Heart As A Pump 2

Question 1

What work is done by the heart?

Answer 1

1. Stroke work: contracting and pumping blood into aorta (and pulmonary artery)
2. Kinetic work: Accelerating the blood through the valves into aorta (and pulmonary arteries)

Kinetic work is about 1% of total work done (usually ignored)

Work done by the heart= work done in ejecting a volume of blood (SV) into aorta

Question 2

Define work

Answer 2

Force applied to an object times the distance the object moves

Work done= force x distance (force= pressure x area)

Therefore, stroke work= pressure x area x distance
(Area x distance)= volume

Stroke work= volume x pressure

Question 3

Summarize work in the heart

Answer 3

Work done is the force (ventricular pressure) applied to a volume of blood (stroke volume) to eject it into the aorta

(Cannot measure ventricular pressure easily but since it is the same as aortic pressure)

Stroke work= stroke volume x mean arterial pressure

Stroke work= area of represented by the pressure- volume loop

Question 4

Contrast the work done on both sides of the heart

Answer 4

• LV works 6x harder than RV
• (RV doesn’t need to generate so much pressure to expel blood because pulmonary circulation is a low resistance circulation
• Kinetic energy because significant when valves are stenosis
• (Heart needs to work harder to push blood through narrowed valves)
• Large amount of work is converted to heat (“tension heart”)
• Heart consuming energy during Isovolumetric contractions but no external work is being done. Energy expended ends up as heat.

Question 5

Describe the fitting in the pressure volume loop on the ventricular function curve

Answer 5

Peak isometric curve /ESPVR- this line/curve is analogous to the peak isometric tension curve for isolated muscle.

• it limits how far shortening can occur.
• In the whole heart it sets the limit to how much blood can be ejected by a single contraction

Resting tension = myocardial muscle fiber length/ end diastolic volume

Question 6

What is the significance of ESPVR/ Peak isometric curve?

Answer 6

-In the whole heart, the peak isometric tension curve is equivalent to the ventricular pressure developed in the ventricles and is called the End-Systolic Pressure Volume Relationship(ESPVR)

The ESPVR defines the maximal pressure that can be generated at any given volume under a given inotropic state-equivalent to the peak isometric tension curve

The resting tension is related to myocardial muscle fiber length which is related to the EDV

Question 7

How is preload changed?

Answer 7

Changed by altering EDV

• EDV is altered by changing VR to the heart
• VR is altered by altering blood volume or by venoconstriction/venodilation or by slowing heart rate

Question 8

How is afterload changed in the body?

Answer 8

Changed by altering aortic pressure or changing total peripheral resistance

Question 9

How is contractility changed in the body?

Answer 9

CGH anger by altering sympathetic activity, or by giving drugs which alter inotropic state

Question 10

What are the effects of increasing preload?

Answer 10

E.g. an acute response to an increase in VR
IMMEDIATE effects due to Starlings mechanism

Increased VR = increased EDV ( = increased preload)
Increased preload = increased stroke volume

Effect of changes in LVEDV on stroke volume at constant arterial pressure (afterload) and inotropic state. Frank-Starling relationship

The greater the LVEDV the greater the SV

Question 11

What is the effect of increasing contractility ?

Answer 11

Changes in contractility change the slope of the ESPVR

ESPVR becomes steeper

SV is increased because muscle can shorten more. End systolic volume is reduced

Increased contractility—> increased stroke volume (stroke work) and ejection fraction

Effect of inotropic state on stroke volume at a given LVEDV & arterial pressure (afterload). Increasing the inotropic state (contractility) of the heart increases SV from a given LVEDV

Question 12

What are the effects of increasing afterload?

Answer 12

E.g. increased aortic pressure
SV is reduced. Therefore ejection fraction is reduced.
Increased afterload = decreased stroke volume and decreased ejection fraction

Afterload has a negative impact on SV. All cardiac cycles here are starting from same LVEDV and inotropic state but proceed against 3 different afterloads.

Ventricle cannot open the aortic valve until the LV pressure reaches the higher aortic pressure. Because ventricle has had to develop more isometric tension, it’s capacity to shorten is reduced and the ventricles eject less blood

Question 13

What are the graphical changes in increasing preload in pressure loop?

Answer 13

D and C pushed outward—> increased stroke volume

Point E is a little higher

Question 14

What are the graphical changes to pressure-loop in increasing contractility?

Answer 14

Points A, F & E are pushed back—> larger stroke volume

Question 15

What are the graphical changes in increasing afterload in the pressure-volume loop?

Answer 15

Points E and F pushed upwards

F and A pushed inward

Afterload increases as stroke volume is reduced

Question 16

How can Starling’s law compensate for fall in SV ?

Answer 16

By increasing SV on the next cycle

Question 17

What are the effects of exercise on the pressure-volume loop?

Answer 17

Exercise has two methods of effect:
1. Increasing sympathetic activity—> increased contractility—> increased stroke volume

2. Increasing sympathetic activity—> increased venomotor tone—> increased venous return —> increased EDV —> increased Preload—> increased stroke volume

Combined, both of these lead to a very large increase in SV