Physiology: Force Generation by the Heart Flashcards
Describe the organisation of cardiac muscle
- Striated, due to regular protein arrangement
- No neuromuscular junctions
List and describe the connections between cardiac myocytes
Gap junctions:
- Protein channels
- Allow low resistance electrical communication between neighbouring cells
Desmosomes:
- Provide mechanical adhesion between cells
- Ensure that tension produced by one cell is transmitted to the next
Describe the All-or-none Law of the heart
If the stimulus exceeds the threshold potential, heart will give a complete response, otherwise there is no response
Describe a myfibril
- Contractile units of muscle
- Alternating segments of actin and myosin
Describe the appearance of actin filaments in a myofibril
- Thin
- Lighter colour
Describe the appearance of myosin filaments in a myofibril
- Thick
- Darker colour
Describe a sarcomere
- A subunit of a myofibril
- Smallest contractile subunit
- From one Z line to the next
What is the basic principle of how muscle tension is produced?
By actin filaments sliding on myosin filaments
e.g. Sarcomeres shorten
This uses ATP
Describe the process by which myosin binds to actin
- Troponin-tropomyosin blocks the myosin cross bridge binding sites
- Ca2+ binds to troponin, causing a conformational change
- Myosin binding sites exposed
- Myosin cross bridge binds to actin via binding sites
Give another term for a muscle fibre
Muscle cell (myocyte)
Describe the sarcoplasmic reticulum (SR)
- Stores Ca2+ for release during contraction mechanism
- Forms a mesh enclosing the myofibrils
- Has transverse tubules (T-tubule) connected by lateral sacks
Define the sarcolemma
The membrane that envelops myocytes
Define transverse tubules (T-tubules)
Extensions of the sarcolemma that penetrate into the centre of the myocyte
Describe the purpose of the transverse tubules (T-tubules)
To bring the membrane potential closer to the myofibrils (and thus sarcomeres)
Describe the mechanism by which adequate Ca2+ are acquired to free up the myosin cross bridge binding sites
Ca2+ induced Ca2+ release (CICR):
- Ca2+ influx during phase 2 of action potential
- Ca2+ influx induces Ca2+ stores in the Sarcoplasmic reticulum to be released
- Enough Ca2+ present to full expose the myosin cross bridge binding sites
Is there enough Ca2+ influx during phase 2 of the action potential to allow the myosin cross bridge binding sites to move?
No, it requires Ca2+ release from the sarcoplasmic reticulum
This occurs via Ca2+ - induced Ca2+ release (CICR)
Define the refractory period of a cardiac myocyte
The period after an action potential in which it is impossible to produce another action potential
Describe the importance of the long refractory period of cardiac myocytes
Prevents tetanic contractions
Define tetanic contractions
Sustained muscle contraction due to very rapidly occurring action potentials
What factors contribute to the existence of the refractory period?
- The Na+ channels are closed after phase 0, preventing further depolarisation
- Phase 2 lasts a long time due to the slowly inactivating L-type Ca2+ channels
- In phase 3 the outflux of K+ prevents another depolarisation
Define the stroke volume (SV) of the heart
The volume of blood ejected a ventricle during systole
Give an equation for determining stroke volume from the end volumes of systole and diastole
SV = EDV - ESV
Define the end diastolic volume (EDV)
The volume of blood within the ventricle at the end of diastole
i.e. the max volume of blood in the ventricle
What determines the end diastolic volume?
The venous return of to the heart
Define cardiac preload
The initial stretching of the cardiac myocytes prior to contraction
It is determined by the end diastolic volume (how full the ventricle gets)
Define the end systolic volume (ESV)
The volume of blood within the ventricle at the end of systole
Describe the Frank-Starling Mechanism (Starling’s Law)
- The relationship between end diastolic volume and stroke volume
- The more blood in the ventricle during diastole (EDV), the greater the volume of blood ejected during systolic contraction (SV)
What conditions are required to achieve optimal force generation from the heart?
- Optimal fibre length
Does the the myocyte fibre length increase past the optimal fibre length for maximising stroke volume
Not in a healthy heart
Give the effect that myocyte fibre stretch has on troponin affinity for Ca2+
Fibre stretch increases the affinity of troponin for Ca2+
Compare the optimum muscle fibre lengths of skeletal and cardiac muscle
Skeletal:
- Unstretched
Cardiac:
- After stretching
Describe why the optimum muscle fibre length of cardiac muscle is achieved after stretch
- As stretch increases the affinity of troponin for Ca2+
- Leading to more cross bridge formation
- More cross-bridges better contraction
Define the venous return of to the heart
The blood that returns to the an atrium of the heart
Can refer to either the right or left atria
Describe the effect of increased venous return into the right atrium on:
- The EDV of the right ventricle
- Stroke volume into the pulmonary artery
EDV increases
so
Stroke volume increases
Describe the effect of increased venous return into the left atrium:
- The EDV of the left ventricle
- Stroke volume into the aorta on the EDV of the left ventricle
EDV increases
so
Stroke volume increases
Define cardiac afterload
The resistance into which the heart is pumping
Is imposed after contraction
Describe the heart’s response to an increased cardiac afterload
- At first the heart cannot eject the full stroke volume
So - EDV increases
Then - The force on contraction increases via the Frank-Starling mechanism
Describe the outcome of continued increases afterload
e.g. hypertension
Ventricular hypertrophy
To increase contractile force to overcome the increased afterload
List the 2 types of extrinsic control of stroke volume
- Hormonal
- Nervous
Describe the role of sympathetic nervous stimulation in controlling stroke volume
- Ventricular muscle is supplied by sympathetic nerves
- Stimulation increases the contraction force (+ve inotropic effect)
- Thus the peak ventricular pressure also increases
- Causes increased rate of contraction and relaxation as well
Describe the effect of sympathetic nervous stimulation on the rate of ventricular contraction and relaxation
- Increased rate of contraction
- Increased rate of relaxation
Describe the impact of increased rate of contraction and increased rate of relaxation
Increased rate of contraction:
- Reduces systole duration
Increased rate of relaxation:
- Reduces diastole duration
Thus it has a +ve chronotropic effect
Why does sympathetic stimulation increase ventricular contraction force?
- Activation of Ca2+ channels
- Greater influx of Ca2+
Describe the effect sympathetic stimulation has on the the Frank-Starling Mechanism
- Shifts the graph to the left and upwards
- A greater stroke volume is achieved at the same EDV
Describe the impact of a +ve and a -ve inotropic effect on the the Frank-Starling Mechanism
A +ve inotropic effect:
- A greater stroke volume is achieved at the same EDV
- Graph moves upwards
A -ve inotropic effect:
- A lower stroke volume is achieved at the same EDV
- Graph moves downwards
Describe the role of sympathetic nervous stimulation in controlling stroke volume
- Very little innervation of ventricles by vagus nerve
- Therefore little effect of stroke volume
Describe the role of hormones in controlling stroke volume
- Adrenaline and noradrenaline have a +ve inotropic and chronotropic effect
- They are released from the adrenal medulla
- Have minor effects compared to that of sympathetic nerves
Define cardiac output (CO)
The volume of blood pumped by each ventricle per minute
Give an equation to calculate cardiac output from stroke volume and heart rate
CO = SV x HR
What is an average healthy cardiac output?
~5 litres