Intrinsic regulation of the heart: preload and afterload Flashcards

1
Q

what is preload?

A

defined as the initial stretching of the ventricular cardiac myocytes prior to contraction
* related to muscle sarcomere length

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2
Q

Why is end-diastolic volume an index of preload?

A
  • as increased stretch increases contractile force, so stroke volume increases with EDV
  • ie the greater the stretch (preload), the greater the contractile force and therefore the greater the stroke volume
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3
Q

What is the end diastolic volume?

A
  • It is the volume of blood in the left or right ventricle at the end of filling in diastole (ie the amount of blood in the ventricles before systole(contraction)
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4
Q

what is Starling’s law/frank starling mechanism of the heart?

A
  • This law represents the relationship between** stroke volume and end-dystolic volume **
  • the law states that the stroke volume of the heart** increases** in response to an increase in the volume of blood in the ventricles before contraction (ie EDV)
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5
Q

Describe the mechanism of the active tension - length relation in cardiac muscle

A
  • sarcomeres within the cardiac myocytes stretch when cardiac muscle is stretched, the maximal force for a sarcomere is 2.2-2.3um and further stretching beyond this point reduces contractile force
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6
Q

what essential function does the starling mechanism have on the right and left ventricular output?

give example

A
  • the frank starling mechanism prevents the left and right ventricular outputs from being greater than eachother
  • it** equalises the outputs **
  • if for eg, the right ventricular output was increased, this would increase the pulmonary volume and therefore increase the pressure in the pulmonary veins which will increase the filling of the left ventricle - therefore the LVO will increase until balance is restored
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7
Q

what is the sarcomere length at normal end diastolic volume?

A
  • 1.8-2.0um
  • cardiac muscle operates on the ascending phase of the length tension curve
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8
Q

Explain the degree of stretch of the sarcomeres and its** relation to contractile force** along the active tension-length curve

A
  • at the** ascending phase **of the active tension - length curve, the length of the sarcomeres is normal
  • after the ascending phase, the length of the sarcomeres is too long and the contractile force starts to decrease
  • ie the more you stretch the sarcomeres, the less actin and myosin overlap and therefore a cross bridge cannot be generated & contractile force decreases
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9
Q

what is an increased stretch of the sarcomere associated with?

A
  • increased stretch is associated with increased Ca2+ sensitivity of the contractile apparatus (ie troponin)
  • if there is higher Ca2+ sensitivity & stretch, then there is more space for actin and myosin to bind and form cross bridges
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10
Q

what is a determinant of preload?

A

CVP - central venous pressure, not venous return as that is a flow rate and is dependent on the cardiac output

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11
Q

how dos CVP affect preload?

A
  • changes in CVP affect the right ventricular muscle preload (stretching before contraction)
  • if CVP is raised, the EDV and volume increase and this increases the stretching of the ventriculsr myocytes (ie preload)
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12
Q

What factors affect CVP (recap)?

A
  • gravity (ie if sitting upright from a supine position )
  • blood volume (decrease in blood volume = decrease in CVP)
  • skeletal muscle pump
  • sympathetic nerves
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13
Q

Explain how the CVP influences the right and left ventricular EDV

A
  • the CVP determines the right ventricular EDV
  • the** right ventricular output depends on the right EDV**
  • the right ventricular output determines the pulmonary blood flow which in turn influences left atrial pressure (as pulmonary blood flow enters here)
  • the left atrial pressure determines the left ventricular EDV and therefore the** left ventricular output ** (SV)
  • therefore CVP determines the SV of the left ventricle
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14
Q

what effect does a raised extracardial pressure (intrathoracic pressure) have on the heart?

eg coughing

A

this will decrease ventricular filling, SV and CO as it will make the heart stiffer

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15
Q

what is afterload?

A
  • the ‘load’ that the heart must eject blood against
  • the arterial pressure that the ventricles of the heart pump against
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16
Q

what is a major determinant of afterload?

A

arterial pressures

17
Q

what are examples of clinical conditions associated with increased afterload?

A
  • arterial hypertension
  • aortic stenosis ( narrowing of the aortic valve - ie the exit from the left ventricles)
18
Q

what is laplaces law?

A
  • internal (intraventricular pressure in this case) is proportional to the wall tension T and inversely proportional to the internal radius
  • P=2T/r
  • acts in opposition of the starling forces
19
Q

what is ventricular wall tension?

A
  • tension generated by myocytes that results in a given intraventricular pressure at a particular ventricular radius
  • ventricular contraction raises wall tension
20
Q

What are the 3 determinants of afterload?

A
  • arterial pressure
  • ventricular radius
  • ventricular wall thickness