14. Cardiac Output & Contractility Flashcards
what meds are used to treat heart failure
cardiac glycosides
how do cardiac glycosides work
- meds inhibit Na/K ATPase binding K binding site
- increase [intracellular Na]
- decrease Ca thru Ca/Na exchanger (bc less gradient)
- increase [intracell Ca]
- positive inotropic effect
what is the traditional formula for CO
HR * SV
what is positive inotropic effect
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
what is the negative inotropic effect
decreased contractility
what is the relationship of Ca and CO
CO proportional to amount of Ca that is available to troponin on actin filaments of contractile apparatus
what is preload
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 are length-tension relationship & preload
preload = EDV = related to venous return
==> so CO = venous return
what is the frank-starling relationship
volume of blood ejected by the ventricle depends on the vol present in the ventrilcle at the end of diastole
what is afterload
for LV - related to aortic P
=force opposing contraction aka pressure required to eject blood
How is velocity of shortening and afterload related
velocity of shortening decrease as afterload increase
=greatest when afterload = 0
what is the equation for SV & what is the normal value
SV = EDV - ESV
around 70 mL
=vol of blood ejected by ventricle w/ each beat
what is ejection fraction
=SV/EDV = 55%
= fraction of EDV ejected in each SV
-measure efficiency and contractility
what is normal CO
around 5 L/min
what happens to CO and contractility as preload increases
both increase
what happens to CO and contractility with increased afterload
decreased CO
increase contractility or increase HR to overcome the decreased CO
how are chronotropic and inotropic effect related
increase HR (pos chronotropic effect) –> increase contractility (pos inotropic effect)
explain the positive staircase effect
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
what is post-extrasystolc potentiation
if a signal present out of synch –> then the next one is stronger
how do sympathetics affect contractility
positive inotropic effect
beta-1 –> cAMP –> pka –> phosphorylate
- sarcolemma Ca channel –> increase Ca inward current during plateu and increase SR release
- phospholamban –> stimulatory
- troponin I –> inhibit inhibitory
how do parasyms affect contactility
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
what is 1 - 2
1 = EDV (low P bc ventricles relaxed)
1 –> 2: increaes LV P to where aortic valve opens (2)
=isovolumetric contraction
what occurs from 2 to 3
= ventricular ejection ; P remains high bc ventricle contracting
= SV
3 = ESV
when is isovolumetric relaxation occuring
3 to 4
3 = end of systole, ventricles relax *aortic valve closed bc decreased P
-volume - constant
4 = AV valve opens
what happens from 4 to 1
ventricular filling
what happens if preload increases
greater EDV - increase VR & increase BV
afterload & contractility = constant
increased SV
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)
what happens with increased contractility
–> increase tention and P in ventricle during systole –> eject a large vol
increase SV & EF%
decreaese ESV
what is volume work
cardiac output
what is pressure work
aortic P
what is minute work
CO * aortic P
what is stroke work
performed by LV =
stroke vole * aortic P
what is the largest % of O2 consumption for
pressure work (rather than CO)
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
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
what does the cardiac fxn curve show
VR increase –> P(ra) increase
EDV & end diastolic diber length increased
what is the vascular fxn curve
VR & P(ra) inversely related
depends on P gradient - increase P(ra) = less gradient –> decrease VR
what is the relationship of the CO and venous return
at equilibrium –> CO =VR
only occur at specific preload
what is the mean systemic pressure
P(ra) where venous return or CO = 0
–> depends entirely on vascular compliance & BV
what happens to CO and P(ra) with positive inotropic effect
increase contractility –> increase SV –>
increase CO
decrease P(ra)
what happens with increased TPR
increased TPR
–> increase P(arterial) –> Increase afterload –> decrease CO
–> decrease VR
-P(ra) doesnt change
what happens with increased BV
increase CO & P(ra)
