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CV physio Larmon - S.Horvath > control of cardiac output > Flashcards

control of cardiac output Flashcards

1
Q

the cardiac output is controlled mainly by

A

the sum of all the local tissue flows

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2
Q

cardiac output

A

the quantity of blood pumped into the aorta each minute

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3
Q

venous return

A

the quantity of blood flowing from the veins into the right atrium each minute

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4
Q

CO =

A

HR x SV

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5
Q

SV =

A

EDV - ESV

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6
Q

EF =

A

SF/EDV = EDV-ESV/EDV

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7
Q

end diastolic volume - end systolic volume =

A

stroke volume

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8
Q

which affects CO more? HR or SV?

A

HR. changes in HR alone inversely affect stroke volume

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9
Q

at low HR, increase in HR is greater than

A

decrement in SV

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10
Q

Bowditch (Treppe or staircase phenomenon)

A

an increase in HR will also cause positive ionotrpy duets an increase in intracellular Ca+++ with a higher HR

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11
Q

preload

A

the initial stretching of the cardiac myocytes prior to contraction. it is related to the sarcomere length at the end of diastole.

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12
Q

what are the indirect ways to measure preload

A

LVEDV, LVEDP, PCWP, CVP

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13
Q

determinants of preload

A

venous BP, vasomotor tone, venous volume, venous retur, total blood volume, respiration, excerise, filling time (HR), ventricular compliance, atrial contraction, inflows outflow resistance, ventricular systolic failure

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14
Q

Frank-Starling Mechanism

A

When venous return to the heart is increased, ventricular filling increases, as does preload. This stretching of the myocytes causes an increase in force generation, which enables the heart to eject the additional venous return and thereby increase stroke volume.
(the heart pumps the blood that is returned it)

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15
Q

increasing venous return and ventricular preload leads to

A

increase in stroke volume

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16
Q

Afterload is closely related to

A

aortic pressure

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17
Q

afterload is

A

the “load” that the heart must eject blood against

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18
Q

LaPlace’s Law is for which concept

A

after load

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19
Q

what is LaPlace’s Law

A

wall stress = Pr/h. p is ventricular pressure, R is ventricular radius, h is wall thickness

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20
Q

aortic pressure does what to afterload

A

increased aortic pressure increases afterload

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21
Q

SVR does what to afterload

A

increased SVR increases afterload

22
Q

aortic valve stenosis effect on afterload

A

increases

23
Q

ventricular dilation effect on afterload

A

increases

24
Q

Anrep effect

A

an abrupt increase in afterload can cause a modest increase in inotropy

25
Q

contractility

A

the inherent capacity of the myocardium to contract independently of changes in afterload or preload.

26
Q

alternative name for contractility

A

iontropy

27
Q

changes in contractility are caused by

A

by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length.

28
Q

decreased iontropy does what to stroke volume and LVEDP?

A

decrease SV and increases LVEDP

29
Q

increased iontropy does what to stroke volume and LVEDP

A

increase SV and decrease LVEDP

30
Q

increased afterload does what to contractility

A

increases - anrep effect

31
Q

what are the four major determinants of CO

A

contractility, stroke volume, HR, preload

32
Q

to increase stroke volume, ____ End-diastolic volume

A

increase

33
Q

to increase stroke volume ___, End-systolic volume

A

decrease

34
Q

preload is directly related to _____ because of frank starling

A

CO. preload increases, CO increases. preload decreases, CO decreases

35
Q

What physiologic relationship keeps cardiac output of the ventricle matched with venous return?

A

Frank starling mechanism – allows the heart to readily adapt to changes in venous return. Increasing venous return and preload leads to an increase in SV.

36
Q

What physiologic relationship keeps the cardiac output of the right and left ventricles matched?

A

Frank starling – outputs of the two ventricles are matched over time, otherwise blood volume would shift between the pulm and systemic circulations

37
Q

what parameter is on the y axis of starling curve

A

SV

38
Q

what parameter is on the x axis

A

LVEDP

39
Q

what factors can cause an increased after load?

A

Increased aortic pressure, increased SVR, aortic valve stenosis, ventricular dilation

40
Q

Increasing afterload ____ SV

A

decreasese

41
Q

decreasing afterload ______ sv

A

increases

42
Q

q: during the phase of rapid ventricular filling

A

mitral valve open

43
Q

q: rv preload is increased by ___ HR

A

decreased HR. more time is available for filling at reduced heart rates; therefore preload is increased.

44
Q

effect on decreased atrial contractility, decreased blood volume, and decreased ventricular compliance on preload

A

reduced ventricular filling, reduced preload

45
Q

increase in preload is a _____ in sarcomere length

A

increase

46
Q

as the preload on a ventricular myocyte is increased,

A

active tension development increases

47
Q

LVEDP is ____ by ventricular hypertrophy

A

increased

48
Q

ventricular stroke volume is ____ by decreased ionotropy

A

reduced

49
Q

ventricular stroke volume is ___ by reduced HR

A

increased - more filling

50
Q

left ventricular end-systolic volume is ___ when iontrophy is impaired

A

increased

51
Q

increasing afterload decreases ejection velocity and stroke volume, which leads to an ___ in end-systolic volume

A

increase

52
Q

an increase in end diastolic volume will ____ SV, but stroke volume changes are about 1/4 as effective in changing myocardial oxygen consumption compared to changes in HR, MAP, or ventricular radius

A

increase

CV physio Larmon - S.Horvath (8 decks)

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