fluid volume deficit

body's fluid intake isnt sufficient to meet body's fluid needs

GI suctioningIleostomy or colostomy drainageDraining wounds, burns, or fistulas fluid volume deficit causes (GID VIC) Vomiting or diarrheaIncreased urine output from use of diureticsContinuous GI irrigation ThirstHR increases, thready pulse,and postural hypotensionIncreased specific gravity of urineRapid weight lossDizziness or weaknessDecrease in urine, dark, cloudy, concentrated Flat neck and hand veinPoor skin turgor and dry mucous membranesIncreased hematocrit levelConfusionIncreased hematocrit level
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fluid volume deficit s/s(THIRDD FPIC)

fluid volume deficit interventions(CLM^4T)

Check mucous membranes, skin turgorLactated ringers solutions 0.9% NSMonitor VS, I&O, daily weight, hematocrit & electrolyte levelTest urine for specific gravity

fluid volume excess

exceeds the body's fluid needAKA overhydration and fluid overload

Weight gainIncreased resp & HR, Neck and hand vein distentionDecreased hematocrit level fluid volume excess s/s(WIND CCLIP) ConfusionCough and dyspneaLung CracklesIncreased BP, bounding pulsePitting edema

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fluid volume excess interventions(PAM^4 CPR)

Position client in Semi FowlersAdminister diuretics as prescribedMonitor I&0Monitor weightMonitor VSMonitor hematocrit and electrolyte levels Check for edemaProvide low sodium diet (as prescribed)Restrict fluids (as prescribed)

Potassium (K+) fact

IV bolus of K+ is never administrated. Always diluted

Potassium (K+) value

3.5 to 5.1 mEq/L

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hypokalemia causes(DEVI-US CRAP)

DiarrheaExcessive gastric suction, fistula drainingVomiting Inadequate intake of KtUncontrolled diabetesSyndrome(Cushing) Chronic use of corticosteroidsRenal diseaseAlkalosisParental nutrition

hypokalemia s/s(SHALL PC)

Shallow respirations & thready pulseHypoactive bowel soundsAbsent or decreased reflexesLeg and abdominal crampsLethargy and weakness Postural hypotensionConfusion

hypokalemia reading

P waves- peakedT waves- flatST segment- depressedU waves- depressed

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hyperkalemia causes(TEAM RICE)

Tranfusion of stored blood (the breakdown of older RBC releases K+)Excessive use of K+ based salt substitutesAddisons diseaseMetabolic acidosis Renal failureIntestinal obstructionCell damageExcessive oral and parenteral adm. of K+

FishRaisinsOrangesMushrooms Potassium (K+) food sources(FROM PAST BCC) Potatoes, porkAvocadosSpinach & StrawberriesTomatoes BananasCantaloupesCarrots

hyperkalemia s/s(DHPHM)

DiarrheaHypotensionParesthesiasHyperactive bowel soundsMuscle weakness

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hyperkalemia reading

P waves- flatT waves- peakedST segment- depressedQRS widened complexPR prolonged interval

hypokalemia interventions(GIM^5)

Give with food/juice (causes GI irritation)IV site (watch for phlebitis, infiltration)Monitor VSMonitor I&OMonitor neuromuscular activityMonitor cardiac changesMonitor electrolyte level

hyperkalemia intervention(M^5AP)

Monitor VSMonitor for cardiac changesMonitor I&OMonitor Lab valuesMonitor for calcium and magnesium loss when using KayexalateAdm. sodium polystyrene sulfonate (Kayexalate)Prepare for peritoneal dialysis, hemodialysis (as prescribed)
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sodium levels

135 to 145 mEg/L Irrigation of GI tubes with plain waterNausea and vomiting BurnsIncreased perspirationsGastrointestinal suction

hyponatremia causes(IN BIG DIPER)

Draining skin lesionsInadequate sodium intakePotent diureticsExcessive intake of waterRetention of fluidsSyndrome of inappropriate antidiuretic hormone secretion

Rapid, thready pulseAbdominal crampingWeakness hyponatremia s/s(RAW MAPP) Muscle twitching and seizuresApprehensionPoor skin turgor Postural BP changes

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hyponatremia interventions(RAM^3S)

Restrict water intake and avoid tap water enemasAssess skin turgor and mucous membranesMonitor VSMonitor I&OMonitor weightSaline is used for irrigation rather than sterile water.

Watery diarrheaEnteral and parental nutrition depletes the cells of water hypernatremia causes(WE DECIDED CHF) DehydrationExcessive perspirationCushing SyndromeImpaired renal functionDiabetes inspidusExcessive adm. if sodium bicarbonateDecreased water intakeCorticosteroidsHyperventilationFever

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ConfusionOliguriaMuscles twitchingElevated temperatureSeizures hypernatremia s/s(COMES LFFTD) Loss of skin turgorFlushed skinFatigueThirstDry mucous membranes

hypernatremia interventions(IM^3)

Increase water intake orally (provide water between meals and tube feedings, 8-10 glasses a dayMonitor VSMonitor I&OMonitor electrolyte level

Calcium levels

8.6- 10 mg/dl Acute pancreatitisCrohn's diseaseDiarrheaCalcium excreting medications (diuretics, caffiene, anticonvulsants, heparin, laxatives, nicotine_ Long term immobilization and bone demineralizationInadequate Vit. D consumptionEnd stage
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hypocalcemia causes(ACDC LIE DIE IE)

renal disease Decreased secretion of parathyroid hormoneInhibited absorption of calcium from the intestinal tractExcessive GI losses from diarrhea or wound draining Inadequate intake of calciumExcessive adm. of blood HypotensionHyperactive bowelsCrampsDiarrhea hypocalcemia s/s(HHC TTT PPP ) TachycardiaTwitchingTetany ParesthesiasPositive Chovestek's or Trousseau's signProlongation of QT interval Teach client proper use of antacids or laxativeInstruct client taking calcium excreting meds to check CA levels periodicallyMonitor calcium levels closely Adm. Vit. D (AP) to aid in the digestion of calcium from the intestinal tractAdm. CA 1-2 hours after meal to max. intestinal absorptionMonitor VSProvide quiet environment,
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hypocalcemia interventions(TIM AAMP KIM)

avoid over stimulation Keep 10% calcium gluconate for acute calcium deficitInitiate seizure precautionsMonitor for Chvostek's (contraction of facial muscles in response to a light tap over the facial nerve in front of the ear) Trousseau's )carpal spasm induced by inflating a BP cuff above systolic pressure for a few minutes.) Renal failureHyperparathyroidism hypercalcemia causes(RH AEIU) Adrenal insufficiency Excessive intake of Vit. DIncreased bone resorption of destruction from conditions (tumors, fractures, osteoporosis, & immobility)Use of thiazide, lithium, glucocorticoids

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Muscle weakness (hypotonicity)Increased HR & BPNausea and vomitingDiminished deep tendon reflexes hypercalcemia s/s(MIND ABBCC) Abdominal distentionBounding pulseBradycardia(late stage)ConstipationConfusion, lethargy, and coma

hypercalcemia reading

T wave- widenedQT interval shortened CheeseCollard greensSardinesSpinach

calcium food sources(CCSS MARTY) Milk and soy milkRhubarbTofuYogurt

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MilkMustardLunch meatsKetchup Sodium food sources(MMLK BBCCSS WTPL) BaconButterCanned foodsCheese (american, cottage)Snack foodsSoy sauce White/whole wheat breadTable saltProcessed foodsLunch meats Prepare calcitonin(Calcimar)increase calcium in the bones, and phosphate (AP)Avoid large doses of Vit. D supplements, avoid thiazide diureticIncrease mobilityRestrict calcium intake hypercalcemia interventions(PAIR M^7S Monitor VSMonitor for dysrhythmiasMove clients safely, assist in ROM when ambulation isnt possibleMonitor for dev. of pathological fracturesMonitor for severe flank & abd. pain Monitor LOCMonitor for confusion and neurological changesStrain urine watch for urinary stones 1.6 - 2.6 mg/dl

magnesium level

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Prolonged gastric suctioningAcute pancreatitisChemotherapy MalnutritionAlcoholismCeliac disease hypomagnesemia causes(PAC MAC SED DIC) SepsisEclampsiaDiabetic ketoacidosis DiarrheaIleostomy, colostomy, instestinal fistulasCrohn's disease Confusion TwitchingTetany Tachycardia hypomagnesemia s/s(C TTT SHIPPS) Shallow respirationsHyperactive reflexesIrritabilityParethesiasPositive Chvostek's (contraction of facial nerve..) Trosseaus's (carpal spasm induced by BP cuff...)Seizures T waves- tallST segment- depressed

hypomagnesemia reading

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hypomagnesemia interventions(AIM^6)

