Force generation by the heart Flashcards
what type of muscle is cardiac muscle?
striated
what is the striation caused by?
reglular arrangement of contractile protein
what are the junctions in the heart like?
There is no neuromuscular junctions in the cardiac muscle
But, the cardiac myocytes are electrically coupled by gap junctions
what are gap junctions?
These are protein channels which forms low resistance electrical communication pathways between neighbouring myocytes
what does the presence of these gap junctions allow?
They ensure that each electrical excitation reaches all the cardiac myocyctes
what law is this?
all or none law
what are the other junctions in the heart?
desmosomes
what do the desmosomes do?
provide mechanical adhesion between adjacent cardiac cells
what do desmosomes ensure?
They ensure that the tension developed by one cell is transmitted to the next
where are the dermosomes located?
within the intercalated discs
what does each muscle fibre (one cell) contain many of?
myofibrils.
what are myofibrils ?
the contractile unit of the muscle
describe the myofibrils?
they have alternating segments of thick and thin protein filaments
what makes up the thin filaments and what do they look like?
The ACTIN (thin filaments) causes the lighter appearance in myofibrils and fibers
what makes up the thick filaments and what do they look like?
MYOCYIN (thick filaments) causes the darker appearance
what is the arrangement of actin and myocin called in myofibrils?
sarcomeres
what is a sarcomere?
the smallest functional unit of the heart
how is muscle tension generate?
by sliding the actin filaments on myocin filaments
what does force generation depend on ?
ATP dependent interaction between actin and myocin
Energy is stored in the myocin head but even if ADP and Pi are attached and the head is energised you need another component, what is this?
calcium
what other process involving cross bridges do you need ATP for?
breaking the bridges down
what complex is formed if the cells die?
rigor complex
what does Ca do in the sliding theory?
Ca binds to troponin resulting in a conformational change which takes the troponin away. troponin normally covers the actin binding
where is Ca released from?
the sarcoplasmic reticulum
In cardiac muscle: what is the release of Ca from SR dependent on?
the presence of extra-cellular Ca
in What phase is Ca influx in ventricular muscle AP?
THE PLATEAu phase - ca influx through voltage gated Ca channels
give a summary of the events leading to muscle fibre contraction
Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site; cross-bridge binding occurs
give a summary of the events leading to muscle fibre relaxation
no cross-bridge binding because the cross-bridge binding site on actin is physically covered by the troponin-
tropomyosin complex
what effect does the long refractory period prevent?
generation of tetanic contraction
why does the long refractory period not occur in skeletal muscle cells
because the AP do not have a the plateau
what is the refractory period?
the period following an AP in which it is not possible to produce another action potential
what happens in the plateau phase to generate a refractory period?
the Na channels are in the depolarised closed state i.e. they are not available for opening
what happens in the descending phase of the AP to generate a refractory period?
the K channels are open and the membrane can not be depolarised
what is the definition of SV?
the volume of blood ejected by each ventricle per heart beat
SV =
end diastolic volume (EDV) - end systolic volume (ESV)
what intrinsic mechanisms regulate the SV?
mechanisms within the heart muscle itself
what extrinsic mechanisms regulate the SV?
nervous and hormonal control
Which intrinsic mechanisms change the SV?
they are brought about by changes in the diastolic length of myocardial fibres
what is the diastolic length (end diastolic volume) defined as?
the volume of blood within each ventricle at the end of diastole
what is the EDV dependent on?
venous return
what does the Frank - Starling curve state
the more the ventricle is filled with blood during diastole (end diastolic volume) the greater the volume of ejected blood will be during the resulting systolic contraction (SV)
which factor increases the affinity of troponin for Ca
stretch
In skeletal muscle there is an optimum fibre length at resting muscle length. what happens in cardiac muscle?
this is not true. the optimal length in cardiac muscle is achieved by stretching the muscle (frank starling mechanism)
what happens if the venous return to the right atrium is increased?
starlings law matched the stroke volume of RV and LV
what is the afterload?
this refers to the resistance into which the heart is pumping. It is the extra load imposed after the heart has contracted
what happens as a result of afterload?
at first the heart is unable to eject full SV, so the EDV increases
the force of contraction rises via the starling mechanism.
If increased afterload continues to exist, eventually the ventricular muscle mass increases to overcome the resistance
what is an clinical reason for afterload?
hypertension
what autonomic system innervates the ventricular muscle ?
sympathetic nerve fibres
what is the increase in force by sympathetic innervation called?
positive inotropic effect
how is the increase in force linked to the increase in rate?
the force of contraction increases - get an activation of Ca channels - greater Ca influx. The effect is cAMP mediated. it results in the rate of pressure chande dP/dt during systloe increasing. This reduces the duration of systole
The rate of ventricular relaxation increases (increased rate of Ca pumping. This reduced he duration of diastole.
what is the effect of sympathetic nerve stimulation on ventricular contraction in the starling curve ?
the curve is shifted to the left
what shifts the curve to the right/
hear failure
what is the effect of parasympathetic nerves on ventricular contraction?
vey little innervation of ventricles.
vagal stimulation has a major influence on rate, not force, of contraction
which hormones have an effect on the control of SV?§
adrenaline and noradrenaline have an inotropic and chronotropic effect
