regulation of cardiovascular system Flashcards
Which 4 factors affect venous volume distribution?
- Peripheral Venous Tone
- Gravity
- Skeletal Muscle Pump
- Breathing
What determines the stroke volume?
The amount of blood returning to the heart
What is central venous pressure?
blood pressure in the vena cava, near the right atrium
What does central venous pressure determine?
The amount of blood flowing back to the heart
How is blood flow altered?
Mainly by the arterioles and changing vessel radius
What does the constriction of veins determine?
Its compliance and venous return
What does the constriction of arterioles determine?
Blood flow to the organs they serve, mean arterial blood pressure and the distribution of blood to organs
What is the extent of vascular constriction determined by?
By the pattern of organisation of innervation to particular vascular beds - the number of adrenoreceptors will affect the blood flow to an organ
What are the 3 ways of regulating blood flow?
- Local Mechanisms - intrinsic to the smooth muscle itself or closely associated
- Hormones
- Autonomic Nervous System - innervates arterioles and veins to produce constriction or dilation
Hormones and ANS are extrinsic and local is intrinsic
What is the primary function of extrinsic factors?
To regulate arterial blood pressure by altering systemic vascular resistance
What is autoregulation?
The intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance – this is an example of a local mechanism regulating blood flow
What would happen in the absence of autoregulation if blood pressure fell?
The resistance will increase and flow will decrease
What happens during autoregulation if pressure falls?
There will be a gradual decrease in resistance and hence a gradual increase in flow
What are the two theories suggesting how autoregulation occurs?
Myogenic Theory = smooth muscle fibres respond to stretch and as pressure rises, the muscle fibres start contracting to keep flow constant
Metabolic Theory = if the vessels supplying a particular vascular bed contract, the flow to the vascular bed decreases and the vascular bed produces more metabolites - as more metabolites are produced, it feeds back on the vessel that’s supplying the bed and causes vasodilation and hence allows more flow to the vascular bed and the metabolites which triggered this response are washed away
How can autoregulation be affected by injury?
When a vessel is injured, platelets aggregate and they release serotonin which is a powerful vasoconstrictor which will constrict the injured vessel
Give examples of substances released from the endothelium that can regulate blood flow
Nitric Oxide - vasodilation
Prostacyclin (vasodilator)
Thromboxane A2 (vasoconstrictor)
Endothelins - potent vasoconstrictors
Give examples of hormones that can affect blood flow
Kinins
- Have complex interactions with the Renin-Angiotensin System
- Tend to relax vascular smooth muscle
ANP (Atrial Natriuretic Peptide)
- Circulating peptides that are secreted from the cardiac atria
- As the atria stretch they release more ANP which causes vasodilation
Circulating Vasoconstrictors
- Vasopressin
- Angiotensin II
- Noradrenaline
What is the structure of parasympathetic nerved and what does this mean?
Have a long preganglionic fibre and a short postganglionic fibre - the parasympathetic ganglion will be right beside the sinoatrial node
What are the SNS and PNS important for (heart)?
Sympathetic - generally controls the flow
Parasympathetic - important in regulating heart rate
Which vessels have sympathetic innervation and which don’t?
They innervate all vessels except capillaries (and precapillary sphincters and some metarterioles)
Is the distribution of sympathetic nerves even and what does this mean?
No- more sympathetic nerve fibres innervate vessels supplying the kidney, gut, spleen and skin and fewer innervate the skeletal muscle and the brain so there is more potential to constrict the blood going to these places so that we can divert blood to the organs that we need more
Where does noradrenaline bind and what does it do?
To alpha 1 adrenergic receptors to cause constriction
Where does adrenaline bind and what does it do?
To smooth muscle beta-2-adrenoreceptors to cause vasodilation in some organs
However the effect is very concentration-dependent. At high concentrations, adrenaline can bind to alpha adrenoreceptors which can override the vasodilatory effects of the beta-2-adrenoreceptor stimulation and produce vasoconstriction
Where is the vasomotor centre located and what does it consist of?
Is located bilaterally in the reticular substance of the medulla and the lower third of the pons
The VMC consists of a:
- Vasoconstrictor Area (Pressor)
- Vasodilator Area (Depressor)
- Cardioregulatory Inhibitory Area
What can affect the VMC?
Higher centres in the brain (such as the hypothalamus) can exert excitatory and inhibitory effects on the VMC
What do different areas of the vasomotor centre do?
- Lateral Portions of the VMC controls heart activity by influencing heart rate and contractility
- Medial Portions of the VMC transmits signals via the vagus nerve to the heart that tends to decrease heart rate
- The VMC allows an anticipatory response to exercise: your heart rate and ventilation rate will go up slightly before exercise because of these higher sensors in the brain
How does the nervous system control blood vessel diameter?
