Osmotic Imbalances

SODIUM (Na)135mg 145mEq/L

most important cation in the ECFcontrols S. osmolality levels and H2O retentionmaintains water balance throughout the bodyControls ECF osmolalitygenerates transmission of neuromuscular impulses (muscle & cardiac contractions)essential in the Na+, K+ pump maintains A/B balance

Regulation of Nalost through the skin, git, and gut.Regulated by kidneys through glomerular filtration and tubular reabsorption Regulated by aldosterone and ADH

When ECF Na is, the adrenal glands send aldosterone to the kidneys, where Na is reabsorbed.

HYPONATREMIA< 135 mEq/Lcell swells as water is pulled in from ECF

Etiology:a. Increased Na excretion Excessive diaphoresisDiureticsWound drainage (burns, GIT)Decreased aldosterone secretionHyperlipidemiaRenal disease : scarred convoluted tubuleGIT: NGT suction, diarrhea, or laxative abuse

b. Inadequate Na intakeNPOLow-salt diet

c. Relative Na Deficits / Delution of NaExcessive ingestion of hypotonic fluidsPsychogenic polydipsiaFreshwater drowningRenal failure (NS)Irrigation w/ hypotonic fluids Hyperglycemia CHFAdrenal Insufficiency : aldosterone levels Na reabsoprtion Na excretionSIADH : etio: tumor, head injuries, endocrine & pulmonary disorders, meds

SIADH Excessive ADH activitywater retention dilutional hyponatremia & inappropriate urinary excretion of Na in the presence of hyponatremia

Two Mechanisms involved in Hyponatremia

Na in the Blood & ECF ECF & Cellular Fluid Slower Membrane Depolarization Cell Excitability HYPONATREMIA ECF osmolalityECF moves into ICF cell swells impairs function

CLINICAL MANIFESTATIONSFeeling of exhaustion Poor skin turgor Dry mucousa Decreased saliva production Orthostatic fall in BP GIT : Abdominal cramping, anorexia, nausea and vomiting, hyperactive bowel sounds=d/t abnormal losses of Na or gains in waterRESPIRATORYPulmonary edemaRapid shallow respirationMoist crackles

NEUROLGIC & MUSCULOSKELETAL SYMPTOM (Na

DIAGNOSTIC FINDINGS S. Na level < 135 mEq / L USG =1.002 to 1.004S. osmolarity < 275 mosm/kg (except in azotemia or ingestion of toxin

MEDICAL MANAGEMENT (Na++) a. Drug TherapyOsmotic diuretics excretion of fluids rather than sodiumReplace other electrolyte losses (K, Ca, HCO3) IV Saline for Na and fluid loss2-3% Saline for severe hyponatremia

b. Diet therapy Fluid restriction & Na intake

NURSING MANAGEMENTIdentify high-risk patients :

- diuretic therapy- gastric suctioning- renal disorders- burn injuries- feverNa replacement :

- administer highly hypertonic solution w/ caution to prevent circulatory overload & neurologic complications Osmotic Demyelization - neurologic damage- occurs when Na+ is over-corrected at 140mEq/dL

Highly Hypertonic Solutions:- 3% NaCl 1L (513 mEq Na)- 5% NaCl 1L (855 mEq of Na) Administered only in ICUMonitor for fluid overload (force water to leave ICF to balance Na in ECF causing cellular shrinkage excessive demands on the heart lead to CHF)Relieve acute manifestations of cerebral edema and prevent neurologic symptoms rather than to correct Na+ Na & H2O restriction (800 ml/24) Note for GIT symptoms

Cont Nsg MgtBe alert for CNS changes= lethargy, confusion, muscle twitching, seizuresBe alert for circulatory overload

- patients w/ CVD disease- dyspnea, puffy lids- dependent edema - wt gain in 24Measure I & O & daily weightMonitor V / S & S Na levelsCheck USGEncourage foods & fluids with high Na content Be aware of Na content of common IVF

HYPERNATREMIA Serum Na > 145 mEq/LNa ECF osmolalityICF moves into ECFICF dehydration

ETIOLOGY:a. Decreased Na excretionHyperaldosteronismRenal failureCorticosteroidsCushings syndrome or diseaseDI

b. Increased Na intakeExccessive oral Na ingestionExcessive administration of Na-containing IV fluids

Decreased water intakeNPOFluid deprivation in unconscious patients, old and vey young patients.

