Isotonic, Hypotonic , Hypertonic IV Third Spacing Where Has All the Fluid Gone - [PDF Document] (2024)

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Suppose your patient has edemaindicating that theres enoughfluid inhis bodybut his vital signs and urine

output suggest that hes hypovolemic.Whats going on? Hesexperiencingthird-spacing, a shifting of fluid intointerstitialspaces. Find out whatneeds to be done to get that fluidback whereit belongs.

MARCIA BIXBY, RN, CS, CCRN, MS

Critical Care Nurse Specialist Beth Israel Deaconess

Medical Center Boston, Mass.

Consultant for Critical Care Education Randolph, Mass.

The author has disclosed that she has no significantrelationships with or financialinterest in any commercial companiesthat pertain to this educational activity.

YOURE TAKING REPORT on JohnMiller, who had a colectomy 2 daysagobecause of a ruptured diverticulus. Youlearn that his heart ratehas increased overthe past 24 hours, yet his blood pressure

has been gradually falling and hes hadmarginal urine output (30mL/hr). Mr.Miller weighs 4 kg more than beforesurgery, and he hasgeneralized edema.

The health care team has decided not toincrease Mr. Millersmaintenance intra-venous (I.V.) infusion of lactatedRingerssolution. The nurse from the previous shiftsays not toworry: His fluid will mobilizeand hell make urine soon.

Not sure what she means by that, youhead off to check out Mr.Millers conditionfor yourself.

During your assessment, you find that Mr.

Miller has 2+ edema, warm skin, and palpa-ble peripheral pulses.His heart rate is 108beats/min, his blood pressure is 110/64 mmHg,and his urine output remains marginalat 30 mL/hr. Mr. Millersabdomen is firm

and distended, with hypoactive bowelsounds. He says his pain iswell controlledwith his patient-controlled analgesia infu-sion.

Mr. Millers edema indicates that he hasenough fluid in his body.But his vital signsand urine output seem to tell adifferenttalehypovolemia. How can you reconcilethesedifferences?

Whos on third?Mr. Miller is experiencing third-spacing,whichhappens when fluid is trapped inthe interstitial spaces. It canoccur in the

42 Nursing made Incredibly Easy! September/October 2006

Where has all

Third-spacing:

2.5ANCC/AACN

CONTACT HOURS

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brain, lungs, abdomen, and extremities.Lets look at thephysiology of third-spacingand what you need to know to care forMr.Miller.

You may remember from your patho-

physiology class that fluid moves fromintravascular (inside theblood vessel) toextravascular (outside the blood vessel)spaces andfrom intracellular (inside the cell)to extracellular (outside thecell) spaces (seeFluids 101). Fluid is constantly on the movetomaintain balance (see On the move).

Intravascular-to-extravascular movementof fluid occurs throughdiffusion, which iscontrolled by hydrostatic and capillary plas-maoncotic pressures.

Hydrostatic pressure is the pressure thatfluid places on thewall of a blood vessel. Ifthe vessel wall is strong, as with anartery,

September/October 2006 Nursing made Incredibly Easy! 43

the fluid gone?

On the moveFluids are constantly on the move, seeking to

keep the body in equilibrium. Heres how

they do it.

Diffusion: This is passive movement of mol-

ecules across a membrane from an area of

higher concentration to an area of lower con-

centration.

Osmosis: Water moves through a selective-

ly permeable membrane from an area of

lower concentration of ions to an area of

higher concentration of ions.

Active transport: This is movement of mole-

cules against a concentration as they move

from an area of lower concentration to an

area of higher concentration. The movement

requires energy.

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fluid will be held in. But if the wall is weakor semipermeable,as with a capillary,hydrostatic pressure will force fluid out ofthevessel. Hydrostatic pressure pushes fluidfrom the arterial side ofthe capillary into theinterstitial space.

Intravascular or intracapillary oncotic pres-sure is determinedby plasma proteins in thebloodstream. The proteins keep fluid intheblood vessel, with albumin protein mole-cules doing 70% of thework.

When oncotic pressuregoes badLoss of albumin or protein leads tode-creased oncotic pressure. Fluid can nowleak from theintravascular space into theinterstitial space and stay there,causingedema. Because this fluid is lost from thecirculating bloodvolume, cardiac outputdecreases. You can see albumin loss inpa-tients with liver failure, liver dysfunction,

or malnutrition. The low albumin levelslead to loss of fluidinto the peritoneum,causing ascites.

At some point, a patient with decreased

oncotic pressure might need hypertonic orcolloid fluids, such asalbumin, to pull thefluid in the interstitial space back intotheintravascular space and increase the circulat-ing volume. Givinghypotonic fluids causesfluid to shift from the intravascularspaceinto the interstitial space, increasing intersti-tial fluidand edema. I.V. fluids that are iso-tonic should move in and out ofthe vascularspace equally, so thats what Mr. Miller isreceiving(seeHow fluids affect cells and Quick

guide to I.V. solutions).

And another thingEven when the oncotic pressure and albu-minlevels are normal, fluid can still leak outof the vessels if theresdamage to the capil-lary membranes. Thats what happened toMr.Miller. During surgery, his bowel washandled, poked, and prodded asit was re-paired, damaging tissues and destroying theendothelialcells lining the capillaries. Not

good news for Mr. Miller: Endothelial cellshelp maintainvascular integrity, which facil-itates osmosis, diffusion, andactive trans-port of fluids and electrolytes.

Once Mr. Millers endothelial cells weredestroyed, permeabilityof his capillarymembranes increased, allowing fluid tomove from theintravascular space to theinterstitial space, but not back again.Oncoticpressure fell and fluid was trapped, causingedema. (RememberMr. Millers 2+ general-ized edema?) The excessive fluid in the

abdomen (ascites) causes increased pressureand firmness. Thefluid in the interstitialspace and tissue compliance determinethelevel of pressure.

Periods of hypotension, which causehypoperfusion, along withhypoxia andischemia, can also destroy endothelial cellsand trapfluid in the interstitial space. Thiscan occur in the brain as aresult of a car-diac arrest. In the lungs, fluid accumulationcanlead to cardiogenic or noncardiogenicpulmonary edema. As you sawwith Mr.Miller, excessive fluid in the extremitiesleads toperipheral edema. And if the fluid

44 Nursing made Incredibly Easy! September/October 2006

Those hard-working plasma

proteins helpkeep thingswhere they

belong!

Fluids 101Fluids bring nutrition and oxygen to cells and

take away cell waste for metabolism or

excretion. This important role may be why

60% of an adults weight is fluid. This fluid is

divided into two compartments: intracellular

and extracellular.Intracellular fluid, located inside thecells,

makes up 40% of the bodys total fluid. The

remaining 60% of the bodys total fluid is

extracellular fluid, which is, logically, located

outside the cell. Extracellular fluid is further

divided into interstitial (between cells, in tis-

sue) and intravascular (inside the blood ves-

sels) fluid.

The bodys fluid should be in balance, with

the volume entering the body equal to whats

leaving. Fluid loss can occur through urine,

sweat, stool, and incidental losses from res-

piratory effort.

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Quick guide to I.V. solutionsA solution is isotonic if itsosmolarity falls within (or near) the normal range for serum (240to 340

mOsm/L). A hypotonic solution has a lower osmolarity; ahypertonic solution, a higher osmolarity.

This chart lists common examples of the three types of I.V.solutions and provides key considera-

tions for administering them.

Solution Examples Nursing considerations

Isotonic Lactated Ringers Because isotonic solutions expandthe

(275 mOsm/L) intravascular compartment, closely monitor the

Ringers injection patient for signs of fluid overload,especially if

(275 mOsm/L) he has hypertension or heart failure.

0.9% sodium chloride Because the liver converts lactate tobicarbon-

(308 mOsm/L) ate, dont give lactated Ringers solution if the

5% dextrose in water patients pH exceeds 7.5.

(D5W; 260 mOsm/L) Avoid giving D5W to a patient at risk for

5% albumin increased intracranial pressure (ICP) because it

(308 mOsm/L) acts like a hypotonic solution. (Althoughusually

Hetastarch considered isotonic, D5W is actually isotonic

(310 mOsm/L) only in the container. After administration,dex-

Normosol (295 mOsm/L) trose is quickly metabolized, leavingonly

(295 mOsm/L) watera hypotonic fluid.)

Hypotonic 0.45% sodium chloride Administer cautiously. Hypotonicsolutions

(154 mOsm/L) cause a fluid shift from blood vessels intocells.

0.33% sodium chloride This shift could cause cardiovascularcollapse

(103 mOsm/L) from intravascular fluid depletion andincreased

2.5% dextrose in water ICP from fluid shift into braincells.

