Lecture 15: Regulation of Cardiac Output (Hayward) Flashcards Preview

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Flashcards in Lecture 15: Regulation of Cardiac Output (Hayward) Deck (27):
1

cardiac output =

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

2

parasympathetic or sympathetic input to heart is more quickly reversed?

parasym.

3

Increases in HR are coupled with changes in :

ventricular function

4

Positive lusitropic effects --> HR and rate of relaxation

increases both

5

chronotropic effect

changes HR. Positive chronotropic effect = increased HR

6

lusotropic effect relates to

contractility

7

inotropic effect

regulates myocardial performance.

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

8

Actin and myosin interact during

muscle contraction

9

functional unit of a muscle

sarcomere

10

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

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

11

Active tension in cardiac muscle is dependent on:

starting length of the sarcomeres at the time of activation

12

Total tension +

passive + active tension

13

preload

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)

14

afterload

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

15

end-diastolic volume

volume load during diastole

16

Frank-Starling effect

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

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

aortic pressure

18

isotonic contraction

muscle shortens when total muscle force exceeds external load

19

increased aortic pressure --> stroke volume ?

decreases

20

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

AFTERLOAD and contractility (not preload!)

21

decreased aortic pressure --> stroke volume?

increases

22

contractility

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

23

inotropic changes ***

changes in contractility **

24

Increased NE --> contractility

increases (because more Ca is released) INOTROPIC EFFECT

25

ischemia

lack of perfusion

26

Thyroid hormone ---> Ca reuptake and hypertrophy

Enhances both

27

Increased CO2 --:> myocardial performance

declines (due to lower pH)

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