Increased water lossIncreased rate of metabolismFeverHyperventilationInfectionExcessive diaphoresisWatery diarrheaDehydration

CLINICAL MANIFESTATIONSEarly S/S Renal : Polyuria followed by oliguria, USG GIT: Anorexia, nausea and vomiting = d/t fluid retention in gastric cells

CNS manifestations: d/t sensitivity of brain cells to fluid shiftingRestlessness, Irritability, Muscle weakness

Decrease fluid in the interstitial compartmentsDry, flushed skinDry, sticky mucous membranesTongue furrowsFever = d/t amount of fluid available for dissipating heat.Increased thirst = primary characteristic of Na; primary defender in healthy people

Cardiovascular manifestations NaTachycardia Dysrhythmias Hypovolemic hypernatremia: orthostatic hypotension w/ compensatory tachycardiaHypervolemic hypernatremia: BP, JV distention, prolonged peripheral emptying, generalized edema wt gain

Pulmonary ManifestationsCrackles, dyspnea d/t hydrostatic pressure seen in BV

Na >155 mEq/L Severe neurologic manifestations resulting from shrinkage of brain cells d/t ECF osmolalityConfusionseizurescoma irreversible brain damageMuscle twitching, tremor, hypereflexia seizures = d/t altered neuromuscular contractility and irritabilityRigid paralysis= grave sign

DIAGNOSTIC FINDINGS Na level > 145 mEq/L S. osmolality > 295 mosm / kg kidneys attempt to conserve waterPlasma Cl level > 106 mEq/L = Cl is the major ECF ion that balances w/ NaUSG > 1.025 kidneys attempt to conserve water urine osmolality

POTENTIAL NURSING DIAGNOSISFluid volume deficitHigh risk for injuryFatigueAltered nutrition: less than body requirements

MEDICAL MANAGEMENTDiuretics - poor renal excretion of NaDiabetes Insipidus : Desmopressin acetatE, nasal spray to slow the rate of diuresisPatients w/ CV pulmonary and neurologic manifestations

- Hospitalization- IV hypotonic saline solutionTo decrease total body water and replace fluid loss

- Hypo-osmolar/ hypotonic solution: 0.3 NaCl or 0.45% - D5 W

Diet Therapy Adequate water intake among older adults or those who have no access to waterDietary Na restriction Fluid restriction

POTASSIUM (3.5 5.0 mEq / L)

major cation in the ICF (98%), 2% ECF (neuromuscular function) K+ imbalances are commonly associated with various diseases and:

injuries Medications =diuretics, laxatives, antibiotics special treatments = e.g. TPN & chemotherapyPrimarily regulated by the kidneys Aldosterone increases the excretion of K+ by the kidneys

Functions of PotassiumPlays vital role in the transmission of electric impulses of the nerve, heart, intestinal and lung tissueAssists in regulation of acid-base balance by cellular exchange with H+Works in reciprocal fashion with Na (excessive intake of Na+ results to excretion of K+ and vice versaRegulation of protein synthesis, glucose use & storage

Etiologya. Excessive K lossInappropriate or excessive use of drugs

- Prolonged diuretic tx - K+ follows water & Na across the tubular membrane - Digitalis- Corticosteroids - influence Na retention & reciprocal K+ excretionHyperaldosteronism : Cushing;s syndrome

excessive absorption of Na in the proximal tubules, accounting for accelerated excretion of KCirrhosis, nephritic syndrome, HF, malignant HPNDiarrhea & laxative use

H0kalemiaWound drainage (esp gastrointestinal)Recent Ileostomy -Intestinal fluid may contain as much as 30 mEq / L of K+Prolonged NGT suction, Vomiting : K+ is lost when gastric fluid is lost bile is rich in K+Heat-induced excessive diaphoresisRenal disease impairing reabsorption of potassiumExcessive removal of K+ during peritoneal or hemodialysis

Heat-induced excessive diaphoresisRenal disease impairing reabsorption of potassiumExcessive removal of K+ during peritoneal or hemodialysis

b. Inadequate Potassium intakeNPOInadequate intake & absorption debilitated, elderly, alcoholic, anorexia & bulimia nervosa

c. Alkalosis : Movement of K from ECF to ICF= ICF&ECF shifting of ions= lowered levels of extracellular H ion move out of the cells in alkalotic states to help correct high ph & K+ ions move in to maintain electrically neutral stateHyperinsulinismHyperalimentation/TPNHypertonic glucose solution

d. Villous adenoma tumor of the intestinal tract characterized by excretion of K+-rich mucus

e. Hyperaldosteronismf. Dilution of Serum PotassiumWater intoxicationIV therapy with potassium-poor solution

* Magnesium depletion causes renal K+ loss & must be corrected first; otherwise loss of K+ will continue

Clinical Manifestations (K+ 3mEq/L)Respiratory Manifestations Shallow, ineffective respirations: profound weakness of the skeletal muscles of respiration Diminished breath soundsNR: Assess for breath sounds, ease of respiratory effort, color of nail beds and mucous membranes, rate & depth of respiration. Assess respiratory status q 2 hours because respiratory insufficiency is the major cause of death.

