Regulation of Arterial Blood Pressure Flashcards
What is haemodynamics?
Principles governing blood flow in cardiovascular system
What is diastolic pressure?
Lowest arterial pressure during a cardiac cycle
= arterial pressure during ventricular relaxation (when no blood is being ejected from LV)
What is systolic pressure?
Highest arterial pressure during a cardiac cycle
= arterial pressure after blood ejected from the LV in systole
What is the name of the ‘blip’ in arterial pressure shown here?
Dicrotic notch
Cause of the dicrotic notch?
Closure of aortic valve = brief retrogate flow from aorta to valve (brief dec in aortic press below systolic press)
What is pulse pressure?
-Difference between systolic & diastolic press
-All other factors equal - size of pulse press shows vol of blood ejected from LV in 1 beat/SV
What is mean arterial pressure (Pa/MAP)?
Avg press over 1 cardiac cycle
How is mean arterial pressure calculated?
-DP = diastolic pressure
-(where pulse pressure = diff between diastolic & systolic pressures)
Normal range of mean arterial pressure?
70-100 mmHg
How do systolic, mean arterial & diastolic pressures change with increasing age?
-Dec compliance of arterial walls = inc pulse pressure - BUT same SV = causes inc.s in both systolic & diastolic pressures
Which takes up a larger fraction of the cardiac cycle - diastole or systole?
Diastole (which is why mean arterial pressure puts more weight on diastolic press than systolic)
What are the 2 factors that determine blood flow through a blood vessel or SERIES of blood vessels?
-Pressure difference between the 2 ends of the vessel
-Resistance of the vessel to blood flow
What is an equation that expresses the 2 factors affecting blood flow through blood vessels?
Q = ΔP/R (no need to memorise!)
-Q is blood flow (ml/min)
-ΔP is pressure difference (mm Hg)
-R is resistance (mm Hg/ml/min)
What can be said about 2 values in Q = ΔP/R that are proportional & 2 that aren’t?
-Blood flow (Q) = directly proportional to pressure gradient (ΔP)
–> blood flow direction determined by direction of press grad (blood flows LV -> aorta in vent ej & not other way as press higher in v than aorta)
-Blood flow = inversely proportional to resistance
–> increasing R reduces Q (vice versa)
What is total peripheral resistance (TPR) aka systemic vascular resistance (SVR)?
Resistance of entire systemic vasculature
-Changes in TPR can alter CO
CO = ΔP/R
–> shows inversely proportional relationship between CO & TPR
What is resistance on a smaller scale than TPR?
Resistance in a single organ (same flow, pressure, resistance relationship as TPR - i.e., Q = ΔP/R
How to measure total peripheral resistance?
Relationship between TPR, CO & Pa?
If TPR doubles, CO is almost halved & Pa will increase modestly
What drives blood flow to tissues?
Diffs in pressure between arterial & venous sides of circulation
-So is driven by mean arterial pressure
What are the 2 ways in which resistance can be arranged in the cardiovascular system?
-Series resistance
-Parallel resistance
What is series resistance & how is it calculated?
Arrangement of blood vs WITHIN each organ:
-Supplied w/ blood by major artery & drained by major vein
-In organ blood flows from major artery, smaller arteries, arterioles, capillaries, venules, veins
Arrangement of blood vessels in an organ
R total = R artery + R arterioles + R capillaries + R venules + R vein
What is parallel resistance & how is it calculated?
-Distribution of blood flow AMONG major arteries branching off aorta
-Distribution of blood (on % basis) among organ systems - CO blood via aorta for simultaneous blood flow through each of the circulations (e.g., renal, cerebral…) then venous effluent collects & returns via vena cava
-Pressure in major artery serving each organ is equal to Pa
-Blood flow to each organ = independently regulated by altering resistance of its arteries (via local control mechanisms)
–> so blood flow through each organ = fraction of total blood flow
If each individual resistance = 10, what is the total parallel resistance of 4 blood vessels?
= 2.5
(1/10 + 1/10 + 1/10 + 1/10 = 0.4 –> 1/R total)
1/0.4 = 2.5
Features of parallel arrangement of arteries - in terms of pressure?
