Preload and afterload Flashcards by Jash S

What is cardiac Output?

definition?
what is it proportional to?
equation?

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

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CO of RHS and LHS

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

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CO and BP
relation?
equation?

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

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can cardiac output change? why?

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

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what controls Stroke Volume? (4) and how?

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)

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what is energy of contraction?

what does it depend on?

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

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Function of Stroke Work (2)

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

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preload + afterload relation to energy of work

Preload
‘Increases’ energy of contraction therfore Enhances SV

Afterload
‘Requires’ greater energy of contraction so Opposes SV

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Starling’s Law of the heart

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

‘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)

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Why does stretching a muscle mean greater energy of contraction?

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

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effect of a large intravenous infusion

effect on SV and BP

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

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summary of increase blood volume + starlings law

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

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

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

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

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

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

clinical importance?

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)

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Fluid challenges with starling law and curve

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

dehydration and starling curve

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

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

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?

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

Preload - Roles of Starling’s Law (5)

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

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

Starling Law role - balance output of RV and LV

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

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

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

why? effect of this?

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)

Starling Law role - fall in CO when standing

why and effect of this?

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

Starling Law role - increased CO during exercise

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

What is afterload?

what is it determined by? significance of this?

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

Laplaces Law equation and what does it determine?

Laplaces law describes parameters that determine Afterload/Wall Stress (S): Pressure (P), Radius (r), wall thickness S = P x r / 2w

Laplaces Law and after load what increases after load? decreases it?

Afterload (S): Increased S – produced by increasing Pressure and Radius Reduced S – produced by increasing Wall Thickness

Afterload – Radius and Wall Stress small ventricle radius effect? ejection? larger ventricle radius effect? ejection?

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 ```

Afterload – Pressure and Wall Stress effect on ejection and SV?

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

why does increased arterial pressure lead to reduced ejection? what happens during isovolumetric contraction? effect of this?

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

Consequences of chronic high arterial blood pressure – High Afterload/Wall Stress how does it affect organs? why?

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

Example of increased radius for afterload what is it called? example? what causes increase in radius? why?

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

Example of increase pressure for afterload | effect on heart?

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

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?

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

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

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

Laplaces law opposes starling's law at rest how does it oppose it? what happens in healthy heart? when do you have an issue?

↑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

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?

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

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

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

Effect of preload on left ventricular pressure-volume loop effetc on isovolumetric contraction? why? effect on area? why?

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

Effect of afterload on left ventricular pressure-volume loop effect on isovolumetric contraction? sv? ejection fraction? effect of decreased blood pressure?

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