Blood Pressure Flashcards
haemodynamics
arteries
under high pressure
recieve blood directly from heart
vol of blood = stressed volume (high pressure)
artery is folded when not stretched by blood
haemodynamics
arterioles
smallest branch of arteries
walls have extensive tonicallu active smooth muscle (always contracted)
maintains pressure for effective movement of blood
site of highest resistance to blood flow
resistance changed in response to: sympathetic nerves, circulating catecholamines and other vasoactive substances
extensively innervated by sympathietic adrenergic nerve fibres
alpha 1 adrenergic receptors on arterioles of several vascular beds e.g. skin and splanchnic vasculature
when activated receptors cause contraction/constriction of vascular smooth muscle = dec diameter of arteriole, inc resistance to blood flow
less common beta 2 adrenergic receptors in skeletal muscle arterioles dilate and relax
haemodynamics
capillaries
site of exchange, but not all perfused with blood - less than 25% at rest
controlled by dilation/constriction of arterioles (pre capillary sphincters in mesentry and brain)
regulated by sympathetic innveration of vascular smooth muscle and vasoactive metabolites produced in tissue e.g. angiotensin, bradykinin, histamine, nitric oxide
haemodynamics
venules and veins
walls contain much less elastic tissue than arteries
large capacitance - much more than arteries, capable of accepting/storing large volumes of blood
contain largest %of blood in CV system (unstessed volume)
smooth muscle in walls innervated by sympathetic fibres - can constrict slightly
inc activity via alpha 1 adrenergic receptors - contraction to reduce capacitance - dec in unstressed volume
velocity of blood flow
blood vessels vary in diameter and cross sectional area = large effect on velocity and blood flow
in identical flow - inverse relationship between velocity and cross section area
V = Q/A
Q = flow ml/s
A = cross sectional area cm2
V = velocity cm/s
blood flow determined by…
pressure difference between inlet and outlet, resistance of vessel to blood flow
total peripheral resistance TPR
resistance of entire systemic vasculature
resistance in single organ can be calculated by substituting e.g. renal flow for flow
resistance to blod flow (Poiseuille’s law)
blood vessels and blood offer resistance to flow, factors involved: blood vessel diameter, vessel length, series/parallel arrangement, blood viscosity
resistance to flow = directly proportional to vessel length and blood viscosity (haematocrit)
but indirectly proportional to 4th power of radius
R = 8nl/Pir4
vessel arrangment
series resistance (within organ) total resistance = sum of individual resistance pressure decrease through each sequential component largest decrease in pressure in arterioles - largest resistance: change in pressure = resistance x flow parallel resistance is less than any individual resistance = no loss of pressure
pressures in CVS
blood pressure varies throughout
decrease occurs as blood flows - as energy is consumed overcoming frictional resistance
aorta = high cardiac output and low compliance (highest of arteries)
healthy aorta = more compliant than old/damaged
pressure in arteries
remains high due to high elastic recoil
pressure in arterioles
dramatic fall due to high resistance to flow —> R = 8nl/Pir4
pressure in capillaries
frictional resistance to flow and filtration
pressure in venules and veins
high capacitance and low pressure
arterial pressure - systemic circulation
oscillations in arterial pressure reflect pulsatile activity of the heart
pulsatile
as heart ejects pulse from ventricles
diastolic pressure
lowest arterial pressure during ventricular relaxation
systolic pressure
highest arterial pressure in arteries after blood ejected from ventricle during systole
dicrotic notch
incisura
blip when aortic valve closes - brief period of retrograde backflow
pulse pressure =
systolic - diastolic
reflects blood volume ejected from left ventricle (stroke volume)
mean arterial pressure =
diastolic + 1/3 pulse pressure
average pressure in complete cardiac cycle
pressure changes throughout day
higher in day
lower at night
rapid regulation of blood pressure
baroreceptors - carotid and aortic sinuses in arteries
nucleus tractus solitarius receives info and directs changes in output of para/sympathetic nervous system via cardiovascular centres
CV centres in brainstem are in reticular formations of the medulla and lower pons
parasympathetic control
parasympathetic outflow via vagus nerve on SAN to decrease heart rate and reduce blood pressure
sympathetic control
has 4 components to elevate blood pressure
1 - SAN to increase heart rate
2 - cardiac muscle to increase contractility and stroke volume
3 - arterioles to produce vasoconstriction and increase total peripheral resistance
4 - veins to produce vasoconstriction and decrease unstressed volume
medium/long term control of arterial pressure
Pa
renin-angiotensin-aldosterone system (RAAS) regulates blood volume (hormonal control)
dec Pa —> dec renal perfusion pressure detected by kidney afferent arteriole mechanoreceptors
prorenin —> renin
angiotensinogen — angiotensin 1 —- angiotensin 2
angiotensin II
acts on adrenal cortex to synthesise and secrete aldosterone
inc Na reabsorption, stimulates Na-H exhange in kidney and reab Na and HCO3
acts on hypothalamus to increase thirst and ADHsecretion (inc water reab in collecting ducts)
vasoconstriction of arterioles to increase TPR
Pa = cardiac output x TPR
other regulatory mechanisms for blood pressure homeostasis
chemoreceptors for O2 in carotid and aortic sinus bodies - stimulates arteriole vasoconstriction
chemoreceptors of CO2 in brain - stimulates arteriole vasoconstriction
ADH (AVP): V1 receptors in vascular smooth muscle cells and V2 receptors in collecting dcuts of kidney
atrial natriuretic peptide (ANP): powerful vasodilator, inc diuresis, dec ciruclating volume
chronic hypertenison
densenitises baroreceptors
info from carotid sinus baroreceptors carried to brainstem (joins CN IX)
aortic arch info via CN X
in chronic hypertension baroreceptors reset = hypertension maintained not corrected
hypertension
dont experience nightime ‘blip’
small inc in blood pressure is associated with inc risk of mobility and mortality
if blood pressure is too high - puts strain on other vessels and organs
can lead to:
heart disease - damage on endothelium on coronary arteries
heart attack
strokes
treatments of hypertension
angiotensin-onverting enzyme inhibitors
angiotensin II receptor blockers - stop effects
diuretics - release water
beta blockers - block adrenaline effects
Ca channel blockers - reduces power of contractions
alpha agonists - reduce sympathetic outflow
