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68 Cards in this Set
- Front
- Back
pressure gradient of vessels |
diff btwn beginning and end of vessel not absolute pressure within the vessel |
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resistance is inversely proportional to |
the 4th power of the radius
(1/r^4) |
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microcirculation consists of |
arterioles cappliaries and venules
- need a microscope |
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basic structure of all blood vessels |
- alternating layers of :
-connective tuissue (fibrous and elastic) -smooth muscle cells - epithelial cells
outer layer: collagen-rich connective tissue
in some in between is external elastic lamina
middle layer: thickest, connective tissue/smooth muscle
inner layer: single layer endothelial cells surrounded by basement membrane and in some an internal elastic lamina |
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arteries |
-large radius, little resistance
- pressure resevoir to provide driving force for blood when heart relaxing
- very stretchy walls allow arteries to stretch like ballon when heart contracts and sends blood, then when heart relaxes arteries let loose and shoot blood downstream |
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pulse pressure |
diff between systolic and diastolic |
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mean arterial pressure = |
diastolic pressure + (1/3) pulse pressure
- since at resting heart rate, 2/3 of cardiac cycle is in diastole and 1/3 in systole |
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arterioles |
- major resistance vessels -mean arterial pressure falls from 93 in arteries to about 37 - need it to drive blood to cappilary beds
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vascular tone of arterioles |
- establishes baseline of arteriolar resistance
- 2 factors responsible
1. considerable myogenic activity - self induced contractile activity
2. sympa fibres supplying continually release norepinephrine, further enhancing vascular tone
-keeps it in middle so it can vasodilate/constrict |
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active hyperaemia |
- vasodilation in metabolic needs such as increased metabolic rate where O2 is used up fast, more blood flow needed for O2
- when low metabolic activity and blood not needed, vasoconstriction occurs |
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endothelial cells |
- secrete vasoactive substances that can vasoconstrict/dialate
- secrete substnces stimulating new vessel growth
- exchange across cappilares
- influence formation of platelet plugs, clotting and clot dissolution
- |
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nitric oxide |
- vasodilator of smooth muscle and penis and clit - inhibits entry of calcium |
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endothelin |
- vasoconstricter - smooth muscle contractions |
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histamine |
- allows vasodilation in injured area so increased blood flow can start inflammatory response
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shear stress |
blood flowing over a vessel causes friction, shear stress - causes endothelials to release nitric oxide and vasodilate |
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myogenic response to stretch |
- vasocontricts in response to stretch, resisting
- opposite happens when stretching decreased
|
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reactive hyperaemia |
- blood supply to a region is completely occluded
- reaction to this happens and when pasage opens a huge increase in blood flow provides lots of oxyxgen - reactive hyperaemia |
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autoregulation |
- local arteriolar mechanisms that keep tissue blood flow fairly constant despite wide variations in mean arterial driving pressure
- change in radius |
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mean arterial pressure = |
cardiac output x TPR |
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norepinephrine on arteriolar smooth muscle |
- a1 adrenergic's - vasoconstriction |
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local controls overriding sympathetic vasoconstriction |
- skeletal and cardiac muscles have most powerful control mechanisms to override
- if running, you will get vasodilation to legs for increased blood and oxygen |
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no parasympathetic innervation to arterioles |
- only to penis and clit
- need vasodilation for HARD erection's |
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medullary cardiovasculat control centre (brain stem - medulla)
and hypothalamus |
- main region of brain sympathetically stimulating arterioles
- integrating centre for BP regulation
- hypothalamus controls temp regulation by adjusting blood flow to skin
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epinephrine and norepinephrine |
norepinephrine combines with a1 for vasocontrict
epineprhine combines with b2 and a1 - b2 vasodilates but isnt found on all tissues
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vasopressin and angiotensin ll |
vasopressin - water balance by regulating amount kidneys retain during urine formation
angiotensin ll - (renin-angiotensin- aldosterone) path to regulate salt balance and retains water
- both influense fluid balance influencing plasma volume and BP
-also both potent vasoconstricters - when huge loss of blood these little guys make a vasoconstrict style and retain plasma volume as best they can |
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arterioles- cappilaries- veins analogy |
narrow rive - wide lake - narrow river |
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capillary pores |
- small water soluble sustances can pass thru these junctions btwn cells |
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metarteriole |
part of capillary system - like a larger cappilary that goes straight from arteriole to venule
- whereas capillaries can branch off of metarteriole or join met arteriole |
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precapillary sphincter |
- stopcocks to control blood flow thru particular capillary each one guards
- wrapped around capillary |
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interstitial fluid |
big part in cappilary play
- takes on basically blood composisiton besides plasma proteins when diffusion in cappilaries takes place |
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bulk flow |
- protein-free plasma filters out of the cappilaries, mixes with the surrounding interstitial fluid and is reabsorbed
- stuff moved together in bulk
- helps control balance of ECF with plamsa and interstitial, imprnt in plasma volume |
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ultrafiltration |
- pressure in cappilaries exceeds outside pressure , fluid pushed out thru pores
-most plasma proteins remain inside |
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reabsorption |
when inward driving pressures are dominant, inward movement of interstitial fluid thru pores comes in |
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4 fources influencing bulk flow |
1. cappilary blood pressure 2. plasma-colloid osmotic pressure 3. interstitial fluid hydrostatic pressure 4. interstsitial fluid-colloid osmotic pressure |
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cappilary blood pressure (bulk flow) |
- fluid/hydrostatic pressure exerted on inside of cappilaries by blood
-tends to force fluid out the cappilaries |
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plasma-colloid osmotic pressure (bulk flow) |
- colloidal dispersion of plamsa proteins
- encourages into cappilaries
- b/c proteins only in plasma, water wants to come in from interstitial to even it out |
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interstitial fluid hydrostatic pressure (bulk flow) |
- exterted on outside of cappilary wall by interstitial fluid
- fluid into cappilaries |
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interstitial fluid-colloid osmotic pressure (bulk flow) |
- doesnt contribute that significantly
- from scarce amount proteins that leak thru pores
-fluid comes out from cappilaries into interstitial |
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lymphatic system (general) |
-at rest more filtration than reabsorbtion happens at cappilaries so extra fluid coming out picked up by lymphatic - brings to heart
how lymph flow driven:
- 'lymph pump' rhythmically contracts to push lymph forward - contraction of skeletal muscles around squeeze lymph out of vessles |
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functions of lymphatic system (4) |
1. return of excess filtered fluid
2. defence against disease - ex. bacteria picked up gets phagocytozeddddddd when passing thru lymph nodes
3.transport of absorbed fat
4. return of filtered protein - proteins that leak thru pores would increase the interstitial fluid-colloid osmotic pressure and mess a bulk flow so these are takennnnn care OF style |
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oedema and 4 general categories |
- swelling of tissues because of excess interstitial fluid
1. reduced conc of plasma proteins - decreases plasma-colloid osmotic pressue, allows excess fluid to filter out
2. increased permeability of cappilary walls - allows more plasma proteins than usual to pass from plasma into interstitial
3. increased venous pressure - when blood damns up in veins, increased capillary BP so fluid out
4. blockage of lymph vessels - excess fluid filtered isnt taken and stays in interstitail |
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elephantiasis |
massive oedema in certain extremities like scrotum and feet - very swollen like a HARD ERECTION |
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veins |
- large radius so little resistance to flow
- blood resevoir as little recoil and lots of stretching |
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5 factors incluencing venous return (list) |
1. sympathetically induced vasocontriction
2. skeletal muscle activity
3. effects of venous valves
4. respiratory activty
5. cardiac suction |
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sympathetic activity on venous return |
- vasoconstriction increases venous pressure which drives to atrium
-narrowing of veins squeezes more blood thru |
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effect of skeletal muscle on venous return |
- many large veins lay between skeletal muscles so contraction compresses veins
- decreases venous capacity and increases venous pressure
- squeezes fluid toward heart
- 'skeletal muscle pump'
- increased activity gets more blood to heart |
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countering effects of gravity on venous system |
1. standing up causes fall in mean arterial pressure which fires sympathetic venous vasoconstriction
2. skeletal muscle pump interrupts column of blood by completely emptying given vein segments intermittently so vein isnt subjected to entrie weight of its column all the way from the heart. NICE |
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effect of venous valves on venous return |
- one way valves that close on backflow |
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varicose veins |