b. Cardiovascular Manifestatons Rapid , weak, thready pulse Orthostatic hypotension ST depression, inverted T wave. Prominent U wave, Heart block

NRMonitor for orthostatic hypotension w/c is present in hypokalemia

c. Neuromuscular ManifestationsAnxiety, lethargy, confusion, comaLoss of tactile discriminationGeneral skeletal muscle weaknessDeep tendon hyporeflexiaFlaccid paralysis

d. GIT ManifestationsDecreased motilityHypoactive to active bowel soundsNausea, vomiting, abdominal distentionParalytic ileusConstipation

e. Renal ManifestationsDecreased ability to concentrate urinePolyuriaDecreased specific gravity : inability to concentrate urine

f. Musculoskeletal ManifestationsSevere hypokalemia : death through cardiac arrest Clinical signs rarely develop before the K+ level has fallen below 3 meq/L unless the rate has been rapidK+ depletion depresses the release of insulin & results in glucose intolerance

- Fatigue - Anorexia - Nausea - Vomiting

K+ = required for normal musculoskeletal contractionMuscle weakness & cramps Cardiac dysrhythmiaHypereflexia Drowsiness, lethargy & comaParesthesias bowel motility (which could develop to paralytic ileus)b. DIAGNOSTIC FINDINGS (K+)History S. K+ level < 3.5 mEq / LECG flat T waves/or inverted T waves suggesting ischemia & depressed ST segmentsU wave = specific for hypokalemiaPH elevated above 7.45 = K+ ion move in to maintain an electrically neural state glucose level

serum bicarbonate levels

MEDICAL MANAGEMENTGoal: Promotion of potassium balance Prevention of complications

a. K+ replacement (oral/IV) 40 80 mEq /day (1 mEq/10ml, 5-10 mEq/hr)b. K sparing diuretics : spironolactone, triamterene, amiloridec. Dietary intake of K+ rich foods raisins, bananas, apricots, oranges, vegetables, legumes,whole grains, meat, milk* Oral K+ supplement can produce small bowel lesions, patient must be assessed for abdominal distention, pain or GI bleeding

NURSING MANAGEMENTNursing DiagnosisRisk for Falls r/t skeletal muscle weaknessConstipation r/t smooth muscle atonyDecreased cardiac output r/t dysrhythmiasSelf-Care deficit r/t skeletal muscle weakness

Expected outcomesAbsence of injury & normal serum potassium level.

Nursing Interventions1. Identify high-risk patients 2. Teach patient receiving diuretic therapy at home about hypokalemia & how to manage it3. Patients receiving digitalis should be monitored for digitalis toxicity4. Careful I & O monitoring is necessary = 40 mEq of K is lost for every liter of urine

5. Monitor ECG changes 6. Monitor blood gas analysis check for HCO3 & ph level7. Monitor IV K+ administrationCorrect flow rateIrritation on the insertion siteMix solution thoroughly Rapid K+ administration can cause sudden hyperkalemia & cardiac arrestAdministered only after an adequate urine flow For life threatening hypokalemia 10 mEq K+ + 100 cc IV solution over 1 hour via infusion pump is administered Never give IM or IV pushMonitor V / S ,I&O (20cc/2hrs)Educate pt on the proper way of taking K+ supplement

HYPERKALEMIA (> 5.5 mEq/L)Seldom occurs in patients with normal renal functionOften due to iatrogenic causes (treatment induced)More dangerous because cardiac arrest is more frequently associated with K+ levels

ETIOLOGICAL FACTORS a. Excessive K intakeOver ingestion of potassium-containing foods or medicationsRapid infusion of potassium-containing IV solutionBolus IV potassium injectionsTransfusion of aged whole blood or packed cells.

b. Decreased K excretionAdrenal insufficiency(Addisons disease, adrenalectomy)Renal failure : poor eliminationPotassium-sparing diuretics

c. Movement of K from ICF to ECFTissue damageAcidosis : K+ moves out of the cell into ECF & H ion shifts into the cellHyperuricimia

d. MedicationsKCl, heparin, ACE inhibitor, NSAID

e. Cell lysis - burns, trauma, Ca chemotherapy, severe infection or any condition f. Addisons Dse and hypoaldosteronism - deficient adrenal hormones leading to Na+ loss and K+ retentiong. PsuedohyperkalemiaProlonged tight application of tourniquet for drawing bloodHemolysis of blood sample Drawing blood sample where K+ is infusingLeukocytosis (WBC > 200,000) = Thrombocytosis (pt ct > 1 million)