(126 mOsm/L) Dont give hypotonic solutions to patients at

risk for increased ICP from stroke, head trauma,

or neurosurgery.

Dont give hypotonic solutions to patient at

risk for third-space fluid shifts (abnormal shifts

into the interstitial space)for example, patients

with burns, trauma, or low serum protein levels

from malnutrition or liver disease.

Hypertonic 5% dextrose in 0.45% sodium Because hypertonicsolutions greatly expandchloride (406 mOsm/L) the intravascularspace, administer them by I.V.

5% dextrose in 0.9% sodium pump and closely monitor the patientfor circu-

chloride (560 mOsm/L) latory overload.

5% dextrose in lactated Hypertonic solutions pull fluid from theinter-

Ringers (575 mOsm/L) stit ial space, so dont give them to apatient with

3% sodium chloride a condition that can cause cellulardehydration,

(1,025 mOsm/L) such as diabetic ketoacidosis.

25% albumin Dont give hypertonic solutions to a patient

(1,500 mOsm/L) with impaired heart or kidney functionhissys-

7.5% sodium chloride tem cant handle the extra fluid.

(2,400 mOsm/L)

September/October 2006 Nursing made Incredibly Easy! 45

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accumulates in the abdomen, the patientcan develop edema of thebowel, whichmay result in intra-abdominal hyperten-sion orabdominal compartment syndromeif not reversed over the first 24 to48 hoursafter surgery.

Whats going on insidethe cells?Interstitial fluid trappingcauses compres-sion of the microvasculature in the distal

circulation. As the cells swell and com-press the capillariesaround them, bloodflow is further impaired, leading tohy-poperfusion and ischemia. Anaerobic me-tabolism kicks in (exceptin the brain cells)

to sustain the cells until perfusion is re-stored. But whenanaerobic metabolism

eventually fails, the sodium/potas-sium pump inside the cellstarts tofail too. Sodium and potassium

switch places: Sodium moves into the

intracellular space while potassiummoves into the extracellularspace.An increased level of intracellular

sodium causes water to be pulled intothe cell. The cell wallmembrane stretches

and releases cytokines and other mediators.Once released,mediators become active andcreate local inflammation, whichfurtherdamages the cells.

Mediators also get into the systemic cir-culation, where theblood gives them aride to other parts of the body. This free

ride can lead to systemic inflammatoryresponse syndrome (SIRS).Organ failuremay also occur, which leads to furtherinflammation anddysfunction, release ofmediators, and progression to multipleorgandysfunction syndrome (MODS),which increases the incidence ofmortality(seeMediators of SIRS and MODS). Letshope Mr. Millerdoesnt go down this road!

Back to Mr. MillerNow that you understand more about thefluidchanges that occur with third-spacing,Mr. Millers vital signs arentsurprising.

The shift of fluid into the interstitial tis-sues decreased hisintravascular circulat-ing volume. The baroreceptors in theaortaand carotid arches sensed the lower vol-ume and told thesympathetic nervoussystem (SNS) to get busy. The SNS did itsjob bycausing release of epinephrine andnorepinephrine, which lead tovasocon-striction of the peripheral vessels and anincreasing heartrate. Lets take a closerlook at this process.

Vasoconstriction shunts blood from theperiphery to the majororgans, which cancompromise circulation to theextremities.Compromised circulation may lead tohypoxia, ischemia,and SIRS.

Youll want to keep a sharp eye on Mr.Millers perfusion: Checkperipheral pulses,skin temperature and sensation, and capil-laryreturn on the hands and feet.

An increased heart rate kicks up cardiac out-put so that thebodys oxygen requirements

can be met. But the heart can only do somuch. If myocardialoxygen demand keepsrising, the heart wont be able to supplyenoughoxygen; myocardial ischemia orinfarction may result. Be ready torespondquickly if Mr. Miller shows signs or symp-toms of myocardialischemia, such as chestpain.

Mr. Millers kidneys are doing their part tohelp out. When theysensed the decrease inglomerular filtration rate, which wouldhap-pen with his marginal urine output, they

launched the renin-angiotensin-aldosteronesystem. This systemcauses peripheral vaso-constriction from the effects of angiotensinIIand fluid retention from the release of aldos-terone.Antidiuretic hormone is also releasedin response to low circulatoryvolume, and ittells the kidneys to absorb more sodiumfrom thetubules; this will also increase theabsorption of water. The goalis to increasecirculating volume, thereby boosting cardiacoutputand blood pressure. Without thiscompensatory mechanism, Mr.Millersblood pressure would be lower than it isright now.

