Body Fluids - PHYL1010 001 PDF

Body Fluids Andre S. Bowers, PhD Physiology Section, Dept. of Basic Medical Sciences, UWI, Mona Objectives Major constituent and types of body fluid Major body compartment and minor subdivisions. Mechanisms of fluid transport. Regulation of fluid volume within compartments. Factors affecting fluid c...

Body Fluids Andre S. Bowers, PhD Physiology Section, Dept. of Basic Medical Sciences, UWI, Mona Objectives Major constituent and types of body fluid Major body compartment and minor subdivisions. Mechanisms of fluid transport. Regulation of fluid volume within compartments. Factors affecting fluid composition. Water content Water is the major constituent of body weight: total body water (TBW) 45 – 75%. > in premature live births. o inability to concentrate urine In newborns, unlike other stages of growth: TBW predominantly in ECF - > 50%. ECF constitutes 1/3 in adults. Water content Infants - the major constituent of body weight: > children & adults. 75 – 80 % of TBW. about 50% in adult females + the elderly TBW gradually decreases throughout infancy: postnatal reduction most pronounced during 1st six months. 6 month – 11 yrs.: 53 – 63 % TBW Water content Prevailing theories re TBW distribution in infants: i. ii. greater surface area/volume ratio. kidney relatively undeveloped: o o iii. inability to concentrate urine. rudimentary LOH & counter-current exchange mechanisms. higher metabolic rates. Water content Forms medium for metabolic processes: medium for suspension of body solutes. homeostasis varies with small changes in medium composition: o precise regulation of volume & composition of fluids. Body fluid system not a static system: dynamic steady state with environ. and internally between fluid compartments. Water content Accurate estimation important clinically: pulmonary embolism congestive heart failure Daily body wgt. est. is a useful indicator: reliable est. of the segmental dist. poor. acute changes more practical. Water content Daily water intake: i. ii. ingestion accounts for about 2100 ml/day. the result of oxidation of carbohydrates accounts for about 200 ml/day. Water content Daily water output: i. ii. insensible water loss: evaporation from respiratory tract and skin about 700 ml/day sensible water loss: 1600 mL/day a. b. c. sweat - about 100 mL/day faeces - about100 mL/day urine - about 1.4 L/day Water – gains + losses Table 8-2; pg 168 Gains + losses About 100 mL H O needed per 2 100 mL calories metabolized: 1000 calories : 1000 mL H2O for efficient excretion. Fever: 12% rise in metabolism per 1 ͦ C rise in body temp: o o increase H2O loss. increased resp. rate – further loss. Gains + losses Fluid requirements driven by metabolic rate: oral intake is the main source of gain. metabolism generates a small amt. (150 – 300 ml). parenteral administration. majority of H2O loss via kidneys: o o smaller vol. via skin and GI tract. increased resp. rate. Balance between water intake (2500 ml/day) and output (2500 ml/day) Category Water Men 60% Women 50% Newborn babies 70-75% Water percentage decreases as the person gets older (Why?) Women have low water percentage compared to men (Why?) Body compartments Broadly, 2 major compartments – intracellular & extracellular divisions. Vary markedly in composition: intra- - H2O + solutes forming medium for cell metabolism: o predominantly localized to the cytosol. Body compartments extra- - surrounds cells & serves as medium for cellular exchange processes: o plasma, interstitial, lymph, extra- parts of bone, cartilage and dense connective tissue. Body compartments ⚫ Three compartments: Intracellular - Fluid contained within cells by semi-permeable membrane (27 L - 40% body weight (bw)) Extracellular – 15L (20% bw); divided into: o Extracellular interstitial - Fluid surrounding & bathing cells (12L – 15% bw) o Extracellular intravascular - Fluid outside of cells but within vessels – plasma (3L – 5%) Body compartments Minor sub-division: Transcellular fluid – Not within cells but separated from plasma and interstitium by cell barriers: cerebrospinal, peritoneal, synovial and pleural fluids. vary in electrolyte