Special Circulations Flashcards
the 2 circuation systems of the heart and what leads them?
- pulmonary = supply driven
- systemic = demand led
what side of the heart determines cardiac output
left side
describe the b supply associated with the lungs
- pulmonary artery are superior to the pulmonary veins
- lungs get their own b supply for metabolic needs via the bronchial circulation
what affects special circulations
-special tasks -adaptations -clinical problems
pressure of the RV and LV (systole and diastole)
RV= 15-30 systole
RA 0-8mmHg
LV=100-140mmHg systole
LA=1-10mmHg
why not same systolic pressure in ventricles and atria
b ventricles contract more than the atria (90% gravity)
pressure of Aorta and PA (systole and distale)
A= 100-140mmHg systole A = 60-90 mmHg diastole PA =15-30mmHg systole PA=4-12 mmHg diastole
why is the diastolic pressure the way it is in the aorta
because of the elastic recoil of the , aorta/arteries maintains the bp we have higher diastolic pressure in the aorta compared to the sudden drop in the ventricle
PA-
elastic recoil of the PA maintains that blood pressure
features of the Pcirculation
-lower resistance therefore shorter distance -lots of capillaries - arterioles have relatively little smooth muscle this helps keep lumen one and v resistance so b flow is more readily transported
adap
-very high densities of capillaries in the alveolar wall so large capillary surface area - short diffusion distance i.e capillaries close to alveoli 0.3microm so overall large SA and short distance
what must you match
ventilation and perfusion ratio
wats the V/Q rtion
- matching ventilation of alveoli with its perfusion -0.8
how do you maintain that V/Q ratio
by diverting blood from the alveoli which aren’t ventilated
how does this happen
-response to hypoxia;
hy
-hypoxic pulmonary vasoconstriction - constrict and lumen the of vessel of hypoxia present this optimises -differecne in csytemic sicruclation is vasodialtion
dis
-works well with mucus block -but chronic hypoxia can cause Right ventrciular failure - so if someones living in low altitude, then gt hypoxia wc c vasoconstriction wc increases resistance b RS failed b pressure ^ to try and pump b around the lung
emphysema
- ^ resistance of vessels in lungs so harder for RS to pump c RS ventricular failure
what are the vessels influenced by? what happens in the upright position? how does this work at different levels to the lungs?
-gravity -at upright position there’s greater hydrostatic pressure on vessels in the lower part of the lung -bv above the lung collapse due to the the lower hydrostatic pressure (wc is created by gravity) - below the lungs the vessels distend due to increased hydrostatic pressure (this pressure is due to the effect o gravity)
effect of exercise on pulmonary flow
- ^ exercise = ^ arterial bp so pulmonary arterial bp so the bv above the lungs (apical) are open instead of collapsing and this improves the V/Q ratio -also b flows better through the capillaries w/o impairing gas exchange (goes from 1 second for RBC to flow and undergo gas exchange to 0.3, without resulting in less gas exchange to occur, this is possible d to short diffusion distance and ^ capillaries)
formation of tissue fluid systemic
- Starling’s LAW ; it determines fluid formation , hydrostatic pressure (out) +oncotic pressure (plasma P draws fluid into capillaries) - fluid taken up by lymphatic
what is hydrostatic pressure affected more by?
-venous pressure (5x greater( than arterial pressure changes)
if venous pressure ^
^ hydrostatic pressure
peripheral oedema is seen with what pressure change
venous d more fluid moving out d^ hydrostatic pressure and lymphatic cant take it in
whats the hydrostatic pressure of lungs? and why less likely to form ins
lower hydrostatic pressure / oncotic same / higher intersitial oncotic pressure -but fluid does move out, just less than the systemic , so filtration and resabosprtion in
^ hydrostatic pressure in lungs
- more fluid moves out so get pulmonary oedema -^venous pressure and ^ arterial pressure (this isn’t a thing in the systemic circulation because arterioles don’t contribute much to hydrostatic pressure d lower resistance(?)
what prevents odemea
Low capillary pressure - ^ arterial pressure
pulmonary oedema effecdt
- impair gas exchange -affected by posture, upright okay but speed they get fluid build up d gravity pulling fluid at the base of lungs when upright , so more spread of the fluid during the -also lie down, congenital heart failure, lower p o reabsorption c increasing b volume returning in the heart ^ pressure in the lung c ^ p o
pO tratmetn
-diuretic to v b volume -treat underlying cause
cerebral circulation demand of the brain? and why?
