P: Arterial blood pressure Flashcards
Determinants of mean arterial pressure:
- Rate of inflow (Qh) of blood into arteries during ventricular systole
- Rate of outflow (Qr) through arterioles into capillaries.
- Qh > Qr = MAP increases
- Qh < Qr = MAP decreases
- Increases in CO or peripheral resistance increases MAP
- Compliance of arteries: rigid arteries increase MAP, elastic arteries decreases rate of MAP increase
Where is resistance to blood flow the greatest?
In arterioles and capillaries, due to narrow diameter.
Total peripheral resistance:
Resistance to blood flow through entire arteriolar system –> determines rate of blood flow out of arterial system.
Mean arterial pressure equation
cardiac output x total peripheral resistance.
How stroke volume determines pulse pressure:
- During ventricular ejection, arterial blood volume increases to V2
- Blood pressure increases to P2
- During diastole, peripheral runoff reduces volume to V1 and pressure to P1.
(V2-V1) = (P2-P1) = pulse pressure
Why do lower compliant arteries have higher blood pressure?
- Ejected blood exerts higher pressure on rigid walls than elastic walls
- Ps (systolic pressure) is increased in rigid arteries so pulse pressure also increases
- Aortic compliance decreases with age, Ps and pulse pressure increase as we age
- Compliance with SV is a determinant of pulse pressure.
To measure systolic + diastolic pressure:
- Inflatable cuff & sphygmomanometer measures systolic + diastolic pressure
- Cuff placed over brachial artery
- As cuff is inflated, it exerts increasing inwards pressure on artery
- When cuff pressure > systolic pressure, artery is entirely closed and blood flow stops.
- Cuff pressure is slowly dropped, and artery partially opens
- Blood flow restarts in turbulent fashion through pinched artery
- Causes thumping noise (Korotkoff sounds) which can be detected with stethoscope placed on artery
- When cuff pressure < diastolic pressure, artery is fully open, blood flow is smooth and Korotkoff sounds disappear.
Vascular smooth muscle structure
- No sarcomeres, so not striated
- Filaments form lattice structure around cell periphery
- Long thin filaments attach to cytoplasmic structures - dense bodies
- Smooth muscle contraction dependent mostly on inward diffusion of extracellular Ca2+ through voltage-gated Ca2+ channels
- Calmodulin acts as a Ca2+ sensor –> Ca2+/calmodulin complex binds and activates myosin light chain kinase
Intrinsic control of resistance:
- Vascular smooth muscle undergoes myogenic regulation
- Rapid increase in blood pressure induces reflex contraction of arterioles
- Rapid decrease in blood pressure induces -reflex dilation of arterioles
- Constant blood flow is maintained
Absence of myogenic regulation examples:
- Increase capillary blood pressure: hydrostatic pressure
- Elevated hydrostatic pressure increases capillary filtration causing fluid accumulation in feet and lower legs.
Endothelial-mediated regulation
- Endothelium also releases substances that trigger contraction/ relaxation of VSM
- Increased blood flow causes shear stress to endothelium & induces releases release of nitric oxide (synthesised from L-arginine)
- NO diffuses into VSM cells and activates guanylyl cyclase which increases intracellular [cGMP] –> decreases intracellular calcium in VSM, inducing dilation of blood vessels.
Extrinsic control of peripheral blood flow:
- Post-ganglionic sympathetic nerves innervate VSM of arterioles and veins
- Increased nerve activity mostly causes vasoconstriction while a decrease induces vasodilation.
- Noradrenaline binds to a-adrenergic receptors on VSM cells inducing vasoconstriction
- Adrenaline binds to B2-adrenergic receptors on VSM cells in skeletal blood vessels, inducing vasodilation.
alpha-adrenergic receptors:
- Activate phospholipase C which produces 2nd messengers which increase intracellular calcium
- Results in contraction
B2-adrenergic receptors
Activates adenylate cyclase, increasing [cAMP]I, which inhibits MLCK.
Sympathetic nerve stimulation:
- Reduces blood flow into tissues by constriction of arterioles
- Decreases tissue blood volume by constriction of venules
- Increase in movement of blood towards heart (venous return)
- Redistribution of blood from venous into arterial system
- Reduces capillary hydrostatic pressure.
-Absorption of interstitial fluid into capillaries increases.
Vasomotor centre:
- Located in reticular substance of medulla and lower 1/3 of the Pons
- Transmits impulses via vagus nerve to heart and sympathetic impulses via spinal cord and peripheral sympathetic nerves to heart and arteries, arterioles and veins.
Rostral Ventrolateral medulla (RVLM)
- Stimulates sympathetic nerve activity
- Neurons here send fibres to spinal cord which excite pre-ganglionic neurons of sympathetic nervous system
- Maintains both sympathetic cardiac & vasoconstrictor tone
- Stimulation of RVLM increases BP and HR
Caudal Ventrolateral medulla (CVLM)
- Fibres from these neurons project to RVLM and inhibit its activity, causing vasodilation.
- Depressor region
- Vasodilator area
Nucleus ambigus (NA, AMB) and dorsal motor nucleus of vagus (DMV)
- Origin of vagal projections to the heart
- Vagal centre.
Nucleus of tractus solitarius (NTS)
- NTS receives sensory nerve signals from circulatory system mainly through vagus and glossopharyngeal nerves
- These nerves in turn are stimulated by baroreceptors and cardiopulmonary receptors
- NTS sends output to NA and CVLM
- Stimulation of NTS reduces sympathetic outflow and increases vagal outflow.
NTS in medulla receives sensory impulses from:
- Baroreceptors
- Cardiopulmonary receptors
- Chemoreceptors
- Other brain regions
How are sudden changes in blood pressure detected?
- Stretch-sensitive mechanoreceptors (baroreceptors) are located in walls of carotid artery and aortic arch
- An increase in blood pressure causes the walls of these blood vessels to stretch
- Baroreceptors become more active in response
How do arterial baroreceptors work?
- Stretch receptors located in carotid sinuses and aortic arch
- Afferent pathways: Carotid sinus nerve, glossopharyngeal nerve, NTS, vagus nerve
- Collectively known as Buffer nerves, cause abrupt changes in BP
Sudden reduction in blood pressure causes sympathetic nerve activity to increase and causes:
- Increase cardiac output by increasing heart rate + stroke volume
- Contract venous smooth muscle, promoting venous return
- Stimulate contraction of arterial smooth muscle to increase peripheral resistance
- Vasoconstriction in kidney arterioles also minimises urine formation