Regulation of Stroke Volume Flashcards
Control of heart rate is
Neural
Regulation of stroke volume depends on
Preload
Afterload
Neural
Pathological
Describe the increase of heart rate (5)
- Sympathetic system releases noradrenaline
- Adrenaline from adrenal medulla
- Both act on B1 receptors on sinoatrial node
- Increases slope of the pacemaker potential
- Increases heart rate= tachycardia
What does increasing the slope of the pacemaker mean?
The cell gets the threshold sooner
Describe the decrease of heart rate
- Vagus release Ach
- Acts on muscarinic receptors on sinoatrial node
- Hyperpolarises cells and decreases slope of pacemaker potential
- Decreases heart rate = bradycardia
Stroke volume
The volume of blood in ml ejected from each ventricle due to the contraction of the heart
What does Starling’s law state
The energy of contraction is proportional to the initial length of cardiac muscle fibre
The more stretched the cardiac muscle fibre is
the higher the calcium sensitivity of the myofibrils, causing a greater number of actin-myosin cross-bridges to form within the muscle fibres
Pre load is affected by what
End Diastolic Volume
Increased venous return means (2)
Increased EDV
Increased stroke volume
Decreased venous return means (2)
Decreased EDV
Decreased stroke volume
What is pre load
The load applied to muscles before it contracts
What is after load
The load against which the muscle tries to contract
Aortic pressure is affected by
How much blood is pushed into the aorta (Cardiac output)
How easy it is for the blood to get out of the aorta (TPR)
What happens if the TPR increases
The aortic pressure increases
Ventricles will have to work harder to build pressure to open valve
Less energy for ejecting blood- SV decreases
What is afterload set by
The arterial pressure against which the blood is expelled which is dependent on the TPR
If the TPR increases what happens to the stroke volume
It will go down
Neural regulation to increase stroke volume (5)
- Sympathetic nerves release noradrenaline
- Plus circulating adrenaline from adrenal medulla
- Both act on B1 receptors on myocytes
- Increase contractility
- Stronger but shorter contractions
Inotropic
Strength of contraction
Contractility
How many calcium cells released
Neural regulation to decrease stroke volume
Parasympathetic has little effect as vagus does not innervate the ventricular muscle
Hypercalcemia effect on SV
Shifts curve up and left (Increased SV, reduced EDV- filling phase it cut short)
Hypocalcemia effect on SV
Shifts curve down and right (decreased SV, more time for filling EDV increases)
Ischaemia effect on SV
Shifts curve down and right (lower SV, more filling time)
Barbiturates
Shifts curve down and right
How does the heart compensate for a reduced pumping ability (3)
Works around a bigger EDV
Lowe ejection fraction
Reduced exercise capacity
Control of CO- HR increases (2)
via decreased vagal tone
Increased sympathetic tone
Control of CO- Contractility increases (2)
via increased sympathetic tone
alters inotropic state and shortens systole (more time for filling and increase stroke volume)
Control of CO- venous return increases
Via venoconstruction (alpha 1) and skeletal respiratory pumps Maintains preload
Control of CO- TPR falls (2)
due to arteriolar dilation in muscle, skin and heart
Reduces afterload
