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Fluids in Human Body

I. Fluid Status of Human Body A. Homeostasis: state of the body when maintaining a state of balance in the presence of constantly changing conditions B. Includes balance of fluid, electrolytes, and acid-base balance . Body water inta!e and output appro"imately e#ual $%&'' m()%* hr.+ II. Body Fluid omposition A. ,ater: -'. of body weight B. /lectrolytes: substances that become charged particles in solution 0. ations: positi1ely charged $e.g. 2a3, 43+ %. Anions: negati1ely charged $e.g. l-+ 5. Both are measured in millie#ui1alents per liter $m/#)(+ . 6smolality: concentration of a solution measured in milliosmoles per liter 7. Balance of hydrostatic pressure and osmotic pressure regulates mo1ement of water between intra1ascular and interstitial spaces III. Body Fluid 7istribution: A. % body compartments: 0. Intracellular fluids $I F+: fluids within cells of body 8ma9or intracellular electrolytes: :otassium $43+, ;agnesium $;g 3%+< %. /"tracellular fluids $/ F+: fluid outside cells= 8ma9or e"tracellular electrolytes: Sodium $2a3+, hloride$ l-+<= this is where transportation of nutrients, o"ygen, and waste products occurs B. (ocations of / F: 0. Interstitial: fluid between most cells

%. Intra1ascular: fluid within blood 1essels= also called plasma 5. >ranscellular: fluids of body including urine, digesti1e secretion, cerebrospinal, pleural, syno1ial, intraocular, gonadal, pericardial I?. ;echanisms of Body Fluid ;o1ement $i.e. mo1ement of solutes, sol1ents across different e"tracellular locations+ A. Osmosis: water is mo1er= water mo1es from lower concentration to higher concentration 0. 2ormal 6smolality of I F and / F: %@& A %B& m6sm)!g %. >ypes of solutions according to osmolality a. Isotonic: all solutions with osmolality same as that of plasma Body cells placed in isotonic fluid: neither shrin! nor swell b. Hypertonic: fluid with greater concentration of solutes than plasma ells in hypertonic solution: water in cells mo1es to outside to e#ualiCe concentrations: cells will shrin! c. Hypotonic: fluid with lower concentration of solutes than plasma ells in hypotonic solution: water outside cells mo1es to inside of cells: cells will swell and e1entually burst $hemolyCe+ 5. 7ifferent intra1enous solutions, used to correct some abnormal conditions, categoriCed according to osmolality: a. Hypertonic: &.glucose ,*&. 2a l solution b. Isotonic: B. 2a l, (actated Dingers solution c. Hypotonic: *&. 2a l B. Diffusion: solute molecules mo1e from higher concentration to lower concentration

0. Solute, such as electrolytes, is the mo1er= not the water %. >ypes: simple and facilitated $mo1ement of large water-soluble molecules+ . Filtration: water and solutes mo1e from area of higher hydrostatic pressure to lower hydrostatic pressure 0. Hydrostatic pressure is created by pumping action of heart and gra1ity against capillary wall %. Esually occurs across capillary membranes 7. Active Transport: molecules mo1e across cell membranes against concentration gradient= re#uires energy, e.g. 2a A 4 pump ?. ;echanisms that Degulate Homeostasis: How the body adapts to fluid and electrolyte changes A. Thirst: primary regulator of water inta!e $thirst center in brain+ B. Kidneys: regulator of 1olume and osmolality by controlling e"cretion of water and electrolytes . Renin-angiotension-aldosterone mechanism: response to a drop in blood pressure= results from 1asoconstriction and sodium regulation by aldosterone 7. Antidiuretic hormone: hormone to regulate water e"cretion= responds to osmolality and blood 1olume /. Atrial natriuretic factor: hormone from atrial heart muscle in response to fluid e"cess= causes increased urine output by bloc!ing aldosterone

Fluid and Electrolyte m!alances I" Fluid ?olume 7eficit $too little fluid in body+ A. ommon Stimuli:

0. /"cessi1e fluid loss, e.g. hemorrhage, e"cess loss of FI fluids $1omiting, diarrhea, or wound drainage+ %. Insufficient fluid inta!e, e.g. no access to fluid, unable to drin! 5. Failure of regulatory mechanisms, fluid shifts B. >erminology: 0. 7ehydration: technically loss of water alone $but usually any state of low fluid+ %. Hypo1olemia: decreased circulating blood 1olume 5. >hird Spacing: shift of fluid from 1ascular space $inside blood 1essels+ to another area such as abdomen)bowels, soft tissues $li!e swelling that occurs with a se1ere in9ury Ali!e a twisted an!le+ . Signs)Symptoms ;ore rapid fluid loss, e#uals more rapid de1elopment of symptoms 0. ,eight loss $liter fluid G %.% lb or 0 !g.+ %. 7iminished s!in turgor, tongue turgor $more reliable in elderly+ 5. :ostural $orthostatic+ hypotension: drop of 0&mm Hg of systolic B: with position change from lying to standing *. Flat nec! 1eins when recumbent &. 7iagnostic test findings $usual, not absolute+: a. /lectrolytes: isotonic fluid loss: 2a is within normal limits= if loss of water only, 2a is ele1ated

