenylate cyclase; This causes an increase in levels of cAMP and in turn protein kinase A;
Increase in levels of cAMP = increased pacemaker (funny) inward currents;
Increase in levels of protein kinase A increases Ca2+ inward currents and K+ outwards currents
B-adrenogenic stimulation effect on cardiac myocytes action potentials
Increase Ca2+ inward currents allows for a stronger and faster plateau phase;
Increase K+ outwards currents allow for a faster repolarisation phase;
Protein Kinase A also inhibits phospholamban which regulates the sarcoplasmic reticulum Ca2+ pump allowing more free Ca2+ in the cell and therefore stronger contraction
