CV physiology Flashcards
rates of contraction for SA node, AV node, bundle of his
SA node ~ 70
AV node ~ 40-60
bundle of his ~ 30-40
what is overdrive suppression?
higher frequency of SA node firing will suppress the other pacemaker cells from firing at their inherent rates bc the AP will pass from the SA node down the conduction system to the other cells before they have the chance to fire
what is the consequence of varied regional conduction velocities in the heart?
AV node is the slowest
Purkinje fibers are the fastest
this allows for the AV node to be the “gatekeeper” for the ventricles if the atria are firing too often and it also allows for coordinated ventricular contraction
2 determinants of cardiac membrane potential
ionic gradients, ionic permeabilities
what maintains the RMP of most cells?
Na/K ATPase
what are the 3 types of channels specific to pacemaker cells?
1- Na-HCN
2- t-type Ca
3- K-K(Ach)
what is responsible for the upstroke of AP in SA and AV node pacemaker cells?
Ca influx via L-type Ca channels
recall these cells lack Na channels
what limits the extent of hyperpol in pacemaker cells?
Na-HCN and t-type Ca channels limit hyperpol to -60 mV
what is the consequence of Ca being the ion to cause upstroke in SA and AV node pacemaker APs?
upstroke is slower and lower amplitude
what causes the upstroke in purkinje fiber pacemaker cells?
Na influx
what causes the plateau phase?
K channels open at max depol allowing for K efflux, but then Ca channels open and Ca influx occurs so plateau results
what is different for APs in atrial vs ventricular myocytes?
ventricular myocytes require more forceful contraction so they have longer plateau phases allowing for increased influx of Ca and thus stronger contraction
3 determinants of conduction velocity
cell diameter
gap junctions
amplitude of AP
(increasing all will increase velocity)
what is the clinical effect of Na channel blockers?
Na channel blockers will decrease the amplitude of AP and therefore will decrease conduction velocity
2 main determinants of HR
rate of pacemaker firing
conduction velocity
what causes the refractory period? what reverses it?
Na channel inactivation causes the refractory period, repel reverses it
discuss the differences in sympathetic vs parasympathetic innervation of the heart
sympathetic- diffuse, including SA node and AV node
parasymp- only SA node and AV node
sympathetic effects on Na-HCN channels
uses GaS mechanism epi/NE binds b-adrenergic receptor g protein activated adenyl cyclase activated increases cAMP increased cAMP activates Na-HCN channels activation increases rate of diastolic depol and increases HR
parasympathetic effects on Na-HCN channels
ACh binds M2 receptor
g-protein activated and inhibits adenyl cyclase
decreased cAMP = decreased activation of Na-HCN = decreased HR
differentiate between t-type and l-type Ca channels
t-type: open during hyperpol (with Na-HCN)
l-type: open during depol, allow Ca influx for contraction
sympathetic effects on t-type Ca channel
uses GaS
epi/NE binds b-adrenergic receptor
g protein and adenyl cyclase activated
increases cAMP
cAMP activates PKA
PKA phosphorylates/activates t-type Ca channel
increased Ca influx brings cell to threshold faster and increases HR
parasympathetic effects on t-type Ca channel
ACh binds to M2 receptor
g protein activated and inhibits adenyl cyclase
decreased cAMP = decreased PKA = decreased HR
parasympathetic effects on K-K(ACh) channel
ACh binds muscarinic receptor
g protein activates K-K(Ach) channel opening it
increased K efflux = hyperpol which delays diastolic depol and decreases HR
what is the main controller of HR?
parasymp