Cardiac Physiology Flashcards

1
Q

How do sympathetic innervation influence end diastolic volume (the volume of blood before ventricular ejection)?

A

1) Sympathetic innervation increases cardiac contractility by increasing Ca2+ in the cytoplasm (SNS post ganglionic adrenergic fibers releases ACh into the neuroeffector (heart cell) junction and causing ca2+ channels on the plasma membrane to open, ca2+ induced ca2+ channels in endoplasmic reticulum to release ca2+)
2) Sympathetic innervation causes venoconstriction (increases pressure in the vein returning blood to the heart), thus, promoting venous return.

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2
Q

How do sympathetic innervation increase stroke volume?
What is stroke volume?
how do you calculate stroke volume?

A

Sympathetic stimulation of the SA node can speed up heart rate. SNS releases norepinephrine into the neuroeffector junction increasing cyotsolic ca2+

Sympathetic stimulates the endocrine cells of the adrenal medulla causing epinephrine release into the blood, reinforcing heart rate.

In addition, SNS promote EDV, by stimulating venoconstriction which causes cardiac muscle cells to stretch and leading to more forceful contraction of the ventricle - this result in increase stroke volume.

Stroke volume = EDV - ESV (135-35 = 100 mL)
the amount of blood the ejected by the ventricle into the body in one contraction

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3
Q

What is end diastolic volume?

End systole volume?

A

The volume of blood filling the left ventricle during diastole. Not all blood is ejected.
End systole volume is the amount of blood that is left in the ventricle after the ventricle has contracted.

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4
Q

What is the Frank Starling Mechanism?

A

it describes the end diastolic pressure volume relationship. As the volume of blood in the ventricle increases at end diastole, the end diastolic pressure also increases (aka preload), the heart will automatically adjusts the strength of contraction, thus increasing stroke volume, such that end diastolic volume and stroke volume.
The mechanism of this is explained in the length tension relationship curve for cardiac muscles

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5
Q

What factor causes contractile myocyte to stretch? What theory describes this intrinsic mechanism of the heart

A

the degree of diastolic filling. Greater volume of blood returning to the heart, the larger EDV will be and more stretch that would cause.

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6
Q

What is afterload? How does afterload affect stroke volume? and why is it not good.

A

is the pressure in the aorta that the ventricle muscle overcome to pump blood to the body.

An increase in afterload will decrease stroke volume, as a result, the ventricle will need to work extra hard to overcome this pressure. The heart may compensate this via hypertrophy. The enlargement of the cardiac muscle fibers will allow the left ventricle to generate more pressure in order to eject the same stroke volume…. BUT, this extra workload that this put on the heart, will eventually lead to HEART FAILURE.

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7
Q

What is preload?

A

Is used to describe the pressure in the left ventricle at the end of diastole

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8
Q

What is the length tension curve for cardiac muscles?

A

Is also known as the Frank-Starling curve. This curve shows how stroke volume changes in response to changes in end-diastolic volume.

An increase in the EDV (causes cell to stretch to its ideal length) and as a result, causes stroke volume to increase (muscle cells can generate greater force)

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9
Q

What type of effects do the sympathetic nerve system have on the Frank-Starling curve?

A

Increased in SNS activity to the heart shifts the FrankSTarling curve up a notch. Whereas a decreased in SNS activity shift the curve down a notch.

Y axis = stroke voume
X axis = EDV (mL)

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