PSEUDOHYPYPERKALEMIA Failure to be aware of these causes can lead to aggressive treatment of nonexistent hyperkalemia resulting in serious lowering of serum K+ levels

CLINICAL MANIFESTATIONSNeuromuscular Effects Early: - Twitching of skeletal muscles,tingling, burning Numbness in the hands & feet & around mouth Flaccid paralysis (arms and legs) Flaccid paralysis of trunk, head, respiratory muscles (lethal levels of K)Cardiovascular System Slowed ventricular conduction Bradycardia Hypotension Widened ORS complex Tall, peaked T waves Ventricular fibrillation Cardiac arrest

GIT Nausea Intermittent intestinal colic Increased motility Diarrhea Urine= oliguria anuria

Laboratory FindingsECG changes ABG metabolic acidosis S. K+ - > 5.0 mEq / L Crea, BUN (RF)

MEDICAL MANAGEMENT (K+ )1. Drug therapyLasixAdministration of cation exchange resin (kayexalate ) orally or by retention enema in patients with renal impairment * Not given to patients with paralytic ileus (causes intestinal perforation)Binds with other cations in the GIT causing hypomagnesia & hypocalcemia Causes Na retention & fluid overload

c. Dextrose w/ insulind. Ca gluconate - antagonizes the action of K+ on the heart but does not K+ leveld. Hemodialysis e. NaHCO3 with caution, it can cause Ca++ levels to drop 2. Restriction of dietary K+ & K+ - containing medications

NURSING MANAGEMENTa. History Ask about chronic illness ( renal disease, DM) Ask about drug use (potassium-sparing, ACE inhibitors,) Obtain diet history Collect S/S r/t K

b. Identify high-risk patients (K+ sparing diuretics, K+ supplements, I.V. K+, RF, & metabolic acidosis) Nursing Diagnosis: same w/ KNursing InterventionsAdminister electrolyte-binding and electrolyte excreting resinsCheck urine output & K+ levels before administering any K+ containing medicationsProvide cardiac monitoringMonitor BP to detect hypotension due to rapid administration of the drug

Appearance of bradycardia is an indication to stop the infusion

Cont. Nursing InterventionsMonitor I & OMaintain potassium restrictions.Verify highly abnormal K+ levels maybe erroneousAvoid prolonged use of tourniquet & caution pt not to exercise extremely to avoid false reports & hyperkalemia Deliver blood sample to laboratory hemolysis of blood sample Encourage patient to adhere to prescribed K+ restrictionsProvide health teachings: key to prevention of hyperkalemia and early detection of complications

Funny Video

CALCIUM(8.5 -10.5 mg/dl/ 2.1-2.6mmol/L) 99% in skeletal system, 1 % blood Regulated closely w/ Mg & Phosphorustransmits nerve impulses & help regulate muscle contraction & relaxation plays a role in blood coagulationabsorbed in the GIT & excreted in the urineFiltered in the glomerulus & reabsorbed in the tubulesNeeded for vitamin B12 absorptionDetermines the thickness & strength of cell membraneSources: milk, cheese, dried beans, meats and vegetables

Calcitriol (Vit D) = promotes Ca absorption & limiting Ca excretion when levels are inadequateCalcitonin: moves Ca from plasma to bone when serum level PTH = stimulates release of Ca from bone into the serum to bring serum level to normal

Ca RegulationBlood Ca levelSecretion of Calcitonin by the TGActivation of vit D inhibitedReabsorption of Ca by the kidneysAbsorption of Ca from the intestinesBreakdown of boneBlood Ca level

Ca Regulationblood Ca levelsecretion of PTH by the PGInc. Activation of vit Da. Reabsorption of Ca by the kidneysb. Release of Ca into the blood stream d/t Inc breakdown of bonec. absorption of Ca from the intestinesblood Ca level

ETIOLOGYActual Calcium Deficitsa. Inhibition of Calcium Absorption from the GITInadequate intake of Ca++Lactose IntoleranceMalabsorption syndromes: Celiac dse, Crohns dseInadequate intake of vit D Inadequate exposure to UV w/c hindres conversion of VIT D to its active form (dihydroxycholecalciferol)ESRD : vitamin D not adsorbed which is necessary for the absorption of Ca++

Patients with renal failure has S phosphates which causes a reciprocal drop in S. Ca++ ;level because phosphorous will bind to Ca++, lowering S levelsAlcohol abuse d/t intestinal malabsorption, hypomagnesemia, hypoalbuminemia & pancreatitisMassive administration of citrated blood (as in exchange transfusions in new born)

