congestive cardiac falure

8/14/2019 Congestive Cardiac Falure

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, ,Prin cip les o f N e u ro scie n ce ivth ed K a n d e lE R e t


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Csf from the arachnoid space is then released into the spinalcanal and the current also arises over the brains convexity

thus infusing its entire surface area.

Flow is then diverted along vessels of Virchow Robin spaceswithin sulci and concaves of the cerebral cortex.

Csf and interstitial fluid within this perivascular spacesexchange small solutes via diffusion, generating a current

which enables metabolites to arise from deep within cerebralhemispheres to the ventricular system and corticle

subarachnoid spaces.


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within the subarachnoid spaces, granulation valves aid in asingle directive of CSF towards venous blood. even though

the brain capillaries are permeable to solutes, proteins,

molecules and microorganisms and red blood cells.

the brain is protected by a blood brain barrier made up ofintricately interlinked podocyte foot processes , through

size segregations.

Permeable brain vessels are located within the fenestrated

capillaries of the posterior pituitary and circumventricularorgans of the subfornical and subcommissural organs,

neurohypophysis, area postrema, median eminence and

laminar terminalis.

Another barrier is existent at the choroid plexus epitheliacalls, they function via active transport enabling thecontinuous CSF secretions within the central nervous

system and molecular exports into vessels


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osmotic equilibrium between csf and blood is achieved throughthe creation of an osmotic gradient from the active molecular

transport due to kinetics. main solutes within the CSF are water,protein, glucose, sodium, potassium, calcium, magnesium,

chloride.

Ph is mildly alkali at 7.33.

in comparism to plasma which has less water, lower acidity andhigher concentrates of protein, magnesium, chloride,potassium, bicarbonates, glucose, calcium however the sodium

concentrates are equal.

CSF is turned over iii - iv times a day, at a rate of 0.35 ml / minand 500 ml / day.

fluid switches of ions, metabolites and ions between CSF andblood function as a density separation medium, between cranial

CSF, extra neuronal fluid, cisternal fluid, spinal fluid and bloodcompositions.


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:// . . / / / / / %h ttp w w w p h a rm a in fo n e t file s im a g e s sto rie s a rticle _im a g e s M o rp h o lo g y 2

In te ra ctio n s b e tw e e n C S F a n d b lo o d circu it
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:// . . . / / / / / /http ed u cation vetm ed vt ed u C u rriculu m V M 80 54 Lab s Lab 9 IM A G E S C H O R O
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Homeostatic maintenance of water and solutes is carried out by

the kidneys. water balance and osmolality is regulated by thirstwhile elimination of excess is mediated by the nephronic system.volumes of the vascular system and the extracellular fluids are

sodium chloride dependent, the concentration of which is kidneyregulated. extracellular fluids are maintained within a slim range.

systemic fluids are segregated within differing membrane enclosedcompartments in varying compositions and composites. these

make up xxxxxx % of an entities body weight which is adipocytedependent, a greater content of which reduces fluid retentions.total systemic fluids are both intra and extra cellular, due tocellular compositions, intracellular fluid is more that cellular

externals, they make up ii / iii of total systemic fluid content.

total systemic fluid amounts can be discovered by multiplying apredetermined 0.6 by an entity's weight, the average of which

ought to be about xxxxii litres. while intracellular fluid is reflectedby 0.4 multiplied by body weight, averaging about xxviii litres, andextracellular fluid determined with multiplications of 0.2 by weight,

this is often averaged at xiv litres.


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,R e la tio n sh ip b e tw e e n in tra ce llu la r a n d e x tra ce llu la r flu id s sy ste m icoutreachesS o u rce s a n d e le ctro ly te co n stitu e n ts

:// . . / / / / / / .http w w w na tu re com kijou rn al v7 2 n 4 im a ge s 50 0 22 8 8 f3 jp g
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C a rd ia c p a ssa g e o f in te stitia l flu id th ro u g h ca p illa ry b e d lin ka g e

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:// . . . / / / / - .h ttp w w w m fiku d k PPa u lev cha p ter1 im ag es n 1 4 a jp g
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Pa ssag e o f so lu te s w ith in th e n e p h ro n s fo r o sm o la lity re g u la tio n s:// . . / / / / / - - -http im g m e dscap e com pi em ed ckb spo rts_m ed icin e 84 61 1 8 80 13 8 8 4 8 4 8
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interstitial fluids is fluid surrounding cells within various systemictissue, this includes bone water mass and circulations within

dense connective tissue.