-No loss of pressure in major arteries
–> so pressure in each artery is same as in aorta
-Inc in one ind vessel = inc total resistance
—> if 1 blood v is occluded (blocked) then total parallel resistance = infinite (1/R total = 1/10 + 1/10 + 1/10 + 1/∞)
-Problem e.g., in cerebral circulation = not affect other circulations - are independent/separate
What factors* determine the resistance of a blood vessel to blood flow?
(Poiseuille equation)
R = πL/r4 x 8/π (just understand)
-R = resistance
-π = viscosity* of blood
-L = length* of blood v
-r = radius* of blood v
(when radius dec = resistance inc e.g., halved radius = 16 fold inc in resistance (2x2x2x2)
R = 1/r(to power 4)
How should blood flow in the cardiovascular system?
Laminar flow
What is laminar flow of blood?
When is smooth parabolic profile (think ‘U’ shape on graph) of velocity in a blood vessel
-Velocity highest in centre & lowest towards vessel walls
-Parabolic profile = develops as layer of blood next to v wall adheres to wall & essentially doesn’t move
–> each successive layer of blood towards centre moves faster & adheres less to adjacent layers
-Velocity @ v wall = 0
-Velocity @ v centre = max
(a diff type of flow = turbulent flow)
When does turbulent blood flow occur & what does it involve?
-When get irregularity in blood v = disrupts laminar stream
-Radial & axial mixed stream - so NO parabolic (‘U’ shaped) profile
Compare sound of laminar vs turbulent blood flow?
Laminar = silent
Turbulent = audible
What is Reynolds number?
Used to predict if blood flow will be laminar or turbulent
What does Reynolds number consider?
NR =Reynolds number
ρ=Density of blood
d=Diameter of blood vessel
v=Velocity of blood flow
η=Viscosity of blood
When will blood flow be laminar or turbulent according to Reynolds number?
-Laminar = Reynolds number is less than 2000
-Turbulent = Reynolds number more than 2000
What features of Reynolds equation will increase Reynolds number?
-Decrease in viscosity
-Narrowing blood vessel/diameter (causes… change in velocity below)
-Increase in velocity
–> dependence of velocity is more powerful than diameter on Reynolds number
A man suffers a stroke caused by partial occlusion of his left internal carotid artery. An evaluation of the carotid artery using MRI shows a 50% reduction in its radius. Assuming that blood flow through the left internal carotid artery was 400 ml/min prior to the occlusion,
-How much would resistance increase with 50% occlusion of the artery?
-What is blood flow through the artery after the occlusion?
-Halved radius = resistance inc 16 fold (Poiseuille equation: R = πL/r4 x 8/p - i.e.,
R ∞ 1/r to power4)
-Blood flow = inversely proportional to resistance (Q = ΔP/R)
–> resistance inc 16 fold so blood flow will DEC 16 fold: 400/16 = 25 ml/min
OR 1/16 x 100 = 6.25%
What are the 2 methods that act to restore Pa if it deviates from its set-point?
-Baroreceptor reflex
-Renin–angiotensin II–aldosterone system
Compare the baroreceptor reflex & the renin–angiotensin II–aldosteronesystem (as methods to restore Pa to set-point)?
-Baroreceptor reflex = faster (as is a reflex)
-Renin–angiotensin II–aldosteronesystem = slower (as is hormonally mediated)
Outline the baroreceptor reflex for an increase in arterial pressure.
-Inc in arterial pressure (Pa)
= inc stretch on barorecs in carotid sinus & aortic arch:
-Info from carotid sinus barorecs - carried to brain stem on carotid sinus nerve - joins glossopharyngeal nerve (cranial nerve 9/CN 9)
-Info from aortic arch barorecs - carried to brain stem on vagus nerve (CN 10)
= inc firing rate in carotid sinus nerve (gloss) & afferent fibres in vagus
-CN9 & CN10 enter vasoconstrictor centre - C1 in upper medulla & lower pons (nucleus tractus solitarius) - where gloss & vagus nerve fibres synapse & transmit BP info
-Signals sent out - to cardiac decelerator - to inc parasymp outflow to heart & also signals to dec symp outflow to heart & blood vs
-Efferent nerves leave cardiac decelerator centre –> travel in vagus nerve to heart - synapse on SAN
= dec firing of SAN = dec HR, dec conduction velocity through AVN, dec contractility - dec SV, ej fraction –> eventually dec BP
–> dec HR & cardiac contractility together dec CO (Pa = CO x TPR) = will dec Pa
(cardiac accelerator centres/symp = inhibited - so dec rate of vasomotor/cardiac accelerator impulses = affects tone of blood vs - allows vasodilation - dec TPR of = dec resistance R
Dec CO & R = increases Pa - returns to normal
Outline the baroreceptor reflex for a decrease in arterial pressure.