=Citrate combines with ionized Ca++ & temporarily remove it from circulation

b. Increased Ca excretionRF- polyuric phaseDiarrheaSteatorrheaWound drainage (esp GIT) Large doses of diuretics Ca++ elimination

c. Conditions that decrease the Ionized Fraction OF CalciumHyperproteneinemiaAlkalosis : HCO3 binds to Ca++ resulting to S. levelsCa chelators or binders: citrate, mithramycin, penicillamine, Na cellulose phosphateAcute pancreatitis: inflammation of the pancreas causes breakdown of proteins & lipids to fatty acids which combine with Ca++ ions forming Ca++ soaps & excreted in the GITHyperphosphatemiaImmobility

d. Primary hypoparathyroidism or surgical hypoparathynoidism low PTH Ca++ absorption

CLINICAL MANIFESTATIONS (Ca++)

a. Cardiovascular manifestations heart rate myocardial contractilityDiminished peripheral pulses BPECG abnormalities: prolonged ST interval, prolonged QT interval

b. Neuromuscular ManifestationsAnxiety, irritability, psychosisParesthesias followed by numbnessIrritable skeletal muscles : twitches, cramps, tetany, seizures, tingling of fingertips, mouth (Ca, Mg)Hyperactive deep tendon reflexes - Ca level makes the nerve excitable because lack of Ca increases renal permeability to Na Seizures Ca++ irritability of the CNS & peripheral nerves

Mental changes = depression, impaired memory, confusion, delirium, hallucinationsPositive Trousseaus sign, Chovteks sign

c. GIT manifestations: increased motilityhyperactive bowel sounds, abdominal cramping, diarrhea.

d. Easy bruising & petechiae and excessive bleeding when cut - Ca++ is needed for blood clotting

PATHOPHYSIOLOGYCa is an excitable membrane stabilizer, regulating depolarization and the generation of action potentialsCa decreases Na movement across excitable membrane, decreasing the rate of depolarization.

Low serum Ca levels increase Na movement across excitable membranes, allowing depolarization to occur more easily and at inappropriate times

DIAGNOSTIC TESTS ( Ca++)S. Ca++ level < 8.5 mg / dlHyperphosphatemia Mg = Ca regulated w/MgAlbumin - Ca is bound to itProlonged PT & PTT = Ca for blood clottingXRAY= OsteoporosisSulkowitch test = confirms Ca++ in urineECG = prolonged QT interval due to prolongation of ST segment

MEDICAL MANAGEMENT ( Ca++)

* Acute symptomatic hypocalcemia is life threatening & requires treatment with IV Ca++1. Parenteral Ca salts: Ca gluconate, CaCl & Ca gluceptateCardiac arrest too rapid admininistrationDangerous to patients o n digitalis-may cause toxicityCa w/ D5W & given slowly via infusion pumpCa can cause postural hypotension keep on bed & monitor V/S

2. Vitamin D therapy, PTH supplement = to Ca++ absorption in the intestine3. Aluminum & Ca++ containing antacids to elevated phosphorous levels before treating hypocalcemia for patient with CRF4. dietary intake of Ca++ to 1,000 1,500 mg / day

NURSING MANAGEMENT Nursing DiagnosisRisk for injury r/t bone density loss, mental changesReadiness for Enhanced Nutrition r/t the need to increase Ca intake

InterventionsIdentify patients at risk for hypocalcemia

- thyroid diseases, thyroidectomy. GI problemsMonitor trends in serum Ca levelsMonitor fluid statusAdminister medicationsMonitor for side effects of IV administration of Ca

- soft tissue damage w/ extravasation

Cont. Nursing InterventionsEncourage intake of Ca-rich foods.Provide adequate intake of vit D.Monitor neuromuscular, CV manifestations of hypocalcemia.Monitor for overcorrection of hypocalcemia. Institute cardiac monitoring & secure precautions if the patients Ca level is dangerously lowProvide nutritional counseling if Ca is due to dietary deficiency Instruct the patient that exercise enhances Ca mobilization from bone & will replenish plasma Ca level

HYPERCALCEMIA (> 10.5 mg / dl)

Severe hypercalcemia = mortality rate of 50% if not treated promptly

ETIOLOGY:a. Ca AbsorptionExcessive oral intake of Ca, Vit D

b. Ca Excretion: RF, Thiazide diureticsc. bone resorption- Hyperparathyroidism- Malignancy- Hyperthyroidism : accelerates calcitonin secretion- Immobility : alters bone metabolism- Glucocorticoidsd. Hemoconcentration: dehydration, lithium, adrenal insufficiencyMalignant tumor of parathyroid gland & hyperparathyroidism

E. Malignant tumor of parathyroid gland & hyperparathyroidism HYPERPARATHYROIDISM PTH SECRETION release of Ca from bone & Renal Absorption of Ca Ca++ & Phosphorous >70 Calcification of soft Tissues

