Guyton Kap. 10- Rhythmical Excitation Of The Heart

Front 1

Location of SA- node:

Back 1

Superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of superior vena cava

Front 2

Resting membrane potential of sinus node and ventricular muscle cell:

Back 2

Sinus node: -55 to -60 millivolts

Muscle fiber: -85 to - 90 millivolts

Front 3

Why do the sinus node have a less negative membrane potential then ventricular muscle fiber:

Back 3

Leaking sodium and calcium channels

Front 4

Why are fast sodium channels inactivated in sinus node?

Back 4

Because at any time the membrane potential remain less negative then about -55 millivolts for more then a few milliseconds, the gates are inactivated

Front 5

What causes self- excitation of sinus nodal fibers:

Back 5

Inherent leakiness of sinus nodal fibers to sodium and calcium ions

Front 6

Threshold voltage for action potential in sinus node:

Back 6

-40 millivolts

Front 7

Why does the leaky sodium channels not cause sinus nodal fibers to be depolarized all the time?

Back 7

Because sodium- calcium channels close after 100-150 milliseconds and potassium channels open

Front 8

Spreading of action potential from sinus node to AV- node:

Back 8

Through surrounding atrial muscle fibers through connections with the sinus node

Front 9

Speed of conduction through atrias:

Back 9

0.3m/ sec in most fibers, but 1m/ sec in several small bands of atrial fibers:
- Anterior interatrial band
- Anterior, middle and posterior internodal pathways

Front 10

AV- node and bundle:

Back 10

Conduct action potential through the fibrous cardiac skeleton from atria to ventricles and delay the conduction by 0.13 seconds

Front 11

Delay in conduction from sinus node to AV- node:

Back 11

0.03 seconds

Front 12

Total time for an action potential to travel from sinus node to contractile ventricular muscle fibers:

Back 12

0.16 seconds

Front 13

What slows down conduction through AV- node and bundle?

Back 13

Decreasing number of gap junctions between the cells--> great resistance in conduction of ions

Front 14

Characteristics of Purkinje fibers:

Back 14

Large fibers (larger then ventricular muscle fibers)
Transmission velocity of 4m/ sec, up to 6 times faster then in usual ventricular muscle and 150 times faster then in the AV- node

Front 15

What is the reason for fast transmission through Purkinje fibers:

Back 15

Great number of intercalated disks with gap junctions

Front 16

Can action potential travel backwards through AV- node and bundle from ventricles to atria and cause re-entry cardiac impulses?

Back 16

No, not under normal conditions.

Front 17

Duration of action potential traveling through Purkinje system:

Back 17

0.03 seconds

Front 18

Velocity of conduction through ventricular muscle fibers after end of Purkinje fibers:

Back 18

0.3- 0.5 m/sec, 1/6 of that in the Purkinje fibers

Front 19

Time from transport of signal from endocard in the end of Purkinje fibers to epicardial surface:

Back 19

0.03 seconds

Front 20

Total time from start of bundle branch to epicardial surface:

Back 20

0.06 seconds

Front 21

Rates of rhythmically discharge:

Back 21

Sinus node: 70- 80 times per minute

AV- node: 40- 60 times per minute

Purkinje fibers: 15- 40 times per minute

Front 22

Ectopic pacemaker:

Back 22

A pacemaker elsewhere in the heart than the sinus node that has a rhythmical discharge faster then the sinus node---> Abnormal sequence of contraction

Front 23

Stokes- Adams syndrome:

Back 23

After a sudden AV- block it takes 5- 20 seconds before the Purkinje system "picks up" and emits its intrinsic rhythmical impulses (15- 40 per/min) because it used to be overridden/ suppressed by the faster sinus impulses. This leads to fainting after 4-5 seconds

Front 24

Effect of acetylcholine from vagal nerve endings in vagal stimuli:

Back 24

1. Decrease heart rate rythme of sinus node

2. Decreases excitability of AV- junctional fibers, slowing conduction to the ventricles

Front 25

Vagal stimuli:

Back 25

Slowing or stop of sinus rhythmical excitation depending on the strength of stimulus.
---> impulses are not passed to the ventricles and the ventricles stop beating for 5- 20 seconds before a ventricular escape induce 15- 40 beats/ min from the Purkinje fibers, usually in the ventricular septum portion of AV- bundle

Front 26

Mechanism of vagal stimuli:

Back 26

Acetylcholine greatly increase the permeability of fibers to potassium ions----> more negative inside the fibers (hyperpolarization) ==> Decreased excitability

Front 27

Mechanism of the sympathetic effect on the heart:

Back 27

Sympathetic nerve endings release noreadrenaline which stimulates beta-1 adrenergic receptors ==> increase in heart rate (probably due to increased permeability of sodium and calcium ions)

Increased sodium makes it easier to excite sinus node and by the same reason increase conduction time through the AV- node. Increased calcium increases force of contraction.