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b. Serum 6smolality: isotonic fluid loss: osmolality is within normal limits= loss of water alone, osmolality is ele1ated c. Erine specific gra1ity, urine osmolality: both ele1ated as urine becomes more concentrated as !idneys conser1e water d. Increased hematocrit due to hemoconcentration e. :ossible ele1ated blood urea nitrogen $BE2+ f. ?: $mean pressure in right atrium of heart+ sub normal 7. ompensatory ;echanisms $how the body responds to restore homeostasis+ Foal: to conser1e water and 2a= to maintain circulation 0. >achycardia $may lead to hypotension+ %. ?asoconstriction as e1idenced by pale, cool s!in 5. 7ecrease in urinary output with rise in urine specific gra1ity /. ollaborati1e are 0. :re1ent deficits in clients at ris!: especially aged= anyone with increased fluid loss, such as persons with prolonged 1omiting and diarrhea= during hot weather, those under physical e"ertion without ade#uate fluid replacement %. orrect the deficits and treat the underlying cause a. Deplacement of fluids and electrolytes by oral, I?, or enteral route= Isotonic

electrolyte I? solutions for hypotensi1e clients and those with abnormal losses b. Fluid challenge: :hysician orders a specific amount of I? fluid o1er short period of time $e.g. 5'' m( of isotonic solution o1er 0' minutes+. 6btain baseline assessment of 1ital signs, breath sounds, output, mental status before initiation= compare results after fluid challenge completed= physician re-e1aluates response and orders fluids accordingly c. Assess parameters pertinent to the signs and symptoms, 1ital signs, and le1el of consciousness= reassess lab results d. 2otify physician if urine output H 5' m()hr $client has a foley catheter with hourly output as monitoring+ 5. :ertinent nursing diagnoses a. 7eficit Fluid ?olume b. Ineffecti1e >issue :erfusion c. Dis! for In9ury II.Fluid ?olume /"cess $too much fluid in body+ ,ater and sodium are proportionately e"cessi1e and in e"tracellular compartment A. ommon Stimuli $one or combinations of conditions+ 0. :athophysiology: mechanisms that should maintain homeostasis are impaired: a. Heart failure b. 4idney failure

c. irrhosis of li1er d. Adrenal disorders or corticosteroid administration e. Stress conditions causing release of A7H and aldosterone %. /"cessi1e inta!e of sodium and fluid a. /"cessi1e inta!e of foods high in sodium $salt+ b. /"cessi1e inta!e of I? fluids containing sodium $'.'B. 2a l+ B.>erminology 0. Hyper1olemia: e"cess intra1ascular fluid %. /dema: e"cess interstitial fluid .Signs)Symptoms 0. ,eight gain: I &. of body weight o1er short time %. irculatory o1erload: bounding pulse= S5 heart sound= nec! and peripheral 1ein distention= increased ?:, i.e. mean pressure in right atrium of heart= cough= dyspnea= orthopnea= breath sounds, moist crac!les= pulmonary edema= polyuria= ascites 5. :eripheral edema worse in most dependent body part: pedal, sacral for bed-bound client= anasarca $se1ere generaliCed o1er all body edema+= possibly cerebral edema, i.e. altered mental status *. 7iagnostic test findings: a. hest "ray: 1ariable degrees of pulmonary edema

b. Serum sodium and osmolality: usually within normal range c. Hematocrit and hemoglobin: usually slightly decreased d. 7ecreased blood urea nitrogen $BE2+, in some cases 7. ompensatory ;echanisms Heart failure results when heart is unable to increase wor!load to handle e"cess blood 1olume 0. (eft-side heart failure: pulmonary edema %. Dight-side heart failure: peripheral edema /. ollaborati1e are 0. :re1ent fluid 1olume e"cess in at ris! populations $those recei1ing I? fluids, significant at ris! health histories, elderly+ %. /ffecti1e fluid management: a. Assessment of signs)symptoms of fluid o1erload, lab results b. Fluid restrictions as ordered c. 7ietary management: sodium-restricted diets d. ;onitor inta!e and output, daily weights 5. >reatment with diuretic medications a. (oop diuretics $e.g. Furosemide $(asi"++ b. >hiaCide-type diuretics $e.g. HydrochlorothiaCide $H >J++ c. :otassium-sparing diuretics $e.g. Bumetanide $Bume"++ F. 2ursing 7iagnoses 0. /"cess Fluid ?olume

%. Dis! for Impaired S!in Integrity $related to peripheral edema+ 5. Dis! for Impaired Fas /"change $related to pulmonary congestion and)or edema+ *. Acti1ity Intolerance III. /lectrolyte Imbalances 6ne electrolyte or se1eral= often treat underlying cause= careful obser1ation as o1er treatment may cause additional imbalances A. Sodium 0. haracteristics: a. ;ainly in / F b. Blood normal 1alues: 05& A 0*& m/#)( c. Actions: 0. Degulates 1olume %. Degulates osmolality 5. ;aintains neuromuscular acti1ity d. Sources: dietary inta!e, prescription drugs and self-remedies e. ompensatory mechanisms: !idney e"cretes or conser1es sodium in response to changes in 1ascular 1olume, e.g. drop in blood pressure 0. Stimulates renin-angiotensionaldosterone system %. Degulates A7H secretion 5. ;odulates glomerular filtration rate *. ontrols Atrial natriuretic peptide release $sodium e"cretion+ %. Hyponatremia