Adm. magnesium supplementsInitiate seizure precautionsMonitor VSMonitor for dysrhythmiasMonitor neuromuscular changesMonitor I&OMonitor serum mag levels q. 12-24 hours when receiving mag by IVMonitor for reduced deep tendon reflexes that suggest hypermagnesmia

hypermagnesemia causes(ROT)

Renal insufficiency and renal failureOveruse of antacids or laxative containing magnesiumTreatment of preeclampsia with magnesium

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Weak Bradycardia hypermagnesemia s/s(W B L HRS) Loss of deep tendon reflexes HypotensionRespiratory depressionSweating and flushing

hypermagnesemia reading

PR interval- prolongedQRS complexes- widened

Yogurt Green leafy veggies (spinach, broccoli) magnesium food sources(Y G RAM COP^4) RaisinsAvocadosMilk CauliflowerOatmealPeanut butterPeasPork, beef, chicken, fishPotatoes
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hypermagnesemia interventions(RIIM^5)

Remove the source of excess magnesiumIncrease renal excretion by increasing oral fluids, adm. diuretics(AP)Instruct client to avoid laxative and antacids containing magnesiumMonitor VSMonitor for respiratory depressionMonitor for hypotension, bradycardia, dysrhythmiasMonitor neurological and muscular activityMonitor LOC 2.7 - 4.5 mg/dl HypercalcemiaHyperparathyriodismAlcohol withdrawalRenal failureDiabetic ketoacidosis

phosphorus levels

hypophosphatemia causes(HHARD DRUM)

Decreased intake of phosphorus or malnutritionRespiratory alkalosisUse of mag based, alum hydroxide based antacidsMalignancy

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ConfusionWeakness hypophosphatemia s/s(CW BIIDSS) Bone painIncreased bleeding tendencyImmunosuppressionDecreased deep tendon reflexesShallow respirationsSeizures

hypophosphatemia interventions(CAM^3)

Check the renal system before adm. phosphateAdm. Vit. DMonitor for calcium excess and kidney stonesMonitor calcium, phosphorus, sodium, chloride levelsMonitor hematological changes

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hyperphosphatemia causes(COVER H)

ChemotherapyOveruse of phosphate laxatives or enemasVit. D intoxicationExcessive intake of phosphorusRenal insufficiency Hypoparathyroidism

Hyperactive reflexesTetanyMuscle weakness hyperphosphatemia s/s(HTM PN) Positive Chvostek's, Trousseau's signsNeuromuscular irritability

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hyperphosphatemia interventions(M^4AT)

Monitor neuromuscular irritabilityMonitor for hyperreflexia, tetany,a nd seizuresMonitor for Trosseau's and Chvostek's signMonitor for signs of hypocalcemiaAdm. calcium(AP)if hypocalcemia existsTake with meals or immediately after meals.

NutsOrgan meatsWhole grain breads and cereals phosphorus food sources FishPork, beef, chicken skin(diffusion) 400mlskin(perspiration) 100mllungs 350mlfeces 150mlkidneys 1500ml

daily body fluid excretion or loss

Isotonic solutions

5% dextrose in water5% dextrose in 0.225% salineLactated Ringers Solution0.9% saline

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hypotonic

0.45 saline 5% dextrose in Lactated Ringer solution5% dextrose in 0.45% saline5% dextrose in 0.9% saline10% dextrose in water

hypertonic

Third spacing

The accumulation of trapped extracellular fluid in a body space due to disease or injury

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Acidosis or Alkalosis Sleuthing: Using Blood Values to determine the Cause of Acidosis or Alkalosis