the major variance between plasma and interstitial fluid lies withintheir respective compositions, plasma contains greater

concentrates of proteins, other molecular entities are similar inconcentrations.

the key solutes that contribute towards the osmolality ofextracellular fluids are sodium, chloride and bicarbonate, other

lesser contributors are urea, glucose, potassium, phosphate andcalcium.

intracellular fluids have a ph of vii . i while extracellular fluids aremore alkali at vii. iv, the main cations and anions within are

chloride, bicarbonate, potassium, sodium, calcium, and inorganicphosphate. Ineffective osmoles are mediated by membrane

transversing ions, with water remaining outside due to the lack of


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sodium and anions contribute to effective osmoles theseaffect body fluids and changes systemic osmolality, varyingionic particle concentrates within the extra and intracellular

fluids thus affect their volumes.

the inherent permeability of cell membranes and capillarywalls ensures that water is in an osmotic equilibrium, thusplasma osmolality is in direct synchrony with the osmolality

of extracellular, intracellular and interstitial fluids.

there is minute quantities of sodium within the intracellularfluids, it is mainly just potassium, maintenance is carriedout by a ubiquitous sodium, and potassium ATPase pump.

with intracellular fluid anions less in content than that

inherent within the extracellular, this is due to a lesserconcentrate of chloride, bicarbonate with a greaterconstituent of organic anions, phosphates and proteins.

as water transverses the various compartments smoothly


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as water transverses the various compartments smoothly,this mobility is mainly affected by hydrostatic pressure and

osmotic pressure, the hydrostatic pressure created isgenerated by the pumping heart, gravity upon blood

flowing within veins, , osmotic and oncotic pressure of

plasma proteins, it is an important determination of fluidpressure across capillary walls .

the cellular membrane is highly permeable to water,mediating a high variance between intra and extra cellular

fluids within these regions, thus they are often in osmoticequilibrium, if any changes arise, these are transient,

membrane transports facilitate ionic movements, watermobility affects fluid movements between the intra and

extracellular fluids.

apart from the nephrons, other routes of fluid exit includethe skin, lungs, through sweat, urine and waste these

routes are non regulated. the renal fluid output is tightlyregulated for the maintenance of water balance with intake

a precise match for water loss , if intake is high, there ispositive water loss and osmolality of body fluid declines, if


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a n n e ls w ith in th e m e m b ra n e fo r w ate r a n d io n p a ssa g e

:// . / / / / / .h ttp n o b e lp rize o rg n o b e l_prize s ch e m istry la u re a te s 2 0 0 3 p u b lic htm l
http://nobelprize.org/nobel_prizes/chemistry/laureates/2003/public.htmlhttp://nobelprize.org/nobel_prizes/chemistry/laureates/2003/public.htmlhttp://nobelprize.org/nobel_prizes/chemistry/laureates/2003/public.html


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disorders of water balance change the osmolality of bodyfluids, which can be monitored by measuring plasma

osmolality, major determinants of which include sodium,

chloride and bicarbonate, any changes with in the plasmasodium balance would bring about resultant variations inthe volume of the extra cellular fluid compositions, but will

not affect its osmolality.

hypoosmolality would results in a decline in plasma osmolalitythis shift of fluid within cells causes cellular swellings.,

which brain cells are highly susceptible to.

Thus a speedy decline in plasma osmolality affect neurologicalfunctions inducing nausea, malaise, confusion, headaches,seizures, lethargy and eventually even a comatose state.

vasopressin is the key regulator of kidney osmolality andvolume.

water diuresis and diluted urine would bring about a decline inplasma vasopressin. when vasopressin rises, antidiuresis


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a vasopressin molecule is made up by ix amino acids, this tinypolypeptide is synthesized within neuroendocrine cells

located within the supraoptic paraventricular nuclei of thehypothalamus, storage is within the neurohypophysis

( posterior pituitary ).

vasopressin secretions are influenced by body fluid osmolality,volume, pressure of vascular system, nausea, natriuretic

peptides, angiotensin ii, nicotine, downregulation is broughtabout via ethanol, a dip in blood volume or arterial

pressure.

osmotic receptors senses changes in body fluidosmolalities through swelling and shrinkages, they are

responsive to solutes that are effective osmoles such as

sodium chloride.

when an increase in osmolality occurs, signals are received bythe supraoptic and paraventricular nuclei.

Vasopressin dissolves fast within plasma, thus when releaseceases, circulations come to a halt which is why the


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a so p re ssio n m o le cu le

:// . . / / .tp w w w 3d chem com im ag esofm olecules Va sop re ssin jp g

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. . . .w w w n cbi n lm n ihg o v


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Mechanisms of action and production of vasopressin

:// . . . / . =http www frca co uk article aspx?articleid 100852
http://www.frca.co.uk/article.aspx?articleid=100852http://www.frca.co.uk/article.aspx?articleid=100852http://www.frca.co.uk/article.aspx?articleid=100852


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hemodynamics influences its secretions with receptors

located in both the low pressure site of the left atrium andpulmonary vessels and the high pressure sites at the aortic

arch and carotid sinuses of the circulatory systems.

low pressure receptors are located within the highcompliance sites of the venous system which carries majority

of blood, the high pressure receptors are responsive toarterial pressures, while baroreceptors within the cardiac

zones senses stretch from cardiac atrial and arotic arch walls.

the signals conveyed from these baroreceptors are carriedvia the vagal and glossopharyngeal nerves to the brainstemcontrol centres just beneath the medullary oblongata that

regulate heartbeats and thus blood pressures, signals arethen further relayed from the brainstem region tovasopressin secretary cells of the supraoptic and

paraventricular hypothalamic nuclei, decreases in bloodvolume and arterial pressures which were genetically

predefined , steps it down to lower osmotic values.


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Vasopressin increases the permeability of the collectingduct at the medullary portion which thus becomesreceptive to urea passage, vii receptor bindings upon the

basolateral membranes of a cell, coupled with adenylcycvlase via stimulatory G protein.

vasopressin initiates this receptor bindings, withintracellular levels of cyclic adenosine monophosphate

accumulating and thus activating protein kinase A, thisbrings about an insertion of intracellular vesicles ofaquaporin ii which creates water channels at the apicalmembranes of the cell through exocytosis from within, asvasopressin initiates formation of aquaporins, they

transform non permeable cells into highly permeableentities.

over at the basolateral membraneous region, lie aquaporinii and iv which are always water permeable, water is thus

easily shunted from the apex through the cell and out fromits basal membrane, this results in overall water


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Vasopressin effect upon its ii different receptors thus affecting circulationand arterial pressure

:// . . / / .http www cvpharmacology com vasoconstrictor AVP gif

- . , - - ,
http://www.cvpharmacology.com/vasoconstrictor/AVP.gifhttp://www.cvpharmacology.com/vasoconstrictor/AVP.gifhttp://www.cvpharmacology.com/vasoconstrictor/AVP.gif


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Aquaporins proteins are channels that permit faster transport of water. (through cell membranes Initially discovered in plants during 1994 Maurelet

. ). -al 1994 ii tandems of iii membrane spanning helices linked via connecting, - - ( )loops with an axis of Asn Pro Ala NPA thus creating a central pore passage

for water entry:// . . / / / / / / .http www nature com jcbfm journal v22 n4 fig_tab 9591227f1 html

Translocation of an excessi i h di i i
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proton in either direction is-opposed by a free energy

barrier centered at the NPA.region Both hop and turnsteps of proton translocation

are opposed by theelectrostatic field of the

. , - -channel Notably the 10 12- -kcal per mole barrier to

proton translocation peakingat the NPA region resultsfrom a combination of

.factors These include notonly the orientational

control of water moleculesbut also desolvation

penalties and electrostaticeffects caused by the charge

.distribution in the channel

. , . ,N CHAKRABARTI E TAJKHORSHID

. . .B ROUX and R POMES"Molecular Basis of Proton

"Blockage in AquaporinsStructure12 , - ( ). [65 74 2004PubMed ]
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sensations of thirst arise from the thirst centre within thehypothalamus, this response is triggered by angiotensin ii

and sodium chloride, which would increase body fluidosmolality, decrease blood pressure, an extremely potent

initiator of the thirst response is hyperosmolality, with a ii toiii % increase in plasma osmolarity or a x % decline in bloodvolume or arterial pressure initialising an intense desire for

fluids.

concert and synchrony is thus achieved by vasopressinand the hypothalamic thirst centre for the overall

maintenance of systemic water balance.

