Reflex, hormonal and local blood flow regulation Flashcards
how does blood flow
it flows form a high pressure are to a low pressure area
overall blood flow in adults
around 5000mL/min (cardiac output)
functions of circulatory system
deliver blood to organs deliver oxygen and nutrients removal of CO2 maintenance of ion concentrations delivery of hormones around of body
what is the circulatory system consisted of
a pump - the heart, when it contracts it creates the pressure needed
collecting tubes - veins have low pressure and high volume
extensive system thin vessels - capillaries
how is the circulatory divided (3)
arterial system - from heart to tissues
venous system - from tissues to heart
microcirculation - exchange between tissues
hemodynamics
velocity, pressure, flow, resistance, dimensions of components of systemic circulation
all applied to blood flow
vessels are not rigid tubes
blood changes due to viscosity
arterial blood pressure
development and maintenance adequate to perfuse tissues is base requirement for survival
formula for mean arterial blood pressure
MABP = Cardiac Output (CO) x Total peripheral resistance (TPR)
formula for cardiac output
CO = Heart rate (HR) x Stroke Volume (SV)
formula for flow
Q = Velocity (V) x Cross sectional area (A)
measure of volume per unit of time
Darcy’s Law
Q = Pressure differential / Resistance (R)
Largest cross sectional area
in small capillaries (2500 cm2)
each have a small cross sectional area but there is a lot of them
they decrease the velocity of blood flow
how does the velocity of blood change in relationship with the cross sectional area
as area increases, the velocity decreases
this is due to the extensibility of arteries
resistance is greatest in small vessels
velocity lowest in capillaries to promote exchange
what is shear stress
as blood flows though a blood vessel, it exerts a force on the vessel wall parallel to the wall
is directly proportional to flow rate and viscosity
poiseuille’s law
governs the flow of fluid through cylindrical tubes
steady laminar flow
blood viscosity does not remain constant
poiseuille’s law formula
Q = [pi(Pi-Po)r^4]/8nl
Pi-Po - pressure gradient form the inlet (i) of the tube to the outlet (o)
r - radius of the tube
n - viscosity of the fluid
l length of tube
resistance to blood flow
it is directly proportional to the length of the vessel and viscosity of blood
R= Ln/r^4
Total peripheral resistance (TPR)
sum of all vascular resistance within systemic circulation
how are the arteries supplying blood to organs arranged
in parallel
what is the advantage of the organs not being downstream from another
changes in resistance in one organ directly affect blood flow in only that organ
what alters resistance
contraction of the smooth muscle in the vessel wall
local tissue factors
what is functional/active hyperaemia
increase in organ blood flow associated with increased metabolic activity of an organ or tissue
when cells are active they use more oxygen and fuel
the by-products of metabolism
vasodilators that increase the blood flow: CO2, H+, K+, lactate, adenosine
how does blood flow change in relationship with O2
as O2 consumption increases so does the blood flow
why does reactive hyperaemia occur
occurs due to tissue hypoxia and a build up of vasodilator metabolites to dilate arterioles and decrease vascular resistance
flow is elevated as a result
when does reactive hyperaemia occur
after cessation of blood flow
e.g. after myocardial infarction or stroke
what happens to the tissues in reactive hyperaemia
tissues become reoxygenated and vasodilator metabolites are washed out
the resistance vessels regain normal vascular tone, flow returns to control
what happens to blood flow during reactive hyperaemia
blood flow goes beyond the nasal level (the original level), reaches a peak, and then returns to the basal level due to the washing out of vasodilator metabolites
period of occlusion
induces greater metabolic stimulus for vasodilation
increases in peak and duration of reactive hyperaemia
what controls the innvervation
the autonomic nervous system via the sympathetic and the parasympathetic tone
effect of sympathetic and parasympathetic nervous systems in heart
sympathetic: accelerates heart
parasympathetic: inhibits heart
together: balance
what fires nerve innervation
changes in body fluid volumes - changes in blood volume
the sympathetic innervation consists in
vasoconstriction (alpha-adrenergic stimulation) of vascular smooth muscle
skeletal muscle vasodilation (beta-adrenergic and cholinergic simp. stimulation releasing Ach)
why does the heart accelerates in symp. innveration
SA node is accelerated and increases the contractility due to the beta-adrenergic stimulation
why does the Mean Arterial Pressure (MAP) increases
increased TPR and CO
parasympathetic innervation functions
vasodilator of vascular smooth muscle (few organs)
slows heart rate
less involved in changing TPR
the deceleration of the heart rate is due to
the deceleration of SA node and decreased atrial contractility due to action of muscarinic receptors
what are muscarinic receptors
where Ach from the parasympathetic nervous systems reacts
what can signal the innervation
baroreceptors and chemoreceptors
what are baroreceptors
receptors that respond to vascular stretch
location of baroreceptors
carotid sinus and aortic arch
functions of baroreceptors
vasodilation
restoration of BP to lower level - increased BP leads to parasympathetic stimulation (vagal and glossopharyngeal nerves)
what are chemoreceptors
receptors that respond to chemical signals, changes in pO2, pCO2, pH
where are chemoreceptors located
carotid sinus and aortic arch
where do chemoreceptors act
respiratory centres and vasomotor regions
hormones involved in vasoconstriction
adrenalin, angiotensin II, vasopressin
hormones involved in vasodilation
atrial natriuretic factor, kallikrein-kinin system
action of vasocontriction hormones
increase cardiac output by increasing the heart rate and force heart contractions
cause vasoconstriction of arterioles and veins in the skin and abdominal organs
action of vasodilation hormones
lowers blood pressure by causing vasodilation and by promoting the loss of salts and water in the urine, which reduces blood volume
paracrine agents
Nitric oxide (NO) and Endothelin (ET-1)
action of NO
endothelium derived relaxing factor
- released from endothelium
- vasodilator
- anti-proliferative, anti-thrombotic
- impairment of NO -> thrombus that can lead to stroke
action of ET-1
- released from endothelium
- most potent vasoconstrictor
- release stimulated by Ang II, hypoxia, sheer stress, catecholamines
