Hoofdstuk 9 Flashcards
(140 cards)
1
Q
De rechterhelft van het hart pompt het bloed door
A
de longen
2
Q
de linkerhelft van het hart pompt het bloed door
A
het lichaam via de aorta
3
Q
de functie van de atrium is
A
om het bloed in de ventrikels te pompen
4
Q
pericardium
A
een tweelaags zakje om het hart heen dat het beschermt en het op zijn plek houdt
5
Q
aortaklep plek
A
linkerhelft; kleppen tussen aorta en ventrikel
6
Q
mitralisklep plek
A
linkerhelft; tussen linkeratrium en ventrikel
7
Q
pulmonale kelp plek
A
rechterhelft; tussen ventrikel en de pulmonale slagader
8
Q
tricuspidalisklep plek
A
rechterhelft; tussen atrium en ventrikel
9
Q
inferieure vena cava
A
het bloedvat dat zuurstofarmbloed naar de rechteratrium brengt
10
Q
pulmonaire slagaders
A
hier gaat het bloed van rechterventrikel naar de longen (zuurstofarm)
11
Q
pulmonaire aders
A
hier gaat het bloed van de longen naar de linkeratrium (zuurstofrijk)
12
Q
superior vena cava
A
het bloedvat dat zuurstofarmbloed naar de rechteratrium brengt van hoofd en bovenlichaam
13
Q
de lagen van het pericardium
A
van binnen naar buiten: epicardium pericardiale ruimte (is dus leeg) partiele pericadium vezellig pericardium (buitenste laag)
14
Q
Hoe heet de contractie van het hart
A
hartritme
15
Q
de drie grote cardiale spieren van het hart en manieren van contractie
A
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
16
Q
Hartspier anatomie
A
De vezels splitsen zich, voegen zich dan weer samen etc. Zelfde gestreepte structuur als skeletspieren. Ook kan je geïntercaleerde schijven zien
17
Q
geïntercaleerde schijven functie
A
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.
18
Q
verschil structuur linker en rechterhelft
A
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.
19
Q
apex
A
de punt van het hart/ventrikels
20
Q
richting endocardiale vezels
A
rechts
Oook wel subendocardiale vezels
21
Q
richting epicardiale vezels
A
links
ook wel subepicardiale vezels genoemd
22
Q
systole
A
contractie
23
Q
diastole
A
relaxatie van het hart
24
Q
Hoe gaan actiepotentialen van hartcel naar hartcel
A
door gap junctions in de intercalated disks; ionen kunnen hierdoorheen.
25
syncytium
het hart is een syncytium (bestaat uit vele cellen die samen samentrekken).
26
atriale syncytium
de wanden van de twee atria
27
ventriculae syncytium
de wanden van de twee ventrikels
28
de atria zijn gescheiden van de ventrikels door
vezelachtig weefsel dat om de atrioventriculaire (AV) opening zit tusssen de atria en ventrikels.
29
Hoe gaan actiepotentialen van atrium naar ventrikel
NIET door het vezelachtige weesel, maar door de AV-bundel
30
hoeveelheid mV van ventriculaire spieren
van -85 mV naar +20 mV; 105 mV.
31
Door het plateau in hartspieren contraheren deze
15 keer langer dan in skeletspieren
32
2 redenen voor de plateau in hartspieren
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
33
4 phases actiepotentiaal hartspieren
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
34
snelheid spiervezels
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).
35
snelheid purkinjevezels
4 m/sec
36
purkinje vezels
het geleidingsysteem van het hart
37
refractieperiode hartspieren
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
38
een vroege premature contractie contractiekracht
verminderde contractiekracht
39
late premature contractie contractiekracht
evengrote contractiekracht als normaal
40
hebben hartspieren t-tubules?
Ja
41
verschil excitatie-contractie hartspier met skeletspier
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 .
42
SERCA2
de SERCA pomp in de hartspieren
43
wat zou er gebeuren met de contractiekracht van het hart als er geen t-tubules is?
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.
44
hart in een calcium vrije oplossing
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.
45
hart contractie hangt grotendeels af van
calcium hoeveelheid beschikbaar
46
duratie contractie hartcel
0. 2 in atrium
| 0. 3 in ventrikel
47
cardiale cyclus
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
48
locatie sinus node
in de superieure laterale wand van het rechter atrium dicht bij de superieure vena cava
49
duratie cardiale cyclus
bijv 72x per minuut
| is 1/72 min/beat = 0.0139 min/beat = 0.833 sec/beat
50
ECG
Het elektrocardiogram (ECG) is het registreren van de elektrische activiteit van het hart
51
PCG
Een fonocardiogram is een opname van hartgeluiden die visueel op een fonocardiograafkaart kan worden weergegeven. De hartkleppen hoor je vooral
52
wanneer welke harttonen
1e; begin systole
2; eind systole
3e; halferwege diastole
53
druk ventrikels tijdens ejectie
120 mm Hg
54
druk aorta rust en contractie
rust; 80 mm Hg
| contractie; 120 mm Hg
55
volume ventrikels relaxatie en contractie
relaxatie: 50 ml
contractie: 130 ml
56
diastasis
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.
57
als hartritme verhoogt dan
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
58
volgorde golven ECG
P, Q, R , S T
59
P golf
verspreiding van depolarisatie door de atria en contractie atria (verhoging atria druk na P golf).