composition. Extracellular fluid Mainly responsible for transport of water, electrolytes and waste – plasma + interstitium: plasma has high protein content – role in Starlings Forces (colloid oncotic pressure). interstitium has fewer proteins. High Na+ concentration. K+ ion concentration lower than inside cell. Extracellular Homeostaticfluid functions – transport of oxygen and nutrients and the removal of waste: o o solute balance between in- & outside of cell produces a concentration gradient – osmosis, diffusion etc. Blood flow delivers oxygen and nutrients to vessels: plasma filtration across capillaries into interstitium. Composition controlled by kidneys. Intracellular fluid Separated from ECF by plasma membrane. Mainly responsible for transport of water, electrolytes and waste. It contains small amounts of Na + and Cland almost no Ca2+. Contains large amounts of K and P but moderate amounts of Mg2+. Also contains large amounts of proteins. Extracellular fluid CATIONS (mmol/l) Na K Plasma Interstitial Intracellular 142 139 14 OMPOSITION OF BODY FLUIDS 4.2 4.0 140 1.3 1.2 0 0.8 0.7 20 Cl 108 108 4.0 HCO3 24.0 28.3 10 Protein 1.2 0.2 4.0 HPO4 2.0 2.0 11 Ca Mg ANIONS (mmol/l) Estimation principles Only possible to est. TBW and plasma volume by direct meas. Small vertebrates – meas. of TBW before + after desiccation. blood vol. - exsanguination obviously proscribed for human studies. Problems assoc. with defining limits of various compartments. Estimation principles Indicator dilution technique: robust est. of body water content. A known amt. of indicator substance (Q) is added to H2O in an odd-shaped container of intermediate dimensions: allowed to equilibrate the vol. (V) of the H2O is est. by det. the conc. (C) of indicator. Estimation principles Since Q = VC, then V=Q/C Ideally, an indicator substance should: must be uniquely equilibrated in compartment in question: o o rapid dist. even dist. (TBW) Estimation principles Plasma conc. should be representative of compartment in ques. Metabolic degradation + excretion must be precisely controlled for: o not excreted – not possible!: o correction factor Non-toxic Estimation principles Indicator removal from circulation follows first-order kinetics: rate of disappearance prop. to conc. semi-algorithmic plot yields linear rel. after indicator is uniformly dispersed. Estimation principles non-linear (1st) portion shows initial mixing of indicator upon infusion: o extrapolation to t0 = indicator conc. with instant equilibration; no excretion/metabolism. linear – exponential fall in plasma conc. due to excretion/metabolism. Plasma conc. of indicator substance vs. time Estimation principles Water-soluble indicators generally used: distributed only in aqueous phase of plasma. hence, if 7% is protein, indicator plasma conc. = plasma conc. X 0.93 also, if ionic, affected by Donnan effect. TBW est.: antipyrine – analgesic, antipyretic, cost effective (D20)16 tritiated water (3H2O) – est. in liquid scintillation counter. Estimation principles Plasma & blood vol.: Risa + Evans blue binds avidly to albumin. rapid mixing in circ. – uniformity < 15 min. albumin loss from circ. a modulator. o correction – semi-algorithmic plot Total plasma vol. - approx. 4-5% b.w. Estimation principles Since blood volume is a function of the aqueous + non-aqueous plasma volumes + erythrocyte count: Estimation principles ICF and ECF: both portions limited primarily as there is no clear cut general consensus as to their physical boundaries. makes vol. det. esp. troublesome. penetration by indicator fluid incomplete. Utility: ICF - Fractional decrease in body mass with age. up to 20—25% Mechanism of fluid transport Electrolytes – substances that dissociate in solution, forming charged particles (ions). Na+Cl- Na+ + Cl- Non-electrolytes – do not dissociate into ions – urea & glucose. Attractive forces allow anions to accompany cations: equal amt. of either in body fluids. cation/anion are often exchanged for likecharged ions in vivo.?? Mechanism of fluid transport Diffusion: the random movement of particles in all directions through a solution. Active transport: movement of solutes across