Hoofdstuk 9

Question 1

De rechterhelft van het hart pompt het bloed door

Answer 1

de longen

Question 2

de linkerhelft van het hart pompt het bloed door

Answer 2

het lichaam via de aorta

Question 3

de functie van de atrium is

Answer 3

om het bloed in de ventrikels te pompen

Question 4

pericardium

Answer 4

een tweelaags zakje om het hart heen dat het beschermt en het op zijn plek houdt

Question 5

aortaklep plek

Answer 5

linkerhelft; kleppen tussen aorta en ventrikel

Question 6

mitralisklep plek

Answer 6

linkerhelft; tussen linkeratrium en ventrikel

Question 7

pulmonale kelp plek

Answer 7

rechterhelft; tussen ventrikel en de pulmonale slagader

Question 8

tricuspidalisklep plek

Answer 8

rechterhelft; tussen atrium en ventrikel

Question 9

inferieure vena cava

Answer 9

het bloedvat dat zuurstofarmbloed naar de rechteratrium brengt

Question 10

pulmonaire slagaders

Answer 10

hier gaat het bloed van rechterventrikel naar de longen (zuurstofarm)

Question 11

pulmonaire aders

Answer 11

hier gaat het bloed van de longen naar de linkeratrium (zuurstofrijk)

Question 12

superior vena cava

Answer 12

het bloedvat dat zuurstofarmbloed naar de rechteratrium brengt van hoofd en bovenlichaam

Question 13

de lagen van het pericardium

Answer 13

van binnen naar buiten:
epicardium
pericardiale ruimte (is dus leeg)
partiele pericadium
vezellig pericardium (buitenste laag)

Question 14

Hoe heet de contractie van het hart

Answer 14

hartritme

Question 15

de drie grote cardiale spieren van het hart en manieren van contractie

Answer 15

artiale spier, ventriculaire spier, en excitatoire en geleidende spiervezels
Artiale en ventriculaire spier trekken op dezelfde manier samen als skeletspieren.
De excitatoire en geleidende spiervezels trekken niet veel samen; ze zorgen voor automatische elektrische discharge (actiepotentialen) of conductie hiervan

Question 16

Hartspier anatomie

Answer 16

De vezels splitsen zich, voegen zich dan weer samen etc. Zelfde gestreepte structuur als skeletspieren. Ook kan je geïntercaleerde schijven zien

Question 17

geïntercaleerde schijven functie

Answer 17

Hartspierweefsel bestaat uit individuele hartspiercellen verbonden door intercalaire schijven zodat deze als een geheel orgaan kunnen functioneren. Deze schijven zijn de MEMBRANEN van de individuele cellen die ze van elkaar scheidt. Skeletspierweefsel daarentegen bestaat uit meerkernige spiervezels en bevat geen intercalaire schijven. Intercalaire schijven ondersteunen de gesynchroniseerde samentrekking van hartweefsel. Deze schijven zijn aanwezig op de Z-lijnen van een sarcomeer en zijn makkelijk zichtbaar in een lengtedoorsnede van hartspierweefsel.

Question 18

verschil structuur linker en rechterhelft

Answer 18

De linkerhelft heeft twee vezellagen; endocardiale (binnen) en epicardiale (buiten). Ze lopen beide in een andere richting schuin naar beneden. Hierdoor kan de linkerventrikel in een twist-beweging samentrekken vanuit de punt aan het einde van de systole, waardoor al het bloed naar de aorta wordt gestuurd.

Question 19

apex

Answer 19

de punt van het hart/ventrikels

Question 20

richting endocardiale vezels

Answer 20

rechts

Oook wel subendocardiale vezels

Question 21

richting epicardiale vezels

Answer 21

links

ook wel subepicardiale vezels genoemd

Question 22

systole

Answer 22

contractie

Question 23

diastole

Answer 23

relaxatie van het hart

Question 24

Hoe gaan actiepotentialen van hartcel naar hartcel

Answer 24

door gap junctions in de intercalated disks; ionen kunnen hierdoorheen.

Question 25

syncytium

Answer 25

het hart is een syncytium (bestaat uit vele cellen die samen samentrekken).

