Elctrophysiology of the heart 2

Question 1

how are the SA and AV nodal cells effected by beta adrenergic effects? cholinergic? what are the principal time-dependent and voltage dependent ion currents?

Answer 1

SA- main pacemaker
AV secondary pacemaker
-beta andrenergic effect causes increase in conduction velocity and increase pacemaker rate
-cholinergic effect- decrease conduction velocity and pacemaker rate
-currents: Ca, K, funny current (NA)- b/c nodal cells

Question 2

how are atrial cells effected by beta adrenergic effects? cholinergic? what are the principal time-dependent and voltage dependent ion currents? How is this different from ventricular muscle cells?

Answer 2

-Atrial muscle cells function to get blood out of atria
-beta adrenergic effect- causes increase STRENGTH of contraction
-cholinergic- little effect b/c lack receptors
-ions- Na, K, Ca
=> only difference with ventricular muscle is that beta adrenergic stimulation causes ventricular muscle to INCREASE CONTRACTILITY

Question 3

how are purkinje cells effected by beta adrenergic effects? cholinergic? what are the principal time-dependent and voltage dependent ion currents?

Answer 3

• beta adrenergic- increase pacemaker rate
• cholinergic- decrease pacemaker rate
• Ca, K, I funny, Na

Question 4

how does the beta adrenergic system effect phases of both nodal cells and myocytes? Cholinergic?

Answer 4

Beta adrenergic system- increase permeability of Ca++ so it effects phase 0 while-
Cholinergic -causes a change in the slope of phase four depolarization *** increasing the permeability of K to the cell and letting more K out = repolarization faster

Question 5

walk thru the depolarization of the heart using vectors

Answer 5

1) signal for SA to AV-down and to the left- polarize the atria
2) signal goes up and to the right to depolarize the septum from left to right
3) signal goes down and to the left to depolarize the anteroseptal region of the myocardium toward the apex
4) signal goes from apex to outsides of the heart (split) to depolarize bulk of ventricle from endo to epicardium
5) depolarization then turns vertically up to depolarize the posterior portion of the base of the LV
6) depolarization complete

Question 6

if the it’s taking a while for depolarization to occur, what could be happening conduction-wise?

Answer 6

-there could be some problems with the nodal cells and it may be using an alternate path thru regular, slower myocytes

Question 7

what is the primary pacemaker of the heart and what is it’s normal rhythm? what pathways does it use to spread AP?

Answer 7

-SA node
70-80 bpm
internodal pathways similar to Purkinje fibers in ventricles

Question 8

how does the resting membrane potential differ between myocytes and nodal cells?

Answer 8

-myocytes = -90
nodal= -55 to -60

Question 9

why are pacemaker/nodal cells more permeable to cations at rest?

Answer 9

-because of funny channels

Question 10

why are Na channels not used in nodal cells?

Answer 10

-because the high membrane potential in nodal cells cause the inactivation of Na channels - only slow Ca++ channels used

Question 11

Is there such a thing as a true resting membrane potential for nodal cells?

Answer 11

• no because funny channels allow for a continues influx of Na+ (or Ca++) into the cell until the cell reaches threshold for activation and then CALCIUM channels are able to open and cause depolarization
• K opens to repolarize with slight hyperpolarization

Question 12

AV node
what does it do and why?
how does it do this?

Answer 12

• Delays impulse in order to allow ventricles to fill fully
• electrical impulse is generated and THEN muscle contracts (AP is signal for contraction)
• Fewer gap junctions adjoining cells to allow it to slow down the impulse

Question 13

• what do parasympathetics do to the slope and the time between beats in the nodal cells? sympathetics?

Answer 13

para- decrease the slope and increase the time between beats

sym- increases the slope and decreases the time between beats

Question 14

describe the bundle branches

Answer 14

• AV node to the bundle of his at the ventricles and then split to left and right bundle branch
• right is a straight shot
• left splits into septal fascicle and left posterior fascicle and left anterior fascicle

Question 15

purkinji fibers
what do they do?
signal similar to?
what do they allow for?
what can it also do if there is some conduction issues?

Answer 15

• allow very rapid transmission of electrical impulse-similar to non-myelinated nerve cells
• allow for synchronous contraction
• signal from septum all the way up the sides of the heart, after that, all myocytes (slower)
• can also generate a VERY SLOW rhythm is not stimulated (can serve as a tertiary pacemaker)

Question 16

describe what is known as an ectopic pacemaker. what are the normal/intrinsic rates for the SA, AV and Purkinji fibers?

Answer 16

• ectopic pacemakers are pacemakers that come in and set the pace of the heart if the SA node is not as fast as the AV or purkinji fibers.
• intrinsic rate for SA =60, AV=40, purkinji=20

Question 17

what are some causes of ectopic pacemakers? is it okay for impulses NOT to go thru purkinji?

Answer 17

• either super excitable cells or blockages of signal transmission
• it is not usually okay. it takes a long time and will reduce the contractile effectiveness of the ventricles

Question 18

walk thru the excitation and contraction coupling that allows for contraction

Answer 18

1) action potential enters from adjacent cells via t tubules
2) voltage gated Ca++ channels open and Ca++ enters cell
3) Get a Ca++ induced Ca++ release thru ryanodine receptor channels
4) local release causes Ca++ spark
5) summed Ca++ sparks create a Ca++ signal
6) Ca++ binds troponin to initiate contraction
7) relaxation occurs when Ca++ unbinds troponin
8) Ca++ pumped back into SR for storage
9) Ca++ exchanged with Na+
10) Na+ gradient is maintained by the Na-K ATPase

Question 19

what sets the duration of contraction

Answer 19

the AP

Question 20

what occurs when extracellular K is in excess? limited?

Answer 20

-slows HR, Dilates heart over time, can block conduction thru AV bundle
-does so by decreasing resting membrane potential:
depolarizing the cell membrane causing membrane potential to be less neg which reduces the intensity of the AP produced (meaning it’s a lot easier to depolarize the cell) and makes heart progressively weaker
-too low increases the resting membrane potential and that makes it harder for the cell to be depolarized

Question 21

what occurs when extracellular Ca is in excess? limited?

Answer 21

excess- increases contraction thru direct initiation of cardiac contractile apparatus
deficient calcium- decrease contractile potential of heart

Question 22

what does ach excess do to the heart?

Answer 22

• it increases K permeability during phase 4 causing more K to escape the cell making the membrane more negative (hyperpolarizing) the heart making it harder to generate an action potential for contraction
• decreases excitability of AV nodal cells

Question 23

Norepi effects if in excess in the heart

Answer 23

• increases rate of sinus node discharge and increases rate of conduction and excitability by increasing the slope of the phase 4 (Ca++) influx via making the membrane more permeable to Ca and Na
• increases force of contractions

Question 24

*what effects would a potassium channel blocker have on cardiac action potential?

Answer 24

-it would prolong the AP and extend QT interval

Question 25

*what effects would a calcium (l-type) channel blocker have on cardiac action potential?

Answer 25

-decrease rate of conduction at SA and AV nodes by delaying Ca++ entry (verapamil) -longer time to reach threshold

Question 26

*what effects would a Na channel blocker have on cardiac action potential?

Answer 26

reduces phase 0 and slope depolarization, increases ERP (effective refractory period)
(lidocaine)