membranes; requires energy expenditure. Filtration: transfer of water and solutes through a membrane from a region of high pressure to a region of low pressure. Osmosis: movement of water across a semipermeable membrane from a lesser to a more concentrated solution. Mechanism of fluid transport Diffusion: movement of charged and uncharged particles along conc. gradient: energy is supplied by constant random motion. higher conc. = > constant motion. hence, transfer from higher to lower conc. expressions – mg/dL, mEq/L or mmol/L. Mechanism of fluid transport Osmosis: translocation across semipermeable membrane: freely re H2O, but not solutes. as H2O moves btw. compartments it generates an osmotic pressure. osmotic pull of H2O creates a constant conc. grad. in the ICF & ECF. Osmotic press. = hydrostatic needed to oppose movement across the membrane (mm Hg). Osmole – osmotic activity exerted by nondiffusible particles in pulling H2O across membrane: gram mol. wgt. of non-diffusible non-ionizable substance = 1 osmole. Osmotically-active particles all have similar potential: the # of particles is consequential, but not particle size. Serum osmolarity 275 - 295 mOsm/kg (due to Na+ + attendant Cl- & K+): glucose + BUN – 5%. ?? Mechanism of fluid transport The rate of water movement is the rate of osmosis: Osmole: the total number of particles in a solution. Osmolality if measured by Osmole/Kg of water and Osmolarity if measured in Osmole/L of solution. 80% of total ECF osmolarity is due to Na and Cl. 50% of total ICF osmolarity due to K. - + + Movement across semip membrane Fig 8-2; p. 161 Mechanism of fluid transport Osmotic pressure: water freely permeable among all compartments. dist. det. by extent of its physical forces. tendency to ‘escape’ driven by vapour pressure and chemical potential. moves from higher – lower potential. chemical potential of water increased with hydrostatic and temp: ▪ falls with solute increase: o increased osmolality Osmosis/Diffusion ? Donnan equilibrium Donnan equilibrium Consider compartments A & B separated by membrane – impermeable to proteins but not H2O & small solutes: differing conc. Of Na+Cl- on either sides. rapid bi-directional exchange. Donnan equilibrium Electrical neutrality dictates – no net movement of anion in any direction unless there is comparable cationic displacement: ▪ should culminate in no net flux. Donnan effect results from uneven dist. of non-diffusible ions in vs. outside cells: ▪ ▪ causes uneven ion translocation. aim is electrical neutrality. Donnan equilibrium Now add protein to A: - -vely charged at body pH: since non-diffusible into B, A becomes –ve. electrical neutrality – necessitates > movement of cations into A. hence, electrical charge imposed by proteins dictate that, at equilibrium, an excess of cation must move to A, while diffusible anion transport to is reduced. [Na+]I [Cl-]I = [Na+]II [Cl-]II Fluid pressure (Starling’s Law) Ernest starling – Starling’s principle: also Frank-Starling’s Law. ECF and ICF fluid shifts occur due to changes in pressure within the compartments. Fluid flow only when there is a pressure difference. Fluid pressure (Starling’s Law) Pressure classification according to tonicity into 3 classes: isotonic: IC=EC and solutes can’t leave the cell. hypotonic: has lower concentration of solutes. Water will diffuse out of cell. hypertonic: has higher concentration of solutes. Water move into cell causing swelling. Fluid distribution ECF distribution between plasma and interstitial spaces determined by: Hydrostatic pressure – exertional forces within capillaries. Colloid osmotic – pressure exerted by proteins. The distribution of fluid between IC and EC fluids is determined by osmotic effect of smaller solutes across the cell membrane: osmosis + diffusion. Hydrostatic pressure Exertional force caused by the pressure generated by fluids within system: approx. 