cardiac output Flashcards

1
Q

cardiac output

equation and 4 determinants

A

co = HR x SV with SV being volume at beginning of systole in LV to volume at it’s end
1) preload 2) afterload 3) HR 4) contractility

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2
Q

what is the importance of the frank-starling

A

-investigates the fact that the end diastolic volume can stretch the ventricle to a point where it can’t stretch further and this is the cause of heart failure- not enough strength in the ventricle to push it all out

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3
Q

what happens with you decrease heart rate

A
  • you increase SV by increasing the amount of time the heart can fill before it ejects (longer diastole and increased end diastolic vol)
  • co= SV x HR
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4
Q

what happens with you increase heart rate

A

-decrease the amount of time to fill so decrease diastole, decrease SV and decrease the end diastolic vol
CO = SV x HR

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5
Q

on the frank-starling lV pressure vs volume diagram, walk through the whole cycle

A

(ck slide 12)
A- mitral valve opens building LV volume and pressure leading to …
B- closure of the MV giving us the END DIASTOLIC VOLUME/PRESSURE FOR LV
B to C- give isovolumic contraction (all valves closed)
C- aortic valve opens when ventricle pressure higher than aortic pressure
D- aortic valve closes
D to A- isovolumic relaxation (all valves closed)

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6
Q

if you increase peripheral vascular resistance, what happens to strove volume

A

-decreases because need more pressure to generate enough pressure to overcome the change

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7
Q

what do Sarnoff curves prove

A

that if you increase the heart’s ability to contract, you can increase stroke volume ie. not just heart rate determines SV

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8
Q

what does a positive ionotropic agent do to after load

A

-it shifts the afterload curve up and thus it increases the SV

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9
Q

what are some things that can actually cause systolic dysfunction

A
  • myocardial infarction
  • ischemia
  • dilated cardiomyopathy
  • volume overload
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10
Q

what occurs in diastolic dysfunction? describe what occurs via frank-starling graph

A
  • the pressure of the LV is increased at B (the end diastolic LV pressure)
  • reason is that when the ventricles get bigger, due to hypertrophy, it can’t comply with the filling that needs to be done and so you get this diastolic dysfunction and an upward shift of the line going from A to b
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11
Q

what does an increase in blood volume do to the mean systemic filling pressure

A

-increases it…. opposite is true for loss of bv

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12
Q

what does vaso dilation do to the venous return

A

-increases venous return, not the mean systemic filling pressure

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13
Q

what does vasoconstriction do to the venous return

A

-decreases venous return, not the mean systemic filling pressure

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14
Q

how does the sympathetic nervous system effect the cardiac output

A

-increases Ca permeability in nodal cells to increase the slope of the phase 4 depolarization thus increasing the SA/AV stimulation
-increases permeability of Ca in myocytes causing a chronotropic effect
-norepi also starts glycogenolysis that helps with CO
=increase CO by increasing heart rate (nodal cells) and stroke volume (Ca on myocytes)

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15
Q

what does the parasympathetic nervous system do to the cardiac output

A
  • decreases heart rate via Ach on sa and av nodes

thus decreases CO

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16
Q

sympathetics-wise, what occurs IN SYSTOLE in the heart during acute exercise?

A

*systole- increase glycogenolysis to increase energy mobilization and create an enhanced substrate for contraction
-increased cellular permeability to calcium to have more ca during phase 2 and an increased in contractility
-increase in HR and decrease in filling time
INCREASE CO

17
Q

*sympathetics-wise, what occurs IN DIASTOLE in the heart during acute exercise?

A
  • increased HR and decreased filling time-decreased diastole
  • enhanced Ca efflux
  • increased Ca sequestration
  • shorter relaxation time BUT more efficient and faster filling rate
18
Q

what is the equilibrium point

A

when CO and Venous return are have matching inflow and outflow (cross on CO of Ven return vs RA) graph

19
Q

how do you measure cardiac output

A
  • have oxygen put into pt
  • divide that by difference between arterial sample (post lungs) and venous blood at PA

or

-insert dye and see what comes out other end

or thermal dilution

20
Q

what increases CO

A
  • hyperthyroidism
  • anemia (more watery so less viscosity holding it back, need more oxygen so increase HR and CO)
  • reduced peripheral vascular resistance
  • AV shunt
21
Q

what decreases CO

A
  • heart damage- coronary blockage and valve disease
  • decreased blood vol
  • acute venous dilation and venous obstruction
  • decreased tissue mass or tissue metab