Question 26

atriale syncytium

Answer 26

de wanden van de twee atria

Question 27

ventriculae syncytium

Answer 27

de wanden van de twee ventrikels

Question 28

de atria zijn gescheiden van de ventrikels door

Answer 28

vezelachtig weefsel dat om de atrioventriculaire (AV) opening zit tusssen de atria en ventrikels.

Question 29

Hoe gaan actiepotentialen van atrium naar ventrikel

Answer 29

NIET door het vezelachtige weesel, maar door de AV-bundel

Question 30

hoeveelheid mV van ventriculaire spieren

Answer 30

van -85 mV naar +20 mV; 105 mV.

Question 31

Door het plateau in hartspieren contraheren deze

Answer 31

15 keer langer dan in skeletspieren

Question 32

2 redenen voor de plateau in hartspieren

Answer 32

1) Hier zijn naast snelle natrium kanalen ook langzame calcium kanalen; gaan later open en blijven langer dicht.
2) de permeabiliteit voor kalium neemt af, waardoor de repolarisatie later begint

Question 33

4 phases actiepotentiaal hartspieren

Answer 33

0: depolarisatie; snelle natrium kanalen open. mV naar +20
1: initiale repolarisatie; snelle natrium kanalen dicht en kalium open
2: plateau; calcium kanalen openen en kalium weer dicht
3: snelle repolarisatie; calcium dicht en kalium open.
4: rustpotentiaal

Question 34

snelheid spiervezels

Answer 34

voor zowel de atria en ventrikels is dit 0.3 tot 0.5 m/sec (1/250 van snelle zenuwvezels en 1/10 van skeletspieren).

Question 35

snelheid purkinjevezels

Answer 35

4 m/sec

Question 36

purkinje vezels

Answer 36

het geleidingsysteem van het hart

Question 37

refractieperiode hartspieren

Answer 37

ventrikels: 0.25 tot 0.30; ook nog relatieve refractie periode van 0.05s waar excitatie wel kan maar alleen met sterke actiepotentiaal
atria; 0.15s

Question 38

een vroege premature contractie contractiekracht

Answer 38

verminderde contractiekracht

Question 39

late premature contractie contractiekracht

Answer 39

evengrote contractiekracht als normaal

Question 40

hebben hartspieren t-tubules?

Answer 40

Ja

Question 41

verschil excitatie-contractie hartspier met skeletspier

Answer 41

addition to the calcium ions that are released into the sarcoplasm from the cisternae of the sarcoplasmic reticulum, calcium ions also diffuse into the sarcoplasm from the T tubules at the time of the action potential, which opens voltage-dependent calcium channels in the membrane of the T tubule ( Figure 9-7 ). Calcium entering the cell then activates calcium release channels, also called ryanodine receptor channels, in the sarcoplasmic reticulum membrane, triggering the release of calcium into the sarcoplasm. Calcium ions in the sarcoplasm then interact with troponin to initiate cross-bridge formation and contraction by the same basic mechanism as that described for skeletal muscle in Chapter 6 .

Question 42

SERCA2

Answer 42

de SERCA pomp in de hartspieren

Question 43

wat zou er gebeuren met de contractiekracht van het hart als er geen t-tubules is?

Answer 43

Without the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably because the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle and does not store enough calcium to provide full contraction. The T tubules of cardiac muscle, however, have a diameter five times as great as that of the skeletal muscle tubules, which means a volume 25 times as great. Also, inside the T tubules is a large quantity of mucopolysaccharides that are electronegatively charged and bind an abundant store of calcium ions, keeping them available for diffusion to the interior of the cardiac muscle fiber when a T tubule action potential appears.

Question 44

hart in een calcium vrije oplossing

Answer 44

stopt snel met kloppen
The reason for this response is that the openings of the T tubules pass directly through the cardiac muscle cell membrane into the extracellular spaces surrounding the cells, allowing the same extracellular fluid that is in the cardiac muscle interstitium to percolate through the T tubules. Consequently, the quantity of calcium ions in the T tubule system (i.e., the availability of calcium ions to cause cardiac muscle contraction) depends to a great extent on the extracellular fluid calcium ion concentration.

Question 45

hart contractie hangt grotendeels af van

Answer 45

calcium hoeveelheid beschikbaar

Question 46

duratie contractie hartcel

Answer 46

0. 2 in atrium

0. 3 in ventrikel

Question 47

cardiale cyclus

Answer 47

het begin van een hartslag tot de volgende. Begint met actiepotential generatie door de sinus node. Gaat door beide atria en dan via AV bundel naar ventrikels. Hierdoor is er een vertraging van 0.1s; atria trekken eerst samen en brengen het bloed in de ventrikels

Question 48

locatie sinus node

Answer 48

in de superieure laterale wand van het rechter atrium dicht bij de superieure vena cava

Question 49

duratie cardiale cyclus

Answer 49

bijv 72x per minuut

is 1/72 min/beat = 0.0139 min/beat = 0.833 sec/beat

Question 50

ECG

Answer 50

Het elektrocardiogram (ECG) is het registreren van de elektrische activiteit van het hart

Question 51

PCG

Answer 51

Een fonocardiogram is een opname van hartgeluiden die visueel op een fonocardiograafkaart kan worden weergegeven. De hartkleppen hoor je vooral

Question 52

wanneer welke harttonen

Answer 52

1e; begin systole
2; eind systole
3e; halferwege diastole

Question 53

druk ventrikels tijdens ejectie

Answer 53

120 mm Hg

Question 54

druk aorta rust en contractie

Answer 54

rust; 80 mm Hg

contractie; 120 mm Hg

Question 55

volume ventrikels relaxatie en contractie

Answer 55

relaxatie: 50 ml
contractie: 130 ml

Question 56

diastasis

Answer 56

diastasis is the middle stage of diastole during the cycle of a heartbeat, where the initial passive filling of the heart’s ventricles has slowed, but before the atria contract to complete the active filling.

Question 57

als hartritme verhoogt dan

Answer 57

wordt hartcyclus duratie lager, samen met contractie en relaxatie fase. duratie diastole vooral verlaagd.
systole normaal: 0.4 van cyclys
systole actief: 0.65 van cyclus

Question 58

volgorde golven ECG

Answer 58

P, Q, R , S T

Question 59

P golf

Answer 59

verspreiding van depolarisatie door de atria en contractie atria (verhoging atria druk na P golf).

Question 60

QRS golf

Answer 60

depolarisatie van de ventrikels; net voor de ventriculaire systole

Question 61

T golf

Answer 61

repolarisatie van de ventrikels; net voor het einde van de ventriculaire contractie

Question 62

hoeveel bloed stroomt van de atria naar ventrikel voor contractie en tijdens?

Answer 62

80%, en laatste 20% tijdens contractie. Kan ook zonder deze 20% doen

Question 63

merk je het als je atria niet werken

Answer 63

in rust nee, wel als je gaan sporte

Question 64

atria druk golven

Answer 64

a, c en v

Question 65

a golf

Answer 65

atriale contractie.
Ordinarily, the right atrial pressure increases 4 to 6 mm Hg during atrial contraction, and the left atrial pressure increases about 7 to 8 mm Hg.

Question 66

c golf

Answer 66

wanneer de ventrikels samentrekken. De golf ontstaat doordat een beetje bloed terug geduwd wordt naar de atria, en het buigen van de AV kleppen in de atria.

Question 67

v golf

Answer 67

einde van ventriculaire contractie. it results from slow flow of blood into the atria from the veins while the A-V valves are closed during ventricular contraction. Then, when ventricular contraction is over, the A-V valves open, allowing this stored atrial blood to flow rapidly into the ventricles, causing the v wave to disappear.

Question 68

period of rapid filling of the ventricles

Answer 68

During ventricular systole, large amounts of blood accumulate in the right and left atria because of the closed A-V valves. Therefore, as soon as systole is over, and the ventricular pressures fall again to their low diastolic values, the moderately increased pressures that have developed in the atria during ventricular systole immediately push the A-V valves open and allow blood to flow rapidly into the ventricles, as shown by the rise of the left ventricular volume curve

Question 69

periode snel vullen ventrikels

Answer 69

In a healthy heart, the period of rapid filling lasts for about the first third of diastole. During the middle third of diastole, only a small amount of blood normally flows into the ventricles. This is blood that continues to empty into the atria from the veins and passes through the atria directly into the ventricles. During the last third of diastole, the atria contract and give an additional thrust to the inflow of blood into the ventricles. This mechanism accounts for about 20% of the filling of the ventricles during each heart cycle.

