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CPR Exam 1 > Cardiac Output and Contractility > Flashcards

Cardiac Output and Contractility Flashcards

1
Q

How do cardiac glycosides work?

A

used to treat heart failure

  1. inhibit Na/K ATPase K binding sites
  2. increases Na concentration
  3. decreases Ca efflux through Ca/Na exchanger
  4. increases Ca intracellular
  5. Positive inotropic effect
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2
Q

What is preload?

Another term for this is?

A

Amount of blood ready to be pumped, diasole

End diastolic volume (LV or RV)-related to venous return

think of this as fiber length at the end of diastole

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3
Q

What is the Length-Tension Relationship and Preload?

A

Volume at EDV relates to venous return; so CO = Venous return (steady state)

Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole (relates to Length-Tension to functionality)

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4
Q

What is afterload?

A

For the left ventricle, it is related to aortic pressure

What is really means: Force opposing contraction

AKA pressure required to eject blood (open the aortic valve)

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5
Q

What is stroke volume?

A

volume of blood ejected by ventricle with each beat

SV=EDV-ESV (usually about 70ml)

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6
Q

What is ejection fraction?

A

fraction of the EDV ejected in each stroke volume

measure of efficiency and contractility

EF%=SV/EDV (usually approximately 55% reduced in heart failure)

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7
Q

What is cardiac output?

A

total volime of blood ejected by ventricle per minute

CO=SV+HR

usually about 5L/min

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8
Q

What are coupling factors?

A

Preload, afterload

relate to contractility

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9
Q

What happens when afterload increases?

A

CO decreases

heart must increase contractility to overcome or increase HR to overcome

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10
Q

What happens as preload increases?

A

contractility increases

CO increases

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11
Q

What is the effect of heart rate on contractility?

What is the positive staircase effect?

What happens as a result of post-extrasystolic potentiation?

A

Increased HR (positive chronotropic effect) increases contractility (positive inotropic effect)

More Ca enters cells and is taken up into SR (helps with contractions)

Arrhythmia, extra beat

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12
Q

What is the sympathetic influence on CO?

A

positive inotropic effect via b-adrenergic activation

Pi of sarcolemma Ca channels

pi phospholamban (+)

pi troponin I (-)

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13
Q

What are the effects of the parasympathetics on CO?

A

negative ionotropic effect in ATRIA ONLY

no influence on ventricular myocytes

uses muscarinic receptors to decrease inward Ca current during plateau.

Ach increases outward K flow via K-Ach channel

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14
Q

Describe stage 1 of the ventricular pressure-volume loop

A
  • isovolumetric contraction (1-2)
  • point 1 marks end of diastole, pressure is low
  • ejection is not taking place as pressure rises
  • point 2 marks point where ejection of blood begins (aortic valve opens)
  • 1-Preload
  • 2-Afterload
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15
Q

Describe stage 2 of the ventricular pressure-volume loop

A

pressure does not reach a max. at point 2 or 3, but in between

SV=70ml (140ml-70ml)

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16
Q

What is stage 3 of the ventricular pressure-volume loop?

A

point 3, systole ends and ventricles relax

ventricular pressure falls quickly but volume remains constant

pressure must reach level where tricuspid/mitral valve opens (pt 4)

17
Q

What happens between stages 4-1

A

ventricular filling

18
Q

Understand how the cardiac cycle graph relates to the pressure-volume loop

A

–

19
Q

What happens when you increase preload?

How does the system compensate?

A

more venous return=more blood volume

greated EDV, afterload and contractility remain constant

increased afterload

increased contractility

20
Q

When preload increases, afterload increases, what are the results?

A

aortic stenosis and hypertension

greater pressure is needed

reduced SV and reduced EF%

21
Q

When preload increases, contractility increases to compensate. What are the results?

A

Adrenergic stimulation

increases SV and increased EF%

less blood left in heart

22
Q

What are the following terms synonymous with:

  • volume work
  • pressure work
  • minute work
  • stroke work
A
  • cardiac output
  • aortic pressure
  • COxaortic pressure
  • done by LV, =stroke volume x aortic pressure (area within the pressure volume loop)

PW can be bad, because as it increases, heart enlarges to compensate and has to work harder/get more O2

23
Q

What is the largest percentage of O2 consumption used for in the heart?

A

pressure work rather than cardiac output

the left ventricle must proportionally work harder than the right ventricle despite cardiac output being similar because systemic pressure is greater than pulmonary pressure

this is further accentuated by conditions that increase left ventricular pressure work, such as aortic stenosis or systemic hypertension

24
Q

What is the fick principle?

A

a way to measure cardiac output

O2 consumption=CO x (O2 pulmonary vein)-CO x (O2 pulmonary artery)

(usually around 5000ml, or 5L)

25
Q

describe the cardiac function curve

A

venous return increases

right atrial pressure increases

EDV and end diastolic fiber length increase

At steady state, the volume of blood as cardiac output ejected by the left ventricle equals or matches the volume it receives in venous return

26
Q

when are CO and venous return in equilibrium?

A

at a specific preload

equilibrium point will vary depending on state of CV system

Normal is CO 5L/min and Pra=+2mmHg

27
Q

What will the enhanced cardiac function curve show

A

increased inotropy

increased HR

decreased afterload

28
Q

What will a depressed cardiac function curve show?

A

decreased inotropy

decreased HR

increased afterload

29
Q

Describe mean systemic pressure (mean circulatory filling pressure)

A

when there is no cardiac output and vascular function depends entirely on vascular compliance and blood volume (usually around +7 or +8)

as the Pra starts to fall below 0, the increased CO begins to plateau because the vena cava colapses, thus limiting venous return to the heart

30
Q

What is the relationship between CO and venous return in cardiac failure?

A

decreased inotropy

decreased vascular compliance

increased blood volume

increased SVR/TPR

31
Q

What are the +/- inotropic effects in CO on the cardiac and vascular function curve

A

+ inotropy (beta agonist/adrenergic agonist)

  • increased CO, decrease RA pressure
  • inotropy (beta blocker)
  • decrease CO, increase RA pressure
32
Q

What is the effect on CO on the cardiac and vascular function curve with changes in TPR?

A

Increase TPR

  • increase in afterload, decrease in VFC, decrease CO, no change in contractility

Decrease TPR

  • Decrease afterload, increase VFC, increase CO, no change in contractility
33
Q

What are the changes in the cardiac and vascular function curve based on changes in blood volume?

A

Increase BV

  • shift curve to right

Decrease BV

  • shift curve to left

CPR Exam 1 (31 decks)

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