30 & 10 mm Hg at arterial & venous ends, respectively. in the interstitial space, fluid force acting on the outer capillary wall. Experimental data suggest a –ve interstitial force: promotes movement from capillary – interstitium. exception – capillary venules. Hydrostatic pressure P 164 Colloid osmotic pressure Pulling/suction force caused by the dispersion of particles; proteins: about 28 mm Hg across capillary bed. interstitial colloidal press., 8 mm Hg: o represents few protein leached from cap’. Cap’ colloidal > venous end hydrostatic + interstitial colloidal press.: capillary colloidal largely responsible for reuptake in microcirculatory venules. Colloid osmotic pressure P 164 Lymphatic drainage Accessory system by which a fraction of the interstitial fluid is transported via specialized ducts: lymph – nutrients + immune cells: o drained from the thoracic ducts into the subclavian vein: o spleen – WBC. no autoregulation – muscle + joint pumps. any interstitial protein is removed via lymphatics. Lymphatic removal P 164 Fluid distribution Tissue fluids and plasma in the capillaries exert both hydrostatic forces and colloid osmotic pressure: exertional forces hydrostatic pressure forces fluid and solutes through the capillary walls. similar exertional & colloid forces in interstitium. o what about interstitial oncotic? Fluid distribution If> than hydrostatic press. within capillary is the pressure in the surrounding interstitial space, fluids and solutes within the capillary are forced into the interstitium: net movement driven by compartmental pressure difference. mainstay in determining fluid volume + composition. functions similar to electrical neutrality – net movement from area of high to low potential. except with active processes. Role of albumin Reabsorption prevents detrimental capillary fluid loss. Albumin – no transcellular transport. when fluid filters through the capillary, albumin remains. When the conc. of albumin increases, fluid begins to move back into the capillary wall by osmosis. Colloid oncotic pressure - pulling force of albumin in the intravascular space. Starling’s Forces recap Four classes: Hydrostatic pressure in the capillary (Pc) Hydrostatic pressure in the interstitium (Pi) Oncotic pressure in the capillary (pc) Oncotic pressure in the interstitium (pi) Hydrostatic & colloid osmotic pressure - recap Hydrostatic pressure forces fluid and solutes through the capillary walls. Greater hydrostatic press. inside the capillary vs. the interstitium, forces fluids and solutes into the interstitial space. Hydrostatic & colloid osmotic pressure – recap "... there must be a balance between the hydrostatic pressure of the blood in the capillaries and the osmotic attraction of the blood for the surrounding fluids. "... whereas capillary pressure determines transudation, the osmotic pressure of the proteins of the serum determines absorption." Starling’s Forces ? Exchange between ECF & ICF Marked variation in their ionic compositions. Osmotically active solutes essentially mirror one another: animal cells freely permeable to H2O with no net hydrostatic pressure difference. osmotically active solutes contribute to hydrostatic pressure forces. protein conc. far > intracellularly o active transport mechanisms limit solute content within cells - swelling Exchange between ECF & ICF – osmotic uniformity Na+ Cl- Glucose (200 mOsm/kg) Footnote – [previous fig.] Both compartments are impermeable to Na+, Cl- & glucose but permeable to urea and H20: A - contains glucose @ 200 mOsm/kg in I; Na+Clsolution in E at 200 mOsm/kg compartments are in osmotic equilibrium. B - If more NaCl is added to E, its osmotic potential falls: water transfer to E is induced until uniformity is attained. C - Compartment E expands in the process. both compartments now have higher solute conc. solute conc. in I rises as water is translocated to E, expanding the volume in E, while shrinking I. Capillary/interstitial exchange Transfer btw vascular & interstitium occurs at level of capillaries. Four governing forces control such transfer: capillary filtration pressure (hydrostatic) capillary colloidal pressure (oncotic) interstitial/tissue oncotic pressure interstitial/tissue hydrostatic pressure Net oncotic or hydrostatic pressure determines fluid flux. Capillary filtration pressure Capillary filtration – causes movement due to mechanical rather than osmotic forces: 30 – 40 mm