Pressure/Volume Overload Flashcards

1
Q

hemodynamic burden

A

pressure or volume overload

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

what are the two types of responses that the heart has to hemodynamic burden

A
  1. functional response (short term)
  2. proliferative response (long term)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

functional response

A

short term response (minutes/hours)

responds to immediate changes in burden to attempt to survive the burden

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

proliferative response

A

long term response (weeks/months/years)

responds to chronic stressors by hypertrophy

main compensatory mechanism

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

hyperplasia vs hypertrophy

A

hyperplasia: increase in cell number

hypertrophy: increase cell size

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

does cardiomyocyte hyperplasia occur in adults

A

no - only in fetal myocardium

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

how do cardiomyocytes hypertrophy

A

sarcomere hyperplasia –> results in cardiomyocyte hypertrophy

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

primary vs secondary hypertrophy

A

primary: genetic or idiopathic enlargement (ex. HCM)

secondary: increased workload (pressure vs volume overload)

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

pressure overload

A

increased systolic pressure resulting in increased afterload

causes concentric hypertrophy

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

concentric hypertrophy

A

sarcomeres are added in parallel

causes wall thickening and chamber constriction

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

volume overload

A

increased diastolic pressure resulting in increased preload

causes eccentric hypertrophy

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

eccentric hypertrophy

A

sarcomeres are added in series

causes wall lengthening and chamber dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does athletic training affect cardiomyocytes

A

physiologic, reversible hypertrophy

can be in series, parallel, or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does the type of hypertrophy depend on

A

when the wall stress occurs (systole vs diastole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

mechanism of pressure overload causing concentric hypertrophy

A

increased aortic pressure –> increased afterload (systolic wall stress) –> more difficult to push blood out of ventricle –> stroke volume decreases –> myocytes hypertrophy to compensate

LaPlace’s Law: wall thickness can offset wall stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how does concentric hypertrophy affect chamber size and compliance

A

decrease chamber size and decreased compliance

17
Q

mechanism of volume overload causing eccentric hypertrophy

A

increased EDV –> increased preload (diastolic wall stress) –> more volume to push out of ventricle –> stroke volume increases –> chamber dilates by eccentric hypertrophy

18
Q

how does eccentric hypertrophy affect stroke volume and ejection fraction

A

increases stroke volume
decreases ejection fraction

more net blood leaves during systole, but a lower percentage of blood in the ventricles leaves

19
Q

how is hypertrophy maladaptive

A

proliferative and compensatory growth in response to wall stress provides temporary compensation
BUT
cardiomyocytes can not handle prolonged stressors –> overloads the heart –> cardiomyocytes degenerate and die –> ischemia –> replaced with interstitial fibrosis –> exacerbates maladaptive response + decreases conduction

20
Q

maladapyive outcomes of concentric hypertrophy

A
  1. subendocardial ischemia: caused by thick wall preventing nutrients to reach all the way through
  2. myocardial ischemia & fibrosis: myocardium outgrows blood supply leading to ischemia, myocyte death, and necrosis
21
Q

effect of fibrosis on heart function

A

fibrosis causes loss of compliance –> ventricle cannot hold as much blood –> decreases stroke volume

pressure between atria and ventricles decrease

22
Q

maladaptive outcomes of eccentric hypertrophy

A
  1. progressive dilation: preload leads to chamber dilation and increased filling which leads to more preload and exacerbates the issue
  2. AV valve regurgitation: ventricular wall remodeling causes displacement of papillary muscles, which leads to regurgitation and more preload, and more dilation
  3. impaired ejection: chamber dilation decreases systolic wall pressure, leading to decreased contractility and impaired ejection
23
Q

neurohormones and hypertrophy

A

involved in functional response

neurohormones trigger hypertrophic pathways leading to cell death and fibrosis

24
Q

what is the effect of medication on heart failure

A

decreases load on the heart

does NOT fix heart damage