Question 70

ventrikels worden stijf door

Answer 70

veroudering
ziektes dat zorgen voor cardiale fibrose zoals hoge bloeddruk of diabetes. Hierdoor komt minder bloed in de ventrikels tijdens diastole waardoor meer vulling tijdens artiale contractie

Question 71

Isovolumetrische/isometrische contractie

Answer 71

Immediately after ventricular contraction begins, the ventricular pressure rises abruptly, causing the A-V valves to close. Then, an additional 0.02 to 0.03 second is required for the ventricle to build up sufficient pressure to push the semilunar (aortic and pulmonary) valves open against the pressures in the aorta and pulmonary artery. Therefore, during this period, contraction is occurring in the ventricles, but no emptying
occurs. This period is called the period of isovolumic or isometric contraction , meaning that cardiac muscle tension is increasing but little or no shortening of the muscle fibers is occurring.

Question 72

Period of Ejection

Answer 72

When the left ventricular pressure rises slightly above 80 mm Hg (and the right ventricular pressure rises slightly above 8 mm Hg), the ventricular pressures push the semilunar valves open. Immediately, blood is ejected out of the ventricles into the aorta and pulmonary artery. Approximately 60% of the blood in the ventricles at the end of diastole is ejected during systole; about 70% of this portion flows out during the first third of the ejection period, with the remaining 30% emptying during the next two thirds. Therefore, the first third is called the period of rapid ejection , and the last two thirds is called the period of slow ejection.

Question 73

Period of Isovolumic (Isometric) Relaxation

Answer 73

At the end of systole, ventricular relaxation begins suddenly, allowing both the right and left intraventricular pressures to decrease rapidly. The elevated pressures in the distended large arteries that have just been filled with blood from the contracted ventricles immediately push blood back toward the ventricles, which snaps the aortic and pulmonary valves closed. For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change, giving rise to the period of isovolumic or isometric relaxation. During this period, the intraventricular pressures rapidly decrease back to their low diastolic levels. Then, the A-V valves open to begin a new cycle of ventricular pumping.

Question 74

end-diastolic volume .

Answer 74

During diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120 ml.

Question 75

stroke volume output

Answer 75

as the ventricles empty during systole, the volume decreases by about 70 ml,

Question 76

end-systolic volume.

Answer 76

The remaining volume in each ventricle, about 40 to 50 ml,

Question 77

ejection fraction

Answer 77

he fraction of the end-diastolic volume that is ejected

usually equal to about 0.6 (or 60%)

Question 78

When the heart contracts strongly

Answer 78

the end-systolic volume may decrease to as little as 10 to 20 ml. Conversely, when large amounts of blood flow into the ventricles during diastole, the ventricular end-diastolic volumes can become as much as 150 to 180 ml in the healthy heart. By both increasing the end-diastolic volume and decreasing the end-systolic volume, the stroke volume output can be increased to more than double that which is normal.

Question 79

AV kleppen zijn de

Answer 79

triscuspid en mitrale kleppen

Question 80

functie AV kleppen

Answer 80

voorkomen blackflow van bloed in de atria

Question 81

semilunar kleppen

Answer 81

aortic en pulmonaire slagader kleppen

Question 82

functie semilunaire kleppen

Answer 82

voorkomen blackflow van de aorta en pulmonaire slagader terug in de ventrikels

Question 83

gaan de hartkleppen dicht passief of actief

Answer 83

passief; door druk.
That is, they close when a backward pressure gradient pushes blood backward, and they open when a forward pressure gradient forces blood in the forward direction. For anatomical reasons, the thin A-V valves require almost no backflow to cause closure, whereas the much heavier semilunar valves require rather rapid backflow for a few milliseconds.

Question 84

anatomie mitrale klep

Answer 84

bestaande uit een cusp, die vastzit aan het hart met cordae tendineae (soort pezen) en die zitten vast aan papillary muscles die aan het hart zitten

Question 85

anatomie aortic valve

Answer 85

een cusp (klep)

Question 86

trekken papillaire spieren samen

Answer 86

Ja, tijdens ventrikel contractie. Zorgen er echter NIET voor dat de klep dichtgaan. Ze zorgen ervoor dat de klep niet te ver naar binnen buigt door de druk

Question 87

verschillen in semilunar valves en AV valves

Answer 87

The aortic and pulmonary artery semilunar valves function quite differently from the A-V valves. First, the high pressures in the arteries at the end of systole cause the semilunar valves to snap closed, in contrast to the much softer closure of the A-V valves. Second, because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is much greater than that through the much larger A-V valves. Also, because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary valves are subjected to much greater mechanical abrasion than the A-V valves. Finally, the A-V valves are supported by the chordae tendineae, which is not true for the semilunar valves. It is obvious from the anatomy of the aortic and pulmonary valves that they must be constructed with an especially strong, yet very pliable, fibrous tissue to withstand the extra physical stresses.