Hg @ arterial end. 10 – 15 mm Hg @ venous. balanced @ mid-section. A function of arterial + venous press., pre- + postcapillary resistances and gravitational forces: rise in arterial + venous – > systemic capillary press. gravity causes capillary press. increase while standing. Capillary filtration pressure Upon dependency, the wgt. of blood in vascular column results in a 1 mm Hg press. rise for every 13.6 mm Hg dist. from the heart: this scenario can creates a pressure of up to 90 mm Hg in the feet. the weight exerted by blood in the vascular system when standing is a result of the water constituent of blood. hence, the term hydrostatic pressure. Capillary oncotic/osmotic pressure Generated by plasma proteins; too large to cross capillary barrier: approx. 28 mm Hg. Mechanical pressure within vessels. differs from osmotic pressure at cell membranes: o due to electrolytes + non-electrolytes. Capillary oncotic/osmotic pressure retains capillary integrity – not all fluid is lost – equilibrium. o caused by non-diffusible proteins. o > capillary than interstitial conc., hence pulls fluid into capillary. o some return via lymphatics. Capillary oncotic pressure Interstitial fluid press. & the interstitial oncotic press. determine in & out of the interstitium: interstitial hydrostatic is generally negative. however, value det. by capillary processes in vascular regions. the interstitial oncotic reflects the small amt. of protein in the interstitium. Exchange btw ECF & ICF Not all cells demonstrate isosmotic tonicity with ECF: many secretory cells demonstrate this property. ascending loop of Henle – impermeable to water: o o o secretes ions in accordance with systemic requirements. CD and DT (ADH) – antidiuresis important in determining urine conc. Osmotic asymmetry induce net transfer until uniformity regained: determined by ECF conc. Exchange btw ISF & plasma Transfer from interstitial to vascular ECF driven by capillary hydrostatic and colloid pressures: hydrostatic – forces fluid outwards. oncotic pressure – opposing force. small solutes & ions diffusible – contribute to plasma osmotic forces. impermeable to protein – interstitial protein conc. very low: o Clinical: – curtails the amt. of fluid filtered from the circulation. Exchange btw ISF & plasma At 37°C a solute conc. of 1 mOsm/kg exerts an osmotic pressure = 19.3 mm Hg: since plasma protein conc. = 0.9 mM. plasma protein pressure = 17 mm Hg. Donnan equilibrium – contributes an additional 9 – 10 mm Hg of plasma oncotic capillary pressure. o > translocation to plasma vs. interstitium. total pressure 25 – 30 mm Hg. Exchange between ISF & plasma – Starling’s Forces Fluid exchange - lymphatics Capillaries predominantly a protein barrier. However, small amt. do escape on occasions: channeled to lymphatics – accessory route back to circulation. prevents pooling in interstitium: o o defect – interstitial & plasma colloid pressure the same. plasma colloid osmotic press. = 0. Fluid exchange - Lymphatics Lymphatic fluid volume is always considerable but much > with expanded ISF. Fluid movement propelled by tissue movement and muscular contractions. Smaller vessels anastomose into larger: right thoracic duct – right thorax. left thoracic duct – body regions excluding head, right thorax & neck. Ultimately retuned to general circulation: ducts terminate into subclavian vein. Homeostasis Maintaining ECF volume is critical to maintaining blood pressure ECF osmolarity is of primary importance in long-term regulation of ECF volume ECF osmolarity maintained mainly by NaCl balance: o intake: 10.5g/d output: 10g/d in urine Water and electrolyte balance controlled by the kidneys: regulatory mechanisms include – neural and hormonal. Regulation of ECF volume Mechanisms: Neural Renin-angiotensinaldosterone Atrial natriuretic hormone (ANH) Antidiuretic hormone (ADH) Increased ECF results in: decreased aldosterone secretion. increased ANP secretion. decreased ADH secretion. decreased sympathetic stimulation. Decreased ECF results in: increased aldosterone secretion. decreased ANP secretion. increased ADH secretion. increased sympathetic stimulation. Regulation of Fluid Volume