Cardiac Pacemaker Cells

Question 1

Pacemaker potential

Answer 1

. Spontaneous depolarization during diastole

. Basis of automaticity in pacemaker cells

Question 2

Maximum diastole potential of nodal cells

Answer 2

. Level of maximum repolarization by the slow response cell (most neg. potential that nodal cell reaches during single beat)
. Less negative than RMP of fast response cells
.due to lower density of background K channels than fast response coupled w/ relatively constant background Na current

Question 3

Currents in nodal cells

Answer 3

. Background Na current 
. Funny current 
. T-type and L-type Ca currents 
. Na-Ca exchange current 
. Delayed rectifier K current

Question 4

Background Na current in nodal cells

Answer 4

. Small, significant relatively constant background current

. Not the standard VG fast Na channels responsible for upstroke of fast response cardiac cells

Question 5

Funny current

Answer 5

. Monovalent cation current (conducts Na and K equally)
. Voltage-dependent activated by repolarization/hyperpolarization instead of depolarization
. During repolarization of slow AP this depolarizing current is turned on

Question 6

T-type Ca current in nodal cells

Answer 6

. Activated at more negative potentials than L-type
. Threshold is -55 mV
. Depolarization of nodal cell by this channel causes cell to begin to open some L-type channels

Question 7

L-type Ca current in nodal cells

Answer 7

. Threshold is -40 mV
. Opening caused by depolarization by T-type Ca current
. When enough L-type channels open, upstroke of nodal AP occurs

Question 8

Na-Ca exchange current in nodal cells

Answer 8

. Exchange 3 Na for 1 Ca
. Electrogenic
. Roel unclear

Question 9

Delayed rectifier K current in nodal cells

Answer 9

. Slowly activating K current same as in fast response cells
. Primary repolarizing current in nodal cells

Question 10

Purkinje fiber cells

Answer 10

. Can also exhibit automaticity under certain circumstances in spite of them being fast response cells
. Funny current responsible for automaticity (activation of depolarizing current during repolarization is primary cause of pacemaker potential)

Question 11

Phases in slow response cell APs

Answer 11

Phase 0 and phase 3

Question 12

Phase 0 in nodal cells

Answer 12

. upstroke much slower
. No phase 1 or 2
. Overshoot is less positive than fast response cells
. Upstroke due to L-type current
. There are no VG Na channels in nodal cells

Question 13

Phase 3 in nodal cell APs

Answer 13

. Repolarization due to inactivation of L-type Ca current and activation of delayed rectifier K current

Question 14

Refractory periods in slow response cells

Answer 14

. Has absolute and relative refractory periods
. Relative extends into phase 4 (diastolic depolarization) causing marked delay in cell’s ability to respond to early stimulus
. Recovery of excitability more time-dependent than voltage-dependent
. Puts upper limit on HR

Question 15

Mechanisms that determine rate of firing in nodal cells

Answer 15

. Slope of pacemaker potential: steeper slope of depolarization, faster the AP threshold is reached
. Alterations in channel activity will change slope
. Threshold: doesn’t change
. Max diastolic potential: altering this alters amount of depolarization needed to reach threshold, altering fire is rate

Question 16

ANS modulation on automaticity

Answer 16

. HR w/o innervation is around 90-100 bpm based on intrinsic firing from SA node
. In body around 70 bpm due to innervation
. Sympathetic inc., para dec.

Question 17

Overdrive suppression

Answer 17

. Depression of automaticity of pacemaker cells after period of excitation at high frequencies
. Greater firing rate of SA node causes overdrive suppression of other pacemaker cells in heart
. Depression of automaticity due o hyperpolarization of driven pacemaker cells from higher activation of Na/K=ATPase

Question 18

Ca channel blockers

Answer 18

. Treat hypertension, angina, and some arrhythmias
. Dec. upstroke of slow APs but do not effect upstroke of fast APs
. Side effects: slowed HR and depressed contractility in atrial and ventricular muscle since L-type channels works there