This sodium andpotassium

switcheroo cancause a lot of

trouble!

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Blood vessel

Normal cell

An isotonic solution has the same solute concentration

(or osmolarity) as serum and other body fluids. Infusing

the solution doesnt alter the concentration of serum;

therefore, osmosis doesnt occur. (For osmosis to occur,

there must be a difference in solute concentration

between serum and the interstitial fluid.)

The isotonic solution stays where its infused, inside

the blood vessel, and doesnt affect the size of cells.

Order up lactatedRingers for me and

my buddies; we couldall use some balance.

Thats right.An isotonic

solutionmaintains bodyfluid balance.

Why not?I hear its an

excellent choicefor hydration.

May I suggestan isotonic

I.V. solution?

How fluids affect cells: Isotonic solutions

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How fluids affect cells: Hypertonic solutions

A hypertonic I.V. solution has a solute concentration

higher than the solute concentration of serum.

Infusing a hypertonic solution increases the solute

concentration of serum. Because the solute concen-

tration of serum is now different from the interstitial

fluid, osmosis occurs. Fluid is pulled from the cells

and the interstitial compartment into the blood ves-

sels.Many patients receive hypertonic fluids postoper-

atively. The shift of fluid into the blood vessels

reduces the risk of edema, stabilizes blood pressure,

and regulates urine output.

Blood vessel

Shrunken cell

Great! Thishypertonic solutionwill cause fluid to

flow from the cellsinto the blood

vessels.Gulp! Thishypertonicstuff dries

me out.

Wanna try ahypertonic I.V.

solution?Yeah. I

could standto lose alittle fluid.

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How fluids affect cells: Hypotonic solutions

A hypotonic I.V. solution is the opposite of a hyper-

tonic solution. It has a lower solute concentration

than serum. Infusion of a hypotonic solution causes

the solute concentration of serum to decrease.

Because the solute concentration of serum is now

different from the interstitial fluid, osmosis occurs.

This time, the fluid shift is in the opposite direction

than that of a hypertonic fluid. Fluid shifts out of thebloodvessels and into the cells and interstitial

spaces, where the solute concentration is higher.

Swollen cell

Blood vessel

Have you everhad a hypotonic

solution?

Cant sayI have.

Burp!Great stuff.

But this fluidshift has left mea little bloated.

You should try one. Ahypotonic I.V. solutionhydrates cellswhilereducing fluid in thecirculatory system.

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How doesyour patients

abdominalgirth measure

up?

50 Nursing made Incredibly Easy! September/October 2006

One more thing: Know what Mr. Millersheart rate and bloodpressure normally areso you can determine if his currentreadingsare adequate.

Big bellyOK, now you understand Mr. Millers vi-tal signs, butwhat about his abdomen?Whats causing its distension?

Remember our earlier discussion aboutfluid shifts? Whenfluid

shifts into the interstitialspace of the bowel tissue,as hashappened with Mr.

Miller, the tissue becomesedematous. The

swelling causes thebowel to expand in

the peritoneum.The abdominalskin stretches toaccommodate the

edema, similar to

the way a balloon expands when you blowair into it.

We monitor this effect by measuringabdominal girth, and now wecan also mea-sure bladder pressure to determine theamount ofpressure the edematous bowel isgenerating.

To measure abdominal girth, wrap a tapemeasure around thepatients abdomen atthe umbilicus and record themeasurement.Remeasure abdominal girth every 4 to 8

hours, making sure to place the tape mea-sure on the same spot.Report any increasedmeasurements to the health care team.