-Dec in arterial pressure (Pa)
= dec stretch on barorecs in carotid sinus & aortic arch
-Info from carotid sinus barorecs - carried to brain stem on carotid sinus nerve - joins glossopharyngeal nerve (cranial nerve 9/CN 9)
-Info from aortic arch barorecs - carried to brain stem on vagus nerve (CN 10)
= dec firing rate in carotid sinus nerve (gloss) & afferent fibres in vagus
-CN9 & CN10 enter vasoconstrictor centre - C1 in upper medulla & lower pons (nucleus tractus solitarius) - where gloss & vagus nerve fibres synapse & transmit BP info
-Signals sent out to cardiac accelerator centre to inc symp outflow to heart & also signals to dec parasymp outflow to heart & blood vs
-Efferent nerves leave cardiac accelerator centre
–> travel to spinal cord - synapse in spinal cord, in symp ganglia
-Then travel to heart - synapse on SAN
= inc firing of SAN = inc HR, inc conduction velocity through AVN, inc contractility - inc SV ej fraction –> eventually inc BP
–> inc HR & cardiac contractility together inc CO (Pa = CO x TPR) = will inc Pa
(cardiac decelerator centres/parasymp= inhibited - so dec rate of vasomotor/cardiac decelerator impulses = affects tone of blood vs - vasoconstriction —> inc resistance R)
Inc R & CO = returns Pa to normal (increases)
Summarise the baroreceptor reflex in response to haemorrhage.
(Haemorrhage = dec mean arterial pressure)
(MAP/Pa = BP)
-Pa dec= dec stretch on barorecs & dec firing rate of carotid sinus nerve
-Info received in nucleus tractus solitarius of medulla - produces coordinated decrease in parasymp activity to heart & inc symp activity to heart & blood vs
-Inc HR & contractility –> both inc CO
-There is inc constriction of arterioles = inc in TPR & inc constriction of veins = decreases unstressed vol
-Vein constriction = inc venous return = contributes to inc in CO (Frank-Starling mechanism)
Give all 3 responses to haemorrhage.
What are the implications of reduced Pa - in terms of damage to vital organs (secondary implications)?
-Relates to parallel vascular bed structure
–>
consequence of prolonged vasoconstriction = ischaemia
What is ischaemia (consequence of prolonged vasoconstriction)?
When have decreased BP/MAP/Pa (if bleeding e.g.,) - will get vasoconstriction - so redirect blood to most vital organs:
-Brain (NO vasoconstriction here)
-Heart (NO vasoconstriction here)
-Gut (v. little vasoconstriction here)
-Kidneys (little vasoconstriction here)
–> MOST vasoconstriction in skeletal muscles
Q = ΔP/R or F = ΔP/R
Why is a parallel vascular bed structure better than a series structure one?
Allows ability to prioritise blood low to certain organs/system based upon demand for O2 e.g., brain, heart… = why have varying % blood flows
(if not would all get same)
-Blood flow to vascular beds is arranged in parallel, the blood flow to each organ can be controlled separately by vasoconstriction of arterioles supplying each bed
Q = ΔP/R or F = ΔP/R
What is a carotid sinus massage (CSM)?
Firmly press bulb at top of 1 of carotid artery in neck
How does a carotid sinus massage work - science?
Get more parasymp effect (slowed SA firing)
What is the diving reflex?
-When cold water stimulates sensory recs of trigeminal nerve & recs in nasopharynx & oropharynx
-Body is expecting a period of submersion - responds to conserve the limited O2 supply & to divert it to heart & brain
Explain the processes behind the Valsalva manoeuvre?
