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Pharmacology- Test 3 > Heart Failure > Flashcards

Flashcards in Heart Failure Deck (63)
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1

What is the equation of C.O.?

CO= HR x SV

2

What is HR regulated by?

ANS

3

What is preload (filling pressure)?

The volume of blood flowing back to the heart; i.e. venous return going back to the heart

4

What is the relationship between the preload and the SV?

There is a direct relationship; if you increase the preload, you increase the SV (and opposite)

5

What is afterload (PR)?

The resistance against which the heart has to pump against (the ventricle has to pump the blood into the systemic circulation); the peripheral vascular resistance (i.e. how constricted the arterioles are);

6

What is the relationship between afterload and SV?

Inverse relationship; if you increase the resistance of the flow, the lower the SV will be and vice versa

7

What is contractility?

The amount of force that the ventricle can produce per fixed volume of blood in the ventricle

8

Contractility is regulated by what? When would you get more contractility?

ANS (the ventricles are innervated by sympathetic nerves); when you activate B-1 receptors increases contractility (i.e. if you increase SNS, the pump is going to generate more force into the systemic circulation)

9

What are the 3 things that can alter SV?

(1) Preload
(2) Afterload
(3) Contractility

10

What is the qualitative definition of heart failure?

Inability of heart to pump sufficient blood to meet the metabolic demands of the body

11

What is the quantitative definition of heart failure?

Decreased mechanical efficiency (decrease in contractility); reduced ability to generate force into the systemic circulation

12

Starling's Law

(1) Increase the preload -->
(2) heart is going to dilate to accomodate, and as you do that you increase the volume of blood and the
(3) pump has to generate more force to pump it out (increase pump contractility)

13

What are the two ways the body tries to compensate for heart failure?

(1) Intrinsic- what happens within the heart muscle itself
(2) Extrinsic- the neural-chemical activation

14

What are the two ways that Intrinsic factors try and compensate?

(1) Ventricular dilation
(2) Ventricular hypertrophy

15

Ventricular dilation- why does this happen?

To increase the ventricular volume which increases S.V. (You get venoconstriction (increase contractility) which means that more blood goes back to the heart, which means the preload is increased, which means the heart dilates, and force you have to use to pump out will increase)

16

Ventricular hypertrophy- why does this happen?

Each myocyte grows in size (they don't divide) which increases the number of contractile elements within each cell in the heart's attempt to increase the force of contraction
- net result is cells get bigger= ventricular wall gets bigger

17

Are the intrinsic compensation factors better short term or long term?

short term (acutely)

18

What are the extrinsic compensations of heart failure?

Decrase BP is sensed by the baroreceptors to increase sympathetic nervous system

19

What, in turn from the baroreceptor extrinsic compensation, will happen when you stimulate the sympathetic nervous system?

(1) Increase heart rate- B-1 receptors which increases CO
(2) Increase Preload (A-1 constriction from veins)
(3) Increase Afterload (A-1 constriction of arteries- increase BP)
(4) Increase in Ang-II (B-1 renin release in kidney; stimulates release of aldosterone causing salt and water retention)
(2-3-4) Increases blood volume

20

What will happen if the extrinsic compensation happens chronically?

It will accelerate the progression of heart failure

21

What happens when the sympathetic nerves stimulate the B-1 receptors in the ventricle?

Increases contractility and stimulates growth of the myocytes (hypertrophy and remodeling)

22

What 2 things stimulate myocyte growth in extrinsic compensation pathway which stimulate hypertrophy and remodeling?

(1) B-1 receptor activation in the ventricle
(2) Ang-II receptor bind to myocytes and stimulate growth

23

What is maladaptive/ventricular remodeling?

Alteration in dimension, shape or mass in response to hemodynamic stress/injury in association with neurohormonal activation

24

What happens during maladaptive remodeling? Why is this bad?

The shape of the ventricle changes (goes from elliptical to a circular shape and the wall gets thicker); due to pure physics it doesn't pump as well

25

What are the 4 things that happen during ventricular remodeling?

(1) Myocyte hypertrophy
(2) Myocyte apoptosis- cells die faster
(3) Fibroblast proliferation (collagen)- take over for the myocytes (inactive); reduces ability to pump
(4) Oxidative stress- instead of producing ATP, produces species that will increase cell death

26

What are the mediators involved in ventricular remodeling?

(1) Ang-II
(2) Catecholamines (NE)
(3) Aldosterone (mineralocorticoid receptors in myocytes)
(4) Cytokines

27

How do Inotropic agents work?

Directly act with the heart to increase contractility; useful acutely (once case chronically) but they are going to increase workload on heart

28

How do Beta-blockers work?

Can over time decrease S.V.

29

How do the ACE inhibitors and AII receptor blockers work?

Interferes with the R-A system to block it's effects

30

How do Diuretics work?

lowers blood volume back towards normal