Question 88

When the left ventricle contracts

Answer 88

the ventricular pressure increases rapidly until the aortic valve opens. Then, after the valve opens, the pressure in the ventricle rises much less rapidly, as shown in Figure 9-7 , because blood immediately flows out of the ventricle into the aorta and then into the systemic distribution arteries.

Question 89

verhoging van bloeddruk bij systole in aorta

Answer 89

The entry of blood into the arteries during systole causes the walls of these arteries to stretch and the pressure to increase to about 120 mm Hg. Next, at the end of systole, after the left ventricle stops ejecting blood and the aortic valve closes, the elastic walls of the arteries maintain a high pressure in the arteries, even during diastole.

Question 90

incisura

Answer 90

An incisura occurs in the aortic pressure curve when the aortic valve closes. This is caused by a short period of backward flow of blood immediately before closure of the valve, followed by the sudden cessation of backflow.

Question 91

wanneer de aortic valves dicht gaan

Answer 91

After the aortic valve closes, pressure in the aorta decreases slowly throughout diastole because the blood stored in the distended elastic arteries flows continually through the peripheral vessels back to the veins. Before the ventricle contracts again, the aortic pressure usually has fallen to about 80 mm Hg (diastolic pressure), which is two thirds the maximal pressure of 120 mm Hg (systolic pressure) that occurs in the aorta during ventricular contraction.

Question 92

de druk curve van het rechter ventrikel en pulmonaire slagader zijn hetzelfde als

Answer 92

de curve van de aorta; is alleen 1/6 hiervan

Question 93

Relationship of the Heart Sounds to Heart Pumping

Answer 93

When listening to the heart with a stethoscope, one does not hear the opening of the valves because this is a relatively slow process that normally makes no noise. However, when the valves close, the vanes of the valves and the surrounding fluids vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest.
When the ventricles contract, one first hears a sound caused by closure of the A-V valves. The vibration pitch is low and relatively long-lasting and is known as the first heart sound (S1). When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because these valves close rapidly, and the surroundings vibrate for a short period. This sound is called the second heart sound (S2). The precise causes of the heart sounds are discussed more fully in Chapter 23 in relation to listening to the sounds with the stethoscope

Question 94

stroke work output

Answer 94

is the amount of energy that the heart converts to work during each heartbeat while pumping blood into the arteries.

Question 95

twee vormen work output

Answer 95

First, the major proportion is used to move the blood from the low-pressure veins to the high-pressure arteries. This is called volume-pressure work or external work. Second, a minor proportion of the energy is used to accelerate the blood to its velocity of ejection through the aortic and pulmonary valves, which is the kinetic energy of blood flow component of the work output.

Question 96

rechter ventrikel externe work output

Answer 96

is normally about one-sixth the work output of the left ventricle because of the sixfold difference in systolic pressures pumped by the two ventricles. The additional work output of each ventricle required to create kinetic energy of blood flow is proportional to the mass of blood ejected times the square of velocity of ejection.

Question 97

work output van linker ventrikel

Answer 97

Ordinarily, the work output of the left ventricle required to create kinetic energy of blood flow is only about 1% of the total work output of the ventricle and therefore is ignored in the calculation of the total stroke work output. In certain abnormal conditions, however, such as aortic stenosis, in which blood flows with great velocity through the stenosed valve, more than 50% of the total work output may be required to create kinetic energy of blood flow.

Question 98

diastolische druk curve linker ventrikel afhankelijk van

Answer 98

The diastolic pressure curve is determined by filling the heart with progressively greater volumes of blood and then measuring the diastolic pressure immediately before ventricular contraction occurs, which is the end-diastolic pressure of the ventricle.

Question 99

systolische druk curve linker ventrikel afhankelijk van

Answer 99

The systolic pressure curve is determined by recording the systolic pressure achieved during ventricular contraction at each volume of filling.

