Lecture 15: Regulation of Cardiac Output (Hayward) Flashcards

1
Q

cardiac output =

A

flow. L/min CO = SV * HR **MEMORIZE

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2
Q

parasympathetic or sympathetic input to heart is more quickly reversed?

A

parasym.

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3
Q

Increases in HR are coupled with changes in :

A

ventricular function

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4
Q

Positive lusitropic effects –> HR and rate of relaxation

A

increases both

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5
Q

chronotropic effect

A

changes HR. Positive chronotropic effect = increased HR

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6
Q

lusotropic effect relates to

A

contractility

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7
Q

inotropic effect

A

regulates myocardial performance.

Intrinsic regulation via cardiac muscle
Extrinsic regulation via external force (hormones, sympathetic innervation, pH, etc.)

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8
Q

Actin and myosin interact during

A

muscle contraction

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9
Q

functional unit of a muscle

A

sarcomere

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10
Q

How does stretch in cardiac tissue prior to systole impact contractility?

A

SOME stretch increases capacity to generate force, but too much stretch generates less force

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11
Q

Active tension in cardiac muscle is dependent on:

A

starting length of the sarcomeres at the time of activation

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12
Q

Total tension +

A

passive + active tension

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13
Q

preload

A

the stretch on the cardiac muscle that occurs during the relaxed state. Determines the force generated by the cardiac muscle for the subsequent contraction (length-tension relationship)

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14
Q

afterload

A

P in the outside of the system that heart must work against (i.e. aortic pressure)

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15
Q

end-diastolic volume

A

volume load during diastole

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16
Q

Frank-Starling effect

A

relationship between muscle length and force generated. Uses the intrinsic properties of the muscle w/o any outside influence. Important mech. for equalizing outputs between R and L ventricles

17
Q

main force ventricles have to overcome during volume ejection (isotonic contraction phase)

A

aortic pressure

18
Q

isotonic contraction

A

muscle shortens when total muscle force exceeds external load

19
Q

increased aortic pressure –> stroke volume ?

A

decreases

20
Q

end-systolic length of muscle after contraction is directly related to –>

A

AFTERLOAD and contractility (not preload!)

21
Q

decreased aortic pressure –> stroke volume?

A

increases

22
Q

contractility

A

performance of the heart at a given preload and afterload. Determined by changes in intracellular Ca and rate of contractile protein interaction

23
Q

inotropic changes ***

A

changes in contractility **

24
Q

Increased NE –> contractility

A

increases (because more Ca is released) INOTROPIC EFFECT

25
Q

ischemia

A

lack of perfusion

26
Q

Thyroid hormone —> Ca reuptake and hypertrophy

A

Enhances both

27
Q

Increased CO2 –:> myocardial performance

A

declines (due to lower pH)