Cardiac Electrophysiology

Question 1

Fast-response cardiac muscle cells

Answer 1

. Atrial and ventricular contractile cells
. Purkinje fibers
. Have fast conduction velocity

Question 2

Slow response cardiac muscle cells

Answer 2

. Nodal (pacemaker) cells

. Have slow conduction velocity

Question 3

Initiation of contraction in cardiac cells

Answer 3

. Propagated AP initiates it
. External innervation not needed to initiate, only modulate
. Gap-junctions allow rapid cell-cell communication so muscle acts as 1 unit

Question 4

RMP in cardiac muscle cells

Answer 4

-85
. Close to skeletal muscle
. Greater gK/gNa than neurons

Question 5

AP overshoot in cardiac muscle cells is ___

Answer 5

25 mV

Question 6

Cardiac muscle cell AP

Answer 6

. All or none
. Rapid upstroke in fast response cells
. Plateau phase contributing to longer AP duration (200 ms)
.

Question 7

Ionic basis of cardiac AP in fast response cells

Answer 7

. AP of cell divided into 5 phases (0-4) based on time-dependent changes in ionic conductance

Question 8

Phase 0 of cardiac AP

Answer 8

. Rapid depolarization

. Due to opening of VG Na channels

Question 9

Phase 1 of cardiac AP

Answer 9

. Early repolarization
. Due to inactivation of Na channels and opening of specific K channel that opens rapidly and spontaneously inactivates
. Current called transient outward current (Ito)
. Some contribution from Cl channels
. Magnitude of repolarization here has regional variation (prominent in purkinje and epicardial ventricular cells, small in endocardial ventricular myocardium)

Question 10

T/F transient outward current in cardiac AP only contributes in early repolarization, not ate repolarization

Answer 10

T

Question 11

Phase 2 in cardiac AP

Answer 11

. Plateau phase
. Little change in membrane potential for 100-200 ms
. Reflects balance btw depolarizing and repolarizing currents
. Inward Ca current through L type VG channels
. Small contribution from VG Na channels that don’t close rapidly or reopen (Na window current)
. Decline in Ito contributed somewhat
. Delayed rectifier K current from slowly activating K channels that are similar to repolarizing K channels in neurons

Question 12

L-ty[e Ca current

Answer 12

. Similar to VG Na channels but w/ more depolarized potentials and slower kinetics
. Predominant in heart
. Modulated by ANS, hormones, and drugs
. Exist in other muscle APs but do not contribute

Question 13

Why is Na window current clinically important?

Answer 13

Bloacking of this current is responsible for AP shortening effects of certain anti-arrhythmic agents

Question 14

Phase 3 of cardiac AP

Answer 14

. Primary and final phase of repolarization back to RMP
. Due to inactivation of L-type VG Ca channels and progressive inc. in delayed rectifier K current
. Significant contribution of inwardly rectifying K current as delayed rectifer slowly declines

Question 15

Phase 4 of cardiac cells

Answer 15

. Resting membrane to entail
. Due to inwardly rectifying K current
. Spontaneous opening of these channels causes high background K conductance
. Na conductance very low during this phase
. Small contribution from Na/K-ATPase by maintaining concentration gradient

Question 16

Absolute Refractory periods in cardiac fast response cells

Answer 16

. From phase 0 until halfway through phase 3 (-50 mV)
. During this period there are not enough Na channels recovered to cause a depolarization even if all available ones were opened during large stimulus

Question 17

Relative refractory period in cardiac cells

Answer 17

. From halfway through phase 3 to the end of phase 3 when all Na channels are available for normal depolarization
. Period occurs as progressively more Na channels recover from inactivation to be activated again
.

Question 18

Supernormal period

Answer 18

. Follows relative refractory period sometimes
. Ability of stimulus slightly below normal threshold to elicit AP
. Full recovery time occurs when excitability returns to normal after this period

Question 19

Long Q-T syndrome

Answer 19

. Unusually long ventricular AP duration
. Longer than normal refractory period that disrupts normal electrophysiological timing of heart
. Prone to arrhythmias
. Genetic, result of stroke, starvation, or drug-induced
. Mutations in Gene encoding for delayed rectifer channels or fast Na channels

Question 20

Torsades de Pointes

Answer 20

. Very dangerous ventricular arrhythmia

. More in women than men

Question 21

Romano-ward syndrome

Answer 21

. Has one copy of disease-causing variant (long QT)
. Prone to torsades de Pointes
. Not deaf

Question 22

Jervell and Lange-Nielsen (JLN) syndrome

Answer 22

. 2 copies of disease-causing variant (long QT)
. Prone to torsades de Pointes 
. Deaf 
. More severe heart rhythm problems 
. Appear early in life