Other mechanisms of renal sodium chloride and wateroutput involve fine tuning by the sympathetic nervous

system, when their activities are upregulated, a decline insodium chloride occurs, other aspects of action includedownregulating glomerular filtration rates, upregulating

secretions of rennin and increasing sodium chloride

reabsorptions within the thick ascending loops of henle ,


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re le a se
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H y p o th a la m ic th irst ce n tre w ith in th e h y p o ta la m u s a n d th e o rg a n stargeted

:// . . / / .h ttp w w w cre a tio n o fm a n n e t ch a p te r3 ch a p te r3 _14 htm l
http://www.creationofman.net/chapter3/chapter3_14.htmlhttp://www.creationofman.net/chapter3/chapter3_14.htmlhttp://www.creationofman.net/chapter3/chapter3_14.htmlhttp://www.creationofman.net/chapter3/chapter3_14.html


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:// . . . / / / / - .h ttp w w w m fiku d k PPa u lev cha p ter2 4 im ag es 2 4 6 jp g
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as homeostatic mechanisms are a duo way mechanism ofsignal conveyance, integrations and response, vascularsensors exist for the detecting of varying fluid volumes,

these are alerted by declining pressures and situated within

the cardiac atria and pulmonary vasculatures. an increasein pressure is sensed by receptors within the arotic arches,carotid sinus and juxtaglomerular apparatus of the kidneys,other sensors are located within the central nervous system

and hepatic regions.

congestive heart failure could have been due to a numberof factors such as a congenital heart defects, history of

heart attack, narrowed myocytes arteries, diabetes, alcoholabuse, coronary artery disease, myocardial infarction,

endocarditis of cardiac valves, myocarditis, cardiac fibrosis,high blood pressure, overworked myocytes that have

increased in size and number to a maximal and theirsubsequent necrosis, heart valve disease due to rheumatic

fever or cardiomyopathy.

as the cardiac pump can no longer shunt blood to the

other systemic organs, a couple of characteristic symptomswould be fatigue, pneumonia, reduction in exercise

Congestive cardiacfailure and a


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failure and ahealthy cardiac

(Top) Grossexamination

revealed massivecardiomegaly of

transgenic heart( . ). (1 8 Middle)

-Four chambersection of hearts

( . )1 8 demonstratesmassive

enlargement ofboth ventriclesand atria with

atrial filling by.organized thrombus

(Bottom) Cardiac(histology leftventricular free

, )wall 18 s howsmild edema and,pale hypertrophied

myocytes withoutsignificantinflammation in

.transgenic heart

:// . . / / / / / . .http www pnas org content 94 15 8121 F4 expansion html
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as a characteristic combination of these symptoms areinherent in the patient, congestive heart failure could be a

contributor, however unless systemic confirmations areseen, other probabilities cannot be ruled out as different

configurations of systemic malfunctions or injuries couldresult in the same symptomic set.

confirmations can be carried out via myocardiocyte biopsy,

detecting accumulates of extra fluid in the body by

peripheral edema, breath sounds, size of neck veins orascites as well as an in depth investigation of overall

cardiac condition through measurements of pulse rate,cardiac size, sounds, and murmurs.

an axial essential for confirmation is the echocardiogram,whereby echo location through ultrasound and the resultantbounce back of sound waves as structural contact occurs,this aids in clarity of vision of cardiac zones, pulmonary

state, myocytes, valve structures, blood flow patterns andmorphological variances. apart from being non invasive and

insightful, causes and results are accurately defined.


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A n o th e r via b le m e th o d is v ia ch e st ra d io g ra p h y w h ile p a tie n t is e re ctly. ,p o sitio n e d A t a n e a rly sta g e d u e to d iffe re n ce in th e b lo o d flo w

, ,g ra d ie n t th e p u lm o n a ry lo b e s m ay b e o f a n irre g u lar m o rp h o lo g y w ith, .ex p a n sio n s o f th e u p p e r lo b e s th u s e a sily in d ica te d u p o n th e film s

A s p u lm o n a ry p re ssu re h e ig h te n s fro m flu id b u ild u p fro m a w ea kly,circu la tin g b lo o d stre a m b ro u g h t a b o u t b y th e d a m a g e d le ft v e n tricle

in te rstitia l p u lm o n a ry e d e m a o ccu rs in d ica te d v ia p e rih ila r a n d, ,p e riv a scu la r h a zin e ss p e rib ro n ch ia l cu ffin g a th icke n e d in te rlo b u la r

, - .se p ta a n d a rte ry b ro n ch u s ra tio d e fle ctio n s

.C o n g e stiv e h e a rt fa ilu re e x p a n d s th e ca rd ia c silh o u e tte H o w e v e r b lo o d.e je ctio n h a s little to d o w ith size S tru ctu ra l sh ifts d e p e n d m o re u p o n th e

d e g re e o f d e fle ctio n s o f ca p illa ry w e d g e p re ssu re w h ich is a n in d ire ct,e stim a te o f le ft a tria l p re ssu re in d ica tiv e o f le ft v e n tricle fa ilu re a n d a lso

th e se v e rity o f v a lv e ste n o sis a s th e se a sp e cts slo w m o b ility a n d th u s.a ffe ct pre ssu re w ith in th e le ft a tria l a ffe ctin g th e o v e ra ll re a d in g s