CLINICAL MANIFESTATIONS ( Ca++)Reduced neuromuscular excitability because it suppresses activity at the myoneural junctionMuscle weakness Incoordination Anorexia, nausea, vomiting Hypoactive bowel sounds, abdominal distention Constipation ( tone in smooth and striated muscle).Abdominal pain = peptic ulcer like symptoms; Ca secretion of acid & pepsin by the stomachB. Neurologic manifestations = Ca++ affects conduction across nerve cellsConfusion Personality changes Altered LOC Coma

Other complications DehydrationUrinary calculi = Ca precipitates in the kidneyPathologic fractures Soft-tissue calcification = when Ca level rise & Ca++ binds with phosphorousExcessive urination = d/t disturbed renal tubular function produced by hypercalcemiaExcessive thirst = 2 polyuria Constipation - motility of the intestinesCardiac standstill = Ca++ above 18mg/dl (4.5mmol/LS)

LABORATORY & DIADNOSTIC TEST: ( Ca++) S. Ca levels > 10.5 mg / dlX-ray- bone changes & bone density & urinary calculiECG dysrhythmias & shortening of QST+ interval

& ST segment Double-antibody PTH test

- differentiates primary hyperparathyroidism & malignancy as cause of Ca++- PTH levels are in primary & secondary hyperparathyroidism & suppressed in malignancySulkowitch urine test

- analyzes the amount of Ca in urine - dense precipitation is observed due hypercalcemia

MEDICAL and Nursing MANAGEMENT ( Ca++)Goal: the S Ca++ level reversing the process of hypercalcemia treating the underlying cause is essential Drugs ,Dialysis, OFI, Diet1. Institute measures to prevent hypercalcemiaidentify high-risk pts & instruct them to avoid Ca rich foods Ambulate patient as early as possible

2. Initiate measures to eliminate excess CaAdminister IV NSS

- dilutes Ca++ temporarily- excretion of Ca++ by the kidneys by inhibiting tubular reabsorption of Ca++ - Fluids with Na++ favor Ca++ excretionAdminister loop diuretics = facilitate Ca++ removal

3. Administer Calcitonin as ordered to S. Ca level Calcitonin from salmon - skin test necessary reduces bone resorption, Ca & phosphorous deposit in the bone & urinary excretion of Ca++ & phosphorousAdminister IM not SC = patients with Ca have poor perfusion to SC tissue

4. Administer IV phosphate as ordered - can cause reciprocal drop in S. Ca- used with extreme caution with Ca because it can cause severe calcification in various tissues, hypotension, tetany & ARF

CONT. 5. OFI containing Na++ (if not contraindicated) 3 4 quarts daily6. intake of fiber-rich foods to inhibit absorption of Ca in the intestine & facilitate, prevent constipation7. Monitor for neuromuscular manifestations of hypercalcemia. 8. Assess for sign of digitalis toxicity Ca potentiates effects of digitalis ECG changes PVCs, Paroxysmal atrial tachycardia & heart block can occur Monitor CR & rhythm

9. Monitor V / S & electrolyte status10. Encourage mobilization to prevent bone resorption.

MAGNESIUM

(1.5 2.5 mEq/L or 1.8 3.0 mg/dl)most abundant ICF cation next to K+found in heart, bones, nerves, muscle tissue Only 1% of TBW is ionizedDietary Mg is absorbed in the jejunum & ileum Elimination: kidney; GITRegulated by parathyroid & steroid hormonesSources = vegetables, nuts, fish, whole grain, peas and beans

FunctionsExerts effects on the neuromuscular junction, affecting neuromuscular irritability.Skeletal & muscle contractionMetabolism of CHO & proteinsAdenosine triphosphate (ATP) formationB-complex vitamin activationFacilitates Na & K transport across cell membraneInfluences ICF Ca levelsthrough its effect on parathyroid hormone secretionDNA synthesisContributes to vasodilation: BP; Cardiac output Facilitate Na+ & K+ transport across a cell membrane Ca++ levels should be evaluated with albumin levels; S albumin levels decrease total Mg

HYPOMAGNESEMIA

2. Inadequate intake or absorptionMalnutrition or starvationMalabsorption syndrome: IBD, Pancreatitits, Celiac, Critically ill: no enzymes for absorptionExcessive dietary intake of Ca or vit D

3. Alcohol: GI losses & malabsorption4. Fluid & electrolyte shiftsAdm. of TPN that are Mg deficientCaHigh dose steroid useDKA- 2 to renal excretion during osmotic diuresis & shifting of Mg into the cells with insulin therapySepsisPancreatitis

