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factors that contribute to movement of blood
heart - primary source
gravity
skeletal muscle
diaphragm movements
elastic tissue in arteries
systolic blood pressure
max pressure exerted in arteries when blood ejects into them during systole
contracting phase
diastolic blood pressure
min pressure within arteries when heart relaxes
pulse pressure
measure of strength of pressure wave
systolic BP - diastolic BP
mean arterial pressure (MAP)
average pressure responsible for driving blood forward into tissue thruout cardiac cycle
MAP = diastolic + 1/3(pulse pressure)
what happens to pressure wave when moving to capillaries
loss of energy due to friction = pulse pressure reduced to 0 when reach capillaries
why is MAP important
essential for efficient function and life
low bp = dizziness, organ failure
high bp = stroke, aneurysm
what determines MAP
cardiac output (CO) - depends on stroke volume and heart rate
resistance of peripheral circulation (TPR)
MAP proportional to CO x TPR
hypertension
high blood pressure
hypotension
low blood pressure
regulation when mean arterial pressure gets low
increase cardiac output
constrict aterioles close to capillaries = increases resistance = heart increases pressure
which nervous system effects blood pressure
autonomic
SNS = raises
PNS = lowers
cardiac output
volume of blood pumped by 1 ventricle in given time
CO = heart rate x stroke volume
avg 5 L/min
stroke volume
amount of blood pumped by 1 ventricle during contraction
SV = end diastolic volume - end systolic volume
avg at rest = 135ml - 65ml = 70ml
venous return
volume of blood flowing back into right atrium per minute
determines how much blood we have in heart
end diastolic volume
volume in ventricle at end of diastole
determined by venous return
end systolic volume
volume of blood in ventricle
what determines stroke volume
venous return and contractility of ventricles
what affects venous return
respiratory pump - inhale decreases pressure near heart = draws blood up
skeletal muscle pump - skeletal muscle contract = compress deep veins = push blood up
blood volume
neural control - veins have alpha-1 receptors
what happens when blood volume decreases
venous return decreases > end diastolic volume decreases > lower stroke volume> lower cardiac output > lower arterial mean pressure
frank-starling law
stretch-force relationship
more blood in ventricle = stretches cardiac muscles closer to optimal length = stronger contraction force
modulation of stroke volume
by sympathetic nerves = causes myocytes to contract harder
what affects heart rate
changing rate of depolarisation of autorhythmic pacemaker cells - Ifunny current
how sympathetic modulates heart rate
changes ion permeability = depolarises = reach threshold sooner = faster heart rate
by noradrenaline in Beta-1 receptors\
increases action potentials = reduces conduction thru AV node
parasympathetic modulation of heart rate
changes ion permeability = hyperpolarises = longer to reach threshold = slower heart rate
by muscarinic receptors (Ach)
decreases action potentials = longer conduction thru AV node
how does control over cardiac output and total peripheral resistance differ
TPR = fluctates based on needs of local tissue
CO - autonomic system
when TPR adjusts ANS adjust CO to maintain constant arterial pressure
What happens to MAP when total peripheral resistance decreases
initially MAP decreases = SNS increase stroke volume and heart rate = increase cardiac output = MAP increases
what happens to MAP when standing
pooling of blood in legs = reduced venous return = reduced cardiac output = decreases MAP
regulate by increasing heart rate and SNS causes vasoconstriction = push blood to heart
short-term blood pressure regulation
second to second - predominately neural thru baroreceptor reflex
baroreflex
baroreceptors on carotid sinus (blood to brain) and aortic arch (blood to body)
when blood pressure increases = artery stretches = stimulates baroreceptors = sends signals to brain to adjust accordingly
how baroreflex controls blood pressure
change in blood pressure = baroreceptors detect change = sends info to medulla = corrrects changes thru SNS and ParaNS
BP down = decreased baroreceptor signals = increases SNS and decrease ParaNS
what does parasympathetic control in heart
chronotopy/heart rate and AV conduction time
what does sympathetic control in heart
ventricular contractility = change stroke volume thru beta-1 receptors
diameter of vessels thru alpha-1 receptors = increase TPR to increase MAP and increase venous return by constricting veins
long term blood pressure regulation
changing blood volume thru CO and TPR
CO thru regulating Na+ in extracelllular fluid via excretion in urine
TPR changes due to thickening arterial wall and high levels of vasoconstrictive hormones
low pressure baroreceptors
in right atrium = monitor change in pressure due to changes in blood volume
overview of what determines mean arterial pressure
Blood volume - determined by fluid intake/outake > regulated by kidneys
cardiac output - determined by heart rate and stroke volume
resistance to blood flow - determined by arteriole diameter
distribution of blood between arterys and veins - determined by vein diamter
stroke volume determined by heart contractility and end diastole volume
end diastole volume determined by venous pressure = affects blood volume
venous pressure determined by blood volume
vessel diamter determined by venous pressure redistributing blood
how does blood volume influence venous return
increased blood volume in veins = increases pressure = stretches veins = recoils = pushes blood to heart