Role of the kidneys: capillary pressure forces fluid through the walls and into the tubule. at this point H2O or electrolytes are then either retained or excreted. the urine becomes more dilute or more concentrated based on requirements. Antidiuretic hormone Produced by the hypothalamus. Stored in the pituitary gland. Restores blood volume by decreasing excretion of water. Increased osmolality or decreased blood volume stimulates the release of ADH. Increased permeability of collecting ducts to water – aquaporin. Also may be released by stress, pain, surgery, and some meds. Renin-angiotensinaldosterone system Renin secreted by kidney’s JG cells: amount of renin produced depends on blood flow and amount of Na+ in the blood. Modulates angiotensin II release (vasoconstrictor). Angiotensin causes peripheral vasoconstriction. Angiotensin II stimulates the production of aldosterone. Aldosterone Secreted by the adrenal gland response to angiotensin II. The adrenal gland may also be stimulated by the amount of Na+ and K+ in the blood. Causes the kidneys to retain Na+ and H2O. Leads to increases in fluid volume and Na + levels. Decreases the reabsorption of K+. Maintains BP and fluid balance. Atrial natriuretic peptide (ANP) Released by myocardial cells. Released in response to increased atrial pressure. Opposes the renin-angiotensin-aldosterone system. Stimulates excretion of Na+ and H2O Suppresses renin level. Decreases the release of aldosterone. Decreases ADH release. Reduces vascular resistance by causing vasodilation. Fluid shifting Blood pressure maintenance: slow shift between intra-vascular, interstitium and inter-cellular spaces. interstitium = reservoir of excess fluid fall in capillary pressure result in osmotic influx. reverse for hypertension. 1st space shift- normal distribution of fluid in both the ECF and ICF compartments. Fluid shifting 2nd space shift - excess accumulation of interstitial fluid (oedema) 3rd space shift- fluid accumulation in transcellular space –ascites and pleural effusion. Regulation of fluid volume Factors affecting fluid composition Physiological: adipose Tissue sex age Pathological: dehydration over-hydration Dehydration Loss of water from the body. Includes vomiting, diarrhea, sweating, & polyuria: leads to  in both ECF & ICF volumes.  osmolarity in both ECF & ICF. General signs: dry tongue loss of skin elasticity Dehydration soft eyeballs (due to lowering of intraocular tension).  blood pressure.  Hb, &  Hct. Treated with fluid replacement (orally, or IV). Hypotonic Hydration Cellular over-hydration/ H O intoxication 2 renal insufficiency or an extraordinary H 2O ingested rapidly: ECF is diluted – sodium content is normal but excess H2O. resulting hyponatremia promotes net osmosis into tissue cells - swells. these events must be quickly reversed to prevent severe metabolic disturbances: o particularly in neuronal cells. Oedema Atypical accumulation of fluid in the interstitial space, leading to tissue swelling. Nonspecific – abnormal fluid gain: no delineation between ICF and ECF. mostly ECF – term, therefore, refers to detectably abnormal ECF expansion. Proximate cause – Starling’s force disturbances: localized – inflammatory response. general – mainly due to poor Na+ & H2O retention. Oedema Palpable swelling of the interstitial space. Generally not noticeable until the interstitial fluid has exceeded 2.5 to 3 L. Specific alterations include: 1. increased capillary filtration 2. decreased colloid/osmotic 3. increased capillary permeability 4. lymphatic flow obstruction Oedema Factors that accelerate fluid loss include: increased blood pressure, capillary permeability. incompetent venous valves, localized blood vessel blockage. congestive heart failure, hypertension, high blood volume. altered vascular fluid return usually reflects an imbalance in colloid osmotic pressures: o hypoproteinemia – low levels of plasma proteins. Oedema Simple forms of edema include: varicose veins in lower legs. pressure increase in extremities upon prolonged quiet standing. Flow interruption to the legs: HC pressure at venous end of capillary becomes abnormally elevated. net reabsorption