Cardiac Output and Contractility Flashcards
How do cardiac glycosides work?
used to treat heart failure
- inhibit Na/K ATPase K binding sites
- increases Na concentration
- decreases Ca efflux through Ca/Na exchanger
- increases Ca intracellular
- Positive inotropic effect
What is preload?
Another term for this is?
Amount of blood ready to be pumped, diasole
End diastolic volume (LV or RV)-related to venous return
think of this as fiber length at the end of diastole
What is the Length-Tension Relationship and Preload?
Volume at EDV relates to venous return; so CO = Venous return (steady state)
Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole (relates to Length-Tension to functionality)
What is afterload?
For the left ventricle, it is related to aortic pressure
What is really means: Force opposing contraction
AKA pressure required to eject blood (open the aortic valve)
What is stroke volume?
volume of blood ejected by ventricle with each beat
SV=EDV-ESV (usually about 70ml)
What is ejection fraction?
fraction of the EDV ejected in each stroke volume
measure of efficiency and contractility
EF%=SV/EDV (usually approximately 55% reduced in heart failure)
What is cardiac output?
total volime of blood ejected by ventricle per minute
CO=SV+HR
usually about 5L/min
What are coupling factors?
Preload, afterload
relate to contractility
What happens when afterload increases?
CO decreases
heart must increase contractility to overcome or increase HR to overcome
What happens as preload increases?
contractility increases
CO increases
What is the effect of heart rate on contractility?
What is the positive staircase effect?
What happens as a result of post-extrasystolic potentiation?
Increased HR (positive chronotropic effect) increases contractility (positive inotropic effect)
More Ca enters cells and is taken up into SR (helps with contractions)
Arrhythmia, extra beat
What is the sympathetic influence on CO?
positive inotropic effect via b-adrenergic activation
Pi of sarcolemma Ca channels
pi phospholamban (+)
pi troponin I (-)
What are the effects of the parasympathetics on CO?
negative ionotropic effect in ATRIA ONLY
no influence on ventricular myocytes
uses muscarinic receptors to decrease inward Ca current during plateau.
Ach increases outward K flow via K-Ach channel
Describe stage 1 of the ventricular pressure-volume loop
- isovolumetric contraction (1-2)
- point 1 marks end of diastole, pressure is low
- ejection is not taking place as pressure rises
- point 2 marks point where ejection of blood begins (aortic valve opens)
- 1-Preload
- 2-Afterload
Describe stage 2 of the ventricular pressure-volume loop
pressure does not reach a max. at point 2 or 3, but in between
SV=70ml (140ml-70ml)
What is stage 3 of the ventricular pressure-volume loop?
point 3, systole ends and ventricles relax
ventricular pressure falls quickly but volume remains constant
pressure must reach level where tricuspid/mitral valve opens (pt 4)
What happens between stages 4-1
ventricular filling
Understand how the cardiac cycle graph relates to the pressure-volume loop
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What happens when you increase preload?
How does the system compensate?
more venous return=more blood volume
greated EDV, afterload and contractility remain constant
increased afterload
increased contractility
When preload increases, afterload increases, what are the results?
aortic stenosis and hypertension
greater pressure is needed
reduced SV and reduced EF%
When preload increases, contractility increases to compensate. What are the results?
Adrenergic stimulation
increases SV and increased EF%
less blood left in heart
What are the following terms synonymous with:
- volume work
- pressure work
- minute work
- stroke work
- cardiac output
- aortic pressure
- COxaortic pressure
- done by LV, =stroke volume x aortic pressure (area within the pressure volume loop)
PW can be bad, because as it increases, heart enlarges to compensate and has to work harder/get more O2
What is the largest percentage of O2 consumption used for in the heart?
pressure work rather than cardiac output
the left ventricle must proportionally work harder than the right ventricle despite cardiac output being similar because systemic pressure is greater than pulmonary pressure
this is further accentuated by conditions that increase left ventricular pressure work, such as aortic stenosis or systemic hypertension
What is the fick principle?
a way to measure cardiac output
O2 consumption=CO x (O2 pulmonary vein)-CO x (O2 pulmonary artery)
(usually around 5000ml, or 5L)
describe the cardiac function curve
venous return increases
right atrial pressure increases
EDV and end diastolic fiber length increase
At steady state, the volume of blood as cardiac output ejected by the left ventricle equals or matches the volume it receives in venous return
when are CO and venous return in equilibrium?
at a specific preload
equilibrium point will vary depending on state of CV system
Normal is CO 5L/min and Pra=+2mmHg
What will the enhanced cardiac function curve show
increased inotropy
increased HR
decreased afterload
What will a depressed cardiac function curve show?
decreased inotropy
decreased HR
increased afterload
Describe mean systemic pressure (mean circulatory filling pressure)
when there is no cardiac output and vascular function depends entirely on vascular compliance and blood volume (usually around +7 or +8)
as the Pra starts to fall below 0, the increased CO begins to plateau because the vena cava colapses, thus limiting venous return to the heart
What is the relationship between CO and venous return in cardiac failure?
decreased inotropy
decreased vascular compliance
increased blood volume
increased SVR/TPR
What are the +/- inotropic effects in CO on the cardiac and vascular function curve
+ inotropy (beta agonist/adrenergic agonist)
- increased CO, decrease RA pressure
- inotropy (beta blocker)
- decrease CO, increase RA pressure
What is the effect on CO on the cardiac and vascular function curve with changes in TPR?
Increase TPR
- increase in afterload, decrease in VFC, decrease CO, no change in contractility
Decrease TPR
- Decrease afterload, increase VFC, increase CO, no change in contractility
What are the changes in the cardiac and vascular function curve based on changes in blood volume?
Increase BV
- shift curve to right
Decrease BV
- shift curve to left