If the patient has a urinary catheter inplace, you can measureabdominal pres-sure by obtaining bladder pressure mea-surements (ifyou have the capability ofdoing these measurements). Afterclamp-ing the urinary catheter, aseptically insertan 18-gaugeAngiocath in the catheterssampling port or connect an IAPbladder

pressure monitor. Connect the system to a

Mediators of SIRS and MODSMediator Effects

Tumor necrosis factor Vasodilation

Activation of other proinflammatory mediators

Histamine Intense vasodilation

Increased capillary membrane permeability

Bradykinins Vasodilation Activation of the coagulationcascade

Platelet-activating factor Platelet aggregation

Activation of the coagulation cascade

Myocardial depressant factor Depressed myocardial function

Arachidonic acid cascade,

an inflammation-related

cascade, including:

Leukotrienes Increased tissue permeability

Thromboxanes Vasoconstriction of arterioles

Prostaglandins Vasodilation

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pressure transducer and level the transduc-er to the iliaccrest. Instill 50 mL of sterile0.9% sodium chloride into thebladder, turnthe stopco*ck or valve, and obtain the pres-suremeasurement at end expiration. If theintra-abdominal pressure ismore than 12mm Hg, suspect that the patient has intra-abdominalhypertension (seeMaking thegrade).

Elevated pressure in the abdomen indi-cates increased boweledema. As the bowel

edema progresses (as a result of cellularischemia andhypoperfusion) and theresmore pressure in the abdomen, thebloodreturn to the right side of the heart is im-paired; so isblood flow out of the left ven-tricle. The increased abdominalpressurecan impair lung expansion as well, leadingto respiratorydistress. It can also exertpressure on the renal circulation,leading torenal dysfunction.

Mr. Millers edema happened quickly

because of his surgery, so his skin cantkeep pace with theswelling. Thats whyhis abdomen is firm. Rising pressure intheabdomen from third-spacing compressesthe major blood vesselsrunning throughit, which causes the following problems:

in the vena cava, reduced preload (ve-nous return to the heart),leading to de-creased cardiac output, which results indecreasedblood pressure

in the aorta and the iliac and femoral ar-teries, increasedafterload (pressure in the

peripheral circulation), further reducingcardiac output andblood pressure

in the renal vessels, impaired kidneyfunction in the spleensvasculature, impairedblood flow to the bowel, liver, andspleen.

If the fluid shift isnt corrected and pres-sure keeps rising,Mr. Miller will developintra-abdominal hypertension orabdominalcompartment syndrome. This situationresults in a downwardspiral of bowelischemia and tissue death leading to necro-sis. Soyoull want to watch him closely forsigns of intra-abdominalhypertension and

abdominal compartment syndrome: increas-ing abdominal girth orbladder pressure andincreasing pain not controlled with thepre-vious medication dosing. Early suspicion ofintra-abdominalhypertension or abdominalcompartment syndrome will allow timefor

interventions to prevent or minimize tissuedamage.

Whats next?Mr. Millers vital signs are slightly abnor-mal butstable, so he seems to be tolerat-ing the fluid shifting. Over thenext sev-eral hours (up to 48 hours), the fluid shiftwill beresolved or he will continue to de-velop bowel edema and,eventually, is-chemia.

During this time, closely monitor Mr.

Millers vital signs, urine output, and periph-eral perfusion.Report any changes to thehealth care provider. Here are other areastokeep tabs on: Mental status. Is Mr. Miller responsiveand able tocommunicate and answerquestions appropriately? If not, hisbloodpressure isnt high enough for adequateperfusion.Ventilation/perfusion status. Can hemaintain adequate ventilationto supporthis oxygen needs? Does he have crackles?Is his oxygensaturation greater than 97%on room air, or does he needsupplemen-

September/October 2006 Nursing made Incredibly Easy! 51

Making the gradeA patients intra-abdominal pressure (IAP)determines if he has intra-

abdominal hypertension. In a consensus statement, the WorldSociety of

Abdominal Compartment Syndrome defines intra-abdominalhyperten-

sion as sustained or repeated pathologic elevation of IAP 12 mmHg.

There are four grades of intra-abdominal hypertension, accordingto this

group:

Grade I: IAP of 12 to 15 mm Hg

Grade II: IAP of 16 to 20 mm Hg

Grade III: IAP of 21 to 25 mm Hg

Grade IV: IAP of > 25 mm Hg.The higher the number, the moresevere the condition and the greater

the risk of complications.

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tal oxygen therapy?

Hematocrit and hemoglobin. Risinghematocrit and hemoglobinlevels indicatehemoconcentration of serum due to fluidshifting tothe interstitial space; decreasesin these values may indicatebleedingunless Mr. Millers had several liters offluid replacementsolution, causing a dilu-tional effect.

Serum electrolytes. Increased sodiummay occur withhemoconcentration. Potas-

sium may rise due to intracellular shiftingor if Mr. Miller isdeveloping renal dys-function.