is impaired – fluid pools in interstitial spaces. Oedema Congestive heart failure – impaired pumping capacity: venous pooling. increased peripheral venous pressures. pulmonary + peripheral implications. Simplification of cardiac involvement – by detection of the rise/fall in CO, mechanisms are induced which serve to either promote water retention/excretion: expansion or contraction of the ECF. (In)decrease compartmental osmolarity. Oedema Inflammation: recruitment of inflammatory mediators: increased capillary permeability. facilitate leakage of proteins to interstitium. IO > CO + IH Oncotic (colloid) pressure. net sequestration in the ECFI ensues due to high capillary hydrostatic + high interstitial oncotic pressures. Oedema Similar mechanism for oedema due to lymphatic obstruction: No escape route for the few proteins that reach the interstitium. Increased capillary filtration Rise in filtration press. increases fluid displacement from vasculature; secondary to: i. ii. iii. iv. rise in arterial pressure fall in arterial resistance (R) through capillary sphincters. increased venous pressure increased R to post-cap’ outflow. Increased capillary filtration May be localized or generalized: Localized - allergic reactions s.a. hives. anti-inflammatory mediators + histamine: o cause swelling of pre-cap’ sphincters + arterioles. increased venous pressure. increased R to post-cap’ outflow. Increased capillary filtration Thrombophlebitis: blood clot formation within venous network. affects superficial as well as deep vessels. interruption affects post-capillary vessel outflow. results in supra-normal venous pressures. predominantly localized to lower extremities. Increased capillary filtration Generalized (anasarca) – result of increased vascular volume: related to vasodilation of superficial vessels. H2O + Na+ retention also a feature. Common in conditions assoc. with water retention and/or vascular congestion – congestive heart dis. + right heart failure: fluid pools in vessels – poor return of P.A. swelling of dependent extremities. Decreased capillary colloid oncotic: Osmotic potential due to colloids (plasmatic, large mol. wgt.) and NOT solutes as in general osmosis: albumin (69k), fibrinogen (140k) & globulin (400k). 1g albumin has 2x osmotic’ particles as fibrinogen & 6x globulin, resp.: ▪ ▪ related to lower mol. wgt. albumin (4.5 g/dL) > globulin (3.5 g/dL) > fibrinogen (0.3 mg/dL). Hence, decreased CCOP related to loss of or inadequate protein prod. Decreased capillary colloid oncotic: Acute/chronic hepatic abnormalities: plasma proteins synthesized in liver. impairment can lead to suboptimal protein conc. by virtue of its osmotic potential, albumin is the primary protein related to Starling’s disturbances. Malnutrition – low amino acid bioavailability: impaired protein synthesis. Decreased capillary colloid oncotic: Renal – glomerulonephritis: inflammatory phenotype loss through endothelium (esp. albumin) homogenous dist. of plasma proteins throughout: also, not gravity-related. ▪ produces generalized, NOT dependent oedema: o feet + facial indications. Burns – loss of proteins via skin. Increased capillary permeability: Enlargement of the capillary pores: inflammatory mediators – cytokines & other immune responses. reactive oxygen species proliferation. systemic and/or pulmonary infections. protein leakage into interstitial space: o increases tissue fluid vol., secondary to increased capillary osmotic forces. Lymphatic obstruction Lymphedema – obstruction of lymph nodes: surgical removal of nodes. malignancies An accessory route back to the general circulation: large particles incl.. proteins cannot reenter via capillary wall. may raise OI. Lymphatic obstruction Loss or trapping of ECF in transcellular spaces: serous fluids continual movement of body struc.: ▪ governed by same principles re fluid transport elsewhere. structurally-linked to lymphatics: ▪ pumping action cause by moving parts – drains protein + solutes into lymph, then gen. circ. Lymphatic obstruction Oedema is the accumulation of fluids, predominantly in the ECF but also within the ICF & 3rd fluid spaces, that contribute to