Force Generation by the Heart Flashcards
describe the structure of cardiac muscle
cardiac muscle is striated - striation is caused by regular arrangement of contractile protein
there is no neuromuscular junctions in cardiac muscle
cardiac myocytes are electrically coupled by gap junctions - these are protein channels which form low resistance electrical communication pathways between neighbouring myocytes
they ensure that each electrical excitation reaches all the cardiac myocytes (all or none law of the heart)
the desmosomes within the intercalated discs provide mechanical adhesion between adjacent cardiac cells
they ensure that the tension developed by one cell is transmitted to the next
describe the sliding filament mechanisms of muscle contraction
muscle tension is produced by sliding of actin filaments (thin) on myocin filaments (thick); muscle shortens and produces force
force generation depends upon ATP-dependent interaction between myosin and actin filaments (ATP is required for both contraction and relaxation)
Ca2+ is also required to switch on cross bridge formation - it causes a conformational change by binding to troponin, exposing the myosin binding site of the cross bridge
resting - no cross bridge binding as binding site on actin is physically covered by troponin-tropomyosin complex
+Ca2+ - excitation
binding - Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross bridge binding site => cross bridge binding occurs
bending - binding of actin and myosin cross bridge triggers power stroke that pulls thin filament inward during contraction
fresh ATP available
detachment
energised
describe how excitation of cardiac muscle results in contraction (excitation contraction coupling)
Ca2+ is released from the sarcoplasmic reticulum (SR)
in cardiac muscle the release of Ca2+ from SR is dependent on presence of extracellular Ca2+
describe the source and role of calcium ions in ventricular systole
Ca2+ influx during plateau phase of action potential
this causes Ca2+ induced Ca2+ release from SR
the Ca2+ then activates contractile machinery
describe how ventricular diastole is achieved
when action potential has passed, Ca2+ influx ceases, Ca2+ re-sequestered in SR by Ca2+ ATPase, heart muscle relaxes
intracellular calcium is low (as it is stroked in SR) and so there it is not sufficient to cause a conformational change in the cross bridge
explain the importance of a long refractory peroid to normal cardiac function
prevents generation of tetanic contraction (sustained muscle contraction evoked when the motor nerve that innervates skeletal muscle emits action potentials at a very high rate)
refractory period - period following action potential in which it is not possible to produce another action potential
during plateau phase of ventricular action potential the Na2+ channels are in the depolarised closed state (not available for opening)
during the descending phase of action potential the K+ channels are open and the membrane can not de depolarised
define the term stroke volume
the volume of blood ejected by each ventricle per heart beat
contraction of ventricular muscle ejects the stroke volume
regulated by intrinsic (within heart itself) and extrinsic (nervous and hormonal) mechanisms
what is stroke volume equivalent to
end diastolic volume - end systolic volume
describe changes to ventricular period
leads to changes in stroke volume
frank-starling mechanism - the relationship between venous return, end diastolic volume and stroke volume
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)
stretch also increases the affinity of troponin for Ca2+ -optimal length in cardiac muscle is achieved by stretching the muscle
explain how stroke volume of right and left ventricles are matched
starling’s law matches the stroke volume of right and left ventricles
if venous return to right atrium increases, end diastolic volume of right ventricle increases
starling’s law leads to increased stroke volume into pulmonary artery
venous return to left atrium form pulmonary vein increases, end diastolic volume of left ventricle increases
staling’s law leads to increased stroke volume into aorta
explain the concept of afterload and its effect on stroke volume
frank-starling mechanism partially compensates for decreased stroke volume caused by increased afterload
afterload - resistance into which heart is pumping
extra load is imposed after the heart has contracted
if after load increases - at first, heart is unable to eject full stroke volume so end diastolic volume increases
force of contraction rises by frank-starling mechanism
if increased afterload continue to exist (untreated hypertension) eventually the ventricular muscle mass increases (ventricular hypertrophy) to overcome the resistance
describe how extrinsic control -sympathetic stimulation - influences ventricular contraction
extrinsic control - hormones and nerves
ventricular muscle is supplied by sympathetic nerve fibres
neurotransmitter is noradrenaline
stimulation of sympathetic nerves increases the force of contraction => iontropic effect
(also causes positive chronotropic effect)
force of contraction increases (Activation of Ca2+ channels = greater Ca2+ influx)
effect is cAMP mediated
peak ventricular pressure rises
rate of pressure change (dP/dt) during systole increases - reducing duration of systole
rate of ventricular relaxation increases (increased rate of Ca2+ pumping - reducing duration of diastole
refer PP;
peak ventricular pressure rises - contractility of heart at a given end diastolic volume rises (frank starling curve shifted to left, heart failure shifts curve to right)
define the term cardiac output
volume of blood pumped by each ventricle per minute
resting cardiac output = approx 5 litres per minute (70 stroke volume x 70 BPM)
what is cardiac output equivalent to
stroke volume x heart rate
regulating stroke volume and heart rate will regulate cardiac output
describe the structure of striated muscle fibre
each muscle fibre contains many myofibrils - these are the contractile units of muscle
the myofibrils have alternating segments of thick and thin protein filaments
actin (thin filaments) - causes lighter appearance in myofibrils and fibres
myocyin (thick filaments) - causes darker appearance
within each myofibril - actin and myocin are arranged into sacromeres
