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37 Cards in this Set

  • Front
  • Back
list the components of the myocardial cell
1) myofibrils - provide the contractile elements, surrounded by:
2) the sarcolemma- a complex cell membrane which invaginates and forms:
3) T-tubules - network of tubules that carries electrical signals to the interior of the cell (opening of Ca++ channels)
4) sarcoplasmic reticulum- releases Ca++ to initiate contraction and uptake of Ca++ for relaxation
5) mitochondria- adjacent to myofibrils (more numerous than in skeletal muscle)
what is the myocardial contractile unit?
sarcomere
Z line to Z line, 1.9 to 2.3 microns in length
composed of actin and myosin
describe actin
thin filament, contains reg. proteins (troponin/tropomyosin)
attach to Z lines
describe myosin
thick filaments
provide ATPase activity for contraction
titin
myofibrilar protein, provides elasticity and supports myosin
which direction are subendocardial and subepicardial muscle fibers oriented?
longitudinally
which direction are the mid wall fibers oriented
circumferential, perpendicular to the long axis
describe the geometry of the left ventricle
thick walled, prolate ellipsoid
what are the mechanical properties of the ventricular chamber described in?
pressure and volume (similar to force-length properties of skeletal muscle)
what are the determinants of contraction?
1.intracellular calcium levels
2.neurohumoral stimuli control signals
3. SR regulation of Ca++ uptake and release in response to stimuli
what are the 4 phases of diastole
1.IVR- ACTIVE process
2.Early diastolic filling
3.Diastasis
4.Atrial Systole
does HR have a greater impact on diastole or systole?
diastole
what factors influence diastole?
1. myocardial relaxation
2. ventricular filling
3. AV pressure gradient
4. passive elastic properties of the ventricle
5. HEART RATE
is diastolic dysfunction characterized by an increase of decrease in diastolic filling pressure?
INCREASE (exacerbated by elevated HR)
which kind of disorders is diastolic dysfunction common?
those causing ventricular hypertrophy
what are the determinents of IVR?
1. maximal systolic pressure
2. end-systolic fiber stretch
3. coronary blood flow
4. elastic recoil
how is increased diastolic pressure manifested clinically?
dyspnea
is tau increased or decreased with delayed ventricular relaxation?
increased
when is relaxation complete with regards to the time constant tau
3.5 times tau after aortic valve closure
what is tau?
a time constant used to assess ventricular relaxation
which direction is the diastolic pressure-volume curve shifted in a stiffer, non compliant ventricle?
to the LEFT
when does this occur most often?
situations of ventricular overload and hypertrophy (i.e. hypertension or AS)
what is pre-load
force acting to stretch a resting muscle
how is pre-load definied in the ventricle?
as end diastolic wall stress, the force at the maximal resting length of the sarcomere
which CV indices are used to measure wall stress in vivo?
end diastolic pressue/ end diastolic volume
what is starling's law?
force of contraction is dependent upon initial length of the sarcomere (and therefore extent of overlap between actin and myosin filaments-number of cross bridges that can form)

optimal overlap in cardiac muscle is 2.0 to 2.2 microns
for ventricular geometry, how is wall stress distributed?
two ways:
1. Meridonial stress
2. circumferential stress
define meridonial stress
F acting along the long axis of the ventricle and opposing long axis shortening
define circumferential stress
F acting along the equitorial direction and opposing circumferential fiber shortening
define afterload
F applied to myocardium in systole (for L ventricle it is the aortic P against which it pumps blood)
- influences extent of muscle shortening
how can afterload be defined?
as systolic wall stress
what are the two major components of afterload?
aortic systolic pressure and aortic (arterial compliance)
(T/F) Afterload and shortening are directly related
False they are inversely related. An increase in AL will result in decreased shortening of the muscle fibers.
define contractility (aka inotropism)
instrinsic property of cardiac muscle to develop force at a given muscle length that determines the force and rate of contraction INDEPENDENTLY of afterload and preload
what ion is contractility related to?
Ca++ and it's interaction with contractile proteins.
how is inotropism modulated
neurohumoral factors and the adrenergic nervous system
what is afterload mismatch?
when compensatory mechanisms can no longer normalize wall stress and contractile performance declines leading to decreased contractility, myocyte death and ventricular failure