overall body weight but NOT to the homeostatic fluid reserve or to physiological function. Diagnostic tests for fluid excess (F/E) Urinalysis: Urine pH Urine Specific gravity Urine osmolarity Urine creatinine clearance Urine sodium Urine potassium Blood Studies Serum Hematocrit = 40-54%/men, 3847% for women Blood urea nitrogen = 8-20 mg/dL Serum Creatinine = 0.6 – 1.5 mg/dl Serum osmolality Serum Albumin – 3.5-5.5 g/dL Serum Electrolytes Assessment of F/E Balance History of potential factors which place patient at risk. Vital signs Body weight Skin Mucus membranes Fluid volume deficit Hypovolemia - Dehydration hypertonic ECF isotonic ECF contraction: deficiency of both H2O + electrolytes. caused by decreased intake, vomiting, diarrhea, fluid shift. contraction: deficiency of water. caused by water loss related to high blood glucose, inadequate ADH production, high fever, excess sweating. Assessment of fluid deficit Hypotension Weak rapid pulse Temperature changes Weight loss Skin turgor poor Concentrated urine and blood Fluid volume excess Extracellular: Intracellular: H2O isotonic fluid excess: excess of both water and electrolytes. caused by retention of H2O + electrolytes related to kidney disease; overload with isotonic IV fluids. excess: excess body H2O but not electrolytes. caused by overhydration in the presence of renal failure Transcellular fluids Body fluids which are formed by secretion of epithelial cell. Contained within epithelium lined spaces: Cerebrospinal fluid Peritoneal Synovial Pleural fluids. Cerebrospinal fluid Choroid plexus - constellation of modified ependymal cells @ fourth ventricle of brain: produces CSF. at rate @ 20 ml/hr (adults) CSF flows through the subarachnoid space where a volume of 90 – 150 ml is maintained (adults) neonate volume 10-60 mL Reabsorbed at the Arachnoid villus: eventually reabsorbed into the blood Cerebrospinal fluid CSF - functions As shock absorber. as mechanical buffer. cushion between the brain and cranium. Act as a reservoir and regulates the contents of the cranium. Serves as a medium for nutritional exchange in CNS. Transport hormones and hormone-releasing factors. Removes the metabolic waste products through absorption. Peritoneal fluid Produced in abdominal & pelvic cavities: lubricates peritoneal tissues pathological increase – ascites Contains many enzymes: amylase LDH telomerase Presence generally an indication of ascites or malignancies. Peritoneal fluid Serum-ascites albumin gradient (SAAG) most useful indicator for evaluating peritoneal fluid. SAAG = albumin conc. of serum minus albumin conc. of ascitic fluid. High gradient: > 1.1 g/dL – due to portal hypertension. Important causes of high SAAG (> 1.1 g/dL) include: high protein : heart failure. low protein : cirrhosis of the liver. Synovial fluid Ultrafiltrate of blood plasma combined with hyaluronic acid: produced in the joints space by the synovial cells lining synovial tendon, joints, etc. Composition similar to plasma as small ions and molecules readily pass into the joint space. Reabsorption – lymphatics. Acts as a lubricant and adhesive, and provides nutrients for articular cartilage. Synovial fluid Examination of synovial fluid is essential to differentiate infectious from noninfectious arthritis. Mucin clot test: Add acetic acid to SF → precipitates hyaluronate into a mucin clot which may be graded as good, fair or poor Fair to poor mucin clot → reflects dilution and depolymerization of hyaluronic acid - a nonspecific inflammatory finding. Synovial fluid Pleural fluid Plasma filtrate derived from capillaries of the parietal pleura. Pleural cavity normally contains small amount of fluid that facilitates movement of two membranes against each other. Produced continuously at the rate dependent on capillary hydrostatic pressure, plasma oncotic pressure and capillary permeability. Pleural fluid Reabsorbed – lymphatics and venules of visceral pleura. Volume – about 10ml each. Abnormal fluid accumulation – an effusion, results from imbalance between the fluid production and reabsorption Fluid accumulation in pleural, pericardial and peritoneal cavities → serous effusion Pleural fluid