Cardiac Conduction and Action Potentials Flashcards
The action potential spreads throughout the myocardium in the following sequence:
SA node AV node, bundle of his, purkinje system
slow conduction through the AV node ensures what?
that the ventricles have sufficient time to fill with blood before they are activated and contract
how is the velocity of the cardiac conduction system determined?
cells/fiber with larger diameter are faster (purkinje> atrial and ventricular muscle> AV node
What is phase 0 in the ventricles, atria, and purkinje system known as?
upstroke/ depolarization
what is phase 0 caused by in the ventricles, atria, and purkinje system?
a transient increase in Na + conductance ( I na)
what happens when the Na+ conductance increases?
there is an inward Na+ current, which drives the membrane potential towards +65 mV
what is the majority of phase 0 being driven by?
the opening of voltage gated “fast” Na+ channels activation gate
what happens to the Na+ channels as the cell starts to depolarize?
the inactivation gates on the Na+ channels start to close in response to depolarization
for repolarization to occur, what must happen?
there must be a net outward current
what is phase 1 in the ventricles, atria, and purkinje system known as?
initial repolarization
what is phase 2 in the ventricles, atria, and purkinje system known as?
plateau
how is there a balance of inward and outward currents achieved during the plateau of phase 2 (aka what occurs in phase 2 of the cardiac fast action potential)?
there is opening of the voltage-gated L-type Ca2+ channels; closure of inward rectifying K+ channels; there is outward K+ current
what is phase 3 in the ventricles, atria, and purkinje system?
repolarization
what occurs during phase 3?
closure of the voltage-gated L-type Ca2+ channels; opening of the inward rectifying K+ channels; opening of the voltage-gated K+ channels
what is the big driver of phase 3- repolarization?
the opening of the voltage-gated K+ channels (I Kr (rapid) and I Ks (slow))
what causes Long QT syndrome?
transition from phase 2 to phase 3 is lengthened; it could be acquired or it can be congenital causes influencing I Kr or I Ks
Outward K current makes the membrane potential what?
more negative
in the cardiac fast action potential, what does the resting membrane approach?
the K+ equilibrium potential
what occurs during phase 1 of the cardiac fast action potential?
there is closure of the inactivation gates on the voltage-gated Na+ channels AND opening of the transient outward K+ current
what is phase 4 of the cardiac slow action potential?
resting membrane potential gradually depolarizes until reaches threshold
what acts as the pacemaker of phase 4 of the cardiac slow action potential?
spontaneous depolarization
what causes the spontaneous depolarization of the phase 4 of the cardiac slow action potential?
a slow influx of Na+ through “funny” voltage-gated Na+ channels
when do the funny Na+ channels open?
upon complete repolarization of membrane
what generates/drives the phase 0 of the cardiac slow action potential?
voltage-gated Ca2+ channels
what occurs during the phase 0 of the cardiac slow action potential?
opening of the voltage-gated Ca2+ channels and closure of the inward rectifying K+ channels
what is/ what occurs during phase 3 of the cardiac slow action potential?
closure of the voltage-gated Ca2+ channels and opening of the delayed rectifying K+ channels and closure of inward rectifying K+ channels
what are the parasympathetics to the heart carried by?
the vagus nerve
what is the parasympathetic neurotransmitter that acts on the heart? and what receptors does it act on?
acetylcholine acts on M2/M3
what is the specific effect of the parasympathetics on the heart?
there is slower entry of Na+ through funny Na channels during phase 4; also hyperpolarization of SA node by increasing outward K+ current via special K+-ACh channels
what is the sympathetic neurotransmitter that acts on the heart? and what is its receptor?
norepinephrine - Beta-1 adrenergic receptor
what is a positive chronotropic effect?
speeding up of heart rate
what is a positive inotropic effect?
increased contractility
how specifically does the sympathetics speed up heart rate?
there is a more rapid influx of Na+ through funny Na+ channels
how do the sympathetics increase contractility?
there is increased Ca2+ into myocytes
what happens during the absolute refractory period of the heart?
all voltage-gated Na+ channels are inactivated
what is the supranormal period?
cell is actually more excitable than normal
what effect does hyperkalemia have on the cardiac action potential?
it slows phase 0 and speeds phase 3 (you are more likely to reach threshold)
what effect does hypokalemia have on the resting membrane potential?
it will be more negative- you will need a stronger stimulus