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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
Q

PV relationship: D to A

A

isovolumic ventricular relaxation
- at A, passive filling occurs again
- no change in volume but big change in pressure

26
Q

PV relationship: A, B, C, D in terms of valves opening and closing

A

A= mitral valve opens
B= mitral valve closes
C= aortic valve opens
D= aortic valve closes

27
Q

Stroke volume (SV)

A

= amount of blood pumped by one ventricle during a contraction

avg resting SV= 70mL/beat (135mL-65mL)

28
Q

SV= ….-….

A

end diastolic volume - end systolic volume

29
Q

Cardiac output (CO)

A

= volume of blood pumped by one ventricle in a given period of time

avg resting CO= 5L/min

30
Q

CO= ….x….

A

HR (beats/min) x SV (mL/beat)

31
Q

how much blood do we have in our bodies?

A

5L
your heart pumps all of the blood in your body every single minute

32
Q

autonomic innervation of the heart: stimulating SA node

A

-if we add sympathetic input to SA nose= speed up

-if we add parasympathetic input to SA node= slow down

33
Q

ventricular myocardium ONLY gets — input

A

sympathetic

34
Q

chonotropic effect

A

= autonomic effect on the SA node
-modulation of HR (chronotropic effect)
-parasympathetic or sympathetic

35
Q

Inotropic effect

A

= autonomic effect on ventricular myocytes
- modulation of contractility (inotropic effect)
- only sympathetic

36
Q

in HR increases, contractility…

A

increases
- contractility increases so SV increases

and therefore CO increases

37
Q

chronotropic effect: parasympathetic neuron

A

parasympathetic neuron (ACh on M2 receptor)

-decreases HR

38
Q

chronotropic effect: sympathetic neuron

A

sympathetic neuron (NE on beta 1 receptor)

-increases HR

39
Q

more than 1 heart beat per sec=

A

+ chronotropic effect
fast?

40
Q

less than 1 heart beat per second=

A

Negative chronotropic effect
slow

41
Q

how is SV modulated?

A

SV is proportional to contraction force

contraction force is determined by:
1. sarcomere length (approx EDV)
2. contractility of muscle

42
Q

ideal length for max tension is a skeletal muscle sarcomere=

A

2 microns

43
Q

Frank-Starling Curve

A

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
Q

Frank-Starling Law

A

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
Q

2 factors that increase EDV

A
  1. increased venous return
  2. decreased HR (more filling time)
46
Q

as EDV increases, SV…

A

increases

(increases SV because we increase contractility)

47
Q

effect of SNS on ventricular contractility

A

norepinephrine is spit out onto beta 1 receptors

SNS activity of ventricular myocytes, increase in contractility, increased SV

48
Q

what happens to the Frank Sterling curve with sympathetic input?

A

it gets “bumped up”

49
Q

what happens to the Frank Sterling curve with parasympathetic input?

A

it gets “bumped down”

50
Q

2 effects of (increased – activity) SNS on myocyte contractility

A
  1. increased activity of LTCC (L type calcium channels)
  2. increased activity of SERCA (Sarcoendoplasmic Reticulum Calcium ATPase)
51
Q

how does increased activity of the LTCC affect myocyte contractility?

A

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
Q

How does increased SERCA activity affect myocyte contractility?

A

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
Q

adding sympathetic stimulation (such as the SNS example of epinephrine and norepinephrine) would be an example of an —- effect

A

inotropic effect

205 (19 decks)

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