Guyton Kap. 9- Heart & Valves

Front 1

Three types of cardiac muscle:

Back 1

Atrial muscle
Ventricular muscle
Conductive muscle fibers (do not contract much do to little contractile fibers)

Front 2

Cardiac muscle as a "Syncytium":

Back 2

Cardiac mm. cells are separated by intercalated disks with gap junctions--> Free diffusion of ions and thus action potentials

Front 3

Two functional syncytium:

Back 3

Atrial
Ventricular

Separated by fibrous cardiac skeleton, only connected by AV- bundle

Front 4

Action potential in cardiac mm.:

Back 4

- About 105 millivolts.
- Intracellular potential from -85 to +20
- Membrane is depolarized for 0,2 seconds (plateau)---> ventricular contraction is 15 times longer then in skeletal m.

Front 5

Skeletal VS. Cardiac action potential:

Back 5

1. Skeleteal:
Fast Na+ channels, open for a thousends of a secondm abruplty close--> open of K+ ==> rapid repolarization.
Ca2+ from ER trigger contraction

2. Cardiac:
Fast Na+ channels + Slow Ca2+ channels, open for about 0,2 s--> decreased permeability of K+ (prolonged depolarization/ plateau), absolute refractory. Closing of Ca2+ channels---> increased K+ permeability ==> repolarization

Ca2+ influx through slow Ca2+- channels trigger contraction

Front 6

Velocity of signal conduction in cardiac mm.:

Back 6

Muscle fibers: 0,3- 0,5 m/s

Purkinje fibers: 4m/s

Front 7

Duration of (absolute) refractory period of cardiac m.:

Back 7

0.25- 0.30 second in ventricles and 0.15 in atrias (duration of the prolonged plateau action potential)

Front 8

Duration of relative refractory period:

Back 8

0.05 second

A very strong stimulus can initiate a "early premature contraction"

Front 9

Excitation- contraction coupling:
(The mechanism by which action potential causes myofibrils to contract):

Back 9

1. Action potential:
- Open of voltage gated Ca2+ channels in T- tubules---> inflow of Ca2+
2. Ca2+ inflow trigger ryanodine receptors (calcium release channels) in ER---> release of calcium
3. Ca2+ interact with troponin as normal.

Front 10

T- tubules in cardiac mm:

Back 10

5 times greater diameter and 25 times greater volume then skeletal muscle.

Have direct communication with extracellular environment---> same as ECF.

Front 11

Cardiac mm. contraction is dependent on:

Back 11

Extracellular Ca2+ form T- tubules

Front 12

Transport of Ca2+ back into T- tubules (out of the cells) and into ER (sarcoplasmic reticulum):

Back 12

T- tubules:
Sodium- calcium exchanger. Sodium that accumulates in the cell is transported out by Na+/K+ ATPase.

ER:
CalciumATPase pump.

Front 13

AV- node delay:

Back 13

Action potential is delayed through the AV- node 0,1 second
==> Allows atria to contract ahead of ventricular contraction, pumping blood into the ventricles before the strong ventricular contraction

Front 14

Duration of cardiac cycle:

Back 14

Reciprocal of heart rate:
72 beats/min--> 1/72 beats/min--> 0.0139 minutes/beat ==> 0.833 seconds/ beat

Front 15

Effect of increased heart rate on duration of cardiac cycle:

Back 15

Systole normally is 40 % of the cycle, if heart rate increases 3 times systole is 65 % of the cycle meaning that the diastole is becomes much shorter.

Front 16

Significants of atria:

Back 16

80 % of venous return goes right through the atria to the ventricle.

20 % is pumped by the atria

Front 17

Isovolumic contraction (isometric)

Back 17

Tension is increasing in the muscle but there is little shortening of the muscle fibers (All valves are closed)

Front 18

Opening of semilunar valves:

Back 18

When left ventricle pressure is over 80mmHg and right ventricle pressure is over 8mmHg.

Front 19

Period of rapid ejection:

Back 19

First third of ejecting when 70 % of volume is ejected

Front 20

Period of slow ejection:

Back 20

Last two thirds of ejection when 30 % eject

Front 21

End diastolic volume:

Back 21

110- 120 ml

Front 22

Stroke volume output:

Back 22

70 ml decrease in volume during contraction

Front 23

End- systolic volume:

Back 23

40- 50ml (can be 10- 20ml by strongly increasing contraction force)

Front 24

Ejection fraction:

Back 24

Fraction of end diastolic volume that is ejected.
Usually 60 %

Front 25

Opening and closing of valves:

Back 25

Passively when forward and backward pressure gradient pushed blood backward or forward forcing the valves open or shut.

Front 26

Function of papillary muscles:

Back 26

Holding the A-V valves back, so they will not bulge to much into the atria from the pressure increase during ventricular contraction

Front 27

Diastolic pressure of the aorta:

Back 27

80mmHg

Front 28

Preload:

Back 28

The degree of tension on the muscle when it begins to contract (end- diastolic pressure)

Front 29

Afterload:

Back 29

Load against which the muscle exerts its force.
The pressure in the aorta leading from the ventricle, which corresponds to the systolic pressure. Can also be considered as the resistance in the circulation rather then the pressure.

Front 30

Energy for muscle contraction:

Back 30

70- 90 % from oxidative metabolism of fatty acids, and 10- 30 % from other nutrients as glucose and lactate

Front 31

Tension- time index:

Back 31

Oxygen consumption in the heart muscle is proportional to the tension that occurs in the heart muscle during contraction, multiplied by the duration of time the contraction persist.

Front 32

Why is energy consumption greater in heart failure?

Back 32

Because much more chemical energy is expended when the ventricle is abnormally dilated because heart muscle tension during contraction is proportional to pressure times the diameter of the ventricle.

Front 33

Efficiency of cardiac contraction:

Back 33

Ratio of work output to chemical energy expenditure. Maximum efficiency of the heart is 20- 25 % (5-10 % in heart failure) meaning that 75- 80% of the chemical energy is converted to heat.

Front 34

Regulation of heart pumping:

Back 34

1. Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart

2. Control of heart rate and strength by autonomic nervous system

Front 35

Frank- Sterling mechanism of the heart:

Back 35

The greater the heart muscle is stretched during filling, the greater is the force of contraction and the greater is the quantity of blood pumped into the aorta

Front 36

Effect of stretch of right atrial wall:

Back 36

Directly increase heart rate by 10- 20 %

Front 37

Sympathetic stimulus on heart:

Back 37

Increase of heart rate up to 200- 250 beats/min.
Double force of contraction
==> Increase maximal cardiac output to two or threefold.

Front 38

Removal of sympathetic rhythmic discharge decrease cardiac output by:

Back 38

30 % (By decreasing force and heart rate)

Front 39

Strong vagal stimuli:

Back 39

Can stop heart beats for a few seconds--> escape beats of 20- 40 beats/min (if stimuli persists)

Decrease strength in contraction by 20- 30 % (but innervate mostly atria so it does not effect force so much, but affect sinus node and rate)

Front 40

Effect of increased extracellular potassium on heart:

Back 40

Heart becomes dilated and flaccid, and slow heart rate. Block conduction through AV- bundle. K+ levels 2-3 times above normal level can cause fatal arrhythmia's.

Why? K+ decreases resting membrane potential--> decreases intensity of action potential---> heart weakness.

Front 41

Effect of increased extracellular Ca2+ on the heart:

Back 41

Spastic contraction

Front 42

Why does heart rate increase (maybe double) with increased temperature (fever)?

Back 42

Heat increases the permeability of cardiac muscle membrane to ions that control heart rate, resulting in acceleration of self- excitation process.