Cardiac Function And Venous Return Curves Flashcards

1
Q

As End Diastolic Volume increases on CO

A

The CO increase also

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2
Q

As EDV increases the, on Venous Return

A

The Venous Return stays steady and then decreases

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3
Q

What determines the Venous Return

A

The Right Atrial Pressure

The lower the RAP the more venous return

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4
Q

Another way of saying CO

A

ESCPR (End-Systolic-Venous - pressure- relationship):

=CO AND EDV - curve

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5
Q

What increases the CO and with the EDV staying the same

A

Inotropy (contractility) increases, CO increases and EDV stays the same

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6
Q

When is the venous return and EDV in equilibrium

A

At +2mmHg RAP

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7
Q

When does venous return stay the same

A

Any EDV when the RAP is 0mmHg or less

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8
Q

Pulmonary resistance goes up, what happens to venous return

A

Pulmonary HTN —> RV needs more force to push blood out —> RA increases P so blood can go into high P V——> decreases venous return

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9
Q

Mean Systemic Filling Pressure

A

Psf
= P in vasculature when there is no flow
= 7+ mmHG RAP ——> venous return = 0mmHg

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10
Q

When does the right amount of venous return occur

A

At +2mmHg RAP

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11
Q

Increased TPR on CO and VR

A

Decreases both
(Specifically in arterioles and arteries)
*Psf stays the same

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12
Q

What happens when TPR decreases

A

No change in Psf

Increased CO and VR

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13
Q

What causes the CO, VR, and Psf to increase all together

A
  1. RAPID BLOOD VOLUME INCREASE
  2. Increased venous tone
  3. Venoconstriction (unstressed volume)
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14
Q

When does the CO = Venous Return

A

EQUILIBRIUM = +2mmHg RAP*

(CO=+5 L/min, VR= +5 L/min) *

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15
Q

RAP in heart failure

A
RAP increases
CO decreases (SV decreases, more blood left tin V)
Venous Return (+3mmHG)
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16
Q

Venous return is controlled more by what N

A

Alpha 1

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17
Q

CO is controlled more by what N

A

Beta1

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18
Q

Higher contractility does what to CO, VR, RAP

A
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
19
Q

Increased Blood Volume causes what to CO,VR, RAP

A

RAP increases
CO increases
Venous Return = 6mmHg
Contractility stays the same

20
Q

Blood volume increased
CO
RAP
Psf

A

CO : Increased (13L/min)
RAP : increased (+7mmHg)
Psf : increased to (+16mmHg)

21
Q

Decrease in TPR on
CO, VR
RAP
Psf

A

Increases CO (reduced afterload), increased VR
*new equilibrium at +2mmHG, (VR and CO = 6mmHG)
RAP STAYS THE SAME
Psf stays the same also (+7)

22
Q

Increased TPR (arteriole constriction, blood stays longer in arteries) on
CO, VR
RAP
Psf

A

Decreased CO, decreased VR
= * new equilibrium at +2mmHG (both CO and VR are +3L/min)
RAP and Psf stay the same

23
Q

EDV

ESV

A

Volume in Heart right before contraction

Volume in Heart right after contraction (usually 40%, 120mL-50mL)

24
Q

CO =

A

CO = SV x HR

SV influenced by myocardial contractility

25
CO is influenced by what 4 things
1. HR 2. Contractility (effecting SV) 3. Preload 4. Afterload
26
What is SV
V ejected by Ventricle each beat | SV = EDV -ESV (usually 70mL)
27
What is the ejection fraction
Fraction of EDV ejected (usually 55%) *efficiency and contractility measured this way* EF = SV/EDV
28
What is Cardiac Output (Q)
TOTAL volume of blood ejected by Ventricle PER MINUTE | CO = SV x HR (usually 5L/min)
29
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% ```
30
Preload is what
Amount of blood ready to be pumped (EDV) *effected by Venous Return ——> CO = tension of Ventricular wall tension
31
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
32
Afterload and velocity of myocardial contraction
As afterload increases the velocity of the muscles contracting decreases
33
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
34
Isometric contraction of V has what inside
``` The EDV (end diastolic volume) * valve opens = afterload pressure (around 80mmHG) ```
35
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*)
36
ESPVR represents
Contractility | More contractility = peak of ventricular pressure = INCREASED ESP
37
``` Decrease in PRELOAD does what to EDV ESV SV Afterload Contractility ```
``` EDV: decreased ESV : no change SV : decreased Afterload : no change contractility: no change ```
38
``` increase in AFTERLOAD does what to EDV ESV SV Afterload Contractility ```
EDV : no change ESV : increased SV : decreases Contractility : no change
39
4 things causing increased afterload
1. HTN, (increased TPR) 2. Aortic Stenosis 3. Increased blood viscosity 4. Increased intrathoracic Pressure
40
Causes for decrease in AFTERLOAD
1. Hypotension (low TPR) 2. decrease in blood viscosity 3. A fistula (organs causing decrease resistance of blood in arteries)
41
``` Decrease in AFTERLOAD does what to EDV ESV SV Contractility ```
Stays the same Decrease Increase Stays the same
42
``` 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 ```
43
``` 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 ```