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Serum sodium is lower than normal $Serum 2a H 05& m/#)(+ a. ommon Stimuli 0. ,ater shifts to / F= osmolality changes and cells swell %. (oss of sodium $without water+ a. /"cessi1e through urine $e.g.diuretics, !idney disease+ b. FI $e.g. 1omiting, diarrhea, FI suction+ c. S!in $e.g. sweating, burns+ d. ,ater gain to dilute / F 5. 7iseases: heart or renal failure= cirrhosis= Syndrome of Inappropriate secretion of Anti-7iuretic Hormone $SIA7H+= e"cessi1e hypotonic I? fluids b. Signs and Symptoms $depend on rapidity and se1erity of onset+ 0. /arly: $2a at 0%&+ a. ;uscle cramps, wea!ness, fatigue b. FI: anore"ia, 1omiting, diarrhea, nausea, abdominal cramping %. (ater $2aH0%'+ a. erebral edema symptoms $brain cells swell+ b. Headache, depression, personality changes

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c. (ethargy, muscle twitching, tremors d. Further progress to con1ulsions and coma with se1erely low le1els 5. 7iagnostic test findings a. 7ecreased serum 2a $H05& m/#)(+ b. Serum 6smolality $H%@& m6sm)!g+ c. %*-hour urine collection for 2a used to differentiate cause c. ollaborati1e are Destoration of blood 1olume and sodium le1els 0. ;edications a. Isotonic I? solution $DingerLs, '.B. 2a l+ b. Hypertonic I? 2a solution $5. 2a l+ is used to treat the client with se1ere hyponatremia $2a : 00' A 00& m/#)(+ c. (oop diuretics $e.g. Furosemide+ to promote isotonic diuresis %. Fluid and 7ietary ;anagement a. Increase foods high in sodium b. Destrict fluid in 1olume 5. Assessment of signs)symptoms of hyponatremia, especially

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a. ontinual mental status assessment b. SeiCure precautions c. Strict inta!e and output and monitoring weight daily d. Deassess lab results d. 2ursing 7iagnoses 0. Dis! for Impaired Fluid ?olume %. Dis! for 7ecreased Intracranial Adapti1e apacity 5. Hypernatremia Serum sodium is higher than normal $Serum sodiumI0*& m/#)(+ Hyperosmolality of / F= may occur with fluid 1olume deficit or e"cess a. ommon Stimuli 0. Sodium gained in e"cess of water, e.g. e"cessi1e salt inta!e or hypertonic I? solutions, clients with heat stro!e, near drowning in seawater %. ,ater lost in e"cess of sodium, e.g. clients unable to respond to thirst as with altered mental status or physical disability= diabetes insipidus b. Signs and Symptoms $depend on rapidity and se1erity of onset+ 0. Initially: thirst %. If not responded to: altered neurologic function= lethargy= irritability= seiCures= coma= death

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5. 7iagnostic test findings: a. Serum 2a is greater than 0*& m/#)( b. Serum 6smolality I %B& m6sm)!g c. ollaborati1e are 0. >reatment according to cause with slow correction of 2a to a1oid de1elopment of cerebral edema %. ;edications a. 6ral or intra1enous water replacement $hypotonic I? solutions such as &.de"trose or '.*&. 2a l+ b. 7iuretics for 2a e"cretion 5. Assessment a. 2ursing history for precipitating factors as stimuli b. ?ital signs, including temperature c. ;ental status d. Signs)symptoms consistent with fluid 1olume deficit or e"cess e. Deassess lab results d. 2ursing 7iagnoses: Dis! for In9ury B. :otassium 0. haracteristics a. :rimary intracellular cation

0*

b. 2ormal serum potassium le1el 5.& A &.' m/#)( c. Actions: 1ital role in cellular metabolism, heart function, and neuromuscular function d. 2eed daily inta!e of potassium, usually through food e. 4idneys eliminate potassium from body under regulation by aldosterone f. Shifts in and out of cells in response to concentration of hydrogen ion $pH+ in the blood %. Hypo!alemia Serum potassium is lower than normal $H 5.& m/#)(+ a. ommon Stimuli 0. /"cessi1e loss of potassium a. >hrough !idneys: secondary to drugs, hyperaldosteronism, diabetes mellitus b. >hrough FI tract: se1ere 1omiting, gastric suction, diarrhea or ileostomy drainage %. Inade#uate inta!e a. Enable or unwilling to eat, anore"ia ner1osa b. Alcoholism 5. Shift from e"tracellular to intracellular space b. Signs and Symptoms

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0. Abnormal heart rhythms including atrial and 1entricular :otentiates digitalis to"icity $medication to treat heart failure+ %. ;uscle wea!ness, including leg cramps 5. Slowed abdominal peristalsis *. 7iagnostic test findings: a. Serum 4: if 43G%.& A 5.', moderate= if H %.&, se1ere and probably symptomatic b. Arterial blood gases $hypo!alemia associated with al!alosis, ele1ated pH+ c. /lectrocardiogram changes: flattened or in1erted >, E wa1es c. ollaborati1e are 0. ;edications a. :otassium supplements, oral or parenteral b. 2e1er gi1e potassium I? push, only as I? infusion %. 7ietary management :otassium rich foods $fruits and 1egetables+ 5. Health promotion: :re1ention of hypo!alemia a. Esing balanced electrolyte fluids with FI loss