1 = Inc intrathoracic pressure = inc blood flow from pulmonary circulation into LA = inc LV EDV & SV & is compression of aorta = inc BP
2 = High intrathoracic press = slows venous return = dec SV & so dec BP
During this - is barorec-mediated inc in HR
3 = Manoeuvre released - aorta compression stopped - LV filling pressures is reduced temporarily - as pulmonary vessels re-expand = causes BP dec
4 = VR restored - incs cardiac filling pressures & SV
This incs BP - get barorec reflex-mediated bradycardia & subsequent BP dec to normal levels
(Inc pressure = get bradycardia, dec pressure =
What is the modified Valsalva manoeuvre?
-Do normal Valsalva manoeuvre
-Then lay back with legs up
-Then sit back up
S = Strain (just enough to make the plunger of a 10cc syringe move, equal to 40mmHg)
V = Venous return (supine with passive leg raise)
T = Time (15s at each stage)
Recap the 3 responses to haemorrhage.
Give the stages of the Renin-angiotensin II-aldosterone system (RAAS) - to increase Pa.
Dec Pa - activates RAAS - causes:
-Dec in renal perfusion pressure
–> causes renin release into plasma from JG cells
-Renin catalyses conversion of plasma angiotensinogen to angiotensin I
-Angiotensin I - converted to angiotensin II in lungs & kidneys by ACE
-Angiotensin II = agonist @ AT1 recs (a GPCR) - on many tissues
–>
*On arterioles = vasoconstriction
*On adrenal cortex (zona glomerulosa) = induces aldosterone release
-Aldosterone acts on DCT tubular cells - incs expression of ENaCs on apical memb & Na+ pump on basolateral memb
*On proximal convoluted tubules = stimulates inc Na+, H+ exchange - incs Na+ reabsorption
*On CNS = stimulates hypothalamus to inc thirst & so H2O uptake, AND, pituitary gland to release ADH - decs H2O loss (more water reabsorbed), as upregulates aquaporins in CD of kidney
-BP (inc Pa) incs as:
*have increased TPR (resistance - as diameter dec due to vasoconstriction) = inc BP
*increased Na+ reabsorption = inc ECF vol & blood vol = inc venous return & CO (due to inc blood vol - Frank Sterling relationship) = inc BP
*increased H2O retention = inc body fluid
(ignore 5th branch where ACE2 is!)
Give the process of stages of peripheral chemoreceptors.
-Dec arterial PO2
= increased afferent nerves firing rate from carotid & aortic bodies
= activates sympathetic vasoconstrictor centres
–>
*Causes arteriolar vasoconstriction in skeletal muscle, renal, and splanchnic vascular beds
*Inc parasymp outflow to heart = !transient!dec in HR
(transient slowing of HR as peripheral chemorecs = primarily control breathing)
-PO2 dec also = inc ventilation = decreases parasympathetic outflow to heart = increases HR (lung inflation reflex)
Give the processes of stages of central chemoreceptors.
-PCO2 or pH changes = stimulate medullary chemorecs:
-If brain becomes ischemic (decreased cerebral blood flow) cerebral PCO2rapidly incs & pH decs
-Medullary chemorecs detect these change - cause:
*inc in symp outflow to THE blood vs = arteriolar vasoconstriction in many vascular beds & an inc TPR
-Blood flow = redirected to brain to maintain its perfusion
–> Vasoconstriction = incs Pa dramatically (even to life-threatening levels)
What is ADH secreted by?
Posterior lobe of pituitary gland
What is the basic role of ADH?
Regulates body fluid osmolarity & participates in regulating arterial BP
What are the 2 types of receptor for ADH?
V1 and V2
Where are the 2 types of ADH receptors (V1 & V2) found?
V1 = in vascular smooth muscle
V2 = in principal cells of the renal collecting ducts
What do V1 receptors for ADH cause?
Vasoconstriction of arterioles & increased TPR
What are V2 receptors for ADH involved in?
Water reabsorption in collecting ducts & maintaining body fluid osmolarity
What are the 2 types of stimuli that increases ADH secretion by posterior pituitary?
-Increased serum osmolarity
-Decreased blood vol & BP
