Cardiac Action Potential

Question 0

L-type Ca2+ channels INACTIVAATE very slowly, allowing Ca2+ to enter the myoplasm, and trigger contraction.

Answer 0

.

Question 1

Voltage gated Na+ channels in cardiac, skeletal and smooth muscle all work essentially the same but are encoded by different genes.

Answer 1

.

Question 2

Ca2+ channels occur in densities that are very small relative to the densities of VG N+ channels

Answer 2

..

Question 3

I(k1) - inward rectifier - characteristics

Answer 3

if Vm > -80, linear flow of K out

if Vm < -80, current decreases, non linear flow, channel stops working, (this channel’s) K not moving.

Question 4

K+ current that is primarily responsible for establishing the cardiac myocyte resting potential is actually less during the action potential than when the cell is at rest.

Answer 4

.

Question 5

Ionic conductances during plateau are generally comparable to those during rest (much less than during depol and repol)
Therefore, any small changes can have profound effects!

Answer 5

.

Question 6

I(Ks)- major roles

Answer 6

Gradual decline in plateau potential (phase 2)

Initiation of rapid repolarization to resting potential (phase 3)

Question 7

Voltage gated delayed rectifier K+ channels gradually open during the plateau of the cardiac action potential, eventually leading to membrane repolarization.

Answer 7

.

Question 8

Increased I (Kur) shortens AP plateau (Atrial AP shorter than Ventricular AP). Only difference between atria and ventricle AP

Answer 8

.

Question 9

SA AP v Ventricular AP - differences

Answer 9

Phase 0 slower (smaller slope)
Peak is lower
Phase 4 is spontaneous gradual depolarization and not rest

Question 10

I(f) - actions

Answer 10

Opens when membrane potential does down (as in pacemaker phase 4) - Cause INC Vm
Nonspecific Cation Channel[Na+ and K+ movement]
Opens if Vm less negative than -35mV (closes when too positive)

Question 11

Modifying (increasing) I(f) will make you reach threshold quicker which means more action potentials

Answer 11

.

Question 12

In pacemaker cell there is no Na channels, so depolarization only due to Ca2+ (which has slower effect)

Answer 12

.

Question 13

AV nodal delay - describe, causes

Answer 13

decreased conduction velocity

• absence of Na+ channels
• Low density of Ca2+ channels
• fewer gap junctions

Question 14

Myocardial INfarction - biochemical effects on infarcted area

Answer 14

Decreased ATP

Less negative Vm

Question 15

ordered depol and repol in heart during MI

Answer 15

Area depolarizes too late, make heart more likely o generate arrhythmia delayed repolarization as well

Question 16

I (k, ACh) - location, actions

Answer 16

Pacemaker cells, Atria
Always open but major effect during phase 4
Inc parasympathetic tone -> dec. Vm -> slow depolarization -> dec. HR

Question 17

I(K, ATP) - actions, relevance

Answer 17

closed @ normal ATP
open @ dec. ATP (i.e MI)
- resists depol -> dec. HR in SA -> preserve ATP
-GOOD in short/temp ischemia
-BAD in long ischemia b/c resulting hyperkalemia causing inactivation of Na then Ca channels which severely slows AP conduction

Question 18

I(Cl, cAMP) - E(Cl), location, action (under what conditions), relevance

Answer 18

E(Cl) = -55mV *Mostly Ventricle (some atrial)
If Vm - more positive than - E(Cl) then Cl- enters => dec. Vm towards rest during plateau => dec. AP
- important for high sympathetic tone (i.e. exercise) b/c shorten plateau to get in more beats an more blood

Question 19

ANS innveration of cardiac and smooth muscle modulates them ( it doesn’t initiate electrical or contractile events)

Answer 19

.