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b. 7iet teaching and)or potassium supplements with meds that predispose to hypo!alemia c. Degular monitoring of serum potassium le1els *. Assessment a. 2ursing history for precipitating factors as stimuli b. ;ental status c. ?ital signs d. Deassess lab results d. 2ursing 7iagnoses 0. Acti1ity Intolerance %. 7ecreased ardiac 6utput 5. Dis! for Imbalance Fluid ?olume *. Acute :ain $:otassium can be irritating to 1eins e1en when diluted= ne1er gi1e I? push+ 5" Hyper!alemia Serum potassium is higher than normal $I&.' m/#)(+ a. ommon Stimuli 0. Inade#uate e"cretion of potassium a. Impaired renal e"cretion of potassium $untreated renal failure, adrenal insufficiency+ b. ;edications that impair 43 e"cretion by !idneys $e.g. 43 sparing diuretics+ %. /"cessi1ely high inta!e of potassium

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a. /"cess oral potassium by supplement, salt-substitute b. Dapid I? administration of potassium, transfusion of aged blood 5. Shift from intracellular to e"tracellular space ;ay occur with acidosis, se1ere tissue trauma b. Signs and Symptoms 0. Abnormal heart function: slowing of heart rate and conduction= 1entricular dysrhythmias progress to cardiac arrest %. S!eletal muscle irritability, tremors progress to wea!ness, and paralysis 5. FI disturbances: initially, diarrhea and colic *. 7iagnostic test findings a. Serum 4: I &.' m/#)( b. /lectrocardiogram: pea!ed > wa1es, prolonged conduction :D, MDS c. Arterial blood gases to determine presence of acidosis c. ollaborati1e are 0. ;edications a. Stop all potassium supplements orally and I?, if recei1ing b. ;edications to lower serum potassium and stabiliCe

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conduction system of heart, including 0. Intra1enous alcium Fluconate %. Intra1enous &' gm of glucose and regular insulin $;o1es 43 intracellularly+ 5. Sodium polystyrene sulfonate $4aye"alate+, orally or rectally $binds 43 in FI tract+ c. (oop diuretics $e.g. Furosemide $(asi"++, if ade#uate renal function %. 7ialysis Nartificial !idneyO remo1es e"cess potassium 5. Health promotion: >each clients at ris! to read food and dietary supplements for potassium *. Assessment a. 2ursing history for precipitating factors as stimuli b. ardiac status with continuous cardiac monitoring c. ?ital signs d. Deassess lab results. e. HemolyCed blood sample: if serum 43 is 1ery high and client does not appear ill enough to ha1e a potassium that high, blood should be redrawn and re-

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tested. First blood sample may ha1e been hemolyCed. d. 2ursing 7iagnoses 0. Dis! for Acti1ity Intolerance %. Dis! for 7ecreased ardiac 6utput 5. Dis! for Imbalanced Fluid ?olume . alcium 0. haracteristics a. Abundant in body b. 2ormal serum calcium le1el K.& A 0'.' m/#)( c. BodyLs source is from diet= %'. of calcium ingested is absorbed d. BB. calcium is in bones and teeth and is bound to phosphorus e. /"tracellular, and only ioniCed form is acti1e f. Actions: 0. Degulates muscle contraction and rela"ation, including respiratory muscles %. ;aintains cardiac function 5. Acts in blood clotting process g. alcium le1els are affected by acid-base balance %. Hypocalcemia >otal serum calcium le1el H K.& mg)d( Systemic effects caused by decreased le1els of ioniCed a in e"tracellular fluid a. ommon Stimuli

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0. Hypoparathyroidism $nec! surgery %* A *K hr post op+ %. Acute pancreatitis 5. /lectrolyte imbalances $low magnesium, high phosphate+, al!alosis *. ;alabsorption disorders &. ertain medications, e.g. loop diuretics $Furosemide+ anticon1ulsants $phenytoin $7ilantin++ -. ;assi1e transfusion of ban!ed blood b. Signs and Symptoms 0. 2euromuscular: a. ;ost serious is tetany $tonic muscle spasm+ and con1ulsions b. /arlier: numbness and tingling around mouth, in hands and feet ad1ancing to muscle spasms of face and e"tremities, hyperacti1e deep tendon refle"es $7>DLs+ c. :ositi1e h1oste!Ls sign: face spasm with chee! tapping= positi1e >rousseauLs sign: carpal spasm with inflation of B: cuff on arm %. Despiratory status: muscle spasms can lead to laryngeal spasms

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5. ardiac: hypotension, bradycardia, 1entricular dysrhythmias and cardiac arrest *. 7iagnostic test findings a. >otal serum a H K.& mg)d( b. Serum albumin affects a c. Serum magnesium: low, H 0.mg)d( is associated with low a d. Serum phosphate: ele1ated, I *.& mg)d( is in1ersely related to a e. :arathryoid hormone $:>H+ to detect hyperparathyroidism f. /lectrocardiogram: e1aluate cardiac conduction: such as prolonged S> segment c. ollaborati1e are 0. ;edications a. alcium supplements: b. Se1ere hypocalcemia: intra1enous $ a hloride or aFluconate+ c. hronic asymptomatic= oral forms, sometimes with ?itamin 7 %. 7ietary management includes calcium in diet $mil!, figs, salmon+ 5. Health promotion: >eaching to include pre1ention of osteoporosis

