force generation by the heart

Question 1

what is the structure of a cardiac muscle?

Answer 1

• the cardiac muscle is striated - caused by regular arrangement of contractile protein
• no neuromuscular junctions
• cardiac myocytes are electrically coupled by gap junctions - these are protein channels which form low resistance electrical communication pathways between neighbouring myocytes, these ensure each electrical excitation reaches all cardiac myocytes

Question 2

what do the desmosomes within intercalated discs do?

Answer 2

• they provide mechanical adhesion between adjacent cardiac cells
• ensure that the tension developed by one cell is transmitted to the next

Question 3

what is the structure of a striated muscle fibre?

Answer 3

• myofibrils are contained in each muscle fibre - these are the contractile units of muscle
• they myofibrils have alternating segments of thick and thin protein filaments
• the actin (thin) causes lighter appearance
• within each myofibril, actin and myosin are arranged into sacromeres

Question 4

how is the muscle tension produced?

Answer 4

• by the slidin of actin filaments on myosin filaments - the sliding filament theory
• force generation depends upon ATP - dependent interaction between myosin and actin
• Ca+ is required to switch on cross bridge formation

Question 5

how does action potential switch on cardiac concentration?

Answer 5

• Muscle fiber relaxed; no cross-bridge binding because the cross-bridge binding site on actin is physically covered by the troponin-
  tropomyosin complex
• Muscle fiber excited; Ca2+ binds with troponin, pulling troponin-tropomyosin complex aside to expose cross-bridge binding site; cross-bridge binding occurs
• Binding of actin and myosin cross
  bridge triggers power stroke that pulls
  thin filament inward during contraction

Question 6

what is the refractory period?

Answer 6

a period following an action potential in which it is not possible to produce another action potential

Question 7

what is the importance of a long refractory period to the normal cardiac function?

Answer 7

• during the plateau phase of ventricular action potential, the Na+ channels are in the depolarised closed state so are not available for opening
• during the descending phase, the K+ channels are open and the membrane cant be depolarised
• the long RP is protective for the heart preventing generation of tetanic contractions in the cardiac muscle

Question 8

what is stroke volume?

Answer 8

• the volume of blood ejected by each ventricle per heart beat
• SV = end diastolic volume - end systolic volume
  = volume at end of diastolation (maximum volume)

Question 9

how is stroke volume regulated?

Answer 9

• by intrinsic (within heart) and extrinsic (nervous and hormonal control) mechanisms

Question 10

what is the intrinsic control of stroke volume?

Answer 10

• changes in SV are beough about by changed in the diastolic length/stretch of myocardial fibres
• this is determined by the end diastolic volume
• EDV determines the cardaic preload (length/stretch)
• EDV is determined by the venous return to the heart

Question 11

what is the frank-starling curve?

Answer 11

• it describes the relationship between venous return, EDV and SV
• “the more the ventricle is filled with blood during diastole (EDV), the greater the volume of ejected blood will be during the resulting systolic contraction (SV)

Question 12

how does starling’s law match the SV or RV and LV?

Answer 12

• if venous return to the RA increases, EDV of EV increases
• the lae leads to increased SV into pulmonary artery
• venous return to the LA from the pulmonary vein increases, EDV of LV increases
• the law leads to increased SV into aorta

Question 13

what is afterload? what is extra load?

Answer 13

• the resistance into which the heart is pumping
• ## the extra load imposed after the heart has contracted

Question 14

what happens if the after load is increased?

Answer 14

• at first, heart unable to eject the full SV, so EDV increases
• force by contraction rises by the law
• if increased afterload continues to exist, eventually the ventricular muscle mass increases to overcome the resistance

Question 15

what is extrinsic control of stroke volume?

Answer 15

• eg hormones and nerves
• the ventricular muscle is supplied by sympathetic nerve fibres
• neurotransmitter = noradrenaline
• stimulation of sympa nerves increases the force of contraction = known as a positive inotropic effect
• (stimulation of sympathetic nerve to the heart also causes a positive chronotropic effects ie the heart rate increases)

Question 16

what is the effect of sympathetic stimulation on ventricular contraction?

Answer 16

• force of contraction increases (Ca+ influx increases)
• the effect is cAMP mediated
• the peak ventricular pressure rises
• rate of pressure change during systole increases
• rate of ventricular relaxation increases (increased rate of Ca+ pumping)
• this reduced the duration of diastole

Question 17

when is the starling curve shifted to the left?

Answer 17

• as a result of sympathetic nerve stimulation on ventricular contraction
• peak ventricular pressure rises - contractility of heart at a given EDV rises

Question 18

when does the heart failure curve shift to the right?

Answer 18

• as a result of positive and negative inotropic agents on ventricular contraction

Question 19

what is the effect of parasympathetic nerves on ventricular contraction?

Answer 19

• very little innervation of ventricles by vagus in man, no effect on SV
• vagal stimulation have major influence on rate, not force, of contraction

Question 20

what is the extrinsic control of SV?

Answer 20

• Adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effect
• Effects normally minor c.f. effects of noradrenaline from sympathetic nerves

Question 21

what is cardiac output?

Answer 21

• The volume of blood pumped by each ventricle per minute is known as the Cardiac Output (CO)
• CO = SV x HR