,D urin g sev e re situ a tio n s p le u ra l e ffu sio n s a n d a irw a y e d e m a m ig h t a lso. ,b e in d ica te d In te n siv e ca re u n it p a tie n ts te n d to re fle ct su ch fin d in g s

o th e r su p in e ra d io g ra p h ica l d isco v e rie s m a y in clu d e b ro n ch u s, in te rm e d iu s fib ro sis in cre a se in p u lm o n a ry a rte ry b ro n ch u s ra tio in th e

. .u p p e r vs lo w er lu n g lo b e s d u rin g sup in e ra d io g ra p h A s b lo o d flo w is

,a ffe cte d b y p o stu re th is fa cto r is co n sid e re d a n d fin d in g s th u s


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D i i l i i i i d i h d i h i h fi ld


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D ire ctio n a l n a vig a tio n s is ca rrie d o u t w ith ra d io w a v e s w h ich a re fie ld s,d ire cte d w ith in th e e n clo se d sp a ce cre a tin g m o b ility o f th e p h o to n s

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further diagnostic confirmations could include theelectrocardiogram and chest x-ray to locate cardiac

enlargement, previous cardiac attacks, fibrosis,arrhythmias, and pulmonary fluid accumulates.

an increase in the extracellular fluid volumes, which alsoresults in pulmonary edema as fluid accumulates within thelungs as the pulmonary vasculature is mediated by the left

side of the cardiac zone.

peripheral edema would also occur from the dysfunctionpumping action of the heart, with the legs mostly affected

due to gravity and peripherals are often most susceptible asthey are at the outreaches of the system and blood is thusshunted there less and at a longer duration as compared to

the axial areas.

Which brings about the characteristic swellings at the calfregions in patients of congestive cardiac failure


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this would also weaken the strength of calf musculature andthe smooth muscles within the tunica media which aids in

deoxygenated blood transport back up to the cardiac.

these high performance myocytes are dependent upon thepresence of adequate blood for nutrients, glycogen and ATP

for contractions and subsequent actin and myosin crossbridge release.

as endothelia valves of tunica intima inverginations prevent

pooling of blood and the accompanying fluids, lack of aproper blood supply to these regions might also result in

cellular death, and a reduction in cellular size.

these factors contribute to the eventual shrinkages anddysfunctions of these valves which would impeded

preventions of backflows.

Further contributing to calf edema.


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kidney's retention of sodium chloride and waterwould also increase extracellular volume within the

interstitial fluid compartments, as blood pressure andcardiac output decline, an overall weakness in cardiac

pumping occurs.

these pressure changes are sensed by vasculaturesensors and a response is carried out which increases

kidney sodium chloride and water retention, this is

meant to dilute the blood thus encouraging itsdistribution within the system and preventingcessation of flows.

in congestive heart failure, another main organ which

is heavily blood dependent due to the high volume ofmetabolic activities carried out within- the liver whichis connected to the hepatic artery and portal vein

becomes damaged.

this is the outcome of severe right sided congestivecardiac failure for an extended duration thus leadin

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as venous circulation is affected, blood wouldstagnate within major veins bringing about an

engorged liver.

ascites of large volumes of fluid would alsoaccumulate within the peritoneal cavities in the eventof a worsening condition which would have resulted in

hepatic cirrhosis an advancement of which wouldbring about the pooling of blood within the splanchnic

circulation ( mesenteric and splenic capillary bedsemptying within the hepatic bed) as a damaged liver

would impede the blood drainage from splanchniccirculation via the portal vein.

as the volumes and pressures are reduced withinareas of the vasculature system where sensors arelocated, venous pressures within the portal systems

increase and this deflection in fluid transudates withinthe peritoneal cavities thus arise. thus the kidneys

react to this hike in extracellular volume, increasing

reference


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referencePrinciples of Neuroscience

Iv th editionKandel Eric RSchwartz James HJessell Thomas MMcGraw Hill

2 000

Principles of PhysiologyIv th editionMatthew N. Levy,

Bruce M. Koeppen,Bruce A. StantonElsevier Mosby2006

congestive cardiac falure

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