PIHRefeeding after starvation

5. Renal disease: Mg depending on the disease : Diuretic phase6. Medications: Gentamycin, chemo (esp cisplatin), steroids, Loop, osmotic and thiazide diuretics Aminoglycosides; cyclosporine, cisplatin, diuretics, digitalis, amphoterecin7. Rapid administration of citrated blood

8. Hypernatremia = Cushings syndrome or hyperaldosteronism (inhibits Mg+ reabsorption)9. Sepsis10. Burns11. Antacid overuse = inhibit uptake of Mg+ from intestinal villi

CLINICAL MANIFESTATIONS (Mg)Warm, flushed appearanceDiaphoresisNausea & vomiting/diarrheaDrowsiness, lethargyWeakness and flaccid musclesHeart block and other dysrhythmiasLoss of deep tendon reflexesDepressed respiratory function: slow & shallowHypotensionBradycardia Generalized tonic-clonic or focal seizuresAthetoid movements Coma

B. CARDIOVASCULAR CHANGES (Mg) HypertensionECG changes: prolonged ORS complex, ST segmentCardiac dyrhythmias: PVCs, SVT, VF susceptibility to digitalis toxicity associated with Na+ levelsbecause patients receiving digoxin are also likely to be receiving diuretic therapy, predisposing them to renal loss of Mg.

C. MOOD ALTERATION 1. apathy 2. depression 3. apprehension4. extreme agitation5. ataxia 6. dizziness 7. insomnia 8. confusion 9. delirium10. auditory or visual hallucination11. Frank psychosis may occur

DIAGNOSTIC FINDINGS (Mg) < 1.5 mEq / L or 0.75 mmol /L K+ Ca++, S albuminQRS, ST segment, flatT waves & prominent U wave reflect Mg+, Ca++, K+ deficiencies PVCs, PAT, Heart block can occurTorsades de Pointes (VTac) is associated with Mg levelUrinary Mg levels are measured

NURSING DIAGNOSES High risk for injuryDecreased cardiac outputAltered nutrition less than body requirementsPotential for fluid volume deficitImpaired memoryNURSING INTERVENTIONSIdentify high risk patients: anorexia, nausea & vomiting, diarrheaMonitor patients w/ hypokalemiaMonitor patients with hypokalemia for impending hypomagnesemiaMonitor patients receiving TPN without Mg added

Monitor a patient with Mg who is on digoxin for signs of digitalis toxicityMonitor cardiac statusInitiate seizure precaution Administer Mg replacement with extreme caution & slowly as ordered (infusion pump)Vasodilatory effect (c ardiac output, and O2 consumption in people w/ shock and sepsis)Rapid administration cardiac arrestAssess V/S frequently to detect cardiovascular & respiratory changes ( BP, RR, dysrhythmias)Monitor urine output before, during & after administration (at least 100ml/4hrs)Check deep tendon reflexes before administration (patellar or knee jerk)( - ) Patella reflexes dont give the drug

Ca gluconate must be ready to treat hypocalcemia tetany or hypermagnesiaAssess for stridor - Mg may cause airway obstructionInstruct the patient on diuretics about the danger of MgMonitor for dysphagia the ability to swallow must be tested with water before oral administration of foodsMonitor deep tendon reflexes. urine output

HYPERMAGNESEMIAPlasma level >2.5mEq or 3mg/dlFalse (+) hemolyzed blood

ETIOLOGY: ( Mg)1. Mg gainMg containing antacids: Maalox, Riopan, Mylanta, laxatives, milk of magnesia)Hyperalimentation administrationHemodialysis using hard water dialysate

2. Inadequate excretion = Renal failure 3. F&E shift: ACTH insufficiency (Hypoadrenalism) =Na+ retention w/ Mg+DKA glucose brings cation across cell membrane

CLINICAL MANIFSTATION ( Mg)Mildly elevated Mg level BP due to peripheral dilationNausea & vomiting epigastric pain Soft tissue calcificationFacial flushing & sensation of warmth

B. Higher Mg levels depresses the CNS & peripheral neuromuscular junction or blocked release of acetylcholine from myoneural junction w/c results in muscle cell activityLethargyDifficulty speaking (dysarthria) DrowsinessAbsent deep tendon reflexesMuscle weakness & paralysisDepressed respiratory center (Mg > 10 mEq/L or 5 mmol/L)Coma if Mg is not treated

DIAGNOSTIC FINDINGS ( Mg)2.5 mEq/L or 3.0 mg/dh (1.5 mmol/L) ECG prolonged PR interval, tall T waves, widened QRS complex, prolonged QT interval & AV blocks

POTENTIAL NURSING DIAGNOSESDecreased OutputIneffective breathing pattern

COLLABORATIVE MANAGEMENTPrevent Mg (early detection of high-risk patients)Provide appropriate patient education.

