Preload and afterload

Question 1

What is cardiac Output?

definition?
what is it proportional to?
equation?

Answer 1

Cardiac output (CO) – volume of blood ejected from the heart per minute

Proportional to how often the heart beats per minute (heart rate, HR) and how much blood is ejected per beat (Stroke volume, SV)

CO = HR x SV

Question 2

CO of RHS and LHS

Answer 2

Cardiac output from right side (via pulmonary artery) and left side (via aorta) are the same

Question 3

CO and BP
relation?
equation?

Answer 3

Cardiac output determines blood pressure and blood flow
BP = CO x TPR
Blood flow (CO) = BP / TPR

Question 4

can cardiac output change? why?

Answer 4

Cardiac output changes according to demand :
rest 70 bpm x 70 ml = 5 litres/min
Vigorous exercise 180 bpm x 120 ml = 22 litres/min

Question 5

what controls Stroke Volume? (4) and how?

Answer 5

Preload - Stretching of heart in diastole, increases SV - Starling’s law (relates to filling pressure)

Heart rate – Sympathetic and parasympathetic nerves
Contractility – Strength of contraction at a given diastolic loading, due to sympathetic nerves + circulating adrenaline increasing [Ca2+ ]i

Afterload – Opposes ejection, reduces SV - Laplaces law (increase in pressure means heart has to work harder to eject blood)

Question 6

what is energy of contraction?

what does it depend on?

Answer 6

Energy of contraction is the amount of work
required to generate stroke volume
Depends on Starling’s Law and Contractility

Question 7

Function of Stroke Work (2)

Answer 7

(1) Increases chamber pressure > aortic pressure (isovolumetric contraction) (to open valve for ejection)
(2) Ejection

Question 8

preload + afterload relation to energy of work

Answer 8

Preload
‘Increases’ energy of contraction therfore Enhances SV

Afterload
‘Requires’ greater energy of contraction so Opposes SV

Question 9

Starling’s Law of the heart

what is it in relation to?
what kind of property is it?

Answer 9

‘Energy of contraction of cardiac muscle is
proportional to the muscle fibre length at rest’

Greater stretch of ventricle in diastole (resting muscle), greater energy of contraction, greater SV achieved in systole (contracting muscle)

Intrinsic property of cardiac muscle (nerves, hormones etc. not involved)

Question 10

Why does stretching a muscle mean greater energy of contraction?

Answer 10

stretching a muscle fibre at rest will mean its longer therefore it can contract even more (become shorter) therefore there is a greater energy of contraction hence more SV

Question 11

effect of a large intravenous infusion

effect on SV and BP

Answer 11

CVP (central venous pressure will increase) hence increased venous/blood voume return to heart due to increase blood volume via intravenous perfusion
therefore an increased SV (also EDV and ESV increased) as increased ejection of blood
also increased aortic BP due to increased blood volume

Question 12

summary of increase blood volume + starlings law

Answer 12

increased venous pressure
therfore increased end-diastolic volume
therefore increased stretch of heart at rest
increased strength of cardiac contraction
increased stroke volume

Question 13

describe the initial stage of starling’c curve/ventricular function curve

Answer 13

at normal resting filling pressure, ↑↓ CVP has considerable change in SV

Question 14

describe the plateau stage of starling’c curve/ventricular function curve

Answer 14

as ↑CVP, ↑SV but eventually reach a plateau stage where you have stretched the heart to max and can’t produce any ↑ contraction therefore no ↑SV

Question 15

describe the descending part after the plateau stage of starling’c curve/ventricular function curve

clinical importance?

Answer 15

excess filling can lead to an overstretched heart muscle which leads to decrease in SV
HENCE is a consideration when giving fluids as you don’t want to overfill (this will be a fluid challenge)

Question 16

Fluid challenges with starling law and curve

Answer 16

must find out where patient is on the starling’s curve before giving fluid as you don’t want to give fluids at high CVP stage and lead to overstretching

Question 17

dehydration and starling curve

where on curve? effect on curve in relation to starlings law?

