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205 > lecture 20- mechanical events of the cardiac cycle > Flashcards

lecture 20- mechanical events of the cardiac cycle Flashcards

1
Q

systole

A

contraction

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2
Q

diastole

A

relaxation

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3
Q

during diastole, chambers are

A

filling with blood

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4
Q

most blood enters ventricles during diastole though the

A

open AV valves (80%)

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5
Q

during atrial systole, blood is pumped from —- into —- and —-

A

pumped from ventricles into aorta and pulmonary artery

(20% of blood)

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6
Q

during ventricular systole, blood is pumped from — into — and —

A

pumped from ventricles into aorta and pulmonary artery

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7
Q

5 stages of the mechanical events of 1 cardiac cycle

A
  1. late diastole
  2. atrial systole
  3. isovolumic ventricular contraction
  4. ventricular ejection
  5. isovolumic ventricular relaxation
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8
Q

late diastole

A

heart is completely relaxed
-semilunar valves closed
- AV valves open

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9
Q

atrial systole

A

small amount of blood enters ventricles (15-20%)
-AV valves open bc atria are contracting

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10
Q

isovolumic ventricular contraction

A

ventricular contraction pushes AV valves closed but not enough force to open semilunar valves

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11
Q

ventricular ejection

A

-semilunar valves open and blood is ejected
-AV valves close

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12
Q

isovolumic ventricular relaxation

A

AV valves open/relaxed
–> chambers fill passively

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13
Q

If atrial systole has occurred it would be…

A

the max volume ventricles can contain
= End diastolic volume
= Max

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14
Q

Ventricular ejection has occured…

A

residual blood left in the heart after ventricle has contracted
= End systolic volume
= Min

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15
Q

The wiggers diagram displays

A

pressure in the left ventricle in terms of the electrical and mechanical events of the cardiac cycle

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16
Q

Wiggers: as ventricles contract, there is…

A

a huge increase in pressure in the left ventricle

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17
Q

Wiggers: why does pressure fall off?

A

because blood has been ejected from the heart

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18
Q

approx how many mL of blood is the left ventricle ejecting at rest?

A

70mL

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19
Q

PV relationship: A to A’

A

passive filling
late ventricular diastole
no increase in pressure

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20
Q

PV relationship: A’ to B

A

atrial systole (15-20% blood)
incr P, incr V

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21
Q

PV relationship: B

A

=EDV= 135 mL

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22
Q

PV relationship: B to C

A

no change in volume
big change in pressure
-ventricles contracted bc not enough pressure to open valves
-isovolumic semilunar valves

23
Q

PV relationship: C to D

A

ventricular systole
at C, semilunar open
stroke volume= 70mL at rest/normal

24
Q

PV relationship: D

A

ESV= 65mL
= minimum blood left after ventricular systole

25
PV relationship: D to A
isovolumic ventricular relaxation - at A, passive filling occurs again - no change in volume but big change in pressure
26
PV relationship: A, B, C, D in terms of valves opening and closing
A= mitral valve opens B= mitral valve closes C= aortic valve opens D= aortic valve closes
27
Stroke volume (SV)
= amount of blood pumped by one ventricle during a contraction avg resting SV= 70mL/beat (135mL-65mL)
28
SV= ....-....
end diastolic volume - end systolic volume
29
Cardiac output (CO)
= volume of blood pumped by one ventricle in a given period of time avg resting CO= 5L/min
30
CO= ....x....
HR (beats/min) x SV (mL/beat)
31
how much blood do we have in our bodies?
5L your heart pumps all of the blood in your body every single minute
32
autonomic innervation of the heart: stimulating SA node
-if we add sympathetic input to SA nose= speed up -if we add parasympathetic input to SA node= slow down
33
ventricular myocardium ONLY gets --- input
sympathetic
34
chonotropic effect
= autonomic effect on the SA node -modulation of HR (chronotropic effect) -parasympathetic or sympathetic
35
Inotropic effect
= autonomic effect on ventricular myocytes - modulation of contractility (inotropic effect) - only sympathetic
36
in HR increases, contractility...
increases - contractility increases so SV increases and therefore CO increases
37
chronotropic effect: parasympathetic neuron
parasympathetic neuron (ACh on M2 receptor) -decreases HR
38
chronotropic effect: sympathetic neuron
sympathetic neuron (NE on beta 1 receptor) -increases HR
39
more than 1 heart beat per sec=
+ chronotropic effect fast?
40
less than 1 heart beat per second=
Negative chronotropic effect slow
41
how is SV modulated?
SV is proportional to contraction force contraction force is determined by: 1. sarcomere length (approx EDV) 2. contractility of muscle
42
ideal length for max tension is a skeletal muscle sarcomere=
2 microns
43
Frank-Starling Curve
the length-tension relationship of the heart -SV on y axis, EDV on x axis --> an increase in EDV (EDV prop to length of sarcomere) --> causes SV to increase
44
Frank-Starling Law
the heart pumps all the blood returned to the heart (5L) --> if we stuff in more blood, there will be a more forceful contraction
45
2 factors that increase EDV
1. increased venous return 2. decreased HR (more filling time)
46
as EDV increases, SV...
increases (increases SV because we increase contractility)
47
effect of SNS on ventricular contractility
norepinephrine is spit out onto beta 1 receptors SNS activity of ventricular myocytes, increase in contractility, increased SV
48
what happens to the Frank Sterling curve with sympathetic input?
it gets "bumped up"
49
what happens to the Frank Sterling curve with parasympathetic input?
it gets "bumped down"
50
2 effects of (increased -- activity) SNS on myocyte contractility
1. increased activity of LTCC (L type calcium channels) 2. increased activity of SERCA (Sarcoendoplasmic Reticulum Calcium ATPase)
51
how does increased activity of the LTCC affect myocyte contractility?
epinephrine/norepinephrine bind to beta 1 receptors, activate cAMP, phosphorylation of voltage gated calcium channels... opening time increases increased Ca2+ entry from the ECF then... --> Ca2+ is stored in SR and/or eventually released= MORE FORCEFUL CONTRACTION
52
How does increased SERCA activity affect myocyte contractility?
phospholamban usually inhibits SERCA epinephrine/norepinephrine binds to beta 1 receptors, activate cAMP, phosphorylation of phospholamban when phospholamban is phosphorylated it does and does its own thing SERCA is not inhibited anymore; increased Ca2+ATPase on SR then... --> Ca2+ is stored and/or eventually released= more forceful contraction --> Ca2+ removed from cytosol faster= shortens Ca-troponin binding time= shorter duration of contraction
53
adding sympathetic stimulation (such as the SNS example of epinephrine and norepinephrine) would be an example of an ---- effect
inotropic effect

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