Lecture 9 Flashcards

1
Q

factors that affect stroke volume and the force of ventricular contraction

A
1- Preload
2-inotropism
3- Autonomic NS
4- Intracellular calcium levels
5- Afterload
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2
Q

Preload

A

o Preload is the “load” or “stretch” on the ventricular cardiac muscle before it contracts
o Preload is directly influenced by EDV
o The effects of preload are confirmed by the Frank-Starling Law of the Heart –within physiological limits, the more the ventricles are filled during diastole, the more blood they will eject during systole (i.e. – the greater the preload, the greater the force of contraction)
o This type of control of SV is referred to as heterometric regulation

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3
Q

Cardiac Contractility (Inotropism)

A

o An increase in cardiac contractility is an increase in contractile strength that is independent of Starling’s Law
o The SNS has a positive inotropic effect on the heart, meaning it causes an increase in SV at a constant preload
o Enhanced contractility results in more complete ejection of blood from the heart, hence a lower ESV & greater SV
o This type of regulation is referred to as homometric regulation
o Sympathetic stimulation via b1 receptors [POSITIVE INOTROPIC EFFECT]
o This increases the force of contraction by 2 mechanisms (short version):
• NEP increases the inward Ca+2 current during the plateau of each cardiac action potential
• NEP increases the activity of the SERCA pumps; as a result, more Ca+2 is accumulated by the SR and thus more Ca+2 is available for release in subsequent beats

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4
Q

After load

A

o The “load” the heart must overcome after (and while) it contracts
o Afterload is essentially the back pressure exerted on the aortic & pulmonary semilunar valves by arterial blood in the aorta and pulmonary trunk respectively
o ↑ afterload:
• The ventricle must pump blood against a higher pressure, resulting in a ↓ in stroke volume
o ↓ afterload:
• The ventricle pumps blood against a lower pressure, resulting in an ↑ in stroke volume
o Examples of increased afterload:
• Vasoconstriction (increased systemic vascular resistance)
• Increased blood volume or viscosity
o Vasodilators are often used to decrease afterload
• decreases myocardial oxygen demand

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5
Q

cardiac output or performance is enhanced by

A

o ↑ Preload
o ↑ Inotropy (SNS)
o ↑ Heart rate
o ↓ Afterload

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6
Q

cardiac output or performance is depressed by

A

o ↓ Preload
o ↓ Inotropy (SNS)
o ↓ Heart rate
o ↑ Afterload

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7
Q

Heterometric regulation of stroke volume

A

different volumes (EDV)
o stretching out the ventricles with different volumes of EDV causes a response to different forces of contraction.
• The more the ventricles are filled during diastole, the more blood they will eject during systole. (CO increases)

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8
Q

Homometric regulation of stroke volume

A
same volume (EDV)
o	The SNS can increase the force of contractility independent of EDV. (CO increases)
•	CO can decrease if HR increases too much and ventricles do not have time to fill.
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9
Q

Frank-Starling law of the heart

A
  • Based on the length-tension relationship in the ventricle; increases in EDV cause an increase in ventricular fiber length, which produces an increase in developed tension
  • Additionally, stretch of the myocardium by greater ventricular filling may enhance the affinity of troponin C for Ca+2 and also may increase Ca+2 uptake and release from the SR; hence, these two effects increase developed force and thereby contribute to the increase in force when the cardiac muscle fiber length increases
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10
Q

effects of nitrates on afterload

A
  • Vasodilators are often used to decrease afterload

* decreases myocardial oxygen demand

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11
Q

entricular pressure-volume loops and the effects that preload, inotropism and afterload on these loops

A

• 4 → 1 is left ventricular filling
• 1 → 2 is isovolumetric ventricular contraction
o @ 2, we start to eject blood into the aorta.
• @ 3, the aortic SL valve closes
• 3 → 4 is isovolumetric ventricular relaxation
o @4 the mitral valve opens

  • A = Increase in preload, you see an increase in volume and an increase in ejected blood.
  • B = Increased afterload, you see an increase in required ventricular pressure during contraction and a decrease in ejected blood.
  • C = Decreased afterload, you see an increase in contractility and more blood is ejected
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