Preload + afterload Flashcards

1
Q

Define CO

A

v of blood ejected from heart per minute

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2
Q

Equations w CO?

A
CO = HR x SV
BP = CO x TPR
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3
Q

What’s resting CO?

A

70 bpm x 70 ml = 5 L/min

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4
Q

What’s exercising CO?

A

180 bpm x 120 ml = 22 L/min

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5
Q

What does CO determine?

A

BP + blood flow

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6
Q

What controls SV?

A

preload, HR, contractility, afterload

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7
Q

How does preload control SV?

A

Stretching of heart at rest, increases SV due to Starling’s law

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8
Q

How does HR control SV?

A

Sympathetic + parasympathetic nerves

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9
Q

How does contractility control SV?

A

Strength of contraction at given resting load, due to sympathetic nerves + A increasing [Ca2+ ]

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10
Q

How does afterload control SV?

A

Opposes ejection, reduces SV due to Laplaces law

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11
Q

Define energy of contraction

A

amount of work required to generate SV

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12
Q

What does energy of contraction depend on?

A

Starling’s Law + Contractility

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13
Q

Role of stroke work?

A

Increases chamber p > aorta (isovolumetric contraction)

Ejection

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14
Q

What’s Starling’s law?

A

‘Energy of contraction of cardiac muscle proportional to muscle fibre length at rest’
ie more stretch at rest –> greater contraction

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15
Q

What’s the intrinsic property of heart?

A

can increase strength of cardiac contraction

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16
Q

What happens if ↑CVP?

A

↑venous return to heart
↑EDV (end diastolic v)
↑preload
↑ejection

17
Q

Features of Starling’s curve?

A

filling p mmHg (CVP or end distole p) vs SV (ml)
ascending limb - ↑filling p –> ↑SV
plateau - ↑filling p but no more work

18
Q

Why do a fluid challenge?

A

give fluid, see if makes diff to CO + BP, see if they’re on ascending limb

19
Q

Why does stretching increase energy of contraction?

A

stretched fibre has less overlapping actin/myosi
less mechanical inference
potential for more cross-bridge formation
↑ sensitivity to Ca2+

20
Q

Roles of Starling’s law?

A
  • Balances outputs of RV + LV
  • ↓CO after drop in blood v (eg haemorrhage, sepsis)
  • ↓CO during orthostasis (standing)–>postural hypotension 😵
  • Restores CO in response to intravenous fluid transfusions
  • ↑ CO during exercise
21
Q

What’s afterload determined by?

A

Wall Stress directed via heart wall

22
Q

What does wall stress do?

A

prevent actin-myosin

23
Q

What does Laplaces law describe?

A
Wall Tension (T),  Pressure (P), Radius (r) in ventricle
P = 2T / r 
Tension (T) = Wall Stress (S) and Wall Thickness (w) so:
P = 2Sw / r     or      S = P x r / 2w
24
Q

Why value of 2?

A

chamber has 2 directions of curvature

25
Q

Why does a smaller ventricle radius give better ejection?

A

greater wall curvature
Wall Stress towards centre of chamber not heart wall
less afterload

26
Q

Why does a larger ventricle radius give better ejection?

A

less wall curvature
more Wall Stress directed via heart wall
more Afterload

27
Q

Roles of Laplace’s law?

A

Opposes Starling’s law at rest
Facilitates ejection during contraction
Contributes to failing heart at rest + during contraction

28
Q

How does Laplace’s oppose Starling’s law at rest?

A

↑ Pre-load –> ↑ chamber radius
Laplace’s says it will increase afterload +opposes ejection from full chamber
BUT Starling’s > Laplace’s

29
Q

How does Laplace’s law facilitate ejection during contraction?

A

Ventricular contraction ↓chamber radius
Laplace’s says it will reduce afterload in emptying chamber so helps ejection during reduced ventricular ejection phase 4 of cardiac cycle :)

30
Q

How does Laplace’s law contributes to failing heart at rest + during contraction?

A

failing heart has dilated chambers so ↑ radius

Laplace’s law says increase afterload opposing ejection

31
Q

What does Laplace’s law say if there’s increased arterial BP?

A

↑ Wall Stress –> ↑ Afterload –> ↓ ejection

32
Q

What happens if there’s an acute rise in arterial BP?

A

Starling’s law - ↑ stretch, ↑ contraction, ↑ SV
Intrinsic increase in contractility - Anrep response, local +ve inotropes
Baroreflex -↓ Sym NS, ↓ TPR, ↓ BP

33
Q

How does Laplace’s law explain hypertrophy in heart failure?

A

S = P x r / 2w
↑r - Volume-overload (MI, cardiomyopathies, mitral valve re-gurgitation)
↑P - Pressure-overload (hypertension, aortic stenosis)

↑ afterload –> ↓ejection so heart compensates by increasing Wall Thickness (w) so:
↓ afterload –> ↑ SV/CO
same wall stress over greater area, less wall stress per sarcomere, less opposition to contraction of sarcomeres, greater O2 use, less contractility…

34
Q

What’s the effect of increased afterload on ventricular p-v loop?

A

-↑ BP (Afterload)
-↑ isovolumetric contraction using more energy
-less energy for ejection so↓ SV
More energy used to eject less blood

35
Q

What’s the effect of increased preload on ventricular p-v loop?

A
  • ↑ venous return (exercise,intravenous fluids)
  • ↑ end-diastolic v
  • ↑ Starling’s law
  • ↑ SV for little increase in energy used