Answer 17

dehydration means decreased CVP therefore you can give fluid as it will be on the ascending limg of the curve therfore lead to increased SV due to increased blood volume and stretch of heart
This will lead to increased CO and better filling or organs and will make you feel better

Question 18

molecular level explanation for how does stretching increase energy of contraction?

what is the issue with un-stretched fibre and why weaker contraction?

whats different with stretched fibre? why stronger contraction? what other mechanism does stretched fibre have for stronger contraction?

Answer 18

Un-stretched fibre
Overlapping actin/myosin hence there is Mechanical inference therefore Less cross-bridge formation available for contraction

Stretched fibre
Less overlapping actin/myosin hence there is Less mechanical inference when actin + myosin come together which means MORE slide in filament hypothesis AND Potential for more cross-bridge formation AND more shortening hence MORE contraction

ALSO, stretched fibre has Increased sensitivity to Ca2+ ions therefore don’t need as much rise in Ca2+ for contraction

Both mechanisms lead to MORE contractions

Question 19

Preload - Roles of Starling’s Law (5)

how does it prevent fluid congestion in heart?
effect of haemorrhage?
importance of postural hypotension?
cvp?
exercise?

Answer 19

Balances outputs of the RV and LV – Very important!
Prevents fluid congestion in heart

Responsible for fall in cardiac output following
a drop in blood volume
(e.g. haemorrhage, sepsis)

Responsible for fall in cardiac output during orthostasis (standing)
leading to postural hypotension (dizziness, fainting)

Restores cardiac output in response
to intravenous fluid transfusions

Contributes to increased cardiac output during exercise

Hence breakdown of Starling’s law will contribute
to development of cause heart failure

Question 20

Starling Law role - balance output of RV and LV

what does this mean and if it doesnt happen, problem?

Answer 20

if more blood returns to the RHS, more leaves the RS, more returns to the LS, more ejected from the LS to the body hence input=output

If this isn’t done, it can lead to congestion and heart failure as blood volume centred in chambers where it shouldn’t be

Question 21

Starling Law role - fall in CO following fall in blood volume

why? effect of this?

Answer 21

due to less venous return therefore there is less stretch of heart muscle therefore there is less SV and less CO therefore less blood to end organs
(less blood go in therefore less blood goes out)

Question 22

Starling Law role - fall in CO when standing

why and effect of this?

Answer 22

due to less venous return to heart due to gravity when standing therefore there is less stretch of heart muscle therefore there is less SV and less CO therefore less blood to brain which makes you feel dizzy

Question 23

Starling Law role - increased CO during exercise

Answer 23

More blood venous return to the heart hence more stretch of muscle therefore more SV and more CO

Question 24

What is afterload?

what is it determined by? significance of this?

Answer 24

Afterload opposes ejection of blood from the heart

Afterload is determined by Wall Stress - force through the heart wall
More energy of contraction needed to overcome Wall Stress to produce ejection
Heart doesn’t function as efficiently with Wall Stress

Question 25

Laplaces Law

equation and what does it determine?

Answer 25

Laplaces law describes parameters that determine Afterload/Wall Stress (S):
Pressure (P), Radius (r), wall thickness

S = P x r / 2w

Question 26

Laplaces Law and after load

what increases after load? decreases it?

Answer 26

Afterload (S):

Increased S – produced by increasing Pressure and Radius

Reduced S – produced by increasing Wall Thickness

Question 27

Afterload – Radius and Wall Stress

small ventricle radius effect? ejection?

larger ventricle radius effect? ejection?

Answer 27

Small ventricle radius
Greater wall curvature
More Wall Stress directed towards centre of chamber therefore more pressure in the centre where blood is which will drive blood out
Less wall stress directed through heart wall
Better ejection

Larger ventricle radius
Less wall curvature
More Wall Stress directed through heart wall
Oppose the contraction of the heart
More Afterload
Less Ejection

Question 28

Afterload – Pressure and Wall Stress

effect on ejection and SV?

Answer 28

Laplaces law states that increased arterial blood pressure leads to Increased Afterload/Wall Stress – Reduced ejection

therefore the higher mean arterial pressure is, the lower SV will be

Question 29

why does increased arterial pressure lead to reduced ejection?

what happens during isovolumetric contraction? effect of this?

