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
Sudden elevation in blood pressure stimulates vagus nerve activity which:
- Reduces cardiac output by slowing heart rate
- Inhibition of sympathetic nerve activity reduces cardiac output, causes relaxation of arterial smooth muscle to decrease peripheral resistance
- Kidneys stimulated to excrete more water as urine, reducing total blood volume.
Cardiopulmonary baroreceptor locations
atria, ventricles and pulmonary vessels
Cardiopulmonary baroreceptor functions (what does it mainly act on and how):
- Initiate reflex that lowers arterial blood pressure in response to changes in blood volume
- Mainly acts on kidneys to reduce blood volume by increasing urine output
- Done by reduction of sympathetic nerve activity to kidney, inhibition of release of angiotensin, aldosterone and vasopressin (antidiuretic hormones).
How do saline infusions increase heart rate?
- Increase blood volume increases atrial pressure causing rapid increase in HR
- Mediated by atrial stretch receptors that transmit afferent signals via vagus nerves to NTS
- Efferent signals are transmitted back through vagal and sympathetic nerves to increase heart rate and contractility
- Transfer of blood into arterial circulation
- Prevents damming of blood in veins, atria and pulmonary circulation.
Bainbridge reflex:
Increased blood volume increases atrial pressure, causing rapid increase in HR
How are bainbridge and baroreceptor reflexes antagonistic?
- Increase in blood volume = bainbdirge reflex predominates
- Blood volume decreases: baroreceptor reflex dominates
Chemoreceptor locations:
Central medulla and carotid sinuses & aortic arch
Chemoreceptor reflex
increase in heart rate is a secondary effect of an increase in ventilation.
Anterior hypothalamus function
decreases BP and HR
Posterior and lateral hypothalamus function:
- Alerting reaction
- Increased BP + HR, vasodilation in skeletal muscle
- Vasoconstriction in skin and splanchnic organs
Cerebral cortex
- Involved in motor functions
- Cause vasoconstriction of skin, splanchnic and renal vessels
- Vasodilation in skeletal muscles