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$calcium mo1es from bones= not measured by serum a+ *. Assessment: a. 2ursing history for precipitating factors as stimuli b. 2euro assessment, cardiac status and 1ital signs c. ontinuous cardiac monitoring and airway support, if indicated= d. Deassess lab results d. 2ursing 7iagnoses: Dis! for In9ury 5. Hypercalcemia >otal serum calcium le1el I 0'.' mg)d(. Systemic effects caused by increased le1els of ioniCed a in e"tracellular fluid a. ommon Stimuli 0. Increased reabsorption of calcium from bones a. Hyperparathyroidism b. ;alignancies: cancers with metastasis $bone destruction by the tumor+ c. Desult of immobility and lac! of weight-bearing %. 7iminished elimination of calcium 6ccurs with medications $e.g. thiaCide diuretics, lithium+ b. Signs and Symptoms 0. 7ecreased neuromuscular irritability: muscle wea!ness, depressed deep

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tendon refle"es $7>D+, ad1ances to confusion, lethargy to coma %. FI: anore"ia, nausea, 1omiting, constipation 5. ardiac: heart conduction disturbances: bradycardia, heart bloc! *. :olyuria and increased thirst &. omplications: peptic ulcer disease, pancreatitis, renal calculi $!idney stones+ -. Hypercalcemic crisis= acute a e"cess, can lead to cardiac arrest @. 7iagnostic test findings a. Serum calcium I0'.' mg)d( b. Serum :arathyroid le1el c. /lectrocardiogram: changes including shortened M>, bradycardia, heart bloc!s c. ollaborati1e are Foal: to promote a elimination by !idneys= to reduce a reabsorption from bone 0. ;edications a. Intra1enous fluids: usually isotonic saline b. (oop diuretic $e.g. Furosemide $(asi"+ alcitonin+ c. For hypercalcemic crisis: I? sodium phosphate or potassium phosphate

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d. For inhibiting bone reabsorption: :licamycin $;ithracin+ e. Flucocorticoids %. 7ietary ;anagement: Increase inta!e of acid ash foods, fiber, fluid inta!e 5. Health :romotion a. Identify persons at ris! b. /ncourage weight-bearing acti1ity c. Fluids up to 5 -* #uarts, if not contraindicated d. (imit calcium foods and supplements and calcium containing antacids *. Assessment a. 2ursing history for precipitating factors as stimuli b. ?ital signs c. 2euro assessment d. ardiac status, continuous cardiac monitoring if indicated e. Deassess lab results $increased ris! for digitalis to"icity+ d. 2ursing 7iagnoses 0. Dis! for In9ury %. Dis! for /"cess Fluid ?olume 7.;agnesium 0. haracteristics a. ;ainly intracellular and in bone

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b. 2ormal serum le1el 0.- A %.- mg)d( c. 6btained through diet $green 1egetables, meat, grains, nuts+ d. /"creted by !idneys e. ?ital to cellular processes, enCyme, protein synthesis f. Sedati1e effect on neuromuscular 9unction g. Affected by potassium and calcium le1els %. Hypomagnesemia ;agnesium le1el H 0.- mg)d( ommon in critically ill patients a. ommon stimuli 0. Esually occurs along with 4 and a deficiencies %. (oss of FI fluids as with diarrhea, ileostomy 5. Impaired nutrition absorption from gut= star1ation, 2:6 status *. hronic alcoholism &. ;edications such as loop or thiaCide diuretics, some antibiotics b. Signs and Symptoms 0. Increased neuromuscular e"citability: tremors, hyperacti1e refle"es, tetany, mood changes %. ardiac: dysrhythmias and sudden death= increased ris! of digitalis to"icity 5. FI: nausea, 1omiting, diarrhea, anore"ia, abdominal distention *. 7iagnostic test findings:

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a. /lectrolyte le1els= low magnesium often with low a and 4 b. /lectrocardiogram: delayed conduction with dysrhythmias, cardiac arrest, sudden death c. ollaborati1e are 0. ;edications: if symptomatic, treated with I? ;agnesium Sulfate, and)or oral supplements %. 7ietary ;anagement: encourage balanced diet including green 1egetables, meat, grains, nuts, seafood 5. Health :romotion a. Identify persons at ris! $postsurgery clients, clients with malnutrition, alcoholics+ b. /ncourage well-balanced nutrition *. Assessment a. 2ursing history for precipitating factors as stimuli b. ?ital signs c. 2euro status d. ardiac status, continuous cardiac monitoring e. FI assessment f. Deassess lab results $increased ris! for digitalis to"icity+ d. 2ursing 7iagnoses: Dis! for In9ury

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5. Hypermagnesemia ;agnesium le1el I%.- mg)d( (ess common a. ommon Stimuli: renal failure, especially clients recei1ing parenteral or oral supplements b. Signs and Symptoms 0. 2euromuscular: wea!ness, lethargy leading to wea! or absent deep tendon refle"es $7>D+, drowsiness as le1el rises %. ardio1ascular: hypotension, flushing, sweating, bradydysrhytmias leading to heart bloc!, cardiac arrest as le1el rises= respiratory depression with high le1els 5. FI: nausea and 1omiting *. 7iagnostic test findings a. ;agnesium le1el ele1ated b. /lectorcardiogram: changes with bradycardia, heart bloc! c. ollaborati1e are 0. ;edications a. ,ithhold medications containing magnesium b. 7ialysis for clients with renal failure c. alcium Fluconate I? for re1ersal or neuro and cardiac effects

