CVS: Preload and Afterload Flashcards

1
Q

Define cardiac output

A

Vol blood ejected per min

Proportional to HR + SV ∴ CO = HR + SV

CO from right side (via pulmonary artery) and left side (via aorta) are same

CO determine blood pressure + blood flow

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2
Q

What is preload?

A

Stretching of heart during diastole, increases SV → Regulated by Starling’s law

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3
Q

What is contractility?

A

Strength of contraction at given diastolic loading, due to sympathetic nerves + circulating adrenaline increasing Ca2_

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4
Q

What is energy of contraction?

A

Work required to generate stroke volume, depends on Starling’s law + contractility

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5
Q

What are the 2 functions of stroke work?

A
  • Increases chamber pressure> aortic pressure (isovolumetric contraction
  • Ejection
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6
Q

Define Starling’s law

A

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

This means:

  • 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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7
Q

Describe preload in terms of the molecular basis of Starling’s law

A

Un-stretched fibre:

  • Overlapping actin/myosin - Less mechanical interference, less cross-bridge formation available for contraction

Stretched fibre:

  • Less overlapping actin/myosin - Less mechanical interference, potential for more cross-bridge formation, increased sensitivity to Ca2+ ions
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8
Q

What are the roles of Starling’s Law?

A
  • Balances outputs of RV and LV → Prevents fluid congestion in heart
  • Responsible for fall in CO following drop in blood volume (haemorrhage, sepsis), orthostasis (standing) leading to postural hypotension (dizziness, fainting)
  • Contributes to increased CO during exercise
  • Restores SV and CO in response to intravenous fluid transfusions

Breakdown of Starling’s law contributes to development of heart failure

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9
Q

What is afterload?

A

Force that opposes ejection, reduces SV → Regulated by Laplace’s law

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10
Q

Define Laplace’s law

A

Afterload opposes ejection of blood from the heart

Afterload is determined by Wall Stress → force through heart wall

More energy of contraction needed to overcome Wall Stress to produce ejection → Heart doesn’t function as efficiently with Wall Stress

Laplace’s law describes parameters that determine Afterload/Wall Stress (S):

  • Pressure (P)
  • Radius (r)
  • Wall thickness (W)

Afterload (S) = P x r/2W

Afterload (S):

  • Increased S- Produced by increasing Pressure and Radius
  • Reduced S - Produced by increasing Wall Thickness

Therefore Laplace’s law states increased arterial blood pressure = Increased Afterload/Wall stress resulting in reduced ejection

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11
Q

How does afterload change when there’s smaller ventricular radius?

A
  • Greater wall curvature
    • More Wall Stress directed towards centre of chamber
    • Less Wall stress directed through heart wall
    • Better ejection - therefore less opposing force so decreased afterload
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12
Q

How does afterload change when there’s larger ventricular radius?

A
  • Less wall curvature
  • More wall stress directed through heart wall
  • Greater afterload
  • Less ejection
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13
Q

How does chronic high arterial blood pressure affect afterload?

A
  • ⬆️Afterload/Wall Stress
    • Increased energy expenditure
    • Ultimately decreased SV/CO = Poor blood flow to end organs, poor perfusion of organs
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14
Q

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

A
  • ⬆️r: Volume-overload heart failure
    • E.g. MI causes poor stroke volume/ejection fraction
    • Blood volume remains in heart
  • ⬆️P: Pressure-overload heart failure
    • E.g. Hypertension causes afterload which heart must work against
    • S = P x r/ 2W therefore, increased r or P will increase afterload meaning less ejection
  • To counteract this, the heart must compensate and it does this by:
    • Increased Wall thickness (W) = hypertrophy (greater myocyte size)
    • Same Wall stress but now over greater area (more sarcomeres)
      • Less wall stress per sarcomere and less opposition to contraction of sarcomeres, greater SV/CO
    • But requires more energy (as more sarcomeres used)
      • This means greater O2 is needed, so ultimately contractility decreases, resulting in a circle of heart failure
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15
Q

What is the importance of Laplace’s law?

A
  • Opposes Starling’s law at rest
    • ⬆️Pre-load = ⬆️chamber radius
    • Laplace’s law states that this will increase afterload, which will oppose ejection of blood from a ‘full’ chamber
    • In a healthy heart, Starling’s law overcomes Laplace’s law to maintain good ejection
  • Facilitates ejection during contraction
    • Ventricular contraction = ⬇️chamber radius
    • Laplace’s law states this will reduce afterload in ‘emptying’ chamber
    • Aids ejection during reduced ventricular ejection phase of cardiac cycle
  • Contributes to failing heart
    • In failing heart, chamber often dilated, increasing chamber radius
    • Reduction in ejection as Laplace’s law dictates that there is increased afterload opposing ejection
  • Therefore, laplace’s law is good with small radii, but bad with large radii
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16
Q

How do changes in preload affect LV P-V loops?

A

Increased preload:

  • Events that increase venous return such as venoconstriction during exercise or administration of intravenous fluids
  • Increased end-diastolic volume = Increased Starling’s law = Increased SV

Decreased preload:

  • Events causing loss of blood volume, e.g., haemorrhage, dehydration
  • Decrease in EDV = decrease in Starling’s law = decreased SV
17
Q

How do changes in afterload affect LV P-V loops?

A

Increased afterload:

  • E.g. chronic hypertension
  • Increased isovolumetric contraction to overcome greater aortic pressure and open aortic valves for ejection = Less energy left for ejection = reduced SV

Decreased afterload:

  • E.g. Reduce blood pressure during dynamic exercise (running)
  • Reduce isovolumetric contraction = easier to open aortic valve = more energy for ejection = increased SV