Question 100

tot welk volume in linker ventrikel kan bloed makkelijk hierin stromen en waarom?

Answer 100

tot 150 ml; diastolische druk is dan nog vrij laag.

Question 101

Waarom gaat de diastolische druk op een gegeven moment rap omhoog

Answer 101

door het vezelachtige weesel dat niet verder kan strekken

Question 102

maximale systolische druk linkerhelft bij … ml

Answer 102

150 tot 170 ml

Question 103

maximale systolische druk links en rechts ventrikel

Answer 103

links: 250 tot 300 mm Hg
rechts: 60 tot 80 mm Hg

Question 104

als linkerventrikel meer dan 170 mL vol is

Answer 104

neemt de systolische druk af doordat de myosine en actine zo ver uit elkaar getrokken worden dat contractie niet meer optimaal is

Question 105

vier punten volume-druk diagram

Answer 105

A: openen mitrale kleppen (eind-systole volume)
B: dicht van mitrale kleppen (eind diastole volume)
C: aortic valve open
D: aortic valve dicht

A-B = periode van vullen
B-C = isovolumetrische contractie
C-D = ejectie
D-A = isovolumetrische relaxatie

Question 106

Fase I volume-druk diagram linkerventrikel

Answer 106

Phase I in the volume-pressure diagram begins at a ventricular volume of about 50 ml and a diastolic pressure of 2 to 3 mm Hg. The amount of blood that remains in the ventricle after the previous heartbeat, 50 ml, is called the end-systolic volume . As venous blood flows into the ventricle from the left atrium, the ventricular volume normally increases to about 120 ml, called the end-diastolic volume , an increase of 70 ml. Therefore, the volume-pressure diagram during phase I extends along the line in Figure 9-10 labeled “I” and from point A to point B in Figure 9-11 , with the volume increasing to 120 ml and the diastolic pressure rising to about 5 to 7 mm Hg.

Question 107

Phase II volume druk diagram linker ventrikel

Answer 107

Period of Isovolumic Contraction
During isovolumic contraction, the volume of the ventricle does not change because all valves are closed. However, the pressure inside the ventricle increases to equal the pressure in the aorta, at a pressure value of about 80 mm Hg, as depicted by point C

Question 108

Fase III volume druk diagram linker ventrikel

Answer 108

Period of Ejection
During ejection, the systolic pressure rises even higher because of still more contraction of the ventricle. At the same time, the volume of the ventricle decreases because the aortic valve has now opened, and blood flows out of the ventricle into the aorta. Therefore, in Figure 9-10 , the curve labeled “III,” or “period of ejection,” traces the changes in volume and systolic pressure during this period of ejection.

Question 109

Fase IV volume druk diagram linker ventrikel

Answer 109

Period of Isovolumic Relaxation
At the end of the period of ejection (point D, Figure 9-11 ), the aortic valve closes, and the ventricular pressure falls back to the diastolic pressure level. The line labeled “IV” ( Figure 9-10 ) traces this decrease in intraventricular pressure without any change in volume. Thus, the ventricle returns to its starting point, with about 50 ml of blood left in the ventricle at an atrial pressure of 2 to 3 mm Hg.

Question 110

EW volume-druk

Answer 110

net externe werk output

Question 111

effect meer bloed pompen op volume druk diagram

Answer 111

When the heart pumps large quantities of blood, the area of the work diagram becomes much larger. That is, it extends far to the right because the ventricle fills with more blood during diastole, it rises much higher because the ventricle contracts with greater pressure, and it usually extends farther to the left because the ventricle contracts to a smaller volume—especially if the ventricle is stimulated to increased activity by the sympathetic nervous system.

Question 112

preload

Answer 112

In assessing the contractile properties of muscle, it is important to specify the degree of tension on the muscle when it begins to contract
usually considered to be the end-diastolic pressure when the ventricle has become filled.

Question 113

afterload

Answer 113

to specify the load against which the muscle exerts its contractile force
The afterload of the ventricle is the pressure in the aorta leading from the ventricle. In Figure 9-10 , this corresponds to the systolic pressure described by the phase III curve of the volume-pressure diagram. (Sometimes the afterload is loosely considered to be the resistance in the circulation rather than the pressure.)