%K

%. Health :romotion a. Identify clients at ris! $those with renal failure, recei1ing magnesium supplements+ b. >each to a1oid la"ati1es, antacids, and enemas containing magnesium 5. Assessment a. 2ursing history for precipitating factors as stimuli b. 2euromuscular assessment c. ardiac assessment, continuous cardiac monitoring and airway support if indicated d. Deassess lab results d. 2ursing 7iagnoses 0. 7ecreased ardiac 6utput %. Dis! for Ineffecti1e Breathing :attern 5. Dis! for In9ury /. :hosphate 0. haracteristics a. ;ostly in bone= intracellular anion b. 2ormal serum le1el %.& A *.& mg)d( c. /ssential to intracellular processes, including muscle contraction and ner1e conduction, metabolism, acid base balance d. Source is from diet, e"creted by !idneys e. In1erse relationship with calcium %. Hypophosphatemia

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Serum phosphorus H %.& mg)d( >otal body deficit or cellular shift a. ommon Stimuli 0. Esually iatrogenic $related to treatment+ %. Defeeding syndrome: occurs with beginning enteral or total parenteral feedings to malnourished clients 5. ;edications: intra1enous glucose solutions, diuretics, aluminum or magnesium-based antacids *. Alcoholism &. Hyper1entilation with respiratory al!alosis b. Signs and Symptoms 0. 2euromuscular: irritability, wea!ness, paresthesias, confusion, and seiCures leading to respiratory failure %. ardiac: dysrhythmias, chest pain 5. FI: anore"ia, dysphagia, nausea, 1omiting, decreased FI motility *. 7iagnostic test findings: serum phosphate is H%.& mg)d( c. ollaborati1e are 0. ;edications a. 6ral phosphate supplements $2eutra-:hos+ b. Intra1enous phosphorus such as 2a :hosphate, 4 :hosphate

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c. /liminate phosphate depleting medications, if possible %. 7ietary ;anagement: stress wellbalanced diet 5. Health :romotion a. Identify clients at ris! b. >each, including a1oidance of phosphorus-binding antacids *. Assessment a. 2ursing history for precipitating factors as stimuli b. 2euromuscular c. FI d. ardiac with cardiac monitoring and respiratory support if indicated e. Deassess lab results, especially electrolytes d. 2ursing 7iagnoses 0. Impaired :hysical ;obility %. Ineffecti1e Breathing :attern 5. 7ecreased ardiac 6utput *. Dis! for In9ury 5. Hyperphosphatemia Serum phosphorus I *.& mg)d( Impaired e"cretion, total body e"cess or cellular shift a. ommon Stimuli 0. Acute or chronic renal failure %. /"cess or rapid inta!e of phosphates

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5. :hosphate shifts from chemotherapy, trauma, heat stro!e *. Accompanies altered calcium concentrations b. Signs and Symptoms 0. 2euromuscular: muscle cramps, paresthesias, muscle spasms, tetany %. alcification of soft tissues 5. 7iagnostic test findings: serum phosphate is I*.& mg)d)( c. ollaborati1e are 0. >reat cause %. :romote renal e"cretion by I? saline or dialysis for client in renal failure 5. 7ietary ;anagement: eliminate phosphate rich foods, such as organ meats, mil!, and mil! products *. Health :romotion a. Identify clients at ris! b. >each, including a1oidance of phosphate sources, foods or medications &. Assessment a. 2ursing history for precipitating factors as stimuli b. 2euromuscular c. Deassess lab results, especially electrolytes d. 2ursing 7iagnoses: Dis! for In9ury

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Acid-Base Balance
I. Bac!ground A. Facts and 7efinitions 0. Acid-base homeostasis is necessary to maintain life. %. Acid base balance must be within a definite range for cellular function to occur. 5. >he acidity of a substance, determined by the hydrogen ion $H3+ concentration= is e"pressed as pH. *. Acids a. Delease hydrogen ions into solution b. Ha1e pH H @ &. Al!alines $bases+ a. Accept hydrogen ions into solution b. Ha1e pH I @ B. Body fluids 0. 2ormally slightly al!aline %. 2ormal range is narrow: @.5& A @.*& $pH of @ is neutral+ 5. Arterial blood pH H @.5& is considered acid *. Arterial blood pH I @.*& is considered al!aline : . Acids and Bases in the body 0. Body functions constantly produce acids %. ;ost acids and bases in the body are wea! 5. Acids include a. arbonic acid, which is eliminated as a gas, carbon dio"ide b. (actic, hydrochloric, phosphoric, sulfuric acids, which are metaboliCed or e"creted as fluids *. Bicarbonate is the ma9or base II. Body regulation of acid-base balance

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onstant response to changes in pH to maintain the pH in the normal range 5 systems in the body, with 1arious response times, to maintain acid-base balance :

A. Buffer System 0. Desponds immediately, but has limited capacity to maintain %. Buffers: substances that bind or release hydrogen ions a. ,hen body fluid becomes acid, buffers bind with hydrogen ions to raise pH b. ,hen body fluid becomes al!aline, buffers release hydrogen ions to lower pH 5. Buffer systems a. Bicarbonate-carbonic acid buffer system #O$ % H$& H$#&' H% % H#&'
(ea) acid (ea) !ase

:rocess is re1ersible but the ratio of %' $bicarbonate+ to 0 $hydrogen+ must be maintained b. :rotein buffer system $intracellular and plasma+ c. :hosphates buffer system B. Despiratory System 0. Desponds within minutes %. Includes respiratory center of brain stem and lungs 5. 6ccurs automatically, not under 1oluntary control *. Ad9usts the depth and fre#uency of respiration according to the pH of the blood= increases or decreases the amount of carbon dio"ide in the blood=

