Control of Cardiac Output/Cardiac Cycle Flashcards

1
Q

7 phases of cardiac cyce

A

(Systole 2,3,4)(Diastole 5,6,7,1)
2- Isovolumetric contraction
3- Rapid ejection
4- Reduced ejection
5- Isovolumetric relaxation
6- Rapid filling
7- Diastasis
1- Atrial systole

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2
Q

Phase 1

A

Atrial systole
NOT REQUIRED
20-40% of LV filling
LVEDV=120ml
Possible s4

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3
Q

When are all valves closed?

A

Phase 2- isovolumetric contraction
S1= mitral valve closes
ALSO
Phase 5- isovolumetric relaxation
S2= pulmonic and aortic valves close

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4
Q

When are pulmonic and aortic valves open?

A

Phase 3- rapid ejection
No heart sounds

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5
Q

What percent ejects during phase 3?

A

70%

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6
Q

LVESV

A

50ml

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7
Q

Phase 6

A

Rapid ventricular filling
Possible S3

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8
Q

Phase 7

A

Reduced ventricular filling
Diastasis

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9
Q

Frank sterling law

A

The bigger the preload, the bigger the force of contraction and thus bigger SV (within limits)
When the sarcomere length is increased, more actin and myosin can bind, causing bigger contraction
Cardiac SV responds more to preload than nuerohormonal mechanisms like the intrincsic heart nodes
Matching venous return to cardiac output in BOTH ventricles
Changes force in contraction and SV in response to venous return
Increase volume increases contraction

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10
Q

What is the more independent flow?

A

Arterial is less controlled by blood flow and CO

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11
Q

What is CO? Not the equation

A

Quantity of blood pumped into the aorta each minute

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12
Q

Venous return

A

The amount of blood coming into the RA each minute

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13
Q

What controls CO normally?

A

Venous return, the heart is not the primary controller of CO

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14
Q

SV formula

A

EDV- ESV

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15
Q

EF

A

SV/EDV

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16
Q

What controls heart pumping?

A

ANS
SNS can double CO
ANS can decrease CO to almost 0 by vagal

17
Q

What is more important for changing CO? HR or SV

A

HR

18
Q

Bowditch (Treppe) Effect

A

“staitway effect”
Increase in Hr also increases inotropy
Due to an increase in intracellular CA with higher HR
NaK-ATPase cant keep up with influx of Na, so Na/Ca pump doesnt work well

19
Q

Values for SV, EDV, ESV

A

70ml
120ml
50ml (wont close all the way like alveoli wont), but can decrease to 20 under high inotropy effect, EDV increases, which bumps sv to 150ml

20
Q

Preload and how its measured

A

Tension of cardiac myoctyes
Related to sarcomere length
LVEDV
LVEDP
PCWP
CVP

21
Q

Frank starling curve

A

Looks like small s curve with the same starting point but different end points
Shift right and down- means increased afterload or decreased inotropy
Shift left and up, means increased inotropy or decreased afterload

22
Q

Laplace law

A

T(Wall stress)= P(pressure) R(Radius) /H(thickness

23
Q

What is responsible for the increased CO that follows an increase in afterload? (Primary and delayed)

A
  1. Frank sterling mechanism/Troponin C sensitivity to calcium
  2. CA increase by SR
23
Q

What increases afterload?

A

Aortic pressure
SVR
AV Stenosis
Ventricular dilation

23
Q

What does increased afterload do to LVESV and SV?

A

Increases LVESV, decreases SV

24
Q

What can and cant change heart force?

A

Can:preload- dependent activation, inotropy-independent activation
Cant: recruitment like other skeletal muscles

25
Q

When does CA influx to increase inotropy, what phase?

A

Phase 2

26
Q

What (physiologic) 3 ways to stimulate inotropywith calcium

A

CA influx phase 2 during AP
Increasing CA by SR
Sensitizing Trop-C to CA

27
Q

What does SNS effect mostly in the heart?

A

Inotropy, ventricular and atrial inotropy

28
Q

What does PNS affect mostly in the heart?

A

Negative effect on atria, minimal on ventricles

29
Q

Anrep affect

A

Sudden increase in afterload will increase inotropy
Increasein afterload increases LVEDP, frank starling causes increased inotropy
Only lasts for 15 minutes
Primary- frank starling, trop c sensitize
delayed- SR release of CA

30
Q
A