Elevated blood urea nitrogen (BUN) andcreatinine levels may bedue to hemoconcen-

tration, but a rising creatinine with a normalBUN level maysignal intrarenal dysfunction.

Lactate is produced as a byproduct ofanaerobic metabolism. Inpatients whovehad bowel surgery, an elevated lactate level

may indicate bowel ischemiaunless thepatient has liverdysfunction or failure andreceived several liters of lactatedRingerssolution for fluid resuscitation. The lactate inlactatedRingers solution is converted tobicarbonate in a healthy liver. Butin a dys-functional or diseased liver, lactate isnt con-verted; itremains in the blood. Abdominal pressure. Measure abdomi-nal girthor bladder pressure at leastevery 4 to 8 hours while Mr. Millersvitalsigns are abnormal and his urine outputis low. Fluidresuscitation. Youll continue to

give Mr. Miller amaintenance I.V.infusion of isotonicfluid, aswell as in-termittent bolusesof a colloid, such asalbumin.Albuminwill pull fluid fromthe interstitialspace into thein-travascular space.

If the kidneys cantget rid of the extrafluid on their own,asmall dose of aloop diuretic likefurosemide (Lasix)can help.Remem-ber, colloid fluidsare plasma pro-teins, so theirhighermolecular structures allow you to

give less volume to support Mr. Millersblood pressure.If hishemoglobin is low, infusing blood

products, such as packed red blood cells, asneeded will helpincrease oxygen-carryingcapacity, as well as increaseintravascularoncotic pressure and pull fluid from theinterstitialspace.

What if?If the health care provider suspects bowelischemia ornecrosis, he may order a

kidney-ureter-bladder (KUB) X-ray andcomputed tomography (CT)scan.

A KUB image will show the extent ofbowel edema and any free air,whichwould indicate bowel perforation. A CTscan detects worseningbowel edema, lackof adequate perfusion, or hematomasformed frombleeding.

A patient whose vital signs are deteriorat-ing and who hasdecreasing urine outputand increasing abdominal girth orbladderpressure readings will likely return to theoperating room;he may have a perforatedbowel that needs to be repaired. If thebowel

52 Nursing made Incredibly Easy! September/October 2006

Listen, I knowthings are

shifting right

now, but giveit some timeto resolve.

did youknow?Why does fluid fol-

low a protein like

albumin? Protein

is a large molecule

with a negative

charge. It attracts

the most abundant

extracellular fluid

ionsodium

which has a posi-

tive charge. You

probably remem-

ber that water fol-

lows sodium. So,

sodium follows

protein, and water

follows sodium..

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isnt perforated, the surgeon still may haveto open up theabdomen to allow the edemato subside; itll be closed later.

A trip to the operating room is definitelyin order if thepatients KUB film shows freeair; he needs to have that perforatedbowelrepaired STAT! While theyre in there, thesurgical team willalso explore the abdomenfor any further damage to the bowelrelatedto perforation or edema.

Its up to youYour clinical assessments and index of sus-picionas to what could be going on in Mr.Millers abdomen will help puthim on thepath of continued recovery. And, yes, nowyou know justwhat the nurse on the othershift meant by mobilize fluid.

Learn more about itAmerican Association of Critical-Care Nurses.AACNProcedure Manual for Critical Care, 5th edition.Philadelphia,Pa., Elsevier, 2005.

Klabunde RE. Cardiovascular Physiology Concepts. Philadel-phia,Pa., Lippincott Williams & Wilkins, 2004.

Kruse JA, et al (eds.). Saunders Manual of Critical Care.St.Louis, Mo., W.B. Saunders, 2003.

Macklin D, Chernecky C. Real World Nursing SurvivalGuide: IVTherapy. St. Louis, Mo., W.B. Saunders, 2004.

Malbrain ML, Cheatham ML. Cardiovascular effects andoptimalpreload markers in intra-abdominal hypertension,in Yearbook ofIntensive Care and Emergency Medicine. J-LVincent (ed.). Berlin,Germany, Springer-Verlag, 2004.

Rosenthal K. The whys and wherefores of I.V. fluids.Nursing madeIncredibly Easy! 4(3):8-11, May/June 2006.

Urden LD, et al (eds). Priorities in Critical Care Nursing,4thedition. St. Louis, Mo., Mosby, 2004.

Urden LD, et al. Thelans Critical Care Nursing: DiagnosisandManagement, 5th edition. St. Louis, Mo., Mosby, 2006.