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controls the amount of carbonic acid formed and ad9usts the pH of the blood a. Hyper1entilation: increased depth and fre#uency of respiration= blows off more 6% in response to an acid pH b. Hypo1entilation: decreased depth and fre#uency of respiration= retains more 6% in response to an al!aline pH . Denal $;etabolic+ System 0. Desponds within hours to days %. Ad9usts the amounts of hydrogen and bicarbonate ions a. 4idneys e"crete H3 ions, or generate and reabsorb bicarbonate ions, in response to an acid pH b. 4idneys retain H3 ions, or generate and e"crete bicarbonate ions, in response to an al!aline pH III. 7etermination of Acid-Base Balance: Analysis of Arterial Blood Fases A. pH 0. 2ormal: @.5& A 5.*& %. Acidic: H@.5& 5. Al!aline: I@.*& B. p 6% :ressure of carbon dio"ide= respiratory component 0. 2ormal: 5&-*& mm Hg %. Acidic: I *& mm Hg $carbon dio"ide forms carbonic acid+ Hypercapnia: ele1ated le1els of carbon dio"ide in blood 5. Al!aline: H 5& mm Hg

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Hypocapnia: decreased le1els of carbon dio"ide in blood . H 65 Bicarbonate= renal or metabolic component 0. 2ormal: %% A %- m/#)( %. Acidic: H %% m/#)( 5. Al!aline: I %- m/#)( 7. Base /"cess 0. alculated 1alue for buffer base capacity: the amount of acid or base added to blood to obtain a pH of @.* %. 2ormal: -5 -- 35 /. p6% :ressure of o"ygen in blood 0. Fi1es data about le1el of o"ygenation= not used to calculate acid-base status of blood %. 2ormal: K' A 0'' mm Hg 5. Hypo"emia: H K' mm Hg I?. Acid-Base Imbalance A. lassifications 0. Acidosis or al!alosis a. Acidosis: Hydrogen ion concentration in blood increases abo1e normal and pH is below @.5& b. Al!alosis: Hydrogen ion concentration in blood decreases below normal and pH is abo1e @.*& %. 6rigin of the problem a. From the respiratory system b. From the metabolic system B. 7isorders: Simple or ombined 0. :rimary disorders a. Simple b. 6ne cause, either respiratory or metabolic

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ombined disorders a. ;ore se1ere b. Both the respiratory and metabolic systems are the cause of the same imbalance . ompensation 0. 6nly occurs with primary disorders %. Desponse by the system not causing the imbalance to correct the pH /"ample: with respiratory acidosis, the !idneys would eliminate hydrogen ions in urine to offset the acidosis caused by hypo1entilation of lungs. 5. omplete ompensation occurs if the pH is corrected to the normal range $@.5& A @.*&+ *. :artial ompensation occurs if there is impro1ement in the pH but not to the normal range. &. ompensation can be determined by analysis of the arterial blood gas results. 7. >reatment 0. Ergency a. ;ental ability and le1el of consciousness is often affected b. Brain function usually affected= brain cells need proper conditions to perform cellular functions c. ells cannot function properly if significant acidosis or al!alosis occurs %. Indirect treatment a. >reating and correcting the precipitating condition often corrects the acid-base imbalance b. 7irectly treating the acid-base imbalance, by adding or remo1ing hydrogen or bicarbonate ions, may lead to further imbalances c. 2ot usually first line of treatment

%.

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?. >ypes of Acid-Base Imbalances A. Despiratory Acidosis pH H @.5& p 6% I *& mm Hg $e"cess carbon dio"ide in the blood+ Despiratory system impaired and retaining 6%= causing acidosis 0. ommon Stimuli a. Acute respiratory failure from airway obstruction b. 61er-sedation from anesthesia or narcotics c. Some neuromuscular diseases that affect ability to use chest muscles d. hronic respiratory problems, such as hronic 6bstructi1e (ung 7isease %. Signs and Symptoms a. ompensation: !idneys respond by generating and reabsorbing bicarbonate ions, so H 65 I%mm Hg b. Despiratory: hypo1entilation, slow or shallow respirations c. 2euro: headache, blurred 1ision, irritability, confusion d. Despiratory collapse leads to unconsciousness and cardio1ascular collapse 5. ollaborati1e are a. /arly recognition of respiratory status and treat cause b. Destore 1entilation and gas e"change= :D for respiratory failure with o"ygen supplementation= intubation and 1entilator support if indicated c. >reatment of respiratory infections with bronchodilators, antibiotic therapy d. De1erse e"cess anesthetics and narcotics with medications such as nalo"one $2arcan+

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e.

hronic respiratory conditions a. Breathe in response to low o"ygen le1els b. Ad9usted to high carbon dio"ide le1el through metabolic compensation $therefore, high 6% not a breathing trigger+ c. annot recei1e high le1els of o"ygen, or will ha1e no trigger to breathe= will de1elop carbon dio"ide narcosis d. >reat with no higher than % liters 6% per cannula f. ontinue respiratory assessments, monitor further arterial blood gas results *. 2ursing 7iagnoses a. Impaired Fas /"change b. Ineffecti1e Airway learance B. Despiratory Al!alosis pH H @.5& p 6% H 5& mm Hg. arbon dio"ide deficit, secondary to hyper1entilation 0. ommon Stimuli a. Hyper1entilation with an"iety from uncontrolled fear, pain, stress $e.g. women in labor, trauma 1ictims+ b. High fe1er c. ;echanical 1entilation, during anesthesia %. Signs and Symptoms a. ompensation: !idneys compensate by eliminating bicarbonate ions= decrease in bicarbonate H 65 H %% mm Hg. b. Despiratory: hyper1entilating: shallow, rapid breathing