Note the pH. This tells you whether the person is in acidosis (pH < 7.35) or alkalosis (pH > 7.45); but it does not tell you the cause. Next, check the PCO2 to see if this is the cause of the acid-base imbalance. Because the respiratory system is a fast-acting system, an excessively high or low PCO2 may indicate either that the condition is respiratory systemcaused or that the respiratory system is compensating. For example, if the pH indicates acidosis and: The PCO2 is over 45 mm Hg, the respiratory system is the cause of the problem and the condition is a respiratory acidosis. The PCO2 is below normal limits (below 35 mmHg), the respiratory system is not the cause but is compensating. The PCO2 is within normal limits; the condition is neither caused nor compensated by the respiratory system. Check the bicarbonate level. If step 2 proves that the respiratory system is not responsible for the imbalance, then the condition is metabolic and should be reflected in increased or decreased bicarbonate levels. Metabolic acidosis is indicated by HCO3- values below 22 mEq/L, and metabolic alkalosis by values over 26 mEq/L. Notice that whereas PCO2 vary inversely with blood pH (PCO2 rises as blood pH falls), HCO3- levels vary directly with blood pH (increased HCO3results in increased pH). Beyond this bare-bones approach there is something else to consider when you are assessing acid-base problems. If an imbalance is fully compensated, the pH may be normal even when the pH is normal, carefully scrutinize the PCO2 or HCO3- values for clues to what imbalance may be occurring.

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Causes and Consequences of Acid-Base imbalances

Metabolic acidosis: Uncompensated (uncorrected) HCO3- < 22 mEq/L; pH < 7.4 Severe diarrhea: Bicarbonate-rich intestinal (and pancreatic) secretions rushed through digestive tract before their solutes can be reabsorbed; bicarbonate ions are replaced by renal mechanisms that generate new bicarbonate ions. Renal disease: failure of the kidneys to rid body of acids formed by normal metabolic processes. Untreated diabetes mellitus: lack of insulin or inability of tissue cells to respond to insulin, resulting in inability to use glucose; fats are used as primary energy fuel, and ketoacidosis occurs. Starvation: Lack of dietary nutrients for cellular fuels, body proteins and fat reserves are used for energyboth yield acidic metabolites as they are broken down for energy. High ECF potassium concentrations: Potassium ions compete with H+ for secretion in renal tubules; when ECF levels of K+ are high, H+ secretion is inhibited. Metabolic alkalosis:
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Uncompensated (HCO3- >26 mEq/L; pH > 7.4) Vomiting or gastric suctioning: loss of stomach HCl requires that H+ be withdrawn from blood to replace stomach acids; thus H+ decreases and HCO3- proportionally. Selected diuretics: cause K+ depletion and H2O loss. Low K+ directly stimulates the tubule cells to secrete H+. Reduced blood volume elicits the renin-angiotensin mechanism, which stimulates Na+ reabsorption and H+ secretion. Ingestion of excessive sodium bicarbonate (antacid): bicarbonate moves easily into ECF, where it enhances natural alkaline reserve. Constipation: prolonged retention of feces, resulting in increased amounts of HCO3- being reabsorbed. Excessive aldosterone: (adrenal tumors) promotes excessive reabsorption of Na+, which pulls increased amount of H+ into urine. Hypovolemia promotes the same relative effect because aldosterone secretion is increased to enhance Na+ (and H2O) reabsorption.

Respiratory acidosis: Uncompensated (PCO2 >45 mm Hg; pH <7.4) Impaired gas exchange or lung ventilation (chronic bronchitis, cystic fibrosis, emphysema): Increased airway resistance and decreased expiratory air flow, leading to retention of carbon dioxide. Rapid, shallow breathing: Tidal volume markedly reduced. Narcotic or barbiturate overdose or injury to the brain stem: depression of respiratory centers, resulting in hypoventilation and respiratory arrest.

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Respiratory alkalosis: Uncompensated (PCO2 < 35 mm Hg; pH > 7.4) Direct cause is always hyperventilation: hyperventilation is pain/anxiety, asthma, pneumonia, and at high altitude represents effort to raise PO2 at the expense of excessive carbon dioxide excretion. Brain injury or tumor: abnormality of respiratory controls.

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