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CPR Exam 1 > 14. Cardiac Output & Contractility > Flashcards

14. Cardiac Output & Contractility Flashcards

1
Q

what meds are used to treat heart failure

A

cardiac glycosides

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2
Q

how do cardiac glycosides work

A
  1. meds inhibit Na/K ATPase binding K binding site
  2. increase [intracellular Na]
  3. decrease Ca thru Ca/Na exchanger (bc less gradient)
  4. increase [intracell Ca]
  5. positive inotropic effect
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3
Q

what is the traditional formula for CO

A

HR * SV

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4
Q

what is positive inotropic effect

A

increased contractility

  • increase blood to heart - increase stretching - increase rate of tension development, increase length –> increase Ca sensitivity to troponin C & amount released from SR
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5
Q

what is the negative inotropic effect

A

decreased contractility

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6
Q

what is the relationship of Ca and CO

A

CO proportional to amount of Ca that is available to troponin on actin filaments of contractile apparatus

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7
Q

what is preload

A

amount of blood ready to be pumped at diastole

=LV EDV

  • wall tension in LV just before contraction is initiated
  • related to venous return
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8
Q

how are length-tension relationship & preload

A

preload = EDV = related to venous return

==> so CO = venous return

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9
Q

what is the frank-starling relationship

A

volume of blood ejected by the ventricle depends on the vol present in the ventrilcle at the end of diastole

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10
Q

what is afterload

A

for LV - related to aortic P

=force opposing contraction aka pressure required to eject blood

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11
Q

How is velocity of shortening and afterload related

A

velocity of shortening decrease as afterload increase

=greatest when afterload = 0

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12
Q

what is the equation for SV & what is the normal value

A

SV = EDV - ESV

around 70 mL

=vol of blood ejected by ventricle w/ each beat

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13
Q

what is ejection fraction

A

=SV/EDV = 55%

= fraction of EDV ejected in each SV

-measure efficiency and contractility

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14
Q

what is normal CO

A

around 5 L/min

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15
Q

what happens to CO and contractility as preload increases

A

both increase

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16
Q

what happens to CO and contractility with increased afterload

A

decreased CO

increase contractility or increase HR to overcome the decreased CO

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17
Q

how are chronotropic and inotropic effect related

A

increase HR (pos chronotropic effect) –> increase contractility (pos inotropic effect)

18
Q

explain the positive staircase effect

A

HR increased –> tension increase in stepwise fashion –> Increase AP/time –> increase Ca at the plateu phase and build up in SR

-at first - no increase in tension bc not accumulated yet but then increase tension in a step wise fashion until it reaches the max tension

19
Q

what is post-extrasystolc potentiation

A

if a signal present out of synch –> then the next one is stronger

20
Q

how do sympathetics affect contractility

A

positive inotropic effect

beta-1 –> cAMP –> pka –> phosphorylate

  1. sarcolemma Ca channel –> increase Ca inward current during plateu and increase SR release
  2. phospholamban –> stimulatory
  3. troponin I –> inhibit inhibitory
21
Q

how do parasyms affect contactility

A

negative inotropic effec in ATRIA ONLY

muscarinic receptor

–> decrease inward Ca during plateu –> shorten plateu

–> Ach increase outward K current –> shorten AP duration –> indirectly decrease Ca inward current

22
Q

what is 1 - 2

A

1 = EDV (low P bc ventricles relaxed)

1 –> 2: increaes LV P to where aortic valve opens (2)

=isovolumetric contraction

23
Q

what occurs from 2 to 3

A

= ventricular ejection ; P remains high bc ventricle contracting

= SV

3 = ESV

24
Q

when is isovolumetric relaxation occuring

A

3 to 4

3 = end of systole, ventricles relax *aortic valve closed bc decreased P

-volume - constant

4 = AV valve opens

25
Q

what happens from 4 to 1

A

ventricular filling

26
Q

what happens if preload increases

A

greater EDV - increase VR & increase BV

afterload & contractility = constant

increased SV

27
Q

what happens to the pressure-volume loop with aortic stenosis/HTN

A

increased afterload – greater P needed (shift 2 up)

decrease SV and EF%

increase ESV (harder to pump blood out, so more blood left)

28
Q

what happens with increased contractility

A

–> increase tention and P in ventricle during systole –> eject a large vol

increase SV & EF%

decreaese ESV

29
Q

what is volume work

A

cardiac output

30
Q

what is pressure work

A

aortic P

31
Q

what is minute work

A

CO * aortic P

32
Q

what is stroke work

A

performed by LV =

stroke vole * aortic P

33
Q

what is the largest % of O2 consumption for

A

pressure work (rather than CO)

34
Q

why does the left ventricle have to work harder than the right ventricle

A

has to be proportional

  • LV work harder bc systemic pressure is greated than pul pressure
35
Q

what is the fick principle

A

CO = O2 consumption / ([O2] pulV - [O2] pulA)

O2 consumption = 250 ml/min

[O2] pulV = 0.2

[O2] pul A = 0.15

==> CO = 5 L/min

36
Q

what does the cardiac fxn curve show

A

VR increase –> P(ra) increase

EDV & end diastolic diber length increased

37
Q

what is the vascular fxn curve

A

VR & P(ra) inversely related

depends on P gradient - increase P(ra) = less gradient –> decrease VR

38
Q

what is the relationship of the CO and venous return

A

at equilibrium –> CO =VR

only occur at specific preload

39
Q

what is the mean systemic pressure

A

P(ra) where venous return or CO = 0

–> depends entirely on vascular compliance & BV

40
Q

what happens to CO and P(ra) with positive inotropic effect

A

increase contractility –> increase SV –>

increase CO

decrease P(ra)

41
Q

what happens with increased TPR

A

increased TPR

–> increase P(arterial) –> Increase afterload –> decrease CO

–> decrease VR

-P(ra) doesnt change

42
Q

what happens with increased BV

A

increase CO & P(ra)

CPR Exam 1 (27 decks)

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