basic electrophysiology Flashcards
sodium entry through the fast Na channel is responsible for what phase of the AP?
the rapid upstroke (phase 0) in nonpacemaker cells
when does calcium enter the cell? what does it do?
enters during phase 2. main channel responsible for depolarization of the pacemaker cells
when does potassium exit the cell? what do open K channels contribute to?
exits thru L channel to repolarize cell during phase 3. open channels contribute to resting potential (phase 4) of nonpacemaker cells.
when is the funny channel activated?
during hyperpolarization: hyperpolarization activated cyclic nucleotide gated channel
what is the structure of an ion channel? which subunit senses voltage changes?
6 transmembrane domains, S4 senses voltage changes. there’s also an inactivation gate and sensitivity filter
in resting sodium channel membrane are most channels open or closed?
closed. even though the inactivation gate is open, Na cannot pass because activation gate is closed.
what gate is closed in the closed state?
the inactivation gate is closed (channel pore blocked)
what ion is the resting potential of a cardiac muscle cell determined by?
potassium
which chemical and charge gradients work on K? what’s the nernst potential for a cell?
inside cell = negative d/t high protein concentration. but concentration gradient from inside to outside. -91 mV
how are sodium voltage gated channels modulated?
a-subunits can be phosphorylated by cAMP-dependent kinase (PKA)
what happens to sodium channels if Vm stays positive?
channels start to inactivate
function of gap junctions in cardiac myocytes?
spread depolarization to neighboring cells (initiate depolarization of cardiac myocytes/conduction)
what is the effect of the Ca current?
slower pacemaker activities of SA and AV node (upstroke, phase 0). contributes to delay between SA and AV nodes. slow inactivation (phase 2). CICR to initiate contraction.
what does phase 3 consist of?
repolarizing K current: slow. 2 currents underly Ik, rapid and slow. delayed rectifiers mean it slowly activates. does not inactivate.
what does the early outward K current do?
atrial and ventricular cells activated by depol and rapidly inactivate. contribute to phase 1.
what is g-protein activated K current regulated by? (GIRK) what does it do?
acetylcholine. in SA and AV decreases pacemaker rate and slows conduction thru AV node.
function of SA node? rate of intrinsic depolarization?
pacemaker. spontaneous depol leads to AP generation. fastest intrinsic spontaneous depol.
AV node function?
slowly conducting. introduces delay between atrial and ventricular activation. slows HR.
phases of pacemaker action potential
phase 4 = sodium influx, depol. phase 0 = ca influx. phase 3 = K efflux, repolarization. finally funny current lets more Na in.
what causes spontaneous depol in SA node?
pacemaker channels (HCN).
1) hyperpolarization activated
2) cyclic-nucleotide-gated
3) cation-selective, Ehcn ~ 0 mV
vagus nerve’s actions? releases what onto what? opens what?
ACh is released from vagus nerve onto the SA and AV node. opens GIRK channels: diastolic potential more negative & makes threshold more positive.
what do sympathetic nerves release? act on what to what effect?
norepinephrine/epi. acts on B-adrenergic receptors in SA and AV nodes to increase conduction velocity and pacemaker rate. increases If, makes threshold more negative. no affect on max diastolic potential.
inotropic effect on atrial and ventricular cells.
what are the mechanisms for altering heart rate or rate of nodal depolarization? what are the steps?
parasympathetic vagal release of ACh. (all require more time to reach threshold)
1) decrease RATE of depol
2) decrease MAX diastolic potential
3) increase threshold potential
when is a cell unexcitable to stimulation?
during the absolute refractory period. 250 ms
effect of temperature increase on SA node firing?
increasing temp increases SA node firing by increasing slope of phase 4.
what are the effects of hyperkalemia?
raises resting potential. reduction of P wave amplitude, widening of P-R interval and QRS, decrease in force of ctxn. accelerates repolariation, shortens AP duration. shortens QT interval, CHARACTERISTIC TALL T WAVE PEAKS.
effects of hypokalemia?
decrease in resting membrane potential, slowing of repolarization and prolongation of AP duration. flattening of T wave, prolongation of PR and QT intervals. possible AV block and V fib.
effect of hypocalcemia?
shortens ventricular AP: shortens ST segment, shortens QT interval
effect of hypercalcemia?
prolongs ST segment and therefore QT interval
effect of potassium channel blockers?
increase AP duration
effect of calcium channel blockers?
slows rate in SA and AV nodes
effect of sodium channel blockers?
reduce phase 0 and slope of depol
effect of B-blockers?
prevent calcium entry into the cell. decrease HR, conduction velocity, strength of ctxn
what are b-blockers used to treat?
hypertension, angina/MI, arrhythmias
what are calcium channel blockers used for? how?
angina, HTN, arrhythmias. decrease entry of Ca and delay depol of SA and AV nodes (reduce upstroke of AP, decrease HR)
