Heart Failure Pathophysiology Flashcards

1
Q

what determines preload

A

venous return (EDV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

main components determining afterload

A

vascular resistance

ventricular wall tension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is ionotropy

A

myocardial contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is ionotropy influenced by

A

NOT preload/afterload
Ca!!!
- L type channels (opened by cAMP)
- Na/Ca exchange (inhibited indirectly by cardiac glycosides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ejection fraction in systolic vs diastolic HF

A

systolic: impaired contractility, dec EF <40%

Diastolic: normal EF, impaired diastolic ventricular relaxation and dec filling. –> dec SV and CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name 3 conditions that lead to HF by:
damaging cardiac muscle:
increasing workload on heart:

A

cardiac muscle: IHD, cardiomyopathies, myocarditis

inc workload: hypertension, valvular disease, anaemia, thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

three types of cardiomyopathy

A

dilated (85%) - dilation in ventricle itself. no hypertrophy/thickening. impaired systolic function (change in actin/myosin).
= idiopathic, alcohol toxicity, viral myocarditis, peripartum

hypertrophic (10%) - proliferation of myoblasts put extra muscle down tends to affect IV septum. hypertension can cause.

Restrictive (5%)
- about changes in properties of wall. how it contracts/relaxes. eg. amyloidosis,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

four valvular abnormalities that cause L sided HF?

A
mitral stenosis (rheumatic fever)
mitral regurgitation (acute - no change in v wall. like MS. 
chronic - dilated myocardiopathy. chronic insid increase in EDV.)

aortic stenosis: degenerative calcification (can’t eject same amount, inc LV pressure, hypertrophy to try inc force)

aortic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

four compensatory mechanisms to maintain cardiac output

A

sympathetic nerve activity
renin-angiotensin-aldosterone
Frank-starling
fluid movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

problem with frank starling in HF

A

inc vasc volume causes inc EDV

increases muscle stretch and O2 consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

problem with sympathetic activity in HF

A

causes tachy, vasoconstriction, dec perfusion of tissue, renin release etc.
this all increases workload of heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

problems with RAAS in HF

A

angiotenisin: vascocontrictor, aldosterone releae

increase Na and water reabsorption AND inflammatory responses depositing collagen in ventricles = stiffer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly