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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

resistance is inversely proportional to

the 4th power of the radius



(1/r^4)

microcirculation consists of

arterioles cappliaries and venules



- need a microscope

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

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

pulse pressure

diff between systolic and diastolic

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

arterioles

- major resistance vessels


-mean arterial pressure falls from 93 in arteries to about 37 - need it to drive blood to cappilary beds



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

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

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



-

nitric oxide

- vasodilator of smooth muscle and penis and clit


- inhibits entry of calcium

endothelin

- vasoconstricter


- smooth muscle contractions

histamine

- allows vasodilation in injured area so increased blood flow can start inflammatory response


shear stress

blood flowing over a vessel causes friction, shear stress - causes endothelials to release nitric oxide and vasodilate

myogenic response to stretch

- vasocontricts in response to stretch, resisting



- opposite happens when stretching decreased


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

autoregulation

- local arteriolar mechanisms that keep tissue blood flow fairly constant despite wide variations in mean arterial driving pressure



- change in radius

mean arterial pressure =

cardiac output x TPR

norepinephrine on arteriolar smooth muscle

- a1 adrenergic's


- vasoconstriction

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

no parasympathetic innervation to arterioles

- only to penis and clit



- need vasodilation for HARD erection's

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


epinephrine and norepinephrine

norepinephrine combines with a1 for vasocontrict



epineprhine combines with b2 and a1 - b2 vasodilates but isnt found on all tissues


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

arterioles- cappilaries- veins analogy

narrow rive - wide lake - narrow river

capillary pores

- small water soluble sustances can pass thru these junctions btwn cells

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

precapillary sphincter

- stopcocks to control blood flow thru particular capillary each one guards



- wrapped around capillary

interstitial fluid

big part in cappilary play



- takes on basically blood composisiton besides plasma proteins when diffusion in cappilaries takes place

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

ultrafiltration

- pressure in cappilaries exceeds outside pressure , fluid pushed out thru pores



-most plasma proteins remain inside

reabsorption

when inward driving pressures are dominant, inward movement of interstitial fluid thru pores comes in

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

cappilary blood pressure (bulk flow)

- fluid/hydrostatic pressure exerted on inside of cappilaries by blood



-tends to force fluid out the cappilaries

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

interstitial fluid hydrostatic pressure (bulk flow)

- exterted on outside of cappilary wall by interstitial fluid



- fluid into cappilaries

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

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

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

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

elephantiasis

massive oedema in certain extremities like scrotum and feet - very swollen like a HARD ERECTION

veins

- large radius so little resistance to flow



- blood resevoir as little recoil and lots of stretching

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

sympathetic activity on venous return

- vasoconstriction increases venous pressure which drives to atrium



-narrowing of veins squeezes more blood thru

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

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

effect of venous valves on venous return

- one way valves that close on backflow

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

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

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

2 determinants of mean arterial pressure

CO x TPR

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

left atrial volume receptors and hypothalmic osmoreceptors

- water/salt balance, affect plasma volume

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

cardiovascular responses associated with behaviours/emotions

- mediated thru cerebral cortex-hypothalmic pathways



- widespread change in cardio activity and fight/flight response



- vasodilation doe

'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

hypothalmic control over skin arterioles

- temp regulation takes precedence over cardiovas centre control for this area

hypertension/hypotension (general)

- hyper - 140/90 +



-hypo - 100/60 -

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



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

adaptation of baroreceptors in hypertension

- adapt to operate at high BP



- still funciton but maintain it at a higher mean pressure

complications of hypertension

- stress on heart and blood vessels


- hemmhorages, strokes, congestiveheart failure, rupture of vessels

treatment of hypertension

- weight loss


- drugs manipulating salt/water management


- autonmic activyt alterations



-ultimately reducing plasma volume and TPR

prehypertension

- btwn 120/80 and 139/89



-dietary measures can be taken before further intervention is needed if worsens

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

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

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