World Society on Abdominal CompartmentSyndrome.http://www.wcacs.org. Accessed June 29, 2006.

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1. Third-spacing refers to fluid trapped in the

a. intravascular spaces.b. interstitial spaces.

c. intracellular spaces.

2. Third-spacing typically occurs in the extremities, ab-

domen, and

a. lungs.

b. liver.

c. kidneys.

3. In third-spacing, fluid in the body moves from the

a. intravascular spaces to the extravascular spaces.

b. extravascular spaces to the intracellular spaces.

c. extracellular spaces to the extravascular spaces.

4. Hydrostatic pressure primarily affects the

a. lymph system.

b. veins.

c. capillaries.

5. Loss of albumin or protein can cause

a. increased cardiac output.

b. decreased oncotic pressure.

c. decreased hydrostatic pressure.

6. Ascites is caused by

a. a low albumin level and fluid accumulation in the peri-

toneum.

b. decreased plasma proteins in the peritoneum.c. excess fluidin the intracellular spaces of the liver.

7. Hypertonic I.V. fluids are used as therapy because they

a. pull fluid from intravascular space into interstitialspace.

b. replace lost proteins.

c. increase circulating volume.

8. Normally, the bodys fluid is distributed as

a. 75% intracellular and 25% extracellular.

b. 60% extracellular and 40% intracellular.

c. 20% intracellular and 80% extracellular.

9. Albumin is effective in treating third-spacing because it

a. decreases oncotic pressure.

b. attracts sodium and water.

c. increases hydrostatic pressure.

10. How does third-spacing relate to systemic inflamma-

tory response syndrome (SIRS)?

a. Swollen cells of interstitial edema release mediators.

b. Histamine release causes capillary vasoconstriction.

c. Bradykinin release inhibits the coagulation cascade.

11. Decreased intravascular circulating volume leads to

a. vasoconstriction and increased heart rate.b. vasodilation anddecreased heart rate.

c. vasodilation and increased blood pressure.

12. Compression of the vena cava from abdominal third-

spacing can cause

a. increased blood pressure.

b. decreased cardiac output.

c. increased preload.

13. Which lab finding may indicate postoperative bowel

ischemia?

a. increased sodium

b. increased blood urea nitrogen

c. increased lactate

14. Five percent dextrose in 12 normal saline is classifiedas

a. isotonic.

b. hypotonic.

c. hypertonic.

15. Patients receiving hypertonic I.V. solutions should be

monitored for which adverse effect?

a. circulatory overload

b. increased peripheral edema

c. decreased intravascular volume

16. Signs of abdominal compartment syndrome include

each of the following except

a. increased abdominal girth.

b. decreased bladder pressure.

c. increased pain levels.

17. Rising hemoglobin and hema-

tocrit in a postoperative patient

probably result from

a. acute bleeding.

b. fluid shifts to inter-

stitial space.

c. compensation for

hypoxemia.

Third-spacing: Where has all the fluid gone?GENERAL PURPOSE: Toprovide the registered professional nurse with an overview of thepathophysiology, signs and symptoms,

and nursing care of a patient who is experiencing third-spacingof fluids. LEARNING OBJECTIVES:After reading this article and

taking this test, you should be able to: 1. Describe thepathophysiology and complications of third-spacing. 2. Identifynursing as-

sessments, monitoring, and interventions for patients withthird-spacing.

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Third-spacing: Where has all the fluid gone? (page 42)B. TestAnswers: Darken one circle for your answer to each question.

a b c

1. 2.

3. 4.

a b c

5. 6.

7. 8.

a b c

9. 10.

11. 12.

a b c

13. 14.

15. 16.

a b c

17.

a b c

1. 2.

3. 4.

a b c

5. 6.

7. 8.

a b c

9. 10.

11. 12.

a b c

13. 14.

15. 16.

a b c

17.

a b c

1. 2. 3.

4.

a b c

5. 6. 7.

8.

a b c

9. 10. 11.

12.

a b c

13. 14. 15.

16.

a b c

17.

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Acute pancreatitis: Inflammation gone wild (page 18)B. TestAnswers: Darken one circle for your answer to each question.

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Bad blood: Tips for preventing CR-BSIs (page 30)B. Test Answers:Darken one circle for your answer to each question.

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Test code: NMIE1206

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Test code: NMIE1306

Registration deadline:

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