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c. 2euro: panic!ed, light-headed, tremors, may de1elop tetany, numb hands and feet $related to symptoms of hypocalcemia= with ele1ated pH more a ions are bound to serum albumin and less ioniCed Nacti1eO calcium a1ailable for ner1e and muscle conduction+ d. ;ay progress to seiCures, loss of consciousness $when normal breathing pattern returns+ e. ardiac: palpitations, sensation of chest tightness 5. ollaborati1e are a. >reatment: encourage client to breathe slowly in a paper bag to rebreathe 6% b. Breathe with the patient= pro1ide emotional support and reassurance, anti-an"iety agents, sedation c. 6n 1entilator, ad9ustment of 1entilation settings $decrease rate and tidal 1olume+ d. :re1ention: pre-procedure teaching, pre1entati1e emotional support, monitor blood gases as indicated . ;etabolic Acidosis pH H@.5& 7eficit of bicarbonate in the blood 2aH 65 H%% m/#)( aused by an e"cess of acid, or loss of bicarbonate from the body 0. ommon Stimuli a. Acute lactic acidosis from tissue hypo"ia $lactic acid produced from anaerobic metabolism with shoc!, cardiac arrest+ b. 4etoacidosis $fatty acids are released and con1erted to !etones when fat is used to supply glucose needs as in uncontrolled >ype 0 diabetes or star1ation+

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c. Acute or chronic renal failure $!idneys unable to regulate electrolytes+ d. /"cessi1e bicarbonate loss $se1ere diarrhea, intestinal suction, bowel fistulas+ e. Esually results from some other disease and is often accompanied by electrolyte and fluid imbalances f. Hyper!alemia often occurs as the hydrogen ions enter cells to lower the pH displacing the intracellular potassium= hypercalcemia and hypomagnesemia may occur %. Signs and Symptoms a. ompensation: respiratory system begins to compensate by increasing the depth and rate of respiration in an effort to lower the 6% in the blood= this causes a decreased le1el of carbon dio"ide: p 6% H5& mm HF. b. 2euro changes: headache, wea!ness, fatigue progressing to confusion, stupor, and coma c. ardiac: dysrhythmias and possibly cardiac arrest from hyper!alemia d. FI: anore"ia, nausea, 1omiting e. S!in: warm and flushed f. Despiratory: tries to compensate by hyper1entilation: deep and rapid respirations !nown as 4ussmaulLs respirations g. 7iagnostic test findings: 0. ABF: pH H @.5&, H 65 H %% %. /lectrolytes: Serum 43 I&.' m/#)( 5. Serum a3% I 0'.' mg)d( *. Serum ;g3% H 0.- mg)d( 5. ollaborati1e are a. ;edications: orrecting underlying cause will often impro1e acidosis

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b. Destore fluid balance, pre1ent dehydration with I? fluids c. orrect electrolyte imbalances d. Administer Sodium Bicarbonate I?, if acidosis is se1ere and does not respond rapidly enough to treatment of primary cause. $6ral bicarbonate is sometimes gi1en to clients with chronic metabolic acidosis+ Be careful not to o1ertreat and put client into al!alosis e. As acidosis impro1es, hydrogen ions shift out of cells and potassium mo1es intracellularly. Hyper!alemia may become hypo!alemia and potassium replacement will be needed. f. Assessment 0. ?ital signs %. Inta!e and output 5. 2euro, FI, and respiratory status= *. ardiac monitoring &. Deassess repeated arterial blood gases and electrolytes *. 2ursing 7iagnoses a. 7ecreased ardiac 6utput b. Dis! for /"cess Fluid ?olume c. Dis! for In9ury 7. ;etabolic Al!alosis pH I@.*& H 65 I %- m/#)( aused by a bicarbonate e"cess, due to loss of acid, or a bicarbonate e"cess in the body 0. ommon Stimuli a. (oss of hydrogen and chloride ions through e"cessi1e 1omiting, gastric suctioning, or e"cessi1e diuretic therapy b. Desponse to hypo!alemia

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c. /"cess ingestion of bicarbonate rich antacids or e"cessi1e treatment of acidosis with Sodium Bicarbonate %. Signs and Symptoms a. ompensation: (ungs respond by decreasing the depth and rate of respiration in effort to retain carbon dio"ide and lower pH b. 2euro: altered mental status, numbness and tingling around mouth, fingers, toes, diCCiness, muscle spasms $similar to hypocalcemia due to less ioniCed calcium le1els+ c. Despiratory: shallow, slow breathing d. 7iagnostic test findings 0. ABFLs: pHI @.*&, H 65 I%%. /lectrolytes: Serum 43 H 5.& m/#)( 5. /lectrocardiogram: as with hypo!alemia 5. ollaborati1e are a. orrecting underlying cause will often impro1e al!alosis b. Destore fluid 1olume and correct electrolyte imbalances $usually I? 2a l with 4 (+. c. ,ith se1ere cases, acidifying solution may be administered. d. Assessment 0. ?ital signs %. 2euro, cardiac, respiratory assessment 5. Depeat arterial blood gases and electrolytes *. 2ursing 7iagnoses a. Impaired Fas /"change b. Ineffecti1e Airway learance c. Dis! for In9ury

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