cardiovascular mechanics 3 Flashcards
describe the design of the circulation
in pul circulation blood is oxygenated and loses CO2
in systemic circulation it is pumped to the body
L and r ventricles - separate but coupled pumps ie same organ
the heart as a pump creates a pressure gradient, blood flow from high - low pressure
flow to capillaries for a short diffusion distance
structure of artery
3 layers of muscle: adventitia, media, intima
capillary structure
small, thin wall, largest SA
venuole and vein structure
less muscular, valve for unidirectional flow
pressue through bv
drop in arterioles
small decline in capillaries
proportion of systemic blood in vessel
related to pressure in bv
and compliance
more in veins - capitance vessel - can decrease blood storage I n times of stress
why dos blood flow
follows the pressure difference - diffuses against the length of resistance tube
resistance can be altered to change blood perfusion
what is darcy’s law
pressure difference can change resistance
Q = flow of blood (volumetric flow)
R = resistance through capillaries
pressure difference = Q*R
haemodynamic determinants of blood pressure
MAP = CO - R
MAP stays constant, blood flow modulated by R
assumptions for relationship for CO, MAP and R
steady flow of blood
rigid vessels
R atrial pressure negligible
describe the pressure in the circulation
drops in arterioles
pressure difference allow flow through capillaries
pressure is built up again in pulmonary circulation
describe the resistance to blood flow
depends on viscosity, length of tube, radius
viscosity and length constant
R = 1/R(power of 4)
half radius - decrease flow 16x
when does viscosity change
pathophysiology
climb mountain
describe distribution of blood flow to organ
at rest CO = 5L/min exercise CO= 15L/min change flow by innervating vascular beds increase heart rate decrease storage in veins blood to skeletal muscle
what is lamina flow
blood flow in linear motion
velocity constant at any 1 point and flows in layers
fastest near centre of lumen
slow near walls - resistance when blood cells hit the wall (adhesive forces with the wall)
turbulent flow
flow erratically
form eddys
prone to pooling
pathophysiological changes to endothelial lining of BV
describe blood flow and shear stress
adhesive forces between fluid and surface
draw parabolic velocity profile - draw tangent, gradient of vel profile is the shear rate
shear rate * viscosity is the shear stress
describe lamina shear stress
high sheer stress
promote endothelial survival and quiescence
cells aligned in direction of flow
secretion promote vasodilation and anticoagulation (secretions are important in the coagulation cascade)
describe disturbed shear stress
low shear stress
promote endothelial proliferation, apoptosis and shape change
secretions promote vasoconstriction, coagulation and platelet aggregation - not good, clotting occludes bv
change in shear stress to disturbed is age related in branch near carotid arteries
how is bp measured
cuff occlude arterial pressure at 130mmHg
won’t hear anything
decrease to 120mmHg - hear terbulant because partially occluded - taps every heart beat
decrease occlusion more - vessel completely open
diastolic pressure - lamina flow - disappearance of sound
calculation for MAP (mean arterial pressure)
MAP = DBP +1/3PP(pulse pressure)
why is there a difference in aortic and ventricular pressure
aortic valve close - aortic pressure fall slowly, ventricular pressure fall rapidly
explained by elasticity of aorta - and large arteries which buffer the change in pulse pressure
elasticity of a vessel related to compliance
describe the wind kessel effect
water out of tube is pulsatile - add balloon (representative of elastic aorta) flow is less pulsatile
push still pulsatile - flow sustained because expanded aorta - maintain diastolic pressure
describe arterial compliance and pulse pressure
blood enter aorta faster than leaves them - 40% SV stored by elastic arteries
recoil of arteries pressure fall slow - diastolic flow
if compliance decreases eg become stiffer with age the windkessel effect is reduced - pulse pressure increases
describe the effect of pressure on vessel walls
transmural pressure causes tension that can be described by law of Laplace
T=P*R
Transmural pressure increases because blood flows through vessel cause persistent high circumferential stress = vessel distention
circumferential stress=tension/wall thickness
describe aneurysms
vessel walls weaken - balloon like distension
pathological law of Laplace
aneurysm increase radius - for same internal pressure - inward force must also increase
if fibres weak - force needed cannot be produced - aneurysm expand until ruptured
same process for formation of diverticuli in gut - pocket form so gut can contract less
cure for aneurysm - surgery - put mesh around to maintain vessel continuity
ecophysiological and cardiological ways to detect them
what is compliance and what does it depend on
the relationship between transmural pressure and vessel volume
depend on elasticity
compare venous and arterial compliance
venous 10-20x higher at low pressure
store more blood
how do you change volume stored in veins
increase smooth muscle contraction and synthetic drive, decrease radius, increase pressure
small changes distend veins - increase volume stored in them
how does gravity affect blood flow
different transmural pressure in different body parts
the extend that gravity increases the increases hydrostatic pressure varies with height - approx. 100mmHg
standing increase hydrostatic pressure in legs as a result of gravity
blood transiently pool in veins - high compliance - without compensation this reduced CO and blood pressure - hypotension - faint (syncope)
mechanisms to cope with gravity
stimulate skeletal muscle pump - more blood returns to heart
valves for unidrirectional flow
respiratory pump - ease blood back to the heart as quickly as possible - diaphragm, intrathoracic pressure
what happens if you have incompetent valves
dilated superficial veins in the leg, pool of blood in legs - varicose veins
what happens with prolonged elevation of venous pressure
oedema
even with intact compensatory mechanisms