60
QRS golf
depolarisatie van de ventrikels; net voor de ventriculaire systole
61
T golf
repolarisatie van de ventrikels; net voor het einde van de ventriculaire contractie
62
hoeveel bloed stroomt van de atria naar ventrikel voor contractie en tijdens?
80%, en laatste 20% tijdens contractie. Kan ook zonder deze 20% doen
63
merk je het als je atria niet werken
in rust nee, wel als je gaan sporte
64
atria druk golven
a, c en v
65
a golf
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.
66
c golf
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.
67
v golf
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.
68
period of rapid filling of the ventricles
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
69
periode snel vullen ventrikels
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.
70
ventrikels worden stijf door
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
71
Isovolumetrische/isometrische contractie
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.
72
Period of Ejection
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.
73
Period of Isovolumic (Isometric) Relaxation
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.
74
end-diastolic volume .
During diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120 ml.
75
stroke volume output
as the ventricles empty during systole, the volume decreases by about 70 ml,
76
end-systolic volume.
The remaining volume in each ventricle, about 40 to 50 ml,
77
ejection fraction
he fraction of the end-diastolic volume that is ejected
| usually equal to about 0.6 (or 60%)
78
When the heart contracts strongly
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.
79
AV kleppen zijn de
triscuspid en mitrale kleppen
80
functie AV kleppen
voorkomen blackflow van bloed in de atria
81
semilunar kleppen
aortic en pulmonaire slagader kleppen
82
functie semilunaire kleppen
voorkomen blackflow van de aorta en pulmonaire slagader terug in de ventrikels
83
gaan de hartkleppen dicht passief of actief
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.
84
anatomie mitrale klep
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
85
anatomie aortic valve
een cusp (klep)
86
trekken papillaire spieren samen
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
87
verschillen in semilunar valves en AV valves
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.
88
When the left ventricle contracts
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.
89
verhoging van bloeddruk bij systole in aorta
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.
90
incisura
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.
91
wanneer de aortic valves dicht gaan
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.
92
de druk curve van het rechter ventrikel en pulmonaire slagader zijn hetzelfde als
de curve van de aorta; is alleen 1/6 hiervan
93
Relationship of the Heart Sounds to Heart Pumping
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
94
stroke work output
is the amount of energy that the heart converts to work during each heartbeat while pumping blood into the arteries.
95
twee vormen work output
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.
96
rechter ventrikel externe work output
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.
97
work output van linker ventrikel
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.
98
diastolische druk curve linker ventrikel afhankelijk van
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.
99
systolische druk curve linker ventrikel afhankelijk van
The systolic pressure curve is determined by recording the systolic pressure achieved during ventricular contraction at each volume of filling.
100
tot welk volume in linker ventrikel kan bloed makkelijk hierin stromen en waarom?
tot 150 ml; diastolische druk is dan nog vrij laag.
101
Waarom gaat de diastolische druk op een gegeven moment rap omhoog
door het vezelachtige weesel dat niet verder kan strekken
102
maximale systolische druk linkerhelft bij ... ml
150 tot 170 ml
103
maximale systolische druk links en rechts ventrikel
links: 250 tot 300 mm Hg
rechts: 60 tot 80 mm Hg
104
als linkerventrikel meer dan 170 mL vol is
neemt de systolische druk af doordat de myosine en actine zo ver uit elkaar getrokken worden dat contractie niet meer optimaal is
105
vier punten volume-druk diagram
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
```
106
Fase I volume-druk diagram linkerventrikel
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.
107
Phase II volume druk diagram linker ventrikel
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
108
Fase III volume druk diagram linker ventrikel
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.
109
Fase IV volume druk diagram linker ventrikel
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.
110
EW volume-druk
net externe werk output
111
effect meer bloed pompen op volume druk diagram
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.
112
preload
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.
113
afterload
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.)
114
waar komt de energie vandaan voor hartcontractie
70-90% van oxidatieve metabolisme
| 10-30% glucose en lactaat
115
Waarom is zuurstof consumptie een goede meetmethode voor de chemische energie die vrijkomt door het hart
omdat het vooral gebruik maakt van oxidatieve reacties
116
zuurstof consumptie hart gelijk aan
```
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
```
117
PE
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.
118
concentric hypertrophy
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
119
eccentric hypertrophy
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
120
Cardiac Efficiency
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%.
121
Regulation of Heart Pumping
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.
122
the Frank-Starling Mechanism
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.
123
What Is the Explanation of the Frank-Starling Mechanism?
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%.
124
ventricular function curves.
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
125
ventricular volume output curve
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)
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Pompen van hart wordt beinvloed door
sympathetische en parasympathetische zenuwen
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vagus nervus
parasympathetische
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sympathetische stimulatie kan hartslag verhogen naar
180 tot 250 beats per minutes
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sympathetische stimulatie kan contractie
verdubbelen; verhogen van volume uitgepompt.
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Parasympathetic (Vagal) Stimulation Reduces Heart Rate and Strength of Contraction
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%.
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vagus nervus locaties op hart
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.
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cardiac output maximale sympathetische stimulatie
25 L per min
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cardiac output normale sympathetishe stimulatie
13 L per min
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cardiac output 0 sympathetische stimulatie
11 L per min
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cardiac output parasympathetische stimulatie
7/8 L per min
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Effect of Potassium Ions op het hart
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.
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Effect of Potassium Ions hoe kan dit?
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.
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Effect of Calcium Ions
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.
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Effect of Temperature on Heart Function
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
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Increasing the Arterial Pressure Load (up to a Limit) Does Not Decrease Cardiac Output
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