- Blood vessels receive sympathetic postganglionic innervation
- The neurotransmitter involved is noradrenaline
- There is always some tonic activity
- If you increase the nerve traffic then you can constrict the vessel
- If you decrease the nerve traffic then you can dilate the vessel
- There is not much parasympathetic innervation of the vascular system
How is the heart rate controlled by the nervous system?
- The sinoatrial nodal cells receive sympathetic and parasympathetic innervation (dual)
- Normal resting heart rate is around 70 bpm
- Parasympathetic slows heart rate down because acetylcholine decreases the gradient of the pacemaker potential - this means that the potential takes longer to reach threshold and fire
- Sympathetic increases heart rate because adrenaline and noradrenaline increases the gradient of the pacemaker potential so threshold is reached more quickly
- With no innervation, the normal activity is around 100 bpm
How is the force of heart contraction controlled?
- Force of contraction can be increased by Starling’s Law
- Sympathetic activity will also increase the force of contraction
- Noradrenaline binds to adrenoreceptors which increases the amount of cAMP which activates PKA which phosphorylates the L-type calcium channels and the SR calcium release channel and SERCA
- So you get more calcium influx and more calcium taken back up into the stores
- Action of noradrenaline on beta-1-receptors in the heart will increase contraction
- Strength of contraction can not be changed by parasympathetic activity
How can stroke volume be controlled?
• Stroke volume can be increased by:
- Increased Sympathetic Activity
- Plasma Adrenaline
• Intrinsic control of stroke volume: venous return which sets the end-diastolic volume (stretch) which increases the force of contraction
• We can get more blood back to the heart if we increase respiratory movements - decreasing intrathoracic pressure helps the filling of the heart
When do rapid changes in respiratory movement, plasma adrenaline and increase in sympathetic activity occur?
During the fight/flight response
Where are baroreceptors located and where do they feed back and via what?
- Baroreceptors are in the aortic arch and in the carotid sinus (carotid bodies)
- Baroreceptors in the carotid bodies feedback to the vasomotor centre via the glossopharyngeal nerve
- The aortic arch baroreceptors feedback to the vasomotor centre via the vagus nerve
Baroreceptor activity
- Carotid sinus baroreceptors respond to pressure between 60 and 80 mmHg
- Baroreceptor response to changes in arterial pressure
- Baroreceptor reflex is most sensitive around 90-100 mmHg
What is reciprocal innervation?
- When the baroreceptor sees an increase in pressure it fires more - the nerve activity is increased which mediates an increase in parasympathetic nerve activity (down afferent nerve)
- Simultaneously the afferent nerves are connected to a series of inhibitory interneurones which are joined to the sympathetic nerves. This slows down the tonic activity so an increase in baroreceptor firing = decrease in sympathetic activity
Control of venous return:
1) More activity of sympathetic activity to vein -> higher venous pressure -> higher venous return -> higher atrial pressure
2) More skeletal pump activity -> more respiratory movement -> higher venous pressure -> higher venous return -> higher atrial pressure
Feedback for blood pressure control following a hemorrhage
Haemorrhage:
loss of blood volume -> reduced venous pressure and return to heart so atrial pressure decrease -> ventricular diastolic volume lower - > lower stroke volume, arterial pressure and CO
Baroreceptor feedback and reciprocal innervation -> more sympathetic activity -> more venous constriction and higher venous pressure
What happens following an increase in blood pressure?
- Nerve activity from the baroreceptors reflects a rise or fall in pressure
- Increased Blood Pressure = huge increase in firing activity throughout from the baroreceptor
- The increase in baroreceptor firing is fed back to the vasomotor centre which triggers increased traffic in the vagus nerve
- Increase in parasympathetic activity causes an increase in acetylcholine production in the SAN which decreases the gradient of the pacemaker potential and causes a decrease in heart rate
- Increase in baroreceptor activity also decreases the sympathetic nerve traffic which also brings about a decrease in heart rate
- Sympathetic cardiac nerves also have an effect on the force of contraction - so less innervation from sympathetic nerves leads to a decrease in the force of contraction
- Decrease in sympathetic activity also leads to an increase in vessel radius
- These changes in heart rate, contraction and dilation leads to a decrease in blood pressure
What is an equation relating MAP, CO and TPR
Mean Systemic Arterial Pressure = Cardiac Output x Total Peripheral Resistance
What factors should be considered when thinking about regulation of CVS system?
how can HR, SV and resistance be changed?
MAP= CO* TPR
CO= HR*SV