Answer 29

Increased pressure of aorta means increased pressure of aorta which means increased pressure on wall of heart therefore increased wall stress and more afterload to overcome

Expend more energy in isovolumetric contraction to overcome this hence less energy for ejection
therefore lower SV and lower CO
must lower BP to increase function of heart

Question 30

Consequences of chronic high arterial blood pressure – High Afterload/Wall Stress

how does it affect organs? why?

Answer 30

Increased energy expenditure to maintain SV
Ultimately decreased SV/CO - poor blood flow to end organs
High blood pressure is bad for the heart!

Question 31

Example of increased radius for afterload

what is it called?
example?
what causes increase in radius? why?

Answer 31

Increased radius -> volume-overload heart failure
Myocardial infarction leads to an area of the heart dying therfore leading to an increased radius as
heart doesn’t function as well as there is a decrease in SV and decrease in ejection fraction
therefore more blood remains in heart which dilates the heart causing the increase in radius

Question 32

Example of increase pressure for afterload

effect on heart?

Answer 32

Pressure-overload heart failure could be due to chronic hypotension therfore heart needs to work harder to overcome this

Question 33

How does heart compensate for increase of radius and pressure (therefore increased afterload)?

how does it try to decrease wall stress? what do we see in many failing hearts? net effect of this?

Answer 33

Increased Wall Thickness (w) to try and lower afterload which is why failing hearts have thicker walls
This leads to hypertrophy (greater myocyte size therefore more sarcomeres and more contractile elements)
BUT Same Wall Stress/afterload which is split now over greater area (more sarcomeres)
Less Wall stress (force) per sarcomere hence can spread out force over more area
Less opposition to contraction of sarcomeres
Greater SV/CO

Question 34

why does heart hypertrophy for increased afterload lead to heart failure?

Answer 34

This requires more energy (as more sarcomeres used)
Greater O2 use, ultimately decreases contractility - heart failure as heart can’t meet O2 demands

Vicious circle of heart failure

Question 35

Laplaces law opposes starling’s law at rest

how does it oppose it?
what happens in healthy heart?
when do you have an issue?

Answer 35

↑preload means ↑ EDV + ↑ESV therefore ↑chamber radius which will ↑WS (afterload)
This will opposes ejection of blood from a ‘full’ chamber
In healthy heart - Starling’s Law overcomes Laplaces law, which is why increase in preload leads to increased stretch of heart and increased contraction and increased SV - therfore maintains ejection

IF stretching doesnt lead to increased contraction, you have problems

Question 36

Laplaces law facilitates ejection during contraction

what happens during ventricular contraction? effect on wall stress and ejection?

what part of cardiac cycle does it help?

Answer 36

Ventricular contraction leads to lower chamber radius
Laplace’s law says this will reduce Afterload/Wall Stress in ‘emptying’ chamber
therfore can direct some of the wall stress into centre of the chamber therefore increased pressure to blood therfore increase pressure gradient to eject more blood
Aids ejection during reduced ventricular ejection phase of cardiac cycle

Question 37

Laplace law contributes to failing heart

what happens to a failing heart? why? what does this do to ejection and why?

Answer 37

In a failing heart - chambers often dilated due to volume overload - increased radius which leads to
Reduction in ejection as Laplace’s law dictates that there is increased Afterload/Wall Stress opposing ejection

Question 38

Effect of preload on left ventricular pressure-volume loop

effetc on isovolumetric contraction? why?

effect on area? why?

Answer 38

Increased venous return(e.g. during exercise,
intravenous fluids)
Increased end-diastolic volume which means greater stretch and more contraction due to Increased Starling’s law hence less energy needed for isovolumetric contraction and more energy can be used for ejection

Increased SV for little increase in energy used hence little change in area as the increase in SV is due to stretching leading to more contraction

Question 39

Effect of afterload on left ventricular pressure-volume loop

effect on isovolumetric contraction? sv? ejection fraction?

effect of decreased blood pressure?

Answer 39

Chronic high blood pressure (Afterload)

Increased isovolumetric contraction as Needed to increase pressure greater than aortic pressure to open valves
Less energy left for ejection therefore Decreased SV, more left in chamber and ESV is greater and ejection fraction is lower

Opposite for decreased blood pressure

Less isovolumetric contraction needed as less afterload
More energy for ejection
Greater SV