Question 114

waar komt de energie vandaan voor hartcontractie

Answer 114

70-90% van oxidatieve metabolisme

10-30% glucose en lactaat

Question 115

Waarom is zuurstof consumptie een goede meetmethode voor de chemische energie die vrijkomt door het hart

Answer 115

omdat het vooral gebruik maakt van oxidatieve reacties

Question 116

zuurstof consumptie hart gelijk aan

Answer 116

EW
en spanning in het hart tijdens contractie en de tijd dat dit duurt
T = P x r
T = ventrikel wand spanning
P = linker ventrikel druk
r = radius

Question 117

PE

Answer 117

potentiele energie. Zit bij EW.
The potential energy represents additional work that could be accomplished by contraction of the ventricle if the ventricle could completely empty all the blood in its chamber with each contraction.

Question 118

concentric hypertrophy

Answer 118

When systolic pressure is chronically elevated, wall stress and cardiac workload are also increased, inducing thickening of the left ventricular walls, which can reduce the ventricular chamber radius (concentric hypertrophy) and at least partially relieve the increased wall tension

Question 119

eccentric hypertrophy

Answer 119

Also, much more chemical energy is expended, even at normal systolic pressures, when the ventricle is abnormally dilated (eccentric hypertrophy) because the heart muscle tension during contraction is proportional to pressure times the radius of the ventricle. This

Question 120

Cardiac Efficiency

Answer 120

During heart muscle contraction, most of the expended chemical energy is converted into heat, and a much smaller portion is converted into work output . Cardiac efficiency is the ratio of work output to total chemical energy used to perform the work. Maximum efficiency of the normal heart is between 20% and 25%. In persons with heart failure, this efficiency can decrease to as low as 5%.

Question 121

Regulation of Heart Pumping

Answer 121

When a person is at rest, the heart pumps only 4 to 6 liters of blood each minute. During strenuous exercise, the heart may pump four to seven times this amount. The basic mechanisms for regulating heart pumping are as follows: (1) intrinsic cardiac pumping regulation in response to changes in volume of blood flowing into the heart; and (2) control of heart rate and heart strength by the autonomic nervous system.

Question 122

the Frank-Starling Mechanism

Answer 122

he amount of blood pumped by the heart each minute is normally determined almost entirely by the rate of blood flow into the heart from the veins, which is called venous return. That is, each peripheral tissue of the body controls its own local blood flow, and all the local tissue flows combine and return by way of the veins to the right atrium. The heart, in turn, automatically pumps this incoming blood into the arteries so that it can flow around the circuit again.
This intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank-Starling mechanism of the heart, named in honor of Otto Frank and Ernest Starling, two great physiologists. Basically, the Frank-Starling mechanism means that the more 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. Or, stated another way— within physiological limits, the heart pumps all the blood that returns to it by way of the veins.

Question 123

What Is the Explanation of the Frank-Starling Mechanism?

Answer 123

When an extra amount of blood flows into the ventricles, the cardiac muscle is stretched to a greater length. This stretching causes the muscle to contract with increased force because the actin and myosin filaments are brought to a more nearly optimal degree of overlap for force generation. Therefore, the ventricle, because of its increased pumping, automatically pumps the extra blood into the arteries. This ability of stretched muscle, up to an optimal length, to contract with increased work output is characteristic of all striated muscle, as explained in Chapter 6 , and is not simply a characteristic of cardiac muscle.
In addition to the important effect of lengthening the heart muscle, another factor increases heart pumping when its volume is increased. Stretch of the right atrial wall directly increases the heart rate by 10% to 20%, which also helps increase the amount of blood pumped each minute, although its contribution is much less than that of the Frank-Starling mechanism. As discussed in Chapter 18 , stretch of the atrium also activates stretch receptors and a nervous reflex, the Bainbridge reflex , that is transmitted by the vagus nerve and may increase heart rate an additional 40% to 60%.

Question 124

ventricular function curves.

