Cardiac Function And Venous Return Curves Flashcards
As End Diastolic Volume increases on CO
The CO increase also
As EDV increases the, on Venous Return
The Venous Return stays steady and then decreases
What determines the Venous Return
The Right Atrial Pressure
The lower the RAP the more venous return
Another way of saying CO
ESCPR (End-Systolic-Venous - pressure- relationship):
=CO AND EDV - curve
What increases the CO and with the EDV staying the same
Inotropy (contractility) increases, CO increases and EDV stays the same
When is the venous return and EDV in equilibrium
At +2mmHg RAP
When does venous return stay the same
Any EDV when the RAP is 0mmHg or less
Pulmonary resistance goes up, what happens to venous return
Pulmonary HTN —> RV needs more force to push blood out —> RA increases P so blood can go into high P V——> decreases venous return
Mean Systemic Filling Pressure
Psf
= P in vasculature when there is no flow
= 7+ mmHG RAP ——> venous return = 0mmHg
When does the right amount of venous return occur
At +2mmHg RAP
Increased TPR on CO and VR
Decreases both
(Specifically in arterioles and arteries)
*Psf stays the same
What happens when TPR decreases
No change in Psf
Increased CO and VR
What causes the CO, VR, and Psf to increase all together
- RAPID BLOOD VOLUME INCREASE
- Increased venous tone
- Venoconstriction (unstressed volume)
When does the CO = Venous Return
EQUILIBRIUM = +2mmHg RAP*
(CO=+5 L/min, VR= +5 L/min) *
RAP in heart failure
RAP increases CO decreases (SV decreases, more blood left tin V) Venous Return (+3mmHG)
Venous return is controlled more by what N
Alpha 1
CO is controlled more by what N
Beta1
Higher contractility does what to CO, VR, RAP
RAP decreases (more blood ejected) CO increases (higher SV and, less blood left in V) Increased afterload = 0mmHG RAP, venous return is plateau at 6mmHg
Increased Blood Volume causes what to CO,VR, RAP
RAP increases
CO increases
Venous Return = 6mmHg
Contractility stays the same
Blood volume increased
CO
RAP
Psf
CO : Increased (13L/min)
RAP : increased (+7mmHg)
Psf : increased to (+16mmHg)
Decrease in TPR on
CO, VR
RAP
Psf
Increases CO (reduced afterload), increased VR
*new equilibrium at +2mmHG, (VR and CO = 6mmHG)
RAP STAYS THE SAME
Psf stays the same also (+7)
Increased TPR (arteriole constriction, blood stays longer in arteries) on
CO, VR
RAP
Psf
Decreased CO, decreased VR
= * new equilibrium at +2mmHG (both CO and VR are +3L/min)
RAP and Psf stay the same
EDV
ESV
Volume in Heart right before contraction
Volume in Heart right after contraction (usually 40%, 120mL-50mL)
CO =
CO = SV x HR
SV influenced by myocardial contractility
CO is influenced by what 4 things
- HR
- Contractility (effecting SV)
- Preload
- Afterload
What is SV
V ejected by Ventricle each beat
SV = EDV -ESV (usually 70mL)
What is the ejection fraction
Fraction of EDV ejected (usually 55%)
efficiency and contractility measured this way
EF = SV/EDV
What is Cardiac Output (Q)
TOTAL volume of blood ejected by Ventricle PER MINUTE
CO = SV x HR (usually 5L/min)
EDV is usually
ESV is usually
+ what happens in heart here
EDV = 120mL (*mitral valve closes after SA node) ESV = 50mL (*right before mitral valve opens) SV= 70mL EF= 58%
Preload is what
Amount of blood ready to be pumped (EDV)
*effected by Venous Return ——> CO
= tension of Ventricular wall tension
Afterload is what
Force to push blood out (or open valve)
LV afterload : effected by aortic P
*a little greater then the aortic P, or pulmonary A (for RV)
*estimated to = Diastolic Pressure or person
Afterload and velocity of myocardial contraction
As afterload increases the velocity of the muscles contracting decreases
Diastolic Pressure related to Systolic Pressure
=ESPVR (end systolic pressure volume relationship)
Diastolic P at 110ml - 160mL (in LV) = causes highest systolic pressure and CO
- Titin is the ideal stretch here
- higher and lower V in LV (and P in Diastolic P) will decrease the systolic P = myosin and actin overlap is not ideal
Isometric contraction of V has what inside
The EDV (end diastolic volume) * valve opens = afterload pressure (around 80mmHG)
After SV has been ejected and the aortic valve closes, what happens in the heart
The blood V left in the LV is contestant = isometric relaxation
LV V increases again when mitral valve opens again (when A pressure has increased, and LV pressure has decreased)
ESPVR represents
Contractility
More contractility = peak of ventricular pressure = INCREASED ESP
Decrease in PRELOAD does what to EDV ESV SV Afterload Contractility
EDV: decreased ESV : no change SV : decreased Afterload : no change contractility: no change
increase in AFTERLOAD does what to EDV ESV SV Afterload Contractility
EDV : no change
ESV : increased
SV : decreases
Contractility : no change
4 things causing increased afterload
- HTN, (increased TPR)
- Aortic Stenosis
- Increased blood viscosity
- Increased intrathoracic Pressure
Causes for decrease in AFTERLOAD
- Hypotension (low TPR)
- decrease in blood viscosity
- A fistula (organs causing decrease resistance of blood in arteries)
Decrease in AFTERLOAD does what to EDV ESV SV Contractility
Stays the same
Decrease
Increase
Stays the same
Increase in CONTRACTILITY does what to EDV ESV SV Afterload
EDV : no change ESV : decrease SV: increases Afterload : no change * LV pressure at peak increased some
Decrease in CONTRACTILITY does what to EDV ESV SV Afterload
No change Increase Decrease No change *negative inotropy * LV pressure decreased some at its peak