Hypertrophy Flashcards
Strength =
Mass (# of sarcomeres) x Contractility (force generated by each sarcomere)
Most Important Stimulus for Hypertrophy
Ventricular wall stress/workload. The increased mechanical stress activates growth signals in myocyte
Increased Heart Muscle Mass
Cause by myocyte enlargement via more sarcomeres, NOT myocyte proliferation
Most Powerful Myocyte GF Signallers
NE and Epi
Physiological vs. Pathological Hypertrophy
Path is less regular and more disarray, and has more fibrosis
Ventricular Wall Stress = (what it is and eq, similar to law of laplace)
(Developed Force x Chamber Radius) / Muscle Thickness
Measures actual workload of each myofiber
Hypertrophy Normalizing Wall Stress
MechanRs detect high wall stress, activating intracellular mechs for hypertrophic gene expression, to normalize wall stress
Hypertrophy and Bioenergetic Efficiency
Increases it, thus decreasing oxygen consumption bc normalizes wall stress
BNP
Endocrine marker produced immediately on wall stress increase, so check BNP if thinking about heart failure and if it’s not elevated it’s not the heart
4 Determinants of Cardiac Work
Preload
Compliance
Contractility
Afterload
Very Common Cardiac Work Determinant in Heart Failure
Reduced compliance
3 Kinds of Hypertrophic Hearts
Hypertrophic - concentric, chamber almost gone
Athletic - larger, but chamber larger too so ratio is preserved
Dilated - Eccentric, more wall but way more chamber too
Cardiac Work Equation and 2 Types of Overload’s Effects
Work = Wall Stress x CO
V Overload Increases CO
P Overload increases wall stress
Cardiac Adaptations to V Overload
Acute - ventricular dilation increases diastolic V and invokes Starling forces, r increases but nothing done about it yet
Chronic - Increased wall stress induced cardiac remodeling and hypertrophy, so get eccentric hypertrophy to reduce wall stress
Cardiac Adaptations to Pressure Overload
Acute: energy conservation by reducing sarcomere shortening length/velocity
Chronic: myocyte hypertrophy