- brain wants 20% of (15% of cardiac output d neurones continuously active) - bra
how does the
- ^ capillary density (^SA - v cerebral diffusion (10microm) - ^basal floor - high 02 extraction (more than 35% of the whole body, good diffusion gradient)
why is this 02 demand important in the brain?
- neurones are sensitive to hypoxia - drop of perfusion, loose consciousness and innrevesibel damage to neurones in 4 mins
how is b supply ensured in brain?
-sturctural; anatomies between basilar(from vertebral) and carotid arteries , ‘circle of wills?’ - functionally; myogenic auto regulation maintains perfusion during hypotension / metabolic factors / brainstem regulates flow (of other circulation)
myogenic auto regulation
- the cerebral resistance vessels in the brain have a myogenic response to changes in transmural pressure - ^ bp across body (systemic) = increases b flow to the brain, but don’t want too much, so vessels vasoconstriction to maintain relative b f - b flow v = vasodilation ot ^ b flow to the brain
image
-myogenic response by ^ resistance / v restiane by contracting and dilating to maintain a b f
myogenic response were else found?
-renal, skeletal muscle
metabolic regualtions ?
- hypercapnia ^Co2 vasodilation to remove that - hypercapnia v co2
how does ventilation c syncope?
- v co2 so hypocapnic state, detected by myogenic cerebral vessels wc c vasoconstriction and v bf to therein
what shows regional activity bf differences? more neuronal acitivy what metallic factors released?
- fMRI - ^ pco2,k+,adenosine (vasodilator ),v p02
Cushing’s reflex
-skull doesnt allow expansionists , so ^ cranial pressure (e.g tumour/haemorrhage) c ^ pressure int he brain c vasoconsitricon and implore cerebral b flow - push brain down towards the foramen magnum c bushings reflex ; vasomotor control centre in brain stem, push onto them c ^ SYMP vasomotor action so ^ SYMp to peripheral so activate a-.. c vasoconstriction c ^ arterial bp wc maintains cerebral bp B also detected by baroreceptors os ^ vagus acitivy of heart so you see bradycardia with ^ bp , -it also affects respiratory c irregular breaths
coronary ciruclation rate?
- R L coronary armies come off L R aortic sinuses - at rest 70pbm, but can ^ 5 folds if excercise (so this demand must be met ) - LCA gets flow during diastole
cardiac vs skeletal muscles perfusion
- fibre diameter is smaller in cardiac, continuous patent d NO. released by endothelial,=this maintains ^ basal flow rate , so ^ capillary density -some vessels in seltela are closed and not perfused at rest c v capillary density + also their bv have ^ fibre diametre -endo
metabolic hyperaemia
-metabolic factors acting as vasodilators - adenosine, k+ ^ and vpH c VASODILATION
what are coronary arteriesprone to
angina d few arterio-arterial anatomies
hw does angina occur and what part of life cycle? what else can c angina?
- diastole shortened therefore more b flow reduced -cold and stress
skeletal muscle
^ supply of 02 to meet demands , also regulates arterial b pressure, -resistance vessels have rich innervations by SYM vasoconstriction part of the baroreceptor reflex maintains b p
skeletal muscle
^ supply of 02 to meet demands , also regulates arterial b pressure, -resistance vessels have rich innervations by SYM vasoconstriction part of the baroreceptor reflex maintains b p - capillary density depends on the muscle type , postural ones wc are used 24/7 have more capillary
why does high capillary tone matter in skeletal muscle
- bg increase in flowx20 fad, or great increase in vasodilation
what c increased flow
metabolic hyperaemia ; ^ k, ^ osmolarity, inorganic phosphates, adenosine, ^H -adrenaline wc acts on beta 2 and noradrenaline a1
cutaneous circulation how is body temp regulated?
temp regulation , d vasoconstriction of bv in hehe skins (capillary bed) bradykinin and arterio-venous anatomies -arterio-venous anatomies wc are under vasoconsitricon from sympathetic control, turning it off c vasodilation so lose heat a lot b lose heat through a-venous anastomies and capillary bed -also bradykinin released c vasodilation c loss of heat
