14. Cardiac Output & Contractility Flashcards

1
Q

what meds are used to treat heart failure

A

cardiac glycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is the traditional formula for CO

A

HR * SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the negative inotropic effect

A

decreased contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how are length-tension relationship & preload

A

preload = EDV = related to venous return

==> so CO = venous return

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is afterload

A

for LV - related to aortic P

=force opposing contraction aka pressure required to eject blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is velocity of shortening and afterload related

A

velocity of shortening decrease as afterload increase

=greatest when afterload = 0

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is ejection fraction

A

=SV/EDV = 55%

= fraction of EDV ejected in each SV

-measure efficiency and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is normal CO

A

around 5 L/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what happens to CO and contractility as preload increases

A

both increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens to CO and contractility with increased afterload

A

decreased CO

increase contractility or increase HR to overcome the decreased CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
what happens from 4 to 1
ventricular filling
26
what happens if preload increases
greater EDV - increase VR & increase BV afterload & contractility = constant increased SV
27
what happens to the pressure-volume loop with aortic stenosis/HTN
increased afterload -- greater P needed (shift 2 up) decrease SV and EF% increase ESV (harder to pump blood out, so more blood left)
28
what happens with increased contractility
--\> increase tention and P in ventricle during systole --\> eject a large vol increase SV & EF% decreaese ESV
29
what is volume work
cardiac output
30
what is pressure work
aortic P
31
what is minute work
CO \* aortic P
32
what is stroke work
performed by LV = stroke vole \* aortic P
33
what is the largest % of O2 consumption for
pressure work (rather than CO)
34
why does the left ventricle have to work harder than the right ventricle
has to be proportional - LV work harder bc systemic pressure is greated than pul pressure
35
what is the fick principle
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
what does the cardiac fxn curve show
VR increase --\> P(ra) increase EDV & end diastolic diber length increased
37
what is the vascular fxn curve
VR & P(ra) inversely related depends on P gradient - increase P(ra) = less gradient --\> decrease VR
38
what is the relationship of the CO and venous return
at equilibrium --\> CO =VR only occur at specific preload
39
what is the mean systemic pressure
P(ra) where venous return or CO = 0 --\> depends entirely on vascular compliance & BV
40
what happens to CO and P(ra) with positive inotropic effect
increase contractility --\> increase SV --\> increase CO decrease P(ra)
41
what happens with increased TPR
increased TPR --\> increase P(arterial) --\> Increase afterload --\> decrease CO --\> decrease VR -P(ra) doesnt change
42
what happens with increased BV
increase CO & P(ra)