Answer 124

shows a type of ventricular function curve called the stroke work output curve. Note that as atrial pressure for each side of the heart increases, stroke work output for that side increases until it reaches the limit of the ventricle’s pumping ability.
links: max 40 stroke work
rechts; max 4 stroke work

Question 125

ventricular volume output curve

Answer 125

The two curves of this figure represent function of the two ventricles of the human heart based on data extrapolated from experimental animal studies. As the right and left atrial pressures increase, the respective ventricular volume outputs per minute also increase.
Rechter en linker ventrikel; 13 L/min. Rechts haalt het eerder (0 mm Hg) dan links (8 mm Hg)

Question 126

Pompen van hart wordt beinvloed door

Answer 126

sympathetische en parasympathetische zenuwen

Question 127

vagus nervus

Answer 127

parasympathetische

Question 128

sympathetische stimulatie kan hartslag verhogen naar

Answer 128

180 tot 250 beats per minutes

Question 129

sympathetische stimulatie kan contractie

Answer 129

verdubbelen; verhogen van volume uitgepompt.

Question 130

Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction

Answer 130

Strong stimulation of the parasympathetic nerve fibers in the vagus nerves to the heart can stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a rate of 20 to 40 beats/min as long as the parasympathetic stimulation continues. In addition, strong vagal stimulation can decrease the strength of heart muscle contraction by 20% to 30%.

Question 131

vagus nervus locaties op hart

Answer 131

The vagal fibers are distributed mainly to the atria and not much to the ventricles, where the power contraction of the heart occurs. This distribution explains why the effect of vagal stimulation is mainly to decrease the heart rate rather than to decrease greatly the strength of heart contraction. Nevertheless, the great decrease in heart rate, combined with a slight decrease in heart contraction strength, can decrease ventricular pumping by 50% or more.

Question 132

cardiac output maximale sympathetische stimulatie

Answer 132

25 L per min

Question 133

cardiac output normale sympathetishe stimulatie

Answer 133

13 L per min

Question 134

cardiac output 0 sympathetische stimulatie

Answer 134

11 L per min

Question 135

cardiac output parasympathetische stimulatie

Answer 135

7/8 L per min

Question 136

Effect of Potassium Ions op het hart

Answer 136

Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid and also slows the heart rate. Large quantities of potassium also can block conduction of the cardiac impulse from the atria to the ventricles through the A-V bundle. Elevation of potassium concentration to only 8 to 12 mEq/L—two to three times the normal value—can cause severe weakness of the heart, abnormal rhythm, and death.

Question 137

Effect of Potassium Ions hoe kan dit?

Answer 137

These effects result partially from the fact that a high potassium concentration in the extracellular fluids decreases the resting membrane potential in the cardiac muscle fibers, as explained in Chapter 5 . That is, a high extracellular fluid potassium concentration partially depolarizes the cell membrane, causing the membrane potential to be less negative. As the membrane potential decreases, the intensity of the action potential also decreases, which makes contraction of the heart progressively weaker.

Question 138

Effect of Calcium Ions

Answer 138

Excess calcium ions cause effects almost exactly opposite to those of potassium ions, causing the heart to move toward spastic contraction. This effect is caused by a direct effect of calcium ions to initiate the cardiac contractile process, as explained earlier in this chapter.
Conversely, deficiency of calcium ions causes cardiac weakness, similar to the effect of high potassium. Fortunately, calcium ion levels in the blood normally are regulated within a very narrow range. Therefore, cardiac effects of abnormal calcium concentrations are seldom of clinical concern.

Question 139

Effect of Temperature on Heart Function

Answer 139

Increased body temperature, such as that which occurs during fever, greatly increases the heart rate, sometimes to double the normal rate. Decreased temperature greatly decreases the heart rate, which may fall to as low as a few beats per minute when a person is near death from hypothermia in the body temperature range of 60° to 70°F (15.5°–21°C). These effects presumably result from the fact that heat increases the permeability of the cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self-excitation process.
Contractile strength of the heart often is enhanced temporarily by a moderate increase in temperature, such as that which occurs during body exercise, but prolonged temperature elevation exhausts the metabolic systems of the heart and eventually causes weakness. Therefore, optimal heart function depends greatly on proper control of body temperature by the control mechanisms

Question 140

Increasing the Arterial Pressure Load (up to a Limit) Does Not Decrease Cardiac Output

Answer 140

increasing the arterial pressure in the aorta does not decrease cardiac output until the mean arterial pressure rises above about 160 mm Hg. In other words, during normal heart function at normal systolic arterial pressures (80–140 mm Hg), cardiac output is determined almost entirely by the ease of blood flow through the body’s tissues, which in turn controls venous return of blood to the heart