Pressure/Volume Overload Flashcards
hemodynamic burden
pressure or volume overload
what are the two types of responses that the heart has to hemodynamic burden
- functional response (short term)
- proliferative response (long term)
functional response
short term response (minutes/hours)
responds to immediate changes in burden to attempt to survive the burden
proliferative response
long term response (weeks/months/years)
responds to chronic stressors by hypertrophy
main compensatory mechanism
hyperplasia vs hypertrophy
hyperplasia: increase in cell number
hypertrophy: increase cell size
does cardiomyocyte hyperplasia occur in adults
no - only in fetal myocardium
how do cardiomyocytes hypertrophy
sarcomere hyperplasia –> results in cardiomyocyte hypertrophy
primary vs secondary hypertrophy
primary: genetic or idiopathic enlargement (ex. HCM)
secondary: increased workload (pressure vs volume overload)
pressure overload
increased systolic pressure resulting in increased afterload
causes concentric hypertrophy
concentric hypertrophy
sarcomeres are added in parallel
causes wall thickening and chamber constriction
volume overload
increased diastolic pressure resulting in increased preload
causes eccentric hypertrophy
eccentric hypertrophy
sarcomeres are added in series
causes wall lengthening and chamber dilation
how does athletic training affect cardiomyocytes
physiologic, reversible hypertrophy
can be in series, parallel, or both
what does the type of hypertrophy depend on
when the wall stress occurs (systole vs diastole)
mechanism of pressure overload causing concentric hypertrophy
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 does concentric hypertrophy affect chamber size and compliance
decrease chamber size and decreased compliance
mechanism of volume overload causing eccentric hypertrophy
increased EDV –> increased preload (diastolic wall stress) –> more volume to push out of ventricle –> stroke volume increases –> chamber dilates by eccentric hypertrophy
how does eccentric hypertrophy affect stroke volume and ejection fraction
increases stroke volume
decreases ejection fraction
more net blood leaves during systole, but a lower percentage of blood in the ventricles leaves
how is hypertrophy maladaptive
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
maladapyive outcomes of concentric hypertrophy
- subendocardial ischemia: caused by thick wall preventing nutrients to reach all the way through
- myocardial ischemia & fibrosis: myocardium outgrows blood supply leading to ischemia, myocyte death, and necrosis
effect of fibrosis on heart function
fibrosis causes loss of compliance –> ventricle cannot hold as much blood –> decreases stroke volume
pressure between atria and ventricles decrease
maladaptive outcomes of eccentric hypertrophy
- progressive dilation: preload leads to chamber dilation and increased filling which leads to more preload and exacerbates the issue
- AV valve regurgitation: ventricular wall remodeling causes displacement of papillary muscles, which leads to regurgitation and more preload, and more dilation
- impaired ejection: chamber dilation decreases systolic wall pressure, leading to decreased contractility and impaired ejection
neurohormones and hypertrophy
involved in functional response
neurohormones trigger hypertrophic pathways leading to cell death and fibrosis
what is the effect of medication on heart failure
decreases load on the heart
does NOT fix heart damage
