Week 4 Flashcards
Regulation of cardiac output
CO= HR * SV
SV= EDV-ESV
CO= HR * (EDV-ESV)
Using ~ values = 70 x (120-50)= 5L.min-1
Regulation of stroke volume
EDV- volume in ventricle at end of diastole 120ml
ESV- volume in ventricle at end of systole 50ml
So can increase stroke volume by increasing EDV or deceasing ESV
Excitation-contraction coupling
For cardiac muscle to contract, actin and myosin filament must interact to form cross bridges
In order for the myosin heads to interact with myosin binding site on actin the regulatory troponin complex must undergo conformational change to move out the way:
-calcium that enters cardiac muscle cells during the action potential via L type calcium channels
-this stimulates the release of calcium from the sarcoplasmic reticulum via the ryanodine receptor- the calcium release channels on SR
-this is called calcium induced calcium release
-its the calcium thats released from SR that binds to troponin C and moves the regulatory complex out the way allowing actin and myosin to form cross bridges for contraction to occur
Therefore it is calcium that regulates the number of actin-myosin cross bridges formed and therefore force of ventricular contraction
Force of contraction (no. Of cross bridges formed) can be increased by:
-increasing the calcium sensitivity of the contractile apparatus so you get more cross bridges formed for given concentration of intracellular calcium
-increasing the concentration of intracellular Ca2+ in cell
Relaxation occurs when calcium is pumped back into SR via SERCA (sarcoendoplasmic reticulum calcium ATPase) regulated by phospholamban
Starlings law of the heart: regulation of SV
Important in controlling SV and matching left and right CO
An increase in EDV can lead to increase in SV:
Starlings law relationship between EDV and SV
Intrinsic property of cardiac muscle
When the cardiac muscle is stretched before it is stimulated to contract via depolarisation it contracts with greater force and therefore it can eject more blood and so increase SV
So the more the ventricles are filled with blood the greater the EDV the more the ventricle will be stretched resulting in greater SV
As length of sarcomere increases the force with which it contracts increases this is due to increase in number cross bridges formed
Possible mechanism: increased Ca2+ sensitivity of contractile apparatus increasing rate of cross bridge formations
Not possible to measure length of sarcomere in functioning heart need to use a proxy- EDV usually used, venous return, ED pressure, cardiac filling pressure, CVP
“Force of ventricular contraction is dependent on the length of ventricular muscle fibres in diastole”
Increased EDV leads to increased SV
Stroke volume increases/decreases by same amount as EDV
With increased EDV the ventricular muscle cells are more stretched-> increasing sarcomere length-> greater crossbridge formation-> greater force of contraction-> larger SV
There is a limit to relationship- the force of contraction only increases in a length dependent fashion over a narrow range of sarcomere length
After this the SV falls with an increase in sarcomere length
At EDV of 120ml sarcomere length= 1.5um
Regulation of EDV- venous return and central venous pressure
The filling of the heart and so EDV is influenced by venous return
Venous return influences our central venous pressure (pressure in the central veins at the point they enter the atria)
So an increase in venous return increases central venous pressure increased EDV
Starlings law of heart ensures RSV=LSV
Right side:
-blood comes back from systemic circulation via veins enters right atrium fills right ventricle to give right EDV this stretches heart to give RSV
Left side:
-anything that changes venous return changes pulmonary circulation so after couple beats get changes in filling left side of heart so changes in left ventricular EDV
-so if we increase venous return to right side of heart it increases amount blood going to pulmonary circulation which will increase amount blood entering left side of heart increase left EDV so increase left SV
If RSV>LSV: congestion of pulmonary circulation
If LSV>RSV: congestion of systemic (venous) circulation
Factors affecting venous return to the right ventricle
- blood volume
-skeletal muscle pump
-respiratory pump
-venous tone
-gravity
The venous system acts as a reservoir for blood can hold up to 70% blood volume
So an increase and decreases in overall blood volume can influence the amount of blood stored in venous circulation and hence how much of that is returned to heart
The changes in distribution of blood within the venous circulation and overall capacity of venous circulation can be used to control venous return to Heart
Blood volume
Increased blood volume (eg during renal failure) leads to increase in venous return- increase right ventricular filling- increase SV
Decreased blood volume (dehydration/haemorrhage) leads to decrease venous return decrease EDV and decrease in SV, decrease in CO and arterial blood pressure
Skeletal muscle pump
Blood is pumped through valves by skeletal muscle pump
When skeletal muscle contracts its squashes veins
Above the contracted muscle the blood is propelled back towards the heart
Below the contracted muscle the blood fills cusps of valves causing them to close and preventing further back flow of blood
When muscle then relax the proximal valve closes to prevent back flow of blood from higher segment of veins and distal valve opens allowing vein to fill again
Standing for long period of time without moving skeletal muscle of the legs can compromise venous return resulting in reduced EDV, SV, CO and arterial BP
Patients with incompetent leaky valves in their veins can develop varicose veins-> compromises venous return to heart
Respiratory pump
The action of breathing helps to return blood to the heart
When we breathe in the diaphragm flattens and presses down on abdomen causing an increase in abdominal pressure and chest wall expands so decrease in thoracic pressure
This pressure gradient sucks blood from abdominal vena cava into thoracic vena cava
This will deliver more blood to right side of heart into right ventricle
This increases filling of heart so increase EDV and by starling law of the heart increase SV
Venous tone
Venous return can be increased by mobilising some of this stored blood
Blood is mobilised by constricting venous vessels so they cant store as much blood
This moves blood back to the heart increasing venous return
Venoconstriction:
-mediated by sympathetic nervous system increase in sympathetic activity will evoke venoconstriction
-venoconstriction reduces the volume of blood in the veins at a given pressure
-so theres less blood in the vein more is returned to heart
Gravity
In supine position the venous vessels will be approx same level of the heart
This allows blood to be evenly distributed between all areas of the body
Venous return is unaffected and central venous pressure is maintained
When moving from supine to standing position gravity acts on venous blood:
-redistribution of blood due to gravity
-venous pooling in Lower extremities less blood returned to heart
-reduction in thoracic blood volume
-fall in venous return- decrease in central venous pressure- decrease in cardiac filling- decrease in EDV and SV
-a fall in Rv stroke volume- decrease CO to pulmonary circulation- decrease pulmonary venous return to LV- decrease LV stroke volume
Pre-load
Any factor which influences the stretch of cardiac muscle cells before contraction
Factors include: blood volume, skeletal muscle pump, respiratory pump, venous tone, gravity
Other factors that affect EDV: atrial contraction
At rest atrial contraction contributes only a small amount to ventricular filling (5ml at rest) so doesn’t contribute much to EDV
Atrial and ventricular muscle both innervated by sympathetic nerves
Sympathetic stimulation of atrial muscle can increase the force of atrial contraction which then boosts ventricular filling leading to greater EDV
This mechanism is important for maintaining EDV at a high HR as the rapid passive filling phase of the ventricle is shortened by increase in HR
Other factors that affect EDV: HR (>180bpm)
Very high heart rate when atrial contraction cant compensate
When heart rate >180 the passive filling plus increase in atrial contraction is not sufficient to maintain EDV and therefore SV won’t be able to be maintained
So at HR>180bpm EDV will be reduced so as ventricular muscle wont be stretched as much so SV reduced and CO compromised
