Pressure volume relationships for cardio

Question 1

End systolic pressure volume relationship (ESPVR) describes what?

Answer 1

the maximal pressure that can be developed by the ventricle at any given LV volume. This implies that the PV loop cannot cross over the line defining ESPVR for any given contractile state.
(ESPVR determines the slope of line on the top left of the P-V loop)

Question 2

The slope of ESPVR (Ees=end-systolic elastance) represents a measure of what?

Answer 2

the end-systolic elastance, which provides an index of myocardial contractility.

Elastance= 1/compliance
or reworded, Compliance (C) = 1/stiffness of the ventricle=C= volume/Pressure

so Elastance = Pressure/ volume

therefore: ESPVR= LV Pressure /LV Volume
This is is repressented on the Pressure volume loop for the cardac cycle.

Question 3

Why use P/V loop to ge the ESPVR slope?

The ESPVR is relatively insensitive to changes in preload, afterload and heart rate. This makes it an improved index of?

Answer 3

Systolic function

Improved over other hemodynamic parameters like ejection fraction, cardiac output and stroke volume

Question 4

The ESPVR becomes steeper and shifts to the left when what increases?

Answer 4

Inotropy (contractility)

Question 5

What happens to ESPVR as inotropy decreases?

Answer 5

It becomes flatter and shifts to the right

Decreased contractility, decreased systolic function

Question 6

Hypertension, As, and AI all do what to afterload?

Answer 6

Increase afterload

Question 7

What is the equation to determine preload of the LV?

Answer 7

(LVEDP×LVEDR)/2h
where

LVEDP = left ventricular end diastolic pressure
LVEDR = left ventricular end diastolic radius (at midpoint of ventricle)
h = thickness of ventricle

Preload is described as the stretching of a single cardiac myocyte immediately prior to contraction and is therefore related to the sarcomere length. Since sarcomere length cannot be determined in the intact heart, other indices of preload such as ventricular end diastolic volume or pressure are used.

Question 8

The area enclosed by the PV loop is a measure of?

Answer 8

the ventricular stroke work, which is a product of the stroke volume and the mean aortic or pulmonary artery pressure (afterload), depending on whether one is considering the left or the right ventricle.

Question 9

End diastolic pressure volume relationship (EDPVR) describes which curve?

Answer 9

passive filling curve for the ventricle and thus the passive properties of the myocardium.

Question 10

The slope of the EDPVR at any point along this curve is the reciprocal of ?

Answer 10

ventricular compliance (or ventricular stiffness).
EDVPR = 1/ventricular compliance

Question 11

If ventricular compliance is decreased, such as in ventricular hypertrophy will the the ventricle is be more or less stiff?

Answer 11

A decrease in vent compliance = more stiff ventricle

Question 12

A stiff noncompliant ventricle will (INCREASE OR DECREASE) the end-diastolic pressures (EDP) at any given end-diastolic volume (EDV) ?

Answer 12

INCREASE ventricular end-diastolic pressures (EDP) …..

less compliance = increased EDP

Question 13

For any given EDP, a less compliant ventricle would have a smaller EDV due to?

Answer 13

impaired filling……

less compliance = decreased EDV

Question 14

A less compliant ventricle would (increase/decrease) slope of EDPVR?

Answer 14

increase, or shift to the left and up
EDPVR curve shifts up and to the left with decreased compliance ……
(slope = 1/compliance, dec compliance = inc slope)

Question 15

If ventricular compliance increases (such as in dilated cardiomyopathy where the ventricle becomes highly dilated without appreciable thickening of the wall), what happens to EDV and EDP?

Answer 15

the EDV may be very high but the EDP may not be greatly elevated……
increased compliance = less stffness so can accommodate a large volume without generating much stretch/tension/pressure.

Question 16

Increased ventricular compliance (inc stiffness)shifts the EDPVR slope up or down?

Answer 16

flattens it, shift down and to the right

Question 17

Frank–Starling curves can be used as an indicator of?

Answer 17

muscle contractility (inotropy). 
.....(graphs the SV / LVEDP)

Question 18

On the Starling curve: Increased afterload shifts the curve (up/down and right/left)?

Answer 18

down (less SV) and to the right (increased LVEDP)

Question 19

On the Starling curve: decreased inotropy shifts the curve (up/down and right/left)?

Answer 19

down and to the right

Question 20

On the Starling curve: Decreased afterload shifts the curve (up/down and right/left)?

Answer 20

up (higher SV) and to the left (lower LVEDP)

Question 21

On the Starling curve: increased inotropy shifts the curve (up/down and right/left)?

Answer 21

up and to the left

Question 22

In dilated cardiomyopathy, the ventricle becomes dilated without compensatory?

Answer 22

thickening of the wall.

The LV is unable to pump enough blood to meet the metabolic demands of the organism.

Question 23

ALL of the following slides relate to LVP vs LVV (Pressure Volume loop)

In dilated cardiomyopathy ESPVR and EDPVR curves are shifted right or left?

Answer 23

RIGHT

Question 24

Left ventricular hypertrophy (LVH) is an increase in the thickness and mass of the myocardium usually a response to chronically increased volume load (preload) or increased pressure load (afterload). This will (increase or decrease)
EDV?
SV?
ESV?

Answer 24

Dec EDV and SV
Increase ESV

The thickening of the ventricular muscle results in decreased chamber compliance. As a result, LV pressures are elevated, the ESV is increased and the EDV is decreased, causing an overall reduction in cardiac output.

Question 25

LVH causes ESPVR and EDPVR to shift right or left?

Answer 25

ESPVR left and up

EDPVR left

Question 26

Aortic stenosis shifts LVP vs LVV loop (ESPVR and EDPVR) left/right and up/down?

Answer 26

ESPVR= up up and right
EDPVR= right

Severe aortic stenosis results in

1. reduced ventricular stroke volume due to increased afterload (which decreases ejection velocity)
2. increased end-systolic volume
3. compensatory increase in end-diastolic volume and pressure

Question 27

In mitral stenosis: because end-diastolic volume decreases more than end-systolic volume decreases, the stroke volume (inc or dec)

Answer 27

decreases

Mitral stenosis impairs LV filling so that there is a decrease in end-diastolic volume (preload). This leads to a decrease in stroke volume by the Frank–Starling mechanism and a fall in cardiac output and aortic pressure. This reduction in afterload (particularly aortic diastolic pressure) enables the end-systolic volume to decrease slightly, but not enough to overcome the decline in end-diastolic volume.

Question 28

In mitral stenosis: LVP vs LVV loop shifts (left or right)

Answer 28

left with dec SV

Question 29

In Aortic Regurg/insuff:
The constant backflow of blood through the leaky aortic valve implies that which 2 phases of the P/V loop are blunted?

what does this do to the loop appearance?

Answer 29

No true isovolumic relaxation.
The LV volume is greatly increased due to the enhanced ventricular filling.

No true isovolumetric contraction
When the LV begins to contract and develop pressure, blood is still entering the LV from the aorta (since aortic pressure is higher than LV pressure). Once the LV pressure exceeds the aortic diastolic pressure, the LV begins to eject blood into the aorta.

Question 30

In Aortic Regurg/insuff:

The increased end-diastolic volume EDV (increased preload) activates the Frank–Starling mechanism to do what?

Answer 30

increase the force of contraction, LV systolic pressure, and stroke volume.

Question 31

In AR/AI: what does the LVP/LVV loop look like compared to control loop?

Answer 31

Loop looks like a wide oval (no true isovolumetric contraction or relaxation) and encompassing all of the normal loop as well as extending to the left of normal ( increased preload and SV)