basic electrophysiology

Question 1

sodium entry through the fast Na channel is responsible for what phase of the AP?

Answer 1

the rapid upstroke (phase 0) in nonpacemaker cells

Question 2

when does calcium enter the cell? what does it do?

Answer 2

enters during phase 2. main channel responsible for depolarization of the pacemaker cells

Question 3

when does potassium exit the cell? what do open K channels contribute to?

Answer 3

exits thru L channel to repolarize cell during phase 3. open channels contribute to resting potential (phase 4) of nonpacemaker cells.

Question 4

when is the funny channel activated?

Answer 4

during hyperpolarization: hyperpolarization activated cyclic nucleotide gated channel

Question 5

what is the structure of an ion channel? which subunit senses voltage changes?

Answer 5

6 transmembrane domains, S4 senses voltage changes. there’s also an inactivation gate and sensitivity filter

Question 6

in resting sodium channel membrane are most channels open or closed?

Answer 6

closed. even though the inactivation gate is open, Na cannot pass because activation gate is closed.

Question 7

what gate is closed in the closed state?

Answer 7

the inactivation gate is closed (channel pore blocked)

Question 8

what ion is the resting potential of a cardiac muscle cell determined by?

Answer 8

potassium

Question 9

which chemical and charge gradients work on K? what’s the nernst potential for a cell?

Answer 9

inside cell = negative d/t high protein concentration. but concentration gradient from inside to outside. -91 mV

Question 10

how are sodium voltage gated channels modulated?

Answer 10

a-subunits can be phosphorylated by cAMP-dependent kinase (PKA)

Question 11

what happens to sodium channels if Vm stays positive?

Answer 11

channels start to inactivate

Question 12

function of gap junctions in cardiac myocytes?

Answer 12

spread depolarization to neighboring cells (initiate depolarization of cardiac myocytes/conduction)

Question 13

what is the effect of the Ca current?

Answer 13

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.

Question 14

what does phase 3 consist of?

Answer 14

repolarizing K current: slow. 2 currents underly Ik, rapid and slow. delayed rectifiers mean it slowly activates. does not inactivate.

Question 15

what does the early outward K current do?

Answer 15

atrial and ventricular cells activated by depol and rapidly inactivate. contribute to phase 1.

Question 16

what is g-protein activated K current regulated by? (GIRK) what does it do?

Answer 16

acetylcholine. in SA and AV decreases pacemaker rate and slows conduction thru AV node.

Question 17

function of SA node? rate of intrinsic depolarization?

Answer 17

pacemaker. spontaneous depol leads to AP generation. fastest intrinsic spontaneous depol.

Question 18

AV node function?

Answer 18

slowly conducting. introduces delay between atrial and ventricular activation. slows HR.

Question 19

phases of pacemaker action potential

Answer 19

phase 4 = sodium influx, depol. phase 0 = ca influx. phase 3 = K efflux, repolarization. finally funny current lets more Na in.

Question 20

what causes spontaneous depol in SA node?

Answer 20

pacemaker channels (HCN).

1) hyperpolarization activated
2) cyclic-nucleotide-gated
3) cation-selective, Ehcn ~ 0 mV

Question 21

vagus nerve’s actions? releases what onto what? opens what?

Answer 21

ACh is released from vagus nerve onto the SA and AV node. opens GIRK channels: diastolic potential more negative & makes threshold more positive.

Question 22

what do sympathetic nerves release? act on what to what effect?

Answer 22

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.

Question 23

what are the mechanisms for altering heart rate or rate of nodal depolarization? what are the steps?

Answer 23

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

Question 24

when is a cell unexcitable to stimulation?

Answer 24

during the absolute refractory period. 250 ms

Question 25

effect of temperature increase on SA node firing?

Answer 25

increasing temp increases SA node firing by increasing slope of phase 4.

Question 26

what are the effects of hyperkalemia?

Answer 26

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.

Question 27

effects of hypokalemia?

Answer 27

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.

Question 28

effect of hypocalcemia?

Answer 28

shortens ventricular AP: shortens ST segment, shortens QT interval

Question 29

effect of hypercalcemia?

Answer 29

prolongs ST segment and therefore QT interval

Question 30

effect of potassium channel blockers?

Answer 30

increase AP duration

Question 31

effect of calcium channel blockers?

Answer 31

slows rate in SA and AV nodes

Question 32

effect of sodium channel blockers?

Answer 32

reduce phase 0 and slope of depol

Question 33

effect of B-blockers?

Answer 33

prevent calcium entry into the cell. decrease HR, conduction velocity, strength of ctxn

Question 34

what are b-blockers used to treat?

Answer 34

hypertension, angina/MI, arrhythmias

Question 35

what are calcium channel blockers used for? how?

Answer 35

angina, HTN, arrhythmias. decrease entry of Ca and delay depol of SA and AV nodes (reduce upstroke of AP, decrease HR)