Contractility & Cardiac Output Flashcards

1
Q

What is preload?

A

aka left ventricular end diastolic volume

-amount of blood ready to be pumped

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2
Q

What is preload directly related to?

A

-fiber length @ end of diastole

–> as ventricle fills with more blood, fibers get longer

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3
Q

How does venous return affect preload?

A

> venous return -> > preload

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4
Q

What is the tension relationship & preload?

A

cardiac output = venous return at a steady state

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5
Q

What is frank starling relat?

A

-volume of blood ejected by ventricle depends od the volume present in the ventricle at end of diastole

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6
Q

What is after load?

A

(for LV) the aortic pressure aka the force opposing contraction

–> pressure required to eject blood by opening the aortic valve

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7
Q

What is the relationship b/w velocity of shorting and after load?

A

-velocity of shortening DECREASES as after load INCREASES

greatest if after load = 0

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8
Q

What is stroke volume and how do you calculate for it?

A

volume of blood ejected by ventricle with each beat

SV = EDV - ESV (~70mL)

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9
Q

What is ejection fraction and how do you calculate it?

What does it measure?

A
  • fraction of EDV ejected in each stroke volume
  • measures efficiency and contractility
  • EF% = SV / EDV (~55%)
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10
Q

What physiological state would cause the ejection fraction to decrease?

A

heart failure

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11
Q

What is cardiac output and how to you calculate it?

A

-total volume of blood ejected by ventricle per minute

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12
Q

What are the two coupling factors that contribute to cardiac output?

A
  • preload
  • afterload

both relate to contractility

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13
Q

What happens to contractility as you increase preload?

A

-increase contractility and increase CO

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14
Q

What happens to CO as you increase after load?

A

decrease in CO

heart must overcome by increasing contractility or HR

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15
Q

What is the positive staircase effect?

A

an auto regulation method by which increased HR increases contractility (via more Ca2+ in cell and into SR)

aka positive chronotropic effect creates a positive inotropic effect

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16
Q

How does sympathetic input affect cardiac output?

activation of what which does what?

A
    • iontropic effect via B-AR activation

- phosphorylation of sarcolemma Ca2+ channels, phospholamban (stimulatory), and troponin 1 (inhibititory)

17
Q

How does parasympathetic input affect cardiac output?

A
  • (-) iontropic effect via muscarinic receptor activation
  • decrease inward Ca2+ current during plateau
  • ACh increased outward flow of K+ current via K+-(-)ACh channels
18
Q

What does administering isoproterenol (B-AR agonist ) do ?

A

increases HR and contractility

treats bradycardia

19
Q

What factors can increase preload?

A
  • increased venous return

- high blood volume

20
Q

What factors can increase after load?

A
  • aortic stenosis

- hypertension

21
Q

What factor can increase contractility directly?

A

adrenergic stimulation

22
Q

What is volume work and how do you calculate it?

A

-cardiac output (SV x HR)

23
Q

What is pressure work?

A

aortic pressure

24
Q

How do you calculate minute work?

A

CO x aortic pressure (SV x HR x aortic pressure)

25
Q

How do you calculate stroke work?

A

SV x aortic pressure (LV)

-the area within the volume pressure loop?

26
Q

What is the difference b/w volume work (cardiac output) and stroke work?

A

Stroke work takes into account the pressure in the aorta; volume work factors in HR

27
Q

What is the Fick Principle? (myocardial O2 consumption)

A

States that he largest % of O2 consumption is pressure work rather than CO (SV x HR)

-LV must work proportionally harder than RV due to systemic pressure > aortic pressure

28
Q

What further accents increase LV pressure work ?

A
  • aortic stenosis
  • systemic hypertension

aka the LV myocytes are using more oxygen to accomplish their tasks to overcome a higher after load pressure and thus more “work”

29
Q

How do you calculate Os consumption ?

A

O2 consumption = CO x ( [O2]pulm v. - (CO x [O2]pulm a.) )

CO = O2 consumption / ( [O2]pulm v. -[O2]pulm a. )

30
Q

What 3 factors play major roles on the cardiac function curve?

A
  • venous return
  • RA pressure
  • EDV and end diastolic fiber length
31
Q

What is the relationship of venous return and CO at equilibrium?

A
  • venous return = CO

- aka volume of blood as cardiac output ejected by ventricle matches the volume it reaches in venous return

32
Q

What happens to the RA pressure and venous return when you increase iontropy vs decrease?

A

increase = RA pressure decreases ; CO/venous return increases

Decreases = RA pressure increases ; Venous return decreases

33
Q

What occurs to RA pressure and venous return when you increase TPR vs decrease TPR?

A

increase : RA pressure remains constant ; venous return decreases

decrease : RA pressure remain constant ; Venous return increases

34
Q

What occurs to RA pressure and venous return when you increase blood volume vs decrease blood volume?

A

increase : RA pressure increases ; venous return increases

Decrease : RA pressure decreases; venous return decreases

35
Q

What happens during cardiac failure?

A
  • decrease iontropy (contractility)
  • decrease vascular compliance
  • increase BP
  • increase SVR/TPR
36
Q

What happens to the pressure in the RA and venous return in cardiac failure?

A
  • RA pressure increases
  • cardiac output decreases

-increase in volume, decrease contractility of ventricle , and increase TPR