Cont: COLLABORATIVE MANAGEMENTAssess neuromuscular system for deficitsMonitor BP,RR, CR, dysrhthmiasAvoid administration of Mg to patient with RFCareful monitoring of seriously ill patients receiving Mg saltsPrompt D/C of oral & parenteral Mg salts Hemodialysis of Mg ++ free dialysateLoop diuretics and 0.45% NaCl (half-strength saline) solution = enhance Mg excretion Administer Ca gluconate to antagonize cardiac effects of Mg in the cardiac muscle & temporarily relieve s/sDietary restrictions : meat, nuts, legumes, fish, vegetables, whole-grain serials

PHOSPHOROUSAdults = 2.5 4.5 mg/dl or 0.8 1.5 mmol/L6 mg/dl (1.94 mmol/L) Infants & children, d/t rate of skeletal growth85 % bones & teeth, 14% - soft tissue, < 1 % in the ECFExcitability of nerves & muscles, Ca balance, cell energyCritical component of the phosphate buffer system to aid renal regulation of acids & basesNecessary for the creation of energy (ATP) Maintains cell membrane integrity by binding with lipids to create the phospholipids cell membrane layerCritical for CHO, fats & protein metabolism

PHOSPHOROUSEssential for the function of RBCs, MUSCLES & CNS Component of DNA & RNA (= important in cell division and transmission of hereditary traits)

REGULATIONFiltered by the glomerulus, reabsorbed in the proximal tubule along with Na+ When GFR , P reabsorption & vice versa When PTH is present, tubular reabsorption is inhibited, increasing P excretionCa helps to regulate P+, because P is found in proportions inversely reciprocal to Ca++

SOURCES: most foods but especially in beef, pork, dried peas and beans

HYPOPHOSPHATEMIA

c. Insufficient Phosphorous IntakeMalnutrition/Alcohol abuseStarvationUse of al hydroxide-based antacidsUse of magnesium-based antacids

d. Increased phosphorous ExcretionHyperparathyroidism-K+, Mg r/t urinary losses of PRenal failureMalignancyCushings syndrome =Glucocorticoid production resulting to K+(w/ PO4)Medications: loop diuretics

1. CNS SYMPTOMS OF ATP DEFICIENCY Confusion, Seizures/coma d/t anoxiaFatigue, Ataxia-loss of voluntary movements

2. CARDIOVASCULAR: Decreased contractility Cardiomyopathy (reversible)3. RESPIRATORY: Shallow Respirations d/t muscle fatigue4. Musculoskeletal Manifestations: Fatigue, deep bone pain, muscle weakness / numbness / paresthesia 5. HEMATOLOGIC SYMPTOMSBruising and bleeding from platelet dysfunctionHemolytic anemia

LABORATORY TESTS

COLLABORATIVE MANAGEMENTEnsure early detection by identifying high-risk patientsAssess for signs of Ca, which occurs in the presence of P dietary intake of P milk & milk products, organ meats, nuts, poultry & fish, whole grainsAdminister I.V. P slowly as ordered

EVALUATIONNormal P levelFree from injuryNormal breathing pattern

HYPERPHOSPHATEMIA> 4.5 mg/Dl

ETIO intestinal absorption of Ca d/t excessive vit D intake.Ingestion of excessive quantities of dairy productsP-containing medications (e. g. laxatives)Renal failure most common where hypocalcemia is present & dietary phosphorous is not excreted Cellular destruction = release of P to serum

Ca, chemotherapyTrauma, Rhabdomyolysis, BTHypoparathyroidism PTH levels Ca concentration POsteoporosis removal of P from bone and enters the serum.

CLINICAL MANIFESTATIONS (same w/ Ca)Tetany tingling sensations in the fingertips & around the mouth= P++ cause S.Ca++Muscle spasm, pain, weaknessAnorexia, nausea, vomitingHypereflexiaChevosteks/Trousseaus sign (+)Soft tissue calcification = joinst, BV, cornea

DIAGNOSTIC FINDINGS P > 4.5 mg/dL (> 1.5 mmol /L) adultsX-ray = skeletal changes with abnormal bone development PTH levels in hypoparathyroidismBUN & Crea: assess renal function

POTENTIAL NURSING DIAGNOSESPainDecreased cardiac outputImpaired mobilityHigh risk for injury

COLLABORATIVE MANAGEMENTIdentify high-risk patients (those with Ca++)Administer phosphate-binding medications (al. hydroxide)Administer Ca supplements along with P- binders for a patient with renal related hyperphosphatemiaAdminister diuretics, vit DPrepare for hemodialysis: remove excessive PInstruct the patient to avoid foods & medications containing PDietary restriction, OFI