Cardiovascular control 2 Flashcards
What determines venous return?
central venous pressure
What does venous return affect?
stroke volume and contractility by affecting the preload (Starling’s Law)
What does venoconstriction do?
reduce compliance, reduce venous return
What does arteriolar constriction do?
determines
- blood flow to downstream organs
- MAP
- pattern of blood flow to organs
How do intrinsic (local) mechanisms regulate blood flow?
closely related to smooth muscle
needed for REFLEX LOCAL BLOOD FLOW REGULATION IN ORGAN
What is autoregulation?
intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance
WITHOUT: fall in perfusion pressure causes fall in flow rate with passive constriction leading to increased resistance
WITH: resistance in vessels falls to allow flow to increase
it is a compensatory mechanism
What is the myogenic theory of autoregulation?
some smooth muscle fibres have stretch sensitive receptors and channels that respond to tension in the vessel wall
as pressure decreases, vessels dilate as muscle relaxes
What is the metabolic theory of autoregulation?
blood flow decreases
metabolites accumulate and vessel dilate with the aim of increasing flow to wash these away
How does injury affect autoregulation?
serotonin released from platelets and causes constriction
What is hormonal control of autoregulation?
local endothelium derived hormones also have an influence
What are 2 examples of autoregulators?
VASODILATORS
NO
- from arginine
- diffuse into vascular smooth muscle cells
PGI2 (prostacyclin) - cardioprotective
- antiplatelet/coagulative
- made from PGH2 prostaglandin precursor
What are 2 examples of autoregulators?
VASOCONSTRICTORS
TXA2
- from PGH2
- made heavily in platelets to amplify their activation
ET (endothelins)
- made from nucleus of endothelial cells
- has minor vasodilator effects
How do extrinsic mechanisms regulate blood flow?
these are mechanisms extrinsic to smooth muscle
consist of hormone regulation and autonomic nervous system
What are examples of circulating (non endothelium derived) hormones?
produced by glands elsewhere
- kinins - vasodilator (from cells of atria of heart)
- bind to receptors on endothelial cells
- stimulate NO synthesis - Atrial natriuretic peptide - secreted from atria in response to stretch
- vasodilator
- reduce BP - Vasopressin/ADH - secreted from posterior pituitary with high blood osmolality
- vasoconstrictor
- bind to VI smooth muscle receptors - Nor/adrenaline - from adrenal gland
- vasoconstriction - Angiotensin II - from renin-angiotensin-aldosterone axis
- vasoconstrictor
- stimulate SNS activity and ADH secretion
- produced via ACE (targeted by ACE inhibitors to lower BP)
How does the ANS influence flow?
PNS
- emerge from cranial and sacral spinal cord regions
- control heart rate
SNS
- emerge from thoracic and lumbar vertebra
- control circulation
Describe sympathetic innervation in the body?
SNS fibres innervate heart and all vessels except capillaries, pre-capillary sphincters and some meta-arterioles
Innervation is variable
- more to kidney/gut/spleen/skin
- poor to skeletal muscle and brain
What does noradrenaline do?
binds to alpha 1 receptors
cause smooth muscle contraction –> vasoconstriction
Describe the structure of the vasomotor centre in the brain?
- located bilaterally in reticular substance of medulla, lower third of pons
- made of vasoconstrictor (pressor) and vasodilator (depressor) regions + cardioregulatory inhibitory area + higher centres (anticipatory response when thinking about activity)
What does the VMC do?
transmits impulses distally through the spinal cord to almost all blood vessels
spinal cord modulated processes of ANS
- lateral areas control HR and contractility
- medial portion transmits signals via vagus nerve to the heart (generally decrease HR)
Describe nervous control of blood vessel diameter?
- vessels receive post ganglionic sympathetic nerve innervation with noradrenaline that maintains BASELINE VASCULAR TONE
- increased tonic activity –> vasoconstriction
- decreased tonic activity –> vasodilation
- no PNS innervation to vasculature
What other factors control blood vessel diameter in addition to sympathetic vasoconstrictor nerves?
circulating hormones loca controls (O2, CO2, K, H, osmolality, metabolites)
How is heart rate controlled?
P/SNS both innervate heart - achieve balance between them
There is always some level of tone down nerves supplying the heart so if one of P/SNS cut, other becomes dominant - if both are cut, intrinsic HR takes over (above normal)
How can HR be increased?
increase SNS
decrease PNS
increase plasma adrenaline levels
How can force of contraction be controlled?
- SNS stimulation
- PNS has no effect
- Starling’s Law
How does SNS stimulation increase contractility?
- NA binds to B1 adrenoceptors to increase cAMP
- cAMP activated PKA to phosphorylate LTCC, SERCA and SR Ca release channels
- More Ca influx, more Ca reuptake (more Ca delivered to myofilaments) therefore more Ca delivered to myofilaments
- HR and contractility altered
Where is baroreceptor VMC located?
medulla oblongata
LOCATION OF RECEPTORS:
SNS carotid sinus –> glossopharyngeal nerve –> MO
PNS aortic arch –> vagus nerve –> MO –> efferent to SAN
Describe the nature of BRs in carotid sinus and aortic arch?
both fire more with increased stretch
BRs in carotid sinus response to pressures between 60-180mmHg and is most sensitive from 90-100mmHg
How do baroreceptors work?
- response to changes in arterial pressue
- increase P increases firing
- stimulated PNS and inhibitory neurone that stimulated SNS arm to decrease SNS activity
What nerve type do vessels have?
only SNS efferents
capillaries have nothing
Describe the process of reciprocal innervation?
increase pressure in baroreceptors
increase activity in afferent nerve (cardioregulatory component of VMC in MO)
increase PNS activity via efferent vagus nerve to decrease HR
Decrease SNS activity to inhibit tonic activity by inhibitory interneuron
- decrease activity of SNS
- decrease HR at SAN –> vasoconstriction
How is a reflex controlled by the carotid sinus?
- Increase BP cause increase nerve activity in CS that is fed to VMC
- Build up of traffic in vagus nerve on PNS is increased to stimulate SAN and decrease HR
- RI = increase BR nerve activity causes decrease SNS activity in both aspects (cardiac and vasoconstrictor nerves) that leads to decrease activity in both leading to dilation and drop in HR –> decrease BP
How does ANS affect heart?
increase PNS –> more ACh produced in SAN to decrease gradient of pacemaker potential and decrease HR
decrease SNS activity –> decrease contractility and increase vessel radius
How to increase VR?
increase blood volume
increase SNS activation of veins
increase skeletal muscle pump
increase respiratory movements
Example of changes after a stabbing?
stab - partially severed femoral artery
haemorrhage
reduced blood V –> reduced venous pressure, VR and atrial pressure
reduced EDV, SV, CO and BP
baroreceptors feedback to increase SNS discharge to veins to increase venous constriction to increase venous pressure
