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1

heart failure most commonly characterized by

- fluid retention
- elevations in ventricular filling pressures

2

some causes of heart failure

- hypertension
- MI
- cardiomyopathy
- arrhythmia
- congenital heart disease
- valvular disease

3

the true problem from heart failure results from

- maladaptive neurohormonal responses to decreased cardiac performance

4

pathophys causes of heart failure

- impaired contractility
- increased afterload
- increased volume
- impaired ventricular filling

5

impaired contractility caused by

- ischemic and dilated cardiomyopathy

6

increased afterload caused by

- longstanding hypertension
- aortic stenosis

7

increased volume caused by

- aortic/mitral insufficiency

8

impaired ventricular filling caused by

- hypertrophy

9

what is the most common cause of heart failure

- MI

10

ischemic cardiomyopathy - the primary/secondary disease process

- primary - coronary arteries
- secondary - heart muscle

11

dilated cardiomyopathy - the primary disease process

- primary - heart muscle

12

decreasing contractility has what effect on stroke volume

effect on cardiac output

- decreasing contractility decreases stroke volume

- decreased cardiac output

13

physiological adaptations to decreased stroke volume

- increased preload (frank starling)
- increased wall thickness

14

what happens if we increase preload beyond that of the adaptive response

- we get pulmonary edema

15

most common symptoms of heart failure

- dyspnea

16

how is preload regulated

- venous tone
- blood volume
- body position

17

venous tone is regulated by

- sympathetic activity increasing tension in walls of veins and venules

18

blood volume increased by

- RAS
- Sympathetic nervous system
- ADH
- fluid intake

19

result of increased sympathetic tone

- beta 1 stimulation increases HR and contractility
- alpha 1 stimulation increases venous return and decreases venous compliance
- increased renin release, salt and fluid retention and vasoconstriction

20

cardio response to chronic beta-AR stimulation

- down regulation of beta AR
- energy starvation
- cardiomyocyte death
- ventricular arrhythmias
- fibrosis

21

RAAS response to decreased stroke volume

- kidneys sense decreased EABV
- increase renin from JGA
- increase angiotensin II and aldosterone levels
- increases blood volume and vasoconstriction

22

heart failure result on RAAS

- disrupts negative feedback loop
- excessive fluid retention

23

role of ANP and BNP

- counteract maladaptive hormones

24

how chronic hypertension leads to heart failure

- chronically elevated BP increases LV pressure
- leads to hypertrophy of ventricle
- remodeling and dilation

25

effect of chronic hypertension and aortic stenosis on afterload

- increase afterload

26

what is the easiest component of afterload to modify

- systemic vascular resistance

27

myocyte impact in pathological hypertrophy

- what type of hypertrophy

- increase myocyte width

- concentric hypertrophy

28

myocyte impact in cardiac dilatation

- what type of hypertrophy

- increase myocyte length

- eccentric hypertrophy

29

what defines pathologic remodeling

- fibrosis

30

impact of fibrosis on the heart

- impairs ability to contract and relax
- leads to heart failure