venous valves dont work and and support column of blood above them
- blood pools and edges of valves cant seal
- veins become overly distended and toruous
- doesnt affect cardiac output - compensatory increase in total circulating blood volume
- possiblity of abnormal clot formation |
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effect of respiratory activity on venous return |
- P within chest cavity averages 5 mmHg less than ATM so when blood travels thru chest cavity an external pressure gradient applied and squeezed blood in veins towards chest and heart |
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effect of cardiac suction on venous return |
- during ventricular contraction AV valves drawn downward enlarging atrial cavities and atrial pressure drops below 0 mmHg and increasing vein to atria pressure gradient
- then when ventricles relax it creates negative pressure further sucking in blood from atria and veins |
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2 determinants of mean arterial pressure |
CO x TPR |
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baroreceptor reflex |
receptors: carotid sinus (brain) and aortic arch (major arterial trunk) barorec - mechanosensitive to mean arterial pressure and pulse pressure
-constantly providing info to cardiovascular control centre which alters ratio of para/sympa stim to effector organs (heart and blood vessels)
- high BP leads to para stim and sympa inhibit to vasodilate and reduce BP |
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left atrial volume receptors and hypothalmic osmoreceptors |
- water/salt balance, affect plasma volume |
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chemoreceptors in carotid/aortic arteries |
- sensitive to low O2 or high acid levels in blood
- increase respiratory activty to bringin more O2 and blow off more acid
- also increase BP by sending excitatory to cardiovascular centre |
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cardiovascular responses associated with behaviours/emotions |
- mediated thru cerebral cortex-hypothalmic pathways
- widespread change in cardio activity and fight/flight response
- vasodilation doe |
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'exercise centres in brain' |
- induce appropriate cardiac and vascular changes at onset of excersise and even in anticipation
- reinforced by medullary carrdiovas centre from chemoreceptors in exercising muscles |
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hypothalmic control over skin arterioles |
- temp regulation takes precedence over cardiovas centre control for this area |
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hypertension/hypotension (general) |
- hyper - 140/90 +
-hypo - 100/60 - |
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secondary hypertension (3) |
occurs secondary to another known primary problem
- renal hypertension - reduced blood flow thru kidney, responds with angiotensin increasing plasma volume and BP
- endocrine hypertension - adrenal medullary tumour and secretes crazy nor/epinephrine and vaso contrict and high BP
- neurogenic hypertension - erroneous BP control arising from a defect in cardiovasc contol centa
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primary hypertension (8 causes) |
- induced by stress, obesity smoking, dietary habits
- not usually know which of these causes, probly contribution of a few:
1. defects in salt managemtn by kidneys
2. excessive salt intake
3. diets low in fruits, veg, dairy (low K and Ca)
4. membrane defects (ex. Na/K pump defect)
5. variation in genes encoding angiotensin
6. endogenous digitalis like substances
7. abnormalities in NO, endothelin...other vasoactive chemicals
8. excess vasopressin |
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adaptation of baroreceptors in hypertension |
- adapt to operate at high BP
- still funciton but maintain it at a higher mean pressure |
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complications of hypertension |
- stress on heart and blood vessels - hemmhorages, strokes, congestiveheart failure, rupture of vessels |
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treatment of hypertension |
- weight loss - drugs manipulating salt/water management - autonmic activyt alterations
-ultimately reducing plasma volume and TPR |
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prehypertension |
- btwn 120/80 and 139/89
-dietary measures can be taken before further intervention is needed if worsens |
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orthostatic hypotension |
- insiffiecient compensatory response to gravitational shifts, lying down to standing up
- pooling of blood in legs from gravity reduces venous return and CO and BP
- baroreceptors attempt to fix but if prolonged bedrest they are inactive after prolonged disuse |
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circulatory shock (list 4 types) |
- BP falls so low, adequate blood flow to tissues can no longer be maintained
1. hypovolemic - fall in blood volume
2. cardiogenic - weakened hearts failue to pump blood adequately
3. vasogenic - widespread vasodilation triggered by vasodilator substances - 2 types - septic is vasodilator sbstances released from infective agents and anaphylactic is from exessive histamine release in allergic reactions
- neurogenic - loss of sympatheic tone - lots of vasodilation |
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irreversible shock |
- short term compensations cant continue indefinietly
- fluid volume must be replaced from outside (drinking, transfusion)
- a point may be reached where BP drops so much organ damage ensues
- when cardiovascular starts to fail, vicious positive feedback cycle eventually causes death |