*Physiology 2 (lecture 2) Flashcards
Is cardiac muscle striated or non-striated?
Why?
Striated
Due to the regular arrangement of contractile protein
What part of the intercalated disc provides mechanical adhesion between adjacent cardiac cells?
The desmosomes
What are myocytes made up of?
Myofibrils which contain actin and myosin
Out of actin and myosin, what is the thicker filament and what is the thinner filament?
Thicker = myosin (darker appearance) Thinner = actin (lighter appearance)
What is the actin and myosin in myofibrils arranged into?
Sacromeres
What are sarcomeres?
The functional unit of muscle
Does actin slide over myosin or does myosin slide over actin?
Actin slides over myosin
Is ATP required for the contraction or relaxation of cardiac muscle fibres?
Contraction and relaxation
What happens to the myosin head when ATP is present but there is no Ca2+ present?
It is energised but since there is no Ca2+, it does not bind to actin
What happens to the myosin head when both ATP and Ca2+ are present?
The myosin head is energised and since there is Ca2+ present, it can bind to actin and creates a bending movement called a power stroke causing the release of energy and ADP + Pi
What must be available for myosin to detach from actin?
ATP
What 2 molecules are found attached to actin?
Troponin
Tropomyosin
How does the presence of Ca2+ lead to myosin being able to bind to actin?
Ca2+ binds to topping which causes a conformational change which slides the troponin-tropomyosin complex away from the binding site on actin (if we don’t have Ca2+ this does not happen and therefore the troponin-tropomyosin complex stays covering the binding site)
What is the intracellular store of calcium in a cell?
In the sarcoplasmic reticulum
how is calcium released from the sarcoplasmic reticulum?
Due to the presence of extracellular calcium = calcium induced calcium release
How does the length of the action potential and muscle contraction compare between cardiac smooth muscle and skeletal muscle?
much longer in cardiac smooth muscle (refractory period is also longer)
What is the refractory period?
The period following stimulation in which it is not possible to produce another action potential
Why is the long refractory period good for the heart?
It is protective, preventing generation of titanic (sustained) contraction
What is the stroke volume?
The volume of blood ejected from each ventricle per heart beat
SV = ?
SV = end diastolic volume - end systolic volume
What are the 2 categories of mechanisms by which the stroke volume can be regulated?
Intrinsic (within the heart itself)
Extrinsic (nervous and hormonal control)
What are the intrinsic factors affecting stroke volume?
Changes in diastolic length of myocardial fibres
This is determined by the volume of blood in each ventricle at the end of diastole (end diastolic volume)
What is the cardiac preload?
Length of sarcomeres/ tension in cardiac muscle prior to contraction
What determines the cardiac preload?
The end diastolic volume
What determines the end diastolic volume?
Venous return to the heart
Starling’s law/ Frank-Starling curve?
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 (stroke volume) - as we increase the end diastolic volume, we increase the stroke volume unless we stretch the heart too much
How is the optimal length of cardiac muscle achieved?
By stretching the muscle
What is the afterload?
Resistance into which the heart is pumping
What can happen if an increased afterload persists e.g. untreated hypertension?
the ventricular muscle will increase to overcome the resistance = ventricular hypertrophy
What type of nerve supplies the ventricular muscle?
Sympathetic nerves
What happens when the sympathetic nerves suppying the ventricular muscle is stimulated?
It increases the force of contraction - positive ionotropic effect
How does the force of ventricular contraction increase due to sympathetic stimulation?
What mediates this effect?
Due to increased activation of Ca2+ channels - peak ventricular pressure rises, rate of pressure change during systole also increases, rate of ventricular relaxation also increases due to increased rate of Ca2+ pumping
cAMP
What are the 2 axis on the frank starling curve?
EDV
Stroke volume
What effect does sympathetic stimulation have on the Frank-stirling curve?
Shifts it to the left and peak is increased
What effect does heart failure have on the frank-starling curve?
Shifts it to the right - negative ionotropic effect - less stroke volume for same EDV due to lower force of contraction
Effect of parasympathetic nerve on ventricular contraction?
Very little innervation of ventricles by ages in man therefore little, if any, direct effect on SV (large impact on rate but not force or contraction)
what hormones have a chronotropic and ionotropic effect?
Adrenaline and noradrenaline released from the adrenal medulla (effects normally minor)
What is the cardiac output?
The volume of blood pumped by each ventricles per